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JOHNSON’S
PRACTICAL
ELECTROMYOGRAPHY
FOURTH EDITION

William S. Pease, MD
Ernest W. Johnson Professor and Chairperson
Department of Physical Medicine and Rehabilitation
The Ohio State University
Columbus, Ohio

Henry L. Lew, MD, PhD

Clinical Associate Professor
Division of Physical Medicine and Rehabilitation
Stanford University School of Medicine
Stanford, California

Ernest W. Johnson, MD
Professor Emeritus
Department of Physical Medicine and Rehabilitation
The Ohio State University
Columbus, Ohio
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Acquisitions Editor: Robert Hurley

Developmental Editor: Louise Bierig
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Copyright © 2007 by Lippincott Williams & Wilkins, a WOLTERS KLUWER business

Third edition ©1997 by Williams & Wilkins

First edition © 1980 by Williams & Wilkins

530 Walnut Street

Philadelphia, Pennsylvania 19106 USA

All rights reserved. This book is protected by copyright. No part of this book may be reproduced in any form
or by any means, including photocopying, or utilizing by any information storage and retrieval system with-
out written permission from the copyright owner.

The publisher is not responsible (as a matter of product liability, negligence or otherwise) for an injury resulting
from any material contained herein. This publication contains information relating to general principles of med-
ical care which should not be constructed as specific instruction for individual patients. Manufacturer’s product
information should be reviewed for current information, including contraindications, dosages, and precautions.

Printed in the United States of America

Library of Congress Cataloging-in-Publication Data

Johnson’s practical electromyography.—4th ed. / [edited by] William
S. Pease, Henry L. Lew, Ernest W. Johnson.
p. ; cm.
Rev. ed. of: Practical electromyography. 3rd ed. c1997.
Includes bibliographical references and index.
ISBN-13: 978-0-7817-5285-5
ISBN-10: 0-7817-5285-X
1. Electromyography. 2. Neuromuscular diseases—Diagnosis.
I. Pease, William S. II. Lew, Henry L. III. Johnson, Ernest W.,
1924– . IV. Practical electromyography. V. Title: Practical
electromyography.
[DNLM: 1. Electromyography. 2. Electrodiagnosis.WE 500
J66 2007]
RC77.5.P7 2007
616.7
407547—dc22
2006023084

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vertently overlooked any, they will be pleased to make the necessary arrangements at the first opportunity.

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10 9 8 7 6 5 4 3 2 1
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To our patients who we are honored to serve and

who stimulate us to find new answers.

And to our students, especially the 231 graduates of

the OSU PM&R residency who have all contributed to
the practice and understanding of EMG.

And, to our families who make it all worthwhile.

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TABLE OF CONTENTS

Preface vii
Contributors ix
Acknowledgments xi

I Introduction to Electromyography
(The Essentials of EMG) 1
1. Anatomy for the Electromyographer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
DENISE L. DAVIS AND ERNEST W. JOHNSON

2. The Essentials of the Needle EMG Exam . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

VIVEK KADYAN, ERNEST W. JOHNSON, AND DENISE L. DAVIS

3. Basic Nerve Conduction Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29

ROBERT J. WEBER AND MARGARET TURK

II Technical Aspects of EMG 65

4. Electrophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
JUN KIMURA

5. Instrumentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87
SANJEEV D. NANDEDKAR

6. Advanced Needle EMG Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105

ERIK STÅLBERG

7. Quality Improvement and Reporting in Electrodiagnostic Medicine . . . . . . . 131

WILLIAM S. PEASE

8. Pictorial Guide to Muscles and Surface Anatomy . . . . . . . . . . . . . . . . . . . . . . . 145

HENRY L. LEW AND SU-JU TSAI

9. Pictorial Guide to Nerve Conduction Techniques . . . . . . . . . . . . . . . . . . . . . . 213

HENRY L. LEW AND SU-JU TSAI

III Solving the Problems in Clinical EMG 257

10. Entrapment Neuropathies and Other Focal Neuropathies
(Including Carpal Tunnel Syndrome) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 259
LAWRENCE R. ROBINSON

v
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vi TABLE OF CONTENTS

11. Evaluation of the Patient with Suspected Peripheral Neuropathy . . . . . . . . . 297

JAMES W. ALBERS

12. Electrodiagnostic Approach to Patients with Suspected Radiculopathy . . . . 333

TIMOTHY R. DILLINGHAM

13. Evaluation of the Patient with Suspected Myopathy . . . . . . . . . . . . . . . . . . . . . 353

ALBERT C. CLAIRMONT, BAKRI ELSHEIKH, AND YOUSEF M. MOHAMMAD

14. Neuromuscular Complications of Critical Illness: Evaluation of the

Patient with a Suspected Critical Illness Neuromuscular Disorder . . . . . . . . 363
DANIEL M.CLINCHOT

15. Evaluation of the Patient with Suspected Neuromuscular

Junction Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 377
WILLIAM J. LITCHY

16. Pediatric Considerations in Electromyography . . . . . . . . . . . . . . . . . . . . . . . . . 395

ROSALIND J. BATLEY

IV Appendices 417
Glossary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 419
Abbreviations Commonly Used in Electromyography . . . . . . . . . . . . . . . . . . . 427
The Practical Exam in Electromyography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 429
ERNEST W. JOHNSON AND WILLIAM S. PEASE

Index 439
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PREFACE
In the years since the release of the third edition of
Johnson’s Practical Electromyography, the science of
electrodiagnostic medicine has advanced greatly.
As our understanding leads us to use different,
new, or redefined words it becomes necessary to
replace the old edition. New organizations and
Board certification exams, and new names for old
organizations demonstrate the vitality of this spe-
cial area of medicine. More than just a set of tests,
electromyography in practice is the specialized use
of these tools for the evaluation and treatment of
persons with nerve and muscle pathology. The
electrodiagnostic medicine consultant plays valu-
able roles in the diagnosis and the treatment of
disorders of function of the nervous system. The
physician is then able to translate this knowledge
into improving the motion and function of the
body.
A particularly valuable addition to this edi-
tion began with a chance encounter on the beach
at Hilton Head during a meeting of the Associa-
tion of Academic Physiatrists. Henry Lew began
discussing a special process that he was using to
create digital images to improve learning of the
basic techniques of nerve conduction based upon
surface anatomy. The collaborative process with
Bill and Ernie was accomplished by reviewing
hard copies in person, and making revisions via
email exchanges. We are proud to now share the
results with you.
We are pleased that the new edition recog-
nizes Ernie Johnson for his invaluable contribu-
tions to the field of electromyography. His
continuing observations and insights are seen in
his chapters in the text, and his always-challeng-
ing test in the appendix. You may also challenge
yourself online and earn CME credit for your ef-
forts. We are pleased to include recorded EMG
video clips to further stimulate your learning; re-
member to have the audio on with the videos as
the sounds of many EMG signals is unique and
distinctive.
The book includes contributions from an in-
ternational group known for their intelligence,
teaching ability, and commitment to this specialty.
We are grateful for their participation in this ef-
fort, and more so for their continuing friendships.
—William S. Pease, Henry L. Lew,
and Ernest W. Johnson
vii
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CONTRIBUTORS

James W. Albers, MD, PhD Timothy R. Dillingham, MD, MS

Professor of Neurology
University of Michigan Medical School
Director, Electromyography Laboratory
University of Michigan Health System
Ann Arbor, Michigan
Professor and Chairman
Department of Physical Medicine
and Rehabilitation
The Medical College of Wisconsin
Milwaukee, Wisconsin

Rosalind J. Batley, MD Bakri H. Elsheikh, MBBS, MRCP (UK)

Associate Professor Assistant Professor
Departments of Physical Medicine Department of Neurology
and Rehabilitation, and Pediatrics The Ohio State University
The Ohio State University Columbus, Ohio
Columbus Children’s Hospital
Columbus, Ohio Ernest W. Johnson, MD
Professor Emeritus
Albert C. Clairmont, MD Department of Physical Medicine
Associate Professor and Rehabilitation
Department of Physical Medicine and The Ohio State University
Rehabilitation Columbus, Ohio
The Ohio State University
Columbus, Ohio Vivek Kadyan, MD
Boise, Idaho
Daniel M. Clinchot, MD
Associate Dean for Medical Education Jun Kimura, MD
and Outreach Professor of Neurology
College of Medicine University of Iowa
Associate Professor and Residency Program Iowa City, Iowa
Director
Department of Physical Medicine Henry L. Lew, MD, PhD
and Rehabilitation Clinical Associate Professor
The Ohio State University Stanford University School of Medicine
Columbus, Ohio Stanford, California
Physical Medicine and Rehabilitation Service
Denise L. Davis, MD VA Palo Alto Health Care System
Clinical Assistant Professor Palo Alto, California
Physical Medicine and Rehabilitation
College of Medicine William J. Litchy, MD
The Ohio State University Consultant in Neurology
Columbus, Ohio Department of Neurology
Mayo Clinic
Rochester, Minnesota

ix
90749_FM(i-xii).ps 8/11/06 8:34 AM
x CONTRIBUTORS
Yousef M. Mohammad, MD, MSc
Assistant Professor
Department of Neurology
Ohio State University
Columbus, Ohio
Sanjeev D. Nandedkar, PhD
Clinical Applications Manager
Viasys Health Care
Madison, Wisconsin
William S. Pease, MD
Ernest W. Johnson Professor and Chairperson
Department of Physical Medicine and
Rehabilitation
Medical Director
Dodd Hall Rehabilitation Hospital
The Ohio State University
Columbus, Ohio
Lawrence R. Robinson, MD
Professor of Rehabilitation Medicine
Vice Dean of Clinical Affairs
School of Medicine
University of Washington
Seattle, Washington
Erik Stålberg, MD, PhD
Professor Emeritus
Department of Clinical Neurophysiology
Uppsala University Hospital
Uppsala, Sweden
Page x
Su-Ju Tsai, MD, MS
Assistant Professor
Department of Physical Medicine and
Rehabilitation
Chung Shan Medical University,
College of Medicine
Medical Director
Department of Physical Medicine and
Rehabilitation
Chung Shan Medical University Hospital
Taichung City, Taiwan
Margaret Turk, MD
Professor
Departments of Physical Medicine and
Rehabilitation, and Pediatrics
State University of New York
Upstate Medical University at Syracuse
Syracuse, New York
Robert J. Weber, MD
Professor and Chairman and Residency
Program Director
Department of Physical Medicine
and Rehabilitation
State University of New York
Upstate Medical University at Syracuse
Syracuse, New York
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ACKNOWLEDGMENTS

We wish to acknowledge the valuable contribution Drs. Eunha Lee, James Chen, Jerry Chiang, and
of Christina E. Taddeo, M.D. in providing insight Kristina Liu for their assistance. The office assis-
to us about the new, illustrated sections from her tance of Ruth Miller and Colleen Howells was also
perspective as a resident. The authors also thank appreciated, as always.

xi
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90749_ch01(1-21).ps 8/11/06 11:04 AM Page 1

Introduction to
I
Electromyography
(The Essential of EMG)
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CHAPTER 1
Anatomy for the
Electromyographer
Denise L. Davis and Ernest W. Johnson
INTRODUCTION
Have an anatomy text nearby! This textbook does
not replace it. Know where things are in the
anatomy text.
In our many years of testing the competence
of electromyographers in various settings, a ma-
jor deficiency has been anatomic knowledge of
even basic nerve and muscle locations. There are
over 400 skeletal muscles in the body for assess-
ment by electromyography (EMG). The elec-
tromyographer must know surface anatomy well
and furthermore should check with the anatomy
text frequently for reinforcement of anatomic
landmarks. Chapters 8 and 9 in this text include
photographs to reinforce your learning of surface
anatomy in order to improve your EMG
techniques.
Basic kinesiologic knowledge also is essential
to activate the muscle being investigated. Move-
ments are represented on the motor cortex and
produced by groups of muscles, not by individual
muscles. In a recumbent person, it is very difficult
to elicit a maximal contraction in a two-joint mus-
cle, but it is much easier to have that full effort on
a single-joint muscle. For example, study recruit-
ment in the soleus (ankle joint only) instead of the
gastrocnemius (knee and ankle) with plantarflex-
ion, and evaluate the vastus medialis (knee joint
only) rather than the rectus femoris (hip and knee)
during knee extension.
Tables 1-1 and 1-2 include simple and useful
guides for motor spinal nerve root motor innerva-
tion of the muscles of upper and lower limbs.
When exploring a large muscle for an in-
volved root problem, one should consider the
embryologic pattern to reduce sampling error.
This pattern is that as one moves from cephalad
to caudad, from proximal to distal, from anterior
to posterior, and from medial to lateral, then one
moves downward (caudal) in the levels of spinal
cord root innervation. Similarly, the pattern of
sensory innervation goes from medial to lateral,
anterior to posterior, and proximal to distal as
the roots descend along the spinal cord. The
amplitudes of the sensory and motor responses
in Table 1-3 can be used to evaluate axon
loss caused by proximal injury of their nerves or
roots (1).
More exhaustive lists are at the end of this
chapter for reference (Tables 1-4 to 1-6), but
Tables 1-1 through 1-3 should be memorized.
For suspected radiculopathy, it is always
more efficient and accurate to select a small mus-
cle for better EMG sampling. An example in-
cludes using the tensor fascia lata for L5 instead of
the gluteus medius; both have three root levels,
L4, L5, and S1. Not only can the muscle be sam-
pled more efficiently at rest, but muscle activation
is usually easier to carry out in a small muscle (see
Fig. 8-73). The relatively anterior position of the
tensor fascia lata also allows it to be explored in the
3
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4 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY

T A B L E 1 - 1 Upper Limb Motor T A B L E 1 - 2 Lower Limb Motor

Innervation Innervation

1. No C7 below wrist 1. L2–4 quadriceps and adductors

2. C6 below elbow
Volar: pronator teres
Dorsal: brachioradials
3. C7 above elbow: triceps, anconeus
4. C7 from trunk, acting on upper limb:
latissimus dorsi, serratus anterior,
pectoralis major
5. C8 thenar: abductor pollicis brevis,
adductor pollicis
6. T1 hypothenar: abductor digiti minimi,
opponens digiti minimi
2. L4 below knee: only anterior tibial
3. L5 below ankle: only extensor digito-
rum brevis
4. S1–2 lateral plantar nerve: abductor
digiti quinti
5. S1–2 medial plantar nerve: abductor
hallucis, flexor digitorum brevis
(Figs. 1-1, 1-2)

Figure 1-1 ● The tarsal tunnel and the course of the tibial nerve.
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CHAPTER 1 • ANATOMY FOR THE ELECTROMYOGRAPHER 5

Figure 1-2 ● Sciatic and tibial nerve anatomy showing branches and common sites of focal
neuropathy.
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6 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY

T A B L E 1 - 3 Sensory and Motor Nerve Conduction Study Innervations

Amplitudes of these responses can be used to evaluate axon loss due to proximal injury of their
nerves or roots (1). Muscles are noted for motor nerve studies (Figs. 1-3–1-5).
Nerve and Recording Nerve and Recording
Location Root(s) Location Root(s)

Lateral antebrachial C5, 6 Medial antebrachial C8

cutaneous nerve (Fig. 1-5) (Fig. 1-6) cutaneous nerve (Fig. 1-8)
Median to digit 1 (thumb) C6 Posterior antebrachial C7, 8
(Fig. 1-7) cutaneous nerve (Fig. 1-8)
Median to digit 3 (long) C7 Lateral femoral cutaneous L2, 3
Ulnar to digit 5 (little) C8 nerve
Posterior interosseous nerve C7, 8 Saphenous nerve (Fig. 1-9) L3, 4
(extensor indicis) Sural nerve L5, S1, 2
Anterior interosseous nerve C7, 8
(pronator quadratus)

Figure 1-3 ● Brachial plexus with demonstration of cervical roots and spinal nerves to the
trunks and other components.
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CHAPTER 1 • ANATOMY FOR THE ELECTROMYOGRAPHER 7

Figure 1-4 ● Relationships between the spinal cord, the roots, and the ventral and dorsal
rami. Note that the dorsal root ganglion is at the intervertebral foramen.

Figure 1-5 ● The lumbar plexus with demonstration of its terminal branches to the
periphery. Posterior divisions are shaded. (Reprinted from Waxman SG. Clinical neuroanatomy. New
York: Lange Medical Books/McGraw-Hill, 2003, with permission.)
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8 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
Figure 1-6 ● The radial nerve and its
course through the spiral groove of the
humerus.
supine position, which is helpful when the patient
cannot easily be moved.
It is a common mistake to avoid needle
EMG exploration of the intrinsic muscles of the
feet because of the notion that positive waves and
fibrillation potentials will be invariably present
because of the trauma the feet are exposed to
based upon their anatomic location. This is in-
correct (2): these muscles are excellent sources of
EMG abnormalities in peripheral neuropathies,
but they are also difficult to study because of
their small size. It is easy to advance the EMG
needle electrode into the endplate and record
Figure 1-7 ● Median sensory nerve con-
duction study with recording from thumb
(digit 1). Damage to the axons from the C6
root level will reduce the amplitude of this re-
sponse if the lesion is at or peripheral to the dorsal
root ganglion, which is at the (C5-6) nerve root
foramen.
endplate potentials as positive waves, a phenom-
enon that can be confusing to the electromyogra-
pher who is unaware of this risk of a false-posi-
tive result.
SPECIAL AREAS OF CONCERN TO
THE ELECTROMYOGRAPHER
Cervical Paraspinal Muscles
These are properly explored much more caudally
than has been appreciated. For the muscles in-
nervated by the posterior primary ramus of C6,
the needle electrode must be inserted at the level
of the tip of and lateral to the spinous process of
the C7 cervical vertebra. C7 is at least 2 cm more
caudal and C8 is at the mid-scapular border. This
is because the superficial paracervical muscles
(semispinalis cervicis) attach to the midline spin-
ous processes and descend at a slight angle to in-
sert below on ribs and the lateral processes (Fig.
1-10). Remember that the needle must first pass
through the trapezius before reaching these
paraspinal muscles.
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CHAPTER 1 • ANATOMY FOR THE ELECTROMYOGRAPHER 9

Figure 1-8 ● Schematic representation of the cutaneous nerves of the forearm that also
depicts general locations of electrodes for sensory nerve conduction studies. This is presented
as a learning aid with Table 1-3. Further information on these techniques is in Chapter 9.
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10 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
Figure 1-9 ● Anatomy of the saphenous
nerve showing its origin from the distal
femoral nerve.
Nasalis
This is a useful muscle to record the compound
muscle action potential (CMAP) in facial palsy (cra-
nial nerve VII) and also for repetitive nerve stimu-
lation for neuromuscular junction diseases. Note
that the muscle immediately adjacent to the nasalis
is the levator labialis superioris. The levator labialis
superioris is a longer muscle with the endplate zone
lower near the side of the nares. Unintentionally
recording from the levator labialis superioris can
confuse an unaware electromyographer when the
CMAP is downgoing (positive) on contralateral
stimulation because electrodes are not positioned
precisely over the nasalis as intended (3).
Tongue
This large muscle is best accessed from under-
neath the chin (Fig. 1-11). With the mouth open
and the needle inserted into the tongue, it is diffi-
cult to get complete relaxation. Activation can be
increased for recruitment analysis with tongue
protrusion pressure against the teeth.
Opponens Pollicis
The opponens pollicis is almost completely cov-
ered by the abductor pollicis brevis. The opponens
is often labeled as “muscle explored or recorded”
when it is clear that the muscle that is actually ex-
amined is the more superficial one at the thenar
eminence, the abductor pollicis brevis.
Pronator Quadratus
The pronator quadratus is best accessed by insert-
ing the needle through the interosseus membrane
of the dorsal distal forearm between the ulna and
radius. This is also the preferred place where one
can record this muscle’s CMAP with surface
recording and median nerve stimulation at the el-
bow. Innervation is from roots C7 and C8 and the
anterior interosseus nerve (4).
Vocal Cords
The vagus nerve innervates the muscles of the
vocal cords by way of the superior laryngeal
nerve and the recurrent laryngeal nerve. The su-
perior laryngeal nerve is examined through nee-
dle EMG via the cricothyroid muscle, while the
thyroarytenoid muscle is used to evaluate the re-
current laryngeal nerve. Activation of these mus-
cles for recruitment is accomplished by asking
the patient to vocalize various sounds, including
a musical scale (5).
Diaphragm
This is of concern during needle EMG study be-
cause of the possibility of penetrating the lung,
resulting in a pneumothorax (Fig. 1-12). The di-
aphragm is accessible by intercostal space needle
insertion between the 8th and 9th or 9th and 10th
ribs bilaterally at the anterior axillary line with
relaxation during the expiratory phase of breath-
ing (see Fig. 1-12). Insert the needle electrode as
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CHAPTER 1 • ANATOMY FOR THE ELECTROMYOGRAPHER 11

Figure 1-10 ● Dissection view of semispinalis muscles in the paraspinal region of the neck
and thorax. (Reprinted from Netter FH. Atlas of human anatomy. Summit, NJ: Ciba-Geigy Corp., 1989,
plate 162, with permission.)

Figure 1-11 ● Needle electrode placement to evaluate the tongue.

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12 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY

Figure 1-12 ● Cutaway diagram of the diaphragm in the thorax showing the relationships
between the ribs, the pleura, and the diaphragm. (Reprinted from Netter FH. Atlas of human
anatomy. Summit, NJ: Ciba-Geigy Corp., 1989, plate 182, with permission.)
90749_ch01(1-21).ps 8/11/06 11:04 AM Page 13

CHAPTER 1 • ANATOMY FOR THE ELECTROMYOGRAPHER 13

Posterior Tibial Muscle

The posterior tibialis muscle lies in the center of
the leg (knee to ankle) and is best reached by a
long electrode through the anterior tibial muscle.
A medial insertion can also reach the muscle;
however, a common error is to use a needle elec-
trode that is too short for the medial approach to
the posterior tibialis, resulting in recording from
the flexor digitorum longus or flexor hallucis
longus rather than the posterior tibialis (8). For-
tunately these three muscles share innervation, so
that erroneous diagnosis is not caused by confu-
sion in needle placement.

Anal Sphincter
Figure 1-13 ● Electrode placements for
recording the CMAP from the diaphragm Analysis of the function of the external anal
when stimulating the phrenic nerve. sphincter requires the use of needle EMG. This
circular muscle can be accessed with the patient in
a side-lying position with knees and hips flexed.
Explore four quadrants (right and left of anterior
and posterior portions).
close as possible to the superior edge of the rib. The external anal sphincter is innervated by
Needle placement in the diaphragm can be a branch of the pudendal nerve (S2, S3, S4), the
confirmed during quiet inspiration when a few inferior rectal nerve. The inferior rectal nerve
motor units are activated and firing. An alter- provides motor innervation to the external anal
native method that some recommend is pene-
tration from the lumbar area with a long needle
electrode at the level of T12-L1 lateral to the
transverse process of the L1 vertebra (6). For
recording the diaphragm with surface elec-
trodes when stimulating the phrenic nerve, E1 is
placed over the xiphoid process and E2 over the
lower costal margin of the rib cage at the nipple
line (Fig. 1-13).

Serratus Anterior Muscle

This muscle is best reached with a needle elec-
trode near its origins on the ribs in the midaxillary
line (7). This location is also best position for the
E1 electrode to record the muscle’s response to
stimulation of the long thoracic nerve. The nerve
travels downward from the axilla in the midaxil- Figure 1-14 ● Photo of cadaver dissection
lary line (Fig. 1-14), and posterior placement of the demonstrating the serratus anterior on
stimulator will cause an artifactual response from the axillary view with the long thoracic
the latissimus dorsi. nerve.
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14 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
Figure 1-15 ● The Martin-Gruber anasto-
mosis, a communication in the forearm con-
necting the median nerve to the ulnar.
sphincter muscle and cutaneous innervation to
the skin around the anus. The needle electrode is
inserted approximately 2 cm from the edge of the
rectum, and the muscle displays constant tone.
This motor activity is increased by asking the pa-
tient to contract the sphincter or to tighten the
gluteus maximus muscles (9).
COMMON ANATOMIC ANOMALIES
Upper Limb
Martin-Gruber anastomosis is one of the more
common anomalies of innervation, occurring in
17% to 25% of the general population; one sixth
of these have it bilaterally (10). It involves an
anastomosis between the median and ulnar nerve
motor fibers in the forearm (Fig. 1-15). The C8
or T1 motor nerve fibers initially communicate
from the lower trunk to the middle or upper
trunk or, alternatively, the motor nerve fibers
from the ulnar motor nerve join the median mo-
tor nerve fibers in the arm. In the forearm these
C8 or T1 motor nerve fibers rejoin the ulnar
nerve. Martin-Gruber anastomosis rarely arises
from the anterior interosseous nerve, which also
has C7, C8, and T1 motor nerve fibers (11).
Martin-Gruber anastomosis is important
electrodiagnostically if the individual has carpal
tunnel syndrome (Fig. 1-16) for three reasons:
1. An initial positive deflection of the thenar
CMAP is obtained when stimulating the me-
dian nerve at the elbow.
2. A larger CMAP is obtained when stimulating
the median nerve at the elbow than at the wrist.
3. An artifactually fast median motor nerve con-
duction velocity is calculated for the forearm
segment.
4. However, if the individual is normal (i.e., no
carpal tunnel syndrome), the only finding with
Martin-Gruber anastomosis is a larger CMAP
following elbow stimulation of the median
nerve.
The Riche-Cannieu anastomosis is estimated
to be present to some degree in 77% of the general
population (12). It consists of an anatomic com-
munication in the palm between the recurrent
branch of the median nerve and the deep branch
of the ulnar nerve. This is the anastomosis that
makes possible the “all-ulnar hand.”
Lower Limb
An accessory peroneal nerve is present in up to
22% of the general population (13,14). This nor-
mal variation in nerve supply, which originates
from the superficial peroneal nerve, provides in-
nervation to the extensor digitorum brevis in ad-
dition to the contribution from the deep peroneal
nerve. It is electrodiagnostically important to rec-
ognize because its presence causes the unusual
finding of a smaller CMAP when stimulating at
the ankle than when stimulating at the fibular
head (Figs. 1-17 to 1-19).
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CHAPTER 1 • ANATOMY FOR THE ELECTROMYOGRAPHER 15

Figure 1-16 ● Median nerve anatomy showing branches relative to locations of commonly
occurring focal injuries and entrapments.

Figure 1-17 ● Sensory nerve skin distribution of the peroneal nerve.

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16 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY

Figure 1-18 ● Peroneal nerve anatomic diagram showing branches and common sites of
focal neuropathy. Some texts refer to the deep branch as the anterior tibial nerve and the superficial
branch as the fibular nerve.

T A B L E 1 - 4 Trunk and Lower Limb

Sensory Innervation
Zones and Landmarks

Clavicle T2
Nipple T4
Xiphoid T6
Costal margin T8
Umbilicus T10
Inguinal ligament T12
Dorsal medial foot L5
Dorsal lateral foot and sole S1
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CHAPTER 1 • ANATOMY FOR THE ELECTROMYOGRAPHER 17

Figure 1-19 ● Detail of the superficial branch of the peroneal nerve (or fibular nerve).
90749_ch01(1-21).ps 8/11/06 11:04 AM Page 18

T A B L E 1 - 5 Anatomy Chart 1: Nerve Root Level Innervations

Muscle Spinal Cord Level Muscle Spinal Cord Level

Upper Limb
Trapezius C2, C3, C4 Extensor carpi radialis C6, C7
Supraspinatus C5, C6 longus
Infraspinatus C5, C6 Extensor carpi radialis C7, C8
Diaphragm C3, C4, C5 brevis
Pectoralis major C5, C6 Extensor digitorum C7, C8
(clavicular) Extensor digitorum C7, C8
Pectoralis major (sternal) C7, C8, T1 minimi
Teres minor C5, C6 Extensor carpi ulnaris C7, C8
Biceps brachii C5, C6 Extensor indicis proprius C7, C8
Triceps brachii C7, C8 Extensor pollicis longus C7, C8
Coracobrachialis C5, C6 Abductor pollicis longus C7, C8
Anconeus C7, C8 Extensor pollicis brevis C7, C8
Brachioradialis C5, C6 Abductor pollicis brevis C8, T1
Pronator teres C6, C7 Opponens pollicis C8, T1
Flexor carpi radialis C7, C8 Flexor pollicis brevis
Flexor digitorum sublimis C7, C8 Superficial head C8, T1
Palmaris longus C7, C8 (median)
Flexor digitorum sublimis C8, T1 Deep head (ulnar) C8, T1
(digits IV, V) Lumbricals I, II (median) C8, T1
Flexor digitorum sublimis C7, C8 Lumbricals III, IV (ulnar) C8, T1
(digit II, III) Opponens digiti minimi C8, T1
Flexor digitorum C7, C8 Abductor digiti minimi C8, T1
profundus (digits IV, V) Palmar interossei C8, T1
Flexor digitorum C7, C8 Dorsal interossei C8, T1
profundus (digits II, III) Adductor pollicis C8, T1

Lower Limb
Rectus femoris L2, L3, L4 Extensor digitorum L5, S1
Vastus medialis L2, L3, L4 longus pedis
Adductor longus L2, L3, L4 Peroneus longus L5, S1
Gracilis L2, L3, L4 Peroneus brevis L5, S1
Sartorius L2, L3, L4 Gastrocnemius L5, S1, S2
Semimembranosus L4, L5 Soleus S1, S2
Semitendinosus L4, L5 Posterior tibialis L5, S1
Biceps femoris Flexor digitorum longus L5, S1
Long head L5, S1 Flexor hallucis longus L5, S1
Short head L5, S1 Extensor digitorum brevis L5, S1
Gluteus medius L4, L5, S1 Abductor hallucis S1, S2
Tensor fasciae latae L4, L5, S1 Abductor digiti V S1, S2
Gluteus maximus L5, S1, S2 First dorsal interosseus S1, S2
Anterior tibialis L4, L5 pedis
Extensor hallucis longus L5, S1
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CHAPTER 1 • ANATOMY FOR THE ELECTROMYOGRAPHER 19

T A B L E 1 - 6 Anatomy Chart 2: Peripheral Nerve Innervations

Muscle Peripheral Nerve† Muscle Peripheral Nerve

Upper Limb
Trapezius XI Pronator quadratus Anterior
Supraspinatus Suprascapular interosseus
Infraspinatus Suprascapular Extensor carpi radialis Radial
Diaphragm Phrenic longus
Pectoralis major Medial pectoral Extensor digitorum Radial
(clavicle) communis
Pectoralis major Lateral pectoral Extensor indicis Radial
(sternum) proprius
Teres minor Axillary Extensor digitorum Radial
Coracobrachialis Musculocutaneous digit V
Biceps brachii Musculocutaneous Extensor carpi ulnaris Radial
Triceps brachii Radial Extensor pollicis longus Radial
Anconeus Radial Abductor pollicis longus Radial
Brachioradialis Radial Extensor pollicis brevis Radial
Pronator teres Median Abductor pollicis brevis* Median
Flexor carpi radialis Median Opponens pollicis* Median
Flexor digitorum Median Flexor pollicis brevis
sublimis Superficial head* Median
Palmaris longus Median Deep head* Ulnar
Flexor digitorum Median Adductor pollicis* Ulnar
profundus (digits Lumbricals I and II* Median
II, III) Lumbricals III and IV* Ulnar
Flexor digitorum Ulnar Opponens digiti
profundus (digits minimi* Ulnar
IV, V) Abductor digiti minimi* Ulnar
Flexor pollicis longus Anterior Palmar interosseus* Ulnar
interosseus Dorsal interosseus* Ulnar

Lower Limb
Rectus femoris Femoral Biceps femoris
Vastus medialis Femoral Long head Sciatic
Adductor longus Obturator Short head Sciatic, lateral
Gracilis Obturator division
Sartorius Femoral Gluteus medius Sup. gluteal
Semimembranosus Sciatic Tensor fasciae latae Sup. gluteal
Semitendinosus Sciatic Gluteus maximus Inf. gluteal

(continued)
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20 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY

T A B L E 1 - 6 Anatomy Chart 2: Peripheral Nerve Innervations (continued)

Muscle Peripheral Nerve Muscle Peripheral Nerve

Anterior tibialis Peroneal (deep) Flexor digitorum longus Tibial

Extensor hallucis longus Peroneal (deep) Flexor hallucis longus Tibial
Extensor digitorum Peroneal (deep) Extensor digitorum Peroneal (deep)
longus brevis*
Peroneus longus Peroneal Abductor hallucis* Tibial-medial
(superficial) plantar
Peroneus brevis Peroneal Abductor digiti minimi Lateral plantar
(superficial) pedis*
Gastrocnemius Tibial First dorsal
Soleus Tibial interosseus pedis* Lateral plantar
Posterior tibialis Tibial

* Intrinsic muscles of the extremities.

† Peroneal nerve is also known as fibular nerve.

KEEP AN UP-TO-DATE ANATOMY TEXT
NEARBY AND USE IT!
REFERENCES
1. Johnson EW. Conservative management of cervi-
cal disc disease. In: Dunsker SB, ed. Cervical
spondylosis. New York: Raven Press, 1981:
145–153.
2. Dumitru D, Diaz CA, King JC. Prevalence of
denervation in paraspinal and foot intrinsic
musculature. Am J Phys Med Rehabil 2001;80:
482–490.
3. Ruys-Van Oeyen A, Gert Van Dijk J. Repetitive
nerve stimulation of the nasalis muscle: technique
and normal values. Muscle Nerve 2002;26:279–282.
4. Mysiw WJ, Colachis SC. Electrophysiologic
study of the anterior interosseous nerve. Am J
Phys Med Rehab 1988;67:50–54.
5. Blair RL, Berry H, Briant TD. Laryngeal elec-
tromyography: techniques, application, and a re-
view of personal experience. J Otolaryngol 1977;
6:496–504.
6. Bolton CF. Clinical neurophysiology of the res-
piratory system: AAEE Mini-monograph #40.
Muscle Nerve 1993;16:809–818.
7. DePalma M, Pease WS, Johnson EW, et al. A
novel technique for recording from the serratus
anterior. Arch Phys Med Rehabil 2005;86:17–20.
8. Goodgold J. Anatomical correlates of clinical
electromyography, 2nd ed. Baltimore, London:
Williams & Wilkins, 1984.
9. Bailey JA, Powers JJ, Waylonis GW. A clinical
evaluation of electromyography of the anal sphinc-
ter. Arch Phys Med Rehabil 1970;51: 403–408.
10. Rodriguez-Niedenfuhr M, Vazquez T, Fer-
reira A, et al. Intramuscular Martin-Gruber
anastomosis. Clin Anat 2002;15:129–138.
11. Guttmann L. Median-ulnar nerve communica-
tions and carpal tunnel syndrome. J Neurol
Neurosurg Psychiatry 1977;40:982–986.
12. Harness D, Sekeles E, Chaco J. The double
anastomotic innervation of thenar muscles. J
Anat 1974;117:239–331.
13. Gutmann L. Important anomalous innerva-
tions of the extremities: AAEM Mini-mono-
graph #2. Muscle Nerve 1993;16:339–347.
14. Gutmann L. Atypical deep peroneal neuropa-
thy in presence of accessory deep peroneal
nerve. J Neurol Neurosurg Psychiatry 1970;33:
453–456.
90749_ch02(21-28).ps 8/11/06 11:05 AM Page 21
CHAPTER 2
The Essentials of the Needle
EMG Exam
Vivek Kadyan, Ernest W. Johnson, and Denise L. Davis
WHY REQUEST AN EMG?
An electromyographic (EMG) examination is a
functional evaluation of the motor unit. It can
assess the location, severity, chronology, and prog-
nosis of injuries, diseases, or other compromises of
the motor unit. The motor unit is made up of the
anterior horn cell, its axon, and all of the muscle
fibers innervated. Some wish to characterize elec-
trodiagnosis as synonymous with EMG, and that is
historically and conventionally correct, if not cor-
rect technically. Most electromyographers in the
United States understand that when an EMG is
requested, the referring physician desires a com-
prehensive electrodiagnostic examination, which
is a specialty medical consultation that includes
EMG testing. This testing is performed either by
or under the personal supervision of the physician,
and is guided by the clinical information of the in-
terview and clinical examination. Another impor-
tant point is that the functional evaluation
provided by electrodiagnostic evaluation is com-
plementary to imaging’s structural evaluation, and
electrodiagnosis is essential to evaluate any trauma
or disease affecting the motor unit.
WHAT CONDITIONS SUGGEST THAT EMG
WOULD BE USEFUL IN DIAGNOSIS AND
MANAGEMENT?
If the patient complains of pain, weakness,
fatigue, or numbness (paresthesia) that results in a
differential diagnosis including problems affect-
ing the motor unit or sensory nerves, then an
EMG may be useful. The most frequent com-
plaint of patients presenting in a primary care
office is “pain.” Pain is commonly caused by:
• Radiculopathy
• Entrapped nerve
• Neuritis (generalized or localized)
• A variety of nonneurologic causes
Weakness can be seen as either localized or
generalized, and this clinical impression will
affect the choice of electrodiagnostic tests. Fatigue
is differentiated from weakness as the gradual loss
of strength during repeated or continuous use of
muscle(s).
Paresthesias (numbness) also can be either
localized or generalized to multiple limbs and is a
very common condition leading to EMG.
WHAT IS ELECTROMYOGRAPHY?
Electromyography literally means recording the
electrical activity of the muscle cell membrane.
With a needle electrode inserted in the muscle, the
motor unit potential (MUP) can be recorded. This
represents the summated electrical activity of
action potentials of all of the muscle fibers making
up that motor unit. In the normal situation, the mo-
tor unit (MU) is “all or none” in its expression as a
MUP. In certain circumstances the action potential
21
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22 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
of individual muscle cell membranes can be
recorded. This portion of the EMG is described in
more detail below in the section on Needle EMG.
In more recent usage, the word “electromyogra-
phy” encompasses all the techniques used in evalu-
ating the function of the peripheral nervous system,
including the lower motor neuron and its inner-
vated muscle fibers (the MU), and the associated
sensory nerve fibers. In conditions that affect the
muscle fibers primarily, this MUP will be smaller
and of shorter duration. If the anterior horn cell or
its axon is impaired, then the MUP will be absent.
Also, if the axon is damaged or the sheath (myelin)
is defective, then the resulting MUP will be delayed
in onset, unstable in appearance, or altered in shape
(i.e., increased duration or reduced amplitude).
Another alteration in the MUP will occur if
there is a disease or injury to the endplate area
(where the motor axon terminal synapses on the
muscle fiber). This contact of axon to muscle is
referred to as the neuromuscular junction, and
in certain conditions (e.g., myasthenia gravis,
Lambert-Eaton syndrome, or botulism) the nerve
impulse can be intermittently delayed or blocked
in reaching the muscle fiber, thus changing the
MUP’s characteristic stability.
WHAT IS NERVE CONDUCTION
VELOCITY?
When the motor nerve is maximally stimulated, all
of the MUs in that muscle respond by depolarizing,
and a surface electrode will record the electrical
activity as a compound muscle action potential
(CMAP), which is a fairly good measure of the
number of motor axons and their MUAPs
responding. Some electromyographers (mostly in
Europe) call this procedure “neurography.” While
they maintain this is more accurate, in motor con-
duction it is mostly dependent on the appearance
of the CMAP as well as the latency; thus, myogra-
phy is appropriate. We therefore prefer to use the
shortened but historically valid and generally
accepted term “electromyography” as a reasonable
compromise for all of these neurophysiologic stud-
ies. With the inclusion of late waves such as the F
wave, H reflex, A wave, blink reflex, and so-
matosensory evoked potentials (SEP) in some ex-
aminations, one must also consider using central
and peripheral action potentials in the description.
When a nerve is stimulated the resulting
action potentials can be recorded with surface
electrodes or with “near nerve” needle recording
either proximal or distal to the stimulation site.
The conduction velocity can be calculated by
dividing the distance by the latency time to onset
of the response. A semiquantitative measure of the
number of functioning axons is represented by the
amplitude of the nerve action potential. If a purely
sensory nerve, it is referred to as the sensory nerve
action potential (SNAP); if recorded over a mixed
nerve, it is referred to as the compound nerve
action potential (CNAP). For greater accuracy,
one should subtract 0.1 ms from the latency before
division—this is the “latency of activation,” tech-
nically the time between application of stimulus
and activation of the axon (i.e., velocity
distance
[in mm]/[latency  0.1 (in ms)]). This time does
not present a significant consideration in adults
except in very short distances. However, in new-
borns it could make a difference in small hands
with 1.5- to 2-ms latencies.
NEEDLE EMG
There are over 400 separate muscles in the body
that could be investigated with a needle electrode.
With knowledge of anatomy and the probable
causes of weakness or pain, one can plan the needle
Figure 2-1 ● A small, isolated fascicula-
tion potential is recorded in a patient with
amyotrophic lateral sclerosis. Total time
duration of the recording is 2 s (gain
100 V,
sweep
50 ms).
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CHAPTER 2 • THE ESSENTIALS OF THE NEEDLE EMG EXAM 23

Step I: Needle in Quiet Muscle (at Rest)

Note spontaneous electrical activity:

A. Fasciculation potentials: these are recognized

by their irregular and slow rate of spontaneous
firing (Figs. 2-1 and 2-2) and classified by their
shape: simple (usually diphasic or triphasic);
complex (either the usual polyphasic MUP or
repetitive discharge polyphasic); myokymic
discharges (groups of MUPs firing together)
(Fig. 2-3).
B. Fibrillation potential: this is spontaneous
discharge of a single muscle fiber. It could be
the result of denervation (but do not call it a
“denervation potential”); other reasons for an
unstable muscle cell membrane include
inflammation (e.g., myositis), spinal shock,
myotonia, local muscle trauma and ischemia,
and other causes (Fig. 2-4).

In some central nervous system conditions

Figure 2-2 ● Fasciculation potentials recorded
from the anterior tibial muscle in a person with
amyotrophic lateral sclerosis. In this case many
different potentials are recorded at a single needle loca-
tion (gain
50 V, sweep
10 ms).
where the upper motor neurons have lost their
influence on the muscle cell membrane (i.e.,
flaccid limb), the stability of the membrane can be
lessened, which results in spontaneous discharges,
including fibrillation potentials and positive
waves appearing. Examples include spinal shock
in spinal cord injuries, cerebral vascular accidents
with flaccid muscles, and so forth.

examination to minimize the number of muscles

explored and narrow the diagnostic probabilities.
There are five steps to this needle EMG exam to be
performed and analyzed as each muscle is explored
with the needle electrode.
Step II: Insertional Activity
Electrical activity resulting from moving the
needle electrode through muscle tissue is called
insertional activity. These potentials are also

Figure 2-3 ● Myokymic potentials recorded with a monopolar needle in a patient with
chronic radiation-induced brachial plexus injury. The slow rate of firing (5 Hz) would be unusual
for a MUP under voluntary control. The first and last potentials are associated with short bursts of complex
repetitive discharges (gain
200 V, sweep
100 ms).
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24 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY

referred to as injury potentials. This activity repre-

sents the disruption of the muscle cell membranes
as the exploring needle is moved about and mem-
brane action potentials result. This portion of the
examination is most at risk of misinterpretation.
The duration of the normal insertional activity is
related to the technique of needle movement used
by the physician performing the examination. The
appearance of the resulting burst of action poten-
tials can last from 40 ms to at least as long as 500 ms.
There are a number of pathologic conditions in
which insertional activity is increased:

1. Muscle cell membrane is hyperirritable from

Figure 2-4 ● Fibrillation potentials (F) and
positive sharp waves (PSW) in a photo of
storage oscilloscope (gain
50 V, sweep

10 ms; calibration is indicated by the
slanted row of dots).
inflammation (e.g., myositis).
2. Loss of control from motor axon compromise
resulting in muscle cell denervation
3. Both 1 and 2 can also result in complex repeti-
tive discharges (CRD); these occur by ephapses

Figure 2-5 ● This series of complex repetitive discharges (CRDs) was recorded from a boy
with Duchenne muscular dystrophy. The small amplitudes of the action potentials reflect the atrophy
of the muscle fibers (gain
50 V, sweep
5 ms).

Figure 2-6 ● Complex repetitive discharges (CRDs) recorded from a patient with persistent
weakness caused by neuropathy. The presence of CRD suggests that the neuromuscular process has
been present for a longer period of time or is chronic (gain
100 V, sweep
10 ms).
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CHAPTER 2 • THE ESSENTIALS OF THE NEEDLE EMG EXAM 25

among muscle fibers whose membranes are

extra-excitable (Figs. 2-5 and 2-6).
4. Electrolyte disturbance
5. Local muscle trauma or ischemia

The most common reason for increased

Figure 2-7 ● Endplate spikes and endplate
positive waves are recorded together inter-
mittently as the needle position is changed
slightly (gain
100 V, sweep
10 ms).
insertional activity is that the needle electrode is in
the endplate area of the muscle. This zone, also
known as the motor point, is the region where
muscle fibers are naturally most vulnerable to
irritation and the production of an action potential
(Figs. 2-7 and 2-8).

Figure 2-8 ● A continuous recording shown cut into two segments. Endplate spikes are shown in
the motor point of a healthy muscle, and as the needle is moved, the endplate spikes are shown to appear as positive
sharp wave (PSW) forms. This type of PSW is normal and can be found in any muscle. The endplate PSW is
differentiated from the PSW seen in pathology by its relatively sharply pointed negative (upward) phase, its higher
frequency rate of occurrence, and especially by its appearance with endplate spikes (gain
1 mV, sweep
10 ms).
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26 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY

Figure 2-9 ● Diagram of the origin of the polyphasic MUP occurring within the first 4
weeks after the onset of radiculopathy. The inflamed nerve tissue allows ephaptic activation of axon
membranes, resulting in synchronous MUP appearances.

To perform this portion of the EMG study,
move the needle electrode briskly through the
muscle tissue at different angles. Normally, there
will be an immediate burst of electrical activity
with needle movement. If there are a few positive
sharp waves after needle electrode movement
stops, this is abnormal and represents a mild insta-
bility of the muscle cell membrane, as is seen early
in neurogenic disease or injury (e.g., radiculopa-
thy). If there is no electrical discharge or activity,
then there is edema, fibrous tissue, or no viable
muscle tissue (e.g., infarcted muscle due to
compartment syndrome).
Step III: Minimal Contraction of the Muscle
With the patient just barely contracting the mus-
cle, one examines the MUP in detail and observes
the rate of firing, stability of amplitude, duration,
and shape. The shape will include the amplitude,
duration, and number of phases (MUP is polypha-
sic if more than four phases). The stability of the
MUAP (shape and amplitude) is critical also for
diagnosis. Amplitude instability implies immatu-
rity of a reinnervating MU.
A special type of polyphasic MUAP is the so-
called early polyphasic, which would be better

Figure 2-10 ● The recruitment interval (RI) is shown as the time period between sequential on-
sets of the MUPs just before the occurrence of a secondary MUP. The reciprocal of the recruitment
interval is the recruitment frequency (RF). In this example from healthy muscle, RI
90 ms and RF
11.1 Hz.
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CHAPTER 2 • THE ESSENTIALS OF THE NEEDLE EMG EXAM 27

characterized as “pseudo” because it is two or
more MUAPs that discharge synchronously but
not simultaneously, thus appearing as a polyphasic
MUAP (Fig. 2-9).
Recruitment of the secondary MU should
also be measured. If there are too few MUPs in the
recruitment pattern, then the first MU will fire
more rapidly before the second one is recruited. In
most normal muscles, the secondary MU will ap-
pear when the primary MU is firing repeatedly at
10 to 12 Hz. If, as in a myopathy, there are the nor-
mal number of MUs but each does not contribute
to a normal effort because many muscle fibers are
myopathic, the second MU will be recruited early,
when the first recruited MU is firing at 6 to 10 Hz.
In fact, an early sign of myopathy is the inability to
get a single MUP on the screen.
The recruitment frequency is the rate at which
the primary MU is firing when the secondary MU
appears (Fig. 2-10). This is a fairly good estimate of
the number of MUs available. Normal limb mus-
cles have a recruitment frequency of about 10 to 12
Hz, but in neuropathic conditions the recruitment
frequency is increased: that is, the first MU will be
at a higher rate when the secondary one is activated.
For this strength of effort, the primary MU must
fire faster because there are not enough MUs.
Step IV: Maximal Contraction
It is difficult, if not impossible, to get a maximal
contraction in a two-joint muscle in a recumbent
position, so whenever possible explore single-joint
muscles. For example, explore the vastus medialis
rather than the rectus femoris. Ensure a full effort
by noting the firing rate and listen to the audio
from the speaker, which will be helpful in esti-
mating the effort and number of MUs recruited as
you gain experience in listening.
The screen is filled horizontally and verti-
cally with a normal maximal contraction; the
sound is similar to static on the radio. The screen
is filled horizontally but not vertically in myopa-
thy; the sound will take on a higher pitch and a
hissing quality. The screen is filled vertically but
not horizontally in neuropathy, with a thudding
quality to the sound as individual, large MUPs
stand out from other noise (Fig. 2-11).

Figure 2-11 ● Reduced number of MUPs in the recruitment pattern. In this case of neuro-
pathic disease, polio of remote onset, a single MUP is firing at 16.7 Hz. The amplitude varies, suggesting some
neuromuscular junction failure that is seen commonly in situations of reinnervation. This type of recruitment
is often described as discrete for reporting purposes. Gain
1 mV, sweep
100 ms (top) and 20 ms (lower).
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28 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
Step V: Distribution of Abnormalities
In the diagnosis of a generalized condition, three
areas of the body should be tested and seen to be
abnormal; this counts the head as an area of the
body or “limb.” Needle EMG sampling should be
performed in at least three areas in each muscle
and eight to ten sites (insertion angles and depths)
in each area.
SUMMARY
An electrodiagnostic study can be useful in any
suspected peripheral nerve injury, radiculopathy,
peripheral neuropathy, localized entrapment, or
disease of the MU. Chronology is important in
assessing nerve injury. Wallerian degeneration oc-
curs within 7 to 10 days, and the electrodiagnostic
examination findings will vary as the axon degen-
eration occurs and results in deterioration of the
neuromuscular junction. Generally, it takes 18 to
21 days to develop all of the EMG signs of dener-
vation. However, the nerve will lose its excitabil-
ity in 7 to 10 days. Thus, motor nerve stimulation
studies can give prognostic information after 7
days. If the axon is going to die (Wallerian degen-
eration), it will lose excitability after 5 to 7 days, a
circumstance giving the electromyographer a way
to determine the prognosis by the use of the meas-
urement of the amplitude of the CMAP. Stimula-
tion studies can also prove continuity of injured
nerves by applying a stimulus proximal to the
injury during the first few days after suspected
injury and demonstrating a partial response.
Listing of Motor Unit Conditions
The MU comprises the anterior horn cell, axon
(passing through rootlets and spinal nerve) and its
terminal branches, neuromuscular junctions, and
all of the muscle fibers it innervates. Diseases,
injuries and other conditions can compromise any
or all of these components:
Anterior horn cell (AHC) diseases
Amyotrophic lateral sclerosis
Poliomyelitis, anterior (paralytic)
Shingles (sometimes affect the AHC)
Infantile progressive muscular atrophy
Nerve root injury
Herniated nucleus pulposus (with or without
radiculopathy)
Most herniated discs will compromise the
nerve roots proximal to the dorsal ganglion
within the spinal canal, so the injury will not
alter the SNAP amplitude. An exception is the
situation of the cervical root when it is com-
promised by foraminal encroachment com-
pressing the nerve root at or distal to the dorsal
ganglion; this decreases the SNAP amplitude.
Dural sheath entrapment
This can result in symptoms and electrodiag-
nostic findings in the posterior primary rami
distribution only. Can be seen in diabetic pe-
ripheral neuropathy as multiple lumbar
radiculopathy and often is the early compro-
mise in Guillain-Barré syndrome.
Peripheral nerve (axons)
Various peripheral neuropathies affect the
axons. If the myelin sheath is affected mostly,
conduction will be slow or blocked. If axons are
primarily involved, muscle fibers will be dener-
vated, and the electrodiagnostic examination
will show fibrillation potentials and positive
waves, and nerve conduction velocity testing
will show reduced amplitude of the CMAP.
Neuromuscular junction
Myasthenia gravis
Myasthenic syndrome (Lambert-Eaton
syndrome)
Botulism
Immature neuromuscular junctions during
reinnervation
Muscular diseases
Muscular dystrophy
Myotonic dystrophy (Steinert disease)
Polymyositis
Steroid myopathy and type II atrophy
The ABCs of EMG are:
1. Assessment: Diagnosis and prognosis
2. Baseline: Follow the course (getting better or
worse?)
3. Complementary: The EMG examination is
functional and thus synergistic to all other clin-
ical, imaging, and laboratory evaluations.
90749_ch03(29-64).ps 8/10/06 3:58 PM Page 29
CHAPTER 3
Basic Nerve Conduction
Techniques
Robert J. Weber and Margaret Turk
INTRODUCTION
Nerve conduction studies (NCS) are the back-
bone of the electrodiagnostic evaluation. NCS are
the most objective of the routine measures used
in electrodiagnosis, and, not coincidentally, they
produce the bulk of electrodiagnostic clinical
fees. The accessibility of many peripheral nerves
makes nerve conduction useful for survey ap-
proaches to peripheral nerve involvement in gen-
eralized diseases, for defining the nature of
injury, and for the prognosis in focal peripheral
nerve injuries. NCS are almost embarrassingly
simple in concept: to determine the nerve con-
duction velocity (NCV) between two points
along the nerve, record the amplitude of the re-
sponse, and compare these values to the values of
a normal population. But for the challenge of
proper recording and interpretation, it would be
duck soup! It’s worth noting that pioneer elec-
trodiagnostic investigators would easily recog-
nize current studies despite a half-century of
rapid advances in medical technology. While
much is similar, our understanding is far deeper
and new challenges are always at hand. This
chapter reviews the clinical challenges and
physiologic principals of adult and pediatric
NCVs. Understanding nerve structure and func-
tion at the molecular level is essential to incorpo-
rating the growing knowledge base of genetic
and molecular-level pathology into daily electro-
diagnostic practice.
AXOLEMMA
Electrodiagnosis is the applied physiology of the
peripheral nerve and muscle systems. Only neu-
rons, muscle, and Schwann cells, plus several asso-
ciated structures, directly participate in peripheral
nerve conduction. These structures exhibit only a
limited repertoire of electrodiagnostically de-
tectable responses to injury. As if to emphasize the
simplicity of the NCS, all of the signals used in
clinical NCS are generated by only one structure,
the cell membrane. Beneath this veneer of sim-
plicity lies a billion years of evolutionary adapta-
tion of the cellular structures that generate nerve
signals. If our evolution began in a chemical soup
of increasingly complex proteins and interde-
pendent chemical cycles, then a necessary step to
life is the packaging of this soup within a vessel
that can carry it into less supportive environments.
The cell membrane provides that function, and
the self-assembly characteristic of its phospho-
lipids is likely to have played a key evolutionary
role in creating the living cell. While enclosure can
create an autonomous cell, it also creates a need for
the means to maintain a stable internal environ-
ment.
The cell membrane is composed of a 5-nm-
thick, ordered, bilayer sheet of phospholipid
molecules. Phospholipids are clothespin-shaped
molecules with a charged, hydrophilic phospho-
rus-based head and two uncharged, hydrophobic,
straight-chain hydrocarbon legs. If suspended in
29
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30 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
water, these amphipathic molecules naturally
form into capsule-like micelles with the water-
loving, phosphoric heads outward facing, or they
form into double sheets with each exterior surface
composed of all phosphorus heads and an internal
double layer of the water-avoiding hydrocarbon
legs; thus, the interior of the membrane is highly
hydrophobic. Such membranes are semiperme-
able. They exclude large molecules, water-soluble
molecules, and all charged molecules (e.g., Na
,
K
), while small, unpolarized, lipid-soluble mol-
ecules and some gases can diffuse through the
membrane. The membrane interior is in fact a
liquid, as described in the fluid mosaic membrane
model of Singer and Nicholson (1), with the phos-
pholipids able to move about easily within the
membrane and the interspersed proteins able to
migrate about, albeit more slowly. The phospho-
lipid molecular structure and the type and volume
of proteins seated in the membrane vary among
different cell types. The fluidity of the membrane
is affected by the inclusion of molecules such as
cholesterol into the membrane, which stiffens in a
warm membrane and increases the fluidity of a
cold membrane, and by kinking of the hydrocar-
bon tail chains of the lipoproteins (double-
bonding), which reduces the tight packing of the
lipoprotein sheets by decreasing the Van der
Waals bonding forces between the hydrocarbons
and thus increases membrane fluidity.
Membrane Proteins
With cells enclosed by a barrier membrane that
prevents simple diffusion of many essential sub-
stances such as charged ions, a transport mecha-
nism across the membrane becomes essential for
electrophysiology. This is achieved through the
special association of adapted protein molecules
with the membrane. While it has long been recog-
nized that proteins are a major constituent of the
membrane, their actual structure and functional
organization have only recently been detailed.
Membrane proteins can be described as extrinsic
(peripheral)—that is, merely attached to the mem-
brane surface—or as intrinsic (integral), those
seated into and often completely spanning the
membrane. Integral membrane proteins can
insert into the membrane with their “waist”
compatible with the hydrophobic, internal
environment of the membrane and their terminal
segments compatible with the hydrophilic intra-
cellular and the extracellular environments into
which they project. Those that function as pas-
sageways through the membrane are termed
pores, channels, or pumps. These proteins are able
to transport ions with or against a concentration
gradient and be gated (switched on and off), and
they are highly selective of the substances to be
transported. Transport against an ionic gradient
(active transport) requires added energy expendi-
ture, while transport down a gradient (passive
transport), here termed facilitated diffusion (facil-
itation refers to the channel function of opening a
path through the membrane), uses the stored en-
ergy in the gradient itself. Gating (opening or clos-
ing a channel) can be triggered by many means:
voltage changes, chemicals, Ca

, and mechani-
cal forces. The proteins essential to axon signal
conduction are voltage gated and will be the focus
of discussion; however, recall that the myoneural
junction is chemically gated with neurotransmit-
ters, while muscle is Ca

gated.
One of the core functions of membrane pro-
teins is to maintain the intracellular concentration
of Na
below and K
above that of the external
environment. This condition is essential for life
processes. Signal conduction along the axon uses a
highly adapted exaggeration of this basic cell func-
tion that can produce episodic, very high ionic
fluxes across the membrane. Since cell membranes
are essentially impermeable to charged ions, this
homeostasis is achieved through the active trans-
port of Na
and K
cations across the cell mem-
brane during the “charging” of the membrane
potential and facilitated diffusion during depolar-
ization. The membrane constrains protein anions
from leaving the cell cytoplasm by providing an in-
ternal, positively charged component and prevents
the passive diffusion of Na
, K
, or Ca

cations
back across the membrane in response to their
transmembrane concentration gradients once
these gradients have been established by active
transport of the ions. The concentration difference
(i.e., gradient of each specific ion) across the cell
membrane (inside versus outside the cell) creates
an electrical potential at the cell membrane that
can be summed for the membrane as a whole
through application of the Nernst equation. For
mammalian nerve cells, the sum typically is 70 mV,
90749_ch03(29-64).ps 8/10/06 3:58 PM Page 31
CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES
with the external surface positive in respect to the
interior. Thus, a static electrical potential exists at
the membrane in its normal “charged,” homeosta-
tic state. This potential can do work, including that
of signal conduction.
The work required to transport ions across the
membrane is reduced if the protein structure forms
a physical void on the membrane, thus permitting
ions to diffuse into the cavity and shorten the trans-
port distance. Once an ion transport candidate
enters the portal, protein pumps bind the ion to a
specific site inside the protein and then must pass it
stepwise through the membrane using a series of
conformational changes and sequential binding
sites along the path inside the protein. While this is
cumbersome, it is well suited to propelling the ion
against the gradient, with the added benefit that the
passageway is firmly blocked by its conformation to
prevent passive ion leakage or passage of compet-
ing ions. Channels, in contrast, enable the high
ionic fluxes essential for creating a depolarization
spike by offering a more straight-through path,
with selectivity based on a close match between the
physical characteristics of the ion and those of the
channel, and employing a more limited, charge-
based selectivity. These channels are voltage gated
(i.e., opened by electrical field effects) to alter their
conformation in order to permit a rapid flow of the
selected ions through the pathway.
MacKinnon’s work demonstrated that selec-
tivity of the K
channel results from a filter effect
that uses the significant difference in diameter of
Na
and K
ions, and the geometry of their
respective linkages to water in solution and to the
dipolar oxygen atoms exposed in the internal
protein channel pathway. The fit of K
bound to
water into the similarly scaled, charged environ-
ment of the protein path promotes the energy-free
stripping away of the water and the subsequent
progression of the K
into and through the
channel. This structure provides the model for
high-flow, facilitated-diffusion–type ion channels
that are necessary to produce the sharp, ion-
generated voltage changes needed to open more
membrane channels and propagate axon
membrane depolarization. Actual conduction of
electrical signals along the membrane is accom-
plished by sequential, voltage-dependent opening
of sodium conductance channels along the axon
membrane. Once triggered at any point on the
31
axon, the signal propagates both centrifugally and
centripetally along the full surface and length of
the membrane (axolemma).
Resting Membrane Potential
The axolemma exhibits an electrical charge of 70
mV on its inside compared to its outside surface
when in its resting (i.e., standby) state. This is due
in part to passive and in part to active processes:
membrane permeability, ion gradients, electrical
gradients, and sodium pumps. The membrane
structure absolutely prevents the movement of the
negatively charged protein anions from the cell
(some are physically anchored, and others are too
large to squeeze through pores), creating a perma-
nent, negative charge within the cell that attracts
cations. While the membrane is effective in block-
ing ion passage, there are pores that permit some
passive ion migration. This permeability is very
much greater for K
ions, the relationship being
K
 Cl  Na
. Since the K
ion is the
species most able to diffuse into the cell and its pos-
itive charge is electrically attracted to the nega-
tively charged anions inside the cell, its concentra-
tion inside the cell increases. As the K
ion
concentration inside the cell increases, entry is pro-
gressively opposed by the increasing K
osmotic
gradient across the membrane until the electrical
attraction of K
into the cell equals the concentra-
tion gradient force to move it out. At that point a
relative equilibrium for K
is established. For K

this occurs at a membrane voltage of 90 mV, and
similarly the equilibrium is
60 mV for Na
and
70 mV for Cl. Other factors complicate the pic-
ture, such as increased K
ion positivity inside the
cell provides electrical attraction for Cl and si-
multaneously further impedes Na
entry.
An entirely passive process cannot maintain
the membrane charge, and the active work of
maintaining the axon membrane potential is pro-
vided by the sodium-potassium-ATPase pump.
This membrane protein internally binds three
intracellular Na
ions and a single adenosine
triphosphate (ATP) molecule. Hydrolysis of the
ATP to ADP energizes the change in the protein
conformation, and the three Na
ions are
subsequently exposed to the extracellular environ-
ment and expelled. This external conformation of
the protein then binds two extracellular K
ions,
90749_ch03(29-64).ps 8/10/06 3:58 PM Page 32
32 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
the ADP is released, and the protein reconfigures
such that the K
ions are exposed to the intracellu-
lar environment and released. This series of
reactions by a single membrane protein very neatly
addresses the active transport requirements for the
two key cations involved in axon signal conduction.
Action Potential
The charged, resting membrane stores energy in
the form of its voltage gradient as well as its Na

and K
concentration gradients across the mem-
brane. These stored assets are converted into an
active electrical field (the action potential) by a
sudden influx of sodium ions through the mem-
brane. The propagation of this local potential
along the full length of the axon constitutes nerve
conduction. Hodgkin and Huxley described
the basic physiology of nerve conduction based
on the squid giant axon in a series of papers in 1952.
In the resting state, the negative internal mem-
brane charge and the low intracellular Na
con-
centration present a strong attraction for extracel-
lular Na
ions to enter the axon. However, the
intact membrane precludes Na
entry. Sodium
conductance protein channels are present in the
membrane but remain closed at rest. These chan-
nels are voltage gated, meaning that they open due
to changes in their protein conformation caused by
a sufficient local voltage change. In axons, the Na

channels open if the membrane voltage moves to
approximately 55 mV (changes by 15 mV) in re-
sponse to an applied electrical field. Smaller stim-
ulations are insufficient to open the channels since
the resting membrane potential is stabilized by
compensatory outflows of potassium. Thus, a suf-
ficient stimulus must exceed the compensatory ca-
pacity of the K
ion outflow current. A sufficient
stimulus electrically charges the capacitance fea-
ture of the channel protein, which then conforms
so that its principal extracellular gate is in the open
position. Na
rapidly flows through the mem-
brane, and this ion flux creates an electrical field
that can be recorded with proper instrumentation.
This is the all-or-none aspect of nerve action first
described by Cajal. The free flow of Na
into the
cell alters the membrane charge, creating a further
positive change to
35 mV, a total increase of

105 mV. This large spike will be useful later as
we review the propagation of the depolarization
wave. If left to flow to equilibrium, the Nernst
equation predicts an even higher membrane volt-
age, but two factors blunt this response. First, a
second gated protein formation on the channel
closes after about 1 ms and stops Na
flow cold.
This structure is not voltage sensitive but rather is
a time-dependent reconformation of the protein.
Second, there is a delayed, gated opening of potas-
sium channels accelerating K
efflux from the
axon that offsets the positive Na
spike. K
efflux
continues until the membrane charge actually falls
below the resting value (hyperpolarization) before
returning to baseline status.
Signal propagation transmits information by
moving a coherent signal along the axon to the
endplate or soma. This involves translation of
the active area of the membrane steadily along the
course of the axon. This is possible because the
electrical field generated by the opening of local
Na
channels is sufficiently strong to open adja-
cent channels and thus propagate the signal in a
stepwise manner along the membrane. You’ll re-
call that the local voltage changes at the mem-
brane during the Na
spike described previously
were about 105 mV. This compares very favorably
with the voltage change needed to open a Na

channel of about 15 mV (the threshold voltage is
55 mV). Thus, local ion currents are able to flow
along the axon, spreading from channel to adja-
cent channel once they are initiated. Normal con-
duction signals start at one end of the axon and
propagate to the other, while those initiated at in-
termediate points propagate simultaneously in
both proximal and distal directions.
This can raise the question of why a propa-
gating wave front does not propagate back along
the axon to form a reverberating circuit. This is
prevented by absolute and relative refractory pe-
riods (i.e., a period of complete or reduced axon
response to stimulation), which are present as the
membrane recovers from an action potential
Na
spike. The absolute refractory period lasts
about 1 ms, during which time there is no axon
response regardless of how strong a stimulus is
delivered. This occurs because:
• Every Na
channel in the area was opened dur-
ing the initial (all-or-nothing) action potential.
• Every Na
channel is temporarily blocked
from “recycling” to its ready state.
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CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES
• The second arm of the protein channel that re-
conformed and shut down Na
flow (described
above) still physically blocks the channel.
• The second arm is not sensitive to voltage (re-
member that it switches based only on elapsed
time).
• The second arm is conformed to prevent the
voltage-sensitive gate protein from returning to
its ready position.
In this physiologic refractory state, no matter
what the voltage change, no sodium channels are
available to open. The relative refractory period
begins when Na
channels begin reconfiguring to
their ready state. Reconfiguration occurs after dif-
ferent intervals in different channels. Both the
opening and resetting of these channels are sto-
chastic (i.e., it occurs randomly) once conditions
are possible. What is seen is that progressively
more Na
channels are responsive to stimulation
and the voltage change needed to trigger depolar-
ization gradually returns to normal. Note that hy-
perpolarization of the membrane is not a factor in
the absolute refractory period since it modulates
only the voltage intensity required to stimulate,
not the ability of the membrane to respond. The
refractory period of an axon determines its maxi-
mum firing frequency by setting the minimum in-
terval between conducted signals. This in turn sets
the limit on the amount of information a single
axon can deliver, since the axon’s all-or-nothing
depolarization strategy keeps the amplitude of the
discharge constant and frequency modulation (fir-
ing rate) is the only factor that can be varied for
encoding information.
Conduction velocity is a critical factor in ef-
fective information transmission. The time
required to deliver certain urgent signals can be
critical to the survival of large, complex organ-
isms. The simplest protective reflex response of
the human foot travels a 2-m-long circuit. This
signal must be transmitted along an extremely
thin axon with a diameter of less than 20 m, and
so it has a length-to-diameter ratio of 50,000 to 1 or
more. All of the axon’s structural components and
energy sources are transported from the soma via
a highly structured active transport system. The
most rapid physical movement of moieties down
the axon (rapid transport) requires many hours.
With physical transport of information obviously
33
far too slow, the rapid depolarization wave
method of signaling is a necessity. Both the speed
and the reliability of this signal are important and
are insured through numerous cellular-level
adaptations.
Each opened Na
channel generates a finite
flow of ions and thus a finite electrical field
change. The effective force for opening a distant
channel is the sum of the field forces generated by
currently active channels. Because channel open-
ing is stochastic, it requires a finite time for com-
pletion in any area, and so the electrical field
generation is incremental. Electrical currents
travel at the speed of light, so, practically speaking,
they act instantaneously. Therefore, the speed of
conduction along the axon can be explained in re-
lation to characteristics of the channel protein and
characteristics of the axon. The Na
channel pro-
tein has capacitor-like characteristics in that it
must be electrically charged before changing its
conformation to open. This requires time and af-
fects the conduction of current in the axon. An ad-
ditional time increment is required for the protein
to shift to its open configuration. Since there is a
degree of randomness in the total time required to
complete this transition, it contributes an irre-
ducible component of the limit on conduction
speed. The size of the axon strongly affects con-
duction velocity, with larger-diameter axons con-
ducting faster. This relates to the decrease in elec-
trical resistance through the cytoplasm with
increasing axon cross-sectional area and is similar
to the reduction in electrical resistance seen in
larger-diameter wires. While the electrical cur-
rent generated by the Na
flow travels at the
speed of light, the distance down the axon over
which there is a sufficient stimulus to open
(charge) channels is controlled by the axon charac-
teristics. First, the axon has cable properties (an
electrical insulator, the membrane, sandwiched
between two conductors [the intracellular and ex-
tracellular fluids] makes up a capacitor) and the
current in the axon must charge that capacitance,
giving up energy that might otherwise open chan-
nels. Second, the channels themselves add more
capacitance to the axon; thus, greater channel den-
sity on the membrane further slows conduction
speed. All things being equal, larger axons have
fewer channels per axon volume, lower cable ca-
pacitance and axonal resistance, and faster
90749_ch03(29-64).ps 8/10/06 3:58 PM Page 34
34 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
conduction velocities. Since the channel opening
speed is a constant between axons, conduction ve-
locity in bare (nonmyelinated) axons increases by a
factor of the square root of the diameter (√D).
Thus, doubling the speed of conduction in
unmyelinated axons requires increasing the diam-
eter by four times.
All species scale up the diameter of axons to
attain greater speed. The classic example of in-
creased diameter in nonmyelinated axons is the gi-
ant axon of the squid. This axon functions in the
animal’s propulsion system and is an essential
component for escape from danger, and thus its
conduction speed is vital. It is the largest known
nonmyelinated axon, reaching 1 mm in diameter,
roughly 50 times greater than the largest human
axon. Its size has made it the preferred experi-
mental model for nerve membrane since it
permits easier intracellular instrumentation. Non-
myelinated axons in humans are typically less than
2 m in diameter and conduct at a speed of a few
meters per second (m/s). This is fast enough for
autonomic regulation of internal body functions
but far too slow for critical motor responses or
complex cognitive functions. Axons in humans
used for time-critical signaling can conduct at
over 100 m/s. What are the prospects for scaling
up the axon diameter like the squid to achieve this
speed? The squid giant axon can conduct at 25
m/s, or one fourth of our 100 m/s target. Using the
√D to reach this speed, the “human giant axon”
could increase its velocity 4 times by increasing the
diameter 16 times (i.e., reaching a 16-mm diame-
ter). The cross-sectional area of this axon would be
200 mm2. Assuming that a typical peripheral
nerve has 10,000 axons, a peripheral nerve of hu-
man giant axons could reach to 2 square meters in
area (2,000,000 mm2)—not really a practical
option!
Myelinated axons overcome this limitation by
greatly extending the distance over which the
propagating electrical wave front can open Na

ion channels, thus enabling depolarization to
leapfrog along the membrane in larger segments,
a process known as salutatory conduction. This
results from a beneficial association between the
axon and a specialized neural support, the
Schwann cell. Myelinated axon fibers are concen-
trically wrapped by the Schwann cell’s membrane.
This divides the axon into electrically insulated
segments, one segment per Schwann cell, with
each segment stretching from 0.3 to 2 mm in
length. The Schwann cell membrane has a high-
lipid and low-protein content with little cyto-
plasm in the wrappings, making it an excellent
insulator. Gaps between the segments, called
nodes of Ranvier, contain essentially all of the con-
ductance channels, creating a discrete electrical
field generator. The internode segments covered
by myelin have few protein channels and thus
have reduced capacitance. This myelin cover im-
proves the cable properties of the axon, reducing
resistance and enabling the generators at the nodes
to act at a greater distance. This moves the area of
membrane depolarization two to three nodes
along the nerve. This leapfrogging of the depolar-
ization across nodes is saltatory conduction, and it
greatly speeds conduction. Based on these
changed axonal conditions, the conduction speed
in myelinated axons increases in direct proportion
to axon diameter rather than to the square root of
the diameter, as seen in nonmyelinated axons.
Myelination is critical for normal human nerve
function, and both myelin pathology and the
adaptive changes of the axon membrane in re-
sponse to myelin play key roles in clinical disease
and NCS.
PATHOLOGY
Myelinated axons demonstrate just three states of
altered function: slowing of conduction, segmen-
tal conduction block, and loss of conduction along
the full length of the axon. Myriad subtle modifi-
cations in the cellular chemistry and protein func-
tions that accompany these changes lie beyond the
reach of electrodiagnostic tests, in part obscured
by the “all-or-none” character of axon function.
The terms neurapraxia, neurotmesis, and ax-
onotmesis appear frequently but offer more con-
fusion than explanation. First, they indicate end
effects rather than the underlying pathophysiol-
ogy of nerve dysfunction. Second, they suggest a
single status for the nerve when we usually deal
with mixed pathology—fostering confusion be-
tween the status of individual axons and that of
the total nerve. Finally, they are often simply mis-
used. A more direct approach is to report a de-
scription of the nerve status using estimates of the
90749_ch03(29-64).ps 8/10/06 3:58 PM Page 35
CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES
Figure 3-1 ● Demyelination pictured im-
mediately following the onset of injury (A,
A1) and 6 weeks later (B, B1) after myelin
debris has been removed. The evoked re-
sponses with stimulation proximal (left) to and distal
(right) to the lesion are demonstrated at A1 and B1 at
the bottom. The demyelinated membrane (B) is able
to restore some membrane proteins to restore propa-
gation of the action potential, although at a slow ve-
locity.
proportion of axons exhibiting diffuse slowing, fo-
cal slowing, focal block, or death.
Conduction slowing occurs in three patho-
physiologic conditions: demyelination, in which
(after an interval) function resumes, as in an un-
myelinated axon (Fig. 3-1) (see conduction block);
remyelination, in which internodes are shorter be-
cause the new Schwann cell produces a shorter,
thinner myelin cover; and reinnervation, where
the axon diameter is smaller and Schwann cells
also produce shorter segments (Fig. 3-2). In each
of these cases, conduction time along an axon is in-
creased because reorganization of the membrane
proteins results in higher capacitance in the axon
(see conduction velocity) due to the increased
number of discrete depolarization points (chan-
nels) that must be charged. In practice, many
variations on these extremes are possible: spotty
demyelination, with demyelinated internode
segments interspersed with normal ones; demyeli-
nation mixed with partial or light remyeliniza-
tion; and partial remyelination mixed with nor-
35
mal segments. When myelin is absent along a long
segment, the conduction velocity will be less than
20 m/s. Faster velocities suggest that demyelina-
tion is confined to a short segment that is “diluted
out” by inclusion of a contiguous normal segment
in the test segment, or that a mixed pathophysiol-
ogy exists. When a segment is successfully re-
myelinated, the NCV often remains slightly
slowed and may appear to be electrodiagnostically
identical to large-fiber neuropathy. Compression
neuropathies produce both demyelination and
large axon loss. After surgical decompression both
of these factors can result in residual slowed con-
duction despite “optimal” recovery. Distinguish-
ing this optimal-but-slowed conduction state from
a recurrent or persisting injury has become a cot-
tage industry. In almost all instances this distinc-
tion is possible only with serial conduction studies
that demonstrate change over time, or, in some
instances, an unexpected failure to improve, or
unusually good improvement following decom-
pression.
Conduction block often occurs at a discrete
location along the axon. Frequent causes include
local stretch or compression, ischemia, trauma, or
autoimmune or vascular disease. By definition,
conduction block indicates an injury in which the
axon survives (apraxia) despite the inability to
Figure 3-2 ● Remyelinated axon; note the
decreased internodal distance and de-
creased thickness of myelin. The evoked po-
tential with stimulation above and below the lesion
that would be obtained from a nerve with all axons
remyelinated is seen below. Conduction is slowed,
and the response is temporally dispersed across the
lesion.
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36 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY

disrupted, the surviving portion may die back to an

Figure 3-3 ● Evoked responses from
stimulation proximal (left) and distal (right)
to the lesion (A) immediately after injury,
(B) 7 days after injury, and (C) some weeks
following injury after neurapraxia has re-
solved. Compare to Figure 3-4.
intact node, stabilize, and attempt regeneration.
Wallerian degeneration occurs in the axon seg-
ment distal to the point of axon disruption. Wal-
lerian degeneration is the process of axon necrosis
that dissolves and removes the disrupted neural
segment and reorganizes the metabolism of any vi-
able proximal segment. Axons are dependent on
the neuron cell body to generate the energy and
major subcellular structures needed for their func-
tion. These structures are transported down the
axon as part of axoplasmic flow. Enough critical
materials are present in the axon for it to continue
functioning for several days independently. An
axon cleanly separated from the rest of the neural
cell will continue to conduct an action potential for
3 to 7 days (Figs. 3-4 and 3-5). During this period,
responses of the separated distal axon segment to
an adequate stimulation will remain essentially
normal. This makes it impossible to distinguish

transmit a signal along a local segment. The seg-

ments of the axon above and below the block are
normal and still conduct a signal when appropri-
ately stimulated. Investigators have attributed
conduction block to mechanical distortion of the
axon (2) (Fig. 3-3) and to an impedance mismatch
(3,4) at the junction of the myelinated and the
demyelinated segment. The absence of cell mem-
brane proteins on bare internode segments pro-
vides a convincing mechanism for conduction
block in demyelination (5) since conduction
through the demyelinated region would fail due
to extinction of the Na
depolarization current
when the demyelinated region extends more than
the two or three internodes across which the elec-
trical field of the last intact node of Ranvier is able
to produce an action potential. Thus, an axon ex-
hibits conduction block once a multi-internode
area is denuded. It can resume conducting only if
additional membrane proteins are inserted into
Figure 3-4 ● Axonotmetic lesion with
the membrane so that it can function in a non-
axon changes demonstrated (A) immedi-
myelinated mode, or when it becomes remyeli- ately after injury and (B) 10 days after in-
nated. jury. The evoked responses obtained by stimulation
Axon death results from a wide range of in- proximal (left) and distal (right) to the lesion of the
jury and disease. When the neuron cell body itself corresponding times (A1 and B1) are demonstrated at
dies, there is no possibility of nerve regeneration. the bottom. In contrast to Figure 3-3B, the response
However, when only a portion of the axon has been is absent at 7 to 10 days.
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CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES
Figure 3-5 ● CMAP recorded from the
thenar eminence with median nerve stimu-
lation at the wrist in an individual with sur-
gically demonstrated complete section of
the median nerve following a stab wound
in the upper arm. The top response was recorded
4 days after injury, the middle response 7 days after
injury, and the bottom response 10 days after injury.
(Sweep = 1 ms, gain = 1 mV.)
between a focal conduction block (neurapraxia)
and the early stages of Wallerian degeneration. At
the end of this 3- to 7-day period, axon conduction
abruptly fails—that is, there is not a gradual
decline but rather a precipitous one (recall the all-
or-none rule). Once conduction fails, physical dis-
solution of the axon segment beyond the injury is
rapid. The delay between injury and axon conduc-
tion failure means that electrodiagnostic distinc-
tion between conduction block and axon death can
be made only at some point from 3 to 7 days after
the injury (see Figs. 3-4 and 3-5). Nevertheless,
electrodiagnostic studies should be performed as
early after injury as possible to determine if some
function is preserved and to obtain a baseline
evoked response to compare with subsequent re-
sponses. It is very helpful to see the failure in con-
duction between two studies rather than simply
not see a response in a traumatized limb! Electro-
diagnosis can never determine if a nerve remains in
structural continuity when there is complete loss of
response to distal stimulation (Wallerian degener-
37
ation present), nor in cases of complete conduction
block earlier than 7 days after injury (Wallerian
degeneration not yet certain). Thus, the prognosis
for axon regeneration that depends largely on the
preservation of the nerve “skeleton” can be divined
only by clinical judgment based on the mechanism
of injury or by surgical exploration. By the same
logic, the diagnosis of axonotmesis, which by defi-
nition is complete axonal degeneration with
preservation of neural architecture such that re-
generation can occur (6), cannot be distinguished
electrodiagnostically from neurotmesis (loss of the
neural skeleton).
Up to this point we have worked with single
nerve fibers, either nonmyelinated or myelinated
axons. Single fibers generally exhibit a simple in-
jury picture with only one pathophysiologic
change, such as conduction slowing, conduction
block, or axon death. In contrast, injured nerves in
situ have thousands of individual axons and are
capable of demonstrating combinations of these
changes. Multiple abnormalities may be found
within a short segment, at separate points along
the nerve, or even at separate points on an indi-
vidual axon. Interpretation of NCS can be compli-
cated, and this highlights the importance of inte-
grating the clinical and the electrodiagnostic
examination when formulating the diagnosis.
Evoked responses are signals produced by the
artificial, simultaneous stimulation of the nerve’s
axons, with electronic recording at a site some-
what distant from the stimulation. They represent
the basic data of NCS. Stimulation of a motor
nerve and recording the depolarization of a mus-
cle it supplies produces a compound muscle action
potential (CMAP) (Fig. 3-6). Similarly, stimula-
tion of a sensory nerve and recording the signal of
the nerve depolarization wave from a different
point along the nerve produces a sensory nerve ac-
tion potential (SNAP). Each of these signals has a
distinct, consistent shape (Fig. 3-7) that, except for
amplitude differences, varies little from nerve to
nerve.
The recorded SNAP signal represents the
summated action potentials (both negative and
positive voltage components) from each of the
nerve’s axons. The consistency of the shape comes
from the consistent “normal” distribution of axon
velocities in human nerves, which in turn creates a
typical summation pattern. The summation of
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38 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY

Figure 3-6 ● CMAP with recording electrode over the motor point of a single muscle. Note
initial negative deflection (negative is upward in the figure).

Figure 3-7 ● SNAPs recorded from three different nerves demonstrate similarity of shape
despite anatomic and (mild) pathologic differences. Median nerve recorded from digit 3 after wrist
stimulation (14 cm) shows mild delay (upper) compared to ulnar response from digit 5 at the same distance
(middle), and this latency difference suggests mild entrapment. Lower trace is from a 10-cm segment of the lat-
eral antebrachial cutaneous nerve. (Sweep = 1 ms, gain = 20 V.)
90749_ch03(29-64).ps 8/10/06 3:58 PM Page 39
CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES
individual axon responses into an extended re-
sponse is illustrated in Figure 3-8. If each axon
conducted at the same velocity, then the duration
of the summated evoked response would be the
same as that of a single axon action potential, and
the amplitude of negative and positive components
would be in proportion to the number of axons
(Fig. 3-9A). Conversely, if each axon conducted at
very different velocities, the compound signal over
a sufficiently long segment would be a sawtooth,
with each deflection produced by one individual
axon (see Fig. 3-9B). In the real world, axons
exhibit a relatively narrow range of conduction
velocities, and the pattern of velocity distribution is
consistent among nerves. Although the signals do
not arrive simultaneously from all of the axons, the
variation of their arrival times is well grouped, and
there is significant overlap of the axon signals.
This spreading out of the evoked potential is
called temporal dispersion. This staggered arrival
Figure 3-8 ● Temporal dispersion. Three
axons of various conduction speeds, I (slowest) to III
(fastest), are illustrated. The summated response of
the signals from each of these axons is shown (A–C)
at distances along the nerve. Conduction begins at
the left and proceeds to the right. At point A, the
signals in each axon arrive almost simultaneously,
producing a very compact recorded response. At
point B, the signals are less well synchronized, pro-
ducing a smaller-amplitude and longer-duration
response. This spreading is increased by the time the
signals arrive at point C. The first potential to arrive
establishes the take-off latency time, and delayed
arrivals will increase the response’s duration. The
greater the number of axons contributing to the
signal, the smoother the curve of the recorded
evoked response.
39
of individual axon potentials at a recording elec-
trode produces overlap of positive and negative
components, resulting in cancellation of part of
the signals, which is called phase cancellation
(see Fig. 3-9C). Thus, a nerve with a normal
complement of healthy fibers will produce a sig-
nal with normal temporal dispersion and typical
phase cancellation, resulting in the standard
shape. However, phase cancellation eliminates
any simple correlation between signal amplitude
(or area) and the number of axons contributing to
the response.
It follows that a different mix of individual
fiber velocities would create a different normal
evoked potential shape, which is precisely the
situation seen in nerve pathology (Fig. 3-10).
Computers enable us to mathematically model the
way in which evoked potential shape varies with
the distribution of individual fiber conduction
velocities. These models demonstrate that up to
50% of the amplitude of the evoked potential of a
typical nerve can be eliminated merely by altering
the conduction velocity mix of its fibers. Thus, the
recorded evoked response can be significantly
reduced in nerve injury without any conduction
block. This forces us to abandon the older concept
in NCS that a “significant” (often 10% or 15%) drop
in the size of the evoked potential across a point of
injury indicates conduction block. Evoked poten-
tial decreases of at least 50% can be entirely due to
the increased phase cancellation of increased
temporal dispersion. In typical patients it is likely
that a combination of conduction block and tem-
poral dispersion will be in play, with each axon
suffering a degree of myelin disruption and repair,
or change in diameter. Needle electromyography
can be helpful in separating blocked fibers from
those that are slowed, since blocked axons cannot
contribute to the voluntary recruitment pattern of
motor unit potentials (MUP), whereas axons that
are merely slowed will still activate MUPs and
produce contractile force. Therefore, relatively
good preservation of the recruitment pattern in the
face of a major drop in the size of the evoked
potential across the lesion indicates predominantly
conduction slowing (phase cancellation) rather
than conduction block, while a major-amplitude
drop coupled with a greatly reduced interference
pattern favors conduction block.
Temporal dispersion is an important, normal
aspect of nerve conduction, and its exaggeration in
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40 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY

Figure 3-9 ● Summation and phase cancellation. A. Simultaneous signal arrival (all axons at
same conduction velocity) amplitude and area are a summation of the individual signals, while duration is the
same as a single axon. B. No overlap (all axons have distinct velocities) leads to the greatest duration of signal,
as the difference between the fastest and slowest axon is maximal. C. Phase cancellation due to overlap of neg-
ative and positive components of axons of slightly different velocities.

injury or disease is a key electrodiagnostic finding.

Figure 3-10 ● Hypothenar muscle CMAPs
from ulnar nerve stimulation at the wrist,
below the elbow, and above the elbow.
Note the loss of amplitude and area of the evoked re-
sponse with conduction across the elbow, demonstrat-
ing mixed neurapraxia and conduction slowing with
temporal dispersion. (Sweep = 10 ms, gain = 5 mV.)
This exaggeration cannot only reduce the ampli-
tude of the response and prolong its duration, but
also prolong its duration to such a degree that
additional phases can appear in the response. Sig-
nals recorded directly from nerves (e.g., SNAPs)
are briefer than the CMAP responses of motor
conduction studies recorded over muscle because
they contain only axon depolarization waves. The
CMAP has a longer duration due to the longer
time period of action potential propagation (slower
conduction) of muscle membranes. Normal nerve
evoked responses (SNAPs) are briefer than 2 ms,
whereas motor responses (CMAPs) in hand and
foot intrinsic muscles are less than 5 ms in duration
(negative peak). Evoked responses longer than
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CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES 41

Figure 3-11 ● Median motor CMAP is recorded with E1 over motor point of the abductor
pollicis brevis and stimulation 8 cm away at the wrist (upper trace). Excessive stimulation
without movement of any electrodes activates the ulnar nerve (lower) by volume conduction. This adds the ul-
nar-innervated thenar muscles’ depolarizations to the recorded potential, creating an erroneously large and
misshaped M-wave. (Sweep = 2 ms, gain = 5 mV.)

these indicate increased temporal dispersion, ei-
ther from disease or technical error (Fig. 3-11).
Where Is the Lesion? Intraneural Anatomy
The interior architecture of nerves has evolved
into a clever arrangement that protects against the
catastrophic loss of whole functions from partial
nerve injuries. The arrangement also turns out to
be a key aid to the electromyographer’s ability to
localize the point of injury along the course of the
nerve. A typical telephone or fiberoptic cable has
its individual fibers bundled into subclusters and
the grouping remains unchanged throughout the
length of the cable. All the telephone lines from
“XYZ, Inc.” travel together in one of these small
bundles and may take up the whole bundle. If
someone cuts that bundle, “XYZ, Inc.” loses all of
its telephones, but no other subscriber is affected.
Similarly, neurons are grouped by function both
in the brain and in the spinal cord, where focal
lesions often cause discrete motor losses. If motor
axons were grouped in nerves analogous to the
arrangement in telephone cables, partial nerve in-
jury might completely denervate one or two mus-
cles while leaving others unaffected, even though
their branches arise distal to the injury (Fig. 3-12).
That arrangement also would make it difficult to
locate the site of injury because there would be no
difference in the observed effect of partial injury
regardless of where it was located in the nerve.
Peripheral nerves, like cables, are also parti-
tioned into bundles known as fascicles, and for
much the same reason as cables: to provide better
internal support and strength. However, unlike the
wires in cables, the body employs a different
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42 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY

Figure 3-12 ● Hypothetical nerve in which all axons stay in a single fascicle until they exit
the nerve. Note that a lesion at A or B would appear identical on needle EMG examination of both the dis-
tal muscle and the one innervated by the midforearm branch.

scheme of continually exchanging axons between
the several fascicles within the nerve. This scheme
continuously alters the axons that are traveling
together and their location within the nerve as
they move along its course (Fig. 3-13). With this
arrangement, a partial nerve injury tends to spare
some of the axons to each of the muscles supplied
distal to the injury, since some fibers to each muscle
are likely to be in spared fascicles, which results in
partial function of most muscles. In addition, it is
likely that each of the nerves supplied distal to the
injury will have at least some abnormality, so that
the distribution of abnormalities clearly locates the
point of injury. Intraneural anatomy is thus the key
to both reduce the functional impact of partial
nerve injuries and also to better pinpoint the lesion.
REFERENCE VALUES
Nerve conduction reference values are established
by performing a standardized testing method on a
group of individuals that meet a pre-established
set of qualifications. These usually include sub-
jects who do not have neurologic complaints or
disease; who are in appropriately good general
health and without previous severe injuries or
illness, environmental exposure, or special cir-
cumstances that would affect testing; and who
collectively match the distribution of age, sex, and
other features representative of the population to
be tested. Notice that the group does not match
the total population, but rather the population that
is likely to be tested. If a clinical condition is found
in a specific group, then normals should match
that group if it has general characteristics that
affect NCS values. Testing for chronic toxicity of
an industrial solvent used for 50 years in a plant
would require at least age-matching the subjects.
“Normal” is usually defined statistically as the
mean value plus or minus two standard deviations
(SD). Although this approach is helpful, problems
such as nonparametric distributions of population
characteristics in the reference group can result in
skewed statistics (as Mark Twain said, “There are
statistics, damned statistics, and lies”). Examples
of this type of characteristic are extreme limb
length and height or extremes of age. Though not
an indication of nerve pathology, groups with one
of the characteristics would have mean nerve con-
duction values different from those of the total
population.

Figure 3-13 ● Typical mammalian nerve, illustrating the movement of axons from one
fascicle to another during their course. Here lesions at A and B may be easily distinguished elec-
tromyographically by the fact that lesion A produces changes in the distribution of branch C, whereas the lesion
at B does not.
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CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES 43

Even when unique personal characteristics portions of the clinical signal at each electrode and
are not at issue, the very wide differences in values thus canceling meaningful information. Surface
that fall within normal for the whole population electrodes are used because they capture the most
makes it difficult to detect small abnormalities in complete signal in a way that permits quantitative
a single individual. Conduction values between analysis of the recorded potentials.
individuals in a reference population vary greatly For CMAP recording, E1 is placed over the
when compared to the limited variation in values muscle motor point and E2 is placed distally over
found in different nerves within a single indi- the tendon or another electrically silent area to
vidual. A review of published reference nerve minimize (desired) signal cancellation. The initial
conduction values shows that the reported range deflection of motor responses should be sharply
of variation (mean  2 SD) is equal to approxi- negative, and the signal should be a smooth,
mately 25% of the mean conduction velocity of the biphasic curve (see Fig. 3-6). A signal that shows
subjects. Compare that to side-to-side differences initial positive deflection (Fig. 3-14) is very likely
in specific nerves of individual subjects, which “volume conducted” (i.e., initiated at a distance
have a narrower range. These are typically several away from E1). The initial deflection of the signal
percentage points, and repeat testing in individu- may be more clearly defined by changing the elec-
als consistently gives day-to-day variation below trode placement to obtain a clean negative initial
10%. When using population-based reference deflection, or if that fails using needle recording to
values, an individual whose beginning conduction
speed was at the “fast end” of the normal range
would have to experience conduction slowing of
40% before dropping below the reference range.
The sensitivity of NCS can be increased without
an undue increase in false-positive results if the
tested individual can also serve as the control. This
approach is appropriate for cases of focal injury
or entrapment but has obvious difficulties in
the face of a generalized neuropathic process such
as diabetic neuropathy. An excellent use of this
strategy is side-to-side comparisons and same-side
median-to-ulnar (or radial) nerve comparisons for
carpal tunnel syndrome assessment.

EVOKED POTENTIAL RECORDING

Evoked potentials are recorded using an E1
(recording) and E2 (reference) electrode attached
to the separate inputs of the differential amplifier.
The amplifier subtracts these two simultaneously
received signals and the remainder voltage is
amplified for display. This technique eliminates
signals common to both electrodes: distant signals Figure 3-14 ● Median motor evoked re-
sponse in a patient with carpal tunnel
such as cardiac potentials and stray signals broad-
syndrome recorded at amplifier settings of
cast from the environment are present in each 1 mV (above) and 100 V (below) per divi-
electrode’s signal and are canceled. This clarifies sion (sweep speed is 1 ms). Increased ampli-
the signal but also makes the placement of the two fication makes clear that the potential is actually ini-
electrodes in relation to the signal generator tially positive, and with earlier onset to show that
source (nerve or muscle), and to each other, more measurements of latency can be affected by the
important. Care is required to avoid capturing amplifier gain.
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44 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
confirm that the signal originates in the proper
muscle, since a distorted response may originate
from a “distant” muscle that was also stimulated.
Polyphasic or complex signals may result from si-
multaneous recording of two muscles or from the
effects of abnormal conduction in the nerve being
studied (Fig. 3-15).
For SNAP recording, both the E1 and the E2
electrodes are placed directly along the course of
the nerve, with E1 located closer to the stimulator.
Ground electrode placement can reduce shock
artifact and usually is best located between the
stimulating and the E1 electrode. The impedance
of dry skin is high, and this may result in excessive
shock artifact in these studies since the amplifica-
tion level is high. Standard electrode paste or gel
will often be sufficient to eliminate this difficulty,
but occasionally light abrasion of the skin is neces-
sary to obtain a satisfactory recording, particularly
in short-segment sensory conduction studies.
Separation between the El and E2 electrodes
alters the measured latency and the amplitude
of the recorded potential. For sensory nerve stud-
ies, the optimal distance is 3 to 4 cm. The ideal
separation reduces phase cancellation and maxi-
mizes amplitude, and this ideal depends upon
the actual conduction velocity of the nerve tested.
The sensitivity of the response to electrode separa-
tion and placement results from the wavelength
Figure 3-15 ● Superimposed are CMAPs
recorded at the abductor pollicis brevis
motor point and at a more medial site over
motor point of three thenar hand muscles.
The larger-amplitude response is from the single ab-
ductor pollicis brevis muscle. The separate compo-
nents of the smaller response result from recording
responses from three separate median-innervated
muscles, which causes some cancellation and other
changes.
Figure 3-16 ● Three SNAPs recorded with
increasing separation of the reference (E2)
from the recording (E1) electrode along the
nerve’s length. Separations are 3 cm (largest
amplitude, shortest duration), 6 cm, and 8 cm
(smallest amplitude, longest duration). Optimal sep-
aration is related to the wavelength of the signal, and
in practice for sensory nerve recording the E1 to E2
separation should be 3 to 4 cm.
characteristics of the nerve signal and the phase
cancellation effects. Maximum amplitude results
when the electrode separation is equal to one fourth
the wavelength of the nerve signal (7) (Fig. 3-16).
Embedding the two electrodes in a plastic bar stan-
dardizes the separation and simplifies application.
An alternate recording technique is to place the E1
electrode directly over the nerve, with the E2 elec-
trode approximately 3 cm away from the recording
electrode but perpendicular to the course of the
nerve (8). This monopolar recording results in a
lower-amplitude signal but one less subject to
change from small E1 movements (Fig. 3-17).
Recording the CMAP with an intramuscular
needle electrode can enable the investigator to
ensure that the recorded signal originates from
a specific muscle (not volume conducted from
some distance). Similarly, with near-nerve needle
Figure 3-17 ● SNAP obtained using standard
E1 and E2 electrode placements along the length of
the nerve (large-amplitude response) and off-nerve
placement (monopolar SNAP technique) of the
reference electrode leading to a smaller-amplitude
response.
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CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES
placement, SNAPs that are not otherwise accessible
can be recorded. Using a needle electrode for nerve
stimulation can confine the stimulation to a specific
nerve or access a deep nerve not easily stimulated
from the surface. When placed intramuscularly,
the needle electrode disproportionately records the
muscle fiber potential spikes from motor units
located very close to the needle tip. The negative
rise time of the potential for a fiber located near
the needle tip is fast and of very large amplitude
(Fig. 3-18). Needle recording electrodes are useful
for confirming that the recorded potential origi-
nates in the muscle under investigation, but they
must be used with caution. The large-amplitude
spike response recorded through a needle electrode
originates from a few motor units near the needle
tip, and so motor nerve conduction velocities with
this technique can be erratic in highly denervated
muscles. In addition, the amplitude recorded with
intramuscular needles is not diagnostically useful
because small needle movements can alter it con-
siderably, although this is not the case if the needle
is placed subcutaneously.
In addition to the normal variation among
individuals, three nonpathologic factors signifi-
cantly affect NCS: nerve temperature, subject age,
Figure 3-18 ● CMAP recorded using a
monopolar EMG needle electrode in the
muscle. The initial deflection is of low amplitude
(full screen represents 6 mV), indicating that the
needle tip is not directly against fibers depolarized
by the fastest-conducting axons, while some slower-
conducting axons activate muscle fibers near the
needle with a short rise time and large amplitude.
45
and subject height. Temperature is the most chal-
lenging of these in daily practice because many
factors, such as a cold environment, vasoconstric-
tion, or evaporative cooling from sweating, can
quickly lower the temperature of superficially lo-
cated peripheral nerves. There is a direct relation-
ship between nerve temperature and conduction
velocity. Henriksen reported a drop in conduc-
tion velocity of approximately 2.4 m/s for every
1°C of temperature reduction in the forearm
(measured by a needle thermistor at a depth
of 2 cm) (9). Johnson, using intramuscular
temperature, found a decrease of 5% per 1°C
(10). Haller found a linear correlation in normal
subjects among skin, subcutaneous, and intra-
muscular temperatures of the calf with various in-
duced temperatures (11). He suggested that the
skin temperature be measured 15 cm proximal to
the medial malleolus and that an arithmetic
correction for conduction velocity then be made to
an equivalent of 32°C. Arithmetic correction
for temperature is effective for small variations
from normal but may have inaccuracies beyond a
narrow range. The correlation in normal sub-
jects between temperature and NCV (for sur-
face, subcutaneous, and deep temperatures) has
been well demonstrated in normal subjects, but
these relationships have not been tested in all
pathologic circumstances.
Temperature also affects the size of recorded
potentials (12). The amplitude and duration of
evoked potentials (and therefore the area under the
negative spike) decrease with increasing nerve
temperature throughout the normal physiologic
temperature range. This effect is counterintuitive.
Because higher temperatures cause conduction
velocity to increase, we might expect that this
velocity increase would cause better summation of
the evoked response and thus a larger recorded
amplitude. The unexpected finding can result
from disproportionate change in conduction rates
among the variously sized axons or to the sum-
mated effect of the reduction in individual axon
depolarization durations (13). At the cellular level,
lower temperature is known to slow both ion
diffusion and protein conformational changes.
Slowing conformation changes in the membrane
protein channels alters the time available for ion
flow, particularly Na
since it has a specific time-
dependent closure function, as well as the relative
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46 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
timing of the interdependent gating events. What-
ever the fundamental cause, the net result is that
cooling reduces the magnitude of phase cancella-
tion and thus increases the amplitude and duration
of the recorded sensory potential (Fig. 3-19).
Because temperature significantly affects
nerve conduction velocity and amplitude, and
since arithmetic correction for temperature de-
viation provides no adjustment to amplitude,
limb temperature should be physically controlled
during nerve conduction testing. Recording the
temperature from a standard location during each
examination provides an excellent reference point
for serial studies in individual patients. This extra
step may not be necessary to demonstrate that a
single entrapment (e.g., carpal tunnel syndrome)
is not present when the latency recorded is
normal. However, the information may prove
invaluable for comparison some years later, when
one re-examines the patient for signs of an early
peripheral neuropathy. The amplitude change
caused by temperature is easily masked in clinical
testing since it is superimposed onto the consid-
erable range of what is considered normal for
Figure 3-19 ● Palm-stimulated orthodromic median mixed nerve response (recorded
proximal to the wrist). The amplitude and duration increase with cooling, while the peak latency slows
(lower trace).
sensory and motor conduction studies. It is also
camouflaged by many other factors, such as skin
and electrode impedance, nerve depth, electrode
placement, inadequate stimulation, and nerve or
muscle anatomic variations. Given this variability,
the absolute amplitude value is less useful for
diagnostic purposes than is velocity. The most
helpful diagnostic use for amplitude measure-
ment is along the course of the nerve (i.e., above
and below trauma or entrapment points) and the
serial assessment of amplitude changes occurring
with time following an injury. Test-to-test repro-
ducibility of NCS in single subjects is by far better
than intersubject comparisons. However, care
should be taken to position the electrodes identi-
cally at each session. Right-to-left comparison of
amplitudes of evoked potentials can be helpful in
acute injuries to quantify the degree of potential
axon loss, but even with careful technique, side-
to-side comparisons of CMAPs for the same nerve
can vary by 50% in normal subjects.
Age significantly affects nerve conduction at
the extremes of youth and maturity. At birth,
motor NCVs are approximately half of the veloc-
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CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES 47

ities of a normal adult (see later section for more

on NCS in children). Population-based studies
indicate that aging-related neuronal loss and
nerve conduction slowing are statistically present
by the fourth decade of life (14). This slowing is
small and is obscured by the wide range of the
normal values for the population. It results from
the gradual loss of larger neurons that accompa-
nies aging. Norris found that conduction velocity
decreased by 1.5% per decade after age 60. This
Figure 3-20 ● SNAP recorded from identi-
slowing is seen throughout the body, but some
cal stimulation and recording electrode
authors have reported that unevenly distributed
placements, but with changes in the high-
slowing can occur at common entrapment points frequency filter settings. The largest-ampli-
(15) in a manner similar to other situations where tude response with shortest latency was obtained
entrapment affects nerves that are vulnerable. with the high-frequency filter at 3.2 kHz. Settings at
Although this slowing is gradual on a population 1.6 and 0.8 kHz produced the intermediate- and
basis, our experience has been that some seniors low-amplitude responses, respectively. Note the
beyond 70 years can show accelerated affects. clinically significant shift in the recorded peak
These individuals may show other signs of neu- latency measurement. (Sweep = 1 ms, gain = 20 V.)
ronal loss. Separate reference values based on age
are required for the young and the old.
amplitude, latency, and duration by directly elim-
Height is inversely correlated with NCV.
inating signal components. This alteration in the
Distal conduction slowing is normal in very tall
recorded frequency component is the electrical
subjects (16). This may be due to greater axonal
equivalent of changing the axon velocity distri-
tapering and lighter myelination in the extra-long
bution within the nerve. Filtering out the high
distal segment. Tall individuals may be subject to
frequencies of the SNAP delays the peak latency
greater large-axon loss with aging because of a
enough to affect clinical values (Fig. 3-20) Elimi-
higher metabolic stress related to supplying the
nation of low-frequency components reduces the
more distant axon and nerve endplate. Thus,
amplitude of the CMAP (Fig. 3-21). The ampli-
aging and distal cooling may exaggerate this
fication level of the signal can affect the visual
finding of slower NCV. In elderly and in very tall
estimation of the initial take-off of the evoked
individuals, it is important to test a sufficient
number of nerves to determine if the slowing
recorded at a suspected entrapment point is
merely an accentuation of generalized peripheral
slowing or a clinically significant entrapment. It is
important to temper the diagnosis of generalized
peripheral neuropathy in these individuals. Motor
unit reorganization on needle EMG and other
pathophysiologic changes should be sought to
confirm the diagnosis. Mathematical correction or
the use of a separate reference data set should be
used whenever one encounters extremes of age or
Figure 3-21 ● Motor evoked responses
height. Other biologic factors such as gender (10)
obtained with low-frequency filter cutoffs
are also known to affect NCS values. However, of 16, 32, 160, and 500 Hz (largest to
these factors are not quantitatively sufficient to smallest amplitude response). There is no
require individual correction. shift in the latency of the initial deflection, but the
Technical factors may produce clinically accuracy of identification of the deflection becomes
important changes in the recorded response. more difficult as the amplitude decreases. (Sweep =
Amplifier filters can drastically change recorded 1 ms, gain = 2 mV.)
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48 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
potential response. Computer-based instruments
with their default filter and gain settings and
automatic marker-setting features make these
issues less intrusive in daily testing. However,
less practice with manual settings and markers
results in uncertainty on those occasions when
adjustment is needed. Understanding these issues
is an important part of troubleshooting when
things “just don’t look right.”
Stimulation
Conduction studies begin with an electrical stim-
ulation adequate to simultaneously depolarize
all of the nerve’s axons. Stimulation is typically
accomplished with an electrical current between
two surface electrodes (bipolar stimulation). This
produces an electromagnetic field and axonal
current that opens sufficient axon membrane chan-
nels to initiate depolarization in each axon. The
stimulation electrodes are oriented along the nerve
with the cathode in the direction of the intended
depolarization wave. In a perfect conduction
medium, stimulation would create a symmetric
electromagnetic field in a hemispheric pattern
around the electrodes; however, the irregularity of
body tissue planes and varied tissue conductivity
and impedance distort the field. This field distor-
tion introduces some uncertainty in the point of
initial nerve activation in deeper nerves, so that de-
polarization may not begin directly beneath the
cathode. A supramaximal stimulus is defined as an
intensity 10% greater than the level necessary to
produce the largest observed amplitude in the po-
tential being examined. Accepted testing technique
is to initially stimulate with intensity somewhat
lower than is usually required for maximum re-
sponse and then increase the intensity in 10% to
20% increments until no further increase in the re-
sponse amplitude is seen between stimulations.
Since the depolarization wave proceeds in both
directions along the nerve, various reflex and re-
current late waves are also produced.
Theoretical investigation of the electrical field
produced by bipolar surface stimulation indicates
that it is shaped as a downward-directed cone with
an angle of approximately 70 degrees (Fig. 3-22)
(17). Depolarization of the nerve (or nerves) can
begin anywhere within the volume of this cone.
Distortion of the shape and intensity of the field is
produced in the patient by connective tissue planes,
bones, and other tissue discontinuities. The deeper
the nerve is located and the greater the stimula-
tion intensity used, the larger the volume of the
cone and the more uncertain the exact point on
the nerve at which depolarization begins (see
Fig. 3-22B). This is due both to the increase in
volume covered by the field and to the increased
distortion of the field by the greater tissue irregu-
larity encountered. This small uncertainty in the
point of initial depolarization of the nerve creates a
measurement error in the length of the nerve
segment used in the conduction study (an error that
doubles when two stimulation points are required),
and it contributes to both expanding the reference
normal range for the study and the variance in
repeat testing. In other words, excessive stimulus
intensities increase the size of the stimulation field
and decrease the accuracy of the studies.
Overstimulation also increases the chance
that the stimulus will inadvertently activate other
nearby nerves (see Fig. 3-22D). Unrecognized
stimulation of additional nerves is a major cause
of error in conduction studies. Overstimula-
tion should be considered (in addition to pathol-
ogy and anatomic variation) whenever there is a
change in the configuration of the evoked poten-
tial between two points of stimulation along the
nerve or when the evoked potential shape is not
typical (see Fig. 3-11).
A needle cathode is often effective for the
stimulation of a deep, difficult-to-isolate nerve
(see Fig. 3-22E). A standard monopolar EMG
needle works well, paired with a surface disc
anode. Inserting the needle tip to a point near the
nerve bypasses the high skin impedance. Thus, a
low-voltage, short-duration stimulus (0.05 ms)
often is adequate. Needle electrodes seldom cause
bleeding and present a minimal risk of infection
owing to both their small size (injecting a small
inoculum) and minimal trauma. Theoretical cal-
culations indicate that there is no risk of electri-
cally generated thermal injury to the nerve from
this technique because of low heat generation
and the excellent heat dispersion by the tissue,
combined with the low electrical voltage and
duration of the stimulus (18).
Nerve stimulation is typically uncomfortable
and is perceived as painful by some patients.
Professionalism requires a concern for the patient
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CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES 49

Figure 3-22 ● The cones in each diagram approximate the volume of tissue in which the
electrical field produced by the cathode is sufficient to initiate nerve depolarization. Initial
depolarization may begin anywhere along the nerve within this volume. A. When the intensity of the stimula-
tion field is just adequate to produce nerve depolarization, the initial depolarization point is more likely to be
directly below the cathode. B. Very large stimulation currents increase the uncertainty of this location and re-
sult in activation of a large segment of the nerve, as marked at the dashed lines. C. Stimulation of a nerve at two
locations where the depth of the nerve varies. If the same current is applied to both, the result will be excessive
stimulation (and an uncertain activation point) for the more superficial nerve site (left). D. The high-intensity
stimulation required to produce depolarization of nerve (1) causes unintended depolarization of the nearby
nerve (2). This often occurs when attempting to stimulate a deep-lying nerve from the surface and may result
in an error if a muscle innervated by nerve 2 is near the recording electrodes. An example of this error is shown
in Figure 3-11. E. A needle EMG-type electrode can be used with a surface anode to produce a small, localized
stimulation field (sphere). Needle stimulation can activate a specific nerve (while avoiding others) or permit
stimulation of deep-lying nerves. The lower intensity of the stimulation is better tolerated by many patients.

and practice with the skills necessary to minimize
patient anxiety and discomfort. Explanation and
reassurance during procedures, as well as engaging
the patient in a general conversation during test-
ing, make the experience more acceptable. Also
important is developing an efficient and practiced
approach to frequently performed studies that
minimizes the number and intensity of shocks
delivered. Detailed knowledge of the anatomy
improves placement of electrodes and allows
quick recognition of and adjustment for anatomic
variation. A proactive diagnostic process reduces
the amount of testing required. The standard
stimulation points are both clinically relevant and
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50 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
points where the nerve is relatively accessible.
Firm pressure used to seat the electrodes between
the adjacent structures permits stimulation with
less current. Experience reduces the number of
stimuli needed for a study by providing an edu-
cated guess about the stimulus intensity needed in
an individual. Stimulation with 0.l ms pulse dura-
tion and 150 to 250 V intensity with a constant volt-
age stimulator is usually sufficient. Longer
durations (0.2 to 0.5 ms) are more effective for
larger-diameter axons. Electrical coupling gels
and light skin abrasion reduce the skin impedance
and thus reduce the stimulation intensity required.
Latency
Latency is the time required for the nerve signal
to reach a recording electrode following its stim-
ulation at a single point. Latency, rather than a
calculated velocity, is used to describe conduction
in the terminal segment of motor nerves because
processes other than simple saltatory conduction
are involved that slow the conduction consider-
ably. Motor latencies are obtained by stimulating
near the terminal end of the nerve and recording
the CMAP over the activated muscle. Conduction
across this distal motor latency segment has several
components:
1. Latency of activation: the time between the initi-
ation of the electrical discharge of the stimulator
and the actual beginning of saltatory conduction
Figure 3-23 ● Conduction “environments” of a typical motor nerve, demonstrating the
path of the distal motor latency. From proximal (left) to the motor point of the muscle (right), there
is gradual reduction in the diameter of axons and slowing of the speed of conduction. Finally there is a delay
time for neuromuscular transmission.
along the axon; it represents channel capacitance
charging, channel conformation change, and
initiation of ion flow.
2. Rapid saltatory conduction along the large,
myelinated axons (Fig. 3-23A,B)
3. Slower conduction along the smaller-diameter
myelinated axons as they taper distally (see Fig.
3-23C,D)
4. Still slower conduction along the even smaller-
diameter axons that branch in the muscle (see
Fig. 3-23E)
5. Very slow conduction along the nonmyeli-
nated, terminal twigs of the axon and the end-
plate (see Fig. 3-23F)
6. Exocytosis of the endplate acetylcholine vesi-
cles (see Fig. 3-23G)
7. Diffusion of acetylcholine across the my-
oneural junction, approximately 0.2 to 0.5 ms
(see Fig. 3-23G)
8. Muscle membrane depolarization (see Fig. 3-
23G)
Residual latency is the difference between the
observed distal motor latency and the calculated
time required to conduct along the same terminal
segment distance using the conduction velocity of
the large, myelinated fibers obtained with standard
NCS. For example, if the median nerve forearm
conduction velocity is 50 m/s and the distal segment
used for the motor latency is 8 cm, then the calcu-
lated time for conduction along this segment would
be 0.08 m  50 m/s  0.0016 s  1.6 ms. If the
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CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES 51

actual measured latency is 3.5 ms, then residual
latency is 3.5 ms  1.6 ms  1.9 ms.
In sensory conduction studies the recorded
potential is generated by the nerve, and the latency
consists only of these nerve-related factors:
1. Latency of activation
2. Rapid saltatory conduction along the myeli-
nated axons (Fig. 3-24)
3. Slower saltatory conduction as the axons’ di-
ameter tapers distally
4. Effects of distal nerve cooling
Therefore, since the distal sensory latency
consists only of “nerve factors,” it can be arithmeti-
cally converted into NCV; however, tradition and
practicality favor use of latency, particularly where
comparison to the motor latency is clinically useful.
The distal sensory latency method also eliminates
the chance of arithmetic error. Because motor la-
tencies include the disparate factors that make up
the residual latency, they cannot be arithmetically
converted into meaningful NCVs.
SPECIAL CONDUCTION STUDIES
Late responses allow assessment of very proximal
lesions in problems such as Guillain-Barré syn-
drome, root and plexus injuries, thoracic outlet
syndrome, and sciatic nerve injuries, where access
for standard surface stimulation proximal to these
lesions is not available. Proximal stimulation of
nerves can sometimes be achieved with needle,
magnetic, or high-voltage direct spinal root stim-
ulation techniques. However, late responses, in-
cluding F waves and H reflexes, can provide what
is often a more comfortable and convenient alter-
native.
The F wave results from the recurrent dis-
charge of a small percentage (1% to 5%) of the
alpha motor neurons that are antidromically
activated during peripheral nerve stimulation
(recall that the action potential propagates in
both directions). Upon stimulation of the motor
nerve, the CMAP is produced in the usual manner
by the distal depolarization wave. At the same
time a proximal wave of depolarization eventually
reaches and excites the neuron cell body. The neu-
ron and axon hillock lack the membrane proteins
needed to generate an action potential. Instead,
they produce a generator potential, which is a
voltage flow that does not have a threshold trigger
to the all-or-none firing. The generator potential
produces a sustained voltage elevation that in
some neurons reenters the axon hillock and reini-
tiates the axon’s depolarization following its re-
fractory period. Therefore, the “afferent” and the
efferent arcs of the F wave follow the same alpha
motor neuron axons, passing through all proximal
nerve segments twice (Fig. 3-25). Since different
anterior horn cells redischarge at each stimula-
tion, the latency, shape, and amplitude of the F
wave vary slightly from stimulation to stimulation
(19,20). If a number of stimulations are recorded
and the shortest latency is selected, then a consis-
tent value that represents the fastest-conducting
motor axons is obtained.

Figure 3-24 ● Conduction along a sensory axon. Showing stimulating and recording electrodes
(right). Note the contrast between this rather uniform conducting medium, which involves only rapid salta-
tory conduction, and that illustrated for the motor axon in Figure 3-23.
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52 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY

Figure 3-25 ● F wave represented by a single neuron and its axon. The course of the depo-
larization following stimulation (dot) is shown by the arrows. Initially, depolarization travels both directly to
the muscle fiber, producing the M wave, and retrograde conduction up the axon to the neuron, where the ex-
citation of the neuron causes repropagation in a small percentage of neurons (randomly occurring), resulting
in an action potential returning back down the axon to produce the delayed F wave. The trace below repre-
sents the recording from stimulation (arrow), through M wave (m), and finally the small F wave.

The F wave is not suppressed by higher-
intensity or -frequency stimulation. Its amplitude
is smaller than that of the H reflex or M wave
and is usually less than 500 V. With the small-
amplitude F waves, the initial deflection is hard to
identify, and care must be taken to ensure that the
shortest latency (earliest take-off) of the wave is
used. Recording at least 10 responses is essential
to establish the fastest latency for each analysis
(Fig. 3-26). Proper testing technique also requires
the elimination of voluntary motor unit potential
activity in the nearby muscles.
The F wave occurs in all motor nerves and of-
ten remains present in the face of severe disease.
Weber developed the following formula for pre-
dicting the fastest F wave latency in the ulnar
nerve (3):
0.31  (the distance in centimeters from the
C7 spine to the tip of the ulnar styloid)

(11.05)  (0.123  the forearm velocity
of the ulnar nerve in m/s)
A normal latency will not exceed the pre-
dicted value by more than 2.5 ms (mean  2 SD).
The nomogram provides the upper limit value
(Fig. 3-27) and is conveniently read using a
straightedge. Right-to-left difference for the ulnar
nerve F wave latency should not exceed 1 ms,
and side-to-side comparisons in other nerves are
also within this general range. For this technique,
the ulnar nerve is stimulated at the wrist as for the
8-cm ulnar motor latency, except that the anode
and the cathode positions are reversed (Fig. 3-28).
Stimulation at the wrist avoids the necessity of
recording an F wave on the later phase of the ulnar
M wave or CMAP, since there is considerable time
separating the CMAP and the F wave. With more
proximal nerve stimulation, the arrival times of
the M wave and the F wave become closer and
the F wave can become undetectable in the larger
CMAP. Special collision techniques can be used
to overcome this, but at the cost of considerable
complexity. For testing and for distance measure-
ment, the arm is positioned with the elbow ex-
tended and the shoulder abducted approximately
20 degrees (Fig. 3-29). This position permits testing
of most individuals despite shoulder or other prox-
imal injury.
Because the ulnar forearm NCV is part of the
formula to predict latency, the individual provides
his or her own reference value rather than using a
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CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES 53

Figure 3-26 ● Recording of median F-waves obtained with 10 sequential stimulations of the
nerve. Note that the M wave is very large and is displayed at lower amplification using a split-screen tech-
nique. The F waves on the right vary in latency, amplitude, and shape, as each represents a different subpopula-
tion of the motor neuron pool with axons of different diameters. (Sweep = 5 ms, gain = 500 V [right] and 5 mV
[left].)

general population value. This requires that the
forearm velocity is consistent with the subject’s
other nerves. This approach narrows the range
of the predicted F wave latency value. It also
negates the effect of distal slowing from proximal
entrapment. Therefore, the technique of predict-
ing F wave latency values should be used for prox-
imal entrapments and not for investigation of gen-
eralized neuropathy.
The H reflex is a monosynaptic spinal reflex
response. The afferent axons are the I-a fibers of
the muscle spindle and the alpha motor neuron ax-
ons are the efferents (Fig. 3-30). In infants, the H
reflex is found in many nerves, but it is in only a few
nerves in most adults. The tibial H reflex latency
for a subject is predicted from the formula (21):
(0.46  the length in centimeters from the
midpopliteal crease to the tip of the medial
malleolus)
(0.1  the subject’s age)
(9.14)
Like the F wave normal value above, it
is more easily obtained from the nomogram
(Fig. 3-31). The normal range of variation is
rather large (5.5 ms), but it can be reduced in uni-
lateral problems by comparing the symptomatic
and nonsymptomatic side. The two sides should
vary by no more than 1.2 ms.
90749_ch03(29-64).ps 8/10/06 3:58 PM Page 54

Figure 3-27 ● This nomogram is produced from the linear equation in the text that pre-
dicts the latency time of the fastest of 10 sequential F wave recordings. Connect the distance
(left; measurement method shown in Fig. 3-28) to the forearm NCV (right) and read that line’s intersection in
the center. The range is  2.5 ms (i.e., add 2.5 to the prediction for the maximum normal value). (Reprinted
from Weber RJ, Piero DL. F wave evaluation of thoracic outlet syndrome: a multiple regression derived F
wave latency predicting technique. Arch Phys Med Rehabil 1978;59:464–469, with permission.)

Figure 3-28 ● Distance measurement for ulnar F wave. Record the length (in cm) from the tip
of the C7 spinous process to the tip of the ulnar styloid.
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CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES 55

The H reflex is typically obtained by using a

Figure 3-29 ● Stimulation and recording
technique for obtaining the F wave in the
ulnar nerve. The cathode is placed proximal to
the anode.
longer-duration pulse (1 ms) with stimulation
below that necessary to evoke full muscle con-
traction (M wave) since the larger-diameter I-a
afferent axons are more easily stimulated than are
the motor axons for the F wave. The H reflex
is also suppressed by supramaximal stimulation
intensities and by stimulation frequencies greater
than 1 Hz. Therefore, it can usually be distin-
guished from the F wave by repeated stimulation
while gradually increasing the intensity. The H re-
flex will appear before or near the threshold stim-
ulation intensity for eliciting the M wave. As the
intensity is increased further, the H reflex increases
in amplitude to several mV, and finally diminishes
and disappears as the intensity of the stimulation
increases. At these higher-intensity (supramaxi-
mal) stimulations, the F wave will then be seen
(22).
Late waves are valuable techniques to assess
proximal nerve injury and disease. They can also
be valuable for measuring conduction in very long
nerve segments where multifocal or generalized
slowing is suspected. Late waves can confirm the
presence of distal conduction abnormalities (par-
ticularly for ulnar lesions at the elbow) since late
waves as well as direct conduction must slow
through an entrapment. However, they should
not be used to replace direct stimulation studies

Figure 3-30 ● The H reflex is obtained by stimulation (small arrows) of the afferent sen-
sory fiber (top), resulting in orthodromic conduction to the spinal cord. There, synaptic acti-
vation of the alpha motor neurons occurs, resulting in the H reflex depolarization (H) in the muscle. A few
motor axons are often directly stimulated, producing the rudimentary M wave (m) illustrated. The path is sim-
ilar to a tendon tap, muscle stretch reflex where a small sensory input is amplified to larger motor output; this
is in contrast to the F wave (see Fig. 3-25).
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56 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY

Figure 3-31 ● Nomogram for predicting the H reflex latency based on leg length and age.
Stimulation is at the middle of the popliteal crease and recording from the soleus muscle. Leg length is meas-
ured from the tip of the medial malleolus to the stimulation site. A line from the length to the age will inter-
sect at the predicted latency, and the range is  5.5 ms. Or, as Dr. Johnson often does, one can measure the
H reflex latency and the leg length and then “predict” the person’s age. (Reprinted from Braddom RL, John-
son EW. Standardization of H reflex and diagnostic use in S-1 radiculopathy. Arch Phys Med Rehabil
1974;55:161–166, with permission.)

for segments of nerves that are easily accessible
(e.g., ulnar), since these tests are unnecessarily
complicated by the central nervous system ele-
ments of these circuit. Whereas the F wave is pres-
ent and can be used to test proximal conduction in
most nerves, the H reflex in adults is usually con-
fined to the tibial, median, and femoral nerves
(23).
Spinal Nerve Stimulation
Spinal nerve stimulation (sometimes called nerve
root stimulation) permits conduction testing of the
most proximal portions of the peripheral nervous
system. Johnson has long advocated spinal root
stimulation with monopolar needle electrodes as a
logical way to study plexus and other proximal in-
juries (24). This approach is well standardized for
C8 spinal nerve stimulation (25), and it can be used
at most root levels in reasonably thin individuals.
Both direct measurement of conduction and H-
reflex testing of root or cauda equina function by
spinal nerve stimulation are possible (26). The
spinal root can be stimulated from the surface
using special high-voltage electrical or magnetic
stimulators. We favor needle stimulation of the
root because it causes less patient discomfort than
high-voltage stimulation and is more reliably ac-
complished for deep-lying roots than is magnetic
stimulation.
Spinal nerve stimulation provides both a
direct measure of the conduction velocity and
information about the distribution of velocities
(temporal dispersion) of the full motor axon
complement of the root. This contrasts with the
F wave and H reflex, which can assess only a
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CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES
limited portion of the axons. On the other hand,
the size and shape of the evoked potential gener-
ated by spinal root stimulation cannot be directly
compared with the response generated distal to
the suspected lesion, since the peripheral nerve
contains axons from more than one nerve root.
Because the number of axons that a particular
nerve root contributes to a given peripheral nerve
varies, the normal response generated in a specific
muscle with spinal nerve stimulation also varies
among the population. Nonetheless, considerable
information can be derived from the shape and
temporal dispersion of the response, and from the
conduction velocity calculated from spinal nerve
stimulation.
C8 is the most frequently tested spinal nerve.
The procedure is safe and relatively painless,
particularly if stimulation can be restricted to sev-
eral trials. A standard monopolar, Teflon-coated
EMG needle is used as the cathode, and a large
surface electrode applied near the midline is the
anode. Stimulation can often be obtained with
stimulus durations of 0.05 to 0.10 ms and an
intensity of less than 100 V. The higher stimula-
tion intensities available with commercial EMG
stimulators can be employed without danger of
tissue injury related to electrical or thermal effects.
Figure 3-32 ● Needle placement for stimulation of the C8 spinal nerve. The insertion site is
2.5 cm from the spinous process, with a 30-degree medial angle of the needle.
57
To stimulate C8, the needle should be inserted
approximately 1 inch lateral to the inferior border
of the C7 dorsal spine, angled 30 to 45 degrees to-
ward the midline, and advanced through the
paraspinal muscle until it strikes the transverse
process (Fig. 3-32). If the first attempt at stimula-
tion is not successful, the needle can be slightly
repositioned until a good response is obtained.
With C8 stimulation, the abductor digiti
minimi is usually chosen as the CMAP recording
site because the lower plexus and ulnar nerve
components are most often of interest in proximal
entrapment syndromes. Normal conduction ve-
locity with this method is 68  3 m/s (normal 62
m/s or more). Distance is measured from the point
of needle insertion to the ulnar nerve motor
latency stimulation location at the wrist (8 cm
from E1). The arm is positioned as for the F-wave
study (see Fig. 3-29). When recording from the
abductor pollicis brevis using this C8 stimulation
method to assess the median nerve, the normal
conduction velocity is 70  2.7 m/s (normal 65 m/s
or more). If the latencies for both the median
nerve and the ulnar nerve are measured with this
C8 nerve stimulation method, then the mean
difference between the two latencies is 1.7 ms or
less (27). If the spinal nerve stimulation response is
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58 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
abnormal, it is important that all peripheral
segments be tested in order to localize the point of
abnormality. Spinal nerve root stimulation, F
wave, and H reflex techniques offer a means of
confirming abnormalities in peripheral conduc-
tion across particularly challenging areas, such as
the ulnar groove, because peripheral slowing
should also be detectable by these techniques.
However, these studies of long segments should
not be the primary indicator of abnormality at
these more peripheral locations of short segment
or focal injury.
Stimulation of each of the cervical spinal
nerve roots up through C5 can be performed in a
manner analogous to that for C8. In the lumbar re-
gion (28), the spinal nerve root stimulation also
uses a lateral approach with the needle angled 30 to
45 degrees toward the midline. For S1, the point of
entry is medial to the posterior superior iliac spine
and approximately 3 to 5 cm lateral to the midline.
A 75-mm-long needle electrode may be required
for stimulation of the lumbar or S1 spinal nerves.
Innervation of the anal sphincter can be assessed by
stimulation of a sacral-level spinal nerve with a
needle electrode at the respective sacral foramen
(29). Although this technique of recording the
CMAP from the anal sphincter is well tolerated, it
is helpful to prepare the patient by explaining what
to expect before the stimulus occurs and providing
some counterirritant pressure in the area of the
stimulation to reduce its sensory impact.
COMMON ERRORS
Computerized electrodiagnostic equipment makes
it increasingly easy to capture a nerve response.
Unfortunately, there is no guarantee that the signal
recorded is the one that was sought or that it was
not distorted by technical problems. The increas-
ing automation can protect the subject from some
careless errors with the instrument, but it also can
mask clues that something is amiss. It is a useful
exercise to periodically review the common sources
of error in order to maintain a high vigilance.
Common sources of error include:
1. All stimulations and recorded signals are vol-
ume conducted; they arise in and are carried
through a volume of nearby tissue that conducts
the current. Unintended nerves in the vicinity
can be stimulated, and unintended nerve or
muscle responses can be recorded. Often a slight
initial-positive response is the only clue to a
problem. It results from initial muscle depolar-
ization occurring some distance away from the
E1 electrode. It is surprising how closely an ul-
nar volume-conducted response, recorded over
the thenar muscles (see Fig. 3-11), resembles the
expected median response in the situation
where the median response is absent in a patient
with severe carpal tunnel syndrome. Always
consider volume conduction when response
shape is not crisp and proper.
2. It is easy to mistake a general slowing of
conduction for focal entrapment if you just rush
through the study, do not think about other
diagnostic possibilities, and fail to check several
nerves for comparison. Since nerves can be un-
evenly involved in an early neuropathy, be cer-
tain the others are normal before deciding that
the initially tested nerve is focally entrapped.
3. Cold nerves cause mistakes. Monitor tempera-
ture throughout the examination. Evaporative
cooling and vasoconstriction quickly decrease
temperatures. It is easy to miss the effects of
cool nerves, age, and height when testing using
very short sensory nerve segments.
4. Technical mistakes happen. Sooner or later you
will reverse the stimulator’s cathode and anode,
use the wrong filter or amplifier setting, meas-
ure distance in error, or stimulate the wrong
nerve. If the signal or value does not look right,
take the time to exclude technical error.
5. Rigid adherence to a standardized technique is
essential in NCS. Deviation from the reference
approach, particularly in short segment studies
in which normal ranges are quite tight, is never
a good idea.
6. Always anticipate possible anatomic variation.
The challenge of the Martin-Gruber anasto-
mosis is not only in recognizing the “wildly”
fast median nerve velocity recorded in carpal
tunnel syndrome, but also in seeing the clue of
the change in the ulnar-innervated evoked po-
tential it also produces.
7. Never ignore inconsistencies in the findings
from your recordings. Patients rarely have in-
explicable, inconsistent nerve function, and
neither should your reports.
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CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES
Reporting Numbers
Computer-based instruments can report results to
an extreme number of decimal places. While
values with two or three decimal places seem more
precise, they are, in fact, deceptive. The precision
of any value is limited by the precision of its least
reliable component. Although the elapsed time of
latency can be accurately recorded by the computer
to many decimal places, the value of the number is
limited by the uncertainty in the distance the signal
has traveled, the inherent variability in channel
opening, acetylcholine diffusion, and rise time of
signals that trigger the timing. Measurement
distance is restricted mechanically and by the
inherent uncertainty as to the point of initial
depolarization along the nerve. Clinical studies
have been shown vary by up to 5% when trials
are immediately repeated and by up to 10% if re-
peated after an interval of several days (30). Then
what numbers are meaningful in a report? Whole
numbers are appropriate for reporting velocity. At
50 m/s, a change of 1 m/s is a 2% variation, much
more “precise” than the 5% standard measurement
accuracy underlying the test. Similarly, a distal la-
tency variation of 0.l ms represents a 5.5% variation
for a short segment median sensory (mean median
nerve reference value less than 3.8 ms) conduction
study. While each study has its own technical
aspects affecting accuracy and reproducibility, the
general guideline of reporting conduction veloci-
ties as whole numbers and using increments of
0.1 ms for reporting latencies remains valid.
NERVE CONDUCTION STUDIES IN
CHILDREN
Many electrodiagnosticians limit their practice
to adults because of the perceived technical and
personal demands of examining children. Nev-
ertheless, a well-planned pediatric study is no
more difficult and relies on the same basic
knowledge of pertinent anatomy, neuromuscular
diseases, and nerve and muscle development as an
examination in adults. Depending on the clinical
problem, a focused study in a child can produce the
diagnosis, direct further diagnostic studies, or pro-
vide pertinent information to guide intervention or
prognostication. Using general electrodiagnostic
59
techniques, an adequate pediatric study can be
accomplished with reasonable ease; just a mod-
icum of special techniques or equipment provides
the examiner with extra assistance in completing
the task. True, experience with pediatric studies
allows the examiner more assurance in planning
and performing the studies, but this can be gained
incrementally by beginning with more limited
problems. It is often the fear of the event (for the
child, family, or examiner) rather than the actual
examination that creates the negative experience.
A confidently and efficiently performed study will
reduce the discomfort to all parties and will pro-
vide useful diagnostic information.
Development and Maturation
A number of studies have documented the effect of
age on both motor and sensory nerve conduction
values (31–37). NCVs in newborns are about
half those found in adults. Significant maturation
of the peripheral nervous system occurs in the
first year of life, with rapid changes noted in con-
duction studies (32,35,38). Clinically, maturation
appears to be more rapid in motor than sensory
fibers when comparing amplitudes of response
and conduction velocities (38). In infants and
children under age 2 years, upper and lower
extremity NCVs have similar values. Addition-
ally, each nerve tends to exhibit its own pattern of
conduction maturation. As a rule of thumb, motor
NCVs in infants are usually no less than 20 m/s.
Developmental-based conduction velocity graphs
show the expected increases in velocities with age
(31,35,37). As expected, late responses like F waves
also show maturational changes. The pediatric
median values for conduction velocity in all nerves
continue to gradually increase, reaching adult
values between the ages of 4 to 6 years. When using
published normal values for conduction studies, it
is of the utmost importance that the examination
techniques are precisely the same as those used in
determining the standard values. Proper segment
length measurement and temperature control are
more important than in adults.
As one would anticipate, there are also
changes in distal latencies and in CMAPs with
peripheral nerve maturation. In the newborn,
distal motor latency values obtained at constant
distances decrease with increasing conceptual
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60 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
age (37). Some distal latency measurements re-
ported in children are quicker than those reported
in adults because of the smaller segment distances.
These distal latency values begin to approach
adult values at the same distances after age 2 years.
By age 6 months, CMAPs triple in amplitude by
both peripheral nerve and muscle maturation
(36,38). Recording of mild degrees of abnormal
temporal dispersion of the response may be diffi-
cult in the face of incomplete development of
myelination in infants. Consequently, what may
be noticed is the resultant lowering of the action
potential’s amplitude.
Sensory conduction velocities also increase
with maturation, with an increase of as much as
0.8 m/s per week of conceptional age in neonates
(39). SNAPs also increase significantly in the first
6 months, with a tripling of amplitude. By about
age 3 years, lower limits of adult values are at-
tained. Two-peaked SNAPs have been reported
in neonates.
Techniques in Pediatric Electrodiagnosis
Maintaining proper subject temperature is essen-
tial during NCS. Maintaining body temperature
is critical to the well-being of newborn and
premature infants as well as being important
electrodiagnostically because of the effect of low
subject temperature or poor temperature control
on conduction velocities. Infants can be studied
in the incubator or with an overhead warmer.
Maintaining a skin temperature of 36° to 37°C
produces appropriate near-nerve temperatures of
37° to 38°C and avoids spurious results. In older
children, anxiety or crying can produce limb
cooling due to sweating and evaporation, another
reason to do the conduction studies before the
more painful needle examination.
Conduction studies require meticulous care
because infants have such short extremities and
the segments studied may be only 6 cm in length.
Small stimulators with an interelectrode distance
of 10 to 15 mm are commercially available and
simplify testing of short nerve segments. The elec-
tromyographer must avoid errors in segment
length measurements because a discrepancy of
only 1 cm will produce as much as a 15% velocity
error. Measurement is inherently difficult in
infants since fat often hides bony landmarks and
the skin “shifts” with pressure. The limb should
be properly immobilized throughout the study.
Electrode placement for sensory studies should al-
low at least a 2-cm separation between E1 and E2.
Shock artifact is often a problem when ex-
amining children because of the shortened dis-
tances between the stimulator and the recording
electrodes. Artifact can often be reduced by
cleansing the skin with pumice paste to reduce skin
impedance, thus permitting adequate stimulation
with lower electrical currents. Using minimal
amounts of conduction cream combined with
small-sized surface electrodes is helpful. Shock
artifact may be minimized if the ground electrode
is placed between the stimulating and recording
electrodes. Grounding with a ring electrode posi-
tioned around the wrist or ankle, or taping the
ground disc to the dorsal surface of the hand is
usually sufficient. Use of a needle electrode as the
stimulating cathode when testing infants offers
some advantages: stimulation is accomplished with
as little as 10% of the usual current, there is less
discomfort, and there is more precise localization of
the site of the stimulus (an important feature when
studying very short nerve segments).
Accuracy in technique is necessary to achieve
reliable results and to compare results with pub-
lished normative data. As in adult studies, the
configuration of the evoked potential at the pro-
ximal and distal stimulation points should be
compared to ensure that neither the stimulus has
been volume conducted to another nerve nor a vol-
ume-conducted response has been recorded from a
distant muscle. These errors, like measurement, are
more likely because of the small-sized patient.
In general, NCS should be a part of a routine
electrodiagnostic examination in children. De-
pending on the clinical findings and direction of
the study, at least one sensory and one or two
motor conduction studies should be performed.
The same nerves that are most useful diagnosti-
cally in adults are also the ones most frequently
studied in pediatric examinations. Studies are per-
formed similarly, relying on the same landmarks
to establish stimulation and recording sites. For
motor conduction studies, the peroneal nerve is
the most easily studied of those available in the
lower limb. Distal stimulation requires careful
placement of the ground electrode. The ulnar and
the median nerves are readily available for upper
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CHAPTER 3 • BASIC NERVE CONDUCTION TECHNIQUES
limb evaluation. In evaluation of a generalized
process, at least one sensory nerve study should be
performed. Sensory potentials are easily elicited in
newborns. Conduction velocities can be calculated
for sensory nerves but are no more routinely help-
ful than standardized sensory distal latency in
infants. Both antidromic and orthodromic studies
of median and ulnar nerves can be performed.
Despite its initial triggering of the grasp reflex in
infants, stimulation at the digits or palm is possi-
ble, since there is often accommodation of the
reflex to the stimulus. The musculocutaneous (lat-
eral antebrachial cutaneous) nerve offers another
useful option for a sensory study that avoids the
reflex and size problems of the hands. Sural
sensory responses are easily obtained from the
lower extremities in normal infants.
Late responses can be very helpful in evalua-
tion of the infant peripheral nervous system.
They offer certain advantages: fewer problems
with temperature control, longer distance of
conduction and reduced distance measurement
error, and a single site of stimulation. The H re-
flex can be elicited from any muscle during
infancy, but most are gradually suppressed by the
age of 1 year. The tibial nerve, of course, retains
the H reflex throughout life. Using the standard
adult technique, the recorded latency is related to
both age and leg length (35,40). The F wave can
be elicited in any peripheral motor nerve, and
the latency changes with age, limb length, and
nerve temperature. Correct supramaximal (F)
and submaximal (H) stimulations and appro-
priate waveform identification are essential in
infants, since both the H reflexes and F waves can
be present in most muscles (41), and they can be
confused with one another.
Common Diagnostic Problems
The Newborn
Several focal neuropathies occur with some regu-
larity in the newborn. The most common is
brachial plexus palsy. Birth-related brachial plexus
palsies usually affect the upper trunk but can in-
volve a more significant portion of the plexus. The
mechanism of injury involves the cervical roots as
much if not more than the plexus itself. There have
been reports of membrane instability found on
early examinations (less than 7 to 10 days from
61
birth), but no definitive studies have been pub-
lished to show the onset of membrane changes in
infants following nerve injuries to make accurate
correlations with time of injury (and relationship
to delivery). The palsies can be studied serially at
about 6- to 8-week intervals to assist with diagnos-
tic and prognostic information (42). Conduction
studies with stimulation at Erb’s point and record-
ing of CMAPs from proximal muscles should be
done, especially if no motor units are found on nee-
dle examination. Comparison of the CMAP to the
same muscle on the uninvolved side can be helpful.
Presence or absence of response, reduced ampli-
tude of response, or prolonged latency can provide
information related to the injury. Caution must be
taken in surface stimulation at Erb’s point in
preterm or newborn infants, since first-degree
burns can be produced on their thin, fragile skin.
The needle examination provides the most impor-
tant prognostic information and can help direct
therapy and provide information regarding future
recovery. Follow-up studies have shown that half
of the children develop age-appropriate distal la-
tency and conduction velocities in median and ul-
nar nerves by age 3 years (43).
Childhood and Adolescence
Focal neuropathies are the most common EMG
referrals in childhood and adolescence, often seen
following skeletal fracture, or peripheral entrap-
ment or compression (44). Brachial plexus injuries
and isolated nerve injuries are seen in children and
adolescents who sustain traumatic brain injuries,
with or without fractures. Carpal tunnel syndrome
has been reported in young teenagers (45). Phrenic
nerve injury occurs in up to 10% of pediatric
cardiac surgery cases (46). Electrodiagnostic tech-
niques are the same as those used in adult studies.
Serial testing can provide diagnostic as well as
prognostic information in acute nerve injuries.
Acquired neuropathies secondary to other disease
processes have had only minimal discussion in
the pediatric electrodiagnostic literature. In type 1
diabetes mellitus, motor NCVs of the lower ex-
tremity and sensory NCVs were reduced in 30% to
40% of those tested (47). A correlation was found
between the slowed conduction and the degree of
glycemic control. Changes in conduction velocities
are seen as early as 5 to 6 months after the diagno-
sis of juvenile-onset diabetes mellitus is made (48).
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62 SECTION I • INTRODUCTION TO ELECTROMYOGRAPHY
Less often, electrodiagnostic evaluation dur-
ing childhood is requested for evaluation of a gait
disturbance or because of progressive weakness.
The electromyographer must consider the history,
family history, and clinical examination to det-
ermine a differential diagnosis. Onset of spinal
muscular atrophy type II and type III is seen in this
age group. Hereditary polyneuropathies become
functionally obvious during this time and medical
evaluation is sought. Hereditary motor and sensory
neuropathy type I (previously known as Charcot-
Marie-Tooth) has an onset in early childhood and is
associated with foot deformities, although with
little muscle wasting early on. Marked slowing of
motor conduction velocities, usually to less than
50% of normal, is usually present with hereditary
motor and sensory neuropathy type I (49). Maximal
slowing of motor NCVs develops over the first 3
to 5 years of life (50). Hereditary motor and sensory
neuropathy type II generally has a later age of on-
set; it is largely an axonal disorder, and conductions
are normal or minimally reduced. Additionally, it
is often at this age that the degenerative diseases
of the central nervous system, with associated de-
myelinating polyneuropathies, present. Metachro-
matic leukodystrophy is noted within the first 2
years of life, but later juvenile onset does occur (51).
Duchenne muscular dystrophy must be considered
in boys age 3 to 4 with gait abnormalities, positive
Gower sign, and inability to run. Other etiologies to
be considered in the acute onset of weakness in
childhood are Guillain-Barré syndrome, dermato-
myositis and polymyositis, and myasthenia gravis.
The most common abnormality in motor conduc-
tion velocities in childhood-onset Guillain-Barré
syndrome is a reduction of CMAP amplitude (52).
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and young adults after 5 to 6 mo of IDDM.
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515–519.
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metachromatic leukodystrophy: biochemical
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II
Technical Aspects of EMG
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CHAPTER 4
Electrophysiology
Jun Kimura
ELECTRICAL PROPERTIES OF NERVE
AND MUSCLE
The same basic membrane physiology applies to
both nerve and muscle, although different
anatomic substrates subserve propagation of elec-
trical impulses. The magnitude of the transmem-
brane potential in a steady state dictates the
excitability of the tissues. Thus, understanding
membrane physiology at the cellular level requires
the knowledge of the ionic concentration of cell
plasma and its role in maintaining transmem-
brane potentials. If an external stimulation depo-
larizes the cell to a critical level, called threshold, an
action potential is initiated at the stimulus site,
which then propagates across the membrane. The
interstitial tissues act as a volume conductor when
analyzing extracellular potentials by surface or
needle electrodes in clinical electrodiagnosis. This
chapter summarizes the basic physiology of the
propagating action potential through volume con-
ductors, which dictates the waveform of the
recorded potentials.
Transmembrane Potential
The muscle membrane forms the boundary be-
tween intracellular fluid in cell cytoplasm and ex-
tracellular interstitial fluids. Approximately equal
numbers of ions are dissolved in both compart-
ments, but the cell is negative inside as compared
to outside with a steady transmembrane potential
(Em) of some
90 mV in the human skeletal mus-
cle at rest (1). To maintain the steady-state equi-
librium, the concentration gradient of potassium
(K), sodium (Na), and chloride (Cl
) ions
(Table 4-1) must counter this electrical force (Fig.
4-1). For example, the ionic concentration differ-
ence pushes K from inside to outside the cell, re-
flecting the higher concentration inside, whereas
the negative equilibrium potential pulls the posi-
tively charged K from outside to inside the cell.
Table 4-1 shows the transmembrane poten-
tial of EK (
97 mV), ENa (66 mV), and
ECl
(
90 mV) theoretically required to establish
such equilibrium based solely on their ionic con-
centrations. These compare with the actual trans-
membrane potential (
90 mV) in the example
under consideration. Thus, ionic concentration
and transmembrane potential alone cannot main-
tain these ions in perfect balance. The other fac-
tors of import include selective permeability of the
cell membrane to certain ions and the energy-
dependent sodium-potassium (Na-K) pump.
In the case of K, its inward transport by the
energy-dependent Na-K pump makes up for the
small discrepancy between EK (
97 mV) and Em
(
90 mV). Here, electrical force (
90 mV) plus
the pump transport (approximately equivalent to

7 mV) from outside to inside the cell counteracts
almost exactly the concentration gradient (equiva-
lent to
97 mV) from inside to outside the cell.
Both the concentration gradient and potential dif-
ference (
90 mV) pull the Na from outside to
67
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68 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 4 - 1 Compositions of Extracellular and Intracellular Fluids of Mammalian

Muscle (19)

Extracellular (mmol/l) Intracellular (mmol/l) Equilibrium Potential (mV)

Cations

Na 145 12 66
K 4 5
97
Others 5 - -

Anions

Cl
120 4
90

HCO
3 27 8
32
Others 7 155 -
Potential 0 mV
90

inside the cell, but only a small amount of the ion
moves because of the impermeability of the cell
membrane. Active transport of Na from inside
to outside by the Na-K pump counters the small
inward Na leak to maintain the equilibrium.
Generation and Propagation
of Action Potential
As mentioned above, a voltage-sensitive channel
regulates the conductance of Na and K ions
across the membrane depending on the transmem-
brane potential. In the resting stage, K channels
are open and Na channels are closed. An exter-
nally applied current induces negativity under the
cathode, or negative pole, thus making inside the
axon relatively more positive, or cathodal depolar-
ization. Subthreshold stimulation produces a self-
limited local change in the transmembrane poten-
tial that diminishes with distance. Threshold or
suprathreshold stimulation depolarizes the mem-
brane to a critical level by 15 to 25 mV from
90
mV to
65 to
75 mV in the human muscle cell
(1). This degree of depolarization opens the volt-
age-dependent Na channels, causing a 500-fold
increase in Na permeability, which initiates the
sequence of events leading to nerve excitation.
The increased conductance or permeability
allows Na to enter the cell, further depolarizing
the cell, which in turn accelerates inward move-
ment of this ion. This sequence results in dramatic
change of Na permeability, with an explosive re-
versal of membrane potential from
90 mV to
20 mV. An action potential thus develops in an
all-or-none fashion; that is, the same maximal re-
sponse occurs regardless of the kind or magnitude
of the stimulus (Fig. 4-2). In other words, a switch
from the K to Na equilibrium constitutes the
generation of an action potential. This negative-
to-positive shift of intracellularly recorded mem-
brane potential can be recorded as negative spike
extracellularly, or upward deflection according to
the convention of clinical electrophysiology.
With depolarization of membrane potential,
permeability to K also increases, but only after a
delay of about 1 ms. At about the same time, the
increased Na permeability falls again to near the
resting value with closure or inactivation of Na
channels. Inactivated Na channels cannot be
open for a few milliseconds even if the membrane
is depolarized again above the critical level. This
inactivation forms the basis of the refractory pe-
riod. Inactivation of Na conductance, together
with increased K permeability, results in a rapid
recovery of the cell membrane from depolariza-
tion. After the potential falls precipitously
towards the resting level, a transient increase in
K conductance hyperpolarizes the membrane,
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CHAPTER 4 • ELECTROPHYSIOLOGY
Figure 4-1 ● Simplified scheme of active
and passive fluxes of potassium (K
),
sodium (Na
), and chloride (Cl) in the
steady state, with driving force on each ion
shown by vectors. For K, the efflux along the
concentration gradient equals the influx caused by
the electrical force plus the active influx by the Na-K
pump. For Na, the electrical and chemical gradient
produces only a small influx because of membrane re-
sistance. The sum of the two equals the active efflux
by the Na-K. For chloride, the concentration gradi-
ent almost exactly counters the electrical force. The
ratio of Na and K exchange by a common electro-
genic pump averages 3:2, although this diagram illus-
trates a neutral pump with a ratio of 1:1. (Reprinted
from Kimura J. Electrodiagnosis in diseases of nerve and
muscle: principles and practice. New York: Oxford
University Press, 2001, with permission.)
which then returns slowly to the resting state,
completing the cycle of repolarization. The total
amount of Na influx and K efflux during the
course of an action potential is too small to alter
the concentrations of these two ions in the intra-
cellular and extracellular fluids.
69
An action potential initiated at one point on
the cell membrane sets up an intracellular current
that flows from the positively charged active area
to the adjacent, negatively charged inactive re-
gions. A return current flows from the inactive to
active region through the extracellular fluid, com-
pleting the circuit (2). Thus, the local current en-
ters the cell at the site of depolarization (i.e., sink)
and passes out from the adjacent polarized regions
on both sides of the active area (i.e., sources).
When depolarization at the sources reaches the
threshold, an action potential is generated, form-
ing a new sink, which in turn gives rise to a new
Figure 4-2 ● Schematic diagram of graded
responses after subthreshold stimuli and gen-
eration of action potentials after suprathresh-
old stimuli. Experimental arrangement shows in-
tracellular stimulation (I) and recording electrodes
(E) on top (A) and polarity, strength, and duration of
a constant current on bottom (B). Hyperpolarizing
(1) and subthreshold depolarizing current (2) induce
a nonpropagating local response. Current of just
threshold strength will produce either local change
(3a) or an action potential (3b). Suprathreshold stim-
ulation (4) also generates an action potential but with
a more rapid time course of depolarization.
(Reprinted from Woodbury JW. Action potential:
properties of excitable membranes. In: Ruch TC, ed.
Neurophysiology, 2nd ed. Philadelphia: WB Saunders,
1965:26–57, with permission.)
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70 SECTION II • TECHNICAL ASPECTS OF EMG

Figure 4-3 ● Diagrammatic representation of an action potential in A fibers of the cat with
the spike and negative and positive after potentials drawn in their correct relative size and
true relationships. (Reprinted from Gasser HS. The classification of nerve fibers. Ohio J Sci 1941;41:
145–159, with permission.)

local current in both distal and proximal direc-
tions. This results in orthodromic as well as an-
tidromic volleys of the action potential from the
original site of depolarization.
In an extracellular recording, an action po-
tential consists of an initial negative spike of about
1 ms in duration, representing the intracellular
positive spike of depolarization, and two subse-
quent after-potentials, depolarizing and hyperpo-
larizing (Fig. 4-3). The first externally negative
deflection grafted onto the declining phase of the
negative spike, a supernormal period of excitabil-
ity, presumably represents sustained internodal
positivity and the extracellular accumulation of
K associated with the generation of an action
potential. The subsequent externally positive
after-potential, a prolonged subnormal period of
excitability, reflects the elevated K conductance
at the end of the action potential combined with
an increased rate of the Na-K pump to counter
the internal sodium concentration.
ANATOMY AND PHYSIOLOGY OF THE
NEUROMUSCULAR JUNCTION
The neuromuscular junction consists of the motor
nerve terminal, junctional cleft, and muscle end-
plate. The release of acetylcholine (ACh) ensures
unidirectional conduction from the axon terminal
to the muscle endplate, similar to synaptic trans-
mission in a sequence of neurons. Other charac-
teristics of the chemical mode of transmission in-
clude a synaptic delay of a fraction of a millisecond
and nonpropagating nature of postsynaptic poten-
tials. Such a local potential causes no refractori-
ness, unlike the all-or-none response of the nerve
or muscle action potential. Temporal as well as
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CHAPTER 4 • ELECTROPHYSIOLOGY 71

spatial summation after subliminal stimuli pro-
vides greater flexibility and adaptability for
graded responses. As in a synapse, the mobiliza-
tion store must continuously replenish the liber-
ated transmitter molecules, so that the neuromus-
cular junction would not fail due to depletion of
immediately available molecules.
Motor Endplate
The term “motor endplate” describes the postsy-
naptic membrane of the striated muscle, where
the specialized motor nerve efferent endings ter-
minate. Each muscle fiber usually has only one
endplate, innervated by a branch of the motor
axon. At the nerve terminals, Schwann cells with-
out myelin (teloglial cells) separate the axon from
the surrounding tissue. Thus, the neuromuscular
junction consists of the motor nerve ending,
Schwann cells, and muscle endplate (Fig. 4-4).
After the nerve ending loses the Schwann cells at
the junctional region, the axon terminal forms a
flattened plate within a surface depression of the
sarcolemma. This indentation of the muscle fiber,
measuring about 200 to 500 Å deep, is called a
synaptic gutter or primary synaptic cleft. The

Figure 4-4 ● Motor endplate as seen in histologic sections in the long axis of the muscle
fiber (A) and in surface view (B) under the light microscope, and a section through the mo-
tor endplate (area in the rectangle in A) under the electron microscope (C). The myelin sheath
ends at the junction at which the axon terminal fits into the synaptic cleft. The Schwann (teloglial) cells cover
the remaining portion without extending into the primary cleft. The membrane of axon (axolemma) forms the
presynaptic membrane, and that of muscle fiber (sarcolemma) forms the postsynaptic membrane of the motor
endplate. Interdigitation of the sarcolemma gives rise to the subneural or secondary clefts. The axon terminal
contains synaptic vesicles and mitochondria. (Reprinted from Bloom W, Fawcett DW. A textbook of histology,
10th ed. Philadelphia: WB Saunders, 1975, with permission.)
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72 SECTION II • TECHNICAL ASPECTS OF EMG

thickened postsynaptic membrane in this region
has a large number of mitochondria, nuclei, and
small granules close to the narrow infoldings
called the junctional folds or secondary clefts.
Diseases of neuromuscular transmission alter the
motor endplate profile (Fig. 4-5).
Electron-microscopic studies of the human
external intercostal muscles (3) show clear, round
synaptic vesicles in the axon terminals, mostly
clustered in the regions called active zones. The
vesicles, containing ACh, are released into the
synaptic cleft from this site. Approximately 50
synaptic vesicles are counted per square microm-
eter in a nerve terminal that occupies an area
close to 4 m2. The synaptic basal lamina, inter-
posed between the nerve terminal and muscle
cell, stores acetylcholinesterase (4). The postsy-
naptic membrane area is 10 times larger than the
presynaptic membrane, forming elaborate junc-
tional folds (5). The postsynaptic junctional folds
containing a high concentration of ACh receptors
cover an area about 2.5 times that of the terminal
itself. The nicotinic ACh receptor, an ionotropic
glycoprotein, comprises five subunits,  (alpha)
2,  (beta),  (gamma), and  (delta) in the fe-
tus and 2, , (epsilon), and  in the adult.
Binding of two ACh molecules to the two  sub-
units initiates the opening of the ACh channel,
allowing cations (predominantly Na) to move
through the postsynaptic membrane, with the net
result of depolarization (6).
The presynaptic axoplasm stores the synaptic
vesicles, which are intracellular structures 300 to
500 Å in diameter that encapsulate ACh mole-
cules. The nerve endings also contain high con-
centrations of choline acetyltransferase, which
synthesizes ACh, and acetylcholinesterase, which
hydrolyzes ACh. The presence of the neurotrans-
mitter and the two enzymes in the proximal por-
tions of neurons suggests that enzymatic synthesis
takes place in the cell body before they are trans-
ported to the nerve terminals (7). Each vesicle con-

Figure 4-5 ● Schematic representation of the motor endplates in normal control, myas-
thenia gravis, and myasthenic syndrome drawn to the scale of the mean figure. The dia-
gram shows in simplified form the loss of the postsynaptic membrane in myasthenia gravis and marked hy-
pertrophy in myasthenic syndrome. (Reprinted from Engel AG, Santa T. Histometric analysis of the
ultrastructure of the neuromuscular junction in myasthenia gravis and in the myasthenic syndrome. Ann NY
Acad Sci 1971;183:46–63, with permission.)
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CHAPTER 4 • ELECTROPHYSIOLOGY
tains a quantum (5,000 to 10,000 molecules) of
ACh (8). A small portion of quanta (about 1,000) is
located adjacent to the cell membrane for imme-
diate release; many more (10,000) are contained in
the mobilization store, which moves continuously
toward the membrane to replace liberated ACh.
The remaining and largest portion of quanta
(300,000) forms the main store as a reserve supply
for the mobilization store.
Electrical Activity at the Endplate
Random release of a single quantum of ACh
from the nerve terminal (9) induces a small de-
polarization of the postsynaptic membrane
known as the miniature endplate potential
(MEPP). The MEPP averages 1 mV in ampli-
tude if recorded with a microelectrode inserted
directly into the endplate region, but only 50 to
100 V when registered with an ordinary needle
electrode placed near the endplate of the muscle
fibers. Each ACh vesicle contains a quantum, or
a nearly equal number, of ACh molecules irre-
spective of external factors, thus maintaining the
MEPP amplitude (a measure of quantum size)
relatively constant. In contrast, the release of vesi-
cles, and the occurrence of MEPPs, varies over a
wide range in frequency, such as increasing with
elevated temperatures.
Depolarization of the motor nerve terminal
leads to the influx of calcium (Ca2), enhancing
quantal release by increasing fusion of the ACh
vesicles with the nerve membrane. The resulting
synchronized release of many ACh vesicles results
in summation of MEPPs, giving rise to a localized
endplate potential (EPP). The number of immedi-
ately available ACh quanta and the voltage-
dependent concentration of Ca2 within the axon
terminal together determine the size of the EPP.
The number of quanta emitted per nerve impulse,
or quantum content, averages 25 to 50, based on
the amplitude ratio of EPP/MEPP.
Like MEPPs, EPPs result from depolariza-
tion of the motor endplate by ACh. The opening
of ACh receptors by the synaptic transmitter in-
creases the conductance of positively charged
ions, including Na and K. The diffusion of
these ions down their electrochemical gradients
results in depolarization of the motor endplate.
This nonpropagated local response begins about
0.5 ms after the release of ACh, peaks in about
73
0.8 ms, and decreases exponentially, with a
half-decay time of about 3.0 ms. The EPP, a
graded rather than all-or-none response, in-
creases in proportion to the number of ACh
quanta liberated from the nerve terminal and the
sensitivity of the endplate to ACh molecules. It
declines rapidly with distance from the endplate.
Like the excitatory postsynaptic potential, two or
more subthreshold EPPs, if generated in near
synchrony, can summate to cause a depolariza-
tion exceeding the critical level for generation of
an action potential.
When the EPP exceeds the threshold or the
critical level of depolarization, a molecular change
of the depolarized membrane results in a selective
increase of Na conductance, followed by an in-
crease in K conductance. As mentioned earlier,
this phenomenon, inherent in the muscle mem-
brane, occurs irrespective of the nature of the stim-
ulus as long as depolarization reaches the critical
value. The all-or-none characteristic of the ampli-
tude is dictated by Na channel kinetics. In con-
trast, the speed of initial depolarization alters the la-
tency of the action potential, which forms the
source of jitter in single-fiber studies. A neuromus-
cular block results when the EPP fails to reach the
critical level, either because of insufficient libera-
tion of ACh vesicles from the axon terminal or re-
duced sensitivity of the muscle endplate. The gen-
eration of a muscle action potential is all-or-none
for each muscle fiber, but the compound muscle ac-
tion potential shows a graded response in propor-
tion to the number of activated muscle fibers.
The muscle action potential, once generated
at the endplate, propagates bidirectionally to the
remaining parts of the fiber at a relatively slow
rate of 3 to 5 m/s. The spread of action potential
from the motor endplate to the transverse tubules
initiates the excitation–contraction coupling,
linking the electrical process to muscle contrac-
tion (10,11).
POTENTIALS RECORDED THROUGH A
VOLUME CONDUCTOR
During the clinical study, connective tissue and
interstitial fluid act as a volume conductor sur-
rounding the generator sources (2,12,13). Here,
an electrical field spreads instantaneously from a
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74 SECTION II • TECHNICAL ASPECTS OF EMG
source represented as a dipole (that is, a pair of
positive and negative charges). In a volume con-
ductor, currents move into an infinite number of
pathways between the positive and negative ends
of the dipole, with the greatest current densities
(the number of charges passing through a unit
area per unit time) along the straight path.
Analysis of electrical potential distribution in a
volume conductor requires knowledge on path-
ways of current that generates potential gradi-
ents. Current path is described as current lines
connecting both the current source and sink of
the dipole. The more current lines penetrating a
unit area (or the higher the current density), the
steeper the potential gradient. In other words,
isoelectric lines (points of identical unit poten-
tials), which transect the current lines, become
more crowded. Current pathways are predicted
by a simple law that current tends to flow along
the path of least resistance.
Characteristics of Current Flow
If the current flows in an infinite homogeneous
volume conductor, a potential at a given point can
be calculated mathematically; the potential is in-
versely related to the square of the distance from
the dipole, and proportional to the cosine of the
angle subtended by the point and the orientation
of the dipole. By contrast, the human body
provides a notoriously inhomogeneous and finite-
T A B L E 4 - 2 Volume Conduction in
Inhomogeneous
Media (14)
Medium Resistivity (ohm/cm)
Seawater 20
Cerebrospinal fluid 64
Blood 150
Spinal cord 180–1,200
Cerebral cortex 230–350
White matter 650
Bone 16,000
Skull 20,000
shaped conductor. As a consequence, the analysis
of current lines becomes extremely complicated
and hardly predictable. Various tissues in the body
have their own resistivity (Table 4-2) (14).
The volume conductor has another charac-
teristic of importance for determining the electri-
cal potential. Capacitance is the ability of the
conductor to store charge. If current flows in a
volume, a portion of the current is used to store
positive and negative charges of equal quantity. If
capacitance is high, it takes longer to generate po-
tential difference at a distance. If low, the same
current produces a steeply rising potential. In the
presence of a fixed capacitance, a quick build-up
of current gives rise to a volume-conducted poten-
tial at more distant locations than a slow develop-
ment of the same current (i.e., source currents
with highly synchronized onset tend to generate
greater volume-conducted potentials than those
with gradual onset). Thus, capacitance serves
much like a resistance in the situation with chang-
ing current. The term impedance is used to denote
the total effective resistance acting against the
changing current and includes the combined im-
pact of resistance and capacitance.
Physiologic sources of current comprise
those generated by both synaptic potentials and
action potentials. Action potentials are a propa-
gating source of current with front positivity.
They are always drawn as current lines starting
from this front current source and ending at the
sink just behind, thus producing currents that are
distributed widely. Potentials associated with
these currents can be recorded from a distance in
a volume conductor. Such potential fields are
called open fields.
Some synaptic potentials in central nervous
system nuclei make a spherical dipolar sink
source. The central current sink is juxtaposed
with the source surrounding it. In this case, cur-
rent lines have a short path confined within the
nucleus. As a result, no volume-conducted poten-
tials are recorded at a distance. Such a configura-
tion is termed a closed field distribution.
The current flow decreases in proportion to
the square of the distance from the generator
source. Thus, the effect of the dipole gives rise to
voltage difference between an active recording
electrode in the area of high current density and
a reference electrode at a distance. Whether the
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CHAPTER 4 • ELECTROPHYSIOLOGY
Figure 4-6 ● Diphasic (top) and monopha-
sic recording (bottom) of an action poten-
tial represented by the shaded area. As
the impulse propagates from left to right in the top
series, the two electrodes see no potential difference
in (a), (c), and (e). Relative to the reference electrode
(E2), the active electrode (E1) becomes negative in
(b) and positive in (d), resulting in a diphasic poten-
tial. In the bottom, the darkened area on the right
indicates a killed end with permanent depolariza-
tion, making E1 positive relative to E2 in (a
), (c
), pole, the greatest number of charges passes per unit
and (d
). In (b
), E1 and E2 see no potential differ- time through a unit area along the straight path.
ence, causing upward deflection from the positive
baseline to 0 potential. (Reprinted from Kimura J.
Electrodiagnosis in diseases of nerve and muscle: princi-
ples and practice. New York: Oxford University
Press, 2001, with permission.)
electrode records positive or negative potentials
depends on its spatial orientation to the opposing
charges of the dipole. For example, in an ideal-
ized homogenous volume, the active electrode lo-
cated at a point equidistant from the positive and
negative charge registers no potential, provided
the reference electrode is indifferent. The factors
that determine the amplitude of the recorded
75
potential include charge density (the net charge
per unit area), surface areas of the dipole, and its
proximity to the recording electrode.
Diphasic and Triphasic Waveforms
With a pair of electrodes directly placed on the
surface over a nerve or muscle, the nearest elec-
trode (E1) becomes negative relative to the distant
electrode (E2) as a propagating action potential
reaches the recording site. This results in an up-
ward deflection of the tracing according to the
convention of clinical electrophysiology. The trace
returns to the baseline at the point where the de-
polarized zone affects E1 and E2 equally. With
further passage of the action potential, E2 be-
comes negative relative to E1, or E1 becomes pos-
itive relative to E2. Thus, the trace now shows a
downward deflection until it returns to the base-
line as the nerve activity becomes too distant to
affect the electrical field near the recording elec-
trodes. This produces a diphasic action potential,
as shown in Figure 4-6 (15).
Unlike in animal studies, where recording
can be done directly from the nerve or muscle with
no external conduction medium, a clinical study
must consider the effect of connective tissue and
interstitial fluid, which act as volume conductors
surrounding the generator sources (2,12,13,15). In
a volume conductor, an electrical field spreads
from a source represented as a dipole or a pair of
positive and negative charges (16). Although cur-
rents move along an infinite number of pathways
between the positive and negative ends of the di-
The solid angle subtended by an object
equals the area of its surface divided by the
squared distance from a specific point to the sur-
face (17,18). The resting transmembrane poten-
tial consists of a series of dipoles arranged with
positive charges on the outer surface and negative
charges on the inner surface. Thus, the solid an-
gle increases in proportion to the size of the po-
larized membrane viewed by the electrode and
decreases with the distance between the electrode
and the membrane. Solid angle approximation
closely predicts the voltage potential derived
from a dipole layer, as schematically shown in
Figure 4-7. A leading dipole, visualized as a
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76 SECTION II • TECHNICAL ASPECTS OF EMG
Figure 4-7 ● Potential recorded at P from
a cell with active (dark area) and inactive
region. In (a), total solid angle consists of (1),
(2), and (3). Potential at P subtending solid angles
(1) and (3) equals zero as, in each, the nearer and
farther membranes form a set of dipoles of equal
magnitude but opposite polarity. In (2), however,
cancellation fails because these two dipoles show the
same polarity at the site of depolarization. In (b),
charges of the nearer and farther membranes sub-
tending solid angle (2) are placed on the axial sec-
tion through a cylindrical cell. A dipole sheet equal
in area to the cross-section then represents the onset
of depolarization traveling along the cell from left to
right with positive poles in advance. (Reprinted from
Kimura J. Electrodiagnosis in diseases of nerve and mus-
cle: principles and practice. New York: Oxford Uni-
versity Press, 2001, with permission.)
positively charged wave front, represents the de-
polarization at the cross-section of the nerve at
which the transmembrane potential reverses (19).
A trailing dipole, with negatively charged wave
front, follows, signaling the repolarization of the
activated zone.
Analysis of Triphasic Waveform
A positive–negative–positive triphasic wave re-
sults as the moving fronts of the leading and
trailing dipoles, representing depolarization and
repolarization, approach, reach, and finally pass
beyond the point of the recording electrode (Fig. 4-
8). Thus, an orthodromic sensory action potential
from a deeply situated nerve gives rise to a tripha-
sic waveform in surface recording. In contrast,
when potentials originate in the region near the
electrode, they lack the initial positivity because the
approaching volley is absent (i.e., a compound
muscle action potential recorded with the active
electrode near the endplate region where the vol-
ley initiates). If a pair of electrodes are placed away
from the activated muscle, then the recording of a
positive–negative diphasic action potential indi-
cates that the impulse approaches but does not
reach the recording site.
Triphasic action potentials generated by a mo-
tor unit represent the summation of a few muscle
fiber activities. The waveform of the recorded po-
tential varies with the location of the recording tip
relative to the source of the muscle cells’ potentials
(20–24). Thus, shifting the position of the needle al-
lows recording of multiple, different-appearing
motor unit action potentials from the same motor
unit. A slight withdrawal of the recording tip away
from the discharging motor unit results in a sub-
stantial reduction in amplitude and an increase in
the duration of the positive-to-negative rising
phase, or rise time. The rise time serves as an im-
portant measure of the proximity of the needle tip
to the generator source. The measured amplitude
provides no clue for this purpose, because it may be
decreased with either smaller-diameter muscle
fibers or lower fiber density.
The location of the needle also dictates the
waveform of spontaneous single-fiber discharges,
which may appear as an initially positive triphasic
fibrillation potential, initially negative biphasic
endplate spike, or initially positive biphasic positive
sharp wave. Despite this prevailing unifying con-
cept (25–27), an accurate description of the ob-
served potential plays a useful role in clinical analy-
ses (28,29). For example, positive sharp waves,
recorded in the absence of fibrillation potentials,
may imply subliminal hyperexcitability of single
muscle fibers that “spontaneously” fire only with
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CHAPTER 4 • ELECTROPHYSIOLOGY
Figure 4-8 ● Triphasic potential character-
ized by amplitude, duration (A–D), and rise
time (B–C). A pair of wave fronts of opposite po-
larity represent depolarization and repolarization.
The action potential travels from left to right in a vol-
ume conductor with the recording electrode (E1)
near the active region and the reference electrode (E2)
on a remote inactive point. As shown in (a), E1 ini-
tially sees the positivity of the first dipole, which sub-
tends a greater solid angle (d) than the second di-
pole of negative front (r). In (b), this relationship
reverses, with gradual diminution of d compared
with r, as the active region approaches E1. In (c),
the maximal negativity signals the arrival of the im-
pulse directly under E1, which now sees only negative
ends of the dipoles. In (d), the negativity declines as
E1 begins to register the positive end of the second di-
pole. In (e), the polarity reverses again as r exceeds
d. In (f), the trace returns to the baseline when the
active region moves farther away. The last positive
phase, though smaller in amplitude, lasts longer than
the first, indicating a slower time course of repolar-
ization. (Reprinted from Kimura J. Electrodiagnosis in
diseases of nerve and muscle: principles and practice.
New York: Oxford University Press, 2001, with
permission.)
mechanical irritation of the needle. If the tip of a
needle damages the muscle membrane and blocks
the propagating impulse, then the recorded poten-
tial appears as a positive sharp wave signaling only
the approach of the positive front of depolarization.
77
FAST- AND SLOW-CONDUCTING FIBERS
The onset latency measured in nerve conduction
studies relates to the fastest fibers, allowing calcu-
lation of the maximal motor or sensory velocities.
Waveform analyses help estimate the range of the
functional motor units within the compound
muscle action potentials (CMAPs) or axons within
the sensory nerve action potentials (SNAPs)
(30–32). This aspect of the study provides an
equally important (if not more so) assessment not
only in evaluating peripheral neuropathies with
segmental block, in which surviving axons may
conduct normally (33–42), but also in assessing
spinal cord dysfunction (43,44). In clinical tests of
motor and sensory conduction, the size of the
recorded response approximately parallels the
number of excitable fibers. Any discrepancy be-
tween responses to proximal and distal shocks,
however, does not necessarily imply an abnormal-
ity because of the effect of physiologic temporal
dispersion, which progressively alters the wave-
form of the recorded potentials.
Physiologic and Pathologic
Temporal Dispersion
The impulses of slow-conducting fibers lag in-
creasingly behind those of fast-conducting fibers
over a long conduction path (45–47). Thus, the
size of the recorded response depends to a great
extent on the site of stimulation and recording.
With increasing distance between stimulating and
pickup electrodes, the recorded potential becomes
smaller in both amplitude and area under the
waveform and longer in duration. In fact, stimu-
lation proximally in the axilla or Erb’s point may
normally give rise to a very small SNAP from a
digit, compared to a large response elicited by
stimulation at the wrist or palm (27,48,49). A
physiologic reduction both in amplitude and area
under the waveform shows a linear change (Fig.
4-9) correlated with the length of the nerve seg-
ment (50–52). This linear relationship stands in
contrast to an abrupt diminution attributable to a
focal conduction abnormality located between the
proximal and the distal sites of stimulation.
A slight physiologic latency difference may
cause the positive peaks of the fast fibers to be
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78 SECTION II • TECHNICAL ASPECTS OF EMG
Figure 4-9 ● Simultaneous recordings of
CMAPs from the thenar eminence and
SNAPs from the index finger after stimula-
tion of the median nerve at palm (P), wrist
(W), elbow (E), and axilla (A). The progres-
sively more proximal sites of stimulation elicited
nearly the same muscle response but progressively
smaller sensory responses from the wrist to the axilla.
(Reprinted from Kimura J, Machida M, Ishida T, et
al. Relation between size of compound sensory or
muscle action potentials and length of nerve seg-
ment. Neurology 1986;36:647–652, with permission.)
aligned with the negative peaks of the slow fibers,
canceling both of the short-duration diphasic sen-
sory spikes (Fig. 4-10). This phenomenon alone
can reduce the normal SNAP to below 50% in area
as well as in amplitude, a conservative figure that
is based on computation from a limited number of
nerve fibers available for analysis (53,54). The same
temporal dispersion has less effect (55–57) on
CMAPs since they are longer in duration, and so
they superimpose nearly in phase rather than out
of phase for the same latency shift, resulting in less
cancellation. Thus, when compared to SNAPs,
physiologic phase cancellation results in a limited
reduction in the size of the CMAP (Fig. 4-11). The
duration change of the SNAP, expressed as a per-
centage of the respective baseline values, also far
exceeds that of the CMAP response (50). As ex-
pected from the term “duration-dependent phase
cancellation” (50), a physiologic temporal disper-
sion also reduces the amplitudes of shorter-
duration CMAPs substantially, such as those
recorded from the intrinsic foot muscles.
The separation between E1 and E2 dictates
the duration and waveform of unit discharges,
which in turn determine the degree of overlap be-
tween peaks of opposite polarity (45). A maximal
cancellation results when a waveform contains
negative and positive phases of comparable size. In
a triphasic orthodromic sensory potential,
compared with biphasic antidromic digital poten-
tials, the initial positivity provides an additional
probability for phase cancellation. Changes in
temperature also affect the temporal dispersion,
influencing the fast- and slow-conducting fibers
more or less equally in percentage terms, and
therefore differently in absolute terms (57). For
these reasons, the equations for the best-fit lines in
one study may not necessarily apply to another.
The nerve length and other measurements, how-
ever, nearly always show a linear relation for phys-
iologic changes, which therefore serve as a better
criterion than does an arbitrary limit of percentage
reduction.
Muscle responses can also diminish dramati-
cally based solely on phase cancellation as pre-
dicted by our model (53) and computer simulation
(58) if the latency differences abnormally increase
between normally conducting and pathologically
slow-conducting motor axons. Thus, in patho-
logic temporal dispersion associated with segmen-
tal demyelination, focal phase cancellation could
substantially reduce the amplitude of the muscle
response, giving a false impression of motor con-
duction block. Thus, a sustained reduction in size
of CMAP may result from a pathologic temporal
dispersion rather than a prolonged time period of
neurapraxia (40,53,54). In this case, a reduction in
amplitude of the CMAP following proximal stim-
ulation is consistent with preserved strength and a
relatively normal recruitment pattern of the
motor units.
A Model for Desynchronized Impulses
A shock applied to either the median (Sm) or
ulnar (Su) nerve at the wrist evokes a sensory
potential of the fourth digit as well as a muscle
potential over the thenar eminence. Hence, a con-
comitant application of two stimuli, Sm and Su,
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CHAPTER 4 • ELECTROPHYSIOLOGY 79

Figure 4-10 ● A model for phase cancellation between fast (F) and slow (S) conducting
sensory fibers. With distal stimulation at the arrows, two unit discharges arrive in phase and summate to
produce a sensory action potential twice as large. With proximal stimulation (lower two traces), a delay of the
slow fiber causes phase cancellation between the positive peak of the fast fiber and the negative peak of the slow
fiber, resulting in a 50% reduction in size of the summated response. (Reprinted from Kimura J, Machida M,
Ishida T, et al. Relation between size of compound sensory or muscle action potentials and length of nerve seg-
ment. Neurology 1986;36:647–652, with permission.)

with varying interstimulus intervals simulates the
effect of desynchronized inputs, as seen in patho-
logic temporal dispersion (53) (Figs. 4-12 and 4-
13). In 10 hands, an interstimulus interval on the
order of 1 ms between Sm and Su caused a major
reduction in sensory potential by as much as 50%
but caused little change in CMAP. With further
separation of Sm from Su, the muscle response
began to decrease in amplitude and area, reaching
a minimum at interstimulus intervals of 5 to 6 ms.
The duration is increased in proportion to the in-
terstimulus interval shift, although a gradual
return of the waveform to the baseline made it
difficult to measure this change. An interstimulus
interval slightly less than half the total duration of
the recorded discharge maximized the phase
cancellation between the two components and
consequently the loss of area under the waveform.
Further increase in the interstimulus difference
(simulating the difference in distal latencies be-
tween faster- and slower-conducting fibers)
resulted in complete separation of the two poten-
tials, which precluded phase cancellation. As an
inference, pathologic temporal dispersion may
decrease the size of the SNAPs or CMAPs; how-
ever, it is also possible to see a paradoxical
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80 SECTION II • TECHNICAL ASPECTS OF EMG

Figure 4-11 ● Same arrangements as in Figure 4-10 to show the relationship between fast
(F) and slow (S) conducting motor axons. With distal stimulation, two motor unit potentials summate
to produce a muscle action potential twice as large. With proximal stimulation, the longer-duration motor unit
potentials still superimpose nearly in phase, despite having the same latency time shift of the slow motor fiber
as the sensory fiber shown in Figure 4-10. Thus, a physiologic temporal dispersion alters the size of the muscle
action potential only minimally, if at all. (Reprinted from Kimura J, Machida M, Ishida T, et al. Relation be-
tween size of compound sensory or muscle action potentials and length of nerve segment. Neurology
1986;36:647–652, with permission.)

increase in the responses, caused by elimination of
physiologic phase cancellation.
WAVEFORM ANALYSIS IN
THE CLINICAL DOMAIN
In differentiating physiologic as opposed to patho-
logic temporal dispersion, many variables, such as
the electrode position and the distance between
the two stimulus sites, make the commonly held
criteria based on percentage reduction nearly
untenable (59). A simpler, more practical ap-
proach relies on a linear relationship between the
latency and the size of the recorded responses seen
in physiologic phase cancellation (60) (see Fig. 4-
9). Testing of linearity requires segmental stimu-
lation at more than two sites but enjoys the distinct
advantage of having a built-in internal control for
all recording variables, such as interelectrode
spacing. A nonlinear reduction in amplitude or
area, often associated with waveform changes, in-
dicates either a pathologic temporal dispersion or
conduction block. The distinction between the
two possibilities must depend in part on associated
findings such as muscle strength and motor unit
recruitment.
In summary, physiologic as well as pathologic
temporal dispersion can reduce the area of dipha-
sic or triphasic evoked potentials recorded in bipo-
lar derivation. Segmental studies provide the best
means to differentiate nonlinear pathologic
changes from linear physiologic regression in
amplitudes and areas of the recorded compound
action potentials. An awareness of a duration-
dependent phase cancellation of unit discharges
within the compound action potential helps ana-
lyze dispersed action potentials in identifying
various patterns of neuropathic processes (31). Ref-
erential derivation of a monophasic waveform in a
“killed-end” arrangement conserves the area irre-
spective of stimulus sites. This type of recording,
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CHAPTER 4 • ELECTROPHYSIOLOGY 81

Figure 4-12 ● Antidromic sensory potentials of the fourth digit elicited by stimulation of the
median (Sm) or ulnar (Su) nerve (top two tracings), or by both Sm and Su at interstimulus in-
tervals (ISI) ranging from 0 to 2.0 ms (left). Algebraic sums of the two top tracings (middle) closely
matched the actual recording at each ISI, as evidenced by the small difference shown in computer subtraction
(right). The area under the negative peak reached a minimal value at an ISI of 0.8 ms in actual recordings as well
as in calculated waveforms. (Reprinted from Kimura J, Sakimura Y, Machida M, et al. Effect of desynchronized
inputs on compound sensory and muscle action potentials. Muscle Nerve 1988;11:694–702, with permission.)

however, may register a stationary far-field poten-
tial generated by the propagating impulse crossing
the partition of the volume conductor (61,62). Such
a steady potential could in turn distort the wave-
form of the near-field potentials.
Conduction Block of Motor Fibers
The usual criteria for conduction block in motor
fibers depend on the percentage comparison of a
proximally and a distally elicited CMAP (63–66).
Generally accepted values range from 20% to
50% reduction, with less than 15% increase in
duration of the CMAP elicited by proximal stim-
ulation (67). These criteria, however, do not nec-
essarily apply in all studies because the effects of
temporal dispersion vary depending on the elec-
trode placement. A triple stimulation method
with double collisions allows identification of
motor conduction block in the face of desynchro-
nization (68), but the technique fails if the lesion
is too proximal or if it compromises nerve ex-
citability at stimulus sites as a consequence of de-
myelination or degeneration. Estimating the
number of surviving motor units also has limited
value (69).
The combination of clinical and electrophys-
iologic findings usually circumvents the ambigu-
ity of the criteria based purely on waveform
analysis (70). In the presence of conduction block,
a shock applied distal to the nerve lesion in ques-
tion elicits a vigorous twitch and a large distal
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82 SECTION II • TECHNICAL ASPECTS OF EMG

Figure 4-13 ● CMAPs from the thenar eminence elicited by stimulation of the median (Sm)
and ulnar (Su) nerve (top two tracings), or by both Sm and Su at interstimulus intervals (ISI)
ranging from 0 to l0 ms (left). Algebraic sums of the top two tracings almost, but not exactly, equaled
the actual recordings as shown by computer subtraction at each ISI (right). The area under the negative peak
reached a minimal value at an ISI of 5 ms in actual recordings as well as in calculated waveform. (Reprinted
from Kimura J, Sakimura Y, Machida M, et al. Effect of desynchronized inputs on compound sensory and
muscle action potentials. Muscle Nerve 1988;11:694–702, with permission.)

amplitude despite clinical weakness (27), associ-
ated with paucity of voluntarily activated motor
unit potentials (71). As an exception, the same re-
sult applies to the paresis attributable to upper
motor neuron involvement or hysteria. The same
finding also characterizes any weakness during
the first few days of an axonal lesion before the
distal stump loses excitability (72). The absence of
F-wave responses complements conventional
nerve conduction studies in documenting a con-
duction block, especially if it involves a proximal
segment (73,74). In equivocal cases, the inability
to distinguish between pathologic temporal dis-
persion and conduction block poses no major
practical problems because either finding usually
suggests demyelination, leading to an appropriate
treatment.
In contrast to motor studies, which rely heav-
ily on clinical assessment of weakness to define
conduction block, sensory studies usually depend
solely on waveform analysis of the antidromic re-
sponse elicited by short incremental stimulation.
An alternative method consists of stimulating the
digital nerve and recording the orthodromic sen-
sory potentials at multiple points with a series of
electrodes mounted 1 cm apart on a specially con-
structed flexible strap (31,75). This method, how-
ever, is applicable only to latency studies of a su-
perficially located sensory or mixed nerve, because
varying the depth of the nerve from the skin
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CHAPTER 4 • ELECTROPHYSIOLOGY 83

Figure 4-14 ● A T1-weighted magnetic resonance image (repetition time [TR] 400 ms; echo
time [TE] 13 ms) (left) and a recording of spinal somatosensory evoked potentials (right) ob-
tained from a 65-year-old patient with cervical myelopathy. Epidural stimulation at L2 elicited
a series of potentials recorded unipolarly from the ligamentum flavum of C7–T1 through C1–2. Note the pro-
gressive increase in size of the negative component (arrows pointing up) from C7–T1 (
3) through C5–C6 (
1),
with the abrupt reduction at C4–C5 (0) followed by a monophasic positive wave at C3–C4 (1). The negative
wave doubled in amplitude and quadrupled in area at (
1) compared to (
3). The (0) corresponded to the level
of the spinal cord showing the most prominent compression on the MR image. (Reprinted from Tani T, Ushida
T, Yamamoto H, et al. Waveform changes due to conduction block and their underlying mechanism in spinal
somatosensory evoked potential: a computer simulation. J Neurosurg 1997;86:303–310, with permission.)

surface greatly influences the amplitude of the
surface-recorded SNAP.
Assessment of Spinal Cord Conduction
In contrast to peripheral study, segmental record-
ing registers comparable spinal somatosensory
evoked potentials in intraoperative spinal cord
monitoring. All recording electrodes are nearly
equidistant from the spinal cord if placed in the
subdural or epidural space, the ligamentum
flavum, or the intervertebral disc (76–80).
Figure 4-14 shows unipolar recording from
the ligamentum flavum at multiple levels after
epidural stimulation of the cauda equina in a pa-
tient with cervical spondylotic myelopathy. The
combination of an abrupt loss of the negative
peak at one level, augmentation of the negative
peaks in the leads closely caudal to that level, and
monophasic positive waves at more rostral levels
constitutes a typical pattern of waveform
changes, indicating a complete focal conduction
block. A paradoxically enhanced negative peak
results from resynchronization of physiologically
desynchronized signals because the leading im-
pulses stop traveling when they reach the site of
involvement, whereas the trailing impulses con-
tinue to propagate until they arrive at the same
point. In addition, the fast-conducting fibers lose
their terminal-positive phases, which would have
reduced the negative phases of the slower fibers
by physiologic phase cancellation.
Even when only some of the fibers sustain a
conduction block, the identical mechanism
enhances the negative peak at the points immedi-
ately preceding an incomplete lesion. Thus, the
response consists of positive–negative diphasic
waves with enhanced negativity at points
90749_ch04(65-86).ps 8/11/06 11:08 AM Page 84
84 SECTION II • TECHNICAL ASPECTS OF EMG
immediately preceding the block, a diphasic wave
with reduced negativity at the point of the block,
and initially positive waves alone or abolition of
any wave at points beyond the block (60,81).
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CHAPTER 5
Instrumentation
Sanjeev D. Nandedkar
INTRODUCTION
The primary function of an electromyograph is to
record, amplify, and display a low-amplitude
neurophysiologic signal in the presence of high-
amplitude ambient noise and interference. The
term “noise” usually refers to the internal noise that
is inherent in all electronic devices. “Interference”
represents the potentials introduced from the
surrounding environment (e.g., radio and TV
transmissions). For simplicity, we will refer to both
phenomena as noise. The electromyograph can
selectively amplify the nerve and muscle potentials
while attenuating the ambient noise. This is
described as improving the signal to noise (S/N)
ratio. In modern instruments the S/N ratio is
increased by developing sophisticated hardware
and software. The hardware refers to physical
devices such as amplifier and cables. The software
represents signal-processing algorithms that are
executed using personal computers. The design
and specification of each of these components
affects the noise as well as the signal of interest.
Hence, it is important to understand the role of
instrumentation in electrodiagnostic examination
(EDX). This expertise also allows one to conduct
studies in hostile environments, recognize artifacts,
and perform studies in a fast and efficient manner.
In this chapter we will review the hardware
and software components of a typical commer-
cially available electromyograph. It is not our in-
tention to review sophisticated signal-quantitation
algorithms. Nevertheless, we will discuss the basic
strategy in making measurements manually. One
must be able to recognize failure of automated
algorithms, which occurs quite frequently.
ELECTRODES
The electrodes are sensors that detect electrical
potentials generated by the nerves and muscles.
For good recordings, there should be a good
contact between the signal generators and the
recording electrodes. This is described as having
“low electrode impedance.” In EDX, the intra-
muscular needle electrodes are surrounded by
highly conductive body fluids. This gives a good
contact (i.e., low impedance). In contrast, the
surface electrodes are placed on skin and make a
poor contact to the body (i.e., they have high
impedance). The impedance of surface electrodes
is reduced using many simple strategies.
First, the skin surface at recording site is
cleaned using alcohol-soaked pads. Lotions and
perfumes are poor conductors of electricity, and
these are removed by the cleaning process. A mild
abrasive may be used to remove the dead skin
cells, which have high resistance to electricity.
Finally, electrolytic gel is used to improve the
contact between the electrode and skin. The
impedance measurements are often mandatory in
evoked potential (EP) and electroencephalogra-
phy (EEG) recordings, where one aims to obtain
87
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88 SECTION II • TECHNICAL ASPECTS OF EMG
an impedance of 4 kilo-ohms or even less.
Furthermore, the impedance of all recording
electrodes should be similar (1).
Reusable surface electrodes should be washed
thoroughly to remove any build-up of residues of
the electrolytic gel. Reusable needle electrodes
should be inspected under a microscope for the
presence of burs and hooks, which cause signifi-
cant pain during needle insertion and movement.
These are removed by polishing the needle tip.
Special electrodes such as those used in single-
fiber EMG may require electrolytic treatment.
The details of this procedure can be obtained from
the needle manufacturers.
LEADS AND CABLES
A lead is piece of wire that connects the recording
electrode to the amplifier. A collection of leads
makes a cable. A lead is a piece of wire, just like
an antenna. Hence, the lead also behaves as a
recording electrode, except that it registers noise
and interference. Increasing the length of the
lead will record more noise. Hence, the length of
lead should be kept as small as possible. As
described later, it is desirable that all leads record
the same ambient noise. This is accomplished by
weaving the leads into one another to form a
cable. Such cables containing only two leads are
often called the “twisted pair” leads. Surface
electrodes used for nerve conduction studies are
commercially available in straight and twisted
leads. Shielded cables are useful when a long
cable length is necessary. The shielding reduces
the interference recorded by the leads contained
in them.
All EMG recordings require three electrodes
(described later). Their leads are color-coded by
most manufacturers as Red for Reference (E2),
Green for Ground, and Black for the Active (E1)
electrode. In past the leads terminated into 2- or
4-mm pins that were inserted into the amplifier
receptacle. A few years ago, the U.S. Food and
Drug Administration (FDA) mandated that all
leads must be “touch-proof” to improve patient
safety. Users of old equipment are urged to con-
vert their EMG instruments and accessories to
meet the FDA guidelines.
AMPLIFIER
This is the most important component of the elec-
tromyograph. The amplifiers used in consumer
electronic devices (e.g., radio, TV) need two input
connections. In contrast, EMG amplifiers require
three connections: active, reference, and ground
(Fig. 5-1). The amplifier does not magnify the
signals at individual inputs; rather, it magnifies
the potential difference between the active and
reference inputs. Hence, it is called a differential
amplifier. The use of differential amplification al-
lows us to improve the S/N ratio. In Figure 5-1A,
the active electrode is a monopolar needle and
records a fibrillation potential of 50
V. The
reference electrode is electrically silent. Their
difference is amplified to obtain an output signal
of 500,000
V (or 0.5 Volts). The differential gain
of the amplifier is thus 500,000/50  10,000.
At the same time, there is an ambient noise of
1,000
V. However, this noise is identical at the
active and reference inputs (see Fig. 5-1B). Their
difference is zero, and hence we do not see it at the
amplifier output. In this manner we can record
the low-amplitude electromyographic potentials
in presence of high-amplitude noise.
The concept of noise attenuation in Figure 5-
1B is an idealized viewpoint. Real differential
amplifiers do amplify the signals that are common
(i.e., identical) to active and reference input. In
Figure 5-1C, we find noise amplitude to be 1,000

V at the amplifier output. The amplification of
common signals is called the common gain, and in
Figure 5-1C it is equal to 1. Note that the S/N ratio
at amplifier input and output is 0.05 and 500,
respectively. For the best performance, the
amplifier should have a high differential gain (see
Fig. 5-1A) and a low common mode gain (see Fig.
5-1C). These properties are described by a single
characteristic called the common mode rejection
ratio (CMRR):
CMRR  Differential gain/Common mode gain
Engineers prefer to describe the CMRR in units of
decibels (dB) using the formula:
CMRR (dB)  20 log (Differential
gain/common mode gain)
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CHAPTER 5 • INSTRUMENTATION 89

Figure 5-1 ● Differential amplifier. A. EMG signal appears as differential input and has a gain of
10,000. B. Noise is identical at active and reference inputs. C. The common mode gain is 1.

In the schematic amplifier of Figure 5-1, the
CMRR is 100 dB. Modern commercially available
amplifiers have a CMRR of 100 dB or better.
In Figure 5-1A, we assumed that reference
electrode does not register any electrical activity. In
EMG and nerve conduction studies (NCS), this is
not true. The cannula of a single-fiber EMG
records motor unit activity called the “macro
EMG” motor unit potential (MUP) (2). In motor
NCS, the position of the reference electrode affects
the initial deflection of the compound muscle
action potential (CMAP) (3). In sensory NCS, the
nerve action potential passes under active and
reference electrodes. The sensory nerve action
potential (SNAP) depends on the distance between
the active and reference electrodes. Short distance
will give a lower amplitude and a shorter peak
latency (Fig. 5-2). Hence, one should use a
standard separation between the active and refer-
ence electrodes. Most laboratories use a 2- to 4-cm
distance. Using a bar electrode in a sensory NCS
results in standardized separation of E1 and E2.
The amplifier is also characterized by its
input impedance. In contrast to the recording
electrodes, the input impedance of the differential
amplifier should be high. Low-input impedance
attenuates the physiologic potential. Fortunately,
modern amplifiers have very high impedance
(1,000 MΩ) and do not pose any problems for
this requirement.
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90 SECTION II • TECHNICAL ASPECTS OF EMG
Figure 5-2 ● SNAP is recorded with
active-reference electrode separation of
4 cm and 1.5 cm. Signal from the reference
electrode affects the amplitude and peak latency.
When the electrode leads are in close spatial
proximity, they should record similar ambient
noise. By virtue of differential amplification, this
noise will be attenuated. Hence, twisted paired
leads or shielded cables are recommended in a
hostile environment (e.g., the intensive care unit).
If the recording electrodes have different im-
pedances, the noise they record is slightly different
at the amplifier inputs. This imbalance gives
higher noise despite differential amplification. It is
typically seen in monopolar needle EMG record-
ings where the active recording electrode is intra-
muscular with low impedance. The reference elec-
trode placed on the skin surface has higher
impedance. Higher noise in monopolar EMG can
also result due to spatial separation among the
leads of the needle and surface electrodes.
FILTERS
All EMG amplifiers use a “bandpass” filter to at-
tenuate noise. The filters can be hardware devices
or signal-processing algorithms implemented in
software. The algorithms are called digital filters.
The bandpass filter is characterized by two
frequency settings: low and high. Their effect on
EMG signal (Fig. 5-3A) can be understood easily
from the sound of EMG on the audio monitor.
Adjusting the high-frequency setting is the same
as changing the treble control on a tape or CD
player. When the high-frequency setting is
reduced, the “hiss” decreases. The high-frequency
noise is reduced (see Fig. 5-3B). Changing the
low-frequency setting is the same as adjusting the
bass control. Increasing the low-frequency setting
attenuates the sound of instruments like a tuba or
drum. On EMG, the baseline is stabilized and it
appears “clamped” near the center of the display
(middle trace in Fig. 5-3A–C). By reducing the
bandwidth (i.e., increasing the low-frequency
and/or decreasing the high-frequency setting), the
noise and interference are reduced. The signal is
also affected. Hence, it is necessary to understand
the effect of filters on EMG waveforms.
The needle EMG signals are recorded with a
low-frequency setting of 10 to 20 Hz. The high-
frequency setting is 10 kHz. When a potential
changes rapidly, it is rich in high-frequency com-
ponents. This is seen in the spike component of the
MUP (Fig. 5-4A). Reducing the high-frequency
setting decreases the signal amplitude and increases
its rise time. The peaks appear rounded rather than
sharp (see Fig. 5-4B). The initial and terminal parts
of the MUP change slowly. This gives the low-
frequency components of the signal. Increasing the
low-frequency setting will attenuate the initial and
terminal slow components, thus reducing the MUP
duration (see Fig. 5-4C).
In sensory nerve conduction studies the low-
frequency setting is 10 to 20 Hz. The high-
frequency setting is variable. Some laboratories set
the high frequency at 10 kHz. This gives a SNAP
with higher amplitude and shorter peak latency
(Fig. 5-5). Since the baseline appears “noisy,” other
laboratories set the high-frequency setting to a
lower value (e.g., 2 kHz). This gives a “smooth”
waveform with reduced amplitude and longer
peak latency (see Fig. 5-5). The onset latency is not
significantly affected.
Long duration potentials such as the CMAP
are rich in low-frequency components. Therefore,
increasing the low-frequency setting reduces the
CMAP amplitude (Fig. 5-6). The onset latency
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CHAPTER 5 • INSTRUMENTATION 91

Figure 5-3 ● Principle of signal filtering. A. Low-amplitude signal with low- and high-frequency
noise. B. Reducing the high-frequency setting attenuates the high-frequency noise. C. Increasing the low-fre-
quency setting stabilizes the baseline.

may be slightly longer due to reduced signal am-
plitude. The duration and area of negative peak
are reduced too. The terminal part of the CMAP
is distorted, and one observes an extra negative
phase at the end of CMAP. Decreasing the high-
frequency setting does not significantly affect the
CMAP.
The power line frequency interference is easily
recognized by the five (for 50 Hz) or six (for 60 Hz)
cycles in a 100 ms sweep (Fig. 5-7A). This is
attenuated using a notch filter (see Fig. 5-7B).
Sometimes the interference appears as the second
(100 or 120 Hz) or third (150 or 180 Hz) harmonic
of the power line frequency. It is not attenuated by
the notch filter (see Fig. 5-7C). Dimmer switches
and fluorescent lights also give spikes at 120 Hz fre-
quency (see Fig. 5-7D). When several other
electrical devices are in use (e.g., in the intensive
care unit), the power line interference can have a
very complex shape (see Fig. 5-7E). When the
notch filter is on, the potentials may be slightly
distorted. Hence, this filter should not be used as far
as possible, but in a hostile environment the notch
filter can be very useful to assess low-amplitude
potentials (e.g., fibrillations and positive sharp
waves).
Since the EMG measurements are affected by
filter settings, one should not deviate from the
settings (Table 5-1) used for defining the normal
values. In some instances, filters are changed
deliberately to enhance certain characteristics of
the signal. In needle EMG examination, the low-
frequency setting can be increased to 100 Hz to
stabilize baseline during assessment of insertional
activity (4). Increasing it to 500 Hz or higher
enhances the spike component of the MUP to
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92 SECTION II • TECHNICAL ASPECTS OF EMG
Figure 5-4 ● Effect of filter settings on the motor unit action potential. The filter settings are (A)
3–10,000 Hz, (B) 3–2,000 Hz, and (C) 100–10,000 Hz. Note the change in amplitude (B) and duration (C).
assess its stability (5). In F wave studies, the low-
frequency setting may be raised to 100 Hz for a
faster return of CMAP to baseline (Fig. 5-8). This
makes it easier to recognize the onset of the
F wave. The amplitudes of F waves is reduced,
but this does not significantly affect its onset la-
tency.
ANALOG TO DIGITAL CONVERTER
The analog to digital converter measures the
EMG signals at regular time intervals. Each
measurement is called a sample (Fig. 5-9A). The
samples are plotted in sequential manner and
connected by straight lines to display the digitized
EMG signal. This process is very similar to taping
a video. During the recording phase, the camera
takes 30 static pictures per second. During play-
back, the pictures are displayed in the same order
and at the same rate. This gives the perception of
a smooth or continuous motion, although it is
generated from static pictures. But if the camera is
defective and captures only five frames per
second, we will not see the “normal” motion
during playback; it will appear distorted. Thus,
the number of frames captured per second defines
the quality of the video. One could increase the
number of frames per second to a higher number,
say 200, but this will not significantly improve the
quality of “motion” on video. From experiments,
we find that a rate of 30 frames per second is quite
adequate. This logic also applies to understanding
the concepts of sampling and distortion that
occurs due to poor sampling.
The time interval between successive samples
is called the sampling interval. The reciprocal of
the sampling interval is the sampling rate. If the
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CHAPTER 5 • INSTRUMENTATION 93

Figure 5-5 ● Effect of filter settings on the SNAP. Reducing the high-frequency setting reduces
amplitude and baseline noise while increasing peak latency.

Figure 5-6 ● Effect of filter settings on the CMAP. Increasing the low-frequency setting (bottom
trace) reduces the amplitude and duration of the negative peak. The arrow indicates an extra negative phase at
the end.
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94 SECTION II • TECHNICAL ASPECTS OF EMG

sampling rate is low, the digitized EMG signal

Figure 5-7 ● Noise and interference. The
60-Hz interference in (A) is attenuated by the notch
filter (B). In (C), the second harmonic of power line
frequency appears as 120 Hz interference. In (D),
the dimmer noise appears as sharp spikes. In (E),
the interference has a complex shape but does
demonstrate a 60-Hz frequency. It was generated by
other electrical instruments that were in use at the
time of EMG recording.
will be different from the analog signal (see Fig. 5-
9B). Specifically, the signal amplitude is reduced
and variable. Sharp peaks are attenuated or
missed. This distortion due to poor sampling is
called aliasing. Sampling theory indicates that the
sampling rate must be at least twice the highest
frequency in the signal (i.e., the high-frequency
setting of the filter). Engineers prefer to use a sam-
pling rate that is three to five times the highest fre-
quency. Thus, the needle EMG signal should be
sampled at a rate of at least 20 kHz, preferably 30
to 50 kHz.
The sampling rate is defined in the software,
and it is not easily possible to measure this setting.
However, aliasing can be recognized quite easily.
First, the high-frequency setting of the filter
should be set at 10 kHz for needle EMG record-
ings. Next, discharges of a sharp MUP (with low
rise time) are displayed using a slow sweep (e.g., 50
ms/division). In normal subjects, the MUP ampli-
tude should remain relatively constant (Fig. 5-
10A). If aliasing occurs, the amplitude will appear
variable (see Fig. 5-10B) for normal MUPs. When
the sampling rate is high, amplitude variability
can be seen due to abnormalities of neuromuscu-
lar transmission. The instability or “jiggle” of the
MUP is of great value in assessing reinnervation

T A B L E 5 - 1 Recommended Low- and High-Frequency Settings of the Band Filters for

the Commonly Used Neurodiagnostic Procedures

Test Low Frequency (Hz) High Frequency (Hz)

Motor nerve conduction 3–20 5,000–10,000

Sensory nerve conduction 3–20 2,000–10,000
F wave/H reflex 3–20 5,000–10,000
Routine needle EMG 10–20 5,000–10,000
Quantitative EMG 2–5 10,000–20,000
Single-fiber EMG 500–2,000 10,000–20,000
Sympathetic skin response 0.1 100
Electrocardiogram 10–20 100–200
Brain stem evoked potentials 50–150 10,000
Visual evoked potentials 1–3 100–300
Somatosensory evoked potentials 3–30 3,000
Routine EEG 0.3–1 70–100
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Figure 5-8 ● Effect of filters on F waves. A. 3–10,000 Hz; (B) 100–10,000 Hz. In (B), the F wave
onset can be recognized better due to return of CMAP to baseline.

Figure 5-9 ● Principle of analog to digital conversion. In (A) the analog and digitized signals
are similar. In (B) the sampling rate is reduced by 50%. The digital signal is quite different from the analog
signal in (A). This is called aliasing.
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96 SECTION II • TECHNICAL ASPECTS OF EMG

Figure 5-10 ● A. Amplitude of a normal motor unit action potential is constant on successive discharges
when the sampling rate is high. B. When the sampling rate is reduced, the amplitude of the same motor unit
action potential is variable; this is aliasing. C. Variable amplitude of a motor unit action potential in a patient
with motor neuron disease. The sampling rate is the same as in (A).

(6). Therefore, one must check the sampling rate
of the EMG program before assessing variability
of MUPs.
DISPLAYING SIGNALS
The digitized EMG signals are displayed on a
computer terminal in two different modes: free-
running or triggered. The free-running mode
updates the display continuously, showing the live
EMG signals as they are recorded. This mode is
used in the needle EMG examination. The trig-
gered mode is used when one wishes to record
EMG signals only when a certain event (the trig-
ger) occurs. In NCS, the trigger occurs when the
nerve is stimulated. The computer displays the sig-
nals immediately after the trigger for the duration
of one sweep. This signal stays on the screen until
the user stimulates the nerve again. In this manner,
the trace is available for review for an extended pe-
riod of time and is updated only by the user control.
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CHAPTER 5 • INSTRUMENTATION
Figure 5-11 ● A. The SNAP is time-locked to the stimulus. The noise appears randomly. B. The noise is
reduced by averaging.
The potential resulting from stimulation appears
at the same location on the screen, making it easier
to assess its reproducibility (Fig. 5-11A).
In needle EMG, one can use an amplitude
trigger to display discharges of a single MUP. The
user sets an amplitude level for triggering. When
the EMG signal amplitude is less than the trigger
level, the signal is not displayed (Fig. 5-12A).
When the amplitude exceeds the trigger level, the
system acquires and displays one sweep of EMG
activity (see Fig. 5-12B). The display will be up-
dated when the EMG signal crosses the trigger
level again. The user adjusts the trigger level so
that only one MUP can exceed it. As a result, the
trace is updated only when the largest-amplitude
MUP discharges. Its waveform appears time-
locked on the display (see Fig. 5-12B).
The amplitude trigger allows one to see the
EMG signal after the trigger occurs. The delay
line allows one to see the activity that precedes the
trigger. In case of MUPs, the combination of trig-
ger and delay line gives us the entire MUP wave-
form on the screen in a time-locked manner (see
Fig. 5-12C). Such a display is used in quantitative
analysis of MUPs or jitter in single-fiber EMG.
97
In routine EMG studies, the amplitude trigger is
useful to assess polyphasic MUP waveforms, late
components, MUP stability, and so forth.
SIGNAL AVERAGER
Averaging is a statistical method of improving the
S/N ratio. In sensory nerve conduction studies, the
sweep is triggered by the stimulator. The resulting
SNAP is time-locked to the stimulation and
appears at the same location in the sweep. In
contrast, the noise appears randomly on successive
sweeps (see Fig. 5-11A). When these sweeps are
summated, the positive noise on one sweep will
cancel the negative noise on another trace. The
SNAP being time-locked to the stimulus is not
affected. Thus, averaging several sweeps will
reduce noise without affecting the SNAP (i.e.,
increase the S/N ratio) (see Fig. 5-11B).
The decrease in noise amplitude is propor-
tional to the square root of the number of averaged
sweeps. Thus, most of the improvement in signal
quality occurs in the initial few sweeps of the aver-
age. Averaging should not be used as a substitute
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98 SECTION II • TECHNICAL ASPECTS OF EMG
Figure 5-12 ● A. EMG is shown in a free-running mode. The amplitude trigger level is shown by the dot-
ted line. B. Motor unit potential discharges are time-locked. C. The delay line permits display of the motor unit
potential before the trigger point.
for good-quality EMG recordings: every effort
should be made to minimize the noise before
starting the signal averager. In evoked potential
studies, many systems will automatically reject
sweeps that contain high-amplitude noise (7).
Background EMG activity (Fig. 5-13A) can
easily produce an averaged signal that resembles a
physiologic potential (see Fig. 5-13B). Therefore,
one should observe individual sweeps to ensure
that a time-locked potential exists in the sweep
(see Fig. 5-11). This is sometime not possible due
to a poor S/N ratio. In those situations, one should
obtain two averaged responses and compare them
to assess the reproducibility of the signal (see Fig.
5-13C). This strategy is used routinely in evoked
potential studies.
STIMULATOR
The electrical stimulator is an integral part of the
EMG system. It has two tips: anode and cathode.
The cathode, the negative tip of the stimulator, is
placed over the stimulation site. The stimulator
can be programmed to deliver a constant voltage or
constant current. The current passing through the
stimulator will depend on the impedance between
the stimulator tips. High impedance will require
higher voltage for stimulation. This also generates
a larger artifact on conduction studies. Hence, one
should reduce the impedance at stimulation sites
before beginning the study. The skin surface
should be cleaned at the stimulation site, and elec-
trolytic gel should be applied to the stimulator tips.
The stimulation artifact is generated by spread
of the currents from stimulators to the recording
electrodes. A shorter distance between stimulator
and recording electrodes will give a larger artifact.
Placing the ground electrode between the stimulat-
ing and recording electrodes will reduce the arti-
fact. By rotating the anode, one can alter the spread
of stimulating current to the recording site. This
maneuver can help minimize the artifact.
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CHAPTER 5 • INSTRUMENTATION 99

Figure 5-13 ● A. Sensory NCS, where no time-locked SNAP is seen on successive trials. However, the
background EMG activity in these sweeps was averaged to potential (B) that appeared similar to a SNAP, and
it was automatically marked. C. Two low-amplitude SNAPs are superimposed to demonstrate reproducibil-
ity. Attempting to repeat (B) would prove the error.

When the nerve is deep, superficial stimulation equal to the product of sweep speed and number
can be inadequate as well as painful. Monopolar of horizontal divisions.
needle electrode can be very useful to get close to the The needle EMG examination is usually
nerve. In this approach, one requires a very low conducted with a sweep duration of 100 ms. The
intensity of stimulation (8). signals are shown in a raster manner. If a potential
occurs at roughly the same position on successive
sweeps, the time interval between the two
MAKING MEASUREMENTS
Modern EMG systems can automatically identify
the onset and end of potentials and measure the
amplitude, area, and other features of the signal.
Sometimes the measuring algorithm may fail due
to a poor S/N ratio. In those instances it is neces-
sary to adjust the automated marking. In some
instances (e.g., needle EMG), one may need to
make measurements manually. To facilitate the
subjective assessment, the trace area is divided in a
rectangular grid. The display gain or sensitivity is
amplitude change corresponding to one vertical
division (Fig. 5-14). One measures the vertical
deflection of the signal as the number of divisions
of the grid and multiplies it by display gain to
estimate amplitude.
The time corresponding to one horizontal
division of the grid is called the sweep speed (see
Fig. 5-14). Multiplying the number of horizontal Figure 5-14 ● Display of EMG signals.
divisions by sweep speed, one measures the time. The trace area is divided in a grid to facilitate manual
Some systems indicate the sweep duration; this is measurements.
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100 SECTION II • TECHNICAL ASPECTS OF EMG
Figure 5-15 ● The motor unit action potential firing rate can be assessed from raster
display of EMG signal. The rate is (A) 10 Hz, (B) 10 Hz, (C) 10 Hz, and (D) 20 Hz.
discharges is roughly 100 ms (0.1 second). The
discharge rate, the reciprocal of the time interval,
will be 10 Hz (Fig. 5-15B). If the potential appears
to shift right on successive sweeps, the two dis-
charges are separated by more than one sweep
duration (i.e., interval 100 ms). Hence, the firing
rate is less than 10 Hz. Sometimes we fail to see
a MUP waveform on a sweep (see Fig. 5-15A).
Conversely, a potential that shifts left is discharg-
ing at more than 10 Hz. Sometimes the potential
is seen twice on one trace (see Fig. 5-15C). When
the potential occurs twice on every sweep, the fir-
ing rate will be 20 Hz (see Fig. 5-15D). The firing
rate can be estimated very easily by counting the
number of potential discharges in five consecutive
sweeps of 100 ms duration and multiplying the
number by 2. Many modern EMG systems offer
such a display mode (see Figs. 5-15A–C).
SAFETY
The EMG laboratory should be a safe environment
for the patients as well as the laboratory personnel
(9). The power cord of many low-powered devices
has only two conductors. One conductor connects
to the main power, and the second provides a return
path for the electrical current. The air surrounding
the electronic devices is an insulator. Nevertheless,
some electricity can pass through the air to reach the
system chassis. If the operator or patient touches the
chassis, some current can flow through the opera-
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CHAPTER 5 • INSTRUMENTATION 101

Figure 5-16 ● A. The medical instrument with two conductor power cords is unsafe. B. The leakage cur-
rent passes through the “ground,” making it safe.
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102 SECTION II • TECHNICAL ASPECTS OF EMG
tor’s body (Fig. 5-16A). If the current passes
through the heart, the results could be deadly.
To make the device safe, EMG instruments
use a power cord with three conductors. One end
of the third conductor is connected to the instru-
ment chassis. The other end is usually connected
to a metal pole buried in the ground. This
connection, called the “ground,” provides a very
low-resistance path for leakage current flowing
through the chassis at all times. By preventing
current flow through the operator, the system
becomes safe for operation. Regardless of this
protective mechanism, the leakage current
should be low. The FDA has established stan-
dards for acceptable leakage, and all instrument
manufacturers must follow the standards. It is a
good idea to have the safety of the instrument
tested on a periodic basis.
Sometimes one finds a wall outlet with a
three-pin receptacle. However, the ground con-
nection may be defective or sometimes not even
functional. This will make the system “unsafe.”
Fortunately, absence of ground makes it almost
impossible to record low-amplitude potentials.
Very-high-amplitude interference, especially at
power line frequency, is an indication of a possible
“ungrounded” power connection.
EMG systems also maintain patient records
that are confidential. These records should be ac-
cessible to only authorized personnel. The Health
Insurance Portability and Accountability Act
(HIPPA) has established guidelines to ensure con-
fidentiality. One should also make backups of pa-
tient records on a regular basis.
TACKLING THE NOISE
The best strategy to attenuate noise is to minimize
it in the first place. Here are some useful tips:
1. Reduce the electrode impedance by cleaning
the skin surface and using electrolytic gel.
2. In conduction studies, place the ground electrode
between the stimulating and recording sites.
3. Make sure the instrument is properly grounded.
This also is necessary for safe operation of the
system.
4. Use short cables. If long cables are necessary,
use shielded cables.
5. Keep all recording leads and cables together so
that they record the same ambient noise. Com-
mon noise is attenuated by the differential
amplifier.
6. Keep recording cables away from power cables
and stimulator leads.
7. Use incandescent lights without dimmer
switches. Turn off any fluorescent lights.
8. Turn off all unnecessary electronic instru-
ments. Better yet, unplug them from the wall
socket. The power cord of an instrument
plugged into the main supply behaves as an
antenna radiating at power line frequency even
when the instrument is turned off.
Despite good technique, one may face occa-
sions when the S/N ratio is poor. Under these
conditions, one usually suspects a failure of the
amplifier, but that is not necessarily the problem:
sometimes the noise is high due to high electrode
impedance or bad cables. To assess an amplifier
problem, connect together the active and refer-
ence inputs. Since there is no differential or
common signal, we expect to see a flat, noise-free
signal baseline. If a flat baseline is indeed seen, the
problem is most likely not in the amplifier. One
should change the leads and/or electrodes to get a
better S/N ratio.
The contact between the electrodes and the
leads is often covered by an insulating layer. The
deterioration of this contact due to normal use
may not be recognized by visual inspection. A
poor contact gives high impedance and hence
more noise. A transient noise usually suggests a
failing cable. Replacing the cable resolves the noise
problem, thus confirming the cable failure. Bad
cables should be discarded immediately to prevent
future use, which would waste the clinician’s and
the patient’s time.
When working in a hostile environment (e.g.,
an intensive care unit), higher noise is unavoid-
able. The filter settings can be adjusted to attenu-
ate noise, but be aware of the changes in the EMG
potentials due to the change in filter settings.
A nearby radio or TV station may produce ex-
cessive electromagnetic radiation that cannot be
sufficiently attenuated by the EMG amplifier. One
can hear those signals on the audio monitor and
view them as low-amplitude, high-frequency
spikes on the display. If signal quality improves
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CHAPTER 5 • INSTRUMENTATION
at another location, it is safe to assume that the
instrument is working properly. Sometimes a
different location within the same examination
room is less noisy than others. Transient noise may
also result from the use of heavy equipment, such as
elevators or tools used in construction. If there is no
control over these noise sources, one may need to
build a so-called Faraday cage. This is an expensive
proposition that involves rebuilding the walls of the
examination room.
Finally, the CMRR of an amplifier will
decrease over a few years due to natural deteriora-
tion of the electronic components. This will make
the EMG signals slightly noisy.
REFERENCES
1. Chiappa K. Evoked potentials in clinical medicine.
New York: Raven Press, 1983.
2. Stalberg E. Macro EMG: a new recording tech-
nique. J Neurol Neurophysiol Psychiat 1980;43:
475–482.
103
3. Kincaid JC, Brashear A, Markand ON. The
influence of the reference electrode on CMAP
configuration. Muscle Nerve 1993;16:392–396.
4. Barkhaus P, Nandedkar S. EMG on CD/DVD,
vol. II, 2003. Available at www.casaengineer-
ing.com.
5. Payan P. The blanket principle: a technical note.
Muscle Nerve 1978;1:423–426.
6. Stalberg EV, Soono M. Assessment of variability
in the shape of the motor unit action potential,
the “jiggle” at consecutive discharges. Muscle
Nerve 1994;17:1135–1144.
7. Nandedkar S. Basic instrumentation. In: Brown
W, Bolton C, Aminoff J, eds. Neuromuscular
function and disease. New York: WB Saunders,
2002:709–718.
8. Pease WS, Fatehi MT, Johnson EW. Monopolar
needle stimulation: safety considerations. Arch
Phys Med Rehabil 1989;70:412–412.
9. Styles P. Safety in electromyography laboratory.
In: Brown W, Bolton C, Aminoff J, eds. Neuro-
muscular function and disease. New York: WB
Saunders, 2002:709–718.
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90749_ch06(105-130).ps 8/11/06 11:10 AM Page 105
CHAPTER 6
Advanced Needle
EMG Methods
Erik Stålberg
INTRODUCTION
The organization of muscle fibers within the mo-
tor unit (MU) changes in typical ways in different
nerve and muscle disorders. Many forms of neu-
rogenic conditions are characterized by collateral
sprouting from intramuscular nerve branches of
surviving MUs. This increases the number of
muscle fibers in individual MUs (1). In the rein-
nervated MU, the fibers of the same MU are found
to be clustered together instead of being randomly
distributed, as in the healthy patient. In muscle
biopsy, this is seen as “fiber-type” grouping (2,3).
In primary myopathies, on the other hand, de-
generation of individual fibers causes a reduced
number of muscle fibers within a MU. In addition,
there is often muscle fiber regeneration and fiber
splitting; these tend to increase the number of mus-
cle fibers, which now occur in small clusters (4).
Fibrosis will further change the local topography of
muscle fibers within a MU. In myopathies there is
often an increased variation in diameter of muscle
fibers, from reduced to some large muscle fibers.
These types of MU changes can be studied
not only with morphologic techniques, as referred
to here, but also by electrophysiologic methods.
The electromyography (EMG) signals are de-
pendent upon the number of muscle fibers, the lo-
cal concentration and sizes of the fibers, and neu-
romuscular and axonal transmission of action
potentials. The EMG signal is also affected by the
type of electrode used for recording (Fig. 6-1).
CONVENTIONAL EMG RECORDINGS
In conventional EMG, concentric or monopolar
electrodes are used. With some differences in the
shape and size of the active recording zone, they
record electrical signals from active muscle fibers
within a radius of 2 to 3 mm (5). This recording
zone is small compared to the size of the entire
MU, which has a “territory” typically 3 to 10 mm
in diameter. On the other hand, it is too large to al-
low the selective recording from just one or a few
muscle fibers for detailed analysis. The amplitude
of the normal MU potential (MUP) may be deter-
mined by one to four fibers closest to the tip, and
the duration of the MUP is determined by ap-
proximately 30 fibers within the 2 to 3 mm record-
ing zone. Still, this technique is of great value in
the study of MU characteristics that differentiate
normal from myogenic and neurogenic disorders.
The MUP analysis is becoming quantitative and
automatic. We have developed a technique by
which up to six different MUPs are recorded from
each recording site; this method, called multi-
MUP recording (Fig. 6-2) (6), is based on decom-
position algorithms. This algorithm recognizes
and extracts the individual elements (MUPs) that
occur repeatedly, each time with the same shape.
In this way a given MUP can be identified even
when superimposed with activity from other
MUs. The decomposition can be more or less com-
plete, depending upon clinical or experimental ap-
plication. If an exact firing (recruitment) pattern
105
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106 SECTION II • TECHNICAL ASPECTS OF EMG
Figure 6-1 ● Different types of EMG electrodes. A. Single fiber EMG electrode with one
recording surface. B. Concentric needle electrode. C. Monopolar electrode. D. Macro electrode.
should be studied, a complete decomposition is
necessary. If the aim is to quantitate MUP param-
eters, it is not necessary that each discharge be
identified. Our multi-MUP method is optimized
in speed and accuracy for daily routine use. Simi-
lar methods have been developed by others (7).
Reference values have been collected for a number
of muscles (8), parameters have been added to im-
prove the detection of pathology, and a new way
to express abnormality has been defined (9).
In neurogenic conditions, the MUPs are typi-
cally of increased duration and amplitude because
of the grouping of muscle fibers within the MU. In
addition, they often change in shape at consecutive
discharges (referred to as “jiggle”) (10), particu-
larly during the phase of ongoing reinnervation.
In myopathies, there is a reduction of dura-
tion owing to loss of muscle fibers and fibrosis.
Furthermore, in both neurogenic and myopathic
conditions, there is often an increased number of
complex or polyphasic MUPs. These complex
MUPs are due to an increased variation among
pathologic muscle fiber diameters, causing a
wider range of conduction velocities (along mus-
cle membranes), and to some degree are due to the
scattered positions of endplates after reinnerva-
tion. These two phenomena produce increased
temporal dispersion among individual single-
fiber action potentials, causing the typical changes
in MUP shape (11). Recordings with conventional
needle electrodes do not provide information
about the size of the MU in terms of the number
of total number of muscle fibers or territory.
Other EMG methods, both more and less se-
lective, have been developed to complement the
conventional recordings. This chapter describes
three of these special techniques. The classic
EMG method is presented in other chapters of
this book.
SINGLE-FIBER EMG
In certain cases, essential information may be
obtained by the detailed study of just one or a few
muscle fibers from one MU. Examples of this
include the study of neuromuscular transmission
in individual endplates and investigations of the
distribution of muscle fibers in the MU. For this
purpose, single-fiber EMG (SFEMG) was devel-
oped. After being proven valuable in these situa-
tions, SFEMG has taken its place in clinical
routine work and will be described briefly here.
The interested reader is referred to additional lit-
erature on the topic (12–15).
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CHAPTER 6 • ADVANCED NEEDLE EMG METHODS 107

Figure 6-2 ● MUP recordings from normal, neuropathic, and myopathic muscles using
multi-MUP analysis technique.

SFEMG is based on extracellular recordings of
single muscle fiber action potentials with a small
electrode (25
m in diameter), exposed in a side
port of a steel cannula 0.5 mm in diameter. Because
of the small area of the recording surface and the
reduced amplifier filter bandwidth (set to 500 Hz
to 10 KHz), the recording zone is limited to a hemi-
sphere with a radius of about 300
m, resulting in
high spatial resolution. On consecutive discharges,
a given single-fiber action potential has a well-
defined and reproducible shape that justifies time
measurements with accuracy as high as 0.1 ms.
These recording advantages have been used
over the years to study a number of morphologic
and functional details in the MU. These studies
range from studies of propagation of action po-
tentials along single muscle fibers, membrane
characteristics, neuromuscular transmission of
individual motor endplates, local organization of
muscle fibers in a MU, discharge characteristics
of ventral horn cells, and conduction in corti-
cospinal tract axons. This chapter describes stud-
ies of the neuromuscular transmission and of
local muscle fiber distribution.
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108 SECTION II • TECHNICAL ASPECTS OF EMG

NEUROMUSCULAR TRANSMISSION monopolar electrode is used as a cathode and a

Methods
Voluntary Activation
The neuromuscular transmission is most com-
monly studied during slight voluntary contrac-
tion. The electrode is inserted into the muscle and
a position is sought where two muscle fibers from
the same MU (i.e., discharging synchronously) are
recorded. When triggering the oscilloscope sweep
on one of the spikes in the potential pair, the
interpotential latency to the other varies during
consecutive discharges. This variation of the inter-
potential intervals is called “jitter.” This is due to
the summated variability of neuromuscular junc-
tion transmission time in the two motor endplates
involved in the recordings (Fig. 6-3).
Intramuscular Stimulation
Also used for these studies is microstimulation of
individual muscle fibers and motor axons, either
inside the muscle or in the nerve trunk. A small
surface electrode is used as an anode for intramus-
cular stimulation. Stimulation strength is usually
kept below 10 mAmp and stimulus pulse duration
is typically 0.05 ms. Recording is through a
SFEMG electrode about 20 mm away from the
stimulation point. If a muscle fiber is directly stim-
ulated, the jitter is less than 4 ms, but if an intra-
muscular axon is stimulated, the jitter is more
than 4 ms because of the involvement of the
synapse at the motor endplate (Fig. 6-4). Using
this method, the neuromuscular junction can be
studied under well-standardized conditions and
over long periods of time. The method can also be
used with uncooperative patients, comatose pa-
tients, patients with movement disorders, infants,
or other situations in which voluntary patient
activation is difficult. The technique can also be
used in animal experiments.
Calculation of Jitter
Jitter is expressed as the mean value of the differ-
ence between consecutive interpotential intervals

Figure 6-3 ● A. Schematic presentation of jitter recording during voluntary contraction.

B. Two single-fiber action potentials from fibers of the same MU recorded at high speed. The
sweep is triggered by the first action potential. Several discharges are superimposed, demonstrating the variabil-
ity of the interpotential interval, the neuromuscular jitter. (Reprinted with permission from Stålberg E, Trontelj
JV. Single fiber electromyography in healthy and diseased muscle, 2nd ed. New York: Raven Press, 1994.)
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CHAPTER 6 • ADVANCED NEEDLE EMG METHODS 109

Figure 6-4 ● Intramuscular stimulation. A. Stimulating and recording electrodes (upper). Exam-
ples of typical responses with direct muscle fiber stimulation (low jitter) and with axonal stimulation having
jitter greater than 4 ms (middle). B. Dual distribution of jitter values in the extensor digitorum communis mus-
cle corresponding to direct and axonal stimulation. Dividing line is at 5
s. (Reprinted with permission from
Stålberg E, Trontelj JV. Single fiber electromyography in healthy and diseased muscle, 2nd ed. New York: Raven
Press, 1994.)

(in absolute values). In stimulation studies, the Neuromuscular Transmission in

interval between stimulus artifact and the
resulting single-fiber action potential is used for
calculations. Jitter was initially calculated from
superimposed filmed recordings, but modern
EMG instruments can automatically calculate
jitter.
Healthy Subjects
Jitter during Voluntary Activity
The jitter during voluntary activation is approxi-
mately 5 to 60
s, depending on the muscle and
the patient’s age (Table 6-1). Motor endplates
 110

T A B L E 6 - 1 Jitter Reference Values for Various Age Groups from a Multicenter Study (18)

Jitter values (
s)*

90749_ch06(105-130).ps

Muscle 10 year 20 year 30 year 40 year 50 year 60 year 70 year 80 year 90 year

Frontalis 33.6/49.7 33.9/50.1 34.4/51.3 35.5/53.5 37.3/57.5 40.0/63.9 43.8/74.1

Orbicularis oculi 39.8/54.6 39.8/54.7 40.0/54.7 40.4/54.8 40.9/55.0 41.8/55.3 43.0/55.8
8/11/06

Orbicularis oris 34.7/52.2 34.7/52.7 34.9/53.2 35.3/54.1 36.0/55.7 37.0/58.2 38.3/61.8 40.2/67.0 42.5/74.2
Tongue 32.8/48.6 33.0/49.0 33.6/50.2 34.8/52.5 36.8/56.3 39.8/62.0 44.0/70.0
Sternocleidomastoid 29.1/45.4 29.3/45.8 29.8/46.8 30.8/48.8 32.5/52.4 34.9/58.2 38.4/62.3
Deltoid 32.9/44.4 32.9/44.5 32.9/44.5 32.9/44.6 33.0/44.8 33.0/45.1 33.1/45.6 33.2/46.1 33.3/46.9
11:10 AM

Biceps brachii 29.5/45.2 29.6/45.2 29.6/45.4 29.8/45.7 30.1/46.2 30.5/46.9 31.0/48.0

Extensor digitorum 34.9/50.0 34.9/50.1 35.1/50.5 35.4/51.3 35.9/52.5 36.6/54.4 37.7/57.2 39.1/61.1 40.9/66.5
Abductor digiti V 44.4/63.5 44.7/64.0 45.2/65.5 46.4/68.6 48.2/73.9 51.0/82.7 54.8/96.6
Quadriceps 35.9/47.9 36.0/48.0 36.5/48.2 37.5/48.5 39.0/49.1 41.3/50.0 44.6/51.2
Page 110

Anterior tibialis 49.4/80.0 49.3/79.8 49.2/79.3 48.9/78.3 48.5/76.8 47.9/74.5 47.0/71.4 45.8/67.5 44.3/62.9

Fiber density values† (same subjects as above)

Muscle 10 year 20 year 30 year 40 year 50 year 60 year 70 year 80 year 90 year

Frontalis 1.67 1.67 1.68 1.69 1.70 1.73 1.76

SECTION II • TECHNICAL ASPECTS OF EMG

Tongue 1.78 1.78 1.78 1.78 1.78 1.79 1.79

Sternocleidomastoid 1.89 1.89 1.90 1.92 1.96 2.01 2.08
Deltoid 1.56 1.56 1.57 1.57 1.58 1.59 1.60 1.62 1.65
Biceps brachii 1.52 1.52 1.53 1.54 1.57 1.60 1.65 1.72 1.80
Extensor digitorum 1.77 1.78 1.80 1.83 1.90 1.99 2.12 2.29 2.51
Abductor digiti V 1.99 2.00 2.03 2.08 2.16 2.28 2.46
Quadriceps 1.93 1.94 1.96 1.99 2.05 2.14 2.26
Anterior tibialis 1.94 1.94 1.96 1.98 2.02 2.07 2.15 2.26
Soleus 1.56 1.56 1.56 1.57 1.59 1.62 1.66 1.71
*Data are given as mean of the mean consecutive difference (MCD) 95% upper confidence limit of normal/95% upper confidence limit of normal for individual pairs of single fibers.
†Data are given as mean fiber density 95% upper confidence limit of normal.
Jitter is abnormal if either (1) value for mean MCD of 20 fiber pairs is greater than the 95% upper confidence limit or (2) jitter values in more than 10% of pairs is greater than the 95%
upper confidence limit for action potential pairs. Fiber density is abnormal if mean value of 20 observations is greater than the 95% confidence limit. (From Bromberg MB, Scott DM.
Single fiber EMG reference values: reformatted in tabular form. Muscle Nerve 1994;17:820–821, with permission.)
90749_ch06(105-130).ps 8/11/06 11:10 AM Page 111
CHAPTER 6 • ADVANCED NEEDLE EMG METHODS
within the same MU have different jitter values.
The jitter does not show any appreciable change
for up to 10 minutes of continuous activity with a
mean rate of about 10 Hz. In a study of the safety
factor (16) of individual endplates using regional
curare, it was found that those with higher jitter
were more sensitive to curare than those with ini-
tially low jitter. Thus, it seems justified to say that
the jitter reflects the safety factor (amount of
acetylcholine [ACh] released in excess of that re-
quired for the synapse) of transmission in individ-
ual motor endplates.
It has been discussed whether neuromuscular
blockade owing to local ischemia might be one of
the reasons for muscular fatigue in normal muscle
that develops during prolonged activity. In a study
with ischemia after the inflation of a sphygmo-
manometer cuff around the upper arm, jitter was
measured in the extensor digitorum communis
muscle activated voluntarily (17). Following a few
minutes of continuous activity during ischemia,
the jitter started to increase fairly rapidly and one
or the other of the potentials showed intermittent
blocking, at first rarely and then more frequently
until total block occurred. The time to blocking
was shorter with higher innervation rates. Ap-
proximately 2,000 to 4,000 discharges were re-
quired before the onset of blocking. After release
of the cuff, the transmission recovered quickly and
jitter became close to normal within a few minutes.
Jitter during Electrical Stimulation
The method is described in detail elsewhere (12,14).
Because only one motor endplate is involved, nor-
mal jitter during electrical stimulation is lower
than with voluntary activation. Theoretically, the
values are reduced on average by a factor of √2
lower. This is in accordance with experimental re-
sults. In muscles in which separate reference values
at electrical stimulation are missing, those from vol-
untary activation can be used after dividing by √2.
Most normal endplates display rather con-
stant jitter at different stimulation rates within the
range of physiologic firing frequencies, reflecting
a high safety factor. This has been studied in some
detail (12). At a 50 Hz stimulation rate, a substan-
tial increase in jitter occurred in comparison to the
jitter values at 10 Hz in over two thirds of the
studied motor endplates of healthy subjects. How-
ever, it still did not exceed the upper normal limit
111
for 10 Hz (40
s) in any of the tested endplates.
This suggests a remarkable ability of the presy-
naptic terminals to cope with the increased de-
mand for ACh synthesis and mobilization even at
these high rates.
Normal Jitter Values
Normal jitter values in Table 6-1 are based on
data from a multicenter study, which includes val-
ues from our laboratory (18). Until the individual
laboratory has collected its own reference values,
these values can be used. Jitter values are ex-
tremely reproducible when the standard instru-
mentation protocols are followed.
Jitter: Voluntary Activation
Jitter is expressed as the mean value of consecutive
differences (MCD) of interpotential intervals. In a
multispike recording occurring in a high-fiber-
density situation, only MCD values between one
triggering component and each of the other com-
ponents is measured: that is, when four spikes are
present, three MCD values are obtained.
Abnormality is expressed in two ways:
1. By marking the number of recordings with jit-
ter outside given limits for individual data. If 2
or more recordings in a set of 20 exceed the
limit, the finding is considered abnormal.
2. By the mean MCD value for the whole study in
a muscle. The distribution of individual jitter
values in abnormal conditions is often skewed,
with some extremely high values. Therefore,
the mean MCD is calculated only from data
with a jitter value less than 150
s (unless a ma-
jority of data are abnormal and distributed
near this limit).
Examples of normal values for the extensor
digitorum communis from a multicenter study
(18) that indicates the preference limit for mean
MCD and individual jitter values are shown in
Figure 6-5. For more information on reference
values for these and other muscles, the reader is re-
ferred to a comprehensive text on the subject (12).
Jitter: Axonal Stimulation
The principles given in descriptions on SFEMG
electrical stimulation must be strictly adhered to
in order to avoid pitfalls leading to potentially
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112 SECTION II • TECHNICAL ASPECTS OF EMG

Figure 6-5 ● Graph showing third-highest individual jitter value in each subject (extensor
digitorum communis [EDC]) plotted against age. The upper line corresponds to 95% confidence
limits and is used as upper normal limits for individual data from 20 recordings in an EDC muscle. (Reprinted
with permission from Gilchrist J, Barkhaus PE, Bril V, et al. Single fiber EMG reference values: a collabora-
tive effort. Muscle Nerve 1992;15:151–161.)

serious errors. A minimum of 20 to 30 endplates
are sampled with two or more different positions
of the stimulating needle. The abnormality is ex-
pressed in the same way as in the voluntary jitter
study (as a number or percentage of the abnor-
mal recordings and as the mean of all individual
MCD values in the study). One out of 20 values
above the upper reference limit is accepted in a
normal muscle.
Jitter Studies with Monopolar or
Concentric Needle Electrodes
It has been frequently asked whether conven-
tional EMG needle electrodes can be used for
SFEMG. For fiber density assessment the answer
is no, since the electrodes have a larger uptake area
than the SFEMG electrode and since action po-
tentials from individual fibers sometimes interfere
and cannot be viewed separately. For jitter meas-
urements, experience has shown that it is possible
to obtain reasonably appropriate estimates. The
filters should be set to a bandwidth of 1,000 (or
even 2,000) Hz to 10 kHz. Some components may
superimpose and the jitter may be underesti-
mated, or occasionally slightly overestimated. If
separate spike components are chosen for trigger
and for measurements, then the jitter values are
similar for this type of recording and the SFEMG
electrode. In a study of 10 myasthenic patients, the
authors found no significant difference in the
values, and the interpretation was the same inde-
pendent of the electrode used (19). The recording
quality is actually better with a disposable concen-
tric needle electrode than with a SFEMG
electrode that has been left without maintenance
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CHAPTER 6 • ADVANCED NEEDLE EMG METHODS 113

to keep the recording surface clean and the tip
sharp. The most selective recording is still ob-
tained with a SFEMG electrode of good quality.
Neuromuscular Transmission in Disease
Myasthenia Gravis
The principal neurophysiologic mechanisms and
corresponding structural changes underlying the
transmission defect in myasthenia gravis (MG)
are well known (20). The endplate potential
(EPP) amplitude is reduced because of blocked,
destroyed, or displaced postsynaptic ACh recep-
tors, whereas the number of ACh quanta re-
leased from the presynaptic terminal per nerve
impulse is normal. The resulting reduction of the
safety factor (the normal excess of receptors) for
neuromuscular transmission with slowly rising
EPPs causes an increase in jitter values. When
the EPPs are insufficient to reach the threshold
for the action potential firing, then impulse
blocking occurs, thus giving rise to clinical weak-
ness as there is no depolarization of the affected
muscle fibers.
SFEMG findings in a patient with MG (Fig.
6-6) include recordings with normal jitter values,
jitter values above the normal range but without
impulse blocking, and recordings in more severe
disease with both increased jitter and intermit-
tent impulse blocking, the latter usually first
appearing in association with a jitter of about 100

s (see Fig. 6-6C).
In a large group of patients with MG investi-
gated with SFEMG during voluntary activation,
the extensor digitorum communis muscle was ab-
normal in 89% of those with generalized MG and
99% when more muscles were included. In ocular
MG, 97% of the studies were abnormal when a set
of muscles (usually a limb and a facial muscle)
were investigated (13).
Stimulated SFEMG can be used to study in
detail the rate-dependent changes of the efficiency
of neuromuscular transmission at the individual
endplates. Indeed, MG may be regarded as a nat-
ural model to study the normal function of the
motor nerve terminal. In a study with this method
(21), 58 endplates of 10 myasthenic patients were
observed at different stimulation rates. A majority
of the endplates showed lower jitter and a reduced
incidence of blocking at the lowest stimulation
rates, followed by an increase in both measures at
2 Hz, 5 Hz, or 10 Hz. The normal presynaptic de-
pression of Ach release in the early phase of low
stimulation rates combined with a low safety

Figure 6-6 ● SFEMG jitter recordings from the extensor digitorum communis muscle of a
patient with MG. The oscilloscope sweep is triggered by the first action potential, and the interval vari-
ability between the single-fiber action potentials (the neuromuscular jitter) is shown as a variable position of
the second potential. In the upper part the sweeps are moving downward, and the recordings are superim-
posed below. A. Normal jitter. B. Increased jitter without impulse blocking. C. Increased jitter and occasional
blocking. (Reprinted with permission from Stålberg E, Trontelj JV. Single fiber electromyography in healthy and
diseased muscle, 2nd ed. New York: Raven Press, 1994.)
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114 SECTION II • TECHNICAL ASPECTS OF EMG

factor is the basis of both the decrement during
routine repetitive stimulation and increased jitter.
Stimulation rates of 20 Hz resulted in a return to
lower jitter values, associated with a decreased
incidence of blocking. This improvement is con-
sidered to be due to an increase in ACh released
per stimulus (i.e., intratetanic potentiation) (Fig.
6-7). The size of the response in the repetitive
nerve stimulation test represents the net result of
these two opposing processes.
Lambert-Eaton Myasthenic Syndrome
This neuromuscular transmission disorder has
been shown to be a result of an autoimmune at-
tack against calcium channels in the presynaptic
nerve terminal, resulting in impaired transmitter
release. The jitter is often grossly abnormal. In
stimulated SFEMG there is a dramatic reduction
of jitter and blocking as the stimulation rate is in-
creased from 1 Hz to 2 Hz up to 10 Hz to 20 Hz
(21), since Ach release is facilitated by increased
frequency of depolarization.
Reinnervation
In cases of ongoing reinnervation, the jitter value
is typically increased. This is probably because of
functional immaturity of the newly formed motor
endplates, both pre- and postsynaptically. After
acute nerve damage, transmission is first estab-
lished in the new endplates after about 3 weeks
(depending upon the site of lesion in relation to its
target muscle). After about 6 months, the jitter

Figure 6-7 ● Stimulated SFEMG. Top: Jitter and frequency of blocking in a sample of 40 myasthenic
endplates at different stimulation rates. The values belonging to individual motor endplates are connected
with lines. Twelve endplates did not show any blocking. Bottom: Mean values and ranges between the 5th and
95th percentile for 32 endplates studied over the complete range of stimulation rates. (Reprinted with permis-
sion from Trontelj JV, Stålberg E. Single motor end-plates in myasthenia gravis and LEMS at different firing
rates. Muscle Nerve 1991;14:226–232.)
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CHAPTER 6 • ADVANCED NEEDLE EMG METHODS 115

values are normalizing, but it is usually possible to
find some abnormality long after this time. Areas
of prior nerve injury should therefore be avoided
in an examination for later-onset neuromuscular
junction disease.
Transmission Safety in the Intramuscular
Nerve Tree, Axonal Jitter, and Blocking
Transmission in the intramuscular nerve tree can
be studied by SFEMG during electrical stimula-
tion by studying the axon reflex (Fig. 6-8) (22). A
single needle stimulator position can result in
stimulation of two branches from the same axon,
although each branch will respond to stimulus in-
tensity in proportion to its distance from the nee-
dle. Low stimulation strength activates the nearer
intramuscular nerve branch of the axon, which
conducts antidromically to the branch site, and
then the action potential is propagated ortho-
dromically in the second fiber branch. Higher
stimulation strength directly activates the farther
branch, which propagates orthodromically but for
a shorter distance. A difference in jitter in the two
different situations should be caused by the jitter

Figure 6-8 ● Axon reflex. Intramuscular electrical stimulation producing a complex response of
action potentials from five muscle fibers from one MU. Two of the muscle fibers (1 and 2) respond with two
latencies whereby they are always linked together. Note the different time calibrations in (A) and (B) through
(C). In (C), seven discharges were superimposed with each of the two latencies to show their relative con-
stancy. D. Schematic explanation of this phenomenon based upon an axon reflex. The two fibers with dual la-
tency are activated either directly through their own axonal branch (D) or, when the stimulus is subthresh-
old, through the branch to the other three fibers in the recording (A). In this case the antidromically
propagated impulse invades the branch to fibers 2 and 3, and the response appears with a longer latency.
(Reprinted with permission from Stålberg E, Trontelj JV. Demonstration of axon reflexes in human motor
nerve fibres. J Neurol Neurosurg Psychiatry 1970;33:571–579.)
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116 SECTION II • TECHNICAL ASPECTS OF EMG

created in the non-common axon segments and
the branching site, which would include the nodes
of Ranvier. In a normal nerve axon, there is no
extra jitter in the nodes of Ranvier.
Intramuscular axonal transmission can also
be studied during voluntary activation if record-
ings are made from three or more muscle fibers.
Two or more components in a complex recording
may show concomitant jitter relative to other
parts of the action potential complex. Sometimes
concomitant impulse blocking occurs. This usu-
ally is due to unreliable propagation of axonal
impulses or conduction failure in the axon to those
muscle fibers from which the blocking action
potentials are recorded (Fig. 6-9) (23).
As with the neuromuscular blocking encoun-
tered in MG, axonal blocking may increase during
continuous activity and worsen with increasing
activation. This may also give rise to decrement in
the surface-recorded responses to repetitive
stimulation. It may even respond positively to
edrophonium (23); therefore, the presence of a
decrement and a positive edrophonium effect is
not absolute proof of a synaptic transmission
defect.
PROPAGATION VELOCITY
OF SINGLE MUSCLE FIBERS
Propagation velocity of the single muscle fiber ac-
tion potential along the muscle fiber (24) can be
measured using a multi-electrode with two arrays
of recording surfaces. The time between the two
recorded potentials from a single muscle fiber
exactly overlying two electrode surfaces is meas-
ured and the propagation velocity calculated. The
normal muscle fiber propagation velocity value

Figure 6-9 ● Concomitant blocking. A recording from six muscle fibers from the same MU. The
middle four spike components intermittently block together. They also show a large common jitter in relation
to the remaining two components. The block is considered to be situated in the nerve twig common to the four
blocking muscle fibers (between the two arrows). The jitter of greater than 5
s between the four components
indicates that this is not the case of four branches from a split muscle fiber with an abnormal motor endplate,
since split fibers would have jitter of less than 5
s. (Reprinted with permission from Stålberg E, Trontelj JV.
Single fiber electromyography in healthy and diseased muscle, 2nd ed. New York: Raven Press, 1994.)
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CHAPTER 6 • ADVANCED NEEDLE EMG METHODS 117

lies between 1.5 and 6.5 m/s but varies from mus-
cle to muscle and even within a given muscle (24).
Experiments on isolated muscle fibers have shown
that muscle fiber diameter is a major factor deter-
mining the propagation velocity. For the range of
diameters of human muscle fibers, the velocity is
directly proportional to fiber diameter. During
continued activation at a firing rate of approxi-
mately 10 Hz, the propagation velocity usually
decreases and is most pronounced during the first
minute (24) (Fig. 6-10).
This decrease in propagation velocity explains
the change in power spectrum observed with the
conventional needle and surface EMG when the
higher frequencies decrease and the lower fre-
quencies increase during continuous activity. In
the literature, this frequency shift is called fatigue,
which deviates from the traditional definition of
muscular fatigue. The change in propagation ve-
locity also explains, at least in part, a decrease in the
number of turns in an analysis of the EMG inter-
ference pattern during continuous muscle activity.
Propagation velocity, dependent on mem-
brane properties, also depends on the interval to
previous discharge, called the velocity recovery
function (VRF) (24). In certain muscle disorders,
the membrane properties are changed, which can
be seen as abnormal VRF. Propagation velocity of

Figure 6-10 ● Decrease of propagation velocity in four muscle fibers during continued ac-
tivity at 11, 16, 12, and 9 discharges, respectively. In a fifth fiber, tested at an innervation rate of 6
and 16 discharges (the two continuous lines), there is no decrease in propagation velocity (24). (Reprinted with
permission from Stålberg E, Trontelj JV. Single fiber electromyography in healthy and diseased muscle, 2nd ed. New
York: Raven Press, 1994.)
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118 SECTION II • TECHNICAL ASPECTS OF EMG

the muscle cell membrane is not a parameter stud- tions. It reflects the distribution of muscle fibers in
ied in routine EMG. the MU and is found to be a useful complement to
conventional EMG (Fig. 6-11).

FIBER DENSITY Method

Morphologic data indicate that changes from the
normal checkerboard pattern of muscle fibers to a
patchy distribution called fiber-type grouping is
an early sign of pathology. This may occur before
a definite change in number of fibers within other
parts of the MU has occurred. A parameter re-
flecting fiber distribution called fiber density (FD)
has therefore been developed. This parameter is
easier to obtain than jitter and has wider applica-
The electrode is positioned in the muscle so that a
given muscle fiber action potential is obtained with
its amplitude maximized. A count is made of the
number of spike components (including the trig-
gering spike) that are time-locked to the triggering
action potential that have an amplitude exceeding
200
V and a rise time shorter than 300
s when
using a low-frequency filter limit of 500 Hz at the
amplifier (many MU discharges must be observed

Figure 6-11 ● Fiber density. SFEMG recordings in normal and reinnervated muscle. The diagram
illustrates the number of muscle fibers of one MU (blacked in). The uptake hemisphere of the recording elec-
trode is represented as a half circle. In the normal muscle (1 and 2), only action potentials from one or two fibers
are recorded. After reinnervation (3), many fibers’ action potentials are recorded owing to increased fiber density
in the MU. (Reprinted with permission from Stålberg E, Trontelj JV. Single fiber electromyography in healthy and
diseased muscle, 2nd ed. New York: Raven Press, 1994.)
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CHAPTER 6 • ADVANCED NEEDLE EMG METHODS 119

Figure 6-12 ● FD definition. Different “difficult” SFEMG recordings indicated to represent one or
two fibers in FD measurements (indicated for each recording). Two spikes are defined when there is any
change in the slope of the signal. (Reprinted with permission from Stålberg E, Trontelj JV. Single fiber
electromyography in healthy and diseased muscle, 2nd ed. New York: Raven Press, 1994.)

to ascertain that the spikes all belong to the same
MU). The sweep speed should be slow enough to
allow observation of 5 ms, or more if necessary (1–2
ms/cm), both before and after the triggering spike.
In the event that individual single-fiber action
potentials occur nearly simultaneously at the
recording electrode, causing superimposition, the
amplitude criterion for inclusion may be difficult
to use. As a rule of thumb, each of the spikes giving
rise to a change in signal polarity (a notch in the sig-
nal) should be counted (Fig. 6-12). At least 20 esti-
mations are made from different recording sites
with at least three separate skin penetrations.
Occasionally, positive-going, broad, jittering
potentials are generated by the preceding spike
component, and these should not be included in
the count or used for jitter measurements. Also,
monopolar or concentric needle electrodes cannot
be used to obtain the FD value because of the
difference in recording uptake area.
advisable to test a small set of controls subjects for
FD values in, for example, the extensor digitorum
muscle. If this data set coincides with published
data, then the operator can fairly conclude that
his or her technique is consistent with that de-
scribed and used for all reference values, which
therefore can be adopted directly for the other
muscles.
FD Findings in Nerve–Muscle Disorders
In cases of abnormal MU organization (e.g., rein-
nervation), the FD values are increased, corre-
sponding to fiber-type grouping in the biopsy.
High values are also found in myopathies (12,25).
This most likely is due to abnormal fiber distribu-
tion owing to splitting, satellite cells, regeneration,
ephaptic transmission, and, sometimes, secondary
neurogenic changes (25,26).

Normal FD Values Indications for SFEMG in Clinical Studies

The normal FD values vary for different muscles and Research
and, in some muscles, vary with age (Fig. 6-13). Experimental studies of neuromuscula transmission
The typical range of values is 1.3 to 1.8. Reference Neuromuscular transmission in diseases
values for different muscles were obtained in a col- Diagnosis, evaluation, follow-up of
laborative study (see Table 6-1) (12,18). FD values neuromuscular disorders
differ somewhat between laboratories. It may be Myasthenia gravis
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120 SECTION II • TECHNICAL ASPECTS OF EMG

Figure 6-13 ● Normal fiber density data from extensor digitorum muscle, collected from
a multicentre study. (Modified from Gilchrist J, Barkhaus PE, Bril V, et al. Single fiber EMG reference
values: a collaborative effort. Muscle Nerve 1992;15:151–161, with permission.)

Lambert-Eaton myasthenic syndrome MACRO EMG

Other myasthenic syndromes
Botulism To obtain an overall picture of the MU, a special
Other conditions with disturbed technique called Macro EMG has been developed
neuromuscular transmission (27). Macro EMG records the summated action
Spatial organization of motor units in potentials from all of the fibers making up a MU.
diseases
Neurogenic disorders Method
Myopathies
The recording electrode consists of a modified
Firing pattern
SFEMG electrode with the cannula insulated ex-
In studies of normal and disturbed cept for the distal 15 mm. The SFEMG recording
recruitment firing patterns surface is exposed 7.5 mm from the tip (the mid-
Spike triggering point of the bare cannula). Recording is made on
Scanning EMG two channels with the EMG equipment con-
Macro EMG nected to a PC for analysis (Fig. 6-14). On one
Spike triggered averaging for MU electrical channel, the macro EMG signal from the cannula
or mechanical output (E1) (using a surface electrode as E2) is recorded
Propagation velocity of the muscle and fed to an average. On the other channel, the
membrane SFEMG recording is obtained between the 25 µm
Measure of fiber diameter E1 and the cannula E2. Amplifier filters are set to
Membrane parameters 5 Hz to 10 KHz and 500 Hz to 10 KHz for Macro
Fatigue EMG and SFEMG, respectively. The electrode is
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CHAPTER 6 • ADVANCED NEEDLE EMG METHODS 121

Figure 6-14 ● Recording principle of Macro EMG recording. A. Recording connection; channel
1 from cannula and channel 2 from SFEMG surface as E1 (active) electrodes. B. SFEMG channel display. C.
Cannula signal, where the synchronous MUP can be seen, but superimposed on other activity. D. Macro MUP
extracted from cannula signal after averaging, triggered from the SFEMG recording.

inserted into the voluntarily activated muscle and
a position is sought where an acceptable SFEMG
potential is seen. At this moment, the averaging
process begins and continues until a smooth base-
line and a constant Macro MUP is obtained on the
“cannula” channel. Concomitantly, FD of the
triggering action potential is obtained. Averaging
is essential since other MUs are active within the
cannula’s recording volume.
The peak-to-peak amplitude and area of the
Macro EMG signal are positively related to the
number and size of muscle fibers in the entire MU
(28). If there is atrophy of the muscle fibers, the
Macro MUP should become reduced. This effect
is counteracted, however, by the shrinkage of the
MU, which reduces the distance between its fibers
and the electrode, increasing the Macro MUP.
When recordings from the same MU are repeated
using a different muscle fiber as the trigger (which
is separated from the first by several millimeters),
the shape of the Macro EMG signal from one MU
is relatively constant, indicating that the recording
really reflects activity in all fibers of a MU.
Normal Findings
In normal muscle, the general Macro EMG MUP
shape differs from one muscle to the other (27). In
the anterior tibial muscle, the potentials often have
two or more separate peaks, whereas in the
brachial biceps muscle, the potentials usually have
a simple configuration with one or two negative
peaks. There is a great scatter in individual Macro
MUP amplitudes in the normal muscle. The
largest Macro MUP may be up to 10 times larger
than the smallest in the brachial biceps muscle for
individuals under age 60 and up to 20 times in
those over 60 years. A larger range of values can be
90749_ch06(105-130).ps 8/11/06 11:10 AM Page 122
122 SECTION II • TECHNICAL ASPECTS OF EMG
expected if high threshold MUs are included. It is
thus easy to detect the so-called size principle and
to study its changes with age and pathology with
this technique, not easily recognized with conven-
tional EMG recordings (29). The mean Macro
MUP amplitude differs five-fold for MUs re-
cruited at 20% of maximal force compared to
those recruited at lower force, corresponding to
orderly recruitment as judged from their twitches
(30). This makes it important to define reference
values for given ranges of contraction levels and to
perform patient investigation within the same
range of contraction.
Normal values given for a low degree of ac-
tivity (i.e., low-threshold MUs) vary for different
muscles. In some muscles, the values increase with
age, an effect more pronounced in the anterior tib-
ial muscle than in either the brachial biceps or the
vastus lateralis muscles. The change with age re-
flects the enlargement of remaining MUs with the
physiologic loss of neurons and reinnervation by
distal sprouting of survivor axons.
MOTOR UNIT ESTIMATION
McComas et al (31) described a method for esti-
mating the number of MUs by means of graded
electrical stimulation and a surface recording of
the increasing M wave amplitude. From the max-
imal response and the mean value of individual
steps, the number of MUs was estimated. To as-
certain the recording from just one MU at a time,
we performed voluntary activation combined
with the SFEMG technique. An SFEMG elec-
trode-triggered activity from one muscle fiber and
surface electrode as used by McComas et al (31)
were used for recordings. The maximal M wave
amplitude response used for the calculations was
obtained from electrical stimulation. Brown et al
(32) have used this technique extensively and
found it useful. We found that deeply located
MUs in large muscles gave smaller signal ampli-
tudes using surface electrodes, and this led to the
development of Macro EMG to better record the
MU size using intramuscular recording. Macro
MUPs recorded during voluntary contraction and
M wave amplitude obtained from the Macro
EMG electrode have been used to estimate the
number of MUs (33). We have occasionally used
Macro EMG to estimate MU numbers in this way,
mainly in the study of patients with a history of
polio. However, in our routine use of Macro
EMG, the degree of loss of axons is obtained from
the relative Macro MUP amplitude increase,
which is a measure of compensatory reinnervation
(see below in the section on reinnervation).
Findings in Myopathies
As expected, the electrical size of the MU reflected
by the Macro MUP is decreased in myopathies as
a group (Fig. 6-15). In the individual case, values
are often within normal limits. Large-mean-
amplitude Macro MUPs have been found in some
patients with facioscapulohumeral and limb-gir-
dle dystrophy with slight or no clinical involve-
ment (34). This finding may indicate a compensa-
tory hypertrophy, as seen by others (31,35). Macro
MUP parameters by themselves are thus not sen-
sitive enough to detect early myopathic changes.
The reason for the normal or near-normal ampli-
tudes is probably the compensatory mechanisms
with fiber regeneration, fiber splitting, occasional
fiber hypertrophy, and general packing of fibers
due to atrophy. These changes will, however,
cause an increase in the FD value. Therefore, the
finding of increased FD values obtained from the
SFEMG channel during the Macro EMG study,
combined with normal or slightly reduced Macro
MUP values, is a useful indicator of myopathy.
These findings can be used to differentiate my-
opathy from neuropathy in questionable cases
(Table 6-2).
Findings in Reinnervation
During reinnervation by collateral sprouting,
which is the most common type of compensation
in neurogenic conditions, the number of muscle
fibers in a given MU increases. In Macro EMG,
this is seen as increased amplitude of the signal. In
this way, Macro EMG offers the possibility of fol-
lowing reinnervation quantitatively.
The individual Macro MUP in reinnervation
can have an amplitude exceeding the normal mean
by a factor of 10 (Fig. 6-16). In the complex situa-
tion involving patients with amyotrophic lateral
sclerosis (ALS) (36), the picture is variable. In some
patients with rapid progression, the Macro MUPs
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CHAPTER 6 • ADVANCED NEEDLE EMG METHODS 123

Figure 6-15 ● Macro EMG amplitude and area values in patients with muscular dystro-
phy. (Reprinted with permission from Hilton-Brown P, Stålberg E. Motor unit size in muscular dystrophy;
a macro EMG and scanning EMG study. J Neurol Neurosurg Psychiatry 1983;46:996–1005.)

T A B L E 6 - 2 Relationship between Macro EMG Amplitude and Fiber Density

Macro MUP Amplitude Fiber Density

Decr. Normal Incr. Normal Incr.

Small normal MU  
Average MU  
Large normal  
Neuropathy  
Myopathy () () 

Relationship between MU parameters and EMG parameters. Note that an individual EMG finding does not always give a
unique understanding of the MU.
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124 SECTION II • TECHNICAL ASPECTS OF EMG
Figure 6-16 ● Macro MUPs from tibialis anterior in a healthy control and in ALS. Note the
great variation in amplitudes due to reinnervation.
are increased only slightly and the FD is only mod-
erately increased. In cases of slow progression, the
Macro MUPs increase much more, with individual
Macro MUPs 10 to 20 times higher than the upper
normal mean. The Macro MUPs are still in paral-
lel with the increase in FD, indicating a homoge-
neous and effective reinnervation. In later stages of
ALS, the average Macro MUP amplitude may
start to decline although the FD is still high. This
has been interpreted as either fragmentation of
large MUs or an effect of selective dropout of the
largest MUs, leaving the smaller ones preserved.
In patients with a history of polio, Macro
MUP is usually increased dramatically, with indi-
vidual values more than 20 times the normal mean
value. This reflects the preserved capacity for rein-
nervation in these patients, even when there is a
pronounced loss of strength. The late effects of po-
lio have been investigated by Macro EMG. In a
study (37) of 18 patients with two examinations 4
years apart, Macro EMG and biopsy were per-
formed in the vastus lateralis muscle. Force meas-
urements of knee extension were performed. The
Macro EMG MUP amplitudes were increased at
the first investigation by 10 times for the muscles
with stable strength and were increased by 16 times
for the unstable muscles (having new weakness)
group. Four years after the first investigation,
the muscle force was unchanged or decreased,
whereas the Macro MUP amplitude had increased
by 67% (p 0.01) and 35% in the stable and unsta-
ble groups, respectively. This increase could not be
explained by a change in the fiber area, which was
unchanged, but is explained by an increase in the
number of fibers owing to reinnervation. At the
stage of fully utilized reinnervation capacity, addi-
tional loss of MUs cannot be compensated. A con-
tinued loss of MUs will then present clinically as a
new or accelerating decrease of strength over time.
Eight years later, a follow-up study was un-
dertaken in 17 of these patients. The macro MUP
amplitude was larger in 20 of the legs compared
with the initial examination. In contrast, it de-
creased in eight of nine legs from the second to the
third examination when the earlier amplitudes
were greater than 20 times control values (38).
Thus, evidence of ongoing denervation and
reinnervation as well as of failing capacity to
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CHAPTER 6 • ADVANCED NEEDLE EMG METHODS
maintain large MUs was demonstrated. An upper
limit of the compensatory process to maintain
muscle strength can be defined, but with individ-
ual variation in the pattern of contributing factors.
Most EMG studies have failed to depict indi-
vidual EMG parameters that may be used to diag-
nose or predict the so-called post-polio syndrome
(PPS) (39). This is due only partly to the fact that
PPS usually concerns the entire condition of the
patient. Even in studies in which functional tests
concern individual muscles, the EMG changes
were similar in patients with unstable and stable
muscle function (40). The difficulty in finding
predictors for PPS is partly due to the complex re-
lationship between the various causes for reduc-
tion of muscle strength and the compensatory
processes in patients with a history of polio. How-
ever, the muscular component of PPS seems to be
predictable when the Macro MUP is increased in
amplitude by more than 20 times.
Indications for Macro EMG
Estimating MU size in normal muscle
Estimating number of MUs
Recruitment order
Neurogenic conditions
Diagnostic
Quantitative analysis of reinnervation processes
Myopathic conditions
Diagnostic (together with FD)
SCANNING EMG
To investigate the distribution of muscle fibers in
either normal or diseased MUs in some detail, dif-
ferent techniques can be used. One is by means of
glycogen depletion of individual MUs. This
method can hardly be applied in human muscles,
and only a few studies have been reported (41). In
general, the fibers are scattered within the MU
territory, although a nonrandom distribution pat-
tern of muscle fibers has been suggested and fibers
are arranged in a more orderly fashion than statis-
tically expected. Electrophysiologically the terri-
tory was first studied by Buchthal et al by means
of multi-electrodes containing 12 1.5 mm-long
leads distributed over a distance of 25 mm (42).
125
With another multi-electrode technique the
territory of the MU was defined by Stålberg et al
(43) using a multi-electrode with 14 different 25

m electrodes in a special arrangement, allowing
44 recording sites spaced 300
m apart recording
over 14 mm. The fibers were found to scatter in a
manner similar to that shown by others in experi-
mental glycogen depletion studies (i.e., without
evidence of grouping).
Another technique with a higher spatial reso-
lution has been developed to obtain a more detailed
electrophysiologic cross-section of the MU. Called
scanning EMG (44), the method gives an enhanced
spatial resolution of the MU compared to the
multi-electrode techniques because the recording
is made from many more sites, spaced 50
m apart.
It gives a new electrophysiologic dimension to the
MU structure in both normal and pathologic con-
ditions (45,46). It is likely that in cases of slight
changes in MU character, the pathology will be
seen only in portion of a MU, which may be missed
by conventional EMG due to sampling error.
Method
This method has been described in related jour-
nals (46–48). In brief, a SFEMG electrode is used
to trigger the activity from one MU during slight
voluntary contraction (i.e., low-threshold MUs are
studied preferentially). As an exploring electrode,
the “scanning electrode,” a concentric needle elec-
trode, is usually used, but any EMG electrode may
be used (Fig. 6-17). The electrode must be in opti-
mal condition, with a sharp tip and no irregulari-
ties along the shaft, to facilitate a smooth move-
ment through the muscle without jumping. Small
jumps may still occur because of friction and will
cause minor errors in terms of sudden changes in
action potential shape or in territory measures,
probably less than 1 mm. The scanning electrode
is inserted 20 mm away from the triggering elec-
trode, along the longitudinal axis of the muscle
and perpendicular to the direction of the muscle
fibers. A position is sought where one can obtain
synchronous activity with that from the triggering
electrode. The scanning electrode is then pushed
through the triggering MU until a position is
reached where no further trigger-locked spike
components are detected.
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126 SECTION II • TECHNICAL ASPECTS OF EMG

Figure 6-17 ● Principles of scanning EMG. An SFEMG electrode is used for triggering action
potentials from one muscle fiber. A separate EMG electrode is pulled in small steps through the MU, with the
recording time locked to the triggering signal. A picture is obtained of the distribution of one MU under study.

Positioning of the two electrodes usually
takes less than 1 minute. The scanning electrode is
connected to a pulling step-motor (digital linear
actuator), which is controlled by a computer sys-
tem. The motor is mounted in a holder with an
electrode grip and a wide footplate. During the
recording the footplate is held by hand steadily
against the skin over the muscle. The recording is
canceled if the position of the holder is visually
changed in relation to the muscle. The signal
recorded from the single-fiber electrode triggers
the oscilloscope sweep for display and also pro-
duces a short trigger pulse to start the analog-to-
digital conversion process (sampling frequency 20
kHz). A sweep length of 25 ms is stored each time.
The signal is displayed on the computer screen.
When the entire signal has been stored, the step-
motor is initiated to pull the concentric electrode
50
m or multiples thereof. The process is re-
peated until the scanning electrode has passed
through the entire MU cross-section, up to a max-
imum of 20 mm. Unless the patient has pro-
nounced tremor, he or she can usually cooperate
well and can produce a slight steady voluntary
contraction during the recording procedure,
which takes less than 1 minute. The entire proce-
dure from positioning the electrodes to recording
from one MU takes less than 5 minutes.
Three-dimensional plots and color plots of
the amplitude distribution of the MU activity are
produced by the PC. In this way, one obtains a
cross-section and distribution of the MU activity.
The following parameters may be analyzed:
• Diameter of MU cross-section: the measured dis-
tance from first to last record with MU activity
• Number of MU fractions: portions of MU
activity having clearly separated amplitude
maximum in time or in scanning direction
• Number and length of silent portions: record-
ings with no activity that occur between the
fractions
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CHAPTER 6 • ADVANCED NEEDLE EMG METHODS 127

Figure 6-18 ● Normal scanning EMG from tibialis muscle. Five fractions are seen and no silent
areas. The time delay between fractions depends on different endplate zones and on difference in conduction
times in the nerve terminals.

• Number of polyphasic or complex portions
within the MU: number of sections where the
activity has more than four phases or five turns
• Length of polyphasic or complex portion of the
MU: sections with more than four phases or five
turns
Findings in Healthy Subjects
The scanning EMG often shows more than one
amplitude maximum. These may be separated by
areas of very low amplitudes, which are then
called fractions (Fig. 6-18). These probably corre-
spond to muscle fibers innervated by one major
intramuscular nerve branch. If these fractions are
separated in time, a recording position between
them may give rise to early or late satellite compo-
nents. The fractions correspond to the peaks in the
Macro EMG signal.
When scanning is performed with a concen-
tric needle electrode, a “cannula” signal is often ob-
served. This occurs in the situation in which active
muscle fibers are recorded from the cannula but not
from the tip. In this way a slow, positive-going
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128 SECTION II • TECHNICAL ASPECTS OF EMG
component occurs that may be difficult to differen-
tiate from the normal onset or end of the slow phase
of the MUP. Scanning EMG also reveals that many
MUs have at least some portion with polyphasic
signals. It should be noted that a conventional
EMG recording represents only one trace of the
scanning EMG. If a MU contains only a few areas
of polyphasic sections, there is less chance that a
conventional recording is performed in that area,
and therefore less chance that a polyphasic MUP is
recorded. Some parameters obtained from the nor-
mal muscle are presented in a separate report (46).
Findings in Patients with Myopathy
or Neurogenic Conditions
Some typical differences between findings in con-
trol subjects and in patients are shown in Figure 6-
18. The most prominent findings are summarized
as follows:
1. The mean length of cross-section of the MU
was nearly the same in all groups.
2. The mean number of fractions was slightly but
significantly increased in both patient groups.
3. In the myopathic conditions, there were a larger
number of recordings with silent sections than
in either normal or neurogenic conditions.
4. The most striking finding was the increase of
the mean length and number of polyphasic
sections in both patient groups, particularly in
myopathies.
Summarizing the individual findings, we
found that individual scanning recordings were
abnormal in some respect in 81% and 37% of all
recordings in the neurogenic group and in 53%
and 47% of all recordings in the myogenic group
in the biceps and tibialis anterior muscles, respec-
tively. We could not find any correlation between
patient age and any of the scanning parameters in
the patient groups or in the controls.
Indication for Scanning EMG
No clinical indications at present
Research uses:
Mapping MU topography
Mapping distribution of electrical activity in
the muscle
Studies of MUP shapes
Studies of volume conduction parameters
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40. Ravits J, Hallett M, Baker M, et al. Clinical and
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41. Garnett RAF, O’Donovan MJ, Stephens JA, et
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unit territory in different human muscles. Acta
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mal MU in man. J Neurol Sci 1976;27:291–301.
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CHAPTER 7
Quality Improvement and
Reporting in Electrodiagnostic
Medicine
William S. Pease
WHAT IS QUALITY?
Physicians and healthcare institutions are expected
to put their best efforts into improving quality of
care and minimizing the risks to the patient. The
latter concept dates to Hippocrates, and the former
is almost as old in its relationship to the lifelong
learning that is the basis for professional work.
Now it is common to find quality-related health-
care data on the Internet and in the press. For
example, the Leapfrog Group (www.leapfrog-
group.org) and many other institutions are insist-
ing upon improvements in healthcare quality and
safety.
While some aspects of quality are considered
subjective or individual, there is consensus in the
Joint Commission on Accreditation of Healthcare
Organizations (JCAHO, commonly pronounced
“Jayco”) approach, whose goals are to increase the
likelihood of desired health outcomes. A quality
improvement (QI) program should address all
processes of care that affect the patient and other
stakeholders in the EMG evaluation program (1).
The first steps in developing a QI program are to
assign responsibility, ensure accountability, and
support delegation of authority as appropriate (2).
One must then systematically examine the quality
of care that is provided. This must always be
viewed as a continuous process of managing and
improving the patient care in each facility. The
scopes of care for the area must be delineated and
the key functions in the area identified that are
likely to have the greatest impact on the patient.
Measurable indicators are developed and a data-
monitoring system is created so that information
can be shared with the group and with the inter-
ested stakeholders. The data serve as feedback in
the system to trigger improvements in the
processes and also to monitor the outcome of the
changes. Actions may be directed toward achiev-
ing outcomes above a certain target created inter-
nally or related to an external benchmark.
An important overall indicator of quality is
patient satisfaction. It is also important to assess
the satisfaction of physicians and agencies that
refer patients and use the reports in their reviews.
Some examples of quality indicators used to meas-
ure patient satisfaction include the following:
1. Were the services performed on a timely basis?
2. Was the staff courteous and professional?
3. Is the office area safe and accessible?
4. Did the physician communicate well before
and after the procedures?
Data on patient satisfaction can be collected
either in the office at departure or (more com-
monly) by mail survey sent to an adequate sample,
typically 20% of the patients. Surveying for quality
purposes is not considered scientific medical re-
search and does not require research ethics or insti-
tutional review board (IRB) review and approval.
131
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132 SECTION II • TECHNICAL ASPECTS OF EMG
In internal peer review of EMG reports, sev-
eral factors might be considered, such as the
following:
• Appropriate clinical information was included.
• Correct nerves and muscles were studied in re-
lation to the presenting and final diagnoses.
• There is internal consistency of the data that
suggests accuracy in measurement.
• A rational discussion, impression, and recom-
mendation section is included that provides
useful information to the referring physician.
Peer review is strongly encouraged as part of
the QI process, with a review of 10 reports per
quarter from each physician.
QUALIFICATIONS OF THE ELECTRODIAG-
NOSTIC MEDICAL CONSULTANT
The overall responsibility for the testing in an
electrodiagnostic medicine (or EMG) laboratory
should be assigned to a physician medical director
who has appropriate board certification in the
field and who also keeps abreast of the field
through continuing education (3,4). Education
and training in electrodiagnostic medicine occurs
within the framework of residency in physical
medicine and rehabilitation, as well as most neu-
rology programs in the United States and Canada.
Consensus guidelines for education followed by
both specialties have been developed by the
American Association of Neuromuscular and
Electrodiagnostic Medicine (AANEM, formerly
AAEM). The educational requirements include
broad knowledge of neuromuscular diseases and
injuries, as well as the performance of at least 200
patient EMG evaluations as a trainee. Some physi-
cians also pursue subspecialty fellowship training
in EMG after residency. Certification of compe-
tence in electrodiagnosis is included in certifica-
tion of the American Board of Physical Medicine
and Rehabilitation. The American Board of Elec-
trodiagnostic Medicine (ABEM) has a testing and
certification program operated in a relationship
with the AANEM that is highly regarded. The
ABEM examination requires at least 1 year of ex-
perience after training and the performance of an
additional 200 examinations for eligibility. EMG
competence is also a component of the training
and testing in the subspecialties of Clinical Neuro-
physiology and Neuromuscular Medicine (new in
2005), which are under the auspices of the Ameri-
can Board of Psychiatry and Neurology. All of
these certifying programs include maintenance of
certification programs of continuing education
and periodic retesting.
Staff of the EMG laboratory may include
technicians who assist the electrodiagnostic medi-
cine physicians and who also perform nerve con-
duction studies under the direct supervision of the
medical staff. The American Association of Elec-
trodiagnostic Technologists has developed train-
ing guidelines and a board-certification process
for the technicians.
THE ELECTRODIAGNOSTIC
MEDICAL CONSULTATION
The EMG evaluation is an extension of the physi-
cal examination of the patient, using electronic
amplifiers to extend our sensory ability into the
realm of “perceiving” the action potentials of
nerves and muscles. The consultant uses the elec-
trophysiologic methods to diagnose, evaluate the
severity of, and manage the treatment of patients
with neuromuscular problems.
Evaluation of possible proximal nerve injury
affecting a limb usually begins with a clinical eval-
uation suggesting nerve root or plexus injury. Nee-
dle EMG examination is recommended as the test
modality with the best sensitivity and specificity
for these diagnoses (5,6). Selection of the appropri-
ate muscles to be tested is based upon the roots or
nerves thought most likely to be affected based
upon the clinical evaluation (7), as well as the pa-
tient’s tolerance and the examiner’s abilities and
training. The muscle selections later in the study
are also guided by any abnormal findings that are
seen. In general, a screening examination is used
when the patient’s presentation does not limit the
possibilities. This screening examination of five or
six muscles (5,6) is designed so that each root and
plexus component is evaluated based upon the
usual innervation patterns (myotomes). As abnor-
malities are identified, additional muscles are
selected to confirm that an injury exists and that
other neural components are not affected in the
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CHAPTER 7 • QUALITY IMPROVEMENT AND REPORTING
same anatomic region. This approach is referred to
as “surrounding the focal abnormality with a ring
of normal findings.” When the screening exami-
nation produces no abnormalities (a situation we
physicians paradoxically refer to as “negative”),
then the differential diagnosis is refined, and this
might lead to alternate testing. The classic abnor-
malities described in the pathologic states dis-
cussed in other chapters are usually found in
muscles with mild to moderate weakness.
For patients suspected of having peripheral
nerve dysfunction such as polyneuropathy or en-
trapment, the EMG laboratory evaluation usually
begins with sensory and motor nerve conduction
studies. The specific nerves tested and possible ad-
dition of F waves to the studies depends upon the
diagnoses under consideration (8), as discussed in
detail in other chapters of this text. Appropriate se-
lection of nerves and stimulation sites will allow
identification of distal, proximal, or segmental
slowing, as well as identifying reduced amplitude
or conduction block. All of these parameters are
necessary for the appropriate analysis of the
patient’s diagnosis, severity, and prognosis (8). Di-
agnostic information is most likely to result from
testing areas that are moderately affected, result-
ing in measurable but markedly abnormal
electrical recordings.
SAFETY
Patient safety in the EMG laboratory involves
risks of infection, bleeding, electrical injury, and
penetration of the chest or abdomen (9). Infection
is managed by the use of universal precaution
standards, including barriers such as gloves and
disinfection, as well as through the use of dispos-
able supplies. Hemorrhage (Fig. 7-1) is reported
rarely but can occur even in the patient without
coagulopathy. The physician should not perform
needle EMG studies in patients at a high risk of
bleeding, such as those with poorly controlled co-
agulopathy or INR values above the therapeutic
range. The patient on appropriate levels of ther-
apeutic anticoagulants can be safely studied with
added pressure for hemostasis being applied at
the needle site after withdrawal. In the case illus-
trated in Figure 7-1, the examiner reports using
concentric EMG needles (0.46 mm in diameter)
133
and asked the patient to activate the paraspinal
muscles for evaluation of motor unit potentials
(MUPs) (10). As mentioned elsewhere, MUP
evaluation is not recommended in the paraspinal
muscles. In addition, routine use of thinner,
monopolar needles (typically 0.33 to 0.40 mm) is
suggested as less painful and less likely to cause
hemorrhage.
EMG equipment should be inspected regu-
larly for leakage current and ground electrodes
(third lead) should be used consistently. Stimula-
tion near pacemakers and catheters leading to ma-
jor vessels is avoided, or supervised by an appro-
priate specialist when necessary. In general, the
risk of electrical injury is greatest in the presence
of a wire or fluid-filled catheter that penetrates the
skin (creating a current path), in contrast to the
lower risk of stimulation near a fully implanted
pump or pacemaker (9). The electrodiagnostic
consultant should practice within his or her train-
ing or experience when examining around the
torso so as to avoid an unnecessary risk of pneu-
mothorax or peritonitis.
Figure 7-1 ● Axial T2-weighted magnetic
resonance view of the L5 level of the spine
revealing right-sided hematoma as a hy-
perintense white mass in the paraspinal
muscle following concentric needle EMG
examination in the area. The MR scan was
scheduled prior to performance of the EMG and the
bleeding was not suspected based upon clinical eval-
uation of the patient. (Reprinted from Caress JB,
Rutkove SB, Carlin M, et al. Paraspinal muscle
hematoma after electromyography. Neurology
1996;47:269–272, with permission.)
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134 SECTION II • TECHNICAL ASPECTS OF EMG

SATISFACTION: PATIENTS AND while they are under anesthesia. Obviously, this
REFERRAL SOURCES approach to consent in EMG is different when the
decision is made to sedate someone for the EMG
procedures, as well as in a pediatric practice set-
First impressions are important, and patients’ con-
ting (see Chapter 16). Verbal or written consent to
fidence in the provider and trust in the advice re-
procedures and medical care carries with it the ob-
ceived will be improved if they see a friendly and
ligation to educate (inform) patients so that they
efficient office staff when they enter the facility.
can make a decision that is in their interest. When
Smiles and respectful attitudes make the relative
the patient asks the EMG examiner to stop, then
drudgery of registration and billing paperwork a
there is also an obligation to educate him or her on
bit easier and encourage patients to relax in an un-
the consequences of stopping the procedure, while
familiar environment. Addressing patients by
always recognizing his or her right to abandon the
their surname or full name is recommended
testing.
rather than using the first name, especially on
their first visit to the office. Staff should not shout
names or use over-friendly terms such as “Baby”
or “Sweetie.”
COMFORT
Referring physicians and their key staff
The secondary benefit of performing the brief his-
members are valuable partners for the electrodi-
tory and examination of the patient prior to test-
agnostic medicine consultant because they can se-
ing is to develop rapport with the patient and gain
lect the appropriate patients who can be helped
his or her confidence as one proceeds to the un-
through testing and can influence these patients’
comfortable portions of the examination. I will of-
perceptions as they prepare for the visit. Contin-
ten explain that I am crazy enough to perform
ued communication with them, in the form of re-
EMG and nerve conduction study techniques on
ports that clearly explain the findings as well as
myself, unless there is a student available to “vol-
verbal communication in unusual cases, is impor-
unteer,” of course. Many probably doubt the truth
tant to these relationships. Electromyographers
of this (although it surely is true), but the little bit
can also provide formal or informal education
of laughter always goes a long way in relieving the
about the medical management of neuromuscular
anxiety of the patient, and we know that anxiety
problems, as well as patient education materials
and pain are closely related. Having noticed that
describing how to prepare for an EMG test. The
many of my teachers were gifted with the ability
knowledge of the referral source and his or her
to keep up a steady conversation to distract the pa-
ability to transmit it and properly prepare the
tient during testing, I have tried to develop this
patient for the procedure greatly improves the pa-
skill and recommend it. When sensory nerve con-
tient’s perceptions and response to the unusual sit-
duction studies are indicated, I begin with them,
uation of the EMG laboratory.
since they are the least noxious of the EMG labo-
ratory procedures. The examination proceeds
with motor nerve stimulations, followed by the
CONSENT monopolar needle study of muscles, taking advan-
tage of impaired sensation for the initial insertions
An electrodiagnostic medical consultation is a (if available) and saving examination of already-
multistep, iterative process during which the typi- tender locations for the last.
cal patient is alert (not sedated) and able to contin-
uously consent to each step of the procedures. Pa-
tients are not usually asked to sign written consent REPORTING
for EMG testing, in part because the consent
would be moot as soon as they told the examiner What will be remembered from the EMG that
to “stop.” This is in contrast to a surgical proce- you just performed on an interesting patient? A
dure, in which patients may be asked to consent to surgeon taught me that the patient gets to see only
sedation and to decisions that need to be made one part of the surgery: the dressing. (This advice
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CHAPTER 7 • QUALITY IMPROVEMENT AND REPORTING
predated videotaped, minimally invasive surgery,
of course.) He advised us to make sure that the pa-
tient thought that you did neat, clean, and careful
work on the inside by showing him that on the
outside.
Similarly, the referring physician will not
know the discipline and care that you put into the
techniques and measurements of your electrodi-
agnostic studies; he or she will see only the report.
The documentation in the report leads to the real-
ization of the full potential of the electrodiagnos-
tic tests and reduces the need for repeat testing
(11). Will the report show a careful discipline as-
sociated with attention to measurement accuracy?
Will it show thoughtful analysis resulting from a
well-planned and thorough examination with at-
tention to the needs of both the patient and physi-
cian? Will it provide him or her with information
that will improve the care of that patient and en-
courage future referrals? The printed or elec-
tronic report of the electrodiagnostic consultation
is the enduring documentation for the medical
record and for proper reimbursement. Modern
equipment allows automated capture of many im-
portant EMG and nerve response parameters into
a typed and tabulated document. These reports
can include images of the waveforms and re-
sponses as well. This also acknowledges that sur-
geons are usually visually oriented and like to see
the pictures and will want to relate them to the
anatomy. This type of reporting is now the pre-
ferred and expected format for a professional re-
port, and it also facilitates progress into the elec-
tronic medical record (EMR).
A well-organized report is readable by any
physician in any specialty. It avoids jargon, such as
the abbreviations seen in this book that are famil-
iar to the electrodiagnostic medicine community
(e.g., SNAP amplitude or MUP duration). Tables
are common in the area of computer-generated
reports and have come to be expected. These ta-
bles can be organized in any number of ways but
should provide easy-to-read data with clear head-
ings, descriptors, and measurement units.
Reported data should be presented with the ap-
propriate number of significant digits (usually two
or three), and not with numbers like 3.124 ms for
a distal latency or 51.568 m/s for conduction veloc-
ity that suggest an impossible degree of accuracy
in vivo; these should be reported as 3.1 ms and 51.6
135
m/s, respectively. Including figures with wave-
forms demonstrates that you are confident that if
another reviewer sees your raw data, then he or
she will reach the same conclusions. In your con-
clusions, you will draw relationships between
physiology and anatomy. Reports should also pro-
vide the information needed to compare future
and past EMG testing to your report that can pro-
vide objective information about changes in the
patient’s condition.
The language in the report should be consis-
tent, and the report should use language included
in the glossary appendix of this text as well as that
published by AANEM (12). Common examples
and potential problems follow:
• The term “increased insertional activity” is dis-
couraged in favor of columns noting the ap-
pearance of positive sharp waves and fibrilla-
tion potentials, since these terms are more
objective and pathologic (Fig. 7-2).
• “Denervation potentials” and other terms that
suggest diagnostic specificity are strongly dis-
couraged since, for example, we now know that
the potentials previously defined as “denerva-
tion” are commonly found in myopathic condi-
tions. Similarly the old term “myopathic motor
unit potentials” had to be abandoned when it
was learned that similar MUPs occurred in
neuromuscular junction diseases.
Some of your referrals will require an EMG
and some nerve conductions with straightforward
reporting of the results to a specialist, such as a
hand surgeon, who is fairly knowledgeable in us-
ing the information in his or her area of interest.
Other patients will be sent for consultation and
opinions that require far more than the electrodi-
agnostic testing and reporting of data. In some of
these situations you may be able to appropriately
bill for evaluation and management (E&M) serv-
ices in addition to EMG. These reports will, of
course, need to document the expected elements of
an E&M visit, including the application of decision
making in planning additional diagnostic testing
and treatment regimens.
As noted above, the EMG evaluation is an ex-
tension of the physical examination of the patient,
using electronic sensors to extend our sensory abil-
ity into the realm of “perceiving” the action poten-
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Figure 7-2 ● Report for an EMG examination. Note that this includes a space for Social Security
Number, which is now discouraged in keeping with privacy concerns. This complicated case justified a good
deal of clinical information but probably does not justify E&M code billing since the physician did not take re-
sponsibility for a final diagnosis and care plan, other than referral.
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CHAPTER 7 • QUALITY IMPROVEMENT AND REPORTING 137

Figure 7-2 ● Report for an EMG examination. (continued)

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138 SECTION II • TECHNICAL ASPECTS OF EMG
tials of nerves and muscles. The report of the
interaction should document that the patient’s
medical history and clinical examination findings
have been incorporated into the planning and test-
ing processes. It is critical that each evaluation be
individualized to the patient’s situation, but we
also recognize that common problems occur
frequently, and guidelines for testing are available
that are applicable to approximately 90% of
situations (13).
Nerve conduction data presentations must
include the measured distance for each nerve seg-
ment studied, in addition to location names of
each stimulus and recording site. Clear reference
to the use of peak or onset latency values should be
provided, since this is a major area of accepted
practice variation. Amplitude values are also nec-
essary for interpretation and should be reported as
measured from baseline to negative peak, or
clearly designated if measured differently.
Tabular presentation of the data from the
needle EMG study is also preferred. There is not
typically a graphical presentation of this data.
Each muscle (and side) should be identified, and
the table should include information about inser-
tional activity, spontaneous activity, motor unit
morphology, and recruitment for each muscle.
Needle EMG studies are most commonly
performed using sterile, disposable monopolar
needles in the United States and Canada, and this
is the default expectation if the report does not
specify. If concentric, reusable, or other specialty
needles are used, there should be a documented
description and explanation.
CLAIMS AND CODING
The document should also include complete in-
formation needed to affirm compliance with
CPT® coding and billing regulations, as well as
adherence to appropriate practice guidelines. At a
minimum, the nerve conduction test reporting
should identify each point of stimulation and
recording, using conventional nerve and muscle
nomenclature. For needle EMG, each muscle
should be named (with side) and full reporting of
the findings in its individual study (Figs. 7-2 and
7-3). Insurers will expect to see appropriate diag-
nostic codes using the International Classification
of Diseases (ICD) that reflect the medical necessity
of performing the EMG testing. When the study
is nondiagnostic, then it is proper to use codes rep-
resenting the patient’s symptoms, such as pares-
thesia (782.0) or limb pain (729.5), or signs, such as
ataxia (781.3). One must pay constant attention to
changes in coding regulations.
Current CPT® coding guidelines require
that at least five muscles of a limb (which may in-
clude the paraspinal muscles as one muscle) be
studied in order to use the code 95860 for a one-
extremity needle EMG. This is consistent with re-
search on the sensitivity and specificity of these
techniques for common problems such as radicu-
lopathy (5,14). Nerve conduction study coding
standards currently require that a uniquely bill-
able test for coding purposes (i.e., 1 unit of service)
is produced by the repositioning of both the
recording and stimulating electrodes. One unit of
service for either motor or sensory nerve testing
could include recording from multiple stimula-
tion sites, such as the inching technique, as well as
when multiple recording sites are used. An F
wave is considered an add-on service to a motor
nerve conduction study and includes the routine
motor study with latency, conduction velocity,
and amplitude data in addition to 10 F-wave
recordings with reporting of at least the fastest la-
tency (this is sometimes referred to as a “bundled
service” in coding jargon). A common problem in
claims processing is the failure of the insurer to
pay for multiple units of the same CPT-coded
service and respond with an error code such as
“duplicate service.” Adding modifiers for the side
of service (RT or LT), using the modifier 59 for
“distinct service,” and using names of nerves in the
claim are useful ways to improve “clean claim”
processing (see Fig. 7-2). Some payers will still re-
quest a copy of the report, however. The CPT
codes reported for Figure 7-2 are in Table 7-1.
According to the Centers for Medicare and
Medicaid Services (15), nerve conduction testing
codes are among the most frequently used codes,
ranking in the top 200 codes used in frequency in
2004. Sensory nerve conduction (95904) was used
2.8 million times, motor nerve conduction with F-
wave (95903) 1.6 million, and motor nerve con-
duction (95900) 1.4 million times that year. The
total allowed charges on these three codes ex-
ceeded $300 million in 2004, so consultants can ex-
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CHAPTER 7 • QUALITY IMPROVEMENT AND REPORTING 139

Figure 7-3 ● Report of an EMG examination including display of nerve conduction re-
sponse waveforms, which facilitates understanding of the results as well as improving the
ability to reinterpret the results or compare them to additional studies at a later time.
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140 SECTION II • TECHNICAL ASPECTS OF EMG

Figure 7-3 ● Report of an EMG examination including display of nerve conduction re-
sponse waveforms, which facilitates understanding of the results as well as improving the
ability to reinterpret the results or compare them to additional studies at a later time. (con-
tinued)
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CHAPTER 7 • QUALITY IMPROVEMENT AND REPORTING 141

T A B L E 7 - 1 CPT Coding for Billing Purposes Documented by the Report in Figure 7-2

CPT® Units of Service Description

Code

95863 1 3 extremity EMG

95900-59 1 Motor nerve conduction (LT Peroneal)
95903-RT 1 Motor nerve conduction with F-wave (RT Peroneal)
95903-LT 1 Motor nerve conduction with F-wave (LT Tibial)
95903-RT 1 Motor nerve conduction with F-wave (RT Ulnar)
95904 1 Sensory nerve conduction
To avoid rejection because of duplicate codes, many offices employ the modifiers “RT” and “LT” to clarify that a nerve was
studied separately on both sides, or the modifier “59” to designate a distinct service. In this example, the use of the modifier
“59” helps to avoid confusion about whether the 95900 should be “bundled” with one of the 95903 claims. Including the
name of each nerve in the detail of the bill often facilitates processing of the claim. Our office does not use modifier “50” to
designate bilateral testing. Note that since three of the four motor nerve conduction studies included the F wave, only one
unit of 95900 is charged.

pect continued scrutiny of this cost and should use
these procedures always and only when they will
benefit the patient.
INFORMATION CONTENT
All reports must clearly identify the patient by
name, date of birth, and local registration number
(which should not be the U.S. Social Security
Number). In practice, the referring physician’s
name is an added identifier, as well as being an
important contact regarding the patient.
Many practitioners include a listing of their
laboratory’s normal reference values for the com-
mon tests performed. We do not recommend this
approach, since a number of factors can influence
the relevance of these values in an individual pa-
tient. This can lead to inappropriate reinterpreta-
tion of the data by those who were not present at its
collection and who fail to appreciate the modifying
factors. Among others, the factors can include age,
height, weight, temperature, and, most impor-
tantly, considerations of comparing the results
with others from the same patient, including con-
tralateral recordings. For example, a median re-
sponse from the left median motor nerve study
recorded at the abductor pollicis brevis might be
7 mV and considered normal in amplitude, but
when compared to the contralateral study showing
19 mV it would be considered small, since it is less
than 50%. Temperature effects are often easy to
discern, since only cooling causes the combination
of slowed conduction (prolonged latency) in asso-
ciation with increased amplitude and duration; if
only latency times are reported without tempera-
ture measures, we are left to worry about temper-
ature-related errors, leading to misdiagnosis.
The EMG report should include an interpre-
tation or discussion section. This summary should
identify each abnormal test result and place each
in the context of the other test findings as well as
the clinical condition of the patient. A hallmark of
an accurately performed group of measurements
is that the findings are internally consistent and
deviations from this consistency should be
explained in relation to the unusual pathology
present. The report should then build a rational
argument to support a single diagnosis supported
independently by more than one finding during
the evaluation. In an unusual case, the presenta-
tion will be of a single EMG abnormality, and this
usually results in some uncertainty as to both the
accuracy of the result and the diagnosis. Equally
rare is the new finding of two independent disease
processes in one person, and these unusual situa-
tions certainly lead to the need for some special
testing.
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142 SECTION II • TECHNICAL ASPECTS OF EMG
The discussion will relate the findings to the
anatomic and physiologic correlates of the disease
or injury. Anatomic variation will influence the
interpretation of the findings, and these variations
need to be explained clearly, especially when they
are the cause for added test procedures.
In some cases the patient’s ability to tolerate
the testing will affect the choice of procedures and
modify the interpretation because of missing data.
Identification of these situations should be re-
ported, as well as guidance in proceeding with
other testing or repeat electrodiagnostic testing
with special preparation needed, such as sedation
or analgesia. Comments should also be made
about other local factors that might influence the
results, such as temperature, skin abnormalities,
and height and weight, if there is deviation from
the usual range of values that influences the inter-
pretation.
The concluding impression should include
the electrophysiologic diagnosis as well as the
most likely clinical diagnosis (or the refined dif-
ferential diagnosis) after taking into account all of
the available clinical information. A concluding
comment may be used to indicate whether addi-
tion EMG testing in the future is recommended.
EXAMPLE REPORTS
The report of the electrodiagnostic medicine con-
sultation in Figure 7-2 demonstrates appropriate
content, including the demographic data, except
that the Social Security Number should not be
included. A focused patient history and clinical
examination is included, which leads to the appro-
priate testing sequence. Data are presented in
clear tables, a point made especially important
when testing is this extensive. Muscle names and
their innervations are included in tables, although
it is recommended that “quadriceps” be replaced
with the more specific “vastus medialis” as appro-
priate. The use of terms that imply diagnosis such
as “neuropathic” is also to be avoided, and the di-
agnostic interpretations should be left to the dis-
cussion and impression sections at the end. Nerve
stimulation and recording sites are included and
all relevant parameters are reported with nota-
tions about abnormality. The listing of normal
reference values in the tables is discouraged, since
these apply to a broad range of the population and
could encourage overinterpretation by someone
unfamiliar with the testing situation.
Figure 7-3 shows a report of a new, focal in-
jury complicating a longstanding neuromuscular
problem. The patient had been the subject of nu-
merous previous EMG studies and it was not nec-
essary to extensively redocument her polio at this
time, so this receives only passing mention in the
discussion. The report adds the nerve stimulation
response waveforms to the tabulated data, which
is a desirable format if space is not constrained.
Previously our EMR could not contain figures, for
example, but that has now been corrected. One
should honestly show the problems of shock arti-
fact and other situations in which measurements
may be subject to inaccuracy. More importantly,
the visual picture of the severity of the problem
improves the understanding of the numeric data.
Note that the median sensory peak latency from
digit 3 with wrist stimulation at 14 cm is consid-
ered abnormal because it is more than 0.5 ms
greater than the comparable ulnar response, even
though its value is below the upper limit of the
population normal of 3.7 ms.
COMMON ERRORS IN REPORTS
A common error in EMG reporting is the diagno-
sis of multiple nerve root injuries rather than
properly refining the conclusion to a single nerve
root. The problem is found in both lumbar and
cervical radiculopathy studies. The problem
sometimes appears to be in relating the spinal
anatomy to the nerves. For example, the disk be-
tween the fourth and fifth lumbar vertebrae is cor-
rectly termed the L4-5 disk. However, the nerve
roots exiting the spine at this level are the right
and left L4 nerves. The term “L4-5 nerve root” is
an incorrect term (16). In most cases a careful
evaluation of the muscles in the various myotomes
will allow the diagnosis to be located to a single
root with high reliability, and this specificity of the
report will serve the interests of the patient as the
EMG result is considered with imaging studies
and the full clinical picture.
Another problem with EMG reports in the
area of nerve root injury is the examination of the
paraspinal musculature. The table of data result-
90749_ch07(131-144).ps 8/10/06 3:45 PM Page 143
CHAPTER 7 • QUALITY IMPROVEMENT AND REPORTING
ing from study of this muscle group should not
make reference to motor unit potentials or re-
cruitment but rather should be confined to inser-
tional and resting activity (5,14). The complex
muscle layer anatomy of the paraspinal muscula-
ture and the difficulty producing controlled acti-
vation of these muscles have made it impossible to
develop a reference database of normal values for
motor unit configurations and amplitudes. In ad-
dition, many patients with back and neck pain
will not tolerate this procedure, and it has been re-
ported in association with injury to the muscles
and hematoma (10).
Reports often mention the needle EMG or
nerve conduction study of the opponens pollicis
muscle (17). This muscle is almost completely cov-
ered by the abductor pollicis brevis muscle and is
very difficult and painful to investigate; the name
is likely being used inappropriately when the APB
has actually been investigated. It is very infre-
quent that these muscles, either the APB or oppo-
nens, need to be studied.
REFERENCES
1. Elixhauser A, Pancholi M, Clancy CM. Using
the AHRQ quality indicators to improve health
care quality. Joint Commission Journal on Quality
and Patient Safety 2005;31:533–538.
2. Monga T. Guidelines for the establishment of a
quality assurance program in an electrodiagnos-
tic laboratory. Muscle Nerve 1999;22:S33–S39.
3. American Association of Electrodiagnostic
Medicine. The scope of electrodiagnostic medi-
cine. Muscle Nerve 1999;22:S5–S12.
4. Dillingham TR, Pezzin LE. Underrecognition of
polyneuropathy in persons with diabetes by non-
physician electrodiagnostic services providers. Am
J Phys Med Rehabil 2005;84:399–406.
5. Dillingham TR, Lauder TD, Andary M, et al.
Identifying lumbosacral radiculopathies: an op-
timal electromyographic screen. Am J Phys Med
Rehabil 2000;79:496–503.
143
6. Wilbourn AJ, Aminoff MJ. AAEM mini-mono-
graph #32: the electrodiagnostic examination in
patients with radiculopathies. Muscle Nerve
1998;21:1612–1631.
7. Lauder TD, Dillingham TR, Andary M, et al.
Effect of history and physical exam in predicting
electrodiagnostic outcome with suspected lum-
bosacral radiculopathy. Am J Phys Med Rehabil
2000;79:60–68.
8. England JD, Gronseth GS, Franklin G, et al.
Distal symmetrical polyneuropathy: a definition
for clinical research. Arch Phys Med Rehabil
2005;86:167–174.
9. Al-Sheklee A, Shapiro BE, Preston DC. Iatro-
genic complications and risks of nerve conduc-
tion studies and needle electromyography. Mus-
cle Nerve 2003;27:517–526.
10. Caress JB, Rutkove SB, Carlin M, et al.
Paraspinal muscle hematoma after electromyog-
raphy. Neurology 1996;47:269–272.
11. Jablecki CK, Busis NA, Brandstater MA, et al.
Reporting the results of needle EMG and nerve
conduction studies: an educational report. Mus-
cle Nerve 2005;32:682–685.
12. American Association of Electrodiagnostic Medi-
cine. Glossary of terms in electrodiagnostic medi-
cine. Muscle Nerve 2001;24(suppl 10):S5–S28.
13. American Association of Electrodiagnostic
Medicine. Practice parameter for electrodiag-
nostic studies in carpal tunnel syndrome. Muscle
Nerve 1999;22:S141–S143.
14. Dillingham TR, Lauder TD, Andary M, et al.
Identification of cervical radiculopathies: opti-
mizing the electromyographic screen. Am J Phys
Med Rehabil 2001;80:84–91.
15. CMS. Part B Physician/Supplier National Data:
CY2004, Top 200 Level I Current Procedural
Terminology (HCPCS/CPT) Codes. Available
at: http://www.cms.hhs.gov/MedicareFeeforSvc
PartsAB/ Downloads/LEVEL1SERV04.pdf. Ac-
cessed March 25, 2006.
16. Iverson C, Flanagin A, Fontanarosa PB, et al.
AMA manual of style, 9th ed. Philadelphia: Lip-
pincott Williams & Wilkins, 1998:437–443.
17. Johnson EW, Fallon TJ, Wolfe CV. Errors in
EMG reporting. Arch Phys Med Rehabil 1976;57:
30–32.
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CHAPTER 8

Pictorial Guide to Muscles

and Surface Anatomy

Henry L. Lew and Su-Ju Tsai

TABLE 8-1 Masseter (Fig. 8-1)

Innervation Mandibular division of the

trigeminal nerve (cranial nerve V),
mesencephalon
Origin Lower and medial aspect of the
zygomatic arch
Insertion Lateral aspect of the mandibular
ramus
Action Elevation of the mandible for
mastication
Position Supine with the head turned to the
other side or lateral decubitus
Figure 8-1 • Masseter muscle Activation Teeth clenching
Needle This muscle is midway between the
placement angle of the jaw and the temporo-
mandibular joint.
Notes 1. Needle is held at oblique angle of
20 degrees from the skin. Muscles
are too thin for perpendicular
insertion.
2. Motor unit potentials are smaller
in both amplitude and duration
than those seen in limb muscles.

145
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146 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-2 Temporalis (Fig. 8-2)

Innervation Deep temporal nerve—mandibular

division of the trigeminal nerve
(cranial nerve V), mesencephalon
Origin Bony floor of the temporal fossa and
the deep surface of the temporal
fascia
Insertion Coronoid process and anterior
border of the ramus of the mandible
Action Elevation and retraction of the
mandible
Position Supine with the head turned to the
Figure 8-2 • Temporalis
other side or lateral decubitus
Activation Teeth clenching
Needle Vertically above its insertion at the
placement mandible, insert 1–2 cm below the
skull ridge from which it arises.
Palpate temporal artery to avoid.
Notes See notes in Table 8-1.

TABLE 8-3 Auricularis Posterior (Fig. 8-3)

Innervation Facial nerve (cranial nerve VII), pons

Origin Mastoid process
Insertion Cartilage of the ear
Action Retraction of the earlobe
Position Supine with the head turned to the
other side or lateral decubitus
Needle Posterior to the midpoint of the ear;
placement can be absent and some patients
cannot activate voluntarily
Notes See notes in Table 8-1.

Figure 8-3 • Auricularis posterior

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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 147

TABLE 8-4 Frontalis (Fig. 8-4)

Innervation Temporal branch of the facial nerve

(cranial nerve VII), pons
Origin Frontal skin and superficial fascia of
the eyebrow
Insertion Epicranial aponeurosis
Action Raise the eyebrows
Position Supine
Activation Raise the eyebrows or look upward.
Needle The frontalis muscle is 5 cm above
placement the eyebrow, superior to most of the
wrinkles on the forehead that it
Figure 8-4 • Frontalis
makes.
Notes See notes in Table 8-1.

TABLE 8-5 Orbicularis Oculi (Fig. 8-5)

Innervation Temporal and zygomatic branches of

the facial nerve (cranial nerve VII),
pons
Origin Medial palpebral ligament and
adjacent bones
Insertion Lateral palpebral raphe and adjacent
tissues
Action Closure of the eyelids and dilatation
of the lacrimal sac
Position Supine
Activation Close eyes, resist opening.
Figure 8-5 • Orbicularis oculi
Needle Palpate the margin of the orbital
placement fossa, and insert the needle in 20°
lateral to the margin. Direct the
needle to avoid the eyeball.
Notes See notes in Table 8-1.
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148 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-6 Nasalis (Fig. 8-6)

Innervation Buccal branch of the facial nerve

(cranial nerve VII), pons
Origin Maxilla
Insertion Ala of the nose
Action Widening of the nasal aperture
Position Supine
Activation Deep inspiration through the nostril
Needle Study this muscle just below the
placement bone–cartilage junction of the nose.
Notes See notes in Table 8-1.
Figure 8-6 • Nasalis

TABLE 8-7 Mentalis (Fig. 8-7)

Innervation Mandibular branch of the facial

nerve (cranial nerve VII), pons
Origin Mandible
Insertion Skin on the chin
Action Protrusion of the lower lip
Position Supine
Activation Protrude the lower lip; “pucker.”
Needle Just above the corners of the
placement anterior jaw
Notes See notes in Table 8-1.
Figure 8-7 • Mentalis
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 149

TABLE 8-8 Orbicularis Oris (Fig. 8-8)

Innervation Buccal and mandibular branches of

the facial nerve (cranial nerve VII),
pons
Origin Encircling fibers from the deep
surface of the skin, the buccinator
Insertion Skin and mucous membrane lining
the inner surface of the lips
Action Compressing the lips together
Position Supine
Activation Lip pucker
Needle This is the deepest-lying of the facial
Figure 8-8 • Orbicularis oris
placement muscles; insert just lateral to mouth
angle, with 30° angle for deeper
penetration.
Note See notes in Table 8-1.

TABLE 8-9 Sternocleidomastoid (Fig. 8-9)

Innervation Spinal accessory nerve (cranial nerve

XI) and the anterior rami of the C2
and C3 nerves, medulla
Origin Upper portion of the sternum and
the medial third of the upper surface
of the clavicle
Insertion Mastoid process and lateral portion
of the superior nuchal line of the
occipital bone
Action Tilting of the head to the same side,
and turning the chin to the opposite
side
Position Supine
Activation Rotate the head to opposite side.
Figure 8-9 • Sternocleidomastoid
Needle Midway between the mastoid and
placement the clavicle; pinch muscle and lift to
avoid penetrating too deeply.
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150 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-10 Trapezius (Fig. 8-10)

Innervation Spinal accessory nerve (cranial nerve

XI), C3 and C4 cervical nerves,
medulla
Origin External occipital protuberance,
ligamentum nuchae, and spinous
processes of the C7 and T1–T12
vertebrae
Insertion Lateral third of the clavicle, the
acromion, and the spine of the
scapula
Action Adduction and rotation (elevating
the acromion) of the scapula
Figure 8-10 • Trapezius
Position Prone, lateral decubitus, or sitting
Activation Shrug shoulders.
Needle Draw a line from the C7 spinous
placement process to the acromion and insert in
the center of this line.

TABLE 8-11 Tongue (Fig. 8-11)

Innervation Hypoglossal nerve (cranial nerve

XII), medulla
Origin Superior genial spine of the mandible
Insertion Inferior portion of the tongue
blending with other tongue muscles
Action Protrusion and lateral movement of
apex of the tongue
Position Supine with the head turned to the
other side
Activation Tongue protrusion or contralateral
Figure 8-11 • Tongue movement
Needle Insert vertically upward 1 cm
placement posterior to the (posterior) edge of
the mental portion of the mandible
and 1 cm from center.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 151

TABLE 8-12 Diaphragm (Fig. 8-12)

Innervation Phrenic nerve: C3, C4, C5

Origin Lower six ribs, internal surface of
xiphoid process, medial and lateral
arcuate ligaments from transverse
processes of L1 and L2 vertebrae
Insertion Central tendon of the diaphragm
Action Inspiration (depression of the
diaphragm)

Figure 8-12 • Diaphragm Position Supine

Activation Rapid inspiration with pursed lips
for resistance
Needle From the costal margin, palpate the
placement intercostal space below the 9th rib.
Insert the needle perpendicular to the
skin 1 cm lateral to the anterior
articulation and close to the superior
edge of the 10th rib. Keep amplifier
on and observe the intercostal muscle
EMG activity and the respiratory
pattern. Penetrate deeper with the
needle reaching the diaphragm,
which is active only on inspiration.
Note: For COPD patients with a
depressed diaphragm at rest, insert
the needle below the costal margin in
the angle between the xiphoid
process and the rib.
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152 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-13 Levator Scapulae (Fig. 8-13)

Innervation Dorsal scapular nerve, branches

from C3 and C4
Origin Transverse processes of atlas, axis,
C3, and C4
Insertion Medial border of the scapula,
superior to the root of the spine
Action Elevation of the scapula
Position Prone, lateral decubitus, or sitting
Activation Shrug shoulder.
Needle Insert into the muscle above the
Figure 8-13 • Levator scapulae
placement medial-superior aspect of the
scapula and activate with elevation
of the shoulder.
Note When activating muscles for motor
unit evaluation, use isometric
contraction.

TABLE 8-14 Rhomboid Major (Fig. 8-14)

Innervation Dorsal scapular nerve—C5

Origin Spinous processes of the T2–T5
vertebrae
Insertion Medial border of the scapula, inferior
to the spine
Action Adduction, retraction, and rotation
of the scapula (acromion down)
Position Prone, lateral decubitus, or sitting
Activation Retraction (adduction) of the scapula
Needle Just medial to the inferior third of
placement the scapula; this is a “keep-amplifier-
on” muscle studied with retraction of
the scapula.
Figure 8-14 • Rhomboid major
Note “Keep-amplifier-on” refers to
switching on the preamplifier with
the needle tip in the dermis or sub-
cutaneous layers. The tip is slowly
advanced until the needle enters the
muscle. This avoids accidental pene-
tration through the intercostal space.
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TABLE 8-15 Rhomboid Minor (Fig. 8-15)

Innervation Dorsal scapular nerve—C5

Origin Spinous processes of the C7 vertebra
and the T1 vertebra
Insertion Medial border of the scapula at the
base of the spine of the scapula
Action Adduction, retraction, and elevation
of the scapula
Position Prone, lateral decubitus, or sitting
Activation Retraction of the scapula
Needle Immediately medial to the scapular
placement spine, this is studied with retraction-
elevation of the scapula as a “keep-
Figure 8-15 • Rhomboid minor
amplifier-on” muscle.
Note See notes in Table 8-14.

TABLE 8-16 Serratus Anterior (Fig. 8-16)

Innervation Long thoracic nerve—C5, C6, C7

Origin Anterior and upper surfaces of the
upper eight to nine ribs
Insertion Anterior surface of the medial border
of the scapula
Action Abduction and protraction of the
scapula
Position Lateral decubitus or supine
Activation Forward flexion or protraction of
shoulder
Needle Palpating ribs 6 and 7 in the mid-
placement axillary line will show this muscle,
which protracts the scapula. Place
fingers in the intercostal spaces while
you insert the needle toward the rib
between the fingers.

Figure 8-16 • Serratus anterior

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154 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-17 Supraspinatus (Fig. 8-17)

Innervation Suprascapular nerve—upper

trunk—C5, C6
Origin Supraspinous fossa of the scapula
Insertion Greater tubercle of the humerus
Action Abduction and external rotation of
the shoulder
Position Prone, lateral decubitus, or sitting
Activation Abduction or external rotation of the
shoulder
Needle Just above the spine of the scapula
placement and 2 cm from its medial border.
Avoid the narrow lateral half of the
scapula, which overlies apical lung
Figure 8-17 • Supraspinatus tissue. By inserting the needle down
to the bone, one is assured of passing
through the trapezius completely.

TABLE 8-18 Infraspinatus (Fig. 8-18)

Innervation Suprascapular nerve—upper

trunk—C5, C6
Origin Infraspinous fossa of scapula
Insertion Greater tubercle of the humerus
Action External rotation of the shoulder
Position Prone, lateral decubitus, or sitting
Activation Externally rotate the shoulder.
Needle Halfway between the inferior angle
placement of the scapula and its spine, insert
the needle 3 cm from the medial
edge of the bone.
Figure 8-18 • Infraspinatus
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 155

TABLE 8-19 Teres Major (Fig. 8-19)

Innervation Lower subscapular nerve—posterior

cord—posterior division—upper
trunk—C5, C6
Origin Lower third lateral border of the
scapula
Insertion Medial lip of bicipital groove of the
humerus
Action Adduction, extension, and internal
rotation of the arm
Position Prone, lateral decubitus, or sitting
Activation Internally rotate the shoulder.
Needle Along the lateral scapula, 2–3 cm
placement above the inferior angle. This is a
Figure 8-19 • Teres major
“keep-amplifier-on” muscle so that
you do not pass through it.
Note See notes in Table 8-14.

TABLE 8-20 Pectoralis Major—Clavicular Head (Fig. 8-20)

Innervation Lateral pectoral nerve—lateral

Figure 8-20 • Pectoralis major—
clavicular head
cord—anterior division—upper
trunk—C5, C6
Origin Sternal half of the clavicle
Insertion Lateral lip of the bicipital groove of
the humerus
Action Adduction, flexion, and internal
rotation of the shoulder
Position Supine or sitting
Activation Internally rotate the shoulder.
Needle Study can be done lateral with
placement shoulder externally rotated to extend
and expose the muscle. Insert medial
to the neck of the humerus. Alterna-
tively, insert just below the middle of
the clavicle.
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156 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-21 Biceps Brachii (Fig. 8-21)

Innervation Musculocutaneous nerve—lateral

cord—anterior division—upper
trunk—C5, C6
Origin Long head: supraglenoid tuberosity
of the scapula
Short head: tip of coracoid process of
the scapula
Insertion Bicipital tuberosity of the radius
Action Supination of the forearm and elbow
flexion
Position Supination of the forearm (elbow
flexion preferentially activates
Figure 8-21 • Biceps brachii brachialis)
Activation Supination of the forearm
Needle Insert into middle of superficial
placement muscle belly. Fully supinate the
forearm to bring this muscle anterior.

TABLE 8-22 Brachialis (Fig. 8-22)

Innervation Musculocutaneous nerve—lateral

cord—anterior division—upper
trunk—C5, C6
Origin Lower two thirds of anterior surface
of the humerus
Insertion Anterior aspect of coronoid process
and tuberosity of the ulna
Action Flexion of the elbow
Position Pronation and extension of the
forearm, supine
Activation Flex the elbow.
Needle This is the primary muscle for elbow
Figure 8-22 • Brachialis
placement flexion. Approach from lateral at the
distal third of the arm.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 157

TABLE 8-23 Coracobrachialis (Fig. 8-23)

Innervation Musculocutaneous nerve—lateral

cord—anterior division—upper and
middle trunk—C6, C7
Origin Tip of the coracoid process of the
scapula
Insertion Middle of medial border of the
humerus
Action Flexion and adduction of the
shoulder
Position Arm at side, supine
Activation Flex the shoulder.
Needle Insert into the anterior axillary fold.
Figure 8-23 • Coracobrachialis
placement Follow muscle line out from the
inferior edge of the coracoid to
midhumerus.

TABLE 8-24 Latissimus Dorsi (Fig. 8-24)

Innervation Thoracodorsal nerve—posterior

cord—posterior division—upper,
middle, and lower trunk—C6, C7,
C8
Origin Spinous processes of lower six
thoracic vertebrae, all lumber and
sacral vertebrae, and posterior iliac
crest
Insertion Floor of the bicipital groove of the
humerus
Action Adduction, extension, and medial
rotation of the shoulder
Position Prone or lateral decubitus, full
shoulder flexion
Activation Resist shoulder extension.
Needle The posterior axillary fold contains
placement this larger muscle. An anterior
Figure 8-24 • Latissimus dorsi
approach helps to avoid the lower
trapezius.
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TABLE 8-25 Deltoid (Fig. 8-25)

Innervation Axillary nerve (posterior and anterior

branches)—posterior cord—posterior
division—upper trunk—C5, C6
Origin Lateral third of the clavicle, upper
aspect of acromion, and spine of the
scapula
Insertion Deltoid tuberosity of the humerus
Action Abduction of the shoulder (assists
with flexion and extension)
Position Anterior and middle heads: supine,
lateral decubitus, or sitting
Posterior head: prone, lateral
decubitus, or sitting
Activation Abduct the shoulder (flexion,
anterior; extension, posterior).
Needle For the anterior head, insert 1 cm
placement lateral to the coracoid process. Insert
midway between acromion and the
Figure 8-25 • Deltoid
tubercle for the middle head. The
posterior head is below the posterior
aspect of the glenoid.
Note Posterior branch—posterior head

TABLE 8-26 Teres Minor (Fig. 8-26)

Innervation Axillary nerve (posterior branch)—

posterior cord—posterior division—
upper trunk—C5, C6
Origin Upper two thirds of the lateral border
of the scapula
Insertion Greater tubercle of the humerus,
capsule of the shoulder joint
Action Adduction and external rotation of
the shoulder
Position Prone, lateral decubitus, or sitting
Activation Externally rotate the shoulder.
Needle This muscle overlies the upper two
placement thirds of the lateral border of the
Figure 8-26 • Teres minor
scapula and the lower portion of the
glenohumeral joint.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 159

TABLE 8-27 Brachioradialis (Fig. 8-27)

Innervation Radial nerve—posterior cord—posterior

division—upper trunk—C5, C6
Origin Proximal two thirds of lateral supracondylar
ridge of the humerus
Insertion Base of styloid process of the radius
Action Flexion of the forearm elbow
Position Half-pronation of the wrist, elbow flexed
Activation Flex the elbow.
Needle Place your thumb into the antecubital space and
placement pinch the muscle lateral to your thumb. Insert
2 cm distal to this point.

Figure 8-27 • Brachioradialis

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160 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-28 Extensor Carpi Radialis (Fig. 8-28)

Innervation Radial nerve—posterior cord—

posterior division—upper and
middle trunk—C6, C7
Origin Lower third of lateral supracondylar
ridge of the humerus, lateral
epicondyle of the humerus, and
radial collateral ligament of the
elbow
Insertion Extensor carpi radialis longus:
posterior aspect of base of the second
metacarpal
Extensor carpi radialis brevis:
posterior aspect of base of the third
metacarpal
Action Extension and radial abduction of
the wrist
Position Pronation of the forearm
Activation Make a fist (this avoids activation of
extensor digitorum).
Needle Palpate the muscle adjacent to the
Figure 8-28 • Extensor carpi
placement brachioradialis on the dorsal forearm
radialis
and insert one third of the distance
from the lateral epicondyle to the
wrist.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 161

TABLE 8-29 Supinator (Fig. 8-29)

Innervation Posterior interosseous nerve*—ra-

dial nerve—posterior cord—poste-
rior division—upper trunk—C6, C7
Origin Lateral epicondyle of the humerus,
lateral ligament of elbow joint,
annular ligament of the radius
Insertion Radial and anterior aspect of upper
third of the radius
Action Supination of the forearm
Position Pronation of the forearm
Activation Supinate the forearm.
Needle With the forearm pronated to extend
placement this muscle, insert 4 cm distal to the
lateral epicondyle and deep (you
have gone only a little too far when
you hit the bone).

Figure 8-29 • Supinator * Also known as deep radial nerve.

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162 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-30 Triceps Brachii (Fig. 8-30)

Innervation Radial nerve—posterior cord—

posterior division—middle and
lower trunk—C7, C8
Origin Long head: infraglenoid tuberosity
of the scapula
Lateral head: lateral and posterior
aspect of the humerus
Medial head: lower posterior aspect
Figure 8-30 • Triceps brachii of the humerus
Insertion Upper posterior aspect of olecranon
process of the ulna
Action Extension of the elbow
Position Supine or lateral decubitus, elbow
flexed
Activation Extend the elbow.
Needle Insert needle into each head as shown
placement in figure. A thick fat pad overlies this
muscle, making it much deeper than
other muscles of the upper limb.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 163

TABLE 8-31 Anconeus (Fig. 8-31)

Innervation Radial nerve—posterior cord—

posterior division—middle and
lower trunk—C7, C8
Origin Lateral epicondyle of the humerus,
posterior ligament of the elbow
Insertion Lateral aspect of the olecranon and
posterior aspect of the ulna
Action Extension of the elbow
Position Pronation of the forearm with flexed
elbow
Activation Extend the elbow.
Needle This muscle lies between the lateral
placement epicondyle and the ulna just below
the olecranon. It is the key to
separating radial nerve injuries
above and below the elbow.

Figure 8-31 • Anconeus

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164 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-32 Extensor Digitorum (Fig. 8-32)

Innervation Posterior interosseous nerve*—radial

nerve—posterior cord—posterior
division—middle and lower
trunk—C7, C8
Origin Common extensor tendon from
lateral epicondyle of the humerus,
and intermuscular septa
Insertion Radial and posterior aspect of
phalanges of the four fingers
Action Extension of the four fingers aids in
extension of the wrist
Position Pronation of the forearm with slight
flexion of the elbow
Activation Hold digits straight, resist flexion.
Needle Between the extensor carpi radialis
placement and the extensor carpi ulnaris. Since
needle study is well tolerated, this
muscle is frequently chosen for
quantitative MUP study and single-
fiber EMG.
Figure 8-32 • Extensor digitorum
* Also known as deep radial nerve.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 165

TABLE 8-33 Extensor Carpi Ulnaris (Fig. 8-33)

Innervation Posterior interosseous nerve*—

posterior cord—posterior division—
upper, middle, and lower trunk—C7,
C8
Origin Common extensor tendon from
lateral epicondyle of the humerus,
posterior border of the ulna
Insertion Ulnar aspect of base of the fifth
metacarpal
Action Extension and adduction of the wrist
Position Pronation of the forearm
Activation Extend the wrist with ulnar
deviation.
Needle The extensor carpi ulnaris is
placement immediately dorsal to the ulna at the
proximal third of the forearm.

* Also known as deep radial nerve.

Figure 8-33 • Extensor carpi ulnaris

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166 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-34 Abductor Pollicis Longus (Fig. 8-34)

Innervation Posterior interosseous nerve*—

radial nerve—posterior cord—
posterior division—middle and
lower trunk—C7, C8
Origin Posterior aspect of the ulna,
interosseous membrane, and middle
third of posterior aspect of the radius
Insertion Radial aspect of base of the first
metacarpal
Action Long abduction of the thumb and
the wrist
Position Pronation of the forearm
Activation Abduct the thumb in palmar plane.
Needle Midforearm in the dorsum, this is
placement a deep-lying muscle; pass by the
tendon of the extensor carpi radialis.

Figure 8-34 • Abductor pollicis

longus * Also known as deep radial nerve.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 167

TABLE 8-35 Extensor Pollicis Longus (Fig. 8-35)

Innervation Posterior interosseous nerve*—radial

nerve—posterior cord—posterior
division—middle and lower
trunk—C7, C8
Origin Middle third of the ulna and
interosseous membrane
Insertion Base of the distal phalanx of the
thumb
Action Extension of the distal phalanx of
the thumb
Position Pronation of the forearm
Activation Extend thumb interphalangeal joint.
Needle This muscle lies between the extensor
placement indicis proprius and the abductor
pollicis longus, midlength of forearm.

Figure 8-35 • Extensor pollicis

longus * Also known as deep radial nerve.
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168 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-36 Extensor Pollicis Brevis (Fig. 8-36)

Innervation Posterior interosseous nerve*—radial

nerve—posterior cord—posterior
division—middle and lower
trunk—C7, C8
Origin Posterior aspect of the radius and
interosseous membrane
Insertion Base of the metacarpophalangeal
joint of the thumb
Action Extension of the proximal phalanx
of the thumb
Position Pronation of the forearm
Activation Extend thumb at the metacarpopha-
langeal joint.
Needle In the distal-third segment of the
placement dorsal forearm, this muscle overlies
the radius.

Figure 8-36 • Extensor pollicis

brevis * Also known as deep radial nerve.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 169

TABLE 8-37 Extensor Indicis Proprius (Fig. 8-37)

Innervation Posterior interosseous nerve*—radial

nerve—posterior cord—posterior
division—middle and lower
trunk—C7, C8
Origin Posterior aspect of lower half of ulna
Insertion Dorsum of the proximal phalanx of
the index finger
Action Extension of the metacarpopha-
langeal joint of the index finger
Position Pronation of the forearm
Activation Extend the index finger.
Needle At the distal third of the ulna on its
placement dorsoradial surface. This is the most
distal motor branch of the radial
nerve, so it is an important muscle to
test for a radial nerve injury.

Figure 8-37 • Extensor indicis

proprius * Also known as deep radial nerve.
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170 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-38 Pronator Teres (Fig. 8-38)

Innervation Median nerve—lateral cord—anterior

division—upper and middle trunk—C6, C7
Origin Humeral head: common flexor tendon from
medial epicondyle of the humerus
Ulnar head: medial aspect of coronoid process
of the ulna
Insertion Middle of radial aspect of the radius
Action Pronation of the forearm, assists with elbow
flexion
Position Supination of the forearm
Activation Resist pronation of forearm.
Needle Draw a line from the medial epicondyle,
placement which intersects the sagittal plane at 45° and
crosses the forearm. Insert at the center of
this line. This is the most superficial of the
volar muscles.

Figure 8-38 • Pronator teres

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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 171

TABLE 8-39 Flexor Carpi Radialis (Fig. 8-39)

Innervation Median nerve—lateral cord—anterior

division—upper and middle trunk—C6, C7
Origin Common flexor tendon from medial
epicondyle of the humerus
Insertion Base of the second and third metacarpals
Action Flexion and abduction of the wrist
Position Supination of the forearm
Activation Wrist flexion with radial deviation
Needle Draw a line from the medial epicondyle of
placement the humerus to the radial styloid. Measure one
third of the distance along this line from the
elbow to the needle insertion point.

Figure 8-39 • Flexor carpi

radialis
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172 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-40 Palmaris Longus (Fig. 8-40)

Innervation Median nerve—lateral and medial cord—

anterior division—middle and lower trunk—
C7, C8
Origin Common flexor tendon from medial
epicondyle of the humerus
Insertion Flexor retinaculum and palmar aponeurosis
Action Flexion of the wrist
Position Supination of the forearm
Activation Flex the wrist.
Needle Deep to the flexor carpi radialis site
placement

Figure 8-40 • Palmaris longus

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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 173

TABLE 8-41 Flexor Digitorum Superficialis (Fig. 8-41)

Innervation Median nerve—lateral and medial cord—

anterior division—middle and lower
trunk—C8, T1
Origin Humeral head: common flexor tendon from
medial epicondyle of the humerus
Ulnar head: coronoid process of the ulna
Radial head: oblique line of the radius
Insertion Palmar surfaces of bases of middle phalanx
of all four fingers
Action Flexion metacarpophalangeal and proximal
interphalangeal joints of all four fingers; aids
in flexing wrist and forearm
Position Supination of the forearm
Activation Flex the proximal interphalangeal joints of
fingers.
Needle Locate needle site at the middle- to distal-
placement third level of the forearm, avoiding the wrist
flexors.

Figure 8-41 • Flexor

digitorum superficialis
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174 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-42 Flexor Pollicis Longus (Fig. 8-42)

Innervation Anterior interosseous nerve—median nerve—lateral

and medial cords—anterior division—middle and
lower trunk—C7, C8
Origin Volar aspect of radius, adjacent interosseous
membrane, and medial border of coronoid process
of the ulna
Insertion Base of distal phalanx of the thumb on palmar
aspect
Action Flexion of the interphalangeal joint of the thumb
Position Supination of the forearm
Activation Flex the thumb’s interphalangeal joint.
Needle At the junction of the middle- and distal-third
placement segments of the forearm, immediately anterior to the
radius. Insert needle from the lateral direction to
avoid the radial artery. This is a very good muscle to
study motor units and recruitment, since the average
person has skillful control of the distal thumb.

Figure 8-42 • Flexor

pollicis longus
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 175

TABLE 8-43 Pronator Quadratus (Fig. 8-43)

Innervation Anterior interosseous nerve—

median nerve—lateral and medial
cords—anteriordivision—middle
and lower trunk—C7, C8
Origin Distal fourth of anterior aspect of
the ulna
Insertion Distal fourth of radial border on
anterior aspect of the radius
Action Pronation of the forearm
Position Pronation of the forearm
Activation Pronate the forearm.
Needle Approach the pronator quadratus
placement from a dorsal approach. Three
centimeters proximal to the ulnar
styloid and midway between the
radius and the ulna. Feel for the
penetration of the interosseous
membrane.

Figure 8-43 • Pronator quadratus

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176 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-44 Abductor Pollicis Brevis (Fig. 8-44)

Innervation Median nerve—medial cord—

anterior division—lower trunk—
C8, T1
Origin Flexor retinaculum, scaphoid, and
trapezium
Insertion Radial aspect of the base of the
proximal phalanx of the thumb
Action Thumb short abduction
Position Supination of the hand
Activation “Post” thumb perpendicular to plane
of palm or pinch tip-to-tip with little
finger.
Needle Draw a line from the center of the
placement distal wrist crease to the lateral edge
Figure 8-44 • Abductor pollicis of the first metacarpophalangeal
brevis joint. The center of this line is the
motor point/center of the abductor
pollicis brevis. Insert slightly lateral.

TABLE 8-45 Opponens Pollicis (Fig. 8-45)

Innervation Median nerve—medial cord—

anterior division—lower trunk—
C8, T1
Origin Trapezium and flexor retinaculum
Insertion Whole radial surface of the first
metacarpal bone
Action Thumb opposition
Position Supination of the forearm
Activation Oppose the thumb.
Needle Deep and slightly media to the
placement abductor pollicis brevis; differentiat-
ing the two muscles is difficult.

Figure 8-45 • Opponens pollicis

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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 177

TABLE 8-46 Lumbricals (Fig. 8-46)

Innervation The radial two lumbricals: median

nerve—medial cord—anterior
division—lower trunk—C8, T1
The ulnar two lumbricals: deep
palmar branch—ulnar nerve—
medial cord—anterior division—
lower trunk—C8, T1
Origin Radial aspect of tendons of flexor
digitorum profundus
Insertion Radial lateral band of the dorsal
digital expansion of the medial four
fingers
Action Flexion of the metacarpophalangeal
joints and extension of the
interphalangeal joints in the four
Figure 8-46 • Lumbricals fingers
Position Supination of the hand, fingers
extended
Activation Extend proximal interphalangeal
joint.
Needle Lumbricals lie medial to the heads of
placement the metacarpals. Use the distal
palmar crease(s) as a guide, as these
muscles lie under this crease.
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178 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-47 Pectoralis Minor (Fig. 8-47)

Innervation Medial pectoral nerve—medial

cord—anterior division—middle
and lower trunk—C7, C8
Origin Anterior aspect of the third to fifth
ribs
Insertion Coracoid process of the scapula
Action Depression and protraction of the
shoulder

Figure 8-47 • Pectoralis minor Position Supine or sitting

Activation Shoulder depression
Needle Palpate the third or fourth rib in the
placement midclavicular line. Keep your finger
in the intercostal space and insert the
needle toward the bone to avoid in-
tercostal penetration.

TABLE 8-48 Pectoralis Major—Sternocostal Head (Fig. 8-48)

Innervation Medial pectoral nerve—medial

Figure 8-48 • Pectoralis major—
sternocostal head
cord—anterior division—middle
and lower trunk—C7, C8
Origin Anterior aspect of the sternum and
cartilages of the upper six ribs
Insertion Lateral lip of the bicipital groove of
the humerus
Action Adduction, flexion, and internal
rotation of the shoulder
Position Supine or sitting
Activation Flex or internally rotate the shoulder.
Needle This muscle is easiest to identify as
placement the lower-medial edge of the anterior
axillary fold.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 179

TABLE 8-49 Flexor Digitorum Profundus (Fig. 8-49)

Innervation Digits II, III: anterior interosseous

Figure 8-49 • Flexor digitorum
profundus
nerve—median nerve—medial
cord—anterior division—middle and
lower trunk—C8, T1
Digits IV, V: ulnar nerve—medial
cord—anterior division—lower
trunk—C8, T1
Origin Anteromedial surface of the ulna,
interosseous membrane, and deep
fascia of the forearm
Insertion Anterior aspect of the distal
phalanges of the medial four fingers
Action Flexion of distal interphalangeal
joints of the four fingers
Position Flexion of the elbow with pronation
of the forearm
Activation Flex the distal interphalangeal joints
of fingers.
Needle Always remember that the medial
placement portion of the flexor digitorum
profundus muscle is superficial.
Insert at the proximal third of the
forearm (between the proximal and
distal segments) 1 cm from the ulna.
Advance needle deep, anterior to
ulna, to enter median innervated
portion.
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180 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-50 Flexor Carpi Ulnaris (Fig. 8-50)

Innervation Ulnar nerve—medial cord—anterior

division—lower trunk—C7, C8, T1
Origin Humeral head: common flexor tendon from
medial epicondyle of the humerus
Ulnar head: olecranon and dorsal border of
the ulna
Insertion Anterior aspect of pisiform, hook of hamate,
and base of the fifth metacarpal
Position Flexion of the wrist aids in adduction of wrist
and flexion of the forearm.
Position Supination of the forearm
Activation Wrist flexion with ulnar deviation
Needle With the forearm fully supinated, palpate the
placement greatest medial prominence of the middle to
proximal third of the forearm.

Figure 8-50 • Flexor carpi

ulnaris
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 181

TABLE 8-51 Abductor Digiti Minimi (Fig. 8-51)

Innervation Ulnar nerve (hypothenar branch)—

medial cord—anterior division—
lower trunk—C8, T1
Origin Tendon of the flexor carpi ulnaris
and pisiform
Insertion Ulnar aspect of the base of the
proximal phalanx of the little finger
Action Abduction of the little finger
Position Supination or pronation of the hand
Activation Abduction of the little finger
Needle Ulnar aspect of the fifth metacarpal,
placement at midshaft

Figure 8-51 • Abductor digiti

minimi

TABLE 8-52 Opponens Digiti Minimi (Fig. 8-52)

Innervation Ulnar nerve (hypothenar branch)—

medial cord—anterior division—
lower trunk—C8, T1
Origin Flexor retinaculum, hook of hamate
Insertion Ulnar border of the fifth metacarpal
Action Opposition of the little finger
Position Supination of the hand
Activation Opposition of the little finger
Needle Deeply inserted toward inner edge of
placement fifth metacarpal bone

Figure 8-52 ● Opponens digiti

minimi
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TABLE 8-53 First Palmar Interosseous (Fig. 8-53)

Innervation Ulnar nerve (deep branch)—medial

cord—anterior division—lower
trunk—C8, T1
Origin Ulnar aspect of the second metacarpal
Insertion Ulnar aspect of the proximal phalanx
of the index
Action Adduction of the index toward the
long finger
Position Supination of the hand
Activation Pinch index and long fingers
together.
Needle Insert at the midshaft level of the
placement metacarpal. This is best palpated
from the dorsum. Insert the needle
Figure 8-53 ● First palmar from the palm, just proximal to the
interosseous palmar crease.

TABLE 8-54 Adductor Pollicis (Fig. 8-54)

Innervation Ulnar nerve (deep branch)—medial

cord—anterior division—lower
trunk—C8, T1
Origin Oblique head: trapezium, trapezoid,
capitate, base of the second and third
metacarpals
Transverse head: palmar aspect of
the third metacarpal
Insertion Ulnar side of the base of the proximal
phalanx of the thumb
Action Adduction of the thumb
Position Pronation of the hand
Activation Pinch thumb to index.
Needle Insert by dorsal approach at the
placement midshaft level of the second
metacarpal, radial side; penetrate
deep to the first dorsal interosseous.

Figure 8-54 ● Adductor pollicis

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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 183

TABLE 8-55 First Dorsal Interosseous (Manus) (Fig. 8-55)

Innervation Ulnar nerve (deep branch)—medial

cord—anterior division—lower
trunk—C8, T1
Origin Lateral and medial heads arise from
adjacent sides of the first and second
metacarpal bones.
Insertion Radial side of the proximal phalanx
of the index
Action Abduction of the index
Position Half-pronation of the hand
Activation Spread fingers apart.
Needle Insert dorsal into the web space close
placement to the second metacarpal and 1 cm
distal to its base at the metacarpopha-
langeal joint.

Figure 8-55 ● First dorsal

interosseous (Manus)
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184 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-56 Cervical Paraspinal Muscles/Multifidi (Fig. 8-56)

Innervation Dorsal rami of the cervical

spinal nerves
Origin Transverse processes of
the cervical vertebrae, two
to four segments in
superior and medial
direction
Insertion Spinous processes of the
cervical vertebrae
Action Extension of the neck
Position Neck flexion in lateral
decubitus or prone
Figure 8-56 ● Cervical paraspinal
Relaxation Gentle active flexion of
muscles/multifidi
the spine
Needle In the cervical and
placement thoracic levels, the initial
needle insertion should be
perpendicular and 1 cm
lateral to the spinous
process. Be aware of the
need to pass through the
trapezius before entering
the paraspinal.
Note Motor unit analysis and
recruitment are not
performed in paraspinal
muscles.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 185

TABLE 8-57 Lumbosacral Paraspinal Muscles/Multifidi (Fig. 8-57)

Innervation Dorsal rami of the lumbosacral spinal

Figure 8-57 ● Lumbosacral
paraspinal muscles/multifidi
nerves
Origin Transverse processes of the
lumbosacral vertebrae, two to four
segments in superior and medial
direction
Insertion Spinous processes of the lumbosacral
vertebrae
Action Extension of the back
Position Round back (kyphosis) in lateral
decubitus or prone with pillow under
abdomen
Relaxation Tense abdominal muscles (spine
flexors).
Needle In the lumbar region, the needle
placement should be inserted 2–3 cm lateral to
the spinous process since the muscle
mass is greater and there is less
worry about the needle producing
injury with too-deep penetration.
Note See note in Table 8-56.
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TABLE 8-58 Intercostalis—External and Internal (Fig. 8-58)

Innervation Anterior division of the spinal

nerves—T1–T11
Origin Inferior border of the rib above
Insertion Superior border of the rib below
Action Inspiration
Position Supine
Activation Ask patient to inspire with pursed
lips for resistance.
Needle The intercostal spaces are best
placement exposed anteriorly. Insert the needle
at a low angle (20 degrees from skin)
near and parallel to the superior edge
of the rib to which you are closest.
This angle allows the needle a longer
track within this thin muscle. Keep
amplifier on and observe respiratory
movements.

Figure 8-58 ● Intercostalis—

external and internal.

TABLE 8-59 Rectus Abdominis (Fig. 8-59)

Innervation Intercostal nerves—T7–T12

Origin Pubic crest and symphysis pubis
Insertion Xiphoid process and the fifth to
seventh costal cartilages
Action Flexion of the trunk
Position Supine
Activation Raise head (flex neck).
Needle Palpate the segments of the muscles
placement as you carefully examine for any
signs of hernia in this area. There is
no need to penetrate deeply, and so
there is little chance of hitting the
peritoneum.
Figure 8-59 ● Rectus abdominis
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 187

TABLE 8-60 External Anal Sphincter (Fig. 8-60)

Innervation Inferior rectal nerve—pudendal

nerve—sacral plexus—S2, S3, S4
Origin Coccygeal apex and anococcygeal
raphe
Insertion Perineal body
Action Contraction of the anal sphincter
Activation Ask patient to contract the sphincter
or tense gluteus maximus.
Needle Sphincter: Insert needle at mucocu-
placement taneous junction (the edge of the
pink) in each of the four quadrants
(anterior/posterior, right/left).

Figure 8-60 ● External anal

sphincter
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188 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-61 Gracilis (Fig. 8-61)

Innervation Obturator nerve—anterior division

of lumbar plexus—L2, L3, L4
Origin Lower half of the symphysis pubis
and the pubic arch
Insertion Proximal part of medial surface of
the tibia, behind the insertion of the
sartorius
Action Flexion and internal rotation of the
knee, adduction of the thigh
Position Supine with flexion, abduction, and
external rotation of the thigh
Activation Flex hip while in external rotation or
Figure 8-61 ● Gracilis
raise knee in position shown.
Needle In the distal third of the medial thigh,
placement this muscle is just anterior to the
medial hamstring tendon. This is the
most superficial of the adductor
muscles.

TABLE 8-62 Adductor Longus (Fig. 8-62)

Innervation Obturator nerve—anterior division

of lumbar plexus—L2, L3, L4
Origin Pubic tubercle
Insertion Middle half of medial lip of linea
aspera of the femur
Action Adduction and flexion of the hip
Position Supine with abduction of the hip
Activation Adduct the hip, or external rotate
and flex hip.
Needle Very deep in the proximal thigh, this
placement muscle is found below its origin at
Figure 8-62 ● Adductor longus the pubis.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 189

TABLE 8-63 Adductor Magnus (Fig. 8-63)

Innervation Anterior fibers: obturator

nerve—anterior division
of lumbar plexus—L2,
L3, L4, L5
Posterior fibers: tibial
portion of sciatic nerve—
posterior division of
lumbar plexus—L4, L5
Origin Anterior fibers: ischial
Figure 8-63 ● Adductor magnus ramus and inferior pubic
ramus
Posterior fibers: ischial
tuberosity
Insertion Anterior fibers: linea
aspera
Posterior fibers: adductor
tubercle of the femur
Action Adduction and flexion
(anterior fibers)/extension
(posterior fibers) of the hip
Position Supine with flexion and
external rotation of the hip
Activation Adduct the hip.
Needle In the abducted thigh,
placement behind the gracilis muscle
at the proximal third
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190 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 8-64 Iliopsoas (Fig. 8-64) (Iliacus and psoas muscles combined near
insertion)

Innervation Femoral nerve—posterior division

of lumbar plexus—L2, L3, L4
Origin Transverse processes and bodies of
lumbar vertebrae, iliac crest, iliac
fossa, anterior sacroiliac, lumbosacral,
iliolumbar ligaments, and ala of the
sacrum
Insertion Lesser trochanter of the femur, hip
joint capsule, and femoral body
Action Flexion of the hip
Position Supine
Activation Flex the hip.
Needle Palpate the anterior superior iliac
placement spine (ASIS) and insert the needle
1 cm medial-inferior to this bony
prominence. To reach muscle fibers
that are part of the psoas, insert the
Figure 8-64 ● Iliopsoas needle more medial, midway
between the pulse of the femoral
artery and the ASIS.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 191

TABLE 8-65 Pectineus (Fig. 8-65)

Innervation Femoral nerve—posterior division

of lumbar plexus—L2, L3, L4
Origin Pectineal line of the superior ramus
of the pubis
Insertion Proximal portion of the pectineal
line of the femur
Action Adduction, flexion, and medial
rotation of the hip
Position Supine
Activation Internally rotate the hip.
Needle Two to three cm inferior and lateral
placement to the pubic ramus, and 2 cm medial
to the femoral artery

Figure 8-65 ● Pectineus

TABLE 8-66 Sartorius (Fig. 8-66)

Innervation Femoral nerve—posterior division

Figure 8-66 ● Sartorius
of lumbar plexus—L2, L3, L4
Origin Anterior superior iliac spine (ASIS)
Insertion Proximal part of medial surface of
the tibia
Action Flexion, abduction, and external
rotation of the hip, flexion of the
knee
Position Supine, flexion, and external rotation
of the hip with flexion of the knee
Activation Flex the knee and hip.
Needle The muscle is usually visible below
placement its attachment at the ASIS when the
hip is externally rotated and
abducted.
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TABLE 8-67 Vastus Medialis (Fig. 8-67)

Innervation Femoral nerve—posterior division

of lumbar plexus—L2, L3, L4
Origin Distal half of the intertrochanteric
line, medial lip of the linea aspera of
the femur
Insertion Medial border of the patella, tibial
tuberosity by the patellar ligament
Action Extension of the knee
Position Supine
Activation Flex hip, keeping knee straight (lift
foot).
Needle About 6 cm above the patella; this
placement large muscle is anterior and medial
in the thigh.

Figure 8-67 ● Vastus medialis

T A B L E 8 - 6 8 Vastus Lateralis (Fig. 8-68)

Innervation Femoral nerve—posterior division

of lumbar plexus—L2, L3, L4
Origin Hip joint capsule, intertrochanteric
line, greater trochanter, gluteal
tuberosity, and linea aspera of the
femur
Insertion Lateral border of the patella, tibial
tuberosity by the patellar ligament
Action Extension of the knee
Position Supine
Activation Flex hip, keeping knee straight;
direct patient to raise heel off table.
Needle At a level 8–10 cm proximal to the
placement patella, and anterior and lateral in
the thigh

Figure 8-68 ● Vastus lateralis

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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 193

T A B L E 8 - 6 9 Rectus Femoris (Fig. 8-69)

Innervation Femoral nerve—posterior division of

lumbar plexus—L2, L3, L4
Origin Anterior inferior iliac spine and
superior brim of the acetabulum
Insertion Patella and tibial tuberosity by the
patellar ligament
Action Flexion of the hip and extension of
the knee
Position Supine
Activation Flex the hip and extend the knee;
direct patient to raise heel from
table.
Needle Midway along a line from the ante-
placement rior superior iliac spine to the
patella. The muscle lies below a
thick layer of fat in many persons.

Figure 8-69 ● Rectus femoris

T A B L E 8 - 7 0 Quadratus Femoris (Fig. 8-70)

Innervation Nerve to the quadratus femoris—

tibial portion of sciatic nerve—
anterior division of lumbosacral
plexus—L4, L5, S1
Origin Outer part of the ischial tuberosity
Insertion Quadrate tubercle of the femur
Action Adduction and external rotation of
the hip
Position Prone or lateral decubitus
Activation Externally rotate the hip.
Needle This deep muscle has well-defined
placement bony landmarks. Palpate the ischial
tuberosity and the greater trochanter
of the femur, and insert the needle
halfway between.

Figure 8-70 ● Quadratus femoris

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194 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 8 - 7 1 Piriformis (Fig. 8-71)

Innervation Nerve to the piriformis—S1, S2

Origin Anterior aspect of the sacrum,
margin of the greater sciatic foramen,
the sacrotuberous ligament
Insertion Superior border of the greater
trochanter of the femur
Action External rotation and abduction of
the hip
Position Prone or lateral decubitus
Activation Externally rotate the hip.
Needle Deep and small, this muscle is
placement difficult to approach. If the posterior
inferior iliac spine can be palpated,
then insert the needle 1 cm inferior
and lateral to that point.

Figure 8-71 ● Piriformis

T A B L E 8 - 7 2 Gluteus Maximus (Fig. 8-72)

Innervation Inferior gluteal nerve—posterior

Figure 8-72 ● Gluteus maximus
division of lumbosacral plexus—L5,
S1, S2
Origin Posterior gluteal line, posterior
surface of the sacrum and coccyx,
sacroiliac joint
Insertion Gluteal tuberosity and linea aspera
of the femur, iliotibial tract
Action Extension, adduction, and external
rotation of the hip
Position Prone or lateral decubitus
Activation Externally rotate the hip in side-
lying position (with hip and knee
flexed, raise the knee lateral while
keeping the foot down).
Needle Palpate the sacroiliac joint, which is
placement this muscle’s origin. Insert the needle
1–2 cm lateral to the sacroiliac joint.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 195

T A B L E 8 - 7 3 Tensor Fasciae Latae (Fig. 8-73)

Innervation Superior gluteal nerve—posterior

division of lumbosacral plexus—L4,
L5, S1
Origin Outer lip of the anterior part of iliac
crest
Insertion Lateral condyle of the tibia and the
iliotibial tract
Action Flexion, abduction, and internal
rotation of the hip
Position Supine or lateral decubitus
Activation Internally rotate the hip.
Needle The tensor fasciae latae is 3 cm
placement anterior to the greater trochanter of
the femur on a line inferior from its
origin on the lateral anterior superior
iliac spine.

Figure 8-73 ● Tensor fasciae latae

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196 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 8 - 7 4 Gluteus Medius (Fig. 8-74)

Innervation Superior gluteal nerve—posterior

division of lumbosacral plexus—L4,
L5, S1
Origin Iliac crest, between posterior and
anterior gluteal line of the ilium
Insertion Greater trochanter
Action Abduction and internal rotation of
the hip
Position Prone or lateral decubitus
Activation Abduct the hip.
Needle The muscle is found 3 cm inferior to
placement the midpoint of the iliac crest.

Figure 8-74 ● Gluteus medius

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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 197

T A B L E 8 - 7 5 Biceps Femoris—Short Head (Fig. 8-75)

Innervation Fibular* portion (lateral division) of

sciatic nerve—posterior division of
lumbosacral plexus—L5, S1, S2
Origin Lateral lip of the linea aspera of the
femur, lateral supracondylar line
Insertion Fibular head and lateral condyle of
the tibia
Action Flexion of the knee
Position Prone or lateral decubitus
Activation Flex the knee.
Needle Four centimeters proximal to the
placement popliteal crease, insert the needle so
that the point is deep to the lateral
hamstring tendon. Can enter the
skin either medial or lateral to the
tendon.

Figure 8-75 ● Biceps femoris—

short head * Also known as peroneal.
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198 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 8 - 7 6 Tibialis Anterior (Fig. 8-76)

Innervation Deep fibular nerve—common

peroneal nerve—sciatic nerve—
posterior division of lumbosacral
plexus—L4, L5
Origin Lateral condyle and lateral surface
of the tibia, anterior interosseous
membrane
Insertion Medial and plantar aspect of the
medial cuneiform bone and base of
the first metatarsal bone
Action Dorsiflexion and inversion of the
ankle
Position Supine
Activation Ankle dorsiflexion
Needle One third of the distance from the
placement knee (tibial plateau) to the ankle
(malleolus) and 1 cm lateral to the
tibial crest

Figure 8-76 ● Tibialis anterior

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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 199

T A B L E 8 - 7 7 Extensor Digitorum Longus (Fig. 8-77)

Innervation Deep fibular nerve—common

peroneal nerve—sciatic nerve—
posterior division of lumbosacral
plexus—L5, S1
Origin Lateral condyle of the tibia, proximal
three fourths of anterior surface of
the fibula, and anterior interosseous
membrane
Insertion Dorsal aspects of middle and distal
phalanges of the lateral four toes
Action Extension of metatarsophalangeal
joints of the lateral four toes
Position Supine
Activation Extend the toes.
Needle One third of the distance from the
placement knee (tibial plateau) to the ankle
(malleolus) and 2.5 cm lateral to the
tibial crest

Figure 8-77 ● Extensor digitorum

longus
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200 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 8 - 7 8 Peroneus Tertius (Fig. 8-78)

Innervation Deep fibular nerve—common

peroneal nerve—sciatic nerve—
posterior division of lumbosacral
plexus—L5, S1
Origin Distal third of anterior surface of the
fibula
Insertion Dorsal aspect of the fifth metatarsal
bone
Action Dorsiflexion and eversion of the
ankle
Position Supine
Activation Dorsiflex and evert the ankle.
Needle Just lateral to the extensor hallucis
placement longus, the muscle lies anterior to
the fibula in its distal third.

Figure 8-78 ● Peroneus tertius

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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 201

T A B L E 8 - 7 9 Extensor Hallucis Longus (Fig. 8-79)

Innervation Deep fibular nerve—common

peroneal nerve—sciatic nerve—
posterior division of lumbosacral
plexus—L5, S1
Origin Middle half of anterior surface of the
fibula and adjacent interosseous
membrane
Insertion Base of the distal phalanx of the
great toe
Action Extension of the great toe
Position Supine
Activation Extend the great toe.
Needle Measure one third of the way from
placement the ankle (lateral malleolus) to the
knee (head of the fibula) and insert
the needle midway between the tibia
and the fibula.

Figure 8-79 ● Extensor hallucis

longus
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T A B L E 8 - 8 0 Extensor Digitorum Brevis (Fig. 8-80)

Innervation Deep fibular nerve—common

peroneal nerve—sciatic nerve—
posterior division of lumbosacral
plexus—L5, S1
Origin Upper and lateral aspect of the
calcaneus
Insertion The first tendon: dorsal aspect of the
base of the proximal phalanx of the
Figure 8-80 ● Extensor digitorum
brevis great toe
The second to fourth tendons: lateral
aspects of the tendons of the extensor
digitorum longus
Action Extension of the great toe and middle
three toes
Position Supine
Activation Extend the toes.
Needle Palpate this muscle from its bony
placement origin on the calcaneus. Insert 1–2
cm distal to the bony prominence.

T A B L E 8 - 8 1 Peroneus Longus (Fig. 8-81)

Innervation Superficial fibular nerve—common

peroneal nerve—sciatic nerve—pos-
terior division of lumbosacral
plexus—L5, S1
Origin Head and upper two thirds of the
lateral surface of the fibula and
lateral condyle of the tibia
Insertion Lateral side of the medial cuneiform
bone and base of the first metatarsal
bone
Action Plantarflexion and eversion of the
ankle
Position Supine or lateral decubitus
Activation Evert the ankle with plantarflexion.
Needle Aligned next the extensor digitorum
Figure 8-81 ● Peroneus longus
placement longus, this muscle is about 4 cm
lateral to the tibial crest at its
proximal third.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 203

T A B L E 8 - 8 2 Peroneus Brevis (Fig. 8-82)

Innervation Superficial fibular nerve—common

peroneal nerve—sciatic nerve—
posterior division of lumbosacral
plexus—L5, S1
Origin Lateral surface of the lower two
thirds of the fibula
Insertion Lateral side of base of the fifth
metatarsal bone
Action Plantarflexion and eversion of the
ankle
Position Supine or lateral decubitus
Activation Evert the ankle with plantarflexion.
Needle At the distal third of the fibula, this
placement muscle lies beneath the peroneus
longus. The needle should aim for
the center of the fibula.

Figure 8-82 ● Peroneus brevis

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204 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 8 - 8 3 Semitendinosus (Fig. 8-83)

Innervation Tibial portion (medial division) of

sciatic nerve—anterior division of
lumbosacral plexus—L5, S1
Origin Ischial tuberosity
Insertion Proximal part of medial surface of
the tibia, behind the insertion of the
sartorius and the gracilis
Action Flexion of the knee, extension of the
hip
Position Prone or lateral decubitus
Activation Flex the knee.
Needle Approach this muscle at the proximal
placement third along its line to the ischium
from the medial hamstring tendon.

Figure 8-83 ● Semitendinosus

T A B L E 8 - 8 4 Semimembranosus (Fig. 8-84)

Innervation Tibial portion of sciatic nerve—

anterior division of lumbosacral
plexus—L5, S1
Origin Ischial tuberosity
Insertion Medial aspect of posterior surface of
medial condyle of the tibia
Action Flexion and internal rotation of the
knee, extension of the hip
Position Prone or lateral decubitus
Activation Flex the knee.
Needle This muscle is deep to the semi-
placement tendinosus and best approached in
the distal third of the thigh.

Figure 8-84 ● Semimembranosus

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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 205

T A B L E 8 - 8 5 Biceps Femoris—Long Head (Fig. 8-85)

Innervation Tibial portion of sciatic nerve—

anterior division of lumbosacral
plexus—L5, S1
Origin Ischial tuberosity
Insertion Fibular head
Action Flexion of the knee, extension of the
hip
Position Prone or lateral decubitus
Activation Flex the knee.
Needle On the line of the muscle from the
placement fibular head to the ischium, insert
the needle near the midpoint.

Figure 8-85 ● Biceps femoris—

long head
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206 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 8 - 8 6 Tibialis Posterior (Fig. 8-86)

Innervation Tibial nerve—sciatic nerve—

Figure 8-86 ● Tibialis posterior
anterior division of lumbosacral
plexus—L5, S1
Origin Lateral part of posterior surface
of the tibia, posterior aspect of
interosseous membrane, and upper
two thirds of medial surface of the
fibula
Insertion Tuberosity of the navicular bone,
plantar surface of all cuneiform
bones, base of the second to fourth
metatarsal bones, cuboid bone, and
sustentaculum tali
Action Plantarflexion and inversion of the
ankle
Position Supine or lateral decubitus
Activation Invert the ankle.
Needle This deepest muscle of the leg is
placement found by inserting the needle from a
medial approach, 1 cm behind the
tibia at its distal third, through the
flexor digitorum longus until the tip
of the needle is midway through the
leg. The thick fascia between the
muscles is usually felt as it is
penetrated.
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 207

T A B L E 8 - 8 7 Flexor Digitorum Longus (Fig. 8-87)

Innervation Tibial nerve—sciatic nerve—

anterior division of lumbosacral
plexus—L5, S1
Origin Middle of posterior surface of the
tibia
Insertion Plantar surface of base of distal
phalanges of the lateral four toes
Action Flexion of the lateral four toes
Position Supine or lateral decubitus
Activation Flex the lateral four toes.
Needle Insert medially into this muscle,
placement which is found half the distance
from the ankle to the knee and 1 cm
posterior to the tibia. With the
patient supine, the needle should be
Figure 8-87 ● Flexor digitorum
aligned in the coronal plane.
longus
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208 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 8 - 8 8 Gastrocnemius (Fig. 8-88)

Innervation Tibial nerve—sciatic nerve—anterior division of

sacral plexus—L5, S1, S2
Origin Two heads from medial and lateral femoral
condyles, adjacent femur, and knee joint capsule
Insertion Calcaneus as Achilles tendon
Action Plantarflexion of the ankle and flexion of the
knee
Position Prone or lateral decubitus
Activation Plantarflexion of the ankle with knee extended
(difficult to activate fully)
Needle Insert the needle deeply into these large muscle
placement bellies, since the subcutaneous layer can be thick
here. They are easily palpated in the proximal
calf.

Figure 8-88 ● Gastrocnemius

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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY
T A B L E 8 - 8 9 Soleus (Fig. 8-89)
Figure 8-89 ● Soleus
T A B L E 8 - 9 0 Abductor Hallucis (Fig. 8-90)
Figure 8-90 ● Abductor hallucis
Page 209
209
Innervation Tibial nerve—sciatic nerve—
anterior division of lumbosacral
plexus—S1, S2
Origin Posterior surface of head and upper
third of the fibula, middle third of
the medial border of the tibia, and
tendinous arch between the tibia and
the fibula
Insertion Calcaneus as Achilles tendon
Action Plantarflexion of the ankle
Position Prone or lateral decubitus
Activation Plantarflexion of the ankle against
resistance (easier to activate than
gastrocnemius)
Needle Insert into this muscle from medial,
placement although it also has lateral exposure.
Palpating the inferior edge of the
medial gastrocnemius will lead to
the area where the soleus is just
below its tendinous fibers, at the
middle to lower third of the calf.
Innervation Medial plantar nerve—tibial
nerve—sciatic nerve—anterior
division of sacral plexus—S1, S2
Origin Medial process of calcaneal
tuberosity, plantar aponeurosis,
and flexor retinaculum
Insertion Medial side of the base of the
proximal phalanx of the great toe
Action Abduction (spread) of the great toe
Position Supine with external rotation of the
knee
Activation Fan toes out or resist extension and
flexion.
Needle One centimeter inferior to the
placement prominence of the navicular bone
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210 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 8 - 9 1 First Dorsal Interosseous (Pedis) (Fig. 8-91)

Innervation Lateral plantar nerve—tibial nerve—sciatic

nerve—anterior division of sacral plexus—
S1, S2
Origin Adjacent surfaces of the first and the second
metatarsal bones
Insertion Medial aspect of the base of the proximal
phalanx of the second toe
Action Abduction of the second toe
Position Supine
Activation Fan toes out or try to pinch pencil between
first two toes.
Needle At the level of the midpoint of the second
placement metatarsal bone, insert needle from dorsal
and between the metatarsal bones.

Figure 8-91 ● First dorsal

interosseous (pedis)
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CHAPTER 8 • PICTORIAL GUIDE TO MUSCLES AND SURFACE ANATOMY 211

T A B L E 8 - 9 2 Flexor Hallucis Brevis (Fig. 8-92)

Innervation Medial plantar nerve—tibial nerve—

sciatic nerve—anterior division of sacral
plexus—S1, S2
Origin Medial aspect of plantar surface of the
cuboid bone, adjacent lateral cuneiform
bone, and the tendinous insertion of the
tibialis posterior
Insertion Medial and lateral aspect of the proximal
phalanx of the great toe
Action Flexion of the great toe
Position Supine with external rotation of the knee
Activation Flex the great toe.
Needle Medial aspect of plantar surface of the
placement first metatarsal, 2 cm proximal to the
tarsometatarsal joint

Figure 8-92 ● Flexor hallucis

brevis
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212 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 8 - 9 3 Flexor Digitorum Brevis (Fig. 8-93)

Innervation Medial plantar nerve—tibial nerve—sciatic

nerve—anterior division of sacral plexus—
S1, S2
Origin Medial process of the calcaneal tuberosity
and plantar aponeurosis
Insertion Middle phalanges of the lateral four toes
Action Flexion of middle phalanges of the lateral
four toes
Position Supine with external rotation of the knee
Activation Flex the toes.
Needle At the midpoint between the calcaneus and
placement the third metatarsophalangeal joint. This is
an uncomfortable location; consider icing
the skin first if you need the information.

Figure 8-93 ● Flexor digitorum

brevis

T A B L E 8 - 9 4 Abductor Digiti Minimi (Fig. 8-94)

Innervation Lateral plantar nerve—tibial

nerve—sciatic nerve—anterior
division of sacral plexus—S1, S2
Origin Lateral processes of the calcaneal
tuberosity
Insertion Lateral aspect of the proximal
phalanx of the little toe
Figure 8-94 ● Abductor digiti Action Abduction (spread) and flexion of
minimi the little toe
Position Supine with internal rotation of the
knee
Activation Fan toes out.
Needle Locate a site 1 cm proximal to the
placement fifth tarsometatarsal joint.
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CHAPTER 9

Pictorial Guide to Nerve

Conduction Techniques

Henry L. Lew and Su-Ju Tsai

Abbreviations for the electrode placement are as follows:

E1 Placement of the active electrode

E2 Placement of the reference electrode
G Placement of the ground electrode
S • Cathode Placement of the cathode for stimulation
• Anode Relation of stimulator anode to the cathode

CRANIAL NERVES

TABLE 9-1 Cranial Nerve VII to Nasalis (Fig. 9-1)

Electrode placement

E1 Over nasalis (lateral side of midnose)

E2 Over contralateral nasalis
G On the cheek or chin
S Postauricular stimulation—behind the
lower ear, below the mastoid process and
behind the neck of the mandible

Normal values

Mean
SD Normal limit

Onset latency (1) 3.5
0.4 ms 4.2 ms
Amplitude (2) 1 mV
Note: Alternate recording sites from other facial muscles as needed
Figure 9-1 • Cranial nerve VII to evaluate specific branches of CN VII.

213
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214 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 9-2 Blink Reflex (Fig. 9-2)

Electrode placement

E1 Over bilateral orbicularis oculi muscle,

lower lateral portion
E2 Medial inferior orbit
G Chin
S Cathode At the supraorbital notch
Anode Superiorly

Normal values (3) (n  83)

Mean
SD Side-to-side
Figure 9-2 • Blink reflex
(Normal limit) difference
(Normal limit)
R1 latency 10.5
0.8 ms 0.3
0.9 ms
(13.0 ms) (1.2 ms)
Ipsilateral R2 30.5
3.4 ms 1.0
3.4 ms
latency (41.0 ms) (4.4 ms )
Contralateral 30.5
4.4 ms
R2 latency (44.0 ms)
Note: Amplitudes are variable.

TABLE 9-3 Cranial Nerve XI to Trapezius (Fig. 9-3)

Electrode placement

E1 Over the upper trapezius, midway between

C7 spinous process and acromion.
E2 On acromion
G Medial clavicle
S Cathode At the posterior edge of the
sternocleidomastoid muscle
Anode Superiorly

Figure 9-3 • Cranial nerve XI Normal values (4,5) (n  30)

Mean
SD Normal limit

Onset latency 2.2
0.4 ms  3.0 ms
Peak 3.9
1.6 mV  1.0 mV
amplitude
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 215

UPPER BODY

Upper Body: Motor Nerves

TABLE 9-4 Phrenic Nerve (Fig. 9-4)

Electrode placement

E1 On the xiphoid process

E2 On the costal margin, at anterior axillary line
G Medial sternum
S Cathode 3 cm above the clavicle, along
the posterior border of the
sternocleidomastoid muscle
Anode Superiorly
Figure 9-4 • Phrenic nerve

Normal values (6) (n  50)

Mean
SD Normal limit
Onset latency 6.3
0.8 ms 8.6 ms
Amplitude 597
139 V 400 V
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216 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 9-5A Long Thoracic Nerve-1 to Serratus Anterior (Fig. 9-5A)

Electrode placement (7) (Fig. 9-5A)

E1 Self-adhesive, 8.0  0.5-cm, ring-type

electrode—cranial end at nipple level (5 cm
distal to the bipolar stimulator) in line with
the bipolar stimulator contact points and the
anterior superior iliac spine
E2 Self-adhesive surface electrode over the
seventh rib distal to the pectoralis muscle
G Over the ipsilateral latissimus dorsi
S In the axilla just anterior to the midaxillary
line

Normal values (7) (n  15, self-adhesive ring-type

Figure 9-5 • A. Long
electrode recording)
thoracic nerve
Side Mean Normal

SD limit

Right 2.3
3.5 ms

0.5 ms
Onset Left 2.3
3.2 ms
latency 0.4 ms
Side-to-side 0.3
0.6 ms
difference 0.2 ms
Right 3.8
1.6 mV
1.9 mV
Left 3.9
1.2 mV
Amplitude
1.9 mV
Side-to-side 0.6
2 mV
difference 0.6 mV
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 217

TABLE 9-5B Long Thoracic Nerve-2 to Serratus Anterior (Fig. 9-5B)

Electrode placement

E1 A needle electrode is placed into the

digitation of the serratus anterior muscle
over the fifth rib, along the midaxillary line.
E2 Two cm distal to the E1 (no need if a con-
centric needle electrode is used for E1)
G Over the 12th rib level at the anterior axillary
line
S Cathode Slightly above the upper
margin of the clavicle lateral to
the clavicular head of the
Figure 9-5 • B. Long thoracic sternocleidomastoid muscle
nerve
Anode Superomedially

Normal values (8) (n  16, concentric needle

recording)
Age (years) Onset latency Normal limit
Mean
SD
20–35 3.6
0.3 ms 4.2 ms
36–50 3.8
0.4 ms 4.4 ms
51–65 4.0
0.4 ms 4.8 ms
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218 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 9-6 Axillary Nerve to Deltoid (Fig. 9-6)

Electrode placement

E1 Midway between acromion and deltoid

tubercle
E2 At deltoid tubercle
G Between the stimulating point and active
electrode
S Cathode Supraclavicular fossa
Anode Superomedially

Normal values (9) (n  62)

Mean
SD Normal limit

Onset latency 3.9
0.5 ms 5.0 ms
Note: No information on amplitude is available (9).

Figure 9-6 • Axillary nerve

TABLE 9-7 Musculocutaneous Nerve to Biceps (Fig. 9-7)

Electrode placement

E1 Midpoint of the biceps brachii muscle belly

E2 Distal biceps tendon
G Over the acromion
S Cathode Supraclavicular fossa
Anode Superomedially

Normal values (9) (n  62)

Figure 9-7 • Musculocutaneous
nerve Mean
SD Normal limit
Onset latency 4.5
0.6 ms 5.7 ms
Note: No information on amplitude is available (9).
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 219

TABLE 9-8 Suprascapular Nerve (Fig. 9-8)

Electrode placement

E1 A concentric recording needle (E2 

reference/outer cannular of needle)
Supraspinatus: Insert the needle just above
the scapular spine at the midpoint. Advance
the needle in a downward and forward
direction until the needle touches the
scapula, then withdraw it 2–3 mm.
Infraspinatus: Insert the needle 3 cm
below the scapular spine and 3 cm lateral
to the medial border of the scapula.
G Over the posterolateral shoulder
S Cathode Supraclavicular fossa
Anode Superomedially
Figure 9-8 • Suprascapular nerve
Normal values (9) (n  62)
Onset latency Mean
SD Normal limit
Supraspinatus 2.7
0.5 ms 3.7 ms
recording
Infraspinatus 3.3
0.5 ms 4.2 ms
recording
Note: No information on amplitude is available (9).
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220 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 9-9 Thoracodorsal Nerve to Latissimus Dorsi (Fig. 9-9)

Electrode placement (10)

E1 Supine position with the arm abducted to 90

degrees. E1 is on the posterior axillary line
at the intersection of the line horizontally
drawn from the inferior angle of the
scapula.
E2 On the posterior axillary line distal to E1
G On the chest wall, between E1 and S1
S1 Cathode In the axilla toward the lateral
margin of the scapula
Anode Superior
S2 Cathode Erb’s point
Figure 9-9 • Thoracodorsal Anode Superior
nerve
Normal values (10) (n  30)

Mean
SD Range

Axilla Onset latency 1.9
0.4 ms 2.7 ms

(S1) Amplitude, 4.1
1.8 mV 1.4 mV
right
Erb’s Onset latency 3.6
0.4 ms 4.5 ms
point Amplitude 6.0
2.0 mV 2.0 mV
(S2)
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 221

TABLE 9-10 Median Nerve to the Abductor Pollicis Brevis (Fig. 9-10)

Electrode placement

E1 Midline between the first metacarpopha-

langeal joint and the first carpometacarpal
Figure 9-10 • Median nerve to joint
the abductor pollicis brevis
E2 Distal to E1 on the first metacarpopha-
langeal joint
G On the dorsum of the hand
S Cathode S1: 8 cm proximal to the E1,
measured first to the midpoint
of the distal wrist crease and
then on the line between the
tendons of the flexor carpi ra-
dialis and the palmaris longus
S2: On the antecubital crease,
at the medial border of the
biceps brachii tendon
Anode Proximal

Normal values (11,12) (n  47)

Mean
SD Normal
limit

Onset latency 3.7
0.3 ms 4.3 ms

Amplitude 13.2
5.0 mV 5.0 mV
Nerve conduction 56.7
3.8 m/s 50 m/s
velocity

Normal values (13) (n  243)

Mean
SD Normal
limit

Onset latency 3.7
0.5 ms 4.7 ms

Amplitude 10.2
3.6 mV 3.0 mV
Nerve conduction 57
5 m/s 47 m/s
velocity
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222 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 9 - 1 1 Median Nerve (Anterior Interosseous Branch) to the Pronator

Quadratus (Fig. 9-11)

Electrode placement

E1 Centrally over the dorsum of the fore-

arm, 3 cm proximal to the ulnar styloid
Figure 9-11 • Median nerve
E2 On the medial dorsum of the wrist over
(anterior interosseous branch) to
the ulnar styloid process
the pronator quadratus
G On the dorsal forearm, between the E1
and stimulating electrodes
S Cathode On the antecubital crease, at
the medial border of the
biceps brachii tendon
Anode Proximally

Normal values (14) (n  52)

Right Left
Onset latency 3.6
0.4 ms 3.5
0.4 ms
Onset to peak 3.1
0.8 mV 3.1
0.8 mV
amplitude
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 223

T A B L E 9 - 1 2 Radial Nerve to the Extensor Digitorum (Fig. 9-12)

Electrode placement

E1 Proximal third from the antecubital crease

Figure 9-12 • Radial nerve to the
extensor digitorum
(S1), over the belly of the extensor digitorum
E2 On the medial dorsum of the wrist over the
ulnar styloid process
G Between the E1 and the S1
S Cathode S1: In the antecubital fossa just
lateral to the biceps tendon as the
tendon crosses the flexor crease
S2: In the axilla between the
coracobrachialis and the long
head of the triceps
Anode Proximally

Normal values (15) (n  30)

Mean
SD Normal
limit
Onset latency 2.6
0.4 ms 3.5 ms
Amplitude 11.2
3.5 mV 4.3 mV
Conduction velocity 68
7.0 m/s 54 m/s
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224 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 9 - 1 3 Radial Nerve to the Extensor Indicis Proprius (Fig. 9-13)

Electrode placement (16)

E1 Concentric needle electrode into the

extensor indicis proprius, at the distal third
of the dorsal forearm and on the dorsum of
the ulna (E2  outer cannula of needle)
G Between E1 and S1, on the dorsum of the
Figure 9-13 • Radial nerve—to
the extensor indicis proprius forearm
S Cathode S1: In pronation of the forearm;
4 cm proximal to the needle
insertion site, radial border of
the extensor carpi ulnaris
muscle
S2: In pronation of the forearm;
5 cm proximal to the lateral
epicondyle, lateral border of the
triceps brachii muscle
S3: Erb Point
Anode Proximally

Normal values (n  49)

Mean
SD Normal limit
Distal latency (17) 2.4
0.5 ms 2.9 ms
Conduction
velocity (16)
S1-S2 61.6
5.9 m/s 50 m/s
S2-S3 72.0
6.3 m/s 60 m/s
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 225

T A B L E 9 - 1 4 Ulnar Nerve to the Abductor Digiti Minimi (ADM) (Fig. 9-14)

Electrode placement

E1 On the border of the palm and dorsum of

the hand, halfway between the wrist crease
and the base of the little finger
E2 Distal to the fifth metacarpophalangeal joint
G On the dorsum of the hand or between the
stimulating and recording electrodes
S Cathode The arm is in a 45 degrees
abducted and externally rotated
position with the elbow moder-
ately flexed to 90–135 degrees
(18).
S1: 2 cm proximal to the E1,
along the radial border of the
tendon of the flexor carpi
ulnaris
S2: 2 cm distal to the ulnar
groove at the elbow
S3: 10 cm proximal to the S2,
Figure 9-14 • Ulnar nerve—to the measured in a curve along the
abductor digiti minimi ulnar groove to a point be-
tween triceps and brachialis
S4: 10 cm proximal to S3 in the
axilla
Anode Proximally

Normal values (n  31)

Mean
SD Normal
limit
Onset latency (18) 3.2
0.5 ms 4.2 ms
Amplitude 6.14
1.90 mV 2.3 mV
Nerve conduction
velocity (18–20)
S1-S2 61.8
5.0 m/s 53 m/s
S2-S3 62.7
5.5 m/s 52 m/s
S3-S4 62.8
6.0 m/s 51 m/s

(continued)
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226 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 9 - 1 4 Ulnar Nerve to the Abductor Digiti Minimi (ADM) (Fig. 9-14)

(continued)

Normal values (21) (n  248)

Mean
SD Normal limit
Distal latency 3.0
0.3 ms 3.6 ms
(21)
Amplitude, 11.6
2.1 mV 7.4 mV
peak to peak
(21)
Conduction
velocity (21)
S1-S2 61
5 m/s 51 m/s
S2-S3 61
9 m/s 43 m/s
S3-S4 61
7 m/s 47 m/s
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 227

T A B L E 9 - 1 5 Ulnar Nerve to the First Dorsal Interosseous (Fig. 9-15)

Electrode placement

E1 On the dorsum of the hand, the first web

space, 1 cm radial to the midpoint of the
second metacarpal bone
E2 Over the first metacarpophalangeal joint
G Between E1 and S1
S Cathode At the ulnar wrist crease, along
the radial border of the tendon
of the flexor carpi ulnaris
Anode Proximally

Figure 9-15 • Ulnar nerve—to the

first dorsal interosseous

Normal values (22) (n  373)

Onset latency Amplitude

Age (years) Mean Limit Mean Limit

20 3.3 ms 4.2 ms 15 mV 8 mV

20–29 3.4 ms 4.1 ms 14 mV 8 mV

30–39 3.3 ms 4.4 ms 15 mV 6 mV

40–49 3.2 ms 4.2 ms 13 mV 6 mV

50–59 3.4 ms 4.4 ms 13 mV 6 mV

60–69 3.6 ms 4.5 ms 12 mV 7 mV

70 3.6 ms 4.2 ms 12 mV 8 mV

Note: No summarized values are available (22).
Mean side-to-side difference, FDI  0.2 ms (0.0–1.3); ipsilateral difference, FDI ADM  0.9 ms (0.2–2.0) (22).
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228 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 9 - 1 6 F Wave in the Upper Extremity (Fig. 9-16)

Electrode placement

E1 Median nerve: over the abductor pollicis

brevis (see Fig. 9-10)
Ulnar nerve: over the abductor digiti
minimi (see Fig. 9-14)
E2 Median nerve: slightly distal to the first
metacarpophalangeal joint
Ulnar nerve: distal to the fifth metacar-
pophalangeal joint
G On the dorsum of the hand
S Cathode Positioned as for standard
wrist stimulation (see Figs. 9-
10 and 9-14)
Anode Distally with supramaximal
stimulation (see Figs. 9-10
Figure 9-16 • F wave in the upper
extremity
and 9-14)

Normal values (23,24) (shortest of 10 stimuli,

minimal latency)

Nerve Range Side-to-side

differences
Median/APB 22–31 ms 2.3 ms
Ulnar/ADM 21–32 ms 2.5 ms
Note: Ulnar F wave latency (25)  [arm length (cm)  0.31] –
[ulnar nerve forearm velocity (m/s)  0.123]
11.05. A prolonga-
tion of 2.5 ms is considered abnormal.
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 229

Upper Body—Sensory Nerves

T A B L E 9 - 1 7 Lateral Antebrachial Cutaneous Sensory Nerve (Fig. 9-17)

Electrode placement (26)

E1 On volar aspect of the forearm, over the

radius bone, 10 cm distal to the stimulating
Figure 9-17 • Lateral antebrachial cathode
cutaneous sensory nerve
E2 3 cm distal to E1
G Between the stimulating and recording
electrodes
S Cathode Just lateral to the biceps tendon
on the antecubital crease
Anode Proximally

Normal values (26) (10-cm distance) (n  213)

Mean
SD Normal limit

Peak latency 2.2
0.2 ms 2.6 ms
Onset to peak 18
10 V 3 V
amplitude

Normal values (27) (10-cm distance) (n  157)

Mean
SD Normal limit

Peak latency 2.8
0.2 ms 3.3 ms
Onset to peak 18.9
9.9 V 8 V
amplitude
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230 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 9 - 1 8 Medial Antebrachial Cutaneous Sensory Nerve (Fig. 9-18)

Electrode placement (27)

E1 On volar aspect of the forearm, over the

ulna bone, 14 cm distal to the stimulating
Figure 9-18 • Medial antebrachial point
cutaneous sensory nerve
E2 3 cm distal to E1
G Between the stimulating and recording
electrodes
S Cathode Along the medial border of the
biceps brachii muscle, 5 cm
proximal to the medial
epicondyle
Anode Proximally

Normal values (27) (n  157)

Mean
SD Normal limit
Peak latency 2.7
0.2 ms 3.3 ms
Onset to peak
amplitude 11.4
5.2 V 5 V
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 231

TABLE 9-19 Median Sensory Nerve to the Second and Third Digits (Fig. 9-19)

Electrode placement

E1 A ring electrode is placed distal to the base

of the second or third digit.
E2 4 cm distal to the active electrode
G On the dorsum of the hand
S Cathode S1: 14 cm proximal to E1 on
the line between the tendons of
the flexor carpi radialis and the
palmaris longus
S2: The midpoint of the line
from E1 to S1
Anode Proximal

Digit 3: Normal values (28) (n  50)

Figure 9-19 • Median sensory
nerve to the second and third digits Mean
SD Normal
limit
Peak S1 3.07
0.2 ms 3.5 ms
latency S2 1.58
0.15 ms 1.88 ms
S2/S1 52
4% 44%
Peak S1 52
13 V 26 V
amplitude S2 67
20 V 37 V
S2/S1 128
29% 186 %

Digit 3: Normal values (29) (n  258)

Mean
SD Normal
limit
Onset S1 2.7
0.3 ms 3.3 ms
latency S2 1.4
0.2 ms 1.8 ms
Peak S1 3.4
0.3 ms 4.1 ms
latency S2 2.0
0.4 ms 2.8 ms
Onset S1 41
20 V 10 V
to peak S2 43
28 V 4 V
amplitude
Peak S1 63
33 V 12 V
to peak S2 66
43 V 5 V
amplitude

(continued)
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232 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 9-19 Median Sensory Nerve to the Second and Third Digits (Fig. 9-19)
(continued)

Digit 2: Normal values (29) (n  258)

Mean
SD Normal
limit
Onset S1 2.6
0.3 ms 3.2 ms
latency S2 1.3
0.2 ms 1.7 ms
Peak S1 3.4
0.3 ms 4.1 ms
latency S2 1.9
0.2 ms 2.4 ms
Onset S1 37
19 V 8 V
to peak S2 38
24 V 4 V
amplitude
Peak S1 56
31 V 9 V
to peak S2 53
36 V 4 V
amplitude
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 233

TABLE 9-20 Median and Radial Sensory Nerves to the Thumb (Fig. 9-20)

Electrode placement (30,31)

E1 Ring electrode, on the proximal phalanx

E2 Ring electrode, on the distal phalanx
G Dorsum of the hand
S Cathode Sm: Median nerve, 10 cm
proximal to E1, in a line meas-
ured first to the midpoint of
the distal wrist crease and then
on the line between the ten-
dons of the flexor carpi radialis
and the palmaris longus
Sr: Radial nerve, over the
lateral radius, 10 cm proximal
to the active electrode

Figure 9-20 • Median and radial Anode Proximal

sensory nerves to the thumb

Normal values (30) (n  78)

Mean
SD Normal
limit
Peak Median 2.5
0.2 ms 2.9 ms
latency Radial 2.4
0.2 ms 2.8 ms
Baseline Median 30
2 V
to peak Radial 12
1 V
amplitude
Note: The upper limit of normal differences between the median
and radial nerve is latency difference 0.3 ms, and amplitude of
median nerve 200% amplitude of radial nerve.
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234 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 9-21 Median and Ulnar Sensory Nerves to the Fourth Digit (Fig. 9-21)

Electrode placement

E1 Ring electrode, on the first metacarpopha-

langeal joint of the fourth digit
E2 Ring electrode, on the distal
interphalangeal joint of the fourth digit
G Dorsum of the hand
S Cathode Sm: Median nerve, 14 cm
proximal to E1, in a line
measured first to the midpoint
of the distal wrist crease and
then to a point on the line
between the tendons of the
flexor carpi radialis and the
palmaris longus
Su: Ulnar nerve, 14 cm
Figure 9-21 • Median and ulnar
proximal to E1, along the
sensory nerves to the fourth digit
radial border of the flexor carpi
ulnaris tendon
Anode Proximally

Normal values (32) (n  37)

Distal Side Mean
SD Normal

Latency limit
Dominant Median 3.14
0.24 ms 3.6 ms
hand Ulnar 3.03
0.21 ms 3.5 ms
Non- Median 3.11
0.32 ms 3.7 ms
dominant Ulnar 3.01
0.32 ms 3.6 ms
hand
Note: The upper limit of normal increase in latency for the median
versus ulnar nerve is 0.5 ms. No information on amplitude is
available (32).
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 235

TABLE 9-22 Radial Sensory Nerve to the Base of the Thumb (Fig. 9-22)

Electrode placement (33)

E1 Over the extensor pollicis longus tendon at

the wrist level
E2 4 cm distal to E1, on the radial side of the
Figure 9-22 • Radial sensory nerve
second metacarpal bone
to the base of the thumb
G Between E1 and the stimulating cathode
S Cathode Over the radius, 10 cm
proximal to E1
Anode Proximally

Electrode placement (34)

First web space recording

E1 Over the tendon of the extensor pollicis
longus tendon at the apex of the first web
space (near the wrist)
E2 On the skin between the heads of the first
and second metacarpal bones
G Dorsal aspect of the hand
S Cathode On the radial side of the
forearm, 10 cm proximal to the
active electrode
Anode Proximally

Thumb recording
E1 Proximal phalanx of the thumb
E2 Distal phalanx of the thumb
G Dorsal aspect of the hand
S Cathode On the radial side of the fore-
arm, 15–17 cm proximal to the
active electrode
Anode Proximally

(continued)
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236 SECTION II • TECHNICAL ASPECTS OF EMG

TABLE 9-22 Radial Sensory Nerve to the Base of the Thumb (Fig. 9-22)
(continued)

Normal values (33) (n  49)

Mean
SD Normal limit

Onset latency 1.8
0.3 ms 2.4 ms
Peak latency 2.3
0.4 ms 3.1 ms
Peak to peak 31
20 V V
amplitude

Normal values (34) (n  20)

First web space recording (10 cm)

Mean
SD Normal limit

Onset latency 1.6
0.1 ms 1.9 ms
Peak to peak 42.2
14.9 V 16.0 V
amplitude

Thumb recording (15–17 cm)

Mean
SD Normal limit

Onset latency 2.8
0.2 ms 3.3 ms
Peak to peak 12.3
4.9 V 5.0 V
amplitude
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 237

T A B L E 9 - 2 3 Ulnar Sensory Nerve to the Fifth Digit (Fig. 9-23)

Electrode placement

E1 Ring electrode, middle of proximal phalanx

of the fifth digit
E2 Ring electrode, on the distal phalanx of the
fifth digit, 4 cm distal to E1
G On the dorsum of the hand
S Cathode S1: 14 cm proximal to E1, along
the radial border of the flexor
carpi ulnaris tendon
S2: At the midpoint of the line
from E1 to S1
Anode Proximally

Normal values (35) (n  100)

Figure 9-23 • Ulnar sensory Mean
SD Normal
nerve to the fifth digit limit
Onset S1 2.6
0.2 ms 3.0 ms
latency S2 1.4
0.2 ms 1.8 ms
Peak S1 3.4
0.3 ms 4.1 ms
latency S2 2.0
0.2 ms 2.5 ms
Onset S1 32
20 V 6 V
to peak S2 33
17 V 3 V
amplitude
Peak S1 50
32 V 4 V
to peak S2 55
36 V 4 V
amplitude
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238 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 9 - 2 4 Ulnar Dorsal Cutaneous Sensory Nerve (Fig. 9-24)

Electrode placement

E1 Over the proximal point of the “V” formed

by the fourth and the fifth metacarpal bones
E2 Over the fifth metacarpophalangeal joint
G On the dorsum of the hand
S Cathode 8–10 cm proximal to E1 between
the ulna and the flexor carpi
ulnaris tendon
Anode Proximally

Normal values (36) (n  54)

Mean
SD Normal
limit
8-cm study: 1.84
0.20 ms 2.3 ms
peak latency
10-cm study: 2.09
0.21 ms 2.7 ms
peak latency

Baseline to 23.5
8.8 V 5.9 V

Figure 9-24 • Ulnar dorsal cuta- peak amplitude
neous sensory nerve
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 239

LOWER BODY

Lower Body—Motor Nerves

T A B L E 9 - 2 5 Femoral Motor Nerve (Fig. 9-25)

Electrode placement for surface recording (37)

E1 About 6 cm above from the superior and

medial border of the patella
E2 Over the quadriceps tendon just proximal
to the patella
G Between E1 and stimulating cathode
S Cathode S1: Above the inguinal ligament
S2: Below the inguinal ligament
The distance between stimula-
tion points across the inguinal
ligament is 5.5
1.6 cm.
Anode Proximally

Normal values (37) (n  100)

Mean
SD Normal
limit
Above the inguinal 7.1
0.7 ms 8.5 ms
Figure 9-25 • Femoral motor ligament latency
nerve Below the inguinal 6.0
0.7 ms 7.4 ms
ligament latency

Delay across the 1.1
0.4 ms 1.9 ms

inguinal ligament

Nerve conduction 66.7
7.4 m/s 50 m/s

velocity above the
inguinal ligament
Note: No amplitude data available (37).

(continued)
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240 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 9 - 2 5 Femoral Motor Nerve (Fig. 9-25) (continued)

Normal values with needle recording (38)

(n  16)
Stimulation at the Mean
SD Normal
inguinal ligament limit
Latency 4.6
0.5 ms 5.5 ms
ligament latency
Amplitude 12.1
1.1 mV 2.5 mV
Note: The bipolar surface stimulation electrodes were placed
lateral to the point of pulsation over the inguinal ligament while a
concentric needle electrode was inserted into the belly of the rectus
femoris.

T A B L E 9 - 2 6 Sciatic Nerve (Fig. 9-26)

Electrode placement (37)

E1 On the extensor digitorum brevis (Fig. 9-27,

peroneal portion), abductor hallucis (Fig. 9-
28A, tibial portion), or abductor digiti min-
imi (Fig. 9-28B, tibial portion)
E2 See Figures 9-27 and 9-28.
G Between E1 and stimulating cathode
S Cathode S1: Surface stimulation in the
popliteal fossa
S2: A long needle electrode in
the midway below the gluteal
fold
Anode Proximally

Normal values (39) (n  18)

Mean
SD Normal
limit
Nerve conduction 51.3
4.4 m/s 42 ms
velocity to abductor
Figure 9-26 • Sciatic nerve digiti minimi
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 241

T A B L E 9 - 2 7 Peroneal* Motor Nerve to EDB (Fig. 9-27)

Electrode placement (40)

E1 On the extensor digitorum brevis muscle,

which is 1 cm distal to the tubercle that is its
origin. This is 2–3 cm distal to the lateral
malleolus.
Figure 9-27 • Tibial nerve
E2 At the fifth metatarsophalangeal joint
G On the dorsum of the foot
S Cathode S1: 8 cm proximal to E1, lateral
to the tibialis anterior tendon
S2: Posterior and inferior to the
fibular head
S3: Approximately 10 cm proxi-
mal to the S2, and medial to the
tendon of the biceps femoris
Anode Proximally

Normal values (41) (n  32)

Mean
SD Normal
limit
Onset latency 4.5
0.8 ms 6.0 ms
Amplitude 4.4
1.2 mV 2.0 mV
Conduction Velocity
S1-S2 49.9
5.9 m/s 40 m/s
S2-S3 51.1
6.3 m/s 40 m/s

Normal values (40) (n  242)

Mean
SD Normal
limit
Onset latency 4.8
0.8 ms 6.4 ms
Amplitude 5.9
2.6 mV 0.7 mV
Conduction Velocity
S1-S2
*Note: 47

No amplitude data available37 4 m/s
. 39 m/s
S2-S3 57
9 m/s 39 m/s
*Peroneal nerve also known as fibular.
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242 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 9 - 2 8 Medial Plantar Motor to Abductor Hallucis (Fig. 9-28A)

Electrode placement

E1 1 cm posterior and 1 cm inferior to the

navicular tubercle, at the junction of plantar
skin and dorsal foot skin
E2 On the first metatarsophalangeal joint
G Over the dorsum of the foot
S Cathode S1: 8 cm proximal to E1, right
Figure 9-28 • A. Tibial nerve
(medial plantar)
behind the medial malleolus
S2: At the popliteal fossa
Anode Proximally

Normal values (42,43) (n  37)

Mean
SD Normal
limit
Onset latency (42) 4.8
0.8 ms 6.4 ms
Amplitude (43) 11.6
4.3 mV 3.0 mV
Conduction 49.8
6.0 m/s 38 m/s
velocity (42)
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 243

T A B L E 9 - 2 8 Lateral Plantar Motor to Abductor Digiti Minimi (Fig. 9-28B)

Electrode placement

E1 Half distance from the sole of the foot to

the tip of the lateral malleolus
E2 On the fifth toe
G Over the dorsum of the foot
S Cathode 8 cm proximal to a site 1 cm
posterior and 1 cm inferior to the
navicular tubercle
Anode Proximally
Figure 9-28 • B. Tibial nerve
(lateral plantar)
Normal values (44) (n  10)

Mean
SD Normal
limit
Onset latency 4.4
0.5 ms 5.4 ms
Amplitude (43) 11.0
3.9 mV 3.2 mV
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244 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 9 - 2 9 F Wave in the Lower Extremity (Fig. 9-29)

Electrode placement

E1 For peroneal nerve: over the extensor

digitorum brevis (see Fig. 9-27)
For tibial nerve: over the abductor hallucis
(see Fig. 9-28A)
E2 For peroneal nerve: at the fifth metatar-
sophalangeal joint
For tibial nerve: at the first metatarsopha-
langeal joint
G Dorsum of the foot
S Cathode For peroneal nerve: 8 cm proxi-
mal to E1, lateral to the tibialis
anterior tendon
For tibial nerve: 8 cm proximal
to E1, and just behind the
medial malleolus
Figure 9-29 • F wave in the lower
extremity Anode Distally

Normal values (45)

Peroneal nerve F wave latency in ms (shortest of
10 stimuli, n  180)

Age Height Mean
SD Normal

(cm) limit
160 43.6
2.5 48.6
19–39 160–169 47.1
3.7 54.5
170 51.5
4.1 59.7
160 45.4
4.8 55.0
40–79 160–169 49.6
4.6 58.8
170 54.6
4.5 63.6

(Reprinted from Buschbacher RM. Peroneal nerve F-wave

recorded from extensor digitorum brevis. Am J Phys Med Rehabil
1999;78:S48–S52, with permission.)

(continued)
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 245

T A B L E 9 - 2 9 F Wave in the Lower Extremity (Fig. 9-29) (continued)

Tibial nerve F wave latency to AH in ms (shortest of

10 stimuli, n  180) (46)

Age Height Mean
SD Normal

(cm) limit
160 43.2
2.2 47.6
19–39 160–169 47.2
3.0 53.2
170–179 52.0
4.0 60.0
180 53.1
4.4 61.9
160 45.4
4.0 53.4
40–59 160–169 49.3
2.2 53.7
170–179 53.6
3.7 61.0
180 58.3
5.3 68.9
160 49.0
4.8 58.6
60–79 160–169 52.8
4.4 61.6
170–179 54.7
3.2 61.1
180 57.3
5.8 68.9
(Modified from Buschbacher RM: Tibial nerve F-wave recorded
from abductor hallucis. Am J Phys Med Rehabil 1999;78;S43–S47,
with permission.)
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246 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 9 - 3 0 H Reflex to the Calf (Soleus) (Fig. 9-30)

Electrode placement

E1 Halfway between the popliteal crease and

the medial malleolus, with subject in prone
position
E2 Over the Achilles tendon
G Between the stimulating and recording
electrodes
S Cathode At the midpopliteal crease
Anode Distal
Stimulation duration  1.0 ms

Normal values: onset latency (ms) (47) (n  251)

Age Height Mean
SD Normal
(cm) limit
160 27.1
1.8 30.7
19–39 160–169 28.6
1.9 32.4
170–179 30.3
1.8 33.9
180 32.0
2.1 36.2
160 27.8
1.1 30.0
40–49 160–169 30.2
1.4 33.0
170–179 31.0
1.6 34.2
180 32.7
2.1 36.9
160 29.3
1.9 33.1
Figure 9-30 • H reflex to the calf
50–79 160–169 31.7
1.6 34.9
170–179 31.9
1.7 35.3
180 33.2
2.5 38.2

Note: The upper limit of increase in latency from one side to the
other is 2.0 ms (47).
Equation to calculate: HLat at 9.1
(0.1  Age)
(0.46  Length)
(48)
(Reprinted from Buschbacher RM. Normal range for H-reflex
recorded from the calf muscles. Am J Phys Med Rehabil
1999;78:S75–S79, with permission.)
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 247

Lower Body—Sensory Nerves

T A B L E 9 - 3 1 Lateral Femoral Cutaneous Sensory Nerve (Fig. 9-31)

Electrode placement

E1 17–20 cm distal to the anterior superior iliac

spine, on the line between the anterior
superior iliac spine and the lateral border of
the patella
E2 3 cm distal to E1
G Between E1 and the stimulating cathode
S Cathode S1: below the inguinal ligament,
1 cm medial to the line between
the anterior superior iliac spine
and the lateral border of the
patella
S2: above the inguinal liga-
ment, 1 cm medial to the
anterior superior iliac spine
Anode Proximally

Normal values (49) (n  20)

Mean
SD Normal
Figure 9-31 • Lateral femoral limit
cutaneous sensory nerve
S1 (14–18 2.5
0.2 ms 2.8 ms
Onset cm)
S2 (17–20 2.8
0.4 ms 3.6 ms
cm)
Peak to S1 7.0
1.8 V 3.4 V
peak
S2 6.0
1.5 V 3.0 V
amplitude

Note: No data on onset to peak amplitude available.

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248 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 9 - 3 2 Posterior Femoral Cutaneous Nerve (Fig. 9-32)

Electrode placement

E1 6 cm proximal to the midpopliteal fossa

E2 3 cm distally
G 3 cm distally
S Cathode 12 cm proximal to E1 on a line be-
tween E1 and the ischia tuberosity
Anode Proximally

Normal values (50) (n  80)

Mean
SD Normal limit
Peak latency 2.8
0.2 ms 3.2 ms
Onset to peak 6.5
1.5 V 3.5 V
amplitude

Figure 9-32 • Posterior femoral

cutaneous nerve
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 249

T A B L E 9 - 3 3 Saphenous Sensory Nerve (Fig. 9-33)

Electrode placement

E1 Slightly anterior to the highest prominence

of the medial malleolus, between the malle-
olus and the tendon of the tibialis anterior
E2 3 cm distal to E1, at the level of the
malleolus
G Between E1 and the stimulating cathode
S Cathode 14 cm proximal to E1 deep to the
medial border of the tibia
Anode Proximally
Figure 9-33 • Saphenous sen-
sory nerve—distal technique Normal values (51) (n  230)
Mean
SD Normal limit
Onset latency 3.2
0.3 ms 3.8 ms
Peak latency 3.8
0.3 ms 4.4 ms
Onset to peak 6.5
3 V 3.5 V
amplitude
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250 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 9 - 3 4 Superficial Peroneal* Nerve: Medial and Intermediate Dorsal

Cutaneous Branches (Fig. 9-34)

Electrode placement

E1 At the level of the ankle

Figure 9-34 • Superficial
peroneal nerve: medial and
intermediate dorsal cutaneous
branches
Medial branch: just lateral to the tendon of
the extensor hallucis longus
Intermediate branch: 1–2 cm medial to the
lateral malleolus
E2 3–4 cm distal to the E1s
G Between E1 and the stimulating cathode
S Cathode 14 cm proximal to E1 on the an-
terolateral aspect of the lower leg
Anode Proximally

Normal values (52) (n  80)

Normal
Branch Mean
SD limit
Peak Medial 3.4
0.4 ms 2.7–4.7 ms
latency Inter- 3.4
0.4 ms 2.8–4.6 ms
mediate
Peak to Medial 18.3
8.0 V 2.3 V
peak am- Inter- 15.1
8.2 V 4 V*
plitude mediate
Onset Inter- 20.5
6.1 V 8.3 V
to peak mediate
ampli-
tude (53)
Nerve Medial 51.2
5.7 m/s 39.8 m/s
conduction Inter- 51.3
5.4 m/s 40.5 m/s
velocity mediate
Note: The value is the smallest value of the range.
*Peroneal nerve also known as fibular.
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 251

T A B L E 9 - 3 5 Tibial Nerve (Mixed Nerve Responses): Medial and Lateral Plantar

Nerves (Fig. 9-35)

Electrode placement

E1 Behind the medial malleolus at the level of

the ankle
E2 Proximally
G Over the dorsum of the foot
S Cathode 1. Medial branch: 10 cm distal to
Figure 9-35 • Tibial nerve:
E1 to the first web space, and
medial and lateral plantar nerves
then 4 cm more distal along
the first web space (total 14 cm
distal to E1)
2. Lateral branch: 14 cm distal
to E1, on the sole between
the fourth and fifth
metatarsals
Anode Distally

Normal values (54) (n  41)

Normal
Branch Mean
SD limit
Peak Medial 3.16
0.26 ms 3.7 ms
Latency Lateral 3.15
0.25 ms 3.7ms
Amplitude Medial 10 V
Lateral 8 V
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252 SECTION II • TECHNICAL ASPECTS OF EMG

T A B L E 9 - 3 6 Sural Sensory Nerve (Fig. 9-36)

Electrode placement

E1 Posterior and inferior to the lateral

malleolus
E2 3 cm distally
Figure 9-36 • Sural sensory
G Between E1 and the stimulating cathode
nerve
S Cathode 14 cm proximal to E1 in the mid-
line or slightly lateral to the mid-
line of the posterior lower leg,
between the two heads of
gastrocnemius
Anode Proximally

Normal values (55) (n  56)

Mean
SD Normal limit
Peak latency 3.5
0.25 4.0 ms
(55)
Baseline to 23.7
3.8 V 10 V
peak amplitude
(53)
Nerve 43.3
4.3 m/s 34.7 m/s
conduction
velocity (54)

Normal values (56) (n  80)

Mean
SD Normal limit
Onset latency 3.1
0.3 ms 3.6 ms
Peak latency 3.8
0.3 ms 4.5 ms
Onset to peak 17
10 V 4 V
amplitude
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CHAPTER 9 • PICTORIAL GUIDE TO NERVE CONDUCTION TECHNIQUES 253

T A B L E 9 - 3 7 Sural Nerve—Lateral Dorsal Cutaneous Branch (Fig. 9-37)

Electrode placement

E1 At the midpoint of the fifth metatarsal and

just lateral to the extensor digitorum brevis
tendon to the fifth toe
E2 Distally
G On the dorsum of the foot
S Cathode 12 cm proximal to E1 behind the
lateral malleolus
Anode Proximally
Figure 9-37 • Sural nerve—
lateral dorsal cutaneous branch
Normal values (57) (n  40)
Mean
SD Normal limit
Onset latency 3.2
0.4 ms 4.0 ms
Peak latency 3.9
0.5 ms 4.9 ms
Baseline to peak 5.8
2.1 V 3 V
amplitude (57)
Nerve 37.6
4.8 m/s 28.0 m/s
conduction
velocity (onset)
Nerve 37.6
4.8 m/s 28.0 m/s
conduction
velocity (peak) 30.7
3.7 m/s 23.3 m/s
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254 SECTION II • TECHNICAL ASPECTS OF EMG
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III
Solving the Problems in
Clinical EMG
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CHAPTER 10
Entrapment Neuropathies and
Other Focal Neuropathies
(Including Carpal Tunnel
Syndrome)
Lawrence R. Robinson
GENERAL APPROACHES TO THE
STUDY OF ENTRAPMENT
There are a number of general considerations
when evaluating any patient with suspected en-
trapment or focal neuropathy. In this chapter, ap-
proaches to the history and physical examination,
timing of electrodiagnostic changes, pathophysiol-
ogy, and principles of localization will be discussed,
as well as initial electrodiagnostic approaches.
History
A directed history is critical to performing the elec-
trodiagnostic medical consultation. It is required
for generating an appropriate list of differential
diagnoses and planning the electrophysiologic ex-
amination. Moreover, many times the electrodiag-
nostic medical consultant has more experience
in the diagnosis of focal neuropathies and other
neuromuscular conditions than the patient’s refer-
ring physician and thus may think of alternative
diagnoses that the referring physician had not
considered.
There are a number of specific components to
the history especially pertinent to the evaluation.
The quality and precise distribution of symptoms,
combined with an intimate knowledge of periph-
eral nervous system anatomy, will usually be very
helpful in developing a sensible differential diag-
nosis. Finding out whether symptoms are inter-
mittent or constant will suggest a likelihood of
finding abnormalities on the electrophysiologic
examination; constant symptoms are more likely
to be associated with electrophysiologic abnormal-
ities than intermittent symptoms. While symp-
toms of entrapment neuropathies are usually
initially reported in one or two limbs, one should
also ask about other limbs to rule out a more gen-
eralized process. The patient presenting with hand
numbness, for example, could have entrapment
neuropathy in the upper limbs; however, if the feet
are also involved, then one might perform a wider
search for a peripheral polyneuropathy. When pa-
tients report the sudden onset of symptoms upon
awakening, this should prompt extensive ques-
tioning about where and how the patient slept and
if he or she was intoxicated or otherwise med-
icated. If there is a recent history of surgery or
trauma, a detailed history may help point to which
areas of the peripheral nervous system might have
been placed at risk.
While an extensive search of the past medical
history is not always productive in the evaluation
for possible entrapment neuropathies, there are
several questions that should always be asked.
One should routinely ask for the medications the
patient is taking. This brings up not only other
prior pertinent diagnoses that may not have been
mentioned (e.g., diabetes mellitus), but also possi-
259
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260 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
ble exposure to neurotoxic agents or anticoagu-
lants. One should elicit any history of systemic dis-
ease that might contribute to the chief complaint,
such as a history of diabetes mellitus, extensive al-
cohol intake, or rheumatologic disease. Also, one
should know whether the presenting symptoms
have occurred in the past so that one is prepared
for the electrophysiologic findings of prior events.
A history of prior trauma may be pertinent, as in
the case of tardy ulnar palsy where an old elbow
injury predisposes to a later ulnar neuropathy.
The patient’s vocational history may play a role in
diagnosis, as many occupations increase the risk of
developing focal entrapment neuropathies.
The family history becomes pertinent when
one is considering congenital diseases. Peripheral
polyneuropathies and myopathies are not uncom-
monly inherited, and it can be very revealing to
find a family history of similar neurologic symp-
toms. There is an autosomally dominant condi-
tion known as familial predisposition to pressure
palsies (1) that may be relevant when considering
entrapment neuropathies.
Physical Examination
While the history often contributes most signifi-
cantly to establishing a differential diagnosis, a di-
rected physical examination is useful in providing
more objective evidence of focal peripheral nerv-
ous system dysfunction. In most cases, the four
most important components of the examination
are muscle strength, sensation, muscle stretch re-
flexes, and provocative signs. The strength exami-
nation should be directed to all four limbs, both to
look for widespread abnormalities as well as to as-
sess any underlying poor effort. Although in some
cases weakness is severe, in most referrals the
weakness is mild or subtle. Optimally, muscles
should be tested at or near their “break” points as
opposed to the large range where resistance cannot
be overcome. Thus, one must be sure to obtain a
maximum mechanical advantage in performing
the muscle strength testing. Useful techniques in-
clude applying force as far as possible from the
joint to obtain a maximal lever arm, putting par-
ticularly strong muscles at added stretch to put
them at a mechanical disadvantage, and using
gravity and body weight as an aid to maximally
stress antigravity muscles. Simply testing dorsi-
flexion or plantarflexion at the ankle against man-
ual resistance, for example, is insufficient to fully
stress the dorsiflexors or plantarflexors. It is prefer-
able to have the patient walk on his heels and on his
toes or perform 10 toe rises on each foot.
Sensory testing should be directed at eliciting
subtle deficits in sensation. As opposed to the pa-
tient with spinal cord injury, where one is looking
for a very gross sensory level, patients with en-
trapment neuropathies often have mild or diffi-
cult-to-elicit sensory losses. Simply finding out
whether the patient can distinguish pinprick from
dull touch is usually insufficient for all but the
most severe deficits. One should compare pin-
prick and light touch sensations in a suspected
area with an asymptomatic area, such as the cheek,
or with the other side if it is not symptomatic. A
useful technique is to touch first the asymptomatic
area and then the symptomatic area, asking the
patient, “If the feeling you have in this (asympto-
matic) area is 100%, how much is it in this (the
symptomatic area)?” Two-point discrimination
often detects milder deficits in sensation that are
missed with simply testing pinprick.
Muscle stretch reflexes are probably the most
objective finding in examination of the peripheral
nervous system, in that they are not easily influ-
enced by patient cooperation or reporting (though
they are by the level of relaxation). Reflexes are
normal in many focal entrapment neuropathies
that are at distal sites, but they will help to rule out
more proximal lesions.
There are several useful provocative tests that
can be used in the physical examination prior to
electrophysiologic studies. Phalen’s test is a mod-
erately sensitive and specific test for detecting me-
dian nerve compression at the wrist. This test is
performed by keeping the wrist in sustained
flexion for 60 seconds and monitoring for repro-
duction of paresthesias. Tinel sign, which was
originally developed for detecting the most distal
site of peripheral nerve regeneration, is sensitive
but not very specific. It can be elicited over the me-
dian nerve at the wrist or ulnar nerve at the elbow
in the case of entrapment, but many asymptomatic
control subjects also have a positive test over unaf-
fected peripheral nerves. The Flick sign is elicited
by asking the patient what he or she does when
awakened at night by symptoms. A Flick sign is
present when the patient “flicks” the wrist in
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES
response to this question. None of the aforemen-
tioned signs is particularly sensitive or specific
when applied to those patients referred to the elec-
trodiagnostic laboratory (2).
Timing
Before embarking upon the electrodiagnostic ex-
amination, it is critical to appreciate the timing
since the onset of symptoms, particularly when
there is trauma or the sudden onset of symptoms.
False-negative or misleading conclusions can re-
sult from not understanding the influence of tim-
ing since the onset of symptoms. Demyelination
and marked axon loss produce electrophysiologic
changes immediately if one can stimulate proxi-
mal and distal to the lesion. More proximal lesions
do not immediately produce changes on distal
nerve conduction studies or needle electromyog-
raphy (EMG) of resting muscle. Whether the le-
sion is proximal or distal, distinction between de-
myelination and axon loss cannot be made until
after the time for Wallerian degeneration has
passed. These concepts, as applied to traumatic
neuropathies, are covered further in other sources
(see Chapter 3) (3).
Day 1 after a Lesion
Immediately after onset of a demyelinating or axon
loss lesion, electrophysiologic changes may be sub-
tle. On needle EMG the only potential abnormality
may be a change in motor unit potential (MUP) re-
cruitment, with reduced or discrete recruitment in
severe lesions. Mild lesions will not produce notice-
able changes in recruitment. Nerve conduction
studies distal to the site of the lesion will not be
changed, but stimulation proximal to a lesion with
distal recording may produce a small-amplitude or
absent response. Otherwise, nerve conduction stud-
ies and EMG will be unremarkable at day 1.
Days 7 to 10
Seven days after a complete nerve lesion, Waller-
ian degeneration will have progressed to the point
where distal stimulation of motor axons elicits no
motor response. Ten days after onset of a complete
lesion, sensory nerve action potentials (SNAPs)
will be absent as well (3). Incomplete lesions will
produce less marked changes, roughly in propor-
tion to the number of axons lost, but with similar
261
timing. Therefore, 7 to 10 days after onset, nerve
conduction studies can distinguish a neurapraxic
injury (in which distal amplitudes will be normal)
from an axon loss lesion (in which distal ampli-
tudes will be reduced or absent).
Days 14 to 21
Two to three weeks after onset of injury, the nee-
dle EMG starts to show fibrillation potentials and
positive sharp waves. Proximal muscles (those
nearest the site of injury) demonstrate these ab-
normalities earlier and distal muscles later. Fibril-
lations and positive sharp waves may be persistent
for several months or even many years after a
single injury, depending on the extent of reinner-
vation. Fibrillation amplitudes are sometimes
helpful in determining the chronology of the le-
sions; fibrillation potentials larger than 100
V
indicate a lesion probably less than 1 year old (4).
Reinnervation
The timing and types of electrophysiologic
changes consequent to reinnervation will depend
in part upon the mechanism of reinnervation.
When reinnervation is a result of axonal regrowth
from the site of the lesion, such as in complete ax-
onal injuries, the appearance of new MUPs will not
occur until motor axons have had sufficient time to
regenerate the distance between the lesion site and
the muscle (usually proceeding at roughly 1 mm
per day or 1 inch per month). When these new ax-
ons first reach the muscle, they will innervate only
a few muscle fibers, producing short-duration,
small-amplitude potentials, formerly referred to as
nascent potentials. With time, as more muscle
fibers join the motor unit, the MUPs will become
larger, more polyphasic, and longer in duration.
MUP changes will also develop when reinner-
vation occurs by axonal sprouting from intact ax-
ons. Polyphasicity and increased duration develop
as newly formed, poorly myelinated sprouts supply
the recently denervated muscle fibers. As the
sprouts mature, large-amplitude, long-duration
MUPs develop and usually persist indefinitely.
Pathophysiology
Whenever possible, provide the referring physi-
cian some indication of the pathophysiology of
the peripheral nerve lesion (e.g., neurapraxia,
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262 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
demyelination, or axon loss). Neurapraxia is best
demonstrated, assuming at least 7 days have
passed, when there is focal conduction block on
nerve conduction studies with a large-amplitude
compound muscle action potential (CMAP) or
SNAP elicited distal to the site of the lesion and a
smaller or absent response with more proximal
stimulation. There is some debate about whether
purely neurapraxic injuries have fibrillation po-
tentials or positive sharp waves on needle EMG.
Some report that positive sharp waves can exist in
purely neurapraxic lesions, while others point out
the difficulty in demonstrating that the lesion is
purely neurapraxic with zero axon loss.
Axon loss lesions are usually demonstrated by
evidence of denervation on needle EMG examina-
tion as well as small-amplitude CMAP and SNAP
responses with stimulation and recording distal to
the site of the lesion. While needle EMG is a more
sensitive indicator for the presence of any motor
axon loss, measurement of the distal CMAP or
SNAP amplitude is a better quantitative measure
of the degree of axon loss and of prognosis. There
is often a mixture of axon loss and neurapraxia in
focal neuropathies.
Demyelination is best demonstrated by slow-
ing of conduction, often with conduction block.
Slowing of conduction may take the form of
slowed conduction velocities, prolonged distal la-
tencies, and increased temporal dispersion. Slow-
ing of conduction does not always mean that
demyelination has occurred; axon loss, particu-
larly of the faster-conducting fibers, will produce
mild slowing of conduction as well.
Estimating Prognosis
Prognosis of a peripheral nerve lesion is related to
the pathophysiologic process that has occurred,
the degree of axon loss, the time since onset, and
the distance between the lesion and the target
muscles. Lesions that have had extensive axon loss
are less likely to have full recovery of function.
Unfortunately, electrophysiologic measures can-
not assess the integrity of supporting structures
around the nerve and hence cannot distinguish
axonotmesis from neurotmesis. Neurotmesis,
which has marked disruption of supporting struc-
tures, carries a much worse prognosis for regener-
ation than axonotmesis, in which the supporting
structures are largely intact. In these cases, careful
periodic EMG re-examination of proximal mus-
cles (those expected to reinnervate first) will give
the best information as to the ultimate prognosis
for full reinnervation.
Lesions that are predominantly neurapraxic
have a much better prognosis; conduction block in
these lesions rarely lasts more than 2 to 3 months.
Demyelinated lesions also have a better prognosis
than axon-loss lesions, but the specific prognosis
will depend upon what intervention is taken, such
as release of entrapment sites.
When axon loss is present, there is a critical
window of 18 to 24 months for peripheral nerve
regeneration to occur before the target muscles
cannot be reinnervated any longer (3). Since pe-
ripheral nerves regenerate roughly 1 inch per
month, proximal lesions with a great deal of axon
loss have a poorer chance of reinnervating distal
hand or foot muscles. Even for proximal muscles,
surgical intervention, if needed, must allow
enough time for axons to grow to the muscle while
reinnervation can still occur (3).
Principles of Localization
There are a number of principles useful for local-
izing peripheral nerve lesions based upon the elec-
trophysiologic examination. Conventionally, in
primarily axonal lesions or in proximal lesions
where one cannot stimulate both proximal and
distal to an entrapment site, needle EMG is often
used to diagnose and localize abnormalities.
Knowing the branch points along the nerve, one
can examine the muscles supplied by each branch
and infer lesion localization based upon the point
at which the muscles change from normal to ab-
normal. Thus, localization is based upon finding
abnormalities distal to a branch point with normal
findings in proximal muscles.
This approach, however, sometimes provides
an erroneous site. Sir Sidney Sunderland (5) has
shown that fascicles within peripheral nerves in-
tertwine considerably as they move proximally
through the limbs. Fascicles supplying the flexor
carpi ulnaris muscle, for example, are not
uniquely placed proximally within the ulnar
nerve as it joins the medial cord of the brachial
plexus. However, fascicles do become organized
within peripheral nerves several centimeters prior
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES
to branch points and, in this example, fascicles
destined to supply the flexor carpi ulnaris become
organized within the ulnar nerve several centime-
ters prior to exiting the nerve to supply the muscle.
Consequently, even though ulnar nerve entrap-
ment at the elbow usually occurs proximal to the
branch to the flexor carpi ulnaris, this muscle is
usually spared in ulnar neuropathy at the elbow,
as the fascicles for this muscle are isolated in a rel-
atively protected area of the nerve at the entrap-
ment site. If one were basing localization only on
needle EMG using the known branch points, one
would erroneously place these lesions distal to the
branch point and in the forearm.
The ulnar nerve is not unique with regard to
the intraneural topography, causing potential
problems in localization. There have been cases
reported of fibular (the peroneal nerve is now
called the fibular nerve) neuropathy occurring
proximal to the popliteal fossa but resulting in
only deep fibular nerve lesions clinically (6). Sci-
atic neuropathies, even occurring near the hip
joint, can result in predominantly common fibular
nerve deficits. The fascicular structure within the
fibular division of the sciatic nerve may make it
more predisposed to injury than the tibial division
(5). Thus, while EMG does make use of known
anatomic branch points to arrive at localization,
the electromyographer should be aware of the in-
traneural topography within the nerve and should
remember that a partial lesion can be misleading.
Nerve conduction studies are best at localiz-
ing the site of pathology when there is demyelina-
tion. Focal slowing and conduction block, when
present, can precisely localize a nerve lesion. A
problem arises with localizing lesions based on
nerve conduction studies when there is predomi-
nantly axon loss and little demyelination. In these
cases conduction velocity throughout the nerve is
mildly slowed due to loss of the faster-conducting
fibers, but it is not focally or markedly slowed.
While there is a diffuse reduction in CMAP or
SNAP amplitude at all sites of stimulation (due to
axon loss and subsequent Wallerian degenera-
tion), there will be no focal drop in amplitude as
one goes across the lesion site. Conduction block,
in which there is a drop in amplitude of the
CMAP as stimulation occurs distal and proximal
to the lesion, is related only to demyelination and
neurapraxia and will not be present in axon-loss
263
lesions once Wallerian degeneration has occurred
(about 7 days after onset).
CARPAL TUNNEL SYNDROME
CASE 1
A 52-year-old woman reports a 6-month history
of right-hand numbness and pain. This involves
the whole hand, and she does not differentiate
whether this is just palmar or also dorsal numb-
ness. She also reports hand weakness, easily drop-
ping small items. The pain and numbness often
awaken her at night. She shakes her hand when
awakened by these symptoms. She denies numb-
ness in her feet. She also denies any neck or prox-
imal upper limb pain. Past medical history is sig-
nificant only for hypothyroidism and obesity. She
works in a chicken-processing plant.
Physical examination is remarkable for nor-
mal strength proximally in the limb, though there
is mild weakness of thumb abduction on the right.
Sensation is reduced on the palmar surface of the
right thumb, index finger, and long finger. Re-
flexes are 2 and symmetric. Phalen’s sign and
Tinel signs are present.
Differential Diagnosis
When presented with a patient with hand numb-
ness, carpal tunnel syndrome (CTS) should usu-
ally be in the differential diagnosis. However, one
should also consider the possibility of more dif-
fuse or more proximal peripheral nervous system
lesions.
When considering diffuse processes such as
peripheral polyneuropathy, one should ask about
symptoms in other limbs. If patients have symp-
toms such as numbness or tingling in the feet, one
should consider polyneuropathy and look for risk
factors in the medical history. Cervical spondylitic
myelopathy could also present with hand and foot
symptoms but should also have myelopathic fea-
tures such as bowel or bladder dysfunction and
hyperactive reflexes.
With diffuse hand numbness (i.e., more than
just the median nerve distribution), one might con-
sider multiple nerve lesions, such as both median
and ulnar nerves. However, it is common for CTS
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264 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
to present with diffuse hand numbness, or with
numbness in the median and ulnar distributions
(7). The differential diagnosis may also include
more proximal median neuropathies, such as
pronator syndrome, ligament of Struthers, flexor
digitorum sublimis arch, and others. All such pa-
tients should be examined for weakness in more
proximal limb muscles, and not just in the distal
median nerve distribution. Brachial plexopathy
and cervical radiculopathy should also be consid-
ered in the differential diagnosis. These would be
more strongly considered if the patient has proxi-
mal limb symptoms or signs, neck pain, or other
predisposing factors.
Clinical Presentation
Patients with CTS typically present with hand
numbness and tingling. As noted above, the symp-
toms often extend outside the median nerve sen-
sory distribution and can even involve the whole
hand in a glove-type distribution (7). Symptoms
are worse at night, and nocturnal awakening is
common. Often when patients are awakened by
their symptoms they shake or “flick” their hands.
Some investigators report this Flick sign (patients
flick their hand when asked what they do at night)
as highly sensitive and specific (8), whereas others
have found it to be of limited utility (2). Driving
and hand use are also precipitating factors for
symptoms.
There are a number of risk factors for CTS.
Medical risk factors include hypothyroidism, obe-
sity, rheumatoid arthritis, osteoarthritis, prior
wrist fracture, diabetes, and pregnancy (9). Occu-
pations that put individuals at risk for CTS are
those that involve high-force or high-repetition
hand movements. Medium- and light-duty indus-
tries commonly have workers with CTS.
The physical examination does not always
show marked abnormalities in CTS. Strength
testing may show weakness or atrophy of thenar
muscles. When testing thenar muscles, one should
be careful to separate these muscles from the long
radial-innervated thumb extensors. The inexperi-
enced examiner will sometimes test thumb exten-
sion rather than thumb abduction (the latter is
perpendicular from the plane of the palm). Sensa-
tion may be reduced in the median distribution to
pinprick or two-point discrimination. Muscle
stretch reflexes are usually normal. Phalen’s test is
performed by flexing the wrist for 1 minute. It is
positive if this produces paresthesia in the median
nerve distribution, reproducing the symptoms.
The Tinel sign was originally developed for de-
tecting nerve regeneration after traumatic neu-
ropathies, but it is frequently applied to peripheral
nerve entrapments such as CTS. This involves
tapping over the nerve at the site of compression;
a positive sign is paresthesia in the median nerve
distribution, reproducing the symptoms. There is
debate about the sensitivity and specificity of
Phalen’s sign and the Tinel sign for detecting
CTS. A recent review has suggested that they are
of limited utility and of less value than thumb ab-
duction strength or distribution of symptoms (10).
Optimal Strategies for Electrodiagnosis
of Carpal Tunnel Syndrome
Although CTS is the most frequently seen entrap-
ment neuropathy in the electrodiagnostic labora-
tory, multiple and varied approaches have been de-
scribed for diagnosing this condition. The lack of
uniformity in approach suggests that there are likely
many unanswered questions on how to best diag-
nose patients with this condition (or, alternatively,
many faculty seeking promotion and tenure!).
Readers are encouraged to read a comprehensive re-
view of methods for diagnosing CTS (11).
The general approach to nerve conduction
studies should include measurement of sensory
and motor conduction in the median nerve across
the wrist, with comparison to nearby nerves that
do not traverse the carpal tunnel. Conduction in
sensory axons is usually affected before motor
axons, though rarely motor axons are preferen-
tially affected, possibly due to focal compression of
the recurrent branch of the median nerve.
While there are many approaches to studying
the median sensory nerve across the wrist, I rely
upon three sensory nerve conduction studies (Fig.
10-1) that have literature support for a high degree
of sensitivity and reasonable specificity in CTS
(Table 10-1). These are comparison of the distal la-
tency of the median and ulnar sensory antidromic
conduction to the ring finger at 14 cm (ringdiff),
comparison of the distal latency of the median and
radial sensory antidromic conduction to the thumb
at 10 cm (thumbdiff), and comparison of the distal
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES
Figure 10-1 ● Three sensory conduction
studies commonly used to evaluate for
carpal tunnel syndrome. From top to bottom:
median and ulnar comparison to the ring finger at 14
cm (ringdiff); median and radial comparison to the
thumb at 10 cm (thumbdiff); and median and ulnar
comparison across the wrist with palmar stimulation
at 8 cm (palmdiff). In this example, as well as all
other references to sensory latency measurement in
this chapter, the time to the peak of the sensory re-
sponse is measured (peak latency).
latency of the median and ulnar orthodromic con-
duction across the wrist with palmar stimulation at
8 cm (palmdiff) (11,12). Reference values can be eas-
ily remembered as “3, 4, 5”: the midpalmar studies
are 0.3 ms or less, the ring finger 0.4 ms or less, and
the thumb studies 0.5 ms or less. Values exceeding
these reference values are suggestive of CTS.
Temperature is well known to slow nerve
conduction latencies and velocities. Thus, obtain-
ing a median sensory latency will be dependent
upon the temperature to a large degree. Much of
this dependency, however, can be reduced by us-
ing comparisons of two nerves within the same
limb (i.e., using the methods suggested above).
265
Thus, to avoid influences of temperature as well
as age, height, and other influential variables, it is
preferable to use comparisons of median nerve
latency to other nerves within the same hand
rather than comparing the median sensory la-
tency against a fixed standard reference value.
Given the number and variety of electrodiag-
nostic tests available for diagnosing CTS, the
question that inevitably comes up is how many
tests should be performed in each patient. At first,
it is tempting to perform many tests so that one is
more likely to detect any problem that might be
subtle or might not be shown on a smaller number
of tests. Also, by performing more tests, one could
argue that one is making a more thorough assess-
ment of different nerve fascicles than one could
with a single test. There are, however, problems
with performing multiple tests. The most signifi-
cant problem is that of multiple comparisons. As
one performs more and more tests, each of which
has a 2.5% false-positive rate (under ideal circum-
stances), the chance of any one of the tests being
abnormal goes up almost additively. Thus, per-
forming two tests yields a 4.9% chance of at least
one test being abnormal in a control population.
For three tests, the false-positive rate is 7.3%; Fig-
ure 10-2 shows the false-positive rate as one per-
forms greater numbers of tests. The false-positive
rate is lower if one requires multiple (two or more)
tests to be abnormal to make a diagnosis, but this
will lower sensitivity. Another practical problem
with performing more testing is simply the time
and cost required to complete the study. Obvi-
ously one would not want to perform tests that do
not add clinical or diagnostic information.
Thus, the question of how many tests to
perform is not a trivial matter. The strategies for
performing multiple tests should be decided upon
before studying the patient and not handled in a
casual manner. To address the question of how to
interpret multiple tests, Robinson et al (13) have
compared strategies of analyzing the three differ-
ent distal sensory latency comparisons described
above for CTS. This strategy is to summate the re-
sults from three tests into a single number. The
combined sensory index is calculated as the sum of
the three latency differences:
Combined sensory index 
palmdiff ringdiff  thumbdiff
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266 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
T A B L E 1 0 - 1 Nerve Conduction Results for Case 1
Sensory and Mixed Nerve Conductions
R/L Nerve (Stim) Record
R Median to ring finger (14 cm)
R Ulnar to ring finger (14 cm)
R Median to thumb (10 cm)
R Radial to thumb (10 cm)
R Median palm to wrist (8 cm)
R Ulnar palm to wrist (8 cm)
Latency (ms)
R Median (wrist) to abductor 4.2
Pollicis brevis
(elbow/forearm) 7.9
This brings in the advantages of multiple tests
(e.g., assessing multiple areas of nerve, enhancing
reproducibility of findings) but does not create the
problem of multiple comparisons. Thus, as long as
one does three tests but only “looks at” the sum-
Figure 10-2 ● The likelihood of having
one abnormal test out of a number of tests
performed based upon random chance.
This calculation assumes a 2.5% false-positive rate
for each test (based upon use of mean 2 SD) and
the independence of each of the tests.
Peak Latency (ms) Amplitude (
V)
3.8 27
3.2 19
3.2 38
2.7 12
2.2 78
1.9 24
Motor Nerve Conductions
Conduction
Amplitude (mV) Velocity (m/s)
6.5
6.4 57
mated result from all three tests, one does not run
into the problem of an additive false-positive rate.
Using this approach, sensitivity is improved, with
specificity still remaining high at 95%. These re-
sults assume a reference value for the combined
sensory index of 0.9 ms or less. Thus, use of the
combined sensory index has advantages of im-
proved sensitivity and high specificity compared
to doing multiple individual tests or even a single
individual test. While this represents an improve-
ment over single tests, it has also been noted that it
might not be necessary to perform all three tests
for the combined sensory index when one or more
are extreme values (14).
Median motor conduction is an essential com-
ponent of the electrodiagnostic evaluation of CTS.
Not only will this allow the examiner to detect mo-
tor slowing across the wrist, but it will also detect
the small number of individuals with CTS limited
to motor slowing. Most commonly, studies are
performed with recording over the abductor pol-
licis brevis (APB) and stimulation at the wrist (8 cm
proximally) and the elbow. Some authors have also
advocated stimulation in the palm to look for
conduction block (neurapraxia) at the wrist; con-
ceptually a much larger-amplitude response at the
palm would suggest focal compression (15). How-
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES
ever, other authors (16) have reported that a sub-
stantial number of asymptomatic individuals have
amplitude changes across the carpal tunnel that
would suggest the presence of CTS. Due to stimu-
lation of the deep ulnar nerve (which on average is
1.2 cm from the recurrent median nerve) (16)
and/or crossing anomalous fibers from median
to ulnar nerves, 53% of healthy control subjects
have a palm/wrist difference in amplitude greater
than reported control values, and 25% of control
subjects have an amplitude ratio (palm/wrist) out-
side the reference range. Nevertheless, clinicians
should consider stimulation of sensory nerves both
proximal and distal to the site of compression (i.e.,
at the wrist and palm) to look for evidence of con-
duction block. This technique is less problematic
than motor nerve stimulation in the palm, since it
is unlikely that ulnar sensory responses will be vol-
ume-conducted to ring electrodes over the median
innervated digits.
The electrodiagnostic examiner should also
be aware of the Martin-Gruber anastomosis when
performing median and ulnar motor conduction
studies. An in-depth description of this can be
found in the literature (17). Briefly, this represents
the presence of an anomalous branch from the me-
dian nerve, or the anterior interosseus nerve, to the
ulnar nerve in the proximal forearm. These cross-
ing fibers typically innervate ulnar muscles, such as
the first dorsal interosseus, but may also innervate
hypothenar muscles or, rarely, thenar muscles.
When stimulating the median nerve at the elbow,
a larger response will be seen from the thenar
recording electrodes than with wrist stimulation
due to coactivation of nearby ulnar muscles via the
crossing fibers. In CTS, the ulnar muscles supplied
by the crossing fibers will be activated before the
thenar muscles (which are slower due to demyeli-
nation at the wrist). Consequently, the elbow stim-
ulation will produce an initial positive deflection
and the measured conduction velocity in the fore-
arm may be unusually fast. There is some evidence
that recording from the first lumbrical (median in-
nervated) and second palmar interosseus (ulnar
innervated) muscles has an advantage over record-
ing from the APB (18,19).
One should take special care in evaluating the
patient with persistent symptoms after carpal tun-
nel release. Improvement in latencies usually oc-
curs after successful release, with maximal im-
267
provement usually present within 6 months of
surgery. However, latencies often do not return to
the normal range (20) despite successful release.
ULNAR NEUROPATHY AT THE ELBOW
CASE 2
A 46-year-old anesthesiologist has gradually
noted mild but progressive weakness in his right
hand and numbness in the ring and little finger.
He comes to you at the prompting of a neurosur-
gical colleague who commented upon his wasting
in the right first web space. The numbness is con-
stant and involves both dorsal and palmar aspects
of the little finger and palm, but does not extend
proximal to the wrist. He denies any symptoms in
the other upper limb or either lower limb. He de-
nies neck pain except when working with selected
surgeons in the operating room.
Physical examination reveals wasting in the
hypothenar and first web space muscles. Strength
is reduced (4/5) in finger abduction and adduction
and in thumb adduction. Strength is otherwise
normal, including wrist flexion and flexion of the
distal interphalangeal joints. Sensation to pin-
prick is decreased over the little finger and ulnar
aspect of the palm on both the dorsal and palmar
surfaces. Muscle stretch reflexes at biceps, bra-
chioradialis, and triceps are active and symmetri-
cal.
The differential diagnosis includes ulnar
neuropathy at the elbow, ulnar neuropathy at the
wrist, and a lower brachial plexus lesion (lower
trunk or medial cord) or C8 radiculopathy. The
presentation is largely compatible with ulnar neu-
ropathy at the elbow. The only findings that may
at first glance appear inconsistent with this diag-
nosis are normal wrist flexion (in part supplied by
the flexor carpi ulnaris) and normal flexor digito-
rum profundus strength. However, these muscles
are often spared in ulnar neuropathy at the elbow.
Ulnar neuropathy at the wrist is unlikely, given
sensory involvement of the dorsal aspect of hand,
supplied by the dorsal ulnar cutaneous nerve,
which branches before the wrist. Normal strength
in the thenar muscles suggests focal ulnar neu-
ropathy rather than lower brachial plexopathy or
C8 radiculopathy.
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268 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
Clinical Presentation
Patients with ulnar neuropathy at the elbow typi-
cally report difficulty with sensation over the ulnar
two digits of the hand. This involves both palmar
and dorsal aspects of the little finger and usually
the ulnar half of the ring finger. There is, however,
substantial variability in the sensory supply to the
hand. In up to 20% of patients there may be sub-
stantial variation where the ulnar nerve may sup-
ply the entire ring finger and the ulnar half of the
middle finger, or just the small finger. Paresthesias
are typically in the same distribution and usually
do not extend above the wrist, although patients
may report some elbow pain. Weakness is often
less common than sensory complaints on initial re-
port, but patients may have difficulty holding on to
objects, especially difficulty with power grasp
(such as using a hammer), since this requires using
the hand in ulnar deviation.
On physical examination, sensory deficits are
usually limited to the little finger and variably the
ring finger and middle finger. Testing two-point
discrimination is more sensitive than simply test-
ing pinprick or light touch for detecting sensory
deficits. In considering the differential diagnosis,
it is important to accurately define the distribution
of the sensory abnormalities. Patients with abnor-
mal sensation limited to the palmar side of the
hand are more likely to have an ulnar nerve lesion
at the wrist, since the dorsal ulnar cutaneous
nerve, supplying the back of the hand, branches
from the ulnar nerve in the distal forearm (proxi-
mal to the wrist). If patients have sensory abnor-
malities extending into the medial forearm, the
area supplied by the medial antebrachial cuta-
neous nerve, ulnar neuropathy is less likely. Since
this sensory branch derives from the medial cord
of the brachial plexus, patients with clear-cut sen-
sory abnormalities over the medial forearm are
more likely to have a lower brachial plexus lesion
or cervical radiculopathy.
Atrophy may be observed in the first dorsal
interosseus and hypothenar muscles, with sparing
of the thenar musculature. The forearm usually
appears normal. In more advanced cases, claw
hand deformity may be present, with the medial
two digits hyperextended at the metacarpopha-
langeal (MCP) joints and flexed at the interpha-
langeal joints. There is variability as to which fin-
gers are involved in claw hand deformity, since
there is often anatomic variation in which lumbri-
cals are supplied by the ulnar and median nerves.
Weakness can be demonstrated in the dorsal
or palmar interossei, as well as the adductor pollicis
muscles. Froment’s sign, difficulty or inability to
perform lateral pinch, is due to weakness of the ad-
ductor pollicis and flexor pollicis brevis, as well as
the first dorsal interosseus. When patients are
asked to perform a lateral pinch between the thumb
and index fingers, they cannot do so, and as the
strength of the pinch increases they compensate by
using their long flexors (flexor pollicis longus and
flexor digitorum profundus). Thus, instead of us-
ing the sides of the thumb and index finger to grasp
an object such as a piece of paper, they use the tips
of the fingers (known as Froment’s sign).
Special note should be made of examining the
strength of the ulnar-innervated muscles in the
presence of a radial neuropathy. Two errors are of-
ten made in this examination. First, many patients
with isolated radial neuropathy are mistakenly
thought to also have ulnar neuropathy because of
weakness in finger abduction. This weakness is sim-
ply an artifact of the weak MCP joint extension pro-
duced by the radial neuropathy. In flexion, finger
abduction is far weaker than it would be when the
MCP joints are fully extended, due to a mechanical
disadvantage. In the presence of a radial neuropa-
thy, these ulnar-innervated muscles must be tested
when the MCP joints are supported in full extension
by placing the hand flat on a table or desk. Con-
versely, patients with a complete isolated radial neu-
ropathy are often thought to have partial radial
nerve sparing because they can extend the interpha-
langeal joints of the fingers. This, however, is a
movement supplied by the ulnar nerve and does not
indicate preservation of radial nerve function.
Many patients with ulnar neuropathy at the
elbow have a positive Tinel sign over the elbow;
however, many patients without ulnar neuropa-
thy at the elbow will also test positive. While the
Tinel sign is a sensitive finding on physical exam-
ination, it is not specific, and many patients with-
out the disease also have a positive finding.
Nerve Conduction Studies
Motor nerve conduction studies are often the
most useful technique for localizing the site of
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES 269

ulnar neuropathy at the elbow and determining however, have found that recording from the first
the pathophysiology of the lesion (Table 10-2). dorsal interosseus muscle, the most distal muscle
Recording from the abductor digiti minimi is the supplied by the ulnar nerve, is more sensitive
most commonly used method. Some authors, (21–23). A two-channel technique may be used to

T A B L E 1 0 - 2 Nerve Conduction and Needle EMG Results for Case 2

Sensory and Mixed Nerve Conductions

R/L Nerve (Stim)

Record Latency (ms) Amplitude (
V)

L Ulnar to small finger 3.4 69

R Ulnar to small finger Absent Absent
R Median to index finger 3.3 45
Motor Nerve Conductions (shown in Fig. 10-3)

Conduction
Latency (ms) Amplitude (mV) Velocity (m/s)

R Ulnar (wrist) to abductor 3.0 7.6

digiti minimi
(below elbow) 7.2 7.1 51
(above elbow to 13.5 3.9 23
below elbow)
Electromyography

R/L Muscle Insertion Spontaneous Voluntary Motor Units

Activity P-wave Fibrillations Other Amp Dur Poly Recruit

R Deltoid N 0 0 0 N N N Full
R Biceps N 0 0 0 N N N Full
brachii
R Triceps N 0 0 0 N N N Full
brachii
R Flexor N 0 0 0 N N N Full
digitorum
profundus
R Abductor N 1 1 0 Incr N Incr Reduced
digiti
minimi
R Abductor N 0 0 0 N N N Full
pollicis
brevis
R First dorsal N 2 1 0 Incr N Incr Reduced
interosseus
Amp, amplitude; dur, duration; incr, increased; poly, polyphasic motor unit potentials; P-wave, positive wave; recruit, re-
cruitment.
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270 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

record from both muscles simultaneously so that
extra stimulations are not required. The recording
site for the first dorsal interosseus is usually de-
scribed as the active electrode over the bulk of
the muscle, with the reference distally over the
MCP joint of the index finger. Such a recording
arrangement often produces an initial positive de-
flection, which is difficult to interpret. An initial
negative deflection is more commonly seen when
the reference is placed over the metacarpopha-
langeal joint of the thumb (see Fig. 9-14).
Stimulation is usually performed at the wrist,
below the elbow, above the elbow, and at the axilla
(Fig. 10-3). While some electromyographers do
not stimulate at the axilla routinely, the advantage
of this technique is that it offers a conduction ve-
locity across one more segment (the arm), which
can be compared with the across-elbow conduc-
tion velocity. Study of the across-elbow segment
requires much care in technique and interpreta-
tion. First, it is well known that the position of the
elbow greatly influences the measured conduction
velocity. When the elbow is extended, it is thought
that the ulnar nerve may become redundant in the
ulnar groove, and that surface measurements do
not reflect the true distance of the underlying
nerve. It is thought that flexing the elbow stretches
the nerve to its full length, and measurement of
the distance over the ulnar groove more closely re-
flects the distance along the nerve (see Fig. 9-14;
Table 10-2) (24,25).
The distance between above- and below-
elbow stimulation sites may also influence the ac-
curacy of the conduction velocity measurement.
Since surface measurements can be in error by
many millimeters, use of short distances between
stimulation sites means that there will be a rela-
tively large percentage error in the distance and
hence conduction velocity measurements. Many
electromyographers recommend using at least a
10 cm across-elbow distance to reduce this meas-
urement error (26), although recent data indicate
that only 6 cm might be needed with the improved
accuracy of today’s EMG instruments (27).
While Martin-Gruber anastomosis is usually
discussed in the context of median nerve conduc-

Figure 10-3 ● Ulnar motor nerve conduction studies reported in Table 10-2. Stimulation of the
ulnar nerve typically occurs at the wrist, below the elbow, and above the elbow. Conduction block (neurapraxia)
at the elbow is shown by the decrease in CMAP amplitude with above-elbow stimulation. Some authors also rec-
ommend stimulation in the axilla (not shown).
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES
tion studies, it is probably far more important to
recognize this anomaly when performing ulnar
nerve conduction studies. When present, this
anomaly will result in a much lower–amplitude
response with below-elbow stimulation compared
to that obtained with wrist stimulation. The inex-
perienced electromyographer may suspect a focal
ulnar neuropathy in the proximal forearm, which
could even be “confirmed” by inching studies as
one inches along the ulnar nerve and across the
anastomosis. However, in all such cases, the pres-
ence of a Martin-Gruber anastomosis can and
should be ruled out very simply by stimulating the
median nerve at the elbow and recording over the
abductor digiti minimi and first dorsal interosseus
muscles. Presence of any significant response with
an initial negative takeoff indicates the presence of
the anomaly.
How much slowing in the across-elbow seg-
ment is sufficient to diagnose ulnar neuropathy?
Some electromyographers compare the across-
elbow velocity to the forearm velocity, allowing a
difference of up to 11 to 15 m/s between the across-
elbow and forearm segments before calling the
finding abnormal (28). Other authors prefer to use
the absolute conduction velocity rather than a com-
parison between segments (22,29). Comparison
with the forearm segment assumes that the forearm
segment remains normal in ulnar neuropathy at the
elbow. However, with axon loss, the distal velocity
often slows, making comparison less useful, which
has led some to study the upper arm segment for
comparison. A recent study has suggested that ab-
solute velocities of less than 48 m/s are suggestive of
ulnar neuropathy at the elbow and that this is supe-
rior to comparison with the forearm velocity (30).
Slowed conduction velocity is not the only
finding that should be considered diagnostic of ul-
nar neuropathy at the elbow. Such patients may
also have a drop in amplitude in the across-elbow
segment or increased temporal dispersion. Some
authors state that an amplitude reduction of more
than 10% in the across-elbow 10 cm segment may
be abnormal (28), but this is more convincing if ac-
companied by focal slowing or temporal dispersion.
Although it was just stated that a 10 cm min-
imum distance across the elbow is recommended
for conduction velocity measurements, it is often
found that study of very short segments yields
a higher sensitivity for very focal lesions. With
271
short-segment studies the injured segment with
demyelination occupies a higher percentage of the
distance studied, when compared to longer
segments in which normal nerve dilutes the meas-
urement. Inching studies (or perhaps more ap-
propriately called centimetering studies) can be
performed by stimulating the nerve at 2 cm incre-
ments across the elbow (31,32). Landmarks are
best established by drawing a line between the me-
dial epicondyle and the olecranon (33), and meas-
uring 2 cm increments distal and proximal to this
line. Stimulation must be carefully performed at
just barely supramaximal, since overstimulation
may cause nerve activation distal to the cathode
and potentially distal to a lesion. Using this tech-
nique, a conduction delay of more than 0.7 ms
across 2 cm segments is probably abnormal (31).
More impressive are accompanying focal changes
in amplitude or waveform morphology across a
segment (Fig. 10-4).
Most of the abnormalities mentioned above
require the presence of demyelination for localiza-
tion. However, in many traumatic ulnar neu-
ropathies in which there is only axon loss without
demyelination, localization of ulnar neuropathy is
far more difficult. In such cases, there will be dif-
fuse mild slowing of conduction velocity without
focal slowing, conduction block, or temporal dis-
persion; thus, there are no focal nerve conduction
changes across the lesion. Needle EMG is only
marginally helpful, since the two ulnar-innervated
muscles in the forearm are often spared (see below)
and there are no ulnar-innervated muscles in the
arm. Therefore, despite one’s best technique, there
are significant numbers of patients with primarily
axonal lesions of the ulnar nerve in whom local-
ization cannot be precisely determined.
Sensory nerve conduction studies are often of
less localizing value than motor conduction studies.
There are several technical problems that make this
response more difficult to interpret. First, with
stimulation of the ulnar nerve and antidromic
recording over the little finger, there is often a
large-amplitude hypothenar motor response vol-
ume conducted to the recording electrodes, which
precludes accurate identification and measurement
of the SNAP. Second, due to phase cancellation
(34), the amplitudes of the sensory responses fall
dramatically over distance, and reductions of 50%
are not unusual or abnormal in the wrist-to-elbow
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272 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

Figure 10-4 ● Inching performed using 2 cm segments across the elbow in a patient with
focal ulnar neuropathy at the elbow. Note the large change in both latency and amplitude between the
medial epicondyle and 2 cm below. Such focal changes indicate demyelination of axons resulting in slowing of
conduction in some axons and conduction block of other axons, and these changes are not seen in pure axon-
loss lesions.

segment. Third, it is much harder to record sensory
responses, particularly with proximal stimulation,
when their amplitudes are reduced by significant
ulnar neuropathy with temporal dispersion.
Nevertheless, sensory responses are often help-
ful for measuring the degree of sensory axon loss.
Reduction in the amplitude of the SNAP after dis-
tal stimulation is probably one of the more sensitive
indicators of the ulnar neuropathy at the elbow (35).
Of course, a low-amplitude sensory response in the
wrist-to-little-finger segment is not localizing and
simply means that there has been sensory axon loss
at or distal to the dorsal root ganglion at C8.
Measurement of SNAPs may be helpful to
exclude lesions other than ulnar neuropathy at the
elbow. When attempting to distinguish ulnar neu-
ropathy at the elbow from ulnar neuropathy at the
wrist, measurement of the dorsal ulnar cutaneous
sensory response can be of help. This nerve is in-
volved with lesions at the elbow, but not at the
wrist (where it bypasses Guyon’s canal). When
this response it normal and symmetrical, it speaks
more for ulnar neuropathy at the wrist. When the
lesion is at the elbow, the dorsal ulnar cutaneous
response is typically reduced in amplitude or absent.
Similarly, the medial antebrachial cutaneous nerve
can be studied to rule out more proximal lesions,
such as a lower brachial plexus lesion. Lower plexus
lesions would be expected to have a small amplitude
or absent medial antebrachial cutaneous nerve re-
sponse, whereas in ulnar neuropathies this nerve
should be spared (see Fig. 9-18).
Needle EMG
Needle electromyography of the ulnar-innervated
muscle is critical, both to determine whether any
axon loss has occurred and to help localize lesions
that are purely axonal in nature. Thus, even if
nerve conduction studies are entirely normal,
when ulnar neuropathy is clinically suspected,
needle EMG should still be performed. The most
helpful hand muscles to assess are the abductor
digiti minimi and first dorsal interosseus, two
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES
muscles commonly involved in ulnar neuropathy
at the elbow (see Table 10-2) (21). Study of the
flexor carpi ulnaris and the ulnar half of the flexor
digitorum profundus is marginally helpful. Al-
though the branch to these muscles usually comes
off distal to most entrapment sites at the elbow,
the fascicles supplying these muscles are in a rela-
tively protected position within the nerve, and
these muscles are consequently often spared.
Needle EMG of non–ulnar-innervated mus-
cles is often useful to rule out other lesions that
may mimic ulnar neuropathy. Examination of
thenar muscles or the extensor indicis proprius of-
fers the opportunity to compare C8-T1 muscles
not innervated by the ulnar nerve. This can be
useful to rule out lower cervical radiculopathies
as well as lower brachial plexopathies. When in-
terpreting abnormalities in the first dorsal in-
terosseus muscle, remember that this is the muscle
most commonly innervated by the Martin-Gruber
anastomosis. Moreover, in many cases of this anas-
tomosis, the anomalous branch is derived from the
anterior interosseus nerve (36). Thus, median neu-
ropathy or anterior interosseus nerve syndrome
should be considered when evidence of axon loss is
found in the first dorsal interosseus and the clini-
cal presentation is not typical of ulnar neuropathy.
Etiology
There are a number of different etiologies of ulnar
neuropathy at the elbow. In cubital tunnel syn-
drome, a relatively common cause, the ulnar nerve
(which normally travels deep to the two heads of
the flexor carpi ulnaris) is entrapped by an
aponeurotic band arising from the medial epi-
condyle of the humerus and attaching to the
medial border of the olecranon. Tardy ulnar palsy
occurs late after fracture or secondary to arthritis.
Many believe that it is secondary to persistent cu-
bitus valgus deformity, putting a chronic stretch
on the ulnar nerve following a fracture (28). Also,
osteophytes from old fractures or synovitis from
rheumatoid arthritis may impinge upon the nerve,
as well as tumors in or around the elbow joint.
In some cases, trauma or external pressure is
the cause of ulnar neuropathy at the elbow. A rela-
tively minor trauma occurring directly over the ul-
nar groove may induce ulnar neuropathy without
significant bony injury. Some believe that ulnar
273
nerve subluxation predisposes to ulnar neuropathy
(37). Childress determined that about 16% of the
population has recurrent subluxation when the
elbow is flexed; such individuals may be more
susceptible to ulnar neuropathy.
Several authors have reported ulnar neuropa-
thy after intrathoracic or intra-abdominal opera-
tions (38,39). While many patients do have ulnar-
innervated hand muscle weakness after surgery, it
is more common for a lower trunk or medial cord
lesion to be responsible for these lesions rather
than ulnar neuropathy (38). In such cases, exami-
nation of median-innervated muscles as well as
the medial antebrachial cutaneous nerve may help
detect a more proximal lesion.
ULNAR NEUROPATHY AT THE WRIST
CASE 3
A 72-year-old man presents with the chief com-
plaint of being unable to cup his left hand suffi-
ciently to apply shaving cream. He denies pain,
sensory loss anywhere, or weakness in any of the
other limbs. He is referred to rule out motor neuron
disease or ulnar neuropathy. Past medical history is
remarkable only for essential hypertension. He is re-
tired. Physical examination reveals marked weak-
ness of the palmar and dorsal interossei in the left
hand, as well as hypothenar muscles. Thenar mus-
cle strength (abduction and opposition) is normal.
Wrist flexion and extension, as well as all proximal
muscle groups, is 5/5 on strength testing. Sensation
is normal to pinprick, light touch, vibration, and
two-point discrimination. Reflexes are active and
symmetrical in the upper and lower limbs.
Differential Diagnosis
The patient presents with painless weakness with-
out sensory loss or complaints in the hand. Motor
neuron disease may also present with painless
weakness, starting in the distal upper or lower
limb muscles, but the absence of hyperreflexia and
the restriction to unilateral ulnar-innervated mus-
cles argues against this, though not definitively.
Spinal cord lesions or cervical root lesions would
also be expected to produce pain or sensory loss in
addition to weakness.
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274 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

Impression
The findings are consistent with ulnar neuropathy at
the wrist affecting only the motor branches. Surgical
evaluation and exploration later reveal a ganglion at
the wrist compressing the ulnar nerve. This is surgi-
cally removed and the patient’s symptoms improve.

Review of Pertinent Anatomy

As the ulnar nerve extends through the distal fore-
arm into the wrist, it gives off several branches.
These include the dorsal ulnar cutaneous nerve,
which innervates the dorsal aspect of the ulnar side
of the hand, and little and ring fingers; the palmar
cutaneous branch, innervating the ulnar side of the
palm; branches to the hypothenar muscles; the dig-
ital sensory branches; and the deep palmar ulnar
branch, innervating the interossei, (non–median-
innervated) lumbricals, and adductor pollicis.
There are a variety of lesions that can occur in this
area, injuring these branches either individually or
in combination. Most commonly, the ulnar nerve is
injured as it passes through Guyon’s canal, whose
boundaries are the transverse carpal ligament and
volar carpal ligament, and on either side the bony
margins of the pisiform bone and the hook of the
hamate. Guyon’s canal contains the ulnar nerve
along with the corresponding artery and vein, but
does not contain any tendons (in contrast to the
carpal tunnel). Since the nerve often divides into its
motor and sensory branches within the canal, it is
possible to have either isolated sensory or motor
loss, or combined motor and sensory deficits. In
addition to the site at Guyon’s canal, it is possible to
have ulnar nerve injury deep within the palm, af-
fecting only the deep ulnar branch, or to have only
isolated involvement of the dorsal ulnar cutaneous
branch of the ulnar nerve.
Clinical Presentation
Clinical presentation of ulnar neuropathy at or near
the wrist will depend upon which branches are af-
fected (Fig. 10-5). Commonly, there is isolated mo-
tor weakness without any sensory loss. When this is
seen in the ulnar distribution, injury at the wrist
should be immediately suspected. Although hy-
pothenar muscles are often involved, if the lesion is
distal enough, these may be spared, and only the in-
terossei, lumbricals, and other distal-innervated
Figure 10-5 ● Branches of the ulnar nerve
and common focal injury sites. Ulnar neuropa-
thy at the wrist can affect either motor or sensory
branches, or both. The branches to the forearm ulnar-
innervated muscles come off after the entrapment site
at the elbow. These two muscles are usually spared in
ulnar neuropathy at the elbow, however, due to place-
ment of these fascicles in a relatively protected part of
the nerve.
muscles may be weakened. Sensory loss will occur
when the sensory branches are affected, either in
isolation or together with the motor branches, and
the sensory distribution will depend upon the
branches that are most severely impaired.
Etiology
The most common etiologies of ulnar nerve en-
trapment at the wrist are ganglia and “occupa-
tional neuritis” (40). Occupational neuritis may be
seen in metal polishers (in which one puts pressure
over Guyon’s canal chronically), pipe cutters, me-
chanics, and bicyclists (40–42). Less common
causes include laceration of the nerve, ulnar artery
disease with thrombosis, and fractures. Dorsal ul-
nar cutaneous nerve lesions are rare. They may be
a result of repetitive wrist motion, handcuff neu-
ropathy (43), or chronic pressure over the ulnar
aspect of the wrist (44).
Nerve Conduction Studies
A combination of motor and sensory nerve con-
duction studies will be helpful in localizing the le-
sion and determining which branches are most se-
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES 275

verely involved. When performing motor nerve
conduction studies, it is critical—if ulnar neuropa-
thy at the wrist is suspected—to record from both
the abductor digiti minimi and first dorsal in-
terosseus muscles. Since hypothenar muscles can
be selectively spared, simply recording from the
abductor digiti minimi and not the first dorsal in-
terosseus would miss a significant percentage of
these lesions (Table 10-3) (45,46). In some patients,
slowing of forearm conduction velocity is also seen,
sometimes confounding the ability to precisely lo-
calize the site of demyelination. This is possibly
due to conduction block or axon loss selectively af-
fecting the fastest fibers at the wrist, allowing
recording from only a slower population of fibers.
Sensory nerve conduction study recording
from the small finger helps determine whether the
digital branches are involved. If an isolated dorsal
ulnar cutaneous nerve lesion is suspected, or if dif-
ferentiation between wrist and elbow lesions is dif-
ficult, recording from the dorsal ulnar cutaneous
nerve will provide additional useful information.

T A B L E 1 0 - 3 Nerve Conduction and Needle EMG Results for Case 3

Sensory and Mixed Nerve Conductions

Nerve (Stim)
R/L Record Latency (ms) Amplitude(
V)

L Ulnar to small finger 3.6 17

R Ulnar to small finger 3.4 22
L Median to index finger 3.1 64
R Median to index finger 3.4 46
L Dorsal ulnar cutaneous 2.2 17

Motor Nerve Conductions

Conduction
Latency (ms) Amplitude (mV) Velocity (m/s)

L Ulnar (wrist) to abductor digiti 5.4 4.9

minimi
(below elbow) 10.2 4.6 52
(above elbow) 12.2 4.3 51
L Ulnar (wrist) to 1st dorsal 6.5 3.7
interosseus
(below elbow) 11.4 3.3 54
(above elbow) 13.3 3.1 53
R Ulnar (wrist) to abductor digiti 2.9 14.2
minimi
(below elbow) 5.6 14.1 59
(above elbow) 7.6 13.3 62
R Ulnar (wrist) to 1st dorsal 3.2 7.1
interosseus
(below elbow) 5.9 6.9 59
(above elbow) 8.1 6.8 56

(continued)
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276 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

T A B L E 1 0 - 3 Nerve Conduction and Needle EMG Results for Case 3 (continued)

Electromyography

R/L Muscle Insertion Spontaneous Voluntary Motor Units

Activity P-wave Fibrillations Other Amp Dur Poly Recruit

L Triceps N 0 0 0 N N N Full
brachii
L Flexor carpi N 0 0 0 N N N Full
ulnaris
L Abductor N 1 1 0 Incr Incr Incr Reduced
digiti
minimi
L First dorsal N 2 1 0 Incr Incr Incr Reduced
interosseus
L Abductor N 0 0 0 N N N Full
pollicis
brevis
Amp, amplitude; dur, duration; incr, increased; poly, polyphasic motor unit potentials; P-wave, positive wave; recruit, re-
cruitment.

Needle electromyography should be per-
formed in ulnar-innervated muscles supplied by the
hypothenar branch as well as the deep ulnar branch
(e.g., abductor digiti minimi, first dorsal inter-
osseus). It should also include ulnar-innervated
forearm muscles and median-innervated muscles to
exclude more proximal lesions.
RADIAL NERVE LESIONS AT THE
SPIRAL GROOVE
CASE 4
A 32-year-old, otherwise healthy man awoke
2 months ago with the sudden onset of right wrist
drop and weakness in finger extension. He was in-
toxicated the night before the onset of symptoms
and remembers waking up with his arm hanging
over the wooden frame of his waterbed. He also
reports mild pain in the midarm and numbness
over the dorsal aspect of the right hand on the ra-
dial side.
Physical examination of the right upper limb
reveals the following strength measurements:
shoulder abduction 5, shoulder flexion 5, shoul-
der extension 5, elbow flexion 5 (but brachioradi-
alis not palpable), elbow extension 5, supination
4, wrist extension 0, wrist flexion 5, MCP exten-
sion 0, interphalangeal joint extension 4, finger
abduction 4. Sensation is reduced over the ra-
dial aspect of the dorsum of the hand but is
otherwise normal. Reflexes are active (2) and
symmetrical at the biceps and triceps. Brachiora-
dialis reflex is absent on the right and active (2)
on the left.
The differential diagnosis in this patient in-
cludes radial neuropathy as well as proximal le-
sions at the posterior cord or C7 root. However,
the presence of normal triceps strength and shoul-
der abduction strength makes these latter two pos-
sibilities less likely. These findings are all consis-
tent with a lesion to the radial nerve (Fig. 10-6) at
the spiral groove distal to the innervation of the
triceps, which starts off at the axilla, and proximal
to the branch of the brachioradialis (Table 10-4).
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES
Figure 10-6 ● Branches of the radial nerve.
The deep radial nerve was formerly called the poste-
rior interosseus nerve.
Clinical Presentation
Radial nerve lesions in the arm typically present
with weakness of wrist extension and finger exten-
sion. Since the radial nerve branch to the triceps
comes off high near the axilla, elbow extension is
spared in most lesions around the spiral groove. Oc-
casional cases of crutch palsy, where the radial nerve
is injured at the axilla, will present with triceps
weakness as well as more distal involvement. Sen-
sory complaints usually involve the dorsum of the
hand, although this distribution is variable; at times
the lateral antebrachial cutaneous nerve supplies the
area of skin often thought of as superficial radial.
On physical examination, localization of the
lesion can often be accomplished by testing the
appropriate radial innervated forearm muscles.
Brachioradialis function can best be assessed by
having the patient flex the elbow in neutral fore-
arm position (thumb pointing up) and palpating
the muscle. Wrist extension and MCP joint exten-
sion are reliably weak in radial neuropathies, since
there are no other muscles to substitute for these
movements. A common error is for the beginning
clinician or electromyographer to mistake inter-
phalangeal joint extension as indicating partial ra-
dial nerve function; this movement is, of course,
produced by intrinsic hand muscles. It is also
sometimes noted that finger abduction appears
weak in the presence of radial neuropathy. This is
277
simply a reflection of the fact that abduction is
often tested when the MCP joints are flexed, in
which position the muscles are at a mechanical
disadvantage. Finger abduction should be tested
when the hand is flat against the table or desk so
that the MCP joints are supported in full exten-
sion during the procedure.
Etiology
The vast majority of radial nerve lesions high in
the arm are a result of trauma, most commonly ex-
ternal compression to the radial nerve as it is pass-
ing through the spiral groove adjacent to the
humerus. “Saturday night palsy,” as in this case,
refers to the condition in which an inebriated indi-
vidual has slept with his arm over a park bench on
Saturday night. When humeral fractures are re-
paired with closed intramedullary nailing, there is
also about a 10% to 15% incidence of radial nerve
injuries (47), which are thought to result from in-
carceration of the radial nerve between fracture
fragments as reduction is accomplished. Improper
use of axillary crutches may also result in radial
nerve lesions, but these are often high, sometimes
involving the triceps muscle as well. Better in-
struction of patients using axillary crutches (i.e.,
not to put weight through the axillary pad) will
reduce the incidence of this neuropathy.
Nerve Conduction Studies
Motor nerve conduction studies for the radial
nerve are difficult to perform and often techni-
cally suboptimal. The greatest problem with the
technique is finding a suitable recording method.
When surface electrodes have been used, it has
been difficult to consistently find a surface record-
ing site that produces a local response and is not
volume-conducted from distant muscles within
the forearm. Needle recording from the extensor
indicis proprius has been more satisfactory but
also has its limitations. Needle recording does not
allow one to interpret the amplitudes obtained,
since they depend greatly on needle position
within the muscle. Moreover, any needle move-
ment during the study (as the muscle contracts
with each stimulus) may make it impossible to
compare results obtained from one site of stimula-
tion to another.
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278 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

T A B L E 1 0 - 4 Nerve Conduction and Needle EMG Results for Case 4

Sensory and Mixed Nerve Conductions

R/L Nerve (Stim) Record Latency (ms) Amplitude (
V)

R Radial to dorsum hand Absent 0

R Ulnar to small finger 3.3 22

Motor Nerve Conductions

Latency (ms) Amplitude (mV) Conduction Velocity (m/s)

R Ulnar (wrist) to abductor 3.5 7.2

digiti minimi
(below elbow) 7.2 6.9 55
(above elbow) 9.1 6.7 62
(axilla) 12.0 6.3 56
R Radial (forearm) to extensor 4.2 2.1
indicis proprius
(above elbow) 8.7 1.9 51
(above spiral groove) Absent 0

Electromyography

Muscle Insertion Spontaneous Voluntary Motor Units

Activity P-wave Fibrillations Other Amp Dur Poly Recruit

Triceps brachii N 0 0 0 N N N N
Brachioradialis Incr 4 2 0 N N Incr Reduced
Extensor carpi radialis Incr 4 3 0 None
Extensor digitorum Incr 4 3 0 None
Extensor carpi ulnaris Incr 4 3 0 None
Extensor indicis Incr 3 2 0 None
proprius
Deltoid N 0 0 0 N N N N
Teres minor N 0 0 0 N N N N
Flexor carpi ulnaris N 0 0 0 N N N N
1st dorsal interosseus N 0 0 0 N N N N
Flexor carpi radialis N 0 0 0 N N N N
Abductor pollicis brevis N 0 0 0 N N N N
Amp, amplitude; dur, duration; incr, increased; poly, polyphasic motor unit potentials; P-wave, positive wave; recruit, re-
cruitment.
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES
Sensory nerve conduction studies may be
performed with stimulation in the forearm and
recording over the dorsal aspect of the hand in the
first web space. While these studies are usually
not of localizing value, a reduced or absent re-
sponse indicates the degree of sensory axon loss
present. In rare cases, the lateral antebrachial cu-
taneous nerve innervates part of the dorsum of
the hand and can contribute to or produce a
SNAP in the presence of complete radial sensory
axon loss.
Needle EMG provides the most useful local-
izing information in most radial neuropathies.
Key muscles to examine include the triceps, bra-
chioradialis, extensor carpi radialis longus and
brevis (these are difficult to distinguish), and
supinator. While the degree of axon loss cannot be
quantitatively estimated based on needle EMG
studies, the distribution of denervation can help
with localization.
DEEP RADIAL (FORMERLY POSTERIOR
INTEROSSEUS) NERVE LESIONS
CASE 5
A 42-year-old man presents with gradual onset
(over 2 weeks) of the inability to extend his fingers,
weak wrist extension, and pain over the dorsal
aspect of the forearm. He denies any sensory loss
or paresthesias. He also denies any antecedent
trauma. On physical examination strength is
shoulder abduction 5, shoulder flexion 5, shoulder
extension 5, elbow flexion 5, elbow extension 5,
supination 5, pronation 5, wrist extension 3 (wrist
deviated radially), wrist flexion 5, MCP extension
2, thumb extension 2, and finger flexion 5. Sen-
sation is normal to light touch, pinprick, and two-
point discrimination. Reflexes are active (2)
and symmetrical at the biceps, brachioradialis,
and triceps.
Differential diagnosis in this case includes ra-
dial neuropathy at the elbow (e.g., deep radial
nerve), high radial nerve lesions, and middle
trunk or C7 root lesions. Presence of normal sen-
sation suggests that the lesion spares the superfi-
cial radial sensory nerve and is affecting only the
deep radial (formerly called posterior interosseus)
nerve branch.
279
Impression
Findings consistent with denervation only in the
distribution of the deep radial nerve (i.e., distal to
the supinator and extensor carpi radialis muscles)
suggest this is only a deep radial nerve lesion
(Table 10-5). The presence of normal and sym-
metrical findings in the radial SNAPs argues
against any higher radial neuropathy, although
they do not exclude a lesion of the root proximal to
the dorsal root ganglion. Normal findings in C7-
innervated muscles outside the deep radial distri-
bution argue against cervical radiculopathy.
Clinical Presentation
Most patients with a deep radial nerve compres-
sion have gradual onset of weakness and pain in
the elbow or proximal forearm over several days
to weeks. Typically, the nerve is compressed as it
enters the supinator muscle under the arcade of
Frohse (see Fig. 10-6). Alternatively, it can be
compressed by tumors, ganglia, or elbow joint
synovitis in this region. Since the radial nerve sup-
plies the brachioradialis, supinator, and extensor
carpi radialis before the site of compression, these
muscles are usually preserved. However, muscles
distal to the site are typically weak or paralyzed.
These distal muscles include the extensor carpi
ulnaris (producing radial deviation with wrist ex-
tension, since the radialis is spared), extensor digi-
torum, extensor indicis proprius, extensor pollicis
longus and brevis, and abductor pollicis longus.
Sensation is usually spared.
The etiology of deep radial nerve syndrome is
most commonly tumors or other mass lesions.
Lipomas are very common in this region and may
be the most frequent cause (48–50); these are usu-
ally painless. Trauma can cause deep radial neu-
ropathy secondary to elbow dislocations, radial
head fractures, or fractures of the ulna with radial
head displacement. Ganglia and rheumatoid el-
bow synovitis have also been reported as causes
(51–53). Entrapment at the arcade of Frohse af-
fects the radial nerve as it passes under the fibrous
tendinous band of the supinator muscle.
Some authors have proposed the existence of ra-
dial tunnel syndrome, also called resistant tennis el-
bow (54–57). This syndrome is controversial but re-
portedly presents predominantly with lateral elbow
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280 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

T A B L E 1 0 - 5 Nerve Conduction and Needle EMG Results for Case 5

Sensory and Mixed Nerve Conductions

R/L Nerve (Stim) Record Latency (ms) Amplitude (
V)

L Radial to dorsum of hand 3.3 15

R Radial to dorsum of hand 3.2 17

Motor Nerve Conductions

Latency (ms) Amplitude (mV) Conduction Velocity (m/s)

R Radial (forearm) to extensor 3.7 1.8

indicis proprius
(above elbow) 7.8 1.7 49
(above spiral groove) 10.9 1.5 47

Electromyography

Muscle Insertion Spontaneous Voluntary Motor Units

Activity P-wave Fibrillations Other Amp Dur Poly Recruit

Triceps brachii N 0 0 0 N N N N
Brachioradialis N 0 0 0 N N N N
Extensor carpi N 0 0 0 N N N N
radialis
Extensor Incr 2 1 0 None
digitorum
Extensor carpi Incr 2 1 0 None
ulnaris
Extensor indicis Incr 3 2 0 None
proprius
Deltoid N 0 0 0 N N N N
Flexor carpi N 0 0 0 N N N N
ulnaris
1st dorsal N 0 0 0 N N N N
interosseus
Flexor carpi N 0 0 0 N N N N
radialis
Abductor pollicis N 0 0 0 N N N N
brevis
Amp, amplitude; dur, duration; incr, increased; poly, polyphasic motor unit potentials; P-wave, positive wave; recruit, re-
cruitment.
90749_ch10(257-296).ps 8/10/06 3:57 PM Page 281
CHAPTER 10 • ENTRAPMENT NEUROPATHIES
pain, although these patients have less marked weak-
ness and less marked electrophysiologic findings
than other patients with deep radial nerve lesions.
Electrodiagnostic Examination
Needle EMG is the most useful part of the elec-
trophysiologic examination, since this can clearly
demonstrate abnormalities in the deep radial dis-
tribution while other muscles supplied by the ra-
dial nerve and C7 root are uninvolved. Although
some studies have demonstrated prolonged motor
latencies from the elbow to the extensor digitorum
(58), it is unclear whether this provides any useful
additional information compared to the needle
EMG. Sensory nerve studies of the radial nerve
should all be within normal limits.
SUPERFICIAL RADIAL NERVE LESIONS
CASE 6
A 52-year-old, 300-pound woman underwent
gallbladder resection at a major teaching hospital.
The medical student, intern, and resident each
failed in attempts to secure intravenous access in
the upper limb, but the attending anesthesiologist
was successful in putting in a central venous access
line. The patient did well during surgery but
awoke postoperatively with pain and numbness
over the radial aspect of the right forearm. While
numbness has been troubling, the dysesthetic pain
has been most disabling.
Physical examination reveals normal strength
in both upper limbs. There is reduced sensation to
pinprick and two-point discrimination over the ra-
dial aspect of the hand on the dorsal surface only.
Muscle stretch reflexes are all active (2) and sym-
metrical. A Tinel sign is present over the radial as-
pect of the distal forearm directly over the radius,
which causes severe pain.
Differential Diagnosis
In the absence of strength and reflex changes, a su-
perficial radial nerve lesion is the most likely diag-
nosis (see Fig. 10-6). Other items in the differential
diagnosis, though, include C6 radiculopathy or
upper brachial plexus lesion, either of which could
be secondary to positioning during surgery.
281
Clinical Presentation
Lesions of the superficial radial nerve (often called
chiralgia paresthetica) can be very painful and dis-
abling. Sensory loss is usually less of a functional
problem than the dysesthetic pain. Neuromas of-
ten form and recur despite repeated resection. The
superficial radial nerve typically supplies the dor-
sum of the hand on the radial aspect, but there is
considerable variation. At times this area can
be supplied largely or wholly by the lateral ante-
brachial cutaneous nerve, the dorsal ulnar cuta-
neous nerve, or in part by the median nerve or its
palmar cutaneous branch (59,60). Although sensa-
tion is abnormal, strength and reflexes are always
preserved in such patients. The Tinel sign is often
present over the injured nerve and may elicit
painful dysesthesias. Prognosis for relief from pain
is poor once neuroma formation has occurred.
By and large, injuries to the superficial branch
of the radial nerve are traumatic in etiology. Tight
casts, wristwatches, or wristbands can be responsi-
ble, as well as handcuffs (61–63). Iatrogenic causes
include complications from de Quervain’s tenosyn-
ovectomy or attempted placement of intravenous
lines or shunts for dialysis, especially near the level
of the wrist.
Electrodiagnostic Evaluation
The only electrodiagnostic study available to assist
in documenting this lesion is the SNAP. This is
often best recorded from the first web space with
proximal stimulation of the radial nerve along the
forearm. The superficial radial nerve can be pal-
pated as it crosses over the extensor pollicis longus
tendon, and the E1 electrode can be placed over
the nerve (see Fig. 9-22). High radial nerve lesions,
brachial plexopathies, and cervical radiculopathies
can best be excluded by performing needle EMG.
ANTERIOR INTEROSSEUS
NERVE SYNDROME
CASE 7
A 40-year-old construction worker presents be-
cause of inability to accurately direct on-site traf-
fic, which is part of his job. He stands behind
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282 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

cement-pouring trucks, directing them as they

back up, and is supposed to give the “OK” sign
with his right hand when they reach a good stop-
ping point. Three weeks ago, he noticed the onset
of right forearm pain and the sudden inability to
make the “OK” sign. He reported that he could
not bend the distal joint of the index finger or the
joint of his thumb sufficiently to make this sign.
He denies any sensory loss or pain other than in
the forearm. Other limbs are all asymptomatic.
Physical examination is remarkable for
weakness of thumb flexion at the interphalangeal
joint and weakness of flexion of the distal inter-
phalangeal joint of the index finger. All other fin-
ger and thumb flexion is normal. Pronation with
the elbow extended is normal, although it seems
mildly weak with the elbow flexed. Sensation is
entirely within normal limits to pinprick, light
touch, and two-point discrimination. Reflexes are
active (2) and symmetrical.
Differential diagnosis includes anterior in-
terosseus nerve syndrome, idiopathic brachial
plexitis (also known as neuralgic amyotrophy or
Parsonage-Turner syndrome), and a proximal
median nerve lesion (Fig. 10-7). The absence of
sensory symptoms or signs argues against a high
median nerve lesion. While the presentation is not
classical for neuralgic amyotrophy, some patients
with this disorder do have symptoms primarily in
the anterior interosseus nerve distribution (64).
Impression
The findings of denervation localized to the ante-
rior interosseus nerve distribution following an ex-
tensive needle examination are most consistent
with anterior interosseus nerve syndrome (Table
10-6). Normal findings in the proximal median-
innervated muscles, as well as muscles supplied by
other branches of the brachial plexus, argue against
a more widespread process. Although there is
some debate as to whether neuralgic amyotrophy
may present with isolated anterior interosseus
nerve deficits (65), there are a number of treatable
causes of this lesion that should be considered (66).
Clinical Presentation
Typically, patients report spontaneous onset of
acute proximal forearm pain lasting several days.
Figure 10-7 ● Branches from the median
nerve and common entrapment sites.
In some cases there is a history of trauma or
overexertion prior to the onset of pain. Weakness
is usually less bothersome to the patient than the
pain, and patients report a decrease in pinch
strength infrequently.
Physical examination shows weakness in the
flexor pollicis longus (interphalangeal joint of the
thumb flexion) and the flexor digitorum profun-
dus, supplying the index finger and sometimes the
middle finger (the latter is sometimes innervated
by the ulnar nerve). The pronator quadratus mus-
cle is best tested by assessing pronation strength
with the elbow maximally flexed to reduce the
contribution from the pronator teres. However,
there are still other muscles that contribute to
pronation (e.g., flexor carpi radialis), and even in
patients with complete denervation of pronator
quadratus, pronation strength may be normal
(66). Since the Martin-Gruber median to ulnar
nerve anastomosis is thought to frequently origi-
nate from the anterior interosseus nerve, patients
with this anomaly as well as anterior interosseus
nerve syndrome may be expected to exhibit weak-
ness in ulnar-innervated hand muscles as well as
those mentioned above.
Etiology
A number of anomalous or accessory muscles and
tendons in the proximal forearm have been impli-
cated in anterior interosseus nerve syndrome, and
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES 283

T A B L E 1 0 - 6 Nerve Conduction and Needle EMG Results for Case 7

Sensory and Mixed Nerve Conduction

R/L Nerve (Stim) Record Latency (ms) Amplitude (
V)

R Median 3.4 23

Motor Nerve Conductions

Latency (ms) Amplitude (mV) Conduction Velocity (m/s)

R Median (wrist) to abductor 3.6 7.8

pollicis brevis
(elbow) 8.9 7.7 55

Electromyography

R/L Muscle Insertion Spontaneous Voluntary Motor Units

Activity P-wave Fibrillations Other Amp Dur Poly Recruit

R Deltoid N 0 0 0 N N N Full
R Pronator Teres N 0 0 0 N N N Full
R Flexor carpi N 0 0 0 N N N Full
radialis
R Flexor pollicis Incr 2 2 0
longus
R Pronator Incr 2 2 0
quadratus
R Abductor N 0 0 0 N N N Full
pollicis brevis
R Extensor carpi N 0 0 0 N N N Full
radialis
R Triceps brachii N 0 0 0 N N N Full
R Extensor indicis N 0 0 0 N N N Full
proprius
Amp, amplitude; dur, duration; incr, increased; poly, polyphasic motor unit potentials; P-wave, positive wave; recruit, re-
cruitment.

these may be responsible for nearly half the lesions
seen (66). Sometimes a repetitive movement or
strenuous use of forearm muscles will provoke the
onset of symptoms (67,68). Trauma from frac-
tures, gunshot wounds, or lacerations has also
been reported (69).
There is debate as to whether neuralgic amy-
otrophy may involve isolated peripheral nerves
rather than simply the brachial plexus. In their
original report of neuralgic amyotrophy, Parson-
age and Turner (70) reported a number of patients
who had weakness limited to the flexor pollicis
longus and median-innervated flexor digitorum
profundus, but they did not recognize that the
weakness was in the anterior interosseus distribu-
tion. Kiloh and Nevin (64) later discussed that this
was within the distribution of a single peripheral
nerve. England and Sumner (65) hypothesized
90749_ch10(257-296).ps 8/10/06 3:57 PM Page 284
284 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
that peripheral nerves (as opposed to only the
brachial plexus) could be affected in neuralgic
amyotrophy and that the anterior interosseus
nerve was one particularly susceptible nerve. A
substantial proportion of patients with anterior
interosseus nerve syndrome may actually have id-
iopathic neuralgic amyotrophy rather than any
extrinsic compression in the forearm.
Electrodiagnostic Examination
Needle EMG is usually the most useful compo-
nent of the evaluation. The diagnosis depends
upon finding evidence of denervation in the
flexor pollicis longus, flexor digitorum profundus
(median half), and pronator quadratus. The latter
muscle can be difficult to examine, but access to
this muscle is greatly facilitated if it is approached
from the dorsal aspect when the forearm is in the
neutral (not pronated) position (66). Muscles out-
side of this distribution are usually normal, al-
though ulnar-innervated muscles may show evi-
dence of denervation if a Martin-Gruber anomaly
is present. Widespread examination of the limb
excludes neuralgic amyotrophy, or more diffuse
nerve or plexus lesions. Motor nerve conduction
studies have been recorded from the pronator
quadratus (67), although it is unclear whether this
presents any additional useful information com-
pared to the needle examination alone. Sensory
nerve conduction studies are typically normal and
are useful to rule out other possible diagnoses.
SCIATIC NEUROPATHY
CASE 8
A 48-year-old woman sustained a left acetabular
fracture during a motor vehicle accident, which
was repaired with open reduction and internal
fixation. Postoperatively, the patient awoke with
a left foot drop. She is referred for electrodiag-
nostic evaluation 3 weeks later. On physical ex-
amination, strength on the left is hip flexion 5,
hip abduction 4, hip extension 5, hip adduction 5,
knee extension 5, knee flexion 4, ankle dorsi-
flexion 1, ankle plantar flexion 4, ankle ever-
sion 3, and ankle inversion 4. Sensation is re-
duced over the dorsum of the foot and the lateral
aspect of the leg. Reflexes are symmetrical and
active (2) at the knee, unelicitable at the medial
hamstring on either side and asymmetrically ab-
sent at the left ankle.
The differential diagnosis includes sciatic
neuropathy (see Fig. 1-2) as a result of the initial
injury or the operative intervention; fibular neu-
ropathy, possibly as a result of prolonged external
rotation in bed or pressure over the nerve; or L5
radiculopathy (hip abduction is weak, but this
could result from the recent surgery).
Impression
The findings in Table 10-7 are consistent with a
sciatic neuropathy predominantly involving the
fibular distribution of the sciatic nerve. Absence of
denervation in the proximal L5 muscles (gluteus
medius or tensor fasciae latae) argues against L5
radiculopathy; however, these muscles can be ab-
normal as a result of the direct trauma of surgery.
Although abnormalities in the tibial distribution
are relatively mild, a predominance of fibular ab-
normalities would not be unexpected for a high
sciatic neuropathy. Sciatic neuropathy in these
cases likely results from stretch on the sciatic nerve
during the retraction required for surgical access
to the hip joint.
Clinical Presentation
Sciatic neuropathies typically present with weak-
ness and sensory loss in the sciatic distribution.
However, it is not unexpected, and is even custom-
ary, for the fibular distribution to be more affected
than the tibial division. This may be related to dif-
ferences in the fascicular structure of the nerve; the
fibular division has a few large fascicles with rela-
tively little intervening fibrous tissue, and the tibial
division carries many small fascicles cushioned by
greater amounts of fibrous tissue (5). In many cases
it is difficult to distinguish sciatic neuropathy from
fibular neuropathy on clinical examination. Help-
ful findings are weakness of knee flexors, absence
of the ankle muscle stretch reflex, and subtle weak-
ness in tibial-innervated muscles. Sensory loss is
similarly greater in the fibular than the tibial dis-
tribution. Characteristically there is sparing of the
saphenous nerve sensory distribution (a branch of
the femoral nerve) along the medial leg and foot.
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES 285

T A B L E 1 0 - 7 Nerve Conduction and Needle EMG Results for Case 8

Sensory and Mixed Nerve Conductions

R/L Nerve (Stim) Record Latency (ms) Amplitude (
V)

L Sural to lateral malleolus 4.3 1

Motor Nerve Conductions

Latency (ms) Amplitude (mV) Conduction Velocity (m/s)

L Fibular (ankle) to extensor 5.6 0.8

digitorum brevis
(below fibular head) 0.7 37
(popliteal crease) 0.65 38
L Peroneal F wave Absent
L Tibial (ankle) to abductor 4.7 2.3
hallucis
(popliteal crease) 1.9 40
L Tibial F wave 57

Electromyography

R/L Muscle Insertion Spontaneous Voluntary Motor Units

Activity P-wave Fibrillations Other Amp Dur Poly Recruit

L Tibialis anterior 3 3 N N Incr Reduced

L Peroneus longus 3 2 N N Incr Reduced
L Medial 1 1 N N N
gastrocnemius
L Soleus 1 0 N N N
L Biceps femoris, 1 1 N N N Reduced
short head
L Semitendinosus 1 0 N N N Full
L Tensor fascia lata 0 0 N N N Full
L Gluteus medius 0 0 N N N Full
L Vastus medialis 0 0 N N N Full
L Lumbar 0 0
paraspinals
Amp, amplitude; dur, duration; incr, increased; poly, polyphasic motor unit potentials; P-wave, positive wave; recruit, re-
cruitment.

Etiology
Sciatic neuropathy can result from hip surgery,
whether it be hip replacement or other types of
surgery where retraction of the sciatic nerve is re-
quired to gain access to the hip (71). Intraoperative
monitoring is often helpful to avoid irreversible
sciatic nerve injury (72). Sciatic nerve injury may
also result from trauma or injections into the
gluteal muscles (73), and is particularly severe
when irritating compounds are injected.
90749_ch10(257-296).ps 8/10/06 3:57 PM Page 286
286 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
Piriformis syndrome is another possible etiol-
ogy of sciatic neuropathy, although debate exists
about its true frequency. In about 6% of cadaver
specimens, the sciatic nerve does pass within the
piriformis muscle (74), though only a small frac-
tion of these can be expected to cause clinical find-
ings of nerve compression. In cadaver specimens,
tension on the muscle produced by hip flexion,
adduction, and internal rotation can cause com-
pression of the sciatic nerve.
Electrodiagnostic Evaluation
Electrodiagnostic studies have several roles in
sciatic neuropathies. They help with localizing
the lesion and assessing the degree of axon loss
and prognosis, and in severe lesions they assess
the degree of reinnervation, allowing an in-
formed decision to be made about operative in-
tervention. Needle EMG is usually the best tool
for localizing the lesion. Key muscles to study in-
clude the fibular- and tibial-innervated muscles
in the leg, the short head of the biceps femoris
(supplied by the fibular division of the sciatic
nerve), other hamstring muscles (supplied by the
tibial division of the sciatic nerve), and the mus-
cles innervated by the gluteal nerves. If the
gluteal muscles are involved, then the diagnosis
is more likely a lumbosacral plexopathy or
radiculopathy rather than simply sciatic neu-
ropathy. Examination of the paraspinal muscles
allows separation of sciatic neuropathy and plex-
opathy from radiculopathy. Needle EMG is also
useful for evaluating reinnervation after com-
plete or very severe lesions. By examining mus-
cles just distal to the lesion, one can note whether
recovery of MUPs is occurring in muscles previ-
ously completely denervated. When there are no
signs of reinnervation by 4 to 6 months after on-
set, surgical nerve grafting may be indicated. Af-
ter nerve grafting or neurolysis procedures, ax-
ons typically grow about 1 inch per month, yet
the muscle remains open to reinnervation for
only about 18 months after denervation. Thus,
peripheral nerve interventions are typically per-
formed by 6 months after onset of the lesion.
Nerve conduction studies are best at determin-
ing the degree of axon loss but are not as good in lo-
calizing the lesion. Abnormalities in both fibular
and tibial motor nerve conduction studies indicate
that the lesion is above the bifurcation of the sciatic
nerve. Similarly, late responses such as the F wave
or the H reflex can help to determine whether both
tibial and fibular divisions are affected.
There are reports of sciatic nerve stimulation
at the gluteal fold, but this technique is difficult in
my experience. Surface stimulation almost never
elicits a response. The absence of a response to
needle stimulation is often difficult to interpret,
and it is unclear how to rule out technical prob-
lems with the procedure. SNAPs of the sural or
superficial fibular nerves are useful to distinguish
a postganglionic lesion (e.g., sciatic nerve or lum-
bosacral plexus) from a pre-ganglionic root or
cauda equina lesion.
FIBULAR (PERONEAL) NEUROPATHY
AT THE KNEE
CASE 9
A 55-year-old woman reports the sudden onset of
right-sided foot drop 3 weeks ago after waking up
from sleeping on a chaise lounge outdoors at a
party where she drank alcohol. She reports diffi-
culty walking and easy falling because of right
foot weakness. She denies any back pain but does
report a sensory loss over the dorsum of the right
foot and the lateral aspect of the right leg. Signifi-
cant history includes intentional weight loss over
the past 3 years, from 220 pounds to 140 pounds
(because of medical complications from being
overweight).
Physical examination reveals right ankle dor-
siflexion strength 0, ankle eversion 2, ankle inver-
sion 5, and ankle plantar flexion 5. Proximal limb
strength is all normal. Sensation is reduced to pin-
prick and light touch over the dorsum of the right
foot, including the first web space, and over the
lateral aspect of the right leg. Reflexes at the knees
and ankles are 2 and symmetrical, and the me-
dial hamstring muscle stretch reflexes are 1 and
symmetrical.
The differential diagnosis includes not only
common fibular neuropathy at the head of the
fibula, but also sciatic neuropathy or L5 radicu-
lopathy. Of interest is the greater involvement of
muscles innervated by the deep fibular nerve dis-
tribution than the superficial fibular branch.
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES 287

Impression ther compression or trauma occurs. The presence

Findings are consistent with fibular neuropathy
(the peroneal nerve is now called the fibular nerve)
at the fibular head, mostly neurapraxic, with a
very good prognosis (Table 10-8). The large-
amplitude response with distal stimulation (3.8
mV) suggests that not much motor axon loss has
occurred and the prognosis for recovery over the
next 2 to 3 months is excellent, assuming no fur-
of abnormalities on needle EMG indicates that
there may be some axon loss, but this is minimal
given the good amplitude of the CMAP.
Clinical Presentation
Patients with fibular neuropathy typically present
with foot drop and weak ankle eversion. Weakness
is usually greater in the ankle dorsiflexors than in

T A B L E 1 0 - 8 Nerve Conduction and Needle EMG Results for Case 9

Motor Nerve Conductions

R/L Nerve (Stim) Record Latency (ms) Amplitude (mV)

L Fibular (ankle) to 5.1 3.8

extensor digitorum
brevis
(below fib. head) 3.7 43
(pop fossa) 0.25 38
L Fibular F wave Absent
L Tibial (ankle) abductor 4.5 5.3
hallucis
(pop fossa) 4.9 42
L Tibial F wave 53.0

Electromyography

Insertion Spontaneous Voluntary Motor Units

R/L Muscle Activity P-wave Fibrillations Other Amp Dur Poly Recruit

L Tibialis anterior 2 2 N N N Discrete

L Peroneus longus 1 1 N N N Discrete
L Medial 0 0 N N N
gastrocnemius
L Soleus 0 0 N N N
L Biceps femoris 0 0 N N N Full
short head
L Semitendinosus 0 0 N N N Full
L Gluteus medius 0 0 N N N Full
L Vastus medialis 0 0 N N N Full
L Lumbar 0 0
paraspinals
Amp, amplitude; dur, duration; incr, increased; poly, polyphasic motor unit potentials; pop fossa, popliteal fossa; P-wave,
positive wave; recruit, recruitment.
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288 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

the everters, consistent with typically greater in- subjects) may cause difficulties in interpretation
volvement of the deep fibular distribution than the (17,77). When this anomaly is present, a larger-
superficial. Ankle inversion and plantar flexion are amplitude response from extensor digitorum bre-
strong in these patients, excluding a sciatic nerve or vis is recorded with stimulation at the fibular head
lumbosacral root lesion. In some cases, only the deep than at the ankle. While this anomaly can be tech-
fibular distribution is clinically affected, resulting in nically confusing, it is not likely to masquerade as
a small or unnoticed sensory loss in the web space conduction block (as opposed to the case of Mar-
between first and second toes, and marked weak- tin-Gruber anastomosis and ulnar neuropathy).
ness of ankle dorsiflexion and toe extension. Recording from the tibialis anterior (Fig. 10-8)
also has advantages and disadvantages. When the
extensor digitorum brevis is absent or gives a very
Etiology
The most common etiology of fibular neuropathy
at the fibular head is acute compression of the
nerve. This can result from improperly fitting
braces or casts, circumferential bandages at the
level of the fibular neck, or lower limbs being
chronically externally rotated in bed while sedated
or unconscious. Improper positioning of the lower
limb during surgical procedures may also be a pre-
disposing factor. Weight loss is common in patients
who develop an acute lesion (75). Occupations that
involve chronic kneeling or squatting may also pre-
dispose to common fibular neuropathy at the fibu-
lar head (76), leading to the name “strawberry
picker’s palsy.” Tumors or Baker cysts (popliteal
space) may occasionally involve the fibular nerve.

Electrodiagnostic Examination
There are a variety of nerve conduction studies
used to localize the site of fibular neuropathy as
well as to assess prognosis. When significant de-
myelination is present in the fibular nerve, motor
nerve conduction studies are often of great value
in terms of localizing the lesion and assessing the
degree of axon loss. Purely axonal lesions are more
difficult to localize.
Recording for motor nerve conduction stud-
ies can be either at the extensor digitorum brevis
or tibialis anterior. The extensor digitorum brevis
is more commonly used, as in Figure 9-27. It has
the advantage of permitting conduction velocity
in the leg segment as well as proximally across the
fibular head. It also is a well-isolated muscle, with
little chance of volume conduction from adjacent
superficial fibular-innervated muscles. On the Figure 10-8 ● Recording from the tibialis an-
other hand, there are disadvantages to using the terior for deep fibular (peroneal) motor nerve
extensor digitorum brevis. The accessory fibular conduction studies. Act, E1 (active) electrode; gnd,
nerve (which is present in about 20% of normal ground electrode; ref, E2 (reference) electrode.
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES
small-amplitude motor response, the tibialis ante-
rior can be a reliable muscle from which to record.
There is some evidence that the response recorded
from the tibialis anterior may be more sensitive at
detecting fibular neuropathy at the fibular head
than when recording from the extensor digitorum
brevis (78–80). In addition, the tibialis anterior is a
more important muscle functionally than the ex-
tensor digitorum brevis; hence, any prognostic
statements are more pertinent to ankle dorsiflexion
function. The biggest problem with recording
from the tibialis anterior, in my experience, is vol-
ume conduction from the nearby peroneus longus.
Since the deep division of the fibular nerve is typi-
cally more affected than the superficial branch, it is
not uncommon to have complete denervation of
the tibialis anterior and preservation of peroneus
longus CMAP. In these cases, despite complete
denervation of tibialis anterior, stimulation of the
common fibular nerve at the fibular head can give
a volume-conducted response from the peroneus
longus recorded by surface electrodes at the tibialis
anterior. In these cases, recording from both the
tibialis anterior and peroneus longus, with both
surface and needle electrodes, can help to sort out
the muscles that are contributing to the surface-
recorded response over the tibialis anterior.
Independent of the recording site, the nerve
should be stimulated both at the fibular head and
in the popliteal fossa. It is critical with popliteal
fossa stimulation to avoid overstimulation activat-
ing the tibial nerve. This becomes apparent when
the amplitude with stimulation at the knee is
larger than that at the fibular head, when an ini-
tial positive deflection appears, or when a nonsen-
sically fast conduction velocity is obtained for the
across-fibular head segment (e.g., 100 m/s). Stim-
ulation in the popliteal fossa should occur later-
ally, just medial to the lateral hamstring tendon.
Evidence of demyelination is the most help-
ful finding for localization. Thus, focal slowing,
conduction block, or temporal dispersion may in-
dicate the site of demyelination. However, in the
majority of axon-loss lesions, amplitudes are small
and conduction velocities mildly slowed through-
out all segments of the nerve. In this event the
diagnosis is made largely on the distribution of
findings with needle EMG.
Inching studies have been reported for the
diagnosis of fibular neuropathy and are probably
289
more sensitive than long-segment studies, similar
to the situation for ulnar neuropathy (81). La-
tency changes over 2 cm segments exceeding 0.7
ms are thought to be abnormal. For amplitude
drop, some authors have recommended using a
50% drop from fibular head to knee stimulation
sites to define abnormal (78), although smaller
decrements are probably abnormal. SNAPs are
useful in demonstrating a postganglionic lesion
and differentiating this from a preganglionic
injury.
Needle EMG may be the only way to localize
a lesion that is purely axonal. The peroneus
longus and tibialis anterior are excellent muscles
to study in this regard. The extensor digitorum
brevis is often thought not to be a reliable mus-
cle for EMG, since many asymptomatic subjects
have fibrillation potentials or positive sharp
waves. Recent evidence, however, suggests that
foot muscles might not be as commonly abnormal
as previously thought (82). To exclude a more
proximal lesion, the short head of biceps femoris,
which is innervated by the fibular division of the
sciatic nerve, and hip abductors (e.g., gluteus
medius and tensor fasciae latae) are helpful. The
tibialis posterior or flexor digitorum longus may
also provide an opportunity to study L5-inner-
vated non-fibular nerve muscles, though it is of-
ten difficult to tell which of these two muscles the
needle is in. Given the preponderance for more
severe involvement of fibular-innervated mus-
cles, both in sciatic neuropathy and L5 radicu-
lopathy, differential diagnosis of these disorders
is not always straightforward and may require
extensive examination.
TARSAL TUNNEL SYNDROMES
CASE 10
A 32-year-old, otherwise healthy woman fell from
a ladder at work and sustained a severe eversion
injury to the left foot. This was diagnosed as an
ankle sprain to the medial ligaments. She was
treated conservatively with casting but soon (sev-
eral weeks) thereafter developed pain and pares-
thesias in the sole of the left foot.
Physical examination revealed normal
strength in the lower limbs, including toe flexion.
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290 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
Sensory testing revealed decreased sensation to
pinprick over the sole of the left foot compared to
the right, but normal sensation elsewhere in the
limb. Muscle stretch reflexes at the knee, medial
hamstring, and ankles were 2 and symmetrical.
The Tinel sign was present with tapping just
posterior to the medial malleolus.
Differential Diagnosis
The symptoms are most suggestive of a focal le-
sion of the tibial nerve at the ankle. While there
are many other causes of foot and ankle pain,
other neurogenic causes include entrapment of the
medial plantar nerve distal to the tarsal tunnel,
where the abductor hallucis originates from the
calcaneus (83), higher tibial nerve lesions at the
knee (such as from a Baker cyst), sciatic nerve, or
S1 root lesions.
Impression
Prolongation of the compound nerve action poten-
tial latency and CMAP latencies unilaterally are
consistent with the diagnosis of tarsal tunnel syn-
drome or tibial neuropathy at the ankle (Table 10-
9). Needle EMG of the intrinsic muscles in the foot
does suggest there may have been some axon loss,
but it is common to see minor abnormalities in oth-
erwise asymptomatic patients and thus is not clearly
indicative of axon loss from a neuropathy. Normal
studies in the proximal tibial, sciatic, and S1 distri-
butions argue against any significant higher lesion.
Clinical Presentations
The frequency of tarsal tunnel syndrome is often
disputed (84). Some authors believe it appears fre-
quently and is often missed electrodiagnostically.
Other authors, including this one, believe that tib-
ial neuropathy at the ankle occurs rarely in the ab-
sence of significant trauma.
Patients with tarsal tunnel syndrome typi-
cally report burning pain over the sole of the foot.
They often report a recent history of significant
injury such as fracture, ankle dislocation, or sprain
(85). Physical examination may show atrophy of
intrinsic foot muscles. Most intrinsic foot muscles
are difficult to test for strength, although toe flex-
ion may be the best maneuver to examine these
muscles. The extensor digitorum brevis should be
spared, since this is innervated by the deep fibular
nerve; it is the only non–tibial-innervated intrinsic
foot muscle (see Fig. 1-18).
Sensory loss is usually restricted to the sole of
the foot. Since the tibial nerve divides into three
branches as it passes through the tarsal tunnel, any
one or a combination of these three branches may
be affected (see Fig. 1-2). The medial plantar
branch supplies the medial sole of the foot and the
first three and a half toes; it can be thought of as
analogous to the median nerve in the hand. The
lateral plantar branch supplies the lateral sole and
lateral one and a half toes; it can be thought of as
analogous to the ulnar nerve in the hand. These
analogies also hold up in general terms when com-
paring muscle innervation. The calcaneal branch
supplies the skin over the plantar surface of the
heel and provides no muscular innervation.
The Tinel sign is often present over the tibial
nerve behind the medial malleolus in patients
with tarsal tunnel syndrome, but this sign is not
specific. Some authors believe that the presence of
a Tinel sign only indicates that there is a nerve un-
der the area being tapped (Jun Kimura, personal
communication).
Etiology
In tarsal tunnel syndrome, the tibial nerve is
thought to be injured as it passes under the reti-
naculum and the lancinate ligament (see Fig. 1-2).
Fractures and dislocations are the usual inciting
events that lead to compression of the nerve (85),
although joint hypermobility (86) may also play a
role. In some cases, masses, varicosities, or in-
flamed tendons can cause tarsal tunnel syndrome
(87). Some investigators report that persistent an-
kle hyperpronation contributes as well, although
this latter point is debatable.
Electrodiagnostic Examination
Since intrinsic foot muscles are thought to fre-
quently show minor abnormalities in asympto-
matic individuals, the majority of the diagnosis
relies on nerve conduction studies. However,
nerve conduction studies are not without technical
difficulties, and right-to-left comparison is cru-
cial. As with any other nerve conduction studies,
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CHAPTER 10 • ENTRAPMENT NEUROPATHIES 291

the absence of a response is less convincing and di-
agnostic than a prolonged latency or other evi-
dence of demyelination. An absent response, espe-
cially if present bilaterally, could be simply due to
technical problems. In these cases, every effort, in-
cluding near-nerve recording, should be made to
obtain a response.
Motor nerve conduction studies are easiest to
obtain yet less sensitive than compound nerve ac-
tion potential studies (see Table 10-9). Stimulation

T A B L E 1 0 - 9 Nerve Conduction and Needle EMG Results for Case 10

Mixed Nerve Conductions

R/L Nerve (Stim) Record Latency (ms) Amplitude (
V)

L Med plant ankle 4.7 5

L Lat plant ankle 4.9 3
R Med plant ankle 3.6 12
R Lat plant ankle 3.7 9

Motor Nerve Conductions

Latency (ms) Amplitude (mV) Conduction Velocity (m/s)

L Med plant (ankle) 6 2.3

abductor hallucis
(pop fossa) 1.9 42
L Lat plant (ankle) abductor 6.3 2.4
digiti minimi pedis
R Med plant (ankle) 4.5 5.3
abductor hallucis
(pop. fossa) 4.9 42
R Lat plant (ankle) abductor 4.5 3.6
digiti minimi pedis

Electromyography

Insertion Spontaneous Voluntary Motor Units

R/L Muscle Activity P-wave Fibrillations Other Amp Dur Poly Recruit

L First dorsal 2 2 Incr Incr Incr

interosseus pedis
L Abductor hallucis 1 1 Incr Incr Incr
L Medial 0 0 N N N
gastrocnemius
L Soleus 0 0 N N N
R First dorsal 1 0 N N N
interosseus pedis
R Abductor hallucis 0 0 Incr Incr Incr
Amp, amplitude; dur, duration; incr, increased; lat, lateral; med, medial; plant, plantar; poly, polyphasic motor unit poten-
tials; pop fossa, popliteal fossa; P-wave, positive wave; recruit, recruitment.
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292 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
Figure 10-9 ● Stimulation of the medial and lateral plantar nerves in the sole with recording at the medial
malleolus. This technique is useful in the evaluation of possible tarsal tunnel syndrome.
is applied behind and superior to the medial
malleolus over the tibial nerve with recording
over the abductor hallucis for the medial plantar
nerve and over the abductor digiti quinti for the
lateral plantar nerve (88). The lateral plantar re-
sponse is usually best recorded when the active
recording electrode is placed over the bulk of the
muscle belly rather than immediately below the
lateral malleolus (see Fig. 9-28).
Measurement of compound nerve action po-
tentials across the tarsal tunnel is more
sensitive than simply measuring motor latencies
but is more problematic (Fig. 10-9). Stimulation
of either nerve can occur at the sole of the foot
14 cm distal to the recording electrode placed pos-
terior and superior to the medial malleolus (89).
This is a compound nerve action potential rather
than a SNAP, since motor fibers supplying intrin-
sic foot muscles are also stimulated antidromically.
The most common technical problems with this
technique are difficulty in stimulation through the
sole of the foot and excessive stimulus artifact.
Pure study of the sensory nerves can be accom-
plished by stimulating the great toe (for the medial
plantar nerve) or little toe (for the lateral plantar
nerve) (90). Since the SNAP from toe stimulation is
very small when recorded over the medial malleo-
lus, it is usually necessary to perform near-nerve
recording with a needle electrode and use signal av-
eraging. Abnormalities may include either a pro-
longed latency or an increase in temporal dispersion
of the potential. The relative sensitivity of these last
two techniques (stimulation at the sole versus the
toes) is not known, and thus it is unclear whether it
is better to stimulate the toes or the sole of the foot,
although the sole seems technically easier.
Needle EMG should be performed to look
for evidence of gross abnormalities. Two muscles
that are best studied are the abductor hallucis (me-
dial plantar innervation) and the first dorsal in-
terosseus (lateral plantar innervation) (see Table
10-9). These muscles are relatively protected from
trauma and have a low incidence of positive sharp
waves and fibrillations in asymptomatic individu-
als compared to other intrinsic foot muscles. Nev-
ertheless, abnormalities in these muscles should
still be interpreted cautiously in the absence of
changes on nerve conduction studies. There is still
some debate as to whether this lesion is due to de-
myelination or primarily axon loss (84). Attempt-
ing to diagnose tarsal tunnel syndrome in the pres-
ence of an underlying polyneuropathy is
exceedingly difficult, if not impossible. Diagnosis
of tarsal tunnel syndrome in such a setting re-
90749_ch10(257-296).ps 8/10/06 3:57 PM Page 293
CHAPTER 10 • ENTRAPMENT NEUROPATHIES
quires demonstration of markedly more severe
changes in one nerve than others or considerably
asymmetry.
CONCLUSIONS
Entrapment neuropathies are a common cause for
presentation to the electrodiagnostic medical con-
sultant. Clinical assessment is critical to forming a
reasonable differential diagnosis. The electrodiag-
nostic evaluation is very helpful for localizing le-
sions, determining the extent of axon loss and
prognosis, and following reinnervation over time
in more complete injuries.
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78. Katirji MB, Wilbourn AJ. Common peroneal
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82. Dumitru D, Diaz CA, King JC. Prevalence of
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CHAPTER 11
Evaluation of the Patient
with Suspected Peripheral
Neuropathy
James W. Albers
INTRODUCTION
The clinical electromyographer is referred a pa-
tient with slowly progressive extremity weakness,
mild sensory loss, and areflexia. The referring
physician asks only, “Does patient have neuropa-
thy?” After evaluation, possible responses could
include “Yes,” “No,” or “I’m not sure,” or the
electromyographer could use his or her combined
clinical and electrodiagnostic skills to help explain
the patient’s symptoms and signs. The evaluation
of patients with suspected polyneuropathy or
peripheral neuropathy (subsequently referred to as
neuropathy) is relatively straightforward. The
evaluation consists of a combination of clinical,
electrophysiologic, and laboratory studies, with
the expectation that the electromyographer will
integrate this combined information in arriving at
a final diagnosis. It is no longer sufficient to simply
confirm the presence of abnormality or to conclude
that findings are consistent with neuropathy.
Evaluation of suspected neuropathy is among
the most frequent investigations performed in the
electromyography (EMG) laboratory, and the elec-
tromyographer plays an important role in estab-
lishing not only the presence but also the etiology
of neuropathy (1). The patient’s history and clinical
findings provide important clues in establishing
the diagnosis or suggesting studies important in
identifying etiology, and the electromyographer’s
role in performing a neuromuscular consultation
includes paying careful attention to relevant
clinical information. Knowledge of potential
exposures (occupational, social, or pharmacologic)
or recognition of a systemic illness may suggest
the cause of a patient’s neuropathy, although
symptomatic neuropathy may precede recognition
of a systemic disorder. The electromyographer
frequently is the clinician most experienced in
making such important associations.
The electrodiagnostic examination is simply
an extension of the neurologic evaluation. It is
derived from sound neurophysiologic principles
and provides objective information useful in con-
firming clinical findings, in addition to localizing
abnormalities to a degree not clinically possible. In
the evaluation of neuropathy, electrodiagnostic
results often suggest the underlying pathophysiol-
ogy, providing additional clues in establishing eti-
ology. A complete electrodiagnostic study includes
evaluation of sensory and motor nerve conduction
studies, late responses, and needle EMG.
Almost all patients with neuropathy demon-
strate large-diameter fiber dysfunction, making
the EMG examination (this term is synonymous
with “electrodiagnostic study” mentioned above)
a powerful clinical tool for evaluating suspected
neuropathy. The presence of large-diameter axon
dysfunction is important since these are the
nerve fibers most easily accessed by the EMG
studies. Classification of neuropathy using electro-
physiologic information focuses the differential
diagnosis and the subsequent evaluation and often
offers a specific diagnosis or class of disorders (2).
297
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298 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
Unfortunately, many neuropathies are character-
ized by nonspecific axonal loss, increasing the
importance of other clinical information in estab-
lishing a specific diagnosis, which often may
include the cause of the neuropathy. Nevertheless,
several of the most common treatable neuropathies
do have characteristic electrodiagnostic features,
yet they were rarely diagnosed until recently.
Awareness of these disorders relates to increased
use of clinical electrophysiology and identification
of characteristic electrodiagnostic features that
result in their recognition.
The following material reviews the underly-
ing pathophysiology associated with neuropathy,
defines expectations of the electromyographer,
outlines a recommended evaluation, and identifies
distinguishing electrophysiologic and clinical
features useful in defining specific classes of neu-
ropathy. For each classification, specific clinical
examples are included.
PATHOPHYSIOLOGIC FEATURES OF
NEUROPATHY
Several major pathophysiologic changes are im-
portant in the clinical electrodiagnostic evaluation
of neuropathy. The most important include ax-
onal degeneration, axonal atrophy, demyelination
(uniform and multifocal), and metabolic or ionic
channel changes that alter nerve conduction (2,3).
Axonal Lesions
Axonal degeneration results from disorders of
the nerve cell (neuronopathy) or axon (axonopa-
thy). Pathophysiologic findings resemble those
associated with nerve transection, varying only in
degree (3). Separation of the distal axon from
the nutritive cell body produces distal axonal
degeneration and breakdown of the myelin sheath
(Wallerian degeneration). Landau reported that
muscle contraction produced by nerve stimulation
distal to the lesion persisted for several days after
transection, but then disappeared (4). Sensory
and motor electrical responses similarly remain
normal for several days, with stimulation distal
to the transection. Within days, sensory nerve
action potential (SNAP) and compound muscle ac-
tion potential (CMAP) motor amplitudes diminish
and ultimately disappear, although conduction
along individual axons remains relatively normal
before disappearance.
Following nerve transection, the needle EMG
examination initially shows absent voluntary
activity but no other findings. Gilliatt and Taylor
(5) demonstrated spontaneous discharge of indi-
vidual muscle fibers (i.e., fibrillation potentials)
beginning 1 to 4 weeks after axonal degeneration,
depending upon proximity to the transection
(first appearing in muscles closest to the lesion).
Fibrillation potentials reflect muscle fiber hy-
persensitivity to acetylcholine (ACh) and are
associated with proliferation and migration of
extrajunctional acetylcholine receptors (AChRs)
on the muscle membrane (6). Initial findings
include increased muscle fiber sensitivity to
mechanical stimulation (typically in the form of
positive waves), followed by sustained sponta-
neous activity (fibrillation potentials) at rest. The
amplitude of fibrillation potentials and positive
waves diminishes over time, proportional to
muscle fiber atrophy, and provides a useful marker
for assessing the duration of partial denervation.
Findings with partial or incomplete axonal le-
sions are similar, with decreased (instead of absent)
sensory and motor responses, normal conduction
along surviving axons, and reduced voluntary
motor unit action potential (MUAP) recruitment
(3). Abnormal spontaneous activity appears in den-
ervated muscle fibers. After partial denervation,
some denervated muscle fibers eventually are
reinnervated by collateral sprouts from surviving
axons, resulting in large motor units when the total
number of motor units remains reduced (7). ACh
hypersensitivity resolves once muscle fibers are
reinnervated, and abnormal spontaneous activity
disappears. Ballantyne and Hansen demonstrated
that regenerating axons produced new motor units
by reinnervating muscle fibers shed by abnormally
large motor units (8).
The most common morphologic response to a
variety of disorders producing neuropathy is a dis-
tal axonopathy (3). A variety of mechanisms exist to
explain distal axonal degeneration in neuropathy,
including failure of axonal transport of some nutri-
ent required for maintenance of the distal axon, as
proposed by Schaumburg et al (9). The concept of
axonal atrophy is controversial, but it may repre-
sent a form of incomplete axonal lesion appearing
before axonal degeneration. It is described at the
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY
terminal axon as a reduced diameter of the distal
axon (axonal stenosis). Because conduction velocity
is proportional to axonal diameter, action potential
propagation is reduced proportional to the size of
the atrophic distal axon. Unlike axonal degenera-
tion, sensory and motor amplitudes are not sub-
stantially reduced in axonal atrophy, and muscle
membrane excitability is unaffected.
Myelin Sheath Lesions
Disorders of the myelin sheath produce conduction
abnormalities similar to those associated with focal
nerve compression, whereby conduction may be
slowed or blocked across the site of compression
without producing axonal degeneration (10,11).
In experimental models using a compressing
tourniquet, Ochoa et al identified localized defects
beneath the edges of the tourniquet, with tele-
scoping of one myelin segment beneath the next
at the node of Ranvier (12,13). This structural
abnormality is thought to reduce or block ionic
current flow by occluding the node, thereby
slowing or preventing action potential propagation
(10). Paranodal demyelination is associated with a
variety of conditions, including focal compression
and neuropathy, and conduction block is attrib-
uted to localized demyelination and intramyelin
edema. Ochoa and Marotte demonstrated that
chronic nerve compression produces similar find-
ings with distorted myelin segments (segmental
demyelination), exposed axon membrane, and
paranodal remyelination with short internodal
distances (11). Membrane excitability does not
increase substantially with demyelinating lesions.
Conduction slowing or block across a compressive
lesion is relevant to the evaluation of generalized
neuropathy, in that findings attributed to acquired
demyelinating neuropathies have similar myelin
abnormalities distributed throughout the periph-
eral nervous system, with combined demyelination
and remyelination, short internodes, and reduced
conduction velocity.
Metabolic Lesions
Reduced conduction velocity does not always
indicate histologic abnormality such as axonal
stenosis or demyelination, because metabolic dis-
orders may produce conduction slowing without
identifiable structural abnormalities (3). Among
299
patients with hyperglycemia, increased conduc-
tion velocity 6 hours after normalizing glucose
levels suggests that nonstructural changes account
partially for conduction slowing (14). In associa-
tion with the neuropathy attributed to chronic
diabetes mellitus, the metabolic pathophysiology is
poorly understood. Hyperglycemia is believed to
produce a decrease in nerve myo-inositol and
increased polyol pathway activity related to the
increased conversion of glucose to sorbitol by
aldose reductase. The reduced nerve myo-inositol
leads to reduced Na
/K
-ATPase activity and a
resultant increase in intracellular Na
(15). In
isolation, the resultant mild depolarization of the
resting membrane potential decreases conduction
velocity independent of structural alteration.
Additional changes, including inactivation of
sodium channels and axoglial disjunction, may
also contribute to conduction velocity abnormali-
ties (16). Finally, coexisting microvascular injury
to the vasa nervorum and diminished production
of nitrous oxide contribute to axonal ischemia and
cellular damage, as may possible autoimmune
damage mediated by antineuronal antibodies (17).
WHAT IS EXPECTED OF THE
ELECTROMYOGRAPHER?
The electromyographer or electrodiagnostic physi-
cian plays an important role in the evaluation of
suspected peripheral nerve disorders. It is expected
that the electromyographer does more than con-
firm the presence of abnormality or conclude that
findings are consistent with a “neuropathy”; possi-
ble etiologies for the neuropathy should be sug-
gested. The electromyographer is a neuromuscular
specialist with experience in the evaluation and
treatment of patients with neuropathy. It is this
clinical experience, combined with electrophysio-
logic information, that is useful in deriving a diag-
nosis and establishing the cause of the problem.
The emphasis of this chapter is on the application
and interpretation of electrodiagnostic informa-
tion. However, the study begins with a focused
history and neurologic examination. Features of
the clinical examination particularly important to
the evaluation of neuropathy are summarized in
Table 11-1.
The electrodiagnostic information is useful
only when collected appropriately. Several com-
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300 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
T A B L E 1 1 - 1 Important Features of the Clinical Examination in Suspected
Neuropathy
General information important to the
evaluation:
• Onset and temporal profile of motor,
sensory, and autonomic complaints
• Type and distribution of paresthesias,
hyperesthesia, and hyperpathia
• Presence and distribution of weakness
and atrophy
• Industrial and medical history for toxin
or drug exposures
• Family history, including bony deformi-
ties such as pes cavus or hammertoes
• Social habits, including recreational
drug use
• Antecedent illness or symptoms of
underlying disease
Clinical examination findings relevant to
neuropathy:
General:
• Findings most prominent in distal lower
limbs
• Relative symmetry
• Look for associated findings, such as
ataxia, tremor, skin lesions, pes cavus, or
hammertoe deformities.
• Palpate peripheral nerves for size, tender-
ness, paresthesias, and hypertrophy.
(Modified from Albers JW. Numbness, tingling, and weakness. Making sense of the neuropathies. AAEM Course for Primary
Care Physicians. Rochester, MN: American Association of Electrodiagnostic Medicine, 1994, with permission.)
ponents of the examination can be standardized.
In the examination, the electromyographer must
attend to these components, which are covered in
the following series of questions:
1. Were the clinical findings considered in de-
signing the electrodiagnostic evaluation?
2. Were the limb temperatures monitored and
cool limbs warmed to at least 31° to 32°C?
3. Were the measurement techniques described?
4. Were normal values provided?
Page 300
Motor (emphasis upon distal muscles):
• Intrinsic hand muscles, finger and wrist
extensors
• Toe extensors and foot dorsiflexors
Sensory:
• Demonstrate distal-to-proximal sensory
loss gradient.
• Identify involved modalities:
• Large fiber: vibration, light-touch,
touch-pressure (common), and joint
position sensation (JPS) (when severe)
• Small fiber: temperature, pin-pain,
and deep pain
• Discriminative sensations less helpful in
peripheral disorders
• Absence of sensory level on the trunk
• Vibratory loss to iliac crest and JPS loss
may suggest spinal cord lesion.
Reflexes:
• Achilles reflexes usually absent
• Diffusely hypoactive reflexes not
necessarily abnormal
• Absence of pathologic reflexes
(e.g., Babinski reflex)
Autonomic nervous system:
• Postural hypotension
• Diminished sweating
5. Was the evaluation sufficient to both document
the problem and exclude alternative explana-
tions (avoiding errors of omission)?
6. Were appropriate negative findings discussed?
7. Was the EMG interpretation consistent with
the clinical signs?
8. Was the referral question(s) adequately ad-
dressed?
Although clinical skills are important in
documenting the distribution and magnitude of
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY 301

a suspected neuropathy, the electromyographer’s Another example is distinguishing neuropathy

role is to help identify the underlying pathophys-
iology and focus the differential diagnosis so that
appropriate laboratory investigations can be
ordered. Basic questions that should be ad-
dressed by the electrodiagnostic study in the eval-
uation of neuropathy are listed in Table 11-2.
These additional questions also extend those ad-
dressed by the clinician prior to performing the
study.
One of the most important tasks of the elec-
tromyographer is to distinguish axonal loss lesions
from lesions characterized by uniform or multifo-
cal demyelination. This allows for the possible
identification of acquired demyelinating neu-
ropathies, which are important because they are
among the most common treatable neuropathies
and because they are frequently associated with a
systemic illness. The electromyographer also must
exclude disorders that mimic neuropathy but
are difficult to identify clinically. For example,
identifying fibrillation potentials in paraspinal
muscles differentiates a distal neuropathy from a
polyradiculopathy or a polyradiculoneuropathy.
from a confluent mononeuritis multiplex. Al-
though clinically difficult, the diagnosis of an
underlying vasculitis may be suggested by asym-
metric EMG findings, distinguishing a vasculitic
neuropathy from other more symmetric forms of
distal neuropathy. The answers to the questions in
Table 11-2 form the basis of the electrodiagnostic
classification of neuropathy, which is described
below.
CLINICAL ELECTROMYOGRAPHY
Nerve conduction studies and needle EMG evalu-
ate slightly different components of the peripheral
nervous system. Nerve conduction studies are
noninvasive and provide the most useful informa-
tion in documenting and establishing the type and
etiology of neuropathy, whereas the needle EMG
examination is more useful in documenting the
magnitude and distribution of axonal loss lesions
and identifying disorders clinically indistinguish-
able from neuropathy.

T A B L E 1 1 - 2 Expectations for the EMG Evaluation of Neuropathy

Document evidence of a peripheral abnormality:

Detect presence.
Document location (diffuse, focal, or multifocal).
Identify which peripheral modalities are involved:
Sensory fibers
Motor fibers
Autonomic fibers
Identify the predominant pathophysiology:
Axonal loss
Uniform demyelination
Multifocal demyelination with partial conduction block or abnormal temporal dispersion
Conduction slowing suggestive of membranopathy
Combination of the above
Establish temporal profile when possible (acute, chronic, old, or ongoing).
Identify accompanying disorders or alternative explanations for findings.
Determine the prognosis.
(Modified from Albers JW. Numbness, tingling, and weakness. Making sense of the neuropathies. AAEM Course for Primary
Care Physicians. Rochester, MN: American Association of Electrodiagnostic Medicine, 1994, with permission.)
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302 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

Nerve Conduction Studies
SNAPs and CMAPs are recorded using surface
electrodes and percutaneous electrical stimulation
(Figs. 11-1 and 11-2) (3). Response amplitudes and
latencies are measured and conduction velocities
are calculated as part of the evaluation. Con-
duction over an entire motor nerve is evaluated
by F wave latency (Fig. 11-3). F wave measures ac-
centuate mild generalized slowing because of the
long conduction distances. Most normal values are
age-dependent and some vary according to patient
size and other factors (18–23). Improper electrode
placement, inaccurate measurements, and failure
to monitor and control limb temperature influ-
ence the results (3). Limb temperature is particu-
larly important in the evaluation of neuropathy.
Cooling decreases conduction velocity and in-
creases amplitude, a combination of findings atyp-
ical for most pathologic processes. Limb tempera-
ture should be monitored, and cool limbs should
be warmed to a surface temperature of between
32° and 36°C (23,24). In the context of the electro-
diagnostic evaluation of neuropathy, failure to
record limb temperature and warm cool limbs
limits the ability to interpret the nerve conduction
study results.
Needle Electromyography
The needle EMG examination plays a limited but
important role in suspected neuropathy (3). The
needle EMG examination evaluates insertional
activity (i.e., positive waves and fibrillation po-
tentials) and volitional MUAP recruitment, size,
and configuration. As a sensitive indicator of
denervation, the needle EMG examination docu-
ments the distribution of axonal lesions, providing
information from muscles inaccessible to nerve
conduction study (e.g., the paraspinal muscles).

Figure 11-1 ● Representative sensory nerve conduction study. Sensory nerve action potentials
recorded from the fifth digit following ulnar nerve stimulation at the wrist and elbow. Calibration: 1 ms and
20 V. (Reprinted from Albers JW, Leonard JA Jr. Nerve conduction and electromyography. In: Crockard A,
Hayward R, Hoff JT, eds. Neurosurgery: the scientific basis of clinical practice, 2nd ed. Oxford: Blackwell Sci-
entific Publications Ltd, 1992:735–757, with permission.)
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY 303

Figure 11-2 ● Representative motor nerve conduction study. Compound muscle action poten-
tials recorded from hypothenar muscles following ulnar nerve stimulation at the wrist, elbow, and clavicle.
Calibration: 2 ms and 5 mV. (Modified from Albers JW, Leonard JA Jr. Nerve conduction and electromyog-
raphy. In: Crockard A, Hayward R, Hoff JT, eds. Neurosurgery: the scientific basis of clinical practice, 2nd ed.
Oxford: Blackwell Scientific Publications Ltd, 1992:735–757, with permission.)

Recruitment refers to the sequential introduction
of additional MUAPs into the interference pattern
as force is increased. In the evaluation of neuropa-
thy, the needle EMG examination provides an in-
dication of ongoing or previous denervation. It also
is used to define the distribution of axonal lesions,
identifying disorders sometimes confused with or
superimposed upon a generalized neuropathy.
The amplitude of positive waves or fibrillation
potentials and the configuration of MUAPs are
used to distinguish acute from chronic disorders
and provide an estimate of the rate of progression
of axonal loss.
ELECTRODIAGNOSTIC EVALUATION IN
SUSPECTED NEUROPATHY
Patients commonly are referred for evaluation
because of symptoms or signs suggestive of neu-
ropathy. Occasionally, asymptomatic patients are
referred because of an underlying illness associ-
ated with neuropathy. Some patients referred for
other reasons are found to have an unsuspected
neuropathy. Regardless of the reason for referral,
the initial evaluation for possible neuropathy
is based upon the patient’s history and clinical
findings. Initial impressions are confirmed or
altered, and the study is modified to accept or re-
ject additional considerations until a final diagno-
sis is achieved.
Protocols for the evaluation of suspected neu-
ropathy are straightforward (Table 11-3). When
signs are mild, the evaluation is directed toward
the most sensitive or susceptible sites (e.g., the
distal lower limb sensory nerves). When severe,
evaluation of less-involved sites is important
because absent responses provide no information
about the presence or absence of conduction
slowing. Bilateral studies are performed on some
nerves to evaluate symmetry, although a super-
imposed focal abnormality should not exclude
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304 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

Figure 11-3 ● Representative F waves following antidromic peroneal nerve stimulation.

(Reprinted with permission from Albers JW. Clinical neurophysiology of generalized polyneuropathy. J Clin
Neurophysiol 1992;10:149–166.)

the diagnosis of neuropathy. The needle EMG
examination provides information supplementary
to that obtained from the conduction studies. The
examination evaluates muscles inaccessible to con-
duction study, such as paraspinal muscles in sus-
pected radiculopathy, and the results are used to
demonstrate a proximal-to-distal abnormality
gradient in neuropathy.
Interpretation of Findings
The initial goals are to determine the presence and
location of sensory or motor involvement (see
Table 11-2). Clinically apparent sensory loss may
reflect a lesion proximal to the dorsal root ganglia,
whereas abnormal SNAPs document peripheral
involvement at or distal to the dorsal ganglia (3).
Weakness and atrophy in combination with low
CMAP amplitudes reflect abnormality of the
lower motor neurons or axons. When present in
isolation, these findings cannot localize the lesion
more precisely (25,26). The distribution of needle
EMG examination abnormalities is helpful in fur-
ther localizing the abnormality.
The next goal is to identify to the extent
possible the primary pathophysiology, such as
axonal degeneration or demyelination (3). Axonal
neuropathies usually are easily identified. They are
characterized by reduced amplitudes, little evidence
of conduction slowing, and neurogenic changes on
needle EMG with evidence of active denervation
and reinnervation (i.e., decreased MUAP recruit-
ment and increased MUAP amplitude, duration,
and polyphasia). Using a computerized model of the
peripheral nerve, expected CMAP responses for a
normal nerve are shown in Figure 11-4. Motor con-
duction abnormalities associated with axonal de-
generation are shown in Figure 11-5. With a loss of
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY 305

T A B L E 1 1 - 3 Representative Electrodiagnostic Protocol for Evaluating

Polyneuropathy

Nerve Conduction Studies

1. Test the most involved site if mild or moderate, the least involved site if severe.
2. Evaluate peroneal motor nerve (extensor digitorum brevis);* stimulate ankle, below fibular
head, and knee. Measure F-wave latency.†
3. If abnormal, evaluate tibial motor nerve (abductor hallucis); stimulate ankle and knee.
Measure F-wave latency.
4. If no responses, evaluate:
a. Peroneal motor nerve (anterior tibialis); stimulate below fibular head and knee.
b. Ulnar motor nerve (hypothenar); stimulate wrist and below elbow. Measure F-wave latency.
c. Median motor nerve (thenar); stimulate wrist and elbow. Measure F-wave latency.
5. Evaluate sural nerve (ankle); stimulate calf.
6. Evaluate median sensory nerve (index finger); stimulate wrist and elbow. If response is absent
or focal entrapment is suspected, record from wrist and stimulate midpalm; evaluate ulnar
sensory nerve (fifth digit); stimulate wrist.
7. If distal CMAP amplitude is substantially larger than proximal CMAP amplitude (15%),
evaluate for abnormal temporal dispersion or partial conduction block.
a. Measure CMAP duration (distal and proximal stimulation) to identify abnormal
dispersion.
b. Evaluate CMAP amplitude and duration over short segments (few mm) to identify partial
conduction block.
c. If capability exists, measure CMAP negative phase area (distal and proximal stimulation).
8. Evaluate additional nerves if findings are equivocal. Definite abnormalities should result in:
a. Evaluation of contralateral extremity
b. Evaluation of specific suspected abnormality (e.g., mononeuropathy or radiculopathy)

Needle Examination

1. Examine anterior tibialis, medial gastrocnemius, abductor hallucis, vastus lateralis, biceps
brachii, first dorsal interosseous (hand), and lumbar paraspinal muscles.
2. Confirm any abnormality by examination of at least one contralateral muscle, looking for
symmetry.
*Muscles in parentheses indicate recording site for conduction studies.
†
All F wave latency measurements are for distal stimulation sites. Record as absent if no response after 10–15 stimulations.
(Modified from Albers JW, Donofrio PD, McGonagle TK. Sequential electrodiagnostic abnormalities in acute inflamma-
tory demyelinating polyradiculoneuropathy. Muscle Nerve 1985;8:528–539, with permission.)

75% of the axons, the CMAP amplitude is markedly
diminished, but conduction velocity is reduced only
to the extent that is associated with the loss of the
largest myelinated axons. There is no evidence of
abnormal temporal dispersion.
Although primary demyelination is char-
acterized by conduction slowing, overemphasis
on mild or focal slowing is a common error in
establishing the presence of demyelination (3).
Important differences exist between hereditary and
acquired demyelination. Hereditary disorders of
peripheral myelin (e.g., hereditary motor sensory
neuropathy type I) have uniform involvement of all
myelinated fibers. Conduction along individual
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306 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
Figure 11-4 ● Peripheral motor nerve con-
duction model demonstrating the resultant
compound muscle action potential (CMAP)
produced by each of eight individual muscle
fiber action potentials and their summation.
Individual axons differ in diameter and therefore con-
duct at different rates. Arrows represent stimulation
sites. Top: CMAP (shown in screen) following distal
stimulation. Bottom: CMAP following proximal
stimulation. (Reprinted from Albers JW. Inflamma-
tory demyelinating polyradiculoneuropathy. In:
Brown WF, Bolton CF, eds. Clinical electromyography.
Boston: Butterworth, 1987:209–244, with permission.)
fibers may be greatly reduced, but slowing is uni-
form; abnormal temporal dispersion is present only
if conduction velocities are markedly slowed and
there is substantial phase cancellation. Conduction
Figure 11-5 ● Model of axonal degener-
ation in motor nerve conduction model de-
scribed in Figure 11-4, demonstrating
CMAPs after random loss of 75% of axons.
Arrows represent stimulation sites. CMAPs follow-
ing distal (upper screen) and proximal (lower screen)
stimulation. (Reprinted from Albers JW. Inflamma-
tory demyelinating polyradiculoneuropathy. In:
Brown WF, Bolton CF, eds. Clinical electromyogra-
phy. Boston: Butterworth, 1987:209–244, with per-
mission.)
slowing is disproportionate to the relatively pre-
served response amplitudes following distal and
proximal stimulation (27). Evidence of conduction
block is not a typical feature of hereditary demyeli-
nation unless conduction velocities are very slow
and produce substantial phase cancellation.
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY 307

Acquired demyelination is characterized by trailing portion of the CMAP, representing the

multifocal, nonuniform abnormalities. The dis-
proportionate involvement of some myelinated
fibers compared to others produces increased
CMAP duration and a characteristic temporal
dispersion of the CMAP (Fig. 11-6) (28). Partial
conduction block results from transmission failure
along the axon. Because the likelihood of conduc-
tion block in any given fiber is length-dependent,
there is abnormal dispersion of the response and
evidence of partial conduction block when the
results of proximal stimulation are compared to
those from distal stimulation. This is demon-
strated in the model in Figure 11-7 after random,
multifocal demyelination, in which propagation is
slowed across a single demyelinated internode and
blocked if two adjacent internodes are demyeli-
nated (shown by the absence of the myelin sheath).
Proximal stimulation produces a CMAP of slightly
reduced amplitude and increased duration because
of increased dispersion. The area beneath the neg-
ative phase of the CMAP is only slightly reduced.
Proximal stimulation produces a low-amplitude,
highly dispersed CMAP because of the variable
amounts of demyelination in some fibers com-
pared to others, producing an increased range of
axonal conduction velocities. The initial compo-
nent of the CMAP is greatly separated from the
fastest- and slowest-conducting axons respectively.
Phase cancellation of the dispersed responses pro-
duces an additional reduction in the proximal
CMAP amplitude. Conduction block in two of the
axons further reduces the CMAP amplitude to a
greater extent than could be explained by abnor-
mal temporal dispersion alone.
Numerous criteria exist to identify acquired
demyelination (Table 11-4), but all of the criteria
have limitations (28–32). In some criteria, con-
duction velocity and distal latency thresholds are
amplitude dependent. In general, conduction
velocities that are less than 70% of the lower limit
of the normal range cannot be attributed to axonal
loss alone (28). The criteria are not intended to
provide strict cutoffs and a “yes-or-no” response.
Rather, the results should be used to raise or reduce
suspicion for a disorder associated with substantial
conduction slowing. The presence of fibrillation
potentials and neurogenic MUAP findings does
not exclude the diagnosis of demyelinating neu-
ropathy because most hereditary and acquired
demyelinating neuropathies have some superim-
posed axonal degeneration.
The remaining goals of the electrodiagnostic
examination are to characterize the neuropathy’s
distribution, severity, rate of progression, and

Figure 11-6 ● Compound muscle action potentials recorded from hypothenar muscles
following ulnar nerve stimulation at distal and proximal sites. Responses are from a patient
with an acquired demyelinating neuropathy and demonstrate abnormal temporal dispersion with partial
conduction block, increased duration, and decreased conduction velocity. (Reprinted from Albers JW, Kelly
JJ Jr. Acquired inflammatory demyelinating polyneuropathies: clinical and electrodiagnostic features. Mus-
cle Nerve 1989;12:435–451, with permission.)
90749_ch11(297-333).ps 8/11/06 11:12 AM Page 308
308 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
Figure 11-7 ● Model of focal demyelina-
tion in motor nerve conduction model de-
scribed in Figure 11-4. Arrows represent stimula-
tion sites. CMAPs following distal (upper screen) and
proximal (lower screen) stimulation. The reduced am-
plitude with proximal stimulation reflects increased
temporal dispersion and conduction block in some ax-
ons where the individual responses are absent.
(Reprinted from Albers JW. Inflammatory demyeli-
nating polyradiculoneuropathy. In: Brown WF,
Bolton CF, eds. Clinical electromyography. Boston: But-
terworth, 1987:209–244, with permission.)
prognosis. The distribution of neuropathy is usu-
ally defined clinically, not electrodiagnosti-
cally, except for the needle EMG examination of
paraspinal muscles in polyradiculopathy or the
intrinsic foot muscles in mild axonal neuropathy.
Neuropathic severity is best related to CMAP and
SNAP amplitudes, because they are proportional
to the extent of abnormality, particularly in axonal
disorders. The needle EMG examination is useful
in documenting very mild axonal neuropathies,
as noted above. Defining severity in demyelinating
neuropathy is difficult because conduction slowing
is not usually associated with functional impair-
ment. Conduction block results in weakness, but
conduction block may be difficult to distinguish
from abnormal temporal dispersion. Serial electro-
physiologic studies are used to estimate the rate of
progression, although a mixture of large- and
small-amplitude fibrillation potentials can suggest
active and chronic denervation.
Electrodiagnostic Classification of
Neuropathy
Neuropathy is classified by a variety of means,
including clinical, biochemical, pathologic, electro-
diagnostic, or a combination thereof. The electrodi-
agnostic results provide information additional
to that obtained from the clinical evaluation and are
used to assign patients with suspected neuropathy
to general categories, thereby directing the subse-
quent clinical and laboratory evaluations. The
classification that follows separates these disorders
into broad categories based on electrodiagnostic
evidence of sensory or motor involvement com-
bined with conduction slowing suggesting the
presence of uniform or multifocal demyelination
versus pure axonal loss lesions (2). This classification
scheme is not inclusive and there is substantial
overlap between categories. This overlap will be
manifest by several forms of neuropathy appearing
in more than one of the tables that follow. There also
is some subjective component to the categorization
scheme, requiring that the electromyographer use
substantial clinical common sense. Nevertheless,
when combined with the clinical history and
examination, the electrodiagnostic results may
suggest a specific diagnosis or direct the subsequent
evaluation. Selected examples are provided in
each category; a more extensive discussion exists
elsewhere (2).
One issue not addressed in this classification
scheme is symmetry. Most forms of peripheral
neuropathy are relatively symmetric. There are
exceptions, however, as noted earlier. The most
common exceptions involve the different forms of
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY 309

T A B L E 1 1 - 4 Electrodiagnostic Criteria Suggestive of Chronic Acquired

Demyelination

Evaluation should satisfy at least three of the following in motor nerves (with exceptions noted
below):
1. Conduction velocity 75% of the lower limit of normal (2 or more nerves)*
2. Distal latency exceeding 130% of upper limit of normal (2 or more nerves)†
3. Evidence of unequivocal temporal dispersion (an increase in negative component duration
exceeding 15% for proximal vs. distal stimulation) or a proximal-to-distal amplitude ratio
0.7 (one or more nerves)†‡
4. F wave latency exceeding 125% of upper limit of normal (one or more nerves)*†
*Excluding isolated ulnar or peroneal nerve abnormalities at the elbow or knee, respectively
†
Excluding isolated median nerve abnormalities at the wrists
‡
Excluding the presence of anomalous innervation (e.g., median-to-ulnar nerve crossover)
(Modified from Albers JW, Kelly JJ Jr. Acquired inflammatory demyelinating polyneuropathies; clinical and electrodiag-
nostic features. Muscle Nerve 1989;12:435–451, with permission.)

vasculitis producing multifocal abnormalities little change in the configuration (amplitude,

that can become confluent. Other examples of
asymmetric diseases include multifocal motor
neuropathy, hereditary neuropathy with liability
to pressure palsy (HNLPP), and the neuropathies
associated with dapsone, porphyria, leprosy, sar-
coidosis, eosinophilia syndromes, and sensory
ganglionopathies.
Motor Greater Than Sensory Neuropathy,
Uniform Conduction Slowing (Table 11-5)
CASE 1
A 23-year-old man presents with a several-year
history of progressive ankle weakness and clum-
siness. Examination reveals that he has distal
weakness of his upper and lower extremities with
footdrop, hammertoe deformities, high arches,
mild sensory loss to vibration and touch, areflexia,
and large firm nerves. Nerve conduction and
needle EMG results, shown in Table 11-6, are
characterized by reduced CMAP and SNAP
amplitudes, prolonged distal and F wave latencies,
and substantially reduced conduction velocities
(well below 50% of the lower limit of normal).
Initial findings of prolonged distal latency that
could have been explained by distal entrapment
were excluded by demonstrating similar abnor-
malities in all the nerves examined. There was
duration, or shape) of the CMAP with distal
and proximal stimulation (i.e., there was no evi-
dence of abnormal temporal dispersion or partial
conduction block). Chronic neurogenic changes
were recorded on needle EMG examination of
distal extremity muscles. The findings provide
electrodiagnostic evidence of a moderately severe
sensorimotor neuropathy of the demyelinating
type, with mild superimposed axonal degenera-
tion. The markedly reduced conduction velocity
without evidence of abnormal temporal dispersion
or partial conduction block is most consistent with
a hereditary neuropathy.
The classic example of a neuropathy char-
acterized by a uniform peripheral myelinopathy
is hereditary motor sensory neuropathy type I
(HMSN I), which is the demyelinating form
of Charcot-Marie-Tooth disease. HMSN I is a
dominantly inherited hypertrophic neuropathy
that presents with the insidious onset of distal
weakness and sensory loss in young adult life. The
diagnosis is clinically suggested by findings of en-
larged nerves, distal weakness with hammertoes
and pes cavus, abnormal vibratory sensation, and
hyporeflexia (33).
The characteristic electrodiagnostic finding
associated with HMSN I is markedly reduced
conduction velocity in all tested nerves, often as low
as 25 m/s or less (33,34). Conduction velocities
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310 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

T A B L E 1 1 - 5 Motor Greater Than Sensory Neuropathy, Uniform Conduction

Slowing

Adrenomyeloneuropathy
Amiodarone
Charcot-Marie-Tooth disease (hereditary motor sensory neuropathy type I)
Congenital hypomyelinating neuropathy
Cytosine arabinoside (ara-C)
Dejerine-Sottas disease (hereditary motor sensory neuropathy type III)
Doxorubicin
Hexacarbons
Metachromatic leukodystrophy
Methyl n-butyl ketone
n-hexane
Perhexiline maleate
Sodium channel blockers (e.g., tetrodotoxin)
Suramin
Tacrolimus
(Modified from Donofrio PD, Albers JW. Polyneuropathy: classification by nerve conduction studies and electromyogra-
phy. Muscle Nerve 1990;13:889–903, with permission.)

typically are below 70% of the lower limit of
normal and therefore cannot be explained by ax-
onal loss alone. Abnormal temporal dispersion and
partial conduction block usually are not present
because of the uniform involvement of the myelin
of all axons. Nevertheless, when conduction ve-
locities are extremely slow, phase cancellation may
result in findings suggestive of abnormal temporal
dispersion (27) (see also Chapter 3). F waves
are present unless the CMAP amplitude is very
reduced, and latencies are prolonged proportional
to conduction velocity slowing. Sensory nerves
demonstrate similar conduction abnormalities,
but low-amplitude responses often preclude con-
duction velocity measurement. Most patients show
at least some degree of axonal loss, and it sometimes
is severe. Needle EMG demonstrates decreased
MUAP recruitment proportional to weakness,
fibrillation potentials and positive waves, and
increased MUAP amplitude and duration reflect-
ing chronic reinnervation. Abnormalities are most
prominent distally. The patient presented was
found to have an asymptomatic sibling with mild
ankle weakness, absent ankle reflexes, equivocal
sensory loss, and definite slowing of motor conduc-
tion velocities.
Disorders other than HMSN I, many of which
also are familial, present with similar electrodiag-
nostic findings (35). Most neuropathies resembling
HMSN I, such as congenital hypomyelinating neu-
ropathy, Dejerine-Sottas disease, and metachro-
matic leukodystrophy, are associated with disorders
of peripheral myelin. Several disorders are not asso-
ciated with primary myelin abnormalities but re-
flect selective loss of large myelinated fiber with
preservation of smaller myelinated axons. One ex-
ample is the neuropathy attributed to amiodarone
(36,37). Amiodarone is associated with a slowly pro-
gressive motor neuropathy with prominent con-
duction slowing, often in the range of 20 to 30 m/s.
Abnormal temporal dispersion and partial conduc-
tion block are not features of this neuropathy, and
slowing reflects preferential loss of the largest
myelinated fibers. Other medications, including the
immunosuppressant tacrolimus (FK506) (38) and
the antineoplastic suramin (39), produce a motor
neuropathy associated with conduction slowing.
The slowing of conduction velocity associated with
FK506 may be sufficient to resemble an acquired
demyelinating neuropathy (40,41). Animal mod-
els of suramin-induced neuropathy suggest the
presence of a length-, dose-, and time-dependent
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY 311

TABLE 11-6 CASE 1

Nerve Conduction Studies

Nerve Conduction Distal F wave
Stimulate (record) Amplitude (V) Velocity (m/s) Latency (ms) Latency (ms)

Motor
R median (thenar)
Wrist 4,000 7.0 44.5
Elbow 3,800 18
R ulnar (hypothenar)
Wrist 6,000 6.1 NR
Elbow 5,700 21
R peroneal
Ankle 400 7.8
Knee 400 17 NR
R tibial
Ankle NR
Sensory
R median (index) 12 23 5.8
R ulnar (fifth) 5 5.2
R sural (ankle) NR

Electromyography

Motor Unit Potential

Muscle Insertional Fibrillation Fasciculation
Activity Potentials Potentials Recruitment Amplitude/Duration
(Fib) (FACS)
R first dorsal
interosseous
(FDI) (hand) Normal 0 0 Reduced Mild increase
R anterior
tibialis Increased
0 Reduced Mild increase
R abductor
hallucis Increased

0 Reduced Moderate increase
L abductor
hallucis Increased

0 Reduced Moderate increase
R vastus
medialis Normal 0 0 Normal Normal
NR, no response. Sensory distal latencies are measured at the peak, and all amplitudes are measured baseline to peak.

sensorimotor neuropathy of the axonal type (42).
However, 15% of patients enrolled in a phase I study
of suramin developed a neuropathy with clinical
and electrophysiologic features suggestive of a
Guillain-Barré syndrome (GBS) (43).
Several hexacarbons are implicated in neu-
ropathy after occupational or recreational expo-
sures (44–47). N-hexane and methyl n-butyl ketone
are metabolized to 2,5-hexanedione, the likely neu-
rotoxic agent. The neuropathy is characterized by
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312 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

progressive distal sensory loss, reduced or absent re-
flexes, and eventual weakness and atrophy. Indi-
viduals who voluntary inhale n-hexane (“huffing”)
sometimes develop a motor loss greater than sen-
sory neuropathy (47). Motor and sensory ampli-
tudes are reduced and conduction is slowed to an
extent suggestive of primary demyelination. How-
ever, conduction slowing is attributed to secondary
myelin damage associated with axonal lesions, and
these neuropathies are characterized by giant ax-
onal swellings filled with neurofilaments (48,49).
Positive waves and fibrillation potentials are
recorded on needle EMG, and motor units are
reduced in number but are of increased amplitude.
The distinction between uniform and multifocal
conduction slowing vis-à-vis abnormal temporal
dispersion and conduction block often is impre-
cise. At times, the neuropathy associated with
n-hexane intoxication may be indistinguishable
from GBS, explaining why this neurotoxicant
appears in more than one of the neuropathy classi-
fication categories.
Neurotoxicants that block sodium channels
include tetrodotoxin derived from the puffer fish
and saxitoxin derived from contaminated shell-
fish (“red tide”) (50). Sodium channel blockade
decreases the local ionic currents associated with
action potential propagation, thereby slowing
conduction velocity. This effect on conduction
velocity is similar to that seen with reduced tem-
perature, which also affects Na
channels. Motor
amplitudes are reduced, but there is no abnormal
temporal dispersion or partial conduction block.
Additional examples of neuropathies that demon-
strate evidence of uniform conduction slowing are
listed in Table 11-5.
Motor Greater Than Sensory Neuropathy,
Multifocal Conduction Slowing
(Table 11-7)
CASE 2
A 42-year-old woman has a 3-year history of pro-
gressive weakness, gait unsteadiness, and painful
dysesthesias in all extremities. On examination,
she has increased skin pigmentation, generalized
distal atrophy and weakness, diminished sensation

T A B L E 1 1 - 7 Motor Greater Than Sensory Neuropathy, Multifocal Conduction

Slowing

Arsenic acute intoxication

Guillain-Barré syndrome
Chronic inflammatory demyelinating polyneuropathy (CIDP)
Chronic disimmune polyneuropathy
Cryoglobulinemia
Castleman’s disease
HIV infection
Lymphoma
Monoclonal gammopathy of undetermined significance (MGUS)
Multiple myeloma
Osteosclerotic myeloma
Systemic lupus erythematosus
Waldenström’s macroglobulinemia
Hereditary neuropathy with liability to pressure palsies (HNLPP)
Multifocal motor neuropathy (MMN) with conduction block
n-hexane
Variants of CIDP (Lewis Sumner syndrome)
(Modified from Donofrio PD, Albers JW. Polyneuropathy: classification by nerve conduction studies and electromyogra-
phy. Muscle Nerve 1990;13:889–903, with permission.)
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY 313

to all modalities except deep pain, and areflexia.
The results of nerve conduction and needle EMG
studies are shown in Table 11-8. An initial median
motor conduction study demonstrated marked
slowing of conduction velocity (approximately
55% of the lower limit of normal), as well as a
prominent change in the CMAP configuration
with proximal compared to distal configuration.
These abnormalities were confirmed in the ulnar
nerve, but lower extremity motor responses were
unobtainable. A representative motor conduction
study, shown in Figure 11-6, demonstrates the
abnormal temporal dispersion and partial con-
duction block that followed stimulation at a distal
and more proximal site. A sural response was
unobtainable, but upper extremity sensory re-
sponses demonstrated low amplitudes, reduced
conduction velocities, and prolonged distal laten-
cies. Needle EMG demonstrated evidence of
chronic partial denervation and reinnervation,
most prominent in the distal lower extremities.
Paraspinal muscles were spared. The combined
studies were interpreted as providing evidence of
an acquired sensorimotor neuropathy of the

TABLE 11-8 CASE 2

Nerve Conduction Studies

Latencies (ms)
Nerve Conduction
Stimulate (record) Amplitude (V) Velocity (m/s) Distal F wave

Motor
R median (thenar)
Wrist 4,000 6.5 42.3
Elbow 1,200 25
R ulnar (hypothenar)
Wrist 3,000 5.6 44.5
Below elbow 1,500 26
R peroneal
Ankle NR
R tibial
Ankle NR
Sensory
R median (index) 8 5.5
R ulnar (fifth) 10 34 5.4
R sural (ankle) NR

Electromyography

Motor Unit Action Potential

Insertional
Muscle Activity Fib Fasc Recruitment Amplitude/Duration

R first dorsal
interosseous (hand) Increased + 0 Reduced Mild increase
R biceps brachii Normal 0 0 Normal Normal
R anterior tibialis Increased ++ 0 Reduced Moderate increase
R abductor hallucis Increased +++ 0 Reduced Severe increase
L abductor hallucis Increased +++ 0 Reduced Severe increase
R vastus medialis Increased + 0 Reduced Mild increase
R gluteus medius Normal 0 0 Normal Normal
R paraspinal (lumbar) Normal 0 0 Normal Normal
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314 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

demyelinating type with superimposed axonal

degeneration.
The presence of abnormal temporal disper-
sion and partial conduction block demonstrated by
this patient is typical of multifocal involvement
and characteristic of an acquired demyelinating
neuropathy such as seen in chronic inflammatory
demyelinating polyneuropathy (CIDP). The ac-
quired inflammatory demyelinating neuropathies
are the prototype disorders associated with multifo-
cal conduction slowing. They are immune diseases
of peripheral nerves and nerve roots. Included are
acute (acute inflammatory demyelinating polyneu-
ropathy or GBS) and chronic (CIDP) forms. CIDP
is thought to be the most common treatable
neuropathy, aside from diabetic neuropathy, evalu-
ated in most neuromuscular clinics. Identification
of CIDP in patients with suspected neuropathy is
important, not only because it is treatable but
also because a subgroup of these patients have an
underlying systemic illness, including plasma cell
dyscrasias, Waldenström’s macroglobulinemia,
gamma heavy-chain disease, cryoglobulinemia,
lymphoma, systemic lupus erythematosus, Castle-
man’s disease, occult malignancy, and human
immunodeficiency virus infection (28). Most ac-
quired demyelinating neuropathies are character-
ized by progressive weakness, areflexia, diminished
sensation, dysautonomia, and elevated levels of
cerebrospinal fluid (CSF) protein (51–53).
The most prominent electrodiagnostic feature
suggestive of an acquired demyelinating neuropathy
is abnormal temporal dispersion or partial
conduction block. Decreases in the ratio of the
CMAP amplitude or the area beneath the negative
potential following proximal and distal stimulation
of up to 50% may result from dispersion and result-
ant phase cancellation (28). Reductions exceeding
50% likely require at least some degree of conduction
block. Changes in the CMAP duration reflect abnor-
mal temporal dispersion, and increases exceeding
15% over short segments and 20% over longer seg-
ments indicate abnormality (29,54). The site of partial
conduction block can sometimes be demonstrated
by making small incremental changes in the stimula-
tion site and observing the resultant CMAP (Fig. 11-
8). Although it is sometimes difficult to distinguish
abnormal temporal dispersion from partial conduc-
tion block, the distinction is clinically unnecessary be-
cause both suggest the presence of acquired demyeli-
Figure 11-8 ● Compound muscle action
potentials (CMAPs) recorded from thenar
muscles following percutaneous stimulation
of median nerve at multiple sites from pa-
tient with an acquired inflammatory de-
myelinating polyneuropathy. The distance
from stimulation to recording site (in mm) is indi-
cated at the left of individual tracings. Although there
is evidence of abnormal temporal dispersion over
long stimulation distances, small incremental
increases in the stimulation distance confirm partial
conduction block with an abrupt decrease in CMAP
amplitude (and area) associated with a small in-
crease in CMAP duration (10%). (Reprinted from
Albers JW. Clinical neurophysiology of generalized
polyneuropathy. J Clin Neurophysiol 1992;10:149–166,
with permission.)
nation. Reduced conduction velocity and prolonged
distal latency also reflect demyelination; however, ab-
normalities must be interpreted in relation to other
information, including response amplitude and dis-
ease duration, and the electromyographer should not
give undue significance to mild conduction slowing.
Whenever possible, the electrodiagnostic evaluation
should include nerves with reasonably preserved
CMAP amplitudes. Absent F responses are a non-
specific finding in isolation; reliance on such findings
is inappropriate (55).
The combination of an abnormal median
sensory response with a normal sural response is a
relatively common finding in acquired demyeli-
nating neuropathy (56). The discrepancy between
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY 315

sural and median sensory responses may be due to
the sural recording site being farther from its
extreme end, because the location of greatest ini-
tial abnormality may involve the most distal,
thinly myelinated fibers. This hypothesis could be
examined by comparing the radial sensory and
sural responses, using comparable recording tech-
niques (57). An abnormal median sensory with
normal sural response occurs more commonly
with GBS (39%) than with CIDP (28%) (28,56).
The needle EMG examination is of second-
ary importance in the evaluation of demyelinating
neuropathy. Most patients develop at least some
evidence of axonal degeneration, and the pres-
ence of fibrillation potentials and positive waves
does not exclude the diagnosis of a demyelinating
neuropathy. The needle EMG examination is use-
ful in estimating the extent, distribution, and
duration of axonal degeneration but is a relatively
insensitive measure of severity (58).
The patient described above was believed to
have an acquired demyelinating neuropathy. The
resultant clinical evaluation disclosed an abnor-
mal skeletal survey (Fig. 11-9) and biopsy evidence
of osteosclerotic myeloma. Her systemic disease
responded dramatically to melphalan and pred-
nisone treatment. Serial electrodiagnostic studies
documented resolution of her neuropathy over
approximately 2 years (59).
Table 11-7 lists several other disorders associ-
ated with a neuropathy characterized by multifocal
or nonuniform conduction slowing. Acute arsenical
neuropathy is interesting for several reasons. Acute
arsenical neuropathy presents as part of a systemic
illness characterized by nausea, vomiting, diarrhea,
dermatitis, cardiomyopathy, pancytopenia with
basophilic stippling, and abnormal liver function
tests. The neurologic deficit progresses over weeks
and may suggest a diagnosis of GBS (60). Because
Mees’ lines (Fig. 11-10) do not appear on the nails

Figure 11-9 ● Multiple scattered sclerotic bone lesions within the right humerus and clav-
icle of case 2. (Reprinted from Donofrio PD, Albers JW, Greenberg SH, et al. Peripheral neuropathy in os-
teosclerotic myeloma: clinical and electrodiagnostic improvement with chemotherapy. Muscle Nerve
1984;7:137–141, with permission.)
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316 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

Figure 11-10 ● Mees’ lines in a patient with documented arsenical neuropathy. Photo-
graph taken approximately 1 month after the most recent acute exposure to arsenic. Note the multiple sets of
Mees’ lines, documenting multiple prior exposures.

until approximately 1 month after exposure to ar-
senic (or any other protoplasmic toxicant), they are
not helpful during the initial phase of the evaluation
if the patient had a single arsenic exposure. As with
GBS, CSF protein levels become elevated several
weeks after onset of arsenical neuropathy, whereas
basophilic stippling, which appears much earlier,
suggests a toxic etiology. Initial EMG studies show
reduced conduction velocity, abnormal temporal
dispersion, partial conduction block, and low-am-
plitude or absent sensory responses. Serial studies
demonstrate a dying-back neuropathy with pro-
gressive axonal degeneration, and initial findings
are probably related to generalized axonal failure.
Several additional disorders in this category are
considered by some to represent variants of CIDP
(e.g., Lewis Sumner syndrome) (61). Multifocal
motor neuropathy is characterized by asymmet-
ric distal weakness associated with partial motor
conduction block, a characteristic of multifocal
demyelination (62,63). On occasion, HNLPP be-
comes confluent, producing findings suggestive of a
diffuse neuropathy (64).
Motor or Motor Greater Than Sensory
Neuropathy, Axonal Loss (Table 11-9)
CASE 3
A 50-year-old man with dermatitis herpetiformis
presented with a 6-month history of painless, pro-
gressive hand weakness and atrophy. Previous elec-
trodiagnostic examinations resulted in a diagnosis
of multiple entrapment neuropathies. His clinical
examination showed profound distal upper limb
weakness and atrophy (Fig. 11-11) and bilateral
weakness of ankle dorsiflexion and intrinsic foot
muscles. Sensation was normal. Reflexes were
hypoactive. Results of nerve conduction and needle
EMG studies are shown in Table 11-10. They
demonstrate relatively symmetric but scattered
reduction of CMAP amplitudes, with some pro-
longed motor distal latencies, minimally reduced
motor conduction velocities, and no sensory abnor-
malities. The needle EMG examination demon-
strates chronic neurogenic changes consisting of
small-amplitude fibrillation potentials, decreased
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY
TABLE 11-9 Motor or Motor Greater
Than Sensory Neuropathy,
Axonal Loss
Charcot-Marie-Tooth disease
(hereditary motor sensory neuropathy
type II)
Dapsone
Disulfiram
Guillain-Barré syndrome (axonal form)
Hyperinsulinism
Multifocal motor neuropathy (axonal
form)
Nitrofurantoin
Organophosphates
Porphyria
Paraneoplastic (lymphoma or carcinoma)
Vinca alkaloids
West Nile virus (neuronopathy)
(Modified from Donofrio PD, Albers JW. Polyneu-
ropathy: classification by nerve conduction studies and
electromyography. Muscle Nerve 1990;13:889–903,
with permission.)
recruitment, and MUAPs of increased amplitude
and duration. The findings were interpreted as
representing a chronic motor neuropathy, although
the findings also are indistinguishable from those
associated with multifocal motor neuron disease.
Motor greater than sensory neuropathies are
relatively uncommon, and identification suggests a
relatively small differential diagnosis. Most neu-
ropathies in the differential have metabolic or toxic
etiologies, often involving medications. The pro-
totype disorder of an axonal motor greater than
sensory neuropathy is hereditary motor sensory
neuropathy type II (HMSN II), the axonal form of
Charcot-Marie-Tooth disease (33). HMSN II is an
autosomal dominant neuropathy characterized by
slowly progressive weakness and sensory loss, usu-
ally beginning in the third or fourth decade of life.
Distal atrophy may be severe, producing an in-
verted-Champagne-bottle appearance to the legs.
Other signs include pes cavus, hammertoe defor-
mities, hyporeflexia, and mild sensory loss. CMAP
317
amplitudes are reduced with normal or minimally
slowed conduction velocities. SNAPs are absent
in about 50% of patients; when SNAPs are pres-
ent, differentiation from a familial progressive
muscular atrophy is difficult. The needle EMG
examination as described by Dyck and Lambert
demonstrates nonspecific neurogenic changes
with a distal predilection (33).
This patient had a negative family history. His
medications, however, included dapsone, a medica-
tion he had taken for over 16 years, with a cumula-
tive dose exceeding 650 g. Dapsone is associated
with a slowly reversible neuropathy that is prima-
rily motor and usually occurs after prolonged
periods (years) of daily use. The neuropathy may
be related to abnormal dapsone metabolism. Dap-
sone is metabolized by N-acetyl transferase, the
same enzyme that acetylates isoniazid, and suscep-
tible patients may be slow acetylators (65). Weak-
ness and wasting sometimes involve the arms
more than the legs, and mild sensory abnormalities
may be present. Electrodiagnostic evaluation is
characterized by low-amplitude CMAPs with
normal sensory studies (66,67). Any conduction
slowing presumably relates to the loss of the largest-
diameter motor axons. Needle EMG examination
demonstrates evidence of chronic denervation and
reinnervation. Dapsone is one of a few recognized
neurotoxicants that produces asymmetric abnor-
malities. The asymmetry and predilection of upper
extremity involvement mimics multiple entrap-
ment neuropathies in terms of distribution, al-
though normal sensory responses would be atypical
for a true mononeuropathy multiplex.
Dapsone was discontinued and initial evi-
dence of improvement was apparent within 4
months, with almost complete resolution over the
next 3 years.
The hepatic porphyrias include acute inter-
mittent porphyria, hereditary coproporphyria,
variegate porphyria, and ALA dehydratase defi-
ciency. They are characterized by the triad of ab-
dominal pain, psychosis, and neuropathy (68–70).
All are associated with variable extrahepatic
gastrointestinal and neuropsychiatric manifesta-
tions, including neuropathy, except for porphyria
cutanea tarda, which does not produce neurologic
manifestations. ALA dehydratase deficiency is
the least common of the hepatic porphyrias, and it
is the only porphyric neuropathy to present in
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318 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
Figure 11-11 ● Photograph of hand of case 3 prior to discontinuing dapsone, demon-
strating severe atrophy of the intrinsic hand muscles.
infancy. It also is the only autosomal recessive he-
patic porphyria (71). Acute hepatic porphyrias are
pharmacogenetic regulatory diseases that are
mainly induced by drugs, sex hormones, fasting, or
alcohol (72). Porphyric neuropathy resembles GBS
with quadriparesis, areflexia, dysautonomia, and
elevated CSF protein levels, but its distinguishing
features include an initial proximal predilection,
asymmetry, and electrophysiologic features of
either an axonal motor or motor greater than
sensory neuropathy, or a polyradiculoneuropathy
(73). Typical findings include reduced CMAP
amplitude, minimally reduced conduction veloc-
ity, profuse fibrillation potentials after the fourth
week, and decreased MUAP recruitment (74).
Some reports exist of patients with porphyric
neuropathy who fulfill the criteria for primary
demyelination, but these results may represent
secondary demyelination associated with axonal
death. Sensory responses occasionally are spared
(75). The early appearance of fibrillation potentials
in paraspinal muscles localizes the lesion to the root
or neuron.
Other axonal motor greater than sensory
neuropathies include the axonal form of GBS
(12,76), the remote-effect motor neuropathy asso-
ciated with lymphoma (77) or carcinoma (78), hy-
poglycemic neuropathy (79,80), and several toxic
neuropathies, including those associated with
disulfiram (81–83), organophosphates (84–87),
nitrofurantoin (88–91), and vinca alkaloids such as
vincristine (92,93). An axonal form of an immune-
mediated multifocal motor neuropathy, without
conduction block or other features of demyelina-
tion, has been proposed (94).
Hypoglycemic neuropathy is associated with
insulin excess and almost always occurs after
hypoglycemic coma (79,80). Like dapsone neu-
ropathy, hypoglycemic neuropathy sometimes in-
volves the upper more than the lower extremities,
and usually involves motor fibers. The etiology
and underlying pathophysiology are poorly under-
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY 319

TABLE 11-10 CASE 3

Nerve Conduction Studies

Latencies (ms)
Nerve Conduction
Stimulate (record) Amplitude (V) Velocity (m/s) Distal F wave

Motor
R median (thenar)
Wrist 400 4.7 NR
Elbow 400 50
L median (thenar)
Wrist 1,200 4.2 NR
R ulnar (hypothenar)
Wrist 5,000 3.1 30.5
Below elbow 4,500 55
R peroneal
Ankle 300 6.2 NR
Below knee 300 42
R tibial
Ankle 2,300 5.4
Sensory
R median (index) 25 64 3.2
R ulnar (fifth) 20 58 3.4
R sural (ankle) 12 44 3.8

Electromyography

Motor Unit Action Potential

Insertional
Muscle Activity Fib Fasc Recruitment Amplitude/Duration

R FDI (hand) Increased ++ 0 Reduced (3+) Moderate increase

L FDI (hand) Increased +++ 0 Reduced (3+) Moderate increase
R abd. pollicis brevis Increased ++++ 0 Reduced (4+) Severe increase
L abd. pollicis brevis Increased ++ 0 Reduced (2+) Moderate increase
R biceps brachii Normal 0 0 Normal Normal
R anterior tibialis Increased + 0 Reduced (1+) Slight increase
R FDI (pedis)s Increased ++++ 0 Reduced (4+) Severe increase
L FDI (pedis)s Increased ++++ 0 Reduced (4+) Severe increase
R vastus medialis Increased 0 0 Normal Normal
R paraspinal (lumbar) Normal 0 0 Normal Normal

stood, but aspects of this neuropathy are consistent
with isolated anterior horn cell involvement. West
Nile virus infection has been associated with an
acute motor neuropathy or neuronopathy charac-
terized by asymmetry, or even an isolated limb
weakness with minimal or no sensory involvement
(95). Disulfiram (Antabuse) is metabolized to ac-
etaldehyde when combined with alcohol, which
should be a deterrent to alcohol use. Disulfiram is
associated with a neuropathy characterized by pre-
dominant weakness, mild sensory involvement,
and areflexia (90). Weakness usually appears
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320 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

slowly, but occasionally onset is abrupt, mimicking result in the progression of neuropathy resembling
GBS (81). Neuropathy develops in approximately the acute toxic neuropathy (102).
0.2% of patients treated with nitrofurantoin (90).
Initial sensory involvement with paresthesias and
sometimes pain is common, although the most Sensory, Axonal Loss Neuropathy or
characteristic feature is rapid onset of severe weak- Neuronopathy (Table 11-11)
ness in elderly women with impaired renal func-
CASE 4
tion and presumably high blood nitrofurantoin
levels (88,89). A 43-year-old woman with ovarian cancer was
Organophosphates are used as pesticides and treated monthly with cisplatin chemotherapy.
nerve gases, producing slowly reversible inactiva- After the sixth and final treatment, she noted the
tion of acetylcholinesterase and leading to acetyl- subacute onset of progressive clumsiness and
choline accumulation in cholinergic neurons profound sensory loss. Examination confirmed the
(84,85,96,97). Muscarinic overactivity results in presence of large-fiber sensory loss (reduced vibra-
miosis, increased secretions, sweating, gastric tion and joint position sensations) and areflexia
hyperactivity, and bradycardia, whereas nicotinic without weakness. Results of nerve conduction and
overactivity results in fasciculations and weakness. needle EMG studies are shown in Table 11-12.
Following resolution of its acute effects, some All sensory amplitudes were unobtainable, but
organophosphates may produce a rapidly progres- motor conduction studies and the needle EMG
sive neuropathy that begins about 1 to 4 weeks after examination were normal, other than the irregular
exposure (85,86,98). Organophosphate-induced activation of MUAPs attributed to poor sensation
delayed neurotoxicity (OPIDN) has been associ-
ated with ingestion of triorthocresyl-phosphate
(TOCP) in adulterated Jamaican ginger extract,
sometimes referred to as Jake paralysis (99), and
contaminated cooking oil in Morocco (100,101).
T A B L E 1 1 - 1 1 Sensory Neuropathy,
OPIDN presents with dysesthesias and progressive
distal greater than proximal weakness. Reflexes are Axonal Loss
reduced at the ankles but may be normal or brisk
Cisplatin
elsewhere, and spasticity may become a late feature,
Congenital
reflecting upper motor neuron involvement. Dur-
ing acute organophosphate intoxication, repetitive CONOMAD
CMAPs occur after a single stimulus, presumably Ethanol
from recurrent postsynaptic depolarization by Friedreich’s ataxia
persistent acetylcholine. Other electrodiagnostic Hereditary sensory
findings are those of axonal degeneration of motor HIV infection
more than sensory fibers. Conduction velocities Idiopathic sensory ganglionitis
remain essentially normal, but evoked amplitudes Sjögren’s syndrome
are reduced and there is needle EMG evidence of Metronidazole
denervation characterized by fibrillation potentials Miller-Fisher variant of GBS
in distal muscles (85,86,98). Vincristine typically Nutritional (vitamin E deficiency)
produces an axonal sensorimotor neuropathy with
Paclitaxel
sensory greater than motor involvement, although
Paraneoplastic
there are reports of weakness rapidly progressing
to a functional quadriplegia associated with vin- Pyridoxine
cristine (92). In some patients, the arms initially Tabes dorsalis
may be involved more than the legs, and the Tacrolimus
disorder resembles a “pure motor” neuropathy or Taxanes
neronopathy. Treatment with standard doses of Thalidomide
neurotoxic antineoplastic medications in patients Thallium (small fiber)
with a pre-existing neuropathy of any cause may
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY 321

TABLE 11-12 CASE 4

Nerve Conduction Studies

Latencies (ms)
Nerve Conduction
Stimulate (record) Amplitude (V) Velocity (m/s) Distal F wave

Motor
R median (thenar) 8,000 63 3.4 26.8
R ulnar (hypothenar) 9,000 61 3.1 28.5
R peroneal 12,000 57 4.8 48.5
Sensory
R median (index) 6 44 4.1
R ulnar (fifth) NR
R radial NR
R sural (ankle) NR

Electromyography

Motor Unit Action Potential

Insertional
Muscle Activity Fib Fasc Recruitment Amplitude/Duration

R FDI (hand) Normal 0 0 Normal Normal

R biceps brachii Normal 0 0 Normal Normal
R anterior tibialis Normal 0 0 Normal Normal
R abductor hallucis Normal 0 0 Normal Normal

(manifest ataxia). Examination of a single sensory
nerve would be insufficient to document a gen-
eralized abnormality of sensory nerves in this
setting, because local entrapment or a variety of
technical factors could result in a false-positive
result. The evaluation of several sensory nerves
provided confirmation that a diffuse abnormality
of peripheral sensory function existed in this
patient. The combined abnormalities were inter-
preted as characteristic of a pure sensory neuropa-
thy or neuronopathy.
Sensory involvement is common in most
forms of neuropathy, but exclusive, severe sensory
involvement is unusual. Acquired axonal sen-
sory neuropathies or neuronopathies include those
associated with pyridoxine (103,104) and cisplatin
(105), as well as those associated with Sjögren’s
syndrome (106), paraneoplastic syndromes (e.g.,
oat cell carcinoma) (107), vitamin E deficiency
(108), tabes dorsalis, idiopathic sensory ganglioni-
tis, Friedreich’s ataxia (109), the Miller-Fisher
variant of GBS (104), and a disorder associated
with chronic ataxic neuropathy, ophthalmoplegia,
IgM paraprotein, cold agglutinins, and disialosyl
antibodies (CANOMAD) (110,111). All of these
conditions present subacutely with unpleasant
paresthesias, evidence of reduced vibration and
joint position sensations, areflexia, and minimally
decreased pain sensation. Pyridoxine (vitamin B6)
is occasionally taken in large amounts to treat a
variety of nonspecific conditions. Schaumburg et
al demonstrated that neurotoxicity is dose related,
owing either to long-term cumulative exposure
or the short-term administration of large doses
(104). With large doses, sensory loss may be
complete and irreversible, including involvement
of facial and mucous membrane areas (112). Cis-
platin is an antineoplastic agent associated with a
dose-dependent sensory neuronopathy (105), as
demonstrated in the case presentation. Cisplatin
sensory neuronopathy is clinically and electrodiag-
nostically indistinguishable from the paraneoplas-
tic sensory neuronopathy associated with small
cell lung carcinoma and antineuronal nuclear
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322 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
antibodies (113). Carcinomatous sensory neuropa-
thy is the most distinctive remote-effect neuropa-
thy (107). It presents with paresthesias and dyses-
thesias, and large-fiber sensory loss in association
with areflexia, gait ataxia, and choreoathetoid
movements. Electrodiagnostic findings include
markedly reduced or absent SNAPs with normal
motor studies. Sequential studies demonstrate a
progressive reduction of SNAP amplitude, with-
out motor conduction abnormality or any needle
EMG evidence of denervation. Paclitaxel is an-
other antineoplastic agent that produces a dose-de-
pendent sensory neuropathy (114,115). Friedre-
ich’s ataxia is characterized by a prominent sensory
neuropathy, but there typically are additional mo-
tor abnormalities consisting of slowing of conduc-
tion velocity related to loss of large myelinated
fibers. There also may be mild chronic neurogenic
changes on needle EMG, differentiating this from
the sensory neuropathies described above.
Thalidomide has been associated with a sen-
sory neuronopathy (116,117). Thalidomide was
initially introduced as a tranquilizer but was rarely
used after 1961 because of teratogenic effects.
Recently, thalidomide has been reintroduced for
the treatment of systemic lupus erythematosus
dermatitis and other conditions. Thalidomide may
produce a length-dependent, sensory more than
motor neuropathy that presents with painful
paresthesias and numbness (117). Although sural
nerve biopsy shows evidence of loss of myelinated
nerve fibers (117), small-fiber more than large-
fiber involvement is attributed to diminished pin
and temperature appreciation in association with
normal reflexes (116). SNAP amplitudes may be
reduced, however, even among asymptomatic
patients receiving thalidomide (116). Metronida-
zole (118), numerous other medications (2), and
ethanol are associated with predominant sensory
neuropathy.
Sensory Greater than Motor Neuropathy,
Axonal Loss (Table 11-13)
CASE 5
A 58-year-old man with a long history of ethanol
abuse complained of an insidious onset of painful
distal paresthesias, numb feet, and clumsiness.
On examination, he had evidence of midline
cerebellar gait ataxia and abnormal heel-to-knee
testing, with distal sensory loss to all modalities,
areflexia, and weakness. Results of nerve conduc-
tion and needle EMG studies are shown in Table
11-14, demonstrating reduced SNAP and CMAP
amplitudes with borderline-prolonged distal la-
tencies but without other evidence of conduction
slowing. An isolated sural abnormality could re-
flect technical factors, as discussed earlier, but the
absent contralateral sural response and the border-
line-low median and ulnar SNAP amplitudes con-
firmed a widespread abnormality of sensory
nerves. Chronic neurogenic changes are present on
needle EMG examination, predominantly involv-
ing the distal lower limbs. The combined findings
were interpreted to represent a nonspecific senso-
rimotor neuropathy of the axonal type. A diagno-
sis of ethanol-associated neuropathy was made,
based in part on the absence of other contributing
factors, the association of other ethanol-related
findings, including midline-cerebellar degenera-
tion (confirmed on cranial magnetic resonance
imaging [MRI]), and the systemic and laboratory
evidence of ethanol toxicity (including abnormal
liver function test results).
The majority of neuropathies of all causes
present with predominant sensory abnormalities
in association with mild but unequivocal motor
abnormalities. Sometimes the motor abnormali-
ties are apparent only on needle EMG examina-
tion. Examples described in the preceding section
that fit into this classification equally well include
neuropathies associated with the Miller-Fisher
variant of GBS, Friedreich’s ataxia, and the
neuropathies associated with rheumatoid arthri-
tis. The vasculitis neuropathies are included in
Table 11-13 under the heading of “connective tis-
sue diseases.” A review of the numerous forms of
vasculitis neuropathy, which include nonsystemic
vasculitis, is beyond the scope of this chapter but
can be found in the referenced materials
(119–122). However, the most distinguishing fea-
ture of most of these neuropathies is the presence
of asymmetry (123).
Most toxic-metabolic neuropathies are char-
acterized by distal axonal degeneration (dying
back) of sensory and motor axons (124). Unfor-
tunately, they are all physiologically similar, limit-
ing the usefulness of electrodiagnostic studies in
establishing etiology. Sensory symptoms and signs
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY 323

T A B L E 1 1 - 1 3 Sensory Greater Than Motor Neuropathy, Axonal Loss

Acromegaly Folate deficiency

Amyloidosis Post-gastrectomy
Critical illness neuropathy Thiamine deficiency
Connective tissue disease Pharmaceuticals
Rheumatoid arthritis Amitriptyline
Periarteritis nodosa Chloramphenicol
Churg-Strauss vasculitis Chloroquine
Degenerative disorders Colchicine
Friedreich’s ataxia Ethambutol
Olivopontocerebellar atrophy Isoniazid
Gout Nitrous oxide
Hypothyroidism Phenytoin
Leprosy Thallium
Lyme disease Statins
Metals Vincristine
Arsenic (chronic) Polycythemia vera
Gold Sarcoidosis
Lithium Toxic
Mercury Acrylamide
Multiple myeloma Carbon disulfide
Myotonic dystrophy Ethyl alcohol
Nutritional Ethylene oxide
B12 deficiency Hexacarbons
(Modified from Donofrio PD, Albers JW. Polyneuropathy: classification by nerve conduction studies and electromyogra-
phy. Muscle Nerve 1990;13:889–903, with permission.)

predominate with dysesthesias, paresthesias, distal
sensory loss, and loss of distal reflexes. Weakness
and atrophy of distal muscles develop subse-
quently. Sensory amplitudes are usually abnormal
early in the course of the disease; motor ampli-
tudes become abnormal later, occurring in the
distal lower limbs first. Conduction velocities
remain essentially normal. Fibrillation potentials
and positive waves appear distally.
Ethyl alcohol is generally identified as one of
the most common causes of neuropathy in the
United States. Neuropathy appears in association
with several neurologic findings related either to the
direct neurotoxic effects of alcohol or its metabo-
lites, nutritional disorders, genetic factors, or com-
binations thereof (125–127). The role of alcohol in
neuropathy is controversial because individuals
who consume large amounts of alcohol often are nu-
tritionally compromised, and clinically similar neu-
ropathies, particularly those involving sensory
nerves, occur with vitamin deficiency states, includ-
ing thiamine and other B vitamins (127). Some
evidence suggests that an alcohol neuropathy can
occur with normal nutrition. Paresthesias and
painful distal dysesthesias are common early symp-
toms. The neuropathy progresses slowly, beginning
with distal sensory loss. Distal weakness, unsteady
gait, and areflexia appear subsequently, often in as-
sociation with dysautonomia. The recognition of
critical illness neuropathy is attributed to the initial
observations of Bolton, who reported development
of neuropathy in association with sepsis and a sys-
temic inflammatory response (128). Distinguishing
involvement of nerve and muscle fibers in the form
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324 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

TABLE 11-14 CASE 5

Nerve Conduction Studies

Latencies (ms)
Nerve Conduction
Stimulate (record) Amplitude (V) Velocity (m/s) Distal F wave

Motor
R median (thenar)
Wrist 5,000 4.1 30.9
Elbow 4,500 55
R ulnar (hypothenar)
Wrist 7,000 3.3 30.1
Below elbow 6,500 57
R peroneal
Ankle 2,000 5.2 NR
Below knee 1,800 44
R tibial
Ankle 2,300 5.4
Sensory
R median (index) 12 54 3.7
R ulnar (fifth) 8 56 3.5
R sural (ankle) NR
L sural (ankle) NR

Electromyography

Motor Unit Action Potential

Insertional
Muscle Activity Fib Fasc Recruitment Amplitude/Duration

R FDI (hand) Increased ++ 0 Reduced (2+) Slight increase

R abd. pollicis brevis Increased ++ 0 Reduced (2+) Slight increase
R extensor digitorum Normal 0 0 Normal Normal
R biceps brachii Normal 0 0 Normal Normal
R anterior tibialis Increased + 0 Reduced (1+) Slight increase
R posterior tibialis Increased ++ 0 Reduced (1+) Slight increase
R FDI (pedis) Increased +++ 0 Reduced (4+) Severe increase
R vastus medialis Increased 0 0 Normal Normal
R paraspinal (lumbar) Normal 0 0 Normal Normal

of critical illness neuropathy or critical illness my-
opathy sometimes is difficult (129).
The electromyographer’s contribution to the
evaluation of axonal sensorimotor neuropathies is
in confirming the presence of neuropathy and
identifying other findings, such as Mees’ lines,
that may suggest a cause for the neuropathy.
Axonal sensorimotor neuropathies with features
suggesting a specific diagnosis include a painful
neuropathy with superimposed carpal tunnel
syndromes in amyloidosis (130), tremor and neu-
ropathy with ithium (131) or mercury intoxication
(132), preservation of reflexes with abnormal cor-
ticospinal tract signs with vitamin B12 deficiency
(133), and the coexistence of neuropathy and
myopathy associated with colchicine use (134).
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY
Familiarity with the associated disorders listed in
Table 11-13 may prove helpful in identifying po-
tential causes for neuropathy in the individual pa-
tient with a nonspecific sensory greater than motor
axonal neuropathy.
Sensory Greater Than Motor Neuropathy,
Conduction Slowing (Table 11-15)
CASE 6
A 32-year-old man with a 12-year history of in-
sulin-dependent diabetes mellitus reported the
gradual onset of very painful distal paresthesias,
numb feet, clumsiness, impotence, and orthosta-
tic lightheadedness. On examination, he had evi-
dence of sensory ataxia, distal sensory loss to all
modalities, absent reflexes, and mild distal weak-
ness. His feet do not appear to sweat, and he had
a 15 mm Hg orthostatic drop in his blood pressure
without an increase in his pulse rate. Nerve con-
duction and needle EMG studies, shown in Table
11-16, demonstrated reduced SNAP amplitudes
and moderate slowing of sensory and motor con-
duction velocities without clear evidence of ab-
normal temporal dispersion or partial conduction
block. F wave latencies were prolonged in upper
and lower extremities. Skin potential responses
were unobtainable. Isolated median abnormali-
ties could have been explained by a focal median
mononeuropathy at the wrist, with the mild con-
duction velocity slowing related to conduction
block of large myelinated fibers. However, simi-
lar findings of borderline-prolonged distal laten-
T A B L E 1 1 - 1 5 Sensory Greater Than
Motor Neuropathy,
Conduction Slowing
Diabetes mellitus
End-stage renal disease
(Modified from Donofrio PD, Albers JW. Polyneu-
ropathy: classification by nerve conduction studies and
electromyography. Muscle Nerve 1990;13:889–903,
with permission.)
325
cies and conduction velocities near the lower limit
of normal were present in all of the motor nerves
examined. The absent skin potential responses,
sometimes called sympathetic skin responses,
provide evidence of autonomic dysfunction but
do not localize the level of abnormality more
precisely. The needle EMG examination demon-
strated chronic neurogenic changes in the distal
lower limbs and fibrillation potentials scattered
throughout the paraspinal muscles. The com-
bined findings were interpreted as those of a
moderately severe sensorimotor neuropathy with
superimposed dysautonomia and polyradi-
culopathy. The conduction slowing was insuffi-
cient to fulfill the criteria for primary demyelina-
tion but was more characteristic of the loss of
large myelinated nerve fibers or of an axonal
membranopathy. The combined abnormalities
were characteristic of those frequently associated
with diabetes mellitus.
Diabetic neuropathy is the most common
cause of neuropathy in the United States. In early
symmetric diabetic neuropathy, sensory com-
plaints and signs predominate with extremity
dysesthesias, paresthesias, and sensory loss. When
present, weakness is most prominent in the distal
lower limbs. Early signs of diabetic neuropathy
include decreased vibration and pain sensations in
the distal lower extremities. Joint position sensa-
tion may be impaired in severe diabetic neuropa-
thy. Ankle reflexes are usually absent, and other
reflexes are hypoactive. Atrophy and weakness of
distal muscles develop, followed by more proxi-
mal involvement.
Most asymptomatic, neurologically intact di-
abetic patients demonstrate conduction slowing
with conduction velocities around the lower limit
of normal (135,136). F wave latencies are typically
prolonged, representing an early and sensitive
finding associated with mild diabetic neuropathy
or membranopathy. As the severity of the neu-
ropathy increases, sensory amplitudes disappear
in the lower extremities and motor amplitudes
become reduced in association with the further
reduction of conduction velocities (136). Abnor-
mal temporal dispersion and partial conduction
block are not prominent. Most patients with iso-
lated sensory abnormalities and all patients with
generalized sensorimotor diabetic neuropathy
have fibrillation potentials distally.
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326 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

TABLE 11-16 CASE 6

Nerve Conduction Studies

Latencies (ms)
Nerve Conduction
Stimulate (record) Amplitude (V) Velocity (m/s) Distal F wave

Motor
R median (thenar)
Wrist 5,000 4.2 33.9
Elbow 4,600 47
R peroneal
Ankle 1,500 6.1 NR
Below knee 1,400 39
R tibial
Ankle 3,300 5.8
40
Sensory
R median (index) 10 49 3.8
R ulnar (fifth) 5 50 3.7
R sural (ankle) NR
Motor Unit Potential
Insertional
Muscle Activity Fib Fasc Recruitment Amplitude/Duration

R FDI (hand) Increased + 0 Reduced Slight increase

R biceps brachii Normal 0 0 Normal Normal
R anterior tibialis Increased + 0 Reduced Slight increase
R median gastrocnemius Increased + 0 Reduced Slight increase
R vastus medialis Increased 0 0 Normal Normal
R FDI (pedis)s Increased ++ 0 Reduced Moderate increase
L FDI (pedis)s Increased ++ 0 Reduced Moderate increase
R paraspinal (lumbar) Increased ++ 0
R paraspinal (thoracic) Increased ++ 0

Electromyographers frequently identify the
presence of what proves to be diabetic neuropathy
among patients referred for evaluation but who
are not known to have diabetes. Consistent with
this observation, about 10% of patients with dia-
betes have evidence of neuropathy at the time of
their diagnosis (137). Similarly, among patients
diagnosed with “idiopathic” neuropathy, labora-
tory glucose evaluation shows that many will have
frank diabetes, whereas as many as 25% will show
impaired glucose tolerance (IGT) in response to a
75 g glucose load (138). The neuropathy associated
with IGT is generally milder than the neuropathy
associated with diabetes mellitus, and small fibers
may be predominantly affected, perhaps explain-
ing the high frequency of patients presenting with
painful sensory neuropathy and IGT (138,139).
The pathogenesis of diabetic neuropathy and
the resultant electrophysiologic abnormalities have
been attributed to a combination of direct axonal
injury due to hyperglycemia, axonal ischemia due
to microvascular injury, and possibly autoimmune
injury associated with development of antineu-
ronal antibodies in response to exposed antigen
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CHAPTER 11 • PATIENT WITH SUSPECTED PERIPHERAL NEUROPATHY
targets (17,140). The pathophysiology of reduced
conduction velocity in symmetric distal diabetic
neuropathy is complex and probably reflects
chronic demyelination with remyelination, axonal
stenosis, and a primary metabolic and ischemic
abnormality. Increased conduction velocity hours
after normalizing glucose levels suggests that
metabolic changes are related to the conduction
abnormalities (14,141). Hyperglycemia activates
aldose reductase, the enzyme that converts glucose
to sorbitol. This is one of several reactions that de-
plete neuronal NADPH, an obligatory cofactor in
oxidative metabolism, limiting the ability of the
nerve to scavenge free radicals and produce nitrous
oxide, thereby producing cellular damage, im-
paired vasodilatation, and nerve ischemia (17). In
addition, decreased nerve myo-inositol and in-
creased polyol pathway activity related to in-
creased conversion of glucose to sorbitol by aldose
reductase are associated with reduced Na
/K
-
ATPase activity, increased intracellular Na
, and
decreased conduction velocity, independent of
structural alteration (15). Axoglial disjunction and
the resultant diminished nodal Na
permeability
also contribute to reduced conduction velocity (16),
and intensive diabetes therapy delays the onset of
clinical neuropathy and the electrophysiologic
attributes of diabetic neuropathy in patients with
Type 1 diabetes mellitus (142).
Patients with renal failure independent of
diabetes mellitus develop a sensorimotor neuropa-
thy characterized by low-amplitude motor and
sensory responses, sometimes in association with
pronounced conduction slowing (143). This is
most apparent in patients with end-stage renal
disease (ESRD). The magnitude of slowing is
greater than that expected from the loss of large
myelinated fibers, and chronic demyelination,
remyelination, and membrane changes contribute
to the slowing (144). Although nerve conduction
studies are important in the diagnosis of ESRD
neuropathy, they are not required to evaluate
the effectiveness of dialysis. Determination of
adequate dialysis is complicated, and the primary
indicators of adequate treatment are clinical and
laboratory, not electrodiagnostic. Dialysis and
renal transplantation are generally effective in
improving ESRD neuropathy, but electrodiag-
nostic improvement is a late finding.
327
SUMMARY
Symptoms associated with peripheral neuropathy
are among the most common neurologic com-
plaints evaluated by the electromyographer.
Although the frequency of neuropathy among the
general population is unknown, it is generally
believed to exceed 5%. During the past 25 years,
the number of identifiable and treatable neu-
ropathies has increased dramatically. Electrodiag-
nostic medicine has contributed to the evaluation
of neuropathy, and most neuromuscular clinicians
use the electrodiagnostic examination as an exten-
sion of their clinical neurologic evaluation. In this
context, the clinical and electrodiagnostic exami-
nations are the most important “tests” used to
evaluate suspected neuropathy. There are few
pathognomonic features for most forms of neu-
ropathy, but the electrodiagnostic evaluation of
neuropathy plays an important role in character-
izing the electrophysiologic features of the neu-
ropathy. Clinical findings are confirmed by the
electrodiagnostic evaluation, and a focused differ-
ential diagnosis is based on the combined clinical
and electrodiagnostic findings. For some forms of
neuropathy, characteristic systemic or pathologic
clues help ascertain identity. For others, addi-
tional laboratory tests are required to establish the
cause of the neuropathy. Establishing the cause of
a neuropathy is a complicated task that depends
on information about the temporal profile of
symptoms and signs, epidemiologic and genetic
information, animal models, and an understand-
ing of systemic disorders and the many substances,
particularly medications, known to produce neu-
ropathy. Of the numerous forms of neuropathy
encountered in clinical practice, the majority re-
spond to treatment directed either at the underly-
ing pathophysiology or the systemic disorder
producing the neuropathy.
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136. Wilbourn AJ. The diabetic neuropathies. In:
Brown WF, Bolton CF, eds. Clinical electromyo-
graphy. Boston: Butterworths, 1987:329–364.
137. Singleton JR, Smith AG, Bromberg MB. In-
creased prevalence of impaired glucose toler-
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thy. Diabetes Care 2001;24:1448–1453.
138. Singleton JR, Smith AG, Bromberg MB.
Painful sensory polyneuropathy associated with
impaired glucose tolerance. Muscle Nerve
2001;24:1225–1228.
139. Sumner CJ, Sheth S, Griffin JW, et al. The
spectrum of neuropathy in diabetes and im-
paired glucose tolerance. Neurology 2003;60:
108–111.
140. Cameron NE, Cotter MA. Metabolic and vascu-
lar factors in the pathogenesis of diabetic neu-
ropathy. Diabetes 1997;46 (Suppl 2):S31–S37.
141. Graf RJ, Halter JB, Pfeifer MA, et al. Glycemic
control and nerve conduction abnormalities in
non-insulin dependent diabetic subjects. Ann
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142. Diabetes Control and Complications Trial Re-
search Group. The effect of intensive diabetic
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of neuropathy. Ann Intern Med 1995;122:
561–568.
143. Dyck PJ, Johnson WJ, Nelson RA, et al. Ure-
mic neuropathy. III. Controlled study of re-
stricted protein and fluid diet and infrequent
hemodialysis versus conventional hemodialysis
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144. Said GH, Boudier L, Selva J, et al. Different
patterns of uremic polyneuropathy. Neurology
1983;33:567–574.
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CHAPTER 12
Electrodiagnostic Approach to
Patients with Suspected
Radiculopathy
Timothy R. Dillingham
INTRODUCTION
Cervical and lumbosacral radiculopathies are con-
ditions involving a pathologic process affecting
the spinal nerve root. Commonly, this is a herni-
ated nucleus pulposus that anatomically com-
presses a nerve root within the spinal canal. An-
other common etiology for radiculopathy is spinal
stenosis resulting from a combination of degener-
ative spondylosis, ligament hypertrophy, and
spondylolisthesis. Inflammatory radiculitis is an-
other pathophysiologic process that can cause
radiculopathy. It is important to remember, how-
ever, that other more ominous processes such as
malignancy and infection can manifest the same
symptoms and signs of radiculopathy as the more
common causes.
This chapter deals with the clinical approach
used in an electrodiagnostic laboratory to evaluate
a person with neck pain, lumbar spine pain, or
limb symptoms suggestive of radiculopathy. The
indications for referring for testing as well as the
limitations of testing are discussed to give a
greater understanding of this important diagnos-
tic procedure.
Given the large differential diagnosis for
limb and spine symptoms, it is important for elec-
trodiagnosticians to develop a conceptual frame-
work for evaluating these referrals with a
standard focused history and physical examina-
tion and a tailored electrodiagnostic approach.
Accurately identifying radiculopathy by means of
electrodiagnosis provides valuable information
that informs planning of treatment and mini-
mizes other invasive and expensive diagnostic and
therapeutic procedures.
SPINE AND NERVE ROOT ANATOMY:
DEVIATIONS FROM THE EXPECTED
Spinal anatomy is discussed in Chapter 1 in
greater detail. From an electrodiagnostic perspec-
tive, however, there are several specific anatomic
issues that merit further discussion.
At all levels the dorsal root ganglion lies in
the intervertebral foramen. This anatomic ar-
rangement has implications for clinical electrodi-
agnosis of radiculopathy, namely that sensory
nerve action potentials (SNAPs) are preserved in
most radiculopathies as the nerve root is affected
proximal to the DRG.
Regarding the cervical nerve roots and the
brachial plexus, there are many anatomic varia-
tions. Perneczky (1) described an anatomic study
of 40 cadavers. In all cases, there were deviations
from accepted cervical root and brachial plexus
anatomy. Levin et al (2) examined the pattern of
abnormalities on electromyography (EMG) in 50
cases of surgically proven cervical root lesions. A
range of needle EMG patterns was found, with
EMG demonstrating less specificity for the C6
root level but more specificity and consistent pat-
terns for C8, C7, and C5 radiculopathies. In
333
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334 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
subjects with C6 radiculopathy, half of the pa-
tients showed findings similar to those with C5
radiculopathy and the other half demonstrated C7
patterns. This surgical group was more severely
affected than patients who did not require surgi-
cal interventions, and this pattern may not hold
for less symptomatic patients.
In the lumbar spine the dorsal and ventral
lumbar roots exit the spinal cord at about the
T11–L1 boney levels and travel in the lumbar
canal as a group of nerve roots in the dural sac.
This is termed the “horse’s tail” or cauda equina.
This poses challenges and limitations to the
EMG examination. A destructive intramedullary
spinal cord lesion at the T11 vertebral level that
damages the anterior horn cells can produce
EMG findings in muscles innervated by any of
the lumbosacral nerve roots and manifest pre-
cisely the same findings on needle EMG as those
seen with a herniated nucleus pulposus at any of
the lumbar disc levels. Likewise, an L2 skeletal
level lesion can affect any of the cauda equina
roots. For this reason, the electromyographer
cannot determine for certain the anatomic loca-
tion of the lumbar intraspinal lesion producing
distal muscle EMG findings in the lower limbs.
The needle EMG examination can identify the
root or roots that are physiologically involved,
but not the precise anatomic site of pathology in
the lumbar spinal canal. This is an important
limitation requiring correlation with imaging
findings to determine which of the possible
anatomic locations is most likely the offending
site. This can be difficult in elderly persons with
foraminal stenosis as well as moderate central
spinal canal stenosis at a more proximal site.
In a prospective study of 100 patients with
lumbosacral radiculopathy who underwent lum-
bar laminectomy, EMG precisely identified the
involved root level 84% of the time (3). Needle
EMG failed to accurately identify the compressed
root in 16%. However, at least half of the failures
were attributable to anomalies of innervation. An-
other component of this study involved intraoper-
ative stimulation of the nerve roots with simulta-
neous recording of muscle activity in the lower
limb using surface electrodes. These investigators
demonstrated variations in root innervations, such
as the L5 root innervating the soleus and medial
gastrocnemius, in 16% of a sample of 50 patients.
Most subjects demonstrated dual innervations for
most muscles (3).
These findings underscore the limitations of
precise localization for root lesions by EMG. The
electrodiagnostician should maintain an apprecia-
tion of these anatomic variations to better convey
the level of certainty with respect to diagnostic
conclusions.
PHYSICAL EXAMINATION
The electrodiagnostic examination is an extension
of the standard clinical examination. The history
and physical examination are vital initial steps in
determining what conditions may be causing the
patient’s symptoms. Most radiculopathies present
with symptoms in one limb. Multiple radicu-
lopathies, such as are seen in cervical spinal steno-
sis or lumbar stenosis, may cause symptoms in
more than one limb. A focused neuromuscular
examination that assesses muscle strength,
reflexes, and sensation in both the affected limb
and the contralateral limb is important, providing
a conceptual framework for electrodiagnostic
assessment.
An algorithmic approach to using physical
examination and symptom information to tailor
the electrodiagnostic evaluation is shown in Fig-
ure 12-1. In this approach, the patient’s symptoms
and physical examination signs of sensory loss and
weakness create a conceptual framework for ap-
proaching these sometimes daunting problems.
Admittedly, there are many exceptions to this ap-
proach, with considerable overlap in conditions
that might fall within multiple categories. Radicu-
lopathies and entrapment neuropathies are exam-
ples of such conditions with a variety of clinical
presentations and physical examination findings,
such that they are included in both focal symptom
categories with and without sensory loss. In the
case of a person with lumbosacral radiculopathy, a
positive straight-leg raise test may be noted in the
absence of motor, reflex, or sensory changes.
Conditions such as myopathies and polyneu-
ropathies better fit this algorithmic approach,
given that symptoms and physical examination
signs are more specific. Figure 12-1 also contains
musculoskeletal disorders and denotes how they
fall into this conceptual framework. The electro-
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CHAPTER 12 • PATIENTS WITH SUSPECTED RADICULOPATHY 335

Patient Presentation
(Pain, Weakness, Gait Disturbance, Sensory Symptoms, Paresthesia)

No sensory loss on Exam Sensory loss on Exam

Generalized Focal Symptoms Generalized Focal

Symptoms Symptoms Symptoms
(With Weakness)

–Multifocal Motor Reduced Reflexes

Neuropathy –Polyneuropathy –Entrapment
–Motor Neuron –Radiculopathy –Bilateral Cervical Neuropathy
Disease –Entrapment Neuropathy Radiculopathy –Radiculopathy
–Myopathy –Mononeuropathy –Bilateral Lumbosacral –Plexopathy
–Neuromuscular –Musculoskeletal disorder Radiculopathy –Other
Junction Disorder –Myofascial pain syndrome (Lumbar Stenosis, Mononeuropathy
Cauda equina syndrome)
Increased Reflexes
Generalized Symptoms
–Cervical Myelopathy
(No Weakness)
–Thoracic Myelopathy
–Fibrositis
–Multiple Sclerosis
–Polymyalgia Rheumatica
–Other Myelopathies

Figure 12-1 ● Algorithmic approach to structuring the electrodiagnostic examination

based upon the patient’s symptoms and physical exam-derived differential diagnosis. Fo-
cal symptoms refer to single-limb symptoms, whereas generalized symptoms are present when the patient
complains of symptoms affecting more than one limb. (Modified from Dillingham TR. Electrodiagnostic ap-
proach to patients with suspected radiculopathy. Phys Med Rehabil Clin North Am 2002;13:567–588, with per-
mission.)

diagnostician must be able to modify the electro-
diagnostic examination in response to nerve con-
duction and EMG findings and adjust the focus of
the examination in light of new information.
The implications of symptoms and signs on
electrodiagnostic findings were investigated by
Lauder et al for both suspected cervical and lum-
bosacral radiculopathies (4,5). Even though physi-
cal examination findings were better at predicting
who would have a radiculopathy, many patients
(18% in the lower limb) with normal examinations
had abnormal lower limb electrodiagnostic stud-
ies, indicating that clinicians should not curtail
electrodiagnostic testing simply because the phys-
ical examination is normal. For lower limb symp-
toms, loss of a reflex or weakness dramatically
increased the likelihood of having a radiculopathy
by EMG. Losing the Achilles reflex, for instance,
resulted in an odds ratio of 8.4 (P
0.01)—in other
words, eight times the likelihood of having a
radiculopathy by EMG with this physical exami-
nation finding (4). Similar findings were noted for
upper limb symptoms. If a reflex was lost or weak-
ness was noted, the likelihood of having a cervical
radiculopathy confirmed by EMG was many
times greater (5). Combinations of findings, par-
ticularly weakness plus sensory loss or weakness
plus reflex changes, resulted in ninefold greater
likelihood of cervical radiculopathy and two to
three times greater likelihood of lumbosacral
radiculopathy (4,5).
ELECTRODIAGNOSTIC TESTING
Electrodiagnostic testing is expensive and uncom-
fortable for patients, and so it is important to un-
derstand why it is performed and the expected
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336 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
outcomes. Electrodiagnostic testing serves several
important purposes:
1. It effectively excludes other conditions that
mimic radiculopathy, such as polyneuropathy
or entrapment neuropathy. Haig et al (6)
demonstrated that the referring diagnostic im-
pression is often altered with electrodiagnostic
testing.
2. Electrodiagnostic testing can to some extent
suggest severity or extent of the disorder be-
yond the clinical symptoms. Involvement of
other extremities can be delineated or the in-
volvement of multiple roots may be demon-
strated, such as in the case of lumbosacral spinal
stenosis.
3. There is utility in solidifying a diagnosis. An
unequivocal radiculopathy on EMG in an eld-
erly patient with nonspecific or mild lumbar
spondylosis or stenosis on MRI reduces diag-
nostic uncertainty and identifies avenues of
management such as lumbar steroid injections
or decompression surgery in certain situations.
4. Outcome prediction may be possible. If surgical
intervention is planned for a lumbosacral
radiculopathy, a positive preoperative EMG
improves the likelihood of a successful outcome
postoperatively (see “Implications of an EMG-
Confirmed Radiculopathy”). This is an area
that deserves more research attention.
Usefulness of Electrodiagnostic Testing
The value of any test depends upon the a priori
certainty of the diagnosis in question, and this
principle applies to electrodiagnostic testing. For a
condition or diagnosis for which there is great cer-
tainty before additional testing, the results of the
subsequent tests are of limited value. The concept
of diminishing returns on the road to diagnostic
certainty is an important one. For instance, an
EMG test will be of limited value in confirming
the diagnosis of radiculopathy in a patient with
acute-onset sciatica while lifting, L5 muscle weak-
ness, a positive straight-leg raise, and an MRI
showing a large extruded L4-5 nucleus pulposus.
This is because the a priori certainty of the diag-
nosis was very high. In contrast, an elderly
diabetic patient with sciatica, limited physical
examination findings, and equivocal or age-re-
lated MRI changes presents an unclear picture. In
this latter case the electrodiagnostic testing is of
high value, placing in perspective the imaging
findings and also excluding diabetic polyneuropa-
thy or plexopathy as confounding conditions.
AANEM Guidelines for
Radiculopathy Evaluation
The American Association of Neuromuscular
and Electrodiagnostic Medicine (AANEM, for-
merly AAEM) guidelines recommend that for an
optimal evaluation of a patient with suspected
radiculopathy, a needle EMG screen of a sufficient
number of muscles and at least one motor and one
sensory nerve conduction study should be per-
formed in the involved limb (7). The nerve con-
duction studies are necessary to exclude polyneu-
ropathy. The sufficiency of the EMG screen and a
recommended number of muscles is discussed in
detail below. An EMG study is considered diag-
nostic for a radiculopathy if EMG abnormalities
are found in two or more muscles innervated by
the same nerve root and different peripheral
nerves, yet muscles innervated by adjacent nerve
roots are normal (8). This assumes, of course, that
other generalized conditions such as polyneuropa-
thy are not present.
EMG study of bilateral limbs is often neces-
sary, particularly if a single limb shows EMG
findings suggestive of radiculopathy and the pa-
tient has symptoms in both the studied and the
contralateral limb. If bilateral limbs are involved,
then the electrodiagnostician should proceed by
studying selected muscles in an upper limb (if the
lower limbs are abnormal on EMG) or a lower
limb (if both upper limbs are abnormal) to exclude
a generalized process such as polyneuropathy or
motor neuron disease. Likewise, additional nerve
conduction studies are appropriate to exclude
other suspected conditions, and the electrodiag-
nostician should have a low threshold for expand-
ing the study.
H Reflex
H reflexes have commonly been used to deter-
mine whether a radiculopathy demonstrates S1
involvement (8). This is a monosynaptic reflex
that is an S1 nerve root-mediated response and can
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CHAPTER 12 • PATIENTS WITH SUSPECTED RADICULOPATHY
differentiate to some extent L5 from S1 radicu-
lopathy. Many researchers have evaluated the sen-
sitivity and specificity of the H reflex with respect
to lumbosacral radiculopathies and generally
found a range of sensitivities from 32% to 88%
(8–13). However, many of these studies suffered
from lack of a control group, imprecise inclusion
criteria, or small sample sizes.
Marin et al (13) prospectively examined the H
reflex and the extensor digitorum brevis muscle
stretch reflex in 53 normal subjects, 17 patients
with L5, and 18 patients with S1 radiculopathy.
Patients in the study had all of the following: low
back pain radiating to the leg; reduced sensation,
weakness, or positive straight leg raise test; and ei-
ther EMG evidence of radiculopathy or structural
changes on MRI or CT. The H reflex maximal
side-to-side latency difference was 1.8 ms, as de-
rived from the normal group. They analyzed the
sensitivity of the H reflex for side-to-side differ-
ences greater than 1.8 ms or a unilaterally absent
H reflex on the affected side. The H reflex
demonstrated only 50% sensitivity for S1 radicu-
lopathy and 6% for L5 radiculopathy but had 91%
specificity. H reflex amplitudes were not assessed
in this study. These results suggest that the H re-
flex has a low sensitivity for S1 root level involve-
ment but may help differentiate L5 from S1 root
involvement.
H reflexes may be useful to identify subtle S1
radiculopathy, yet there are a number of short-
comings related to these responses. They can be
normal with radiculopathy (13), and because they
are mediated over such a long physiologic path-
way, they can be abnormal due to polyneuropathy,
sciatic neuropathy, or plexopathy (8). They are
most useful in the assessment for polyneuropathy.
To interpret a latency or amplitude value,
and to render a judgment as to the probability that
it is abnormal, precise population-based norma-
tive values encompassing a large range of ages of
normal subjects must be available to which to
compare these nerve conduction findings. Falco et
al (14) demonstrated in a group of healthy elderly
subjects (60 to 88 years old) that the tibial H reflex
was present and recorded bilaterally in 92%. Most
elderly persons are expected to have normal H re-
flex studies, and when abnormalities are found in
these persons, the electrodiagnostician should crit-
ically evaluate these findings and the clinical sce-
337
nario before attributing H reflex abnormalities to
the aging process.
In patients with upper limb symptoms sug-
gestive of cervical radiculopathy, H reflexes and F
waves are not useful in diagnosis but rather help
exclude polyneuropathy as an underlying cause of
symptoms. One study by Miller et al (15) exam-
ined the H reflexes in the upper limb in a set of pa-
tients defined by a combination of clinical criteria
(no imaging or EMG studies, however) as having
definite or probable cervical radiculopathy. They
tested the H reflex for the flexor carpi radialis, ex-
tensor carpi radialis, and abductor pollicis brevis
muscles and also evaluated the biceps brachii het-
eronymous reflex. The later reflex is derived by
stimulating the median nerve in the cubital fossa
and recording over the biceps brachii muscle, av-
eraging 40 to 100 trials. These reflex studies had a
72% sensitivity overall for the group, with 100%
for the subset of patients with definite cervical
radiculopathy. In contrast, needle EMG demon-
strated 90% sensitivity for the definite group. Al-
though these findings suggest a possible role for
these upper limb H reflexes, they are highly spe-
cialized, time consuming, and difficult to consis-
tently elicit. They may have a role in sensory
radiculopathies where needle EMG will not be
positive and imaging findings are equivocal. Fur-
ther studies are necessary to clarify whether these
findings of Miller et al (15) can be duplicated in
other centers.
F Wave
F waves are late responses involving the motor ax-
ons and axonal pool at the spinal cord level. They
can be assessed and classified by using the minimal
latency, mean latency, and chronodispersion or
scatter (8). As in the case of H reflexes, F waves
demonstrate low sensitivities and are not specific
for radiculopathy; rather, they are a better test to
screen for polyneuropathy. Published sensitivities
in radiculopathies range from 13% to 69%, but
these studies suffer from many of the shortcom-
ings that are found in the H reflex studies
(9,16,17).
London and England (18) reported two cases
of persons with neurogenic claudication from
lumbosacral spinal stenosis. They demonstrated
that the F wave responses could be reversibly
90749_ch12(333-352).ps 8/10/06 3:49 PM Page 338
338 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
changed after 15 minutes of ambulation that
provoked symptoms. This suggested an ischemia-
induced conduction block in proximal motor neu-
rons. A larger-scale study of this type might find a
use for F waves in the identification of lum-
bosacral spinal stenosis and assist with the delin-
eation of neurogenic from vascular claudication.
Motor and Sensory Nerve
Conduction Studies
Standard motor and sensory nerve conduction
studies are not helpful in identifying a cervical or
lumbosacral radiculopathy; however, they should
be performed to screen for polyneuropathy and to
exclude common entrapment neuropathies if the
patient’s symptoms could be explained by a focal
entrapment. It is important to remember that
based upon the anatomy of the dorsal root gan-
glion, sensory responses should be normal in most
radiculopathies. If they are found to be absent, this
should increase suspicion for another diagnosis,
such as polyneuropathy or plexopathy.
Plexopathies often pose a diagnostic chal-
lenge, as they are similar to radiculopathies in
symptoms and signs. To distinguish plexopathy
from radiculopathy, sensory nerve conduction test
responses that are accessible in a limb should be
tested. In plexopathy, they are likely to be reduced
in amplitude, whereas in radiculopathy they are
generally normal. If substantial axonal loss has oc-
curred at the root level, the compound muscle ac-
tion potential recorded in muscles innervated by
that root may be reduced in both plexopathies and
radiculopathies. This is usually when severe
axonal loss has occurred, such as with cauda
equina lesions or penetrating trauma that severely
injures a nerve root. The distal motor latencies
and conduction velocities are usually preserved as
they reflect the fastest-conducting nerve fibers (8).
Somatosensory Evoked Potentials
and Related Tests
The AANEM guidelines recently examined the
literature and concluded that somatosensory
evoked potentials (SEPs) may be useful for cervi-
cal spondylosis with cord compression. Likewise,
in lumbosacral spinal stenosis, dermatomal SEPs
(DSEPs) may be useful in defining levels of
deficits (7). These tests are not necessary for elec-
trodiagnostic testing for persons with suspected
radiculopathies, and their usefulness is limited to
special circumstances.
DSEPs can document physiologic evidence of
multiple- or single-root involvement in lum-
bosacral spinal stenosis and may be useful in the
case where spinal canal narrowing is minimal and
the patient has symptoms. This testing also com-
plements standard needle EMG. Snowden et al
(19) found that for single-level and multilevel
lumbosacral spinal stenosis, DSEPs revealed 78%
sensitivity relative to spinal imaging. In this well-
designed prospective study, DSEP criteria as well
as inclusion criteria were precisely defined. The
predictive value was 93%. Yiannikas (20) demon-
strated that SEPs may be useful for cervical
myelopathy. In a study of patients with clinical
signs of myelopathy, all 10 had abnormal peroneal
SEPs, and 7 had abnormal median SEPs.
Maertens de Noordhout et al (21) examined
motor evoked potentials (MEPs) and SEPs in 55
persons with unequivocal signs and symptoms of
cervical spinal cord myelopathy. In this group, 87%
showed gait disturbances and 82% showed hyper-
reflexia. MRI was not the diagnostic standard, as
these authors felt that MRI was prone to overdiag-
nosis; rather, metrizamide myelography showed
unequivocal signs of cervical cord compression for
all of these patients. Magnetic stimulation of the
cortex was performed and the responses were
measured with surface electrodes over limb mus-
cles. In these subjects, 89% demonstrated abnor-
malities in MEP to the first dorsal interosseus
muscle, and 93% had one MEP abnormality. At
least one SEP abnormality was noted in 73%.
Tavy et al (22) examined whether MEPs or
SEPs assisted in identifying persons with radio-
logic evidence of cervical cord compression but
who were without clinical markers for myelopa-
thy. All patients had clinical symptoms of cervical
radiculopathy, but not myelopathy. In this group,
MEPs were normal in 92% and SEPs were normal
in 96%. These investigators concluded that MEPs
and SEPs are normal in most cases of persons with
asymptomatic cervical stenosis. This indicates that
abnormal MEPs and SEPs are likely to be true-
positive findings and not false-positives related to
mild cord compression that does not cause symp-
toms. It is important to remember that cervical
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CHAPTER 12 • PATIENTS WITH SUSPECTED RADICULOPATHY
spondylosis is a process that causes a continuum of
problems, including both radiculopathy and
myelopathy.
The inherent variability in SEP recordings
and difficulty in determinations as to what consti-
tutes “normal” prompted investigation. Dumitru et
al (23) examined the variations in latencies with
SEPs. In 29 normal subjects, they examined the
ipsilateral intertrial variations, arithmetic mean
side-to-side differences, and maximum potential
side-to-side differences with stimulation of the su-
perficial peroneal sensory nerve, sural nerve, and
the L5 and S1 dermatomes with respect to P1 and
N1 latencies and peak-to-peak amplitudes. Consid-
erable ipsilateral intertrial variation was observed,
and side-to-side comparisons revealed a further in-
crease in this inherent variation regarding the
above-measured parameters. They suggested an
additional parameter with which to evaluate SEPs:
the maximum side-to-side latency difference.
Dumitru et al (24), in a later study involving
persons with unilateral and unilevel L5 and S1
radiculopathies, evaluated dermatomal and seg-
mental SEPs. History, physical examination, im-
aging studies, and electrodiagnostic medicine
evaluations clearly defined patients with isolated
L5 or S1 nerve root compromise. Regression equa-
tion analysis for cortical P1 latencies evaluating
age and height based on comparable patient and
control reference populations revealed segmental
and dermatomal sensitivities for L5 radicu-
lopathies to be 70% and 50%, respectively, at 90%
confidence intervals. Similar sensitivities were ob-
tained for cortical P1 latencies using the mean  2
standard deviations (SD) method. Side-to-side
cortical P1 latency difference data revealed SEP
and DSEP sensitivities for S1 radiculopathies to be
50% and 10%, respectively, also at 2 SD. These in-
vestigators questioned the clinical utility of both
segmental and dermatomal SEPs in the evalua-
tion of patients with suspected focal L5 or S1
nerve root compromise, finding little utility for
these tests in persons with single-level lum-
bosacral radiculopathy.
In summary, SEPs, DSEPs, and MEPs are
not necessary or recommended for the vast major-
ity of patients referred for possible cervical or lum-
bosacral radiculopathy (7). They can be helpful if
performed in special laboratories skilled in such
testing, with adequate normal values, and in cer-
339
tain clinical situations that can be clarified by such
results.
Needle Electromyography
The need for EMG, particularly in relationship to
imaging of the spine, has been recently high-
lighted (25). Needle EMG is particularly helpful
in view of the fact that the false-positive rates for
MRI of the lumbar spine are high, with 27% of
healthy subjects having a disc protrusion (26). For
the cervical spine the false-positive rate for MRI is
much lower, with 19% of subjects demonstrating
an abnormality, but only 10% showing a herniated
or bulging disc (27). Radiculopathies can occur
without structural findings on MRI, and likewise
without EMG findings. The EMG evaluates only
motor axonal loss or motor axon conduction
block, and for these reasons a radiculopathy af-
fecting the sensory root will not yield abnormali-
ties by EMG. If the rate of denervation is balanced
by reinnervation in the muscle, then spontaneous
activity is less likely to occur and be identified
with needle EMG.
The sensitivity of needle electromyography
for cervical and lumbosacral radiculopathies has
been examined in a number of studies. The results
of some of these studies are shown in Table 12-1.
Table 12-1 lists the “gold standards” for diagnosis
against which these EMG findings were com-
pared. Studies using a clinical standard may re-
flect a less severe group, whereas those using a sur-
gical confirmation may indicate a more severely
involved group. The sensitivity for EMG was
unimpressive, ranging from 49% to 92% in these
studies. EMG is not a sensitive test, yet it likely has
higher specificity. The issue of specificity and its
value in electrodiagnosis was underscored by
Robinson (25). It is apparent that EMG is not a
very good screening test. In terms of screening
tests, MRI is better for identifying subtle struc-
tural abnormalities, with EMG to assess their clin-
ical relevance and to exclude other disorders.
Paraspinal Muscle Examination
Paraspinal muscles are important to study, as they
localize the site of the pathology to the root or
spinal level when positive and they increase the
yield for screening EMG studies of limbs and spine
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340 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

T A B L E 1 2 - 1 Selected Studies Evaluating the Sensitivity of EMG Relative to Various

“Gold Standards” for Diagnosis

Study Sample Size Gold Standard EMG Sensitivity

Lumbosacral Radiculopathy

Weber (28) 42 Clinical  imaging HNP 60%

Nardin (29) 47 Clinical 55%
Kuruoglu (9) 100 Clinical 86%
Khatri (30) 95 Clinical 64%
Tonzola (31) 57 Clinical 49%
Schoedinger (32) 100 Surgically proven 56%
Knutsson (33) 206 Surgically proven 79%
Young (3) 100 Clinical and imaging 84%*
Linden (11) 19 Myelography and CT 78%

Lumbosacral Spinal Stenosis

Hall (34) 68 Clinical  myelogram 92%

Johnsson (35) 64 Clinical  myelogram 88%†

Cervical Radiculopathy

Berger (36) 18 Clinical 61%

Partanen (37) 77 Intraoperative 67%
Leblhuber (10) 24 Clinical  myelogram 67%
So (38) 14 Clinical 71%
Yiannikas (20) 20 Clinical and/or radiographic 50%
Tackman (17) 20 Clinical 95%
Hong (39) 108 Clinical 51%
*Presence of either fibrillation potentials or large motor unit potentials (8 mV) was considered positive.
†This study assessed EMG parameters and used quantitative EMG with a unique grading scale not used in clinical prac-
tice. Fibrillation potentials were reported infrequently. This limits the generalizability of this otherwise strong study.
Unless otherwise stated the EMG parameters used in sensitivity calculations were fibrillation potentials.
(Modified from Dillingham TR. Electrodiagnostic approach to patients with suspected radiculopathy. Phys Med Rehabil
Clin North Am 2002;13:567–588, with permission.)

for radiculopathy. Dumitru et al (40) examined the
lumbosacral paraspinal muscles and intrinsic foot
muscles with monopolar EMG. These investiga-
tors recorded potentials and found that there were
irregularly firing potentials with similar wave-
form characteristics as fibrillations and positive
sharp waves. By excluding irregularly firing
potentials (most likely atypical endplate spikes),
they found much lower false-positive paraspinal
results than other investigators (29,41). Only 4% of
their normal subjects showed regularly firing fib-
rillations or positive sharp wave potentials (40).
They felt that the higher prevalences of sponta-
neous activity previously reported (29,41) were due
to not fully appreciating the similarity between
normal endplate-associated potentials and sponta-
neous single muscle fiber discharges associated
with denervation. This well-designed quantitative
study underscores the need to assess both firing
rate and rhythm as well as discharge morphology
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CHAPTER 12 • PATIENTS WITH SUSPECTED RADICULOPATHY
when evaluating for fibrillations and positive waves
in the lumbar paraspinal muscles. Electrodiagnosti-
cians should take care not to overcall paraspinal
muscle EMG findings by mistaking irregularly fir-
ing endplate spikes for fibrillations.
With respect to paraspinal muscle assessment,
the only relevant findings are fibrillations, positive
sharp waves, complex repetitive discharges,
myokymia, or myotonia. There are no normative
values to which polyphasicity or motor unit mor-
phology can be compared. Electrodiagnosticians
should not identify radiculopathies solely on the ba-
sis of paraspinal polyphasicity, reduced recruit-
ment, or increased insertional activity. Paraspinal
muscles should be considered either normal or pos-
itive if they have fibrillation potentials, positive
sharp waves, or other specific discharges (complex
repetitive discharges, myokymic potentials, or
myotonic potentials). Care must be taken to have the
patient relax these muscles to ensure optimal evalu-
ation of insertional and spontaneous activity.
Paraspinal muscles may be abnormal in
patients with spinal cancers (42–44) or amy-
otrophic lateral sclerosis (45) and in those exam-
ined following spinal surgery (46) or lumbar
puncture (47). In fact, fibrillation potentials can be
found years after lumbar laminectomy (46). The
absence of paraspinal muscle fibrillations in such
patients is helpful, but finding fibrillations in
someone after laminectomy is of uncertain rele-
vance, as these fibrillations may represent either
residual effects from the previous muscle damage
or relatively new denervation.
Investigations over the past decade have
provided insights into better quantification and
examination of lumbosacral paraspinal muscles.
The lumbar paraspinal muscle examination has
been refined through investigations that used
paraspinal mapping (PM) and a grading scale for
the findings (48–51). The “mini PM” score
provides a quantitative means of deriving the de-
gree of paraspinal muscle denervation (51). It dis-
tinguishes normal subjects from persons with
radiculopathy. This novel and quantitative tech-
nique may be able to identify subtle degrees of
radiculopathy or spinal stenosis with greater
precision.
Cervical and lumbar paraspinal muscles
should be examined in most patient EMG evalua-
tions for radiculopathy. Recruitment pattern find-
341
ings and motor unit potential morphology for
these muscles has not been established. Paraspinal
muscles either show spontaneous activity (and
therefore localize the lesion to the root level), or
they do not. There is considerable overlap in
paraspinal muscles with single roots innervating
fibers above and below their anatomic levels. For
this reason, the level of radiculopathy cannot be
delineated by paraspinal EMG alone, but rather is
based upon the root level that best explains the dis-
tribution of limb muscles with fibrillation poten-
tials and other abnormalities.
Identification of Radiculopathy
Electrodiagnostic testing is uncomfortable and ex-
pensive. Because electrodiagnosis is a composite
assessment made up of various tests, a fundamen-
tal question is, “When has the point of diminish-
ing returns been reached?” Some radiculopathies
cannot be confirmed by needle EMG, even though
the signs and symptoms along with imaging re-
sults suggest that radiculopathy is the diagnosis. A
screening EMG study involves determining
whether the radiculopathy can be identified by
EMG. If the radiculopathy cannot be detected by
a predetermined examination of a group of mus-
cles, then presumably no amount of additional
muscles can identify the radiculopathy. If a
radiculopathy can be delineated by EMG, then the
screen should identify this possibility with a high
probability. The process of identification can be
conceptualized as a conditional probability: given
that a radiculopathy can be confirmed by needle
EMG, what is the minimum number of muscles
that must be examined to confidently recognize or
exclude this possibility? This is a fundamentally
different concept from sensitivity. It involves un-
derstanding and defining the limitations of a com-
posite test based upon testing each muscle of a
group.
Radiculopathy Screening: How Many
Muscles to Study?
The concept of a screening EMG encompasses
identifying the possibility of an electrodiagnosti-
cally confirmable radiculopathy. If one of the
muscles in the screen is abnormal, then the testing
must be expanded beyond the screen to exclude
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342 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
other diagnoses and to fully delineate the radicu-
lopathy level. Because of the screening nature of
the EMG examination, electrodiagnosticians with
experience should look for more subtle signs of
denervation, and if these signs are present in the
screening muscles, they should expand the study
to determine whether these findings are limited to
a single nerve root’s myotome or to a peripheral
nerve distribution. If they are limited to a single
muscle, then the clinical significance of the find-
ings is uncertain.
Cervical Radiculopathy Screen
Dillingham et al (52) conducted a prospective
multicenter study evaluating patients referred to
participating electrodiagnostic laboratories with
suspected cervical radiculopathy. A standard set
of muscles was examined by needle EMG for all
patients. Those with electrodiagnostically con-
firmed cervical radiculopathies, based upon EMG
findings, were selected for analysis. The EMG
findings in this prospective study encompassed the
following neuropathic findings: positive sharp
waves; fibrillation potentials; complex repetitive
discharges; high-amplitude, long-duration motor
unit potentials; increased proportion of polyphasic
motor unit potentials; or reduced recruitment of
motor unit potentials.
There were 101 patients with electrodiagnos-
tically confirmed cervical radiculopathies repre-
senting cervical root levels C5 to C8. When
paraspinal muscles were one of the screening mus-
cles, five-muscle screens identified 90% to 98% of
radiculopathies (Table 12-2), six-muscle screens
identified 94% to 99% (Table 12-3), and seven-
muscle screens identified 96% to 100%. When
paraspinal muscles were not part of the screen,
eight distal limb muscles recognized 92% to 95%
of radiculopathies. Six-muscle screening includ-
ing paraspinal muscles yielded consistently high
identification rates, and studying additional mus-
cles led to small marginal increases in identifica-
tion. Individual screens useful to the electromyog-
rapher are listed in Tables 12-2 and 12-3.
In some instances a particular muscle cannot
be studied due to wounds, skin grafts, dressings,
or infections. In such cases the electromyographer
can use an alternative muscle with similar
innervations in the screen with equally high iden-
tification. These findings were consistent
with those derived from a large retrospective
study (53).
Lumbosacral Radiculopathy Screen
A prospective study was conducted at five institu-
tions by Dillingham et al (54). Patients referred to
participating electrodiagnostic laboratories with
suspected lumbosacral radiculopathy were re-
cruited and a standard set of muscles was exam-
ined by needle EMG. Patients with electrodiag-
nostically confirmed lumbosacral radiculopathies,
based upon EMG findings, were selected for
analysis. As described above for the prospective
cervical study, neuropathic findings were ana-
lyzed along with spontaneous activity. There were
102 patients with lumbosacral radiculopathies
representing all lumbosacral root levels. When
paraspinal muscles were one of the screening mus-
cles, four-muscle screens identified 88% to 97%,
five-muscle screens 94% to 98%, and six-muscle
screens 98% to 100% (Tables 12-4, 12-5, and 12-6).
When paraspinal muscles were not part of the
screen, identification rates were lower for all
screens, and eight distal muscles were necessary to
identify 90%. If only four muscles can be tested
due to limited patient tolerance, as seen in Table
12-4, and if one of these muscles is the paraspinals,
few electrodiagnostically detectable radicu-
lopathies will be missed. A large retrospective
study noted consistent findings, concluding that
five muscles identified most electrodiagnostically
confirmable radiculopathies (55).
Dillingham and Dasher (56) reanalyzed data
from a study published almost 40 years earlier by
Knutsson (33). In this detailed study, 206 patients
with sciatica all underwent lumbar surgical explo-
ration. All subjects had undergone standard EMG
by Dr. Knutsson with a set of 14 muscles using
concentric needles. The examiner was blinded to
other test results and physical examination find-
ings. In addition to the EMG and surgical infor-
mation, myelogram and physical examination
data were reviewed. In this reanalysis, screens of
four muscles, with one being the paraspinal mus-
cles, yielded an identification rate of 100%, sensi-
tivity of 92% with respect to the intraoperative
anatomic nerve root compressions, and 89% sensi-
tivity with respect to the clinical inclusion criteria
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CHAPTER 12 • PATIENTS WITH SUSPECTED RADICULOPATHY 343

T A B L E 1 2 - 2 Five-Muscle Screen Identifications of Patients

with Cervical Radiculopathies

Muscle Screen Neuropathic Spontaneous Activity

Without Paraspinals

Deltoid, APB, FCU 92% 65%

Triceps, PT biceps, triceps 85% 54%
ED, FCR, FDI
Deltoid, triceps, 84% 58%
ED, FDI, FCR
Biceps, triceps, 91% 60%
PT, APB, FCU

With Paraspinals

Deltoid, triceps, PT 98% 80%

APB, PSM
Biceps, triceps, ED 95% 73%
FDI, PSM
Deltoid, ED, FDI 90% 73%
PSM, FCU
Biceps, FCR, APB 95% 77%
PT, PSM

The screen detected the patient with cervical radiculopathy if any muscle in the screen was one of the mus-
cles that were abnormal for that patient. Neuropathic findings for non-paraspinal muscles included positive
sharp waves (PSW), fibrillation potentials, increased polyphasic motor unit potentials (MUP), neuropathic
recruitment, increased insertional activity, complex repetitive discharges (CRD), or large-amplitude long-
duration MUPs. For paraspinal muscles the neuropathic category included fibrillations, increased inser-
tional activity, PSWs, or CRDs. Spontaneous activity refers only to fibrillations or PSW.
APB, abductor pollicis brevis; FCU, flexor carpi ulnaris; FCR, flexor carpi radialis; PSM, cervical paraspinal
muscles; FDI, first dorsal interosseus; PT, pronator teres; ED, extensor digitorum.
(Adapted from Dillingham TR, Lauder TD, Andary M, et al. Identification of cervical radiculopathies: op-
timizing the electromyographic screen. Am J Phys Med Rehabil 2001;80(2):84–91, with permission.)

(56). This study, using data from four decades ago,
confirmed that a four-muscle screen provides
high identification. These findings are consistent
with contemporary work showing that screens
with as few as six muscles are adequate.
As described above, these research efforts
were undertaken to refine and streamline the
EMG examination. The strongest studies, con-
temporary prospective multicenter investigations,
provide the best estimates for a sufficient number
of muscles (52,54). In summary, for both cervical
and lumbosacral radiculopathy screens, the opti-
mal number of muscles appears to be six muscles,
including the paraspinal muscles and limb
muscles that represent all root level innervations.
When paraspinal muscles are not accessible or re-
liable, then eight non-paraspinal muscles must be
examined. Another way to think of this is, “To
minimize harm, six in the leg and six in the
arm.”
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344 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

T A B L E 1 2 - 3 Six-Muscle Screen Identifications of the Patients

with Cervical Radiculopathies

Muscle Screen Neuropathic Spontaneous Activity

Without Paraspinals

Deltoid, APB, FCU, triceps, PT, FCR 93% 66%

Biceps, triceps, FCU 87% 55%
ED, FCR, FDI
Deltoid, triceps 89% 64%
ED, FDI, FCR, PT
Biceps, triceps, ED 94% 64%
PT, APB, FCU

With Paraspinals

Deltoid, triceps, PT 99% 83%

APB, ED, PSM
Biceps, triceps, ED 96% 75%
FDI, FCU, PSM
Deltoid, ED, FDI 94% 77%
PSM, FCU, triceps
Biceps, FCR, APB 98% 79%
PT, PSM, triceps
Muscle abbreviations, identification criteria, and definitions are described in Table 12-2. (Adapted from Dillingham
TR, Lauder TD, Andary M, et al. Identification of cervical radiculopathies: optimizing the electromyographic screen.
Am J Phys Med Rehabil 2001;80(2):84–91, with permission.)

Limitations of the EMG Screen
If one of the six muscles studied in the screen is
positive, then there is the possibility of confirming
electrodiagnostically that a radiculopathy is pres-
ent. In this case, the examiner must expand the
study to additional muscles to determine the
radiculopathy level and to exclude a peripheral
mononeuropathy. If the findings are found in only
a single muscle, they remain inconclusive and of
uncertain clinical relevance. If none of the six
muscles is abnormal, the examiner can be confi-
dent of not missing the opportunity to confirm
that a radiculopathy is present, and the painful
needle examination can be curtailed. The patient
may still have a radiculopathy of mild degree
(affecting only a few axons or sensory nerve roots),
but other tests such as MRI will be necessary to
confirm this clinical suspicion. This logic is illus-
trated in Figure 12-2.
These cervical and lumbosacral muscle
screens are not intended to substitute for a clinical
evaluation and differential diagnosis formulation
by the electrodiagnostic consultant. Rather, infor-
mation from the investigations described above al-
lows the electrodiagnostician to streamline the
EMG evaluation and make more informed clini-
cal decisions regarding the probability of missing
an electrodiagnostically confirmable radiculopa-
thy when a given set of muscles is studied. Per-
forming a focused history and physical examina-
tion is essential, and these screens should not
supplant such clinical assessments or a more de-
tailed electrodiagnostic study when circumstances
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CHAPTER 12 • PATIENTS WITH SUSPECTED RADICULOPATHY 345

T A B L E 1 2 - 4 Four-Muscle Screen Identifications of Patients

with Lumbosacral Radiculopathies

Screen Neuropathic Spontaneous Activity

Four Muscles without Paraspinals

ATIB, PTIB, MGAS, RFEM 85% 75%

VMED, TFL, LGAS, PTIB 75% 58%
VLAT, SHBF, LGAS, ADD 52% 35%
ADD, TFL, MGAS, PTIB 80% 67%

Four Muscles with Paraspinals

ATIB, PTIB, MGAS, PSM 97% 90%

VMED, LGAS, PTIB, PSM 91% 81%
VLAT, TFL, LGAS, PSM 88% 77%
ADD, MGAS, PTIB, PSM 94% 86%
The screen identified the patient if any muscle in the screen was abnormal for that patient. The muscle demonstrated either
neuropathic findings or spontaneous activity. Identification criteria and definitions are described in Table 12-2.
PSM, lumbosacral paraspinal muscles; PTIB, posterior tibialis; ATIB, anterior tibialis; MGAS, medial gastrocnemius;
LGAS, lateral gastrocnemius; TFL, tensor fascia lata; SHBF, short head biceps femoris; VMED, vastus medialis; VLAT,
vastus lateralis; RFEM, rectus femoris; ADD, adductor longus.
(Adapted from Dillingham TR, Lauder TD, Andary M, et al. Identifying lumbosacral radiculopathies: an optimal
electromyographic screen. Am J Phys Med Rehabil 2000;79(6):496–503, with permission.)

T A B L E 1 2 - 5 Five-Muscle Screen Identifications of Patients

with Lumbosacral Radiculopathies

Screen Neuropathic Spontaneous Activity

Five Muscles without Paraspinals

ATIB, PTIB, MGAS, RFEM, SHBF 88% 77%

VMED, TFL, LGAS, PTIB, ADD 76% 59%
VLAT, SHBF, LGAS, ADD, TFL 68% 50%
ADD, TFL, MGAS, PTIB, ATIB 86% 78%

Five Muscles with Paraspinals

ATIB, PTIB, MGAS, PSM, VMED 98% 91%

VMED, LGAS, PTIB, PSM, SHBF 97% 84%
VLAT, TFL, LGAS, PSM, ATIB 97% 86%
ADD, MGAS, PTIB, PSM, VLAT 94% 86%
Abbreviations and definitions of muscle abnormalities are the same as in Tables 12-2 and 12-4.
Adapted from Dillingham TR, Lauder TD, Andary M, et al. Identifying lumbosacral radiculopathies: an optimal
electromyographic screen. Am J Phys Med Rehabil 2000;79(6):496–503, with permission.)
90749_ch12(333-352).ps 8/10/06 3:49 PM Page 346

T A B L E 1 2 - 6 Six-Muscle Screen Identifications of Patients with

Lumbosacral Radiculopathies

Screen Neuropathic Spontaneous Activity

Six Muscles without Paraspinals

ATIB, PTIB, MGAS, RFEM, SHBF, LGAS 89% 78%

VMED, TFL, LGAS, PTIB, ADD, MGAS 83% 70%
VLAT, SHBF, LGAS, ADD, TFL, PTIB 79% 62%
ADD, TFL, MGAS, PTIB, ATIB, LGAS 88% 79%

Six Muscles with Paraspinals

ATIB, PTIB, MGAS, PSM, VMED, TFL 99% 93%

VMED, LGAS, PTIB, PSM, SHBF, MGAS 99% 87%
VLAT, TFL, LGAS, PSM, ATIB, SHBF 98% 87%
ADD, MGAS, PTIB, PSM, VLAT, SHBF 99% 89%
VMED, ATIB, PTIB, PSM, SHBF, MGAS 100% 92%
VMED, TFL, LGAS, PSM, ATIB, PTIB 99% 91%
ADD, MGAS, PTIB, PSM, ATIB, SHBF 100% 93%
Abbreviations and definitions of muscle abnormalities are the same as in Tables 12-2 and 12-4.
(Adapted from Dillingham TR, Lauder TD, Andary M, et al. Identifying lumbosacral radiculopathies: an optimal
electromyographic screen. Am J Phys Med Rehabil 2000;79(6):496–503, with permission.)

Suspected Radiculopathy

–Six muscles (with PSM) - lumbar screen

–Six muscles (with PSM) - cervical screen

If one muscle is positive, If all muscles negative, stop

expand study EMG exam in this limb
Determine if EMG reflects; The patient will not have an
1) Radiculopathy (which level), electrodiagnostically confirmable
2) Entrapment neuropathy, radiculopathy
3) Generalized condition, or
They may;
4) Findings that are of uncertain
1) not have radiculopathy, or
relevance
2) have a radiculopathy but you will not
confirm this with EMG. Other
diagnostic tests must be utilized such
as MRI or SNRB.

Figure 12-2 ● Implications of a positive or negative EMG screening evaluation. A positive

result usually warrants further EMG testing to fully define the pathology, and a negative test could lead to
nerve conduction or other testing to consider other diagnoses. PSM, paraspinal muscles; SNRB, selective nerve
root block. (Modified from Dillingham TR. Electrodiagnostic approach to patients with suspected radiculopa-
thy. Phys Med Rehabil Clin North Am 2002;13:567–588, with permission.)
90749_ch12(333-352).ps 8/10/06 3:49 PM Page 347
CHAPTER 12 • PATIENTS WITH SUSPECTED RADICULOPATHY
dictate consideration of diagnoses other than
radiculopathy.
It is important to remember that the EMG
screens for cervical and lumbosacral radicu-
lopathies were validated in a group of patients with
limb symptoms suggestive of radiculopathies.
These screens will not provide sufficient screening
power if a brachial plexopathy is present or if a fo-
cal mononeuropathy such as a suprascapular neu-
ropathy is the cause of the patient’s symptoms. The
electrodiagnostician should always perform EMG
on weak muscles to increase the diagnostic yield.
These screens do not sufficiently screen for my-
opathies or motor neuron disease. It is incumbent
upon the electrodiagnostician to formulate a differ-
ential diagnosis (Fig. 12-1) and methodically evalu-
ate for other diagnostic possibilities when indi-
cated. Structuring the examination as data are
acquired is an important aspect of electrodiagnostic
medicine and one that distinguishes such consulta-
tions from other diagnostic tests.
Lumbar Spinal Stenosis
With the aging population in the United States
and the increasing prevalence of lumbar spinal
stenosis that occurs in the elderly, this condition
takes on greater public health significance. In fact,
an entire edition of Physical Medicine and Rehabil-
itation Clinics of North America was recently dedi-
cated to this complex topic (57). There are few
studies involving spinal stenosis and electromyog-
raphy. For lumbosacral spinal stenosis, Hall et al
(34) showed that 92% of persons with imaging-
confirmed stenosis had a positive EMG. They also
underscored the fact that 46% of persons with a
positive EMG study did not demonstrate
paraspinal muscle abnormalities, only distal mus-
cle findings. For 76%, the EMG showed bilateral
myotomal involvement (34).
In the United States, diabetes is on the rise,
with increasing prevalence and incidence (58). Dia-
betes often confounds the accurate diagnosis of
radiculopathy and spinal stenosis (59,60). Inaccu-
rate recognition of sensory polyneuropathy, dia-
betic amyotrophy, or mononeuropathy can lead to
unnecessary surgical interventions. In a recent
prospective study by Adamova et al (59), the value
of electrodiagnostic testing was assessed. There
were three groups: 29 persons with imaging-
347
confirmed clinical mild lumbar spinal stenosis, 24
subjects with diabetes and polyneuropathy, and an
age-matched control group of 25 persons. In this
well-designed study, sural SNAP amplitudes reli-
ably distinguished the diabetic polyneuropathy
group (an amplitude of 4.2 V or less was found in
47% of diabetic patients and only 17% of stenosis
patients). The ulnar F wave was prolonged in
polyneuropathy patients but not in lumbar stenosis
patients, and likewise the radial nerve SNAP was
reduced in amplitude in polyneuropathy patients
(59). These findings underscore the value of per-
forming sensory testing and F wave testing in the
involved extremity as well as an upper limb to fully
recognize diabetic polyneuropathy and help differ-
entiate this condition from spinal stenosis or
radiculopathy.
Symptom Duration and the Probability
of Fibrillation Potentials
In the past, a well-defined temporal course of
events was thought to occur with radiculopathies
despite the absence of studies supporting such a re-
lationship. It was a commonly held notion that in
acute lumbosacral radiculopathies, the paraspinal
muscles became denervated first, followed by distal
muscles, and that reinnervation started with
paraspinal muscles and then with distal muscles.
This paradigm was recently addressed with a series
of investigations (61–64). For both lumbosacral and
cervical radiculopathies, symptom duration had no
significant relationship to the probability of finding
spontaneous activity in paraspinal or limb muscles.
Based upon the investigations cited above,
there is no evidence of a relationship between the
duration of a patient’s symptoms and the proba-
bility of finding fibrillations in paraspinal or limb
muscles. This simplistic explanation, although
widely quoted in the older literature, does not ex-
plain the complex pathophysiology of radicu-
lopathies. Electrodiagnosticians should not invoke
this relationship to explain the absence or presence
of fibrillations in a particular muscle.
Implications of an EMG-Confirmed
Radiculopathy
The electrodiagnostician must remember that
EMG does not indicate the exact cause of the
90749_ch12(333-352).ps 8/10/06 3:49 PM Page 348
348 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
symptoms, only that axonal loss is taking place. A
spinal tumor, herniated disc, bony spinal stenosis,
chemical radiculitis, or severe spondylolisthesis
can all yield the same EMG findings. This under-
scores the need to image the spine with MRI (in-
cluding gadolinium) to assess for significant struc-
tural causes of electrodiagnostically confirmed
nerve dysfunction. A negative EMG test should
not curtail obtaining an MRI if clinical suspicion
for radiculopathy is high. Given the low sensitivi-
ties of needle EMG, it is not an optimal screening
test, but rather a confirmatory test.
There are few studies that have examined
the outcomes and the usefulness of electrodiag-
nosis in predicting treatment success, the excep-
tion being surgical outcomes for lumbar discec-
tomy. Tullberg et al (65) evaluated 20 patients
with lumbosacral radicular syndromes who un-
derwent single-level surgery for disc herniations.
They evaluated these patients before surgery and
1 year later with lower limb EMG, nerve
conduction studies, F waves, and SEPs. They
showed that the electrodiagnostic findings did
not correlate with the level defined by CT imag-
ing for 15 patients. However, patients in whom
preoperative electrodiagnostic testing was normal
were significantly more likely to have a poor sur-
gical outcome (P
0.01). Although the sample
size in this study was small, the significant corre-
lation of a normal electrodiagnostic study with
poor surgical outcome suggests that this may be a
true relationship.
Spengler and Freeman (66) described an ob-
jective approach to the assessment of patients pre-
operatively for laminectomy and discectomy for
lumbosacral radiculopathy. Spengler et al (67)
confirmed and underscored these findings re-
garding the use of objective methods to assess the
probability of surgical success preoperatively. In
this preoperative screening evaluation, the EMG
findings were combined with imaging, clinical,
and psychological assessments. The EMG find-
ings figured prominently (one quarter of the
scale), and patients with positive EMGs were
more likely to have a better surgical outcome. This
was particularly true when the EMG findings cor-
related with the spinal imaging findings, in a
person without psychological or dysfunctional
personality issues.
SUMMARY
This chapter reviews the electrodiagnostic test-
ing for suspected radiculopathy and the expected
sensitivities that different testing modalities pro-
vide. One cannot overemphasize the importance
of the clinical evaluation and differential diagno-
sis formulation by the electrodiagnostic medical
consultant, which is needed to guide the testing.
The needle EMG examination is the most useful
single electrodiagnostic test but is limited in sen-
sitivity. EMG screening examinations using six
muscles optimize identification while minimiz-
ing patient discomfort. Nerve conduction stud-
ies, H reflexes, and F waves are not very useful
for confirming radiculopathy, but they are useful
to exclude polyneuropathy or mononeuropathy.
Electrodiagnosticians should understand the
strengths and limitations of electrodiagnostic
testing to effectively use this important diagnos-
tic tool when evaluating patients with suspected
radiculopathy.
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CHAPTER 13
Evaluation of the Patient
with Suspected Myopathy
Albert C. Clairmont, Bakri Elsheikh, and Yousef M. Mohammad
INTRODUCTION
Electrodiagnostic findings in myopathy may re-
sult from a number of factors, including abnor-
malities or changes in muscle fibers as well as the
surrounding connective tissue. A wide range of
findings is possible; therefore, the patient pre-
senting with weakness and suspected myopathy
can pose a diagnostic challenge to the elec-
tromyographer. If the abnormal pathology in-
cludes muscle degeneration and regeneration,
one should anticipate abnormal membrane irri-
tability on concentric or monopolar needle elec-
tromyography (EMG). Muscle fiber splitting,
fiber atrophy with little or no degeneration,
errors of muscle maturation syndromes, and im-
paired muscle membrane excitability may have
needle EMG findings that one may not necessar-
ily anticipate based on the underlying pathology.
In this chapter a practical clinical approach to
evaluating a person with weakness and question
of myopathy, using standard electrodiagnostic
techniques, is presented. A proper electrodiag-
nostic consultation includes a detailed history
and physical examination with additional em-
phasis on the neuromuscular examination before
beginning the electrodiagnostic study. After the
electrodiagnostic study, the consultant should
render an impression and make recommenda-
tion(s) for further workup or treatment options
as appropriate.
HISTORY
The history establishes the basis for the entire
evaluation, and thus it is the crucial first step in the
electrodiagnostic study. Every disease has a ca-
dence, and the history elicits the cadence that helps
identify the specific disease. What is the present-
ing complaint? How long have symptoms been
present? In the case of muscle weakness, is the on-
set acute, rapidly progressive, or slowly progres-
sive? One should know if there are exacerbations
and remissions or if the course is stable. It would
be helpful to know if sensory symptoms accom-
pany the weakness and whether or not the sensory
symptoms predated or followed the weakness.
A history of antecedent illness (bacterial or viral)
might lead one toward evaluating for evidence of
neurogenic etiology (e.g., Guillain-Barré syn-
drome) instead of a myopathy. What is the distri-
bution of the weakness (1–4)? Is there a proximal
or distal emphasis? Is the weakness segmental?
Is there a time of day or a specific activity that ag-
gravates the symptoms? Persons with myasthenia
gravis tend to show increasing fatigue and weak-
ness as the day progresses (5). Is there a family his-
tory of muscle weakness that might suggest a
familial etiology for the weakness? Is fatigue an
issue? If fatigue is present, the history must be
expanded to evaluate for other causes of fatigue
that are not necessarily direct muscle function
problems (e.g., depressive illness). Does the person
353
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354 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
complain of weight loss or weight gain? The loss
of muscle fibers that might accompany a myopa-
thy can result in weight loss, although extensive
weight loss should lead one to consider the pos-
sibility of underlying neoplastic disease or neu-
ropathy. In the presence of bulbar or extraocular
weakness, mitochondrial myopathies should be
considered (6).
One should inquire about activities of daily
living. Can the person walk on level ground or
on uneven ground, and can he or she climb stairs
and arise to stand from a normal-height chair or
from a couch? Can the person chew food without
tiring, and is there difficulty swallowing? How
about bathing, dressing, and toileting activities?
The presence or absence of joint and/or muscle
pain must be noted. There may be shortness of
breath as a function of weakness of respiratory
muscles or from lung disease (7) resulting from
the underlying disease process (e.g., pulmonary
fibrosis and pulmonary hypertension in systemic
sclerosis [scleroderma]). Although systemic scle-
rosis is more likely to manifest as an acquired
neuropathy (8), a myopathy can occur in sclero-
derma, from direct extension of fibrosis into
muscle (9). Inflammatory muscle involvement
in scleroderma may show clinical features similar
to polymyositis, with significant proximal mus-
cle weakness and high elevations of muscle
enzymes (7).
PHYSICAL EXAMINATION
The physical examination begins when one greets
the patient or observes the gait as the person walks
into the examining room. Some characteristic
facies may be immediately recognizable because of
obvious wasting of cranial and facial muscles. For
example, in the person with myotonic dystrophy,
the mouth tends to hang open, teeth often are in
disrepair, bitemporal wasting is in evidence, and
frontal balding is noted. A handshake might con-
firm myotonia of grip. In fascioscapulohumeral
muscular dystrophy, facial weakness may show as
the absence or relative absence of furrows, lines, or
creases that would be expected for age. A rash
could suggest inflammatory myopathy. The he-
liotrope rash of dermatomyositis and Groton’s sign
come to mind (10).
NERVE CONDUCTION TESTING
The nerve conduction study in a patient with sus-
pected myopathy should probably include two
motor nerves in the upper limb and one in the
lower. If one chooses to study only one motor
nerve in the upper limb, it would be prudent
to avoid an often-compromised nerve like the
median. We recommend beginning the testing
with one or more sensory nerves in the lower
limb. Suspicion of a neuromuscular junction dis-
order must lead to repetitive stimulation testing at
2 Hz to 3 Hz (11). If Lambert-Eaton myasthenic
syndrome (LEMS) is being considered in the
differential diagnosis, one should deliver single
supramaximal stimulation to the motor nerve be-
ing studied, with the muscle in the rested state (6).
The patient then performs 10 seconds of exercise,
followed immediately by a second supramaximal
electrical stimulus to the motor nerve. Generally,
motor nerve conduction studies are normal in
myopathy. However, substantial muscle wasting
underlying the recording electrode would lead
to abnormally small amplitude of the recorded
compound motor action potential (CMAP). As
alluded to above, an abnormally small CMAP
amplitude should lead one to consider repetitive
nerve stimulation for possible myasthenia gravis
or LEMS (see Chapter 15).
NEEDLE EMG
For needle EMG, we recommend studying two ip-
silateral limbs, preferably on the dominant side, to
allow for possible muscle biopsy evaluation on a
limb that has not been explored with a needle elec-
trode. The most characteristic electrodiagnostic
findings in myopathy are best demonstrated during
needle EMG. The act of inserting the EMG needle
electrode into muscle disturbs a few muscle fibers,
leading to a brief discharge of electrical activity.
The duration of the discharge is to some extent re-
lated to the needle movement of the electromyog-
rapher. In inflammatory myopathy where there
has been extensive muscle necrosis and regenera-
tion, some muscle fibers might undergo functional
denervation and reestablishment of motor end-
plates. The functional denervation manifests as
abnormal membrane irritability with resulting
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CHAPTER 13 • EVALUATION OF THE PATIENT WITH SUSPECTED MYOPATHY
positive sharp waves and fibrillation potentials.
The total number of muscle fibers is decreased in
myopathy, with an increase of connective tissue and
detritus, resulting in an increased distance between
muscle fibers and the exploring needle electrode.
The above combination contributes to the abnor-
mally small amplitude of the motor unit potential
(MUP) in inflammatory myopathy.
MUP duration is a function of the total num-
ber of muscle fibers that are available to contribute
to the MUP. The slow, later phase of the MUP du-
ration is derived from more distant fibers of the
motor unit. In inflammatory and some other my-
opathies, there are smaller numbers of muscle
fibers remaining in the motor units available to
contribute, and the more distant units cannot con-
tribute to the MUP, resulting in the short duration
potential that is a hallmark of myopathy. Another
hallmark of acute inflammatory myopathy is the
presence of polyphasic MUPs. The normal motor
unit comprises muscle fibers of different diame-
ters. Larger muscle fibers tend to have faster prop-
agation velocity along the muscle fiber itself than
do smaller muscle fibers. In inflammatory myopa-
thy there is a greater variation of fiber diameters
than in the normal situation. Some muscle fibers
are sick or damaged and are smaller in diameter
than would be normally expected. This increased
fiber diameter variation is thought to manifest as
slight desynchronization of the MUP, resulting in
polyphasic MUPs (12).
Another characteristic finding on needle
EMG in myopathy is increased recruitment of
MUPs. This is often manifested as the patient’s
inability to voluntarily activate just one single
MUP on command. Because the remaining mo-
tor units are smaller in size, sick, and weak, the
patient’s effort to activate a single motor unit is
unsuccessful. Smaller motor units generate less
force than larger motor units (12). Instead of
a single motor unit, many of the sick and dam-
aged motor units must fire together to produce
enough force to meet the demand for minimal
activation. Therefore, at minimal contraction or
turn-on frequency, many MUPs are immediately
recruited, as recorded by needle EMG. At full
effort of activation, the screen is filled with small-
amplitude, short-duration, polyphasic MUPs that
impart a high-frequency audio cue to the elec-
tromyogram.
355
EXAMPLE CASES
CASE 1
The patient is a 36-year-old right-hand-dominant
Caucasian woman who presents with progressive
muscle weakness. She was well until 3 months
previously when, while working in a toy store, she
could not stack boxes on a shelf a few inches above
her head. Three weeks later she could not climb
stairs without holding on to the side rails. She
blamed her symptoms on exhaustion from work-
ing long hours. However, the week before pre-
senting for electrodiagnostic evaluation, lifting
objects or climbing stairs became impossible. She
had some difficulty swallowing solids.
Physical examination reveals mild bilateral
facial weakness, neck flexor weakness, and sym-
metrical, proximal more than distal limb muscle
weakness. There is no muscle tenderness. There is
no rash, and cardiac and pulmonary functions are
normal. Muscle stretch reflexes and sensory exam-
ination are normal, and motor coordination is also
normal; therefore, a neuropathic process is un-
likely. Levels of creatine kinase (CK) are increased
seven-fold.
Sensory and motor nerve conduction studies
of the right upper and lower limbs are normal.
Repetitive nerve stimulation is normal, thereby
ruling out a myasthenic syndrome. Results of the
needle EMG done on this patient are presented in
Table 13-1.
Summary of Findings
This is a 36-year-old woman with 3-month history
of progressive weakness. Physical examination
suggests a myopathic process. The lack of sensory
symptoms, the preserved reflexes, and the normal
nerve conduction studies exclude a neuropathy. If
sensory and motor nerve conduction study abnor-
malities were recorded in this clinical setting, then
one would consider the possibility of neuromyosi-
tis (13). In neuromyositis, the patient presents with
the usual electrodiagnostic findings of polymyosi-
tis in addition to the presence of abnormalities of
sensory and motor nerve conduction. Abnormal
membrane irritability and normal repetitive nerve
stimulation do not support a neuromuscular junc-
tion disorder. EMG findings of short-duration,
low-amplitude, polyphasic, early recruited MUPs
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356 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

TABLE 13-1 CASE 1

Needle EMG Studies

Muscle Fib. PSW Fasc. CRD Amplitude Duration Polyphasics Recruitment

R Deltoid 3
4
0 Yes Decrease Short Yes Early

R Biceps 2
3
0 Yes Decrease Short Yes Early
R Triceps 1
2
0 No Decrease Short Yes Early
R Pronator teres 1
1
0 No Decrease Short Yes Early
R First dorsal 0 0 0 No Normal Normal No Normal
inteross.
R Cervical 2
3
0 Yes Decrease Short Yes Early
paraspinals
R Adductor 3
4
0 Yes Decrease Short Yes Early
longus
R Rectus 2
3
0 Yes Decrease Short Yes Early
femoris
R Tibialis 1
1
0 No Decrease Short Yes Early
anterior
R Gastrocnemius 1
1
0 No Decrease Normal No Normal
R Lumbar 2
3
0 Yes Decrease Short Yes Early
paraspinals
R Ext. hallucis 1
1
0 No Decrease Normal Yes Early
longus
Fib., fibrillation potentials; PSW, positive sharp waves; Fasc., fasciculation potentials; CRD, complex repetitive discharges.

are typical for myopathy (12,14). Needle EMG also
suggests that the process is more severe proximally
than distally. The presence of abnormal sponta-
neous activity correlates with disease activity (15).
The EMG findings are compatible with a diagno-
sis of inflammatory myopathy. The diagnosis of
polymyositis in this patient is confirmed by muscle
biopsy. Note that the EMG study is done on the pa-
tient’s dominant side to avoid muscle biopsy arti-
facts caused by the EMG needle, since the muscle
biopsy is usually done on the nondominant side.
CASE 2
A 70-year-old, left-hand-dominant, retired male
university professor reported a 2 year history
of progressive painless weakness of the legs. He
gradually lost the ability to get up or down stairs
and later lost the ability to rise from a squat. As time
progressed he realized that he could not open jars.
There was no skin rash or swallowing difficulty.
Weakness was not worse at any particular time of
day. Ocular muscles were not particularly affected.
There was no history of significant weight loss or
sensory complaints. He now presents for electrodi-
agnostic evaluation.
Physical examination demonstrates normal
cranial nerve function and weak elbow flexors,
wrist flexors, finger flexors, hip flexors, knee ex-
tensors, and foot dorsiflexors. Muscle stretch re-
flexes and sensory testing are normal. CK levels
are increased two-fold.
Sensory and motor conduction studies of the
left median and ulnar nerves are normal. The
right peroneal and tibial motor, and superficial
peroneal and sural sensory nerves are also normal.
Results of the needle EMG done on this patient
are presented in Table 13-2.
Summary of Findings
This is a 70-year-old man with a 2 year history of
progressive weakness. The distribution of the
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CHAPTER 13 • EVALUATION OF THE PATIENT WITH SUSPECTED MYOPATHY 357

TABLE 13-2 CASE 2

Needle EMG Studies

Muscle Fib. PSW Fasc. CRD Amplitude Duration Polyphasics Recruitment

L Deltoid 0 0 0 No Normal Normal No Normal

L Biceps 1
1
0 Yes Decrease Short/ Yes Early
Few long
L Brachioradialis 1
1
0 Yes Decrease Short/ Yes Early
Few long
L Triceps 1
2
0 No Decrease Short/ Yes Early
Few long
L Flexor carpi 1
2
0 Yes Decrease Short/ Yes Early
ulnaris Few long
L First dorsal 0 0 0 No Decrease Short/ Yes Early
inteross. Few long
L Iliopsoas 1
1
0 Yes Decrease Short/ Yes Early
Few long
L Gluteus 0 1
0 Yes Decrease Short/ Yes Early
maximus Few long
L Vastus 1
1
0 No Decrease Short/ Yes Early
medialis Few long
L Tibialis 1
2
0 Yes Decrease Short/ Yes Early
anterior Few long
R Medial 0 0 0 No Normal Normal Normal Normal
gastrocnemius
Fib., fibrillation potentials; PSW, positive sharp waves; Fasc., fasciculation potentials; CRD, complex repetitive discharges.

weakness with diffuse proximal and distal mus-
cle involvement is typical of inclusion body
myositis. The lack of sensory symptoms and the
normal nerve conduction studies exclude a neu-
ropathic process. A myasthenic syndrome is un-
likely since the ocular muscles are not involved.
Needle EMG demonstrates abnormal sponta-
neous activity, accompanied by short-duration,
polyphasic, and early recruited MUPs. Some
MUPs are normal, but others are of abnormally
long duration. A mixed pattern including short-
duration, small-amplitude, normal, and long-
duration, high-amplitude MUPs supports the
diagnosis of inclusion body myositis (IBM). Joy et
al defined short duration as less than 6 ms and
low amplitude as less than 500 V; long duration
as more than 18 ms and high amplitude as more
than 5 mV (16). A similar pattern can be seen in
other chronic myopathies. Although the patient
in this case had normal nerve conduction studies,
abnormal nerve conduction studies suggesting a
concurrent neuropathic process as part and parcel
of IBM have been described in some patients
with IBM (16,17). A concurrent neuropathy
would help explain the presence of the long-
duration, high-amplitude MUPs sometimes seen
in patients with IBM. The diagnosis of IBM in
this patient is confirmed by muscle biopsy.
CASE 3
A 30-year-old, right-hand-dominant man pre-
sented to his primary care physician complaining
of longstanding weakness and clumsiness. At
age 12 he often tripped and had some difficulty
keeping up with his peers. Later he developed
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358 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

slowly progressive weakness of the face and hand
muscles. His symptoms did not interfere with his
work as a car salesman. He had no difficulty swal-
lowing. There were no complaints referable to
cardiac or pulmonary systems. During the past 6
months he noticed difficulty in releasing his grip,
causing him to seek medical attention. He noted
that his father and one of his three sisters had
similar complaints.
Physical examination reveals an alert man
with normal speech. He has frontal baldness,
early, dusty cataracts, symmetrical wasting of fa-
cial musculature, and mild bilateral temporalis
muscle weakness and atrophy. His neck flexors,
wrist extensors, intrinsic hand muscles, and an-
kle dorsiflexors are weak. He demonstrates bi-
lateral grip myotonia and percussion myotonia
of the thenar muscles. Sensory examination to
all modalities is normal. His CK level is normal.
Electrocardiogram shows first-degree heart
block.
Sensory conduction studies of the right sural
and ulnar nerves, and motor conduction studies of
the right peroneal and ulnar nerves are normal.
Results of the needle EMG done on this patient
are presented in Table 13-3.

TABLE 13-3 CASE 3

Needle EMG Studies

Myotonic
Muscle Discharges Fib. PSW Fasc. CRD Amplitude Duration Polyphasics Recruitment

R Deltoid Normal 0 0 0 0 Normal Normal No Normal

R Biceps Yes 0 0 0 0 Decrease Short No Normal
R Triceps Yes 0 0 0 0 Decrease Short No Normal
R Extensor Yes 0 0 0 0 Decrease Short No Normal
carpi
ulnaris
R Pronator Yes 0 0 0 0 Decrease Short No Normal
teres
R First Yes 0 0 0 0 Decrease Short Yes Early
dorsal
inteross.
R Abductor Yes 0 0 0 0 Decrease Short Yes Early
pollicis
brevis
R Adductor Normal 0 0 0 0 Normal Normal No Normal
longus
R Rectus Yes 0 0 0 0 Decrease Short No Early
femoris
R Peroneus Yes 0 0 0 0 Decrease Short No Early
longus
Tibialis Yes 0 0 0 0 Decrease Short Yes Early
anterior
R Medial Normal 0 0 0 0 Normal Normal No Normal
gastroc-
nemius
Fib., fibrillation potentials; PSW, positive sharp waves; Fasc., fasciculation potentials; CRD, complex repetitive discharges.
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CHAPTER 13 • EVALUATION OF THE PATIENT WITH SUSPECTED MYOPATHY 359

Summary of Findings with pneumonia. The severity of his pulmonary

condition later required intubation and transfer to
This is a 30-year-old man with slowly progressive,
the intensive care unit (ICU). His ICU course was
predominately distal weakness since age 12. The
prolonged (3 months) and complicated. Attempts
normal nerve conduction studies exclude neuropa-
to wean him off the ventilator were unsuccessful;
thy as a cause of his weakness, although slowing of
therefore, the neurology service was consulted for
conduction velocity has been reported in some
evaluation and recommendations.
cases of myotonic dystrophy (18). The presence of
Neurologic examination reveals diffuse mild
myotonic discharges, a spontaneous discharge of
muscle atrophy and profound generalized muscle
muscle fibers in which both the amplitude and the
weakness, more pronounced proximally than dis-
frequency wax and wane, confirms the clinical
tally. There is no associated muscle tenderness.
finding of myotonia (19). Short-duration, low-
Sensory examination is normal. However, there is
amplitude polyphasic MUPs in myotonic dystro-
a mildly decreased response of the muscle stretch
phy are more easily found in the forearm extensors
reflexes. The CK level is normal. Sensory nerve
and tibialis anterior muscles. The concomitant
conduction studies are normal. Motor nerve con-
myopathic pattern, the preferential involvement of
duction studies show CMAPs of slightly smaller
the distal muscles, and the history of similar prob-
amplitudes than normal, but normal conduction
lems in his father and a sister suggest the diagnosis
velocity. Results of the needle EMG done on this
of myotonic dystrophy (18). The diagnosis in this
patient are presented in Table 13-4.
patient is confirmed by DNA testing.

CASE 4
The patient is a 69-year-old white man with
a known history of diffuse large B-cell non-
Hodgkin’s lymphoma of 6 years’ duration. He
was admitted to the general medicine service for
fever and shortness of breath and was diagnosed
Summary of Findings
This is a 69-year-old man who presents with
respiratory distress, severe pneumonia, and a pro-
longed complicated course in the ICU. Several
attempts to wean him off the ventilator failed.
Neurologic examination is suggestive of a myo-
pathic process, as evidenced by the diffuse muscle

TABLE 13-4 CASE 4

Needle EMG Studies

Muscle Fib. PSW Fasc. CRD Amplitude Duration Polyphasics Recruitment

R Deltoid 0 0 None 0 Decreased Short Yes Early

R Biceps 0 0 None 0 Decreased Short Yes Early
First dorsal 0 0 None 0 Decreased Short Yes Early
inteross.
R Vastus 0 0 None 0 Normal Short Yes Early
medialis
R Iliopsoas 0 0 None 0 Normal Normal Yes Early
Adductor 0 0 None 0 Decreased Short Yes Early
longus
Abductor 0 0 None 0 Decreased Short Yes Early
hallucis
Fib., fibrillation potentials; PSW, positive sharp waves; Fasc., fasciculation potentials; CRD, complex repetitive discharges.
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360 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

atrophy and proximal more than distal muscle
weakness. Diminished muscle stretch reflexes are
proportional to the profound muscle weakness.
Sensory function is normal. The needle EMG
shows some voluntary MUPs of short duration
and low amplitude, but no abnormal membrane
irritability is recorded. The electrodiagnostic pic-
ture is consistent with noninflammatory my-
opathy (20). Neuropathy is ruled out by the lack
of sensory signs and symptoms, and essentially
normal nerve conduction studies. There is neither
clinical nor electromyographic evidence of neuro-
muscular junction disorder (21).
The muscle biopsy shows marked cytoskele-
tal disarray, focal areas of myofibril loss, and occa-
sional muscle fiber necrosis and phagocytosis.
These alterations are compatible with critical
care myopathy. Please review Chapter 14 of this
volume for a more detailed review of critical
illness myopathy.
CASE 5
she had been off steroids. However, 5 years ago
she started to experience generalized myalgias
and weakness described as difficulty with lifting,
getting up from a sitting position, or going up
steps. She described no paresthesias or sensory
problems.
Physical examination reveals some difficulty
getting up from a chair without using her hands.
She cannot walk on her heels or her left toes.
Muscle strength is mildly decreased in the prox-
imal muscles of the upper limbs bilaterally. In the
lower limbs the strength is more profoundly im-
paired in the proximal than the distal muscles.
Sensory examination is normal to light touch and
pin prick. Muscle stretch reflexes are normal ex-
cept at the ankles, where they are reduced bilater-
ally. CK levels are increased three-fold.
Sensory and motor conduction studies are
compatible with mild right carpal tunnel syn-
drome but are otherwise normal. Results of the
needle EMG done on this patient are presented in
Table 13-5.

The patient is a 47-year-old woman with a Summary of Findings

known history of sarcoidosis for 30 years. The This is a 47-year-old woman with a history of
disease was well controlled for many years, and longstanding sarcoidosis who presents with a

TABLE 13-5 CASE 5

Needle EMG Studies

Muscle Fib. PSW Fasc. CRD Amplitude Duration Polyphasics Recruitment

L Deltoid 0 0 None 0 Normal Normal No Normal

L Biceps 1
1
None 0 Decreased Short No Normal
L Triceps 0 0 None 0 Normal Normal No Normal
L Vastus 2
2
None 0 Normal Normal No Normal
medialis
L Vastus 1
1
None 0 Normal Normal No Normal
lateralis
L Gastroc- 0 0 None 0 Decreased Short No Normal
nemius
L Tibialis Rare Rare None 0 Decreased Short No Early
anterior
L Iliopsoas 2
2
None 0 Decreased Short No Early
Fib., fibrillation potentials; PSW, positive sharp waves; Fasc., fasciculation potentials; CRD, complex repetitive discharges.
90749_ch13(353-362).ps 8/10/06 3:54 PM Page 361
CHAPTER 13 • EVALUATION OF THE PATIENT WITH SUSPECTED MYOPATHY
Figure 13-1 ● Normal motor units during
full contraction. Sweep is 10 ms/division. Gain is
2 mV/division.
clinical picture suggestive of myopathy. The
physical examination supports myopathy. Needle
EMG of several muscles in the upper and lower
limb demonstrate patchy abnormal membrane
irritability. Some voluntary MUPs are short in
duration and low in amplitude and show early
Figure 13-2 ● Motor units during full con-
traction in myopathy. Sweep is 10 ms/division.
Gain is 2 mV/division.
361
Figure 13-3 ● Motor units during full con-
traction in neuropathy. Sweep is 10 ms/divi-
sion. Gain is 2 mV/division.
recruitment. The findings are consistent with
patchy inflammatory myopathy (22).
The muscle biopsy is striking for the presence
of focal areas of dense mononuclear cell collections
and granulomatous change compatible with sar-
coid myopathy. Pure sarcoid myopathy is a rare
disease, the diagnostic hallmark of which is the
non-caseating granuloma (23). Three distinct
forms have been described: subacute myositis with
proximal weakness, myalgias, and fever; chronic
myopathy with diffuse atrophy and progressive
symmetrical weakness; and nodular sarcoid my-
opathy with palpable nodes. Sarcoid myopathy
presenting solely with distal weakness has been
reported (24).
Figures 13-1, 13-2, and 13-3 show the relative
amplitudes of MUPs in normal persons and in
those with myopathy and neuropathy, respec-
tively. The recordings were made at the same
amplifier gain and sweep speed settings.
REFERENCES
1. Bohan A, Peter JB. Polymyositis and dermato-
myositis (second of two parts). N Engl J Med
1975;292:403–407.
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2. Bohan A, Peter JB. Polymyositis and dermato-
myositis (first of two parts). N Engl J Med 1975;
292:344–347.
3. Bronner IM, Linssen WH, van der Meulen MF,
et al. Polymyositis: an ongoing discussion about a
disease entity. Arch Neurol 2004;61:132–135.
4. LoVecchio F, Jacobson S. Approach to general-
ized weakness and peripheral neuromuscular
disease. Emerg Med Clin North Am 1997;15:
605–623.
5. Kimura J. Myasthenia gravis and other disorders
of neuromuscular transmission. In: Kimura J,
ed. Electrodiagnosis in diseases of nerve and muscle:
principles and practice, 3rd ed. New York: Oxford
University Press, 2001:754–758.
6. Lacomis D. Electrodiagnostic approach to the
patient with suspected myopathy. Neurol Clin
2002;20:587–603.
7. Smith EA, LeRoy EC. Systemic sclerosis: etiol-
ogy and pathogenesis. In: Klippel JH, Dieppe
PA, eds. Rheumatology, 2nd ed. London: Mosby,
1998:7.10.1–7.10.2.
8. Amato AA, Dumitru D. Acquired neuropathies.
In: Amato AA, Dumitru D, Zwarts MJ, eds. Elec-
trodiagnostic medicine, 2nd ed. Philadelphia: Han-
ley & Belfus, 2002:969–970.
9. Wigley FM. Systemic sclerosis: clinical features.
In: Klippel JH, Dieppe PA, eds. Rheumatology,
2nd ed. London: Mosby, 1998:7.9.7.
10. Medsger TA, Oddis CV. Inflammatory muscle
disease. In: Klippel JH, Dieppe PA, eds.
Rheumatology, 2nd ed. London: Mosby, 1998:
7.13.1–7.13.6.
11. Keesey JC. AAEE Minimonograph #33: Electro-
diagnostic approach to defects of neuromuscular
transmission. Muscle Nerve 1989;12:613–626.
12. Stalberg E. Invited review: Electrodiagnostic as-
sessment and monitoring of motor unit changes
in disease. Muscle Nerve 1991;14:293–303.
13. Milanov I, Ishpekova B. Differential diagno-
sis of chronic idiopathic polymyositis and neu-
romyositis. Electromyogr Clin Neurophysiol 1998;
38:183–187.
14. Kimura J. Myopathies. In: Kimura J, ed. Elec-
trodiagnosis in diseases of nerve and muscles: prin-
ciples and practice, 3rd ed. New York: Oxford
University Press, 2001:798–801.
15. Robinson LR. AAEM case report #22: polymyosi-
tis. Muscle Nerve 1991;14:310–315.
16. Joy JL, Oh SJ, Baysal AI. Electrophysiological
spectrum of inclusion body myositis. Muscle
Nerve 1990;13:949–951.
17. Arnardottir S, Svanborg E, Borg K. Inclusion
body myositis: sensory dysfunction revealed with
quantitative determination of somatosensory
thresholds. Acta Neurol Scand 2003;108:22–27.
18. Streib EW. AAEE minimonograph #27: differ-
ential diagnosis of myotonic syndromes. Muscle
Nerve 1987;10:603–615.
19. Simpson JA, ed. Neuromuscular diseases. Hand-
book of electroencephalography and clinical neuro-
physiology, vol. 16, pt. B. Amsterdam: Elsevier,
1973.
20. Buchthal F. Electromyography in the evaluation
of muscle diseases. Neurol Clin 1985;3:573–598.
21. Howard JF Jr, Sanders DB, Massey JM. The
electrodiagnosis of myasthenia gravis and the
Lambert-Eaton myasthenic syndrome. Neurol
Clin 1994;12:305–330.
22. Takuma H, Murayama S, Watanabe M, et al. A
severe case of subacute sarcoid myositis. J Neurol
Sci 2000;175:140–144.
23. Berger C, Sommer C, Meinck HM. Isolated sar-
coid myopathy. Muscle Nerve 2002;26:553–556.
24. Robberecht W, Theys P, Lammens M, et al. Dis-
tal myopathy as the presenting manifestation of
sarcoidosis. J Neurol Neurosurg Psychiatry 1995;
59:642–643.
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CHAPTER 14
Neuromuscular Complications
of Critical Illness: Evaluation
of the Patient with a Suspected
Critical Illness Neuromuscular
Disorder
Daniel M. Clinchot
INTRODUCTION
Critical illness neuromuscular disorders are more
common than you might first think. The literature
is full of cases of individuals who have survived
being critically ill only to emerge with profound
neuromuscular dysfunction. Critical illness neuro-
muscular disorders are poorly understood, yet they
often have serious clinical and functional impact.
When a patient develops a critical illness neuro-
muscular disorder, there is usually a concomitant
increase in ventilatory time, time in the intensive
care unit (ICU), time in the hospital, and morbid-
ity and mortality; thus demonstrating greatly in-
creased health system costs related to such care.
Spitzer et al reported that 62% of patients with pro-
longed weaning from ventilation had an unsus-
pected neuromuscular disorder (1). The greatest
mortality in patients who develop critical illness
neuromuscular disorder results from the underly-
ing medical condition that resulted in the patient
becoming critically ill. However, patients who be-
come critically ill and survive their ICU stay often
go on to have significant impairment directly re-
lated to a critical illness neuromuscular disorder.
DeJonghe (2) reported on 95 patients who were
ventilated for greater than 7 days and went on to
awaken and improve. The incidence of critical ill-
ness neuromuscular dysfunction in these patients
was 25.3%. Although there is no definitive treat-
ment for these disorders, detection enables the
health care team to intervene and plan appropri-
ately. Specifically, preventing secondary complica-
tions of weakness and altered sensory function will
enable the critical illness neuromuscular disorder
to have the least amount of functional impact once
the patient begins to improve from a medical ill-
ness standpoint. Lastly, familiarity with critical ill-
ness disorders assists the intensive care specialist in
designing and implementing ventilatory weaning
strategies.
Descriptions of neuromuscular complications
of critical illness date as far back as the 1800s, when
Sir William Osler described a syndrome of muscu-
lar wasting in an individual who had survived sep-
sis (3). As the care of the critically ill became more
advanced, so did the spectrum of critical illness
neuromuscular disorders. In the 1960s and 1970s
unexplained neuropathies were described in pa-
tients who had been in a coma or who had been se-
riously burned or septic (4–6). In 1977 Bischoff and
Rich described a polyneuropathy associated with
gentamicin toxicity (7). Aminoglycoside toxicity
has been linked to neuromuscular disorders such
363
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364 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
as disorders of the neuromuscular junction and
neuropathy regardless of whether the patient is
critically ill (8). The term “critical illness polyneu-
ropathy” was not coined until the early 1980s. At
that time the full spectrum of critical illness neuro-
muscular disorders was not yet understood. In the
late 1980s and 1990s we begin to see descriptions of
a neuromuscular syndrome associated with indi-
viduals who have chronic obstructive pulmonary
disease (COPD) or asthma, and who become criti-
cally ill and require intravenous corticosteroid
therapy. Subsequently the association between
nondepolarizing neuromuscular blocking agents
and peripheral neuropathy became clear. In 1998
Coakley et al (9) performed electrophysiologic
studies on 44 patients who were critically ill and
required an ICU stay greater than 7 days. These
electrodiagnostic studies revealed that only 9% of
patients were normal; 43% of these patients had
mixed sensory and motor nerve dysfunction. They
could find no association between the type of criti-
cal illness neuromuscular disorder that developed
and the Acute Physiology and Chronic Health
Evaluation (APACHE II) score, organ failure
score, or the presence or absence of sepsis.
DIAGNOSTIC CONSIDERATIONS
Critically ill patients who require ICU care and
mechanical ventilation are all too often noncom-
municative. They are thus unable to relay feelings
of weakness or sensory abnormalities to the health
care team. It is because of this that the patient
with a critical illness neuromuscular disorder typ-
ically presents when the health care team deter-
mines that there is difficulty weaning from the
ventilator (10). Unfortunately, even in cases with
significant weakness or sensory abnormality, the
critical illness neuromuscular disorder can remain
undiagnosed (11).
When seeing the patient who is critically ill
and weak for an electrodiagnostic medicine consul-
tation, the clinician should recall the broad differ-
ential diagnosis for individuals with weakness. The
articles by Wijdicks et al (12,13) provide a nice
mnemonic of the word “muscle” to support re-
membering the different diagnostic entities that
should be considered when evaluating a patient
with weakness (Fig. 14-1).
The initial electrodiagnostic medicine patient
assessment should include a detailed history and
physical examination. In the history, the clinician
specifically needs to determine:
1. The time course of the critical illness
2. If and when the patient developed multiorgan
dysfunction syndrome or sepsis
3. Bacterial or viral organisms responsible for
infection or sepsis
4. The medications that have been administered
during the course of the critical illness
5. The time course of administering corticos-
teroids, nondepolarizing neuromuscular junc-
tion blocking agents, and aminoglycosides
(these are of particular importance)
6. The premorbid level of function of the person
is important in understanding if the current
level of functioning is a change.
Along with the history, a detailed physical
examination not only serves to confirm weakness
but also allows the clinician to begin to categorize
the process as upper or lower motor neuron, in-
volving sensory and/or motor components or
involving the neuromuscular junction. It is im-
portant for the clinician to examine for muscle
atrophy and tenderness and assess reflexes and
sensation. Although difficult in the noncommu-
nicative patient, making some assessment of mo-
tor strength is important. In the conscious but
uncooperative patient, observation of sponta-
neous limb movements will enable the clinician
to determine if the patient has at least antigravity
strength. Although mental status can be affected
as a prodrome of sepsis and critical illness, criti-
cal illness neuromuscular disorders themselves
typically do not affect mental status. Noting par-
ticular patterns of weakness is important in the
initial patient assessment. Critical illness neuro-
muscular disorders are typically symmetric and
do not involve the face. If cranial nerve involve-
ment is present on physical examination, then the
clinician should be suspicious for a noncritical
illness–related disorder, such as Guillain-Barré
syndrome (GBS). Bolton (14) has developed a
helpful flow chart (Fig. 14-2) to assist the clini-
cian in determining the appropriate process for
evaluating the critically ill patient who develops
weakness.
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CHAPTER 14 • NEUROMUSCULAR COMPLICATIONS 365

M edication (intravenous administration of corticosteroids, panucuronium, vecuronium,

metronidazole, amiodarone, or zidovudine)

U ndiagnosed neuromuscular disorder (PM, DM, ALS, GBS, MG, LEMS, acid maltase
deficiency, mitochondrial myopathy, or muscular dystrophy)

S pinal cord damage (ischemic, compressive hematoma, or trauma)

C ritical illness neuromuscular disorder

L oss of muscle mass (disuse atrophy, rhabdomyolysis, or catabolic state)

E lectrolyte disorders (hypokalemia, hypermagnesemia, or hypophosphatemia)

S ystemic illness (acute prophyria, AIDS, vasculitis neuropathy, or endocrine myopathies)

Figure 14-1 ● Mnemonic for remembering differential diagnosis of weakness in the

critically ill. (Modified from Wijdicks EF, ed. Neurologic complications of critical illness, 2nd ed. New York:
Oxford University Press, 2002:69, with permission.)

In summary, the unexpected failure of ven-
tilatory weaning, accelerated peripheral muscle
atrophy, or an inability to hold the head or a limb
off the bed should be clues to the health care team
that a critical illness neuromuscular disorder is
present. Lack of ventilatory weaning appears to be
the most common patient presentation for a criti-
cal illness disorder. However, the inability to wean
from a ventilator is not only a means of patient
presentation, but in a clinical analysis of patients
with critical illness neuromuscular disorders it was
also found to be independently predicted by the
development of a critical illness neuromuscular
disorder (15).
ETIOLOGIC CONSIDERATIONS
The cause of critical illness neuromuscular disor-
ders is not clear, and it is likely multifactorial. One
thing that has become quite clear is that the sys-
temic inflammatory response syndrome (SIRS)
plays a significant role (16). The SIRS is a severe,
overwhelming systemic response that occurs in
individuals who become critically ill.
The term “SIRS” was coined in 1992 during
a consensus conference between the Society of
Critical Care Medicine and the American College
of Chest Physicians (ACCP) (17). Bolton (16) has
highlighted the significant role that the SIRS has
in the development of critical illness neuromuscu-
lar disorders. The SIRS is a response that consists
of both humoral and cellular components. These
two components act together to create an environ-
ment in which the neuromuscular system becomes
vulnerable to toxic effects. The humoral factors
involved include cytokines, interleukins, arachi-
donic acid, proteases, free oxygen radicals, and
tumor necrosis factor. The cellular responses
typically involve monocytes, lymphocytes, and
macrophages.
The exact trigger for the SIRS can be varied.
Infection, severe trauma, burns, organ transplan-
tation, or other severe bodily assaults can set the
cascade of the SIRS in motion (Fig. 14-3). Once ac-
tivated, the SIRS results in significant vasodilation
and sluggish flow within the most distal compo-
nents of the vascular system. Sluggish flow within
capillaries results in a reduced capacity to remove
toxic substances that are the byproducts of cellular
metabolism. This results in the neuromuscular
system becoming vulnerable. The oxygen debt
within the tissue and inadequate nutrient delivery
create an ideal milieu for injury. In addition, toxic
agents such as nondepolarizing neuromuscular
blocking agents or steroids have greater potential
to cause direct injury to both nerves and muscles
(Fig. 14-4). Thus, when considering aminoglyco-
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366 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

Limb and
respiratory
weakness

Evidence Yes MRI of Yes

of spinal cord spinal cord Abnormal Treat
lesion ?

No No

Electro-
physiology

No No Motor No NMJ No
Normal Neuropathy neuron transmission Myopathy
disease defect

Yes Yes Yes Yes

Muscle bx
No CK etc.
Axonal Demyelinating

Yes

MRI of spinal CIP Motor Cahexia

MG, LEMS
cord, CT of axonal GBS GBS etc. neuron necrosis
drugs, etc.
head, EEG etc. disease etc.

Figure 14-2 ● Flow chart outlining assessment of critically ill patients with weakness.
(Reprinted from Bolton CF. Neuromuscular conditions in the intensive care unit. Intensive Care Med
1996;22:841–843, with permission.)

side toxicity, the activation of the SIRS would be
expected to enhance the development of direct
neurotoxic effects.
Neuromuscular complications of critical ill-
ness can be classified as follows:
• Thick filament myopathy
• Acute necrotizing myopathy of intensive care
• Catabolic myopathy
• Neuromuscular junction abnormalities
• Neuromyopathy

• Neuropathy This classification is helpful for the elec-

• Critical illness polyneuropathy tromyographer in conceptualizing and classifying
• Acute motor neuropathy associated with non- the appropriate diagnosis within the context of the
depolarizing neuromuscular blocking agents clinical and electrodiagnostic findings. This is ex-
• Critical illness myopathy tremely important as the different critical illness
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CHAPTER 14 • NEUROMUSCULAR COMPLICATIONS 367

Infection Trauma

Bacteria, viruses, fungi

Physical, surgical,
burns, chemicals
Sepsis

Systemic inflammatory response syndrome (SIRS)

Single or multiple Neuromuscular Steroid

organ failure blocking agents

Septic Critical illness Critical illness

encephalopathy polyneuropathy myopathy

Figure 14-3 ● Systemic inflammatory response syndrome (SIRS). (Reprinted from Bolton CF.
Neuromuscular manifestations of critical illness. Muscle Nerve 2005;32:140–163, with permission)

Microbial or traumatic
stimulus

Humoral response Cellular response

Rolling neutrophils
Endothelial Increased capillary Fibrin platelet
cell damage permeability Adhesion aggregates
molecules

Deactivated protein C

Increased nitric oxide Sluggish capillary flow

Arteriolar
smooth muscle
vasodilatation

Figure 14-4 ● Microcirculation changes that result from the activation of the SIRS.
(Reprinted from Bolton CF. Neuromuscular manifestations of critical illness. Muscle Nerve 2005;32:140–163,
with permission.)
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368 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
neuromuscular disorders can have very different
functional outcomes (18).
It is also clear that critical illness neuromus-
cular disorders develop in the pediatric popula-
tion. The spectrum of critical illness disorders
mimics those found in adults (19). It is important
to note, however, that the greatest amount of liter-
ature describing critical illness neuromuscular
disorders appears in the adult literature.
NEUROPATHIC CONDITIONS
CASE 1
A 65-year-old woman was admitted to the hospi-
tal with bilateral lobar pneumonia secondary to
Pseudomonas aeruginosa. Her oxygenation pro-
gressively worsened and she developed septic
shock. She required intubation and mechanical
ventilation. During her ICU stay she received
dopamine, amikacin, fentanyl, lorazepam, and
vecuronium. On day 22, as the clinical picture
improved, the nursing staff noted that she had
limb weakness. Neurologic examination revealed
flaccid paralysis and areflexia. After her medical
condition improved she required 3 weeks of in-
patient rehabilitation prior to being able to return
home.
Critical Illness Polyneuropathy
Critical illness polyneuropathy (CIPN) is the best
described and most studied critical illness neuro-
muscular disorder. CIPN is an acute, diffuse,
mainly motor peripheral neuropathy due to axonal
dysfunction. The predominance of motor involve-
ment in CIPN was best described by Hund et al
(20) in a study of 28 patients with moderate to se-
vere CIPN. The electrophysiologic studies on
these patients revealed that 50% of the subjects had
compound muscle unit action potential (CMAP)
amplitudes that were smaller than 50% of the
lower limit of normal (20).
CIPN typically occurs in patients who have
sepsis or multiorgan system dysfunction. The inci-
dence has been reported to be 50% to 75% in indi-
viduals who meet these criteria (16,21,22). The
severity of the peripheral neuropathy has been
found to be proportional to the length of time
an individual has been in the ICU. The typical
presentation of individuals with CIPN is difficulty
weaning from the ventilator. However, it has also
been described as presenting with tetraplegia and
absent deep tendon reflexes. The blood creatine ki-
nase (CK) levels in CIPN are normal.
A period of confusion with impaired atten-
tion, concentration, and orientation has been de-
scribed 2 weeks prior to the onset of CIPN. This
confusional state has been termed “septic en-
cephalopathy” (23). Cerebrospinal fluid studies
during this period have been reported as normal
except for very mild elevations in protein (18,22,24).
In 1987 Zochodne et al (25) reported on 19
patients with CIPN. They found moderate to
severe weakness in 47% of patients, sensory dis-
turbance in 47% of patients, and reduced or absent
reflexes in 68% of patients. Consistent with cur-
rent studies, they found a mortality rate of 58% in
their cohort (25). Lejten et al (10), in a study of
38 patients who were ventilated for greater than
7 days, found that the development and severity
of CIPN were associated with multiple organ
dysfunction syndrome.
There have been numerous studies that have
linked various conditions with the development
of CIPN. Hyperglycemia and hypoalbuminemia
have both been associated with the development
of CIPN (21,25). There has been an association
made with individuals who are receiving par-
enteral nutrition and the development of CIPN
and multiorgan system dysfunction (26). It has
been suggested that artificial nutrition in some
critically ill patients is toxic because of nutrient
intolerance. The specific parameters that indicate
the onset of nutrient intolerance so that artificial
nutrition can be modulated have yet to be delin-
eated. The exact mechanism by which axonal in-
jury occurs is unclear. It has been suggested that
nutritional axonal injury results from glucose-
induced depletion of intracellular phosphate
stores, with subsequent depletion of high-energy
phosphate compounds and the oxidative modifi-
cation of dietary lipids.
The electrodiagnostic findings in CIPN are
typical of an axonal sensory and motor peripheral
neuropathy. The motor and sensory nerve con-
duction velocities and distal latencies are typically
normal, without evidence of conduction block.
There is a mild reduction in the sensory nerve
90749_ch14(363-376).ps 8/10/06 3:55 PM Page 369

CHAPTER 14 • NEUROMUSCULAR COMPLICATIONS 369

Classification of findings in CIPN

Severe SNAP absent, fibrillation potentials in all muscle groups, and
multiple CMAP amplitudes less than 1mv amplitude
Moderate SNAP amplitudes <5 µV, after averaging 20 trials,
multiple CMAP amplitudes between 1 and 3 mV,
fibrillation potentials and positive sharp waves in
distal muscles and occasionally present in
more proximal muscles
Mild SNAP amplitudes >5 µV, CMAP amplitudes >3 mV,
occasional positive sharp waves in distal muscles

Figure 14-5 ● Classification of findings in critical illness polyneuropathy (CIPN). (Modified

from Spitzer AR, Giancarlo T, Maher L, et al. Neuromuscular causes of prolonged ventilator dependency.
Muscle Nerve 1992;15:682–686, with permission.)

action potentials (SNAP) and a significant reduc- multiorgan dysfunction syndrome have failed to
tion in CMAP amplitudes. Repetitive nerve stimu- show any benefit of IVIG with respect to the
lation (RNS) does not show a defect in neuro- development and time course of peripheral neu-
muscular transmission. Needle electromyography ropathy in critical illness (30). The prognosis for
typically reveals positive waves and fibrillation individuals who develop CIPN most closely re-
potentials with neuropathic motor unit potentials lates to the underlying disorder; however, with all
(MUPs) in a proximal-to-distal gradient, with other covariables being equal, the neuropathy typ-
proximal muscles showing greater involvement in ically improves over weeks to months once the pa-
more severe cases. Spitzer et al (1) have proposed a tient’s nutritional status improves. Many patients
way to categorize the electrodiagnostic findings in with severe neuropathy go on to have residual
CIPN as a measure of severity (Fig. 14-5). These functional impairment for years afterward.
categories of severity are expected to reflect the
prognosis for recovery from the neuropathy.
Single-fiber electromyographic studies in pa-
tients with suspected critical illness neuromuscular
disorders have shown an increase in jitter in pa-
tients who develop CIPN (27). It is unclear whether
primary neuromuscular junction dysfunction is
present, since the increased jitter could be caused
by the presence of new endplates as reinnervation
occurs.
Nerve biopsy findings in CIPN typically re-
veal primary axonal degeneration of motor and
sensory fibers that primarily affect the distal seg-
ments (Fig. 14-6). Close examination of slides fails
to reveal any evidence of inflammation. Muscle Figure 14-6 ● Cross-section of a nerve in a
patient with critical illness neuropathy at
biopsy typically shows grouped fiber atrophy, es-
115
magnification showing loss of myeli-
pecially when the neuropathy has been present for
nated fibers. (Reprinted from Kerbaul F, Brousse
a significant period of time (28). M, Collart F, et al. Combination of histopathological
Early studies suggested that the use of in- and electromyographic patterns can help to evaluate
travenous immunoglobulin (IVIG) may help to functional outcome of critical ill patients with neuro-
protect against the development of severe CIPN muscular weakness syndromes. Critical Care 2004;8:
(29). Other open trials in patients with sepsis or 358–365, with permission.)
90749_ch14(363-376).ps 8/10/06 3:55 PM Page 370
370 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
Acute Motor Neuropathy Associated
with Nondepolarizing Neuromuscular
Blocking Agents
This critical illness neuromuscular disorder is typ-
ically associated with the use of nondepolarizing
neuromuscular blocking agents. Its development
has specifically been associated with the adminis-
tration of pancuronium or vecuronium. Each of
these agents has a metabolite that retains neuro-
muscular blocking activity and can accumulate in
the body with prolonged use. The active metabo-
lite of pancuronium is 3-desacetyl-pancuronium;
the active metabolite of vecuronium is 3-desacetyl-
vecuronium. These agents are primarily processed
through the kidneys and liver; thus, they are more
likely to accumulate in individuals with renal dis-
ease, and they accumulate to an even greater extent
in patients who have combined renal and hepato-
biliary disease.
Acute motor neuropathy associated with non-
depolarizing neuromuscular blocking agents likely
results from the direct neurotoxic effects of the
nondepolarizing neuromuscular blocking agents
in association with the SIRS. The triggering of the
SIRS results in microvascular changes that allow
these agents to be in contact with the neuromuscu-
lar system for a greater period of time than they
would be otherwise. Sluggish flow and metabolic
waste buildup further enhance the probability of
nerve or muscle injury. Studies have shown that
the longer these nondepolarizing neuromuscular
blocking agents are used, the more likely that neu-
ropathy will occur (31–33). In fact, the incidence of
acute motor neuropathy associated with nondepo-
larizing neuromuscular blocking agents increases
when nondepolarizing agents are used for greater
than 48 hours (33).
The electrodiagnostic findings in acute motor
neuropathy associated with nondepolarizing neu-
romuscular blocking agents are typical of an ax-
onal motor neuropathy. The motor and sensory
nerve conduction velocities and distal latencies are
typically normal, without evidence of conduction
block. There is a reduction in the CMAP ampli-
tudes with a relative preservation of the SNAP
amplitudes (34). RNS does not show a defect in
neuromuscular transmission. Needle electromyo-
graphy typically reveals positive waves and fibril-
lation potentials with reduced numbers of motor
unit potentials in a neuropathic recruitment pat-
tern. The motor unit potentials are typically of
long duration and polyphasic.
Nerve biopsy findings in acute motor neu-
ropathy associated with nondepolarizing neuro-
muscular blocking agents reveal primary axonal
degeneration of motor fibers. Muscle biopsy typi-
cally shows varying degrees of denervation, fiber
atrophy, and muscle necrosis. The prognosis for
individuals who develop acute motor neuropathy
associated with nondepolarizing neuromuscular
blocking agents appears to be somewhat better
than CIPN (31). Recovery of motor function oc-
curs over weeks to months, with some patients
having functional impairment years after the
development of this neuropathy.
MYOPATHIC CONDITIONS
CASE 2
A 72-year-old man with a history of chronic alco-
holism and COPD was admitted to the hospital in
respiratory failure. He required intubation and
mechanical ventilation. The patient was found to
have pneumonia secondary to Klebsiella pneumo-
niae. He was very difficult to oxygenate. During
his ICU stay he received dexamethasone, methyl-
prednisolone, promethazine, ceftriaxone, gentam-
icin, fentanyl, and vecuronium. After being sta-
bilized it was difficult to wean him from the
ventilator. On day 19 it was noted that he was
alert but not moving his limbs. Facial muscles
were mildly weak and sensory examination was
normal. His CK was elevated at 2,090 IU/L.
As the medical issues resolved, the patient became
stronger. At 6-month follow-up he still needed as-
sistance with activities of daily living, but he was
ambulating short distances with a walker and
assistance.
Thick Filament Myopathy
This critical illness neuromuscular disorder most
often occurs in patients who develop a severe and
sudden asthma or COPD exacerbation. These indi-
viduals typically receive high doses of corticos-
teroids and/or nondepolarizing neuromuscular
blocking agents. There have been associations
90749_ch14(363-376).ps 8/10/06 3:55 PM Page 371
CHAPTER 14 • NEUROMUSCULAR COMPLICATIONS
made between the use of these agents and the
development of the thick filament myopathy. Cor-
ticosteroid use alone can contribute to the develop-
ment of this myopathy. The length of chemical
paralysis, when used in conjunction with corticos-
teroids, has been associated with the development
of thick filament myopathy (35,36).
Douglass et al (37) have shown that the serum
CK level is elevated in 76% of patients with severe
asthma exacerbations who require ventilation.
They also found that 36% of these individuals go
on to develop a symptomatic myopathy. The study
assessed for any metabolic disturbance contribut-
ing to the elevated CK level and did not reveal any
difference between patients who received hydro-
cortisone or dexamethasone. In addition, they
found no association with the dose of corticos-
teroid used and the development of myopathy
(37). Based on the work of Dubois and Almon
(38), there has been some association made with
the development of thick filament myopathy in
patients who receive corticosteroids. Dubois and
Almon found that the number of glucocorticoid
receptors increase to three times normal after
surgical interruption of the nerve supply. This
suggests that a denervated muscle cell may be
hypersensitive to corticosteroids and vulnerable to
catabolism.
Patients with thick filament myopathy typi-
cally present with difficulty to wean from the
ventilator and flaccid limb weakness of both dis-
tal and proximal muscles. The muscles of the
face are typically involved, but to a milder extent
than the limb weakness. Patients with thick fila-
ment neuropathy should have a normal sensory
examination. Muscle stretch reflexes are signifi-
cantly reduced or absent. CK levels are mildly to
moderately increased.
The electrodiagnostic findings in thick fila-
ment myopathy include normal sensory nerve
latencies and conduction velocities and normal
SNAP amplitudes. The motor latency and conduc-
tion velocity are also normal. The CMAP ampli-
tude is reduced in proportion to the severity of the
myopathy, without evidence of conduction block.
RNS does not show a defect in neuromuscular
transmission. Needle electromyography typically
reveals reduced insertional activity with posi-
tive waves and fibrillation potentials. Motor unit
analysis reveals short-duration, low-amplitude
371
Figure 14-7 ● Transmission electron mi-
crograph of patient with thick filament
myopathy (longitudinal section) showing
almost total loss of thick filaments and
vacuoles (arrow). (Reprinted from Stibler H,
Edstrom L, Ahlbeck K, et al. Electrophoretic deter-
mination of the myosin/actin ratio in the diagnosis of
critical illness myopathy. Intensive Care Med 2003;29:
1515–1527, with permission.)
polyphasic motor unit potentials that display an in-
crease in recruitment pattern, which is the pattern
associated with myopathy.
Muscle biopsies in patients with thick fila-
ment myopathy typically show loss of structure
centrally (39). This is thought to be the result of
the destruction of the thick myosin filaments
(Fig. 14-7). There is typically a pattern of fiber at-
rophy, necrosis, and regeneration of both type I
and II muscle fibers in these biopsies. There is lit-
tle or no associated inflammation. The prognosis
for individuals who develop thick filament my-
opathy is typically a gradual recovery of strength.
In severe cases patients have ongoing functional
impairment years after the development of the
myopathy.
Acute Necrotizing Myopathy
of Intensive Care
Acute necrotizing myopathy of intensive care oc-
curs in the presence of overwhelming infections
with organisms such as viruses, Escherichia coli,
Leptospirosis, Legionella, and organisms that can
cause toxic shock syndrome. Patients with this
90749_ch14(363-376).ps 8/10/06 3:55 PM Page 372
372 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
myopathy typically present with fever, severe
weakness, and myalgias in the presence of very
high concentrations of CK and myoglobinuria.
The electrodiagnostic findings in acute
necrotizing myopathy of intensive care include
normal sensory latencies and conduction veloci-
ties, and normal SNAP amplitudes. The motor
conduction velocity is normal; the CMAP ampli-
tude is reduced in proportion to the severity of the
myopathy. Motor conduction studies reveal no
evidence of conduction block. RNS does not show
a defect in neuromuscular transmission. Needle
electromyography typically reveals reduced inser-
tional activity with widespread positive waves
and fibrillation potentials. Motor unit analysis re-
veals short-duration, low-amplitude polyphasic
motor unit potentials that display early recruit-
ment pattern (i.e., myopathic type). Muscle biopsy
in patients with thick filament myopathy typi-
cally shows less severe and widespread fiber
necrosis (Fig. 14-8). There is little or no associated
inflammation.
The prognosis for individuals who develop
acute necrotizing myopathy of intensive care
is similar to that of thick filament myopathy.
Gradual increase in strength and function occurs
over the course of months to years. Most impor-
tantly, patients have a greater mortality than with
thick filament myopathy, but that mortality rate is
Figure 14-8 ● Cross-section of a biopsy
from a patient with acute necrotizing neu-
ropathy of intensive care. (Reprinted from
Kerbaul F, Brousse M, Collart F, et al. Combination
of histopathological and electromyographic patterns
can help to evaluate functional outcome of critical ill
patients with neuromuscular weakness syndromes.
Critical Care 2004;8:358–365, with permission.)
that which is associated with the underlying
pathology.
Catabolic Myopathy
Catabolic myopathy is an ill-defined critical illness
neuromuscular disorder. It is believed to result
from the action of interleukin-1 and tumor necro-
sis factor. Catabolic myopathy is thought to result
from a defect in high-energy metabolites in pa-
tients with respiratory failure, cardiogenic shock,
severe congestive heart failure, gastric bypass, and
sepsis. This myopathy is believed to develop as a
result of severe malnutrition and wasting in the
presence of critical illness. Electrodiagnostic test-
ing typically reveals normal nerve stimulation
studies and needle examination (18).
Muscle biopsy in patients with catabolic my-
opathy typically shows type II muscle fiber atro-
phy. There is no associated inflammation. The
prognosis for individuals who develop catabolic
myopathy of intensive care is directly related to
the outcome of the underlying disorder.
DIFFERENTIATING MYOPATHY
AND NEUROPATHY
It can be difficult for the electromyographer to
distinguish between myopathy and peripheral
neuropathy in the critically ill. The ICU setting
complicates the performance of a complete electro-
diagnostic examination. Interference from sur-
rounding life-sustaining equipment and ICU noise
can reduce the sensitivity of the examination. Di-
rect muscle stimulation has been posed as a means
to assist the electromyographer in distinguishing
between critical illness–related myopathy and neu-
ropathy, especially in cases where a distal CMAP is
unobtainable. Direct muscle stimulation is typically
done by using a monopolar needle as the cathode
and a surface or subdermal needle as the anode.
Stimulation is performed in the distal third of the
muscle in an attempt to avoid the endplate zone.
Beginning with a pulse duration of 0.1 ms at 0.5
Hz, the muscle is stimulated at various depths
while simultaneously increasing the intensity until
a twitch can be palpated at the lowest stimulus in-
tensity. A concentric recording needle is then in-
serted 15 to 25 mm proximal to the stimulating
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CHAPTER 14 • NEUROMUSCULAR COMPLICATIONS
electrode and perpendicular to the skin. This elec-
trode is adjusted until a maximal amplitude is ob-
tained (40,41). In critical illness–related neuropathy
the denervated muscles should retain electrical
excitability and the direct muscle-stimulated
CMAP amplitude should be normal. In critical
illness–related myopathy the muscle fibers lose ex-
citability, and thus the direct muscle-stimulated
CMAP amplitude is reduced (40).
NEUROMUSCULAR JUNCTION
CONDITIONS
Neuromuscular junction abnormalities in critical
illness include a transient, persistent neuromus-
cular blockade that occurs with the use of nonde-
polarizing neuromuscular blocking agents. This
disorder is identified after the medications are
discontinued. This scenario typically develops in
patients who have renal and hepatobiliary dis-
ease. Patients present with failure to wean from
the ventilator and flaccid limbs. Sensation is
normal.
The electrodiagnostic findings in individuals
with persistent neuromuscular blockade include
normal sensory and motor nerve conduction ve-
locities, and the SNAP amplitude and latency is
normal. In severe cases CMAP amplitudes are re-
duced or unobtainable, but the motor conduction
studies reveal no evidence of conduction block.
RNS reveals a neuromuscular transmission defect
through a decremental response at 2 or 3 Hz
stimulation. Needle electromyography typically
reveals normal insertional and membrane activity.
Motor unit analysis reveals normal motor unit
morphology and recruitment patterns, except
in severe cases, where small-amplitude, short-
duration MUPs can appear.
Patients with persistent neuromuscular
blockade typically recover over the course of
weeks to months. The development of persistent
neuromuscular blockade has been associated with
metabolic acidosis, elevated plasma concentra-
tions of magnesium, and female gender. Interest-
ingly, the total dose, rate of administration, and
duration of treatment with nondepolarizing neu-
romuscular blocking agents do not correlate with
the development of persistent neuromuscular
blockade (42).
373
NEUROMYOPATHY
The term “critical illness neuromyopathy” has been
used to describe critically ill patients who develop a
combination of neuropathy and myopathy. This
scenario typically involves CIPN and the acute
necrotizing myopathy of intensive care. It has been
estimated to occur in over 6% of patients with a
critical illness neuromuscular disorder. The pres-
ence of one neuromuscular complication of critical
illness may create an environment that facilitates
the development of a second process. Nates (22) de-
scribes a scenario in which the presence of a
myopathy or neuropathy results in further immo-
bilization and may create an environment that
facilitates the development of the other.
MANAGEMENT
There is no current effective treatment for critical
illness neuromuscular disorders. Prompt identifi-
cation and management of underlying conditions
such as sepsis or multiorgan system dysfunction
will likely result in a decreased incidence of these
syndromes. Control of serum glucose levels can
potentially reduce the incidence of CIPN. Judi-
cious use of corticosteroids and nondepolarizing
neuromuscular blocking agents, as well as reduc-
ing the incidence of hypoalbuminemia, will likely
modulate the incidence and severity of critical
illness neuromuscular disorders.
OUTCOME
The mortality rate in critical illness neuromuscular
disorders ultimately depends on the underlying
conditions, and the development of neuromuscular
pathology does not worsen it. Typically many pa-
tients who develop these syndromes die from the
multiorgan system dysfunction or sepsis. Critical
illness neuromuscular syndromes have important
functional implications for the survivor. Severe
weakness that prolongs recovery and residual mo-
tor and sensory neurologic deficits are extremely
common in survivors of protracted illness. In those
with mild to moderate CIPN or myopathy, recov-
ery is often relatively rapid and complete (weeks to
90749_ch14(363-376).ps 8/10/06 3:55 PM Page 374
374 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
months). In some cases with more severe weakness,
recovery is delayed for years or leaves permanent
deficits. Throughout the recovery process, the
quality of life is often impaired, and in some cases
the severe neuromuscular weakness can contribute
to later deaths. deSeze et al in 2000 completed an in-
teresting study that looked at follow-up in individ-
uals with severe weakness related to CIPN. In 19
patients with severe CIPN, they found that some
patients continued to have severe weakness after 2
years. They also found that complete recovery had
occurred in 21% at 3 months, 52% at 6 months, and
68% at 12 months (43).
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ment. Muscle Nerve 1991;14:1131–1139.
36. Al-Lozi MT, Pestronk A, Yee WC, et al.
Rapidly evolving myopathy with myosin-
deficient muscle fibers. Ann Neurol 1994;35:
273–279.
37. Douglass JA, Tuxen DV, Horne M, et al. My-
opathy in severe asthma. Am Rev Respir Dis
1992;146:517–519.
38. Dubois DC, Almon RA. A possible role for glu-
cocorticoids in denervation atrophy. Muscle
Nerve 1981;4:370–373.
39. Stibler H, Edstrom L, Ahlbeck K, et al. Elec-
trophoretic determination of the myosin/actin
ratio in the diagnosis of critical illness myopathy.
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40. Lefaucheur JP, Nordine T, Rodriguez P, et al.
Origin of ICU acquired paresis determined by
direct muscle stimulation. J Neurol Neurosurg
Psychiatry 2006;77:500–506.
41. Rich MM, Bird SJ, Raps EC, et al. Direct muscle
stimulation in acute quadriplegic myopathy.
Muscle Nerve 1997;20:665–673.
42. Segredo V, Caldwell JE, Matthay MA, et al. Per-
sistent paralysis in critically ill patients after
long-term administration of vecuronium. N
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43. deSeze M, Petit H, Wiart L, et al. Critical
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61–69.
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CHAPTER 15
Evaluation of the Patient with
Suspected Neuromuscular
Junction Disorder
William J. Litchy
INTRODUCTION
The evaluation of the patient with a neuromus-
cular junction (NMJ) disorder has evolved over
recent years. Increased understanding of the
structure and function of the NMJ; the advent of
new and improved electrophysiologic tech-
niques, including patch clamp and endplate noise
analysis; the increased understanding of the im-
munologic characteristics of the NMJ; and the
genetic studies that are identifying increasing
numbers of inherited NMJ disorders have
changed our perspective on this group of disor-
ders. At the same time that more NMJ disorders
have been identified and characterized, treat-
ment options have increased, and the complexity
of the evaluation of the person suspected of hav-
ing a NMJ disorder is greater.
Since Jolly, in 1895, described the physiologic
evaluation of the patient with myasthenia gravis,
there have been advances in the armamentarium
for the electrodiagnostic medicine physician (1).
Improved knowledge of the clinical syndromes
associated with neuromuscular disorders has been
helpful. Although weakness, particularly fluctu-
ating weakness, is the hallmark of NMJ disorders,
further delineation of the symptoms and signs of
these disorders has been important. Increasing
knowledge of the structure and function of the
NMJ has been paramount for furthering the un-
derstanding of NMJ disorders; in this case the
receptors and function have been important.
Advances in immunology and in the knowledge
of the receptors in the NMJ have revolutionized
both the understanding of the pathologic mecha-
nisms of the disease and the diagnostic evaluation
of these disorders. The ability to evaluate the ge-
netic aspects of the NMJ diseases has also led to
many advances. Not only do we now recognize a
large variety of congenital myasthenic syndromes,
but we can also describe the ion channels or mem-
brane receptor impairments and locate the genetic
defect(s) causing the disorder (2–4).
The electrodiagnostic medicine physician’s
tools have also improved and, when combined
with the clinical, immunologic, and genetic infor-
mation, it is possible to interpret the electrophysi-
ologic findings in a more clinically meaningful
manner. The basic tools of the electrodiagnostic
physician are nerve conduction studies and needle
electromyography. The most sensitive nerve con-
duction test for the evaluation of a weak patient
with suspected NMJ disease is repetitive nerve
stimulation. In myasthenia gravis, the most com-
mon disorder of the NMJ, abnormalities of repet-
itive nerve stimulation (RNS) studies may be seen
in up to 90% of people. The specific pattern of ab-
normal, decremental serial responses in these pa-
tients is often characteristic of the disease. Needle
electromyography (EMG), particularly single-
fiber EMG, is also very useful in the evaluation of
the patient. It is a very sensitive test but not specific
for disorders of the NMJ (5,6). Abnormalities can
be observed in disorders of the motor neuron and
377
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378 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
peripheral nerve as well as the muscle fiber that
may be indistinguishable from the observations in
myography (7,8).
The scope of this chapter is to review the ap-
proaches to the evaluation of the patient with a
suspected NMJ disorder in the clinical neurophys-
iology laboratory. The emphasis will be on the
tools used in the electrodiagnostic laboratory. To
understand the value of these tools, a brief discus-
sion of the structure and function of the NMJ is in-
cluded. This will be followed by a discussion of
techniques and approaches to their use. Finally,
observations on some of more commonly encoun-
tered disorders of neuromuscular transmission
(NMT) will be presented.
NEUROMUSCULAR JUNCTION
Structure
The NMJ is a specialized synapse anatomically
and functionally designed to activate muscle fibers
in a controlled manner located at a specialized
area of the muscle membrane called the endplate.
The NMJ is composed of presynaptic and postsy-
naptic membranes separated by the synaptic cleft.
The presynaptic region is the termination of the
motor axon at the endplate, while the postsynaptic
region is the specialized region of the muscle fiber
membrane with multiple junctional folds. Struc-
tural and functional abnormalities of the NMJ re-
sult in numerous clinical disorders, the hallmark
of which are fluctuating weakness and fatigability
(9) (Fig. 15-1).
Presynaptic Terminal
The presynaptic terminal has all of the machinery
required to release the neurotransmitter acetyl-
choline (ACh): mitochondria; synaptic vesicles,
each containing 5,000 to 10,000 ACh molecules;
and a presynaptic membrane that includes active
zones and sodium, potassium, and calcium ion
channels involved in the local depolarization and
subsequent release of synaptic vesicles into the
synaptic cleft (10–13). The synaptic vesicles cluster
at the active zones in preparation for release into
the synaptic cleft. During the depolarization
phase of the presynaptic region, ionic calcium en-
ters the presynaptic terminal. The half-life for
internal Ca2
concentration is approximately 500
ms. The rise in intracellular calcium results in the
vesicular fusion with the presynaptic membrane
and release of ACh into the synaptic cleft (14).
Synaptic Cleft
The synaptic cleft, a space between the pre- and
post-synaptic membranes, is the site where end-
plate-specific acetylcholinesterase (AChE) is lo-
cated on the synaptic basal lamina. The role of
AChE is to inactivate ACh and maintain a steady-
state function of the NMJ.
Postsynaptic Cleft
The postsynaptic membrane is composed of the
specialized region of the muscle membrane formed
into junctional folds with ACh receptors (AChR)
clustered at the tops of the folds at a density of
1,000/um2. At the base of the junctional folds are
voltage-gated Nav1.4 channels. The distribution of
the AChRs and the Nav1.4 into separate areas of the
junctional fold is ideal for the normal function of
the NMJ. Activation of these AChRs by acetyl-
choline, usually two molecules per receptor, results
in a membrane depolarization and activation of
Nav1.4 channels. When this depolarization is suffi-
ciently large, it produces an action potential and a
contraction of the muscle fibers (15).
Function
Under the resting state there is a steady random
release of ACh-filled synaptic vesicles. The ACh
molecules attach to the AChR and generate
miniature endplate potentials (MEPPs) (16–18).
The MEPP is the result of the action of one or a
few synaptic vesicles. A nerve action potential de-
polarizing the nerve terminal results in an influx
of calcium ions into the presynaptic terminal
through voltage-gated calcium channels, causing
a fusion of the synaptic vesicles with the presynap-
tic membrane and release of a large amount of
ACh into the synaptic cleft. The influx of calcium
ions results in an increased probability of addi-
tional release of ACh for a short time (18).
The depolarization the presynaptic mem-
brane by an action potential results in the release of
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CHAPTER 15 • NEUROMUSCULAR JUNCTION DISORDER 379

Figure 15-1 ● ACh is concentrated in synaptic vesicles by a specific vesicular ACh trans-
porter (VAChT). Release of the ACh begins with opening of the calcium channels in the active zone where
ACh-filled vesicles are clustered. The ACh acts by activating the ACh receptors, depolarizing the membrane,
which is then propagated via the Na channels. The action of the ACh is terminated via the action of the acetyl-
cholinesterase (AChE). (Modified from Benarroch EE. Basic neurosciences with clinical applications. Philadel-
phia: Butterworth, Heineman, Elsevier, 2006, with permission.)

many synaptic vesicles and produces an endplate
potential (16,18). When the endplate potentials ex-
ceed the threshold for activating the Nav1.4 chan-
nels, a muscle fiber action potential occurs. The
high concentrations of the AChRs at the top of the
functional fold and the Nav1.4 channels located at
the base of the junctional fold are essential for
normal propagation of the action potential and con-
traction of the muscle fiber. The difference be-
tween the depolarization caused by the AChR acti-
vation and the depolarization required to activate
the Nav1.4 is the safety factor. When the activation
of the AChRs is below the safety factor, the depo-
larization required to activate the muscles will not
occur. All clinical disorders of NMT, whether ac-
quired or congenital, are the result of the endplate
potential being inadequate to activate the Nav1.4 or
else the Nav1.4 channels not responding to normal
endplate potentials (19).
ELECTROPHYSIOLOGIC STUDIES
Electrophysiologic techniques are used to confirm
the clinical suspicion of the disorder of NMJ and to
exclude other disorders in patients with similar
symptoms. The electrophysiologic studies include
routine nerve conduction studies, needle EMG,
RNS, and single-fiber EMG. Although electrodi-
agnostic studies can be very useful in the diagnosis
of a NMJ disorder, and in some cases following the
course of treatment intervention, the absence of
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380 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
electrodiagnostic abnormalities does not preclude a
diagnosis of a NMJ disorder. In autoimmune
myasthenia gravis, for example, 10% of the patients
may not have abnormal results on electrophysio-
logic studies. This percentage is even greater for pa-
tients in early stages of the disorder or those with
primarily ocular myasthenia gravis.
The most frequently used tests in the clinical
neurophysiology laboratory are repetitive stimula-
tion of a motor nerve with recording from its mus-
cle (RNS) and single-fiber EMG. These tests
measure the function of the NMJ indirectly. The
most direct method to study the NMJ is with
endplate analysis techniques. Although in vitro
endplate analysis is clearly the most sensitive and
reliable approach to evaluating the patient with a
suspected NMJ disorder, it requires a muscle
biopsy and a sophisticated analysis. RNS and
single-fiber EMG are more practical, and when
combined with the available immunologic studies,
most patients with NMJ disorders can be evaluated
adequately (20).
Repetitive Nerve Stimulation
RNS is the most frequently used test in the clinical
neurophysiology laboratory to evaluate patients
with a suspected disorder of the NMJ. Although
not as sensitive as single-fiber EMG, it is specific
when an abnormality is found. RNS is a straight-
forward test, but when used incorrectly it can lead
to misdiagnosis or to no diagnosis when a disease
is present. The physiologic characteristics of the
NMJ and the potential for technical errors must
always be considered when evaluating a patient
with suspected NMJ disorders in the clinical neu-
rophysiology laboratory.
The RNS evaluation of the patient with a sus-
pected NMJ disorder requires preparation of the
patient, use of the appropriate equipment, and
studying the correct muscles with the appropriate
stimulation protocols. Although the technique of
RNS stimulation is straightforward, there are nu-
merous physiologic and technical factors that af-
fect test results.
Patient Preparation
For the successful evaluation with RNS, the pa-
tient should be properly prepared for the study.
This preparation includes instructing the patient
in what is expected. The limb must be warm to
avoid unreliable and incorrect results. Also, the
patient should not be taking any medication inter-
fering with the test; specifically, the patient should
not take any anticholinesterase medications prior
to the study, such as pyridostigmine.
Muscles Studied
It is important to study the correct muscles when
doing RNS studies. The criteria for selecting the
nerve and muscle combination are no different
than choosing a nerve or muscle for any other elec-
trodiagnostic test. The muscle studies should be
relevant. There should be a suspicion that it is clin-
ically involved or is useful in excluding a disorder
of the NMJ or other disease. The muscle should be
reliable in that the information one obtains from
the study reflects the function of the NMJ. The re-
sults obtained should be reproducible. If the results
are not similar each time the study is performed, it
is difficult to interpret the results. The test should
be relatively comfortable. RNS is usually uncom-
fortable, so it is helpful to choose a muscle that you
are used to testing and that may be less painful.
The muscles most commonly studied are listed in
Table 15-1, along with the nerve stimulated and
the advantages and disadvantages of studying the
muscle (21,22).
Stimulation Protocols
Before performing repetitive stimulation on a
nerve, it is important to perform routine motor
and sensory nerve conduction studies to exclude
other disorders. A nerve or muscle affected by an-
other pathophysiologic process is unreliable, and
abnormalities observed on RNS are difficult to in-
terpret. RNS is used to demonstrate abnormal
function of the NMJ. Based on the knowledge of
the physiology and the results observed, there are
reasonable approaches to stimulating the nerve in-
nervations of the muscle.
Most frequently, repetitive stimulation is per-
formed by stimulating at 2 Hz in a train of four
stimuli. Longer trains of stimuli, up to 10, and a
higher frequency, 3 Hz, are used in some clinical
neurophysiology laboratories. However, abnor-
malities, when present, are observed with a train
of four stimuli and a lower stimulation frequency
under most circumstances. Shorter stimulus trains
help to reduce the artifact associated with move-
T A B L E 1 5 - 1 Nerves and Muscles Commonly Used in the Evaluation of Patients with Suspected Neuromuscular
Junction Disorders
90749_ch15(377-394).ps

Nerve Muscle Stimulation Site Advantages Disadvantages Immobilization

Axillary Deltoid Supraclavicular Proximal Unstable stimulus, Large Velcro strap

muscle difficult to immobilize or bed sheet
8/10/06

Facial Nasalis Between mastoid Proximal Unstable stimulus, None

and tragus muscle cannot immobilize
3:57 PM

Femoral Rectus femoris Femoral triangle Proximal leg Difficult to immobilize, Lower limb board
muscle may need needle for
stimulation
Median Abductor pollicis Wrist Well Distal muscle may be spared, Hand board
Page 381

brevis tolerated difficult to immobilize

Musculocutaneous Biceps Lower edge axilla Proximal Unstable stimulus, Upper limb board
muscle difficult to immobilize
Peroneal (fibular) Tibialis anterior Popliteal fossa Leg muscle Distal muscle, may be spared Lower limb board
in myasthenia gravis
Radial Anconeus Forearm Forearm Requires a needle None
muscle, for stimulation
comfortable
for the patient
Radial Extensor Elbow Forearm Unstable stimulus, Upper limb board
digitorum muscle muscle artifact
Spinal accessory Trapezius Posterior border Proximal Difficult to immobilize Large Velcro strap
sternocleidomastoid muscle or bed sheet
Ulnar Abductor Wrist Reliably Distal muscle, may be Hand board
CHAPTER 15 • NEUROMUSCULAR JUNCTION DISORDER

digiti minimi immobilized, spared in myasthenia gravis

well tolerated
381
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382 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

ment. Three sets of four stimuli are sometimes
performed to ensure that the recordings are reli-
able and reproducible. These baseline recordings
are used to compare with subsequent studies.
Exercising the muscle studied is a valuable way
to accentuate an abnormality or to observe one that
is not present in the baseline recordings. If there is
an abnormality, brief exercise may repair the decre-
ment, and this is another characteristic feature of a
disorder of the NMJ. In a presynaptic NMJ disor-
der such as Lambert-Eaton myasthenic syndrome,
brief exercise may produce facilitation of the re-
sponse, which, if large enough, may be diagnostic of
this disorder (see later section in this chapter).
Abnormalities on Repetitive Nerve Stimulation
The typical abnormalities observed in NMJ dis-
orders are decrement, repair of the decrement,
postactivation exhaustion, and facilitation. A
decrement of up to 8% has been reported in pa-
tients without NMJ disorders. In autoimmune
myasthenia gravis, a minimal decrement of 10%
should be present in more then one muscle, and
that decrement should repair immediately fol-
lowing exercise (20). The size of the decrement
varies in the muscles studied in the same patient,
reflecting the variation in the NMJ pathology
(Fig. 15-2).

Figure 15-2 ● The results of repetitive stimulation of different nerves in a patient with gen-
eralized myasthenia gravis. Two-Hz repetitive stimulation was performed with the muscle at rest and
a train of four stimuli was recorded (superimposed). The decrement varies with each muscle, with the largest
decrement in the deltoid (62%) and the smallest in the abductor digiti minimi (2%).
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CHAPTER 15 • NEUROMUSCULAR JUNCTION DISORDER 383

Decrement muscle, so a train of 50-Hz stimulation can be used

Decrement is the change in the amplitude (or
area) of the fourth compound muscle action po-
tential (CMAP) compared to the first CMAP in
the train. Decrement is expressed as a percent re-
duction from the first response in the stimulus
train (Fig. 15-3). Although there can be a small
decrement in normal people, a reproducible
decrement of more then 10% is considered abnor-
mal. Besides the amount of decrement, the pattern
of the decrement is important in identifying the
specific cause of the NMJ disorder. In autoim-
mune myasthenia gravis, the largest decrement is
between the first and second response (see Fig. 15-
3). In other disorders of the NMJ, this may not be
the case. Although this pattern is seen in other dis-
eases, a different pattern is due to either technical
problems or other disorders. The amount of the
decrement is also affected by exercise, the time af-
ter exercise when a train of stimuli is given, and
the particular muscle examined (20).
Decrement Repair
A decrement may be lessened, or repaired, imme-
diately after a period of exercise. This repair is ex-
pected in autoimmune myasthenia gravis and
Lambert-Eaton myasthenic syndrome and is most
likely related to the internal concentration of ionic
calcium at the presynaptic membrane. After brief
exercise the accumulated Ca2
increases the proba-
bility of release of ACh and improves the safety fac-
tor for NMT. Under some conditions, for example,
with children, it may not be possible to exercise a
in place of voluntary exercise.
Postactivation Exhaustion
The phenomenon of postactivation exhaustion is
most dramatic 3 to 4 minutes after a period of ex-
ercise. It is manifested by a larger decrement than
that which occurred prior to exercise.
Facilitation
Facilitation refers to the change in amplitude of
the first response in a train of four compared to the
first response in the train of four after exercise
(Fig. 15-4). A small amount of facilitation is ob-
served in normal individuals, but facilitation of
greater than 200% is consistent with the diagnosis
of Lambert-Eaton myasthenic syndrome. Other
presynaptic junction disorders, such as botulism,
may also show facilitation, but not as dramatically
as Lambert-Eaton myasthenic syndrome.
Pitfalls of Repetitive Nerve Stimulation
Although RNS is straightforward and easy to per-
form, there are numerous pitfalls leading to
missed diagnosis and incorrect diagnosis. It is im-
perative to recognize the potential problems when
performing these studies.
Incorrect Electrode Placement
The placement of recording electrodes is as im-
portant for RNS as it is for routine nerve conduc-
tion studies. Care must be taken to place the
recording electrode over the motor point of the

Figure 15-3 ● Decremental response in the trapezius muscle with baseline 2-Hz stimulation
of a patient with myasthenia gravis. The decrement is measured comparing the fourth CMAP with
the first CMAP and is expressed as a percentage of the first CMAP. (Sweep  5 ms, gain  2 mV.)
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384 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

Figure 15-4 ● Facilitation of the CMAP in a patient with Lambert-Eaton myasthenic syn-
drome. Two-Hz stimulation was performed at baseline (A) and immediately after 15 seconds of exercise (B)
recorded from the abductor pollicis brevis muscle. Facilitation is the change in the first response of the baseline
stimulus train compared to the first response of the stimulus train after exercise. (Sweep  2 ms, gain  2 mV.)

muscle and the reference electrode off the muscle.
Placing the stimulating electrode close to the
nerve is also important. If the stimulating elec-
trode is not near the nerve and is not securely
placed to avoid movement during stimulation,
then the amplitude of the response during a stim-
ulus train may vary and suggest a decrement
when there is not one.
Submaximal Stimulation
Stimulation of the nerve at a supramaximal level
is important to make sure the size of the CMAP is
as large as is physiologically possible each time.
Stimulating the nerve at a submaximal level may
lead to changes in the CMAP from one stimulus to
the next. When the variation in CMAP amplitude
is irregular, it suggests a technical problem, but
that may not be the case all of the time.
Movement Artifact
Movement of the limb during the stimulus trains
is difficult to avoid, but bracing the limb can help
to minimize the movement. The movement is
produced by direct activation of the muscles, but
also can be the result of poor relaxation of the pa-
tient (Fig. 15-5). This is particularly true when the
longer train of 10 stimuli is used. Movement of the
limb may result in movement of the stimulating
electrode or even of the recording electrodes. In
the case of the former, the result may be a pattern
like that seen in submaximal stimulation where
the CMAP response is irregular.
Low Temperature
The response of the NMJ to RNS is a physiologic
process and is affected by temperature changes
(23). In a cold muscle, larger amounts of ACh are
released with a single stimulus, the hydrolysis of
the ACh is slower, and the open time of the AChR
is longer. All of these factors lead to a more effec-
tive neurotransmission process and could poten-
tially mask an abnormality of NMT. A decrement
present with RNS in a warm muscle may not be
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CHAPTER 15 • NEUROMUSCULAR JUNCTION DISORDER
Figure 15-5 ● Two- Hz stimulation of the trapezius muscle at baseline. The irregular changes
in the amplitude of the trapezius muscle CMAPs are artifactual, the result of shoulder movement during stim-
ulation. (Sweep  5 ms, gain  2 mV.)
present if the muscle is cold. It is important to
monitor the distal limb temperature during the
nerve conduction studies and maintain a temper-
ature of 31°C or greater.
Medication
Medications can also affect the response of the
muscle to RNS. This is most commonly observed
in patients receiving treatment for myasthenia
gravis with pyridostigmine. If the patient is taking
medication, then the abnormalities that could be
seen with RNS may be masked and a decrement
not observed. It is important that the patient avoid
medication that potentially will interfere with the
testing for at least 4 hours, and longer (12 hours) if
possible.
Needle Electromyography
Standard Needle Electromyography
In the patient with suspected NMJ disease, stan-
dard needle EMG is not used to confirm the diag-
nosis but rather to exclude other disorders of the
motor unit whose symptoms may be similar to the
patient with a NMJ disorder. However, careful
evaluation of the patient with a NMJ disorder may
reveal subtle abnormalities. The variability in am-
plitude and morphology of a motor unit potential
with each firing observed with needle EMG may be
the result of a NMJ disorder. These abnormalities,
385
however, can be observed in many disorders of the
motor unit, including the motor neuron, nerve, and
muscle fiber.
Single-Fiber Electromyography
Single-fiber EMG, developed in the 1960s, pro-
vides additional quantitative information about
the function of the NMJ. Unlike routine needle
EMG, where the electrical activity of many mus-
cle fibers of a motor unit is recorded, in single-
fiber EMG it is possible to measure the action
potentials of a single muscle fiber. The ability to
quantify the synchrony of firing of individual
muscle fibers in a single motor unit is the basis for
the most frequently used measurement made,
jitter (Fig. 15-6). Jitter is considered the most sen-
sitive electrophysiologic measurement for NMJ
disorders, but like routine needle EMG, it is not
specific for these disorders. A more complete de-
scription of single-fiber EMG and use of this tech-
nique and its role is evaluating NMJ disorders can
be reviewed elsewhere (5,6).
Jitter
The jitter, or the measure of synchrony of firing of
muscle fibers, is due in part to small variations in
the endplate potential at the postsynapatic mem-
brane due to AChR dysfunction or Nav1.4 chan-
nel abnormalities producing variability of muscle
fiber action potential firing and variability in the
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386 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

Figure 15-6 ● A voluntary activation single-fiber EMG recording from the frontalis muscle
of a 52-year-old woman with clinically mild autoimmune myasthenia gravis. The first mus-
cle fiber potential is the trigger, and the jitter (a measure of the variability of firing of a pair of muscle fibers in
a single motor unit) is measured from the second muscle fiber potential. A minimal of 50 discharges should be
recorded from 20 muscle fiber pairs. (Sweep  0.5 ms, gain  100 V.)

fluctuations of the firing threshold of the subsy-
naptic sarcolemma. Although this variability can
be observed when performing a routine needle ex-
amination, single-fiber EMG quantifies this
measurement and allows for a comparison with
reference values obtained from people without
NMJ disorders.
The ability to record single muscle fiber ac-
tion potentials is due to several factors, including
special signal filtering, special software for meas-
uring the signals, and a special needle with an ac-
tive recording electrode surface of 25 m exposed
on the side of the needle. Because of the expense
and difficulty involved in maintaining these spe-
cial needles, attempts have been made to use stan-
dard concentric and monopolar needles to meas-
ure the jitter in a muscle. Reference values using
these standard needles are available (24–26).
Voluntary and Stimulated Single-Fiber Elec-
tromyography
Jitter can be measured with voluntarily activated
muscle fibers or from muscle fibers activated by
electrical stimulation of the nerve to the muscle
(27). Both techniques are technically demanding
and have many pitfalls that can cause spurious re-
sults. The sources for error with voluntary single-
fiber EMG include interfering action potentials,
irregularity of the firing rate, split muscle fibers,
and poor electrodes. With stimulated single-fiber
EMG, additional sources of error include below-
threshold stimulation producing spurious block-
ing; direct muscle fiber stimulation producing low
jitter measurements; incorrect stimulation rate;
and axon reflexes, which may create an excessively
high, bimodal jitter.
Observations
The jitter values vary with the muscles studied
and with the age of the patient. Reference values
have been published for voluntary single-fiber
EMG for many muscles using different needles
for recording the single-fiber muscle action poten-
tials (28,29).
Single-fiber MG demonstrates abnormal jit-
ter in most NMJ disorders. In autoimmune myas-
thenia gravis, the sensitivity for making the diag-
nosis varies from 82% to 99%, depending on the
number of muscles. The jitter is usually greatest in
the most clinically weak muscles (30). In Lambert-
Eaton myasthenic syndrome, abnormal jitter is
observed in all patients. Unlike myasthenia gravis,
the amount of jitter in Lambert-Eaton myasthenic
syndrome is often much more severe then ex-
pected with the mild degree of clinical weakness.
Also unlike myasthenia gravis, the jitter will often
decrease with increased muscle action potential
firing rates in Lambert-Eaton myasthenic syn-
drome. Jitter is also increased in many congenital
myasthenic syndromes, as well as in botulism.
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CHAPTER 15 • NEUROMUSCULAR JUNCTION DISORDER
NEUROMUSCULAR JUNCTION
DISORDERS
Myasthenia Gravis
Myasthenia gravis is an acquired, autoimmune
disorder of NMT associated with a decreased
number of AChRs. The first description of this
disorder was by Thomas Willis in the 17th cen-
tury. In 1895 Jolly not only gave the disorder its
name but also described the reduction in tetanic
tension of a muscle with low-frequency stimula-
tion (1). This is the first description of what we
now refer to as RNS.
Myasthenia gravis is a common disorder with
an annual worldwide incidence estimated at 11
million people and a prevalence of up to 150 mil-
lion (31). The incidence in females is higher then
males (3F:2M), and it is more likely to occur at a
younger age, the third decade for women and
sixth for men (32). The predominant clinical fea-
ture is fluctuating weakness and fatigability of
some or all of the voluntary muscles. The symp-
toms may fluctuate through a day, from day to
day, or over longer periods of time. Most com-
monly the ocular muscles are involved initially
and then the symptoms progress to other muscles
in over 80% of the patients. The progression usu-
ally occurs during the first year of the disease.
Spontaneous remissions do occur and last for
varying periods of time (33,34).
The advent of the ability to detect autoanti-
bodies to the AChR has been useful for the diagno-
sis of myasthenia gravis. Although autoantibodies
may be detected in up to 90% of the people with au-
toimmune disorders, they are less likely to be found
in those who are early in the course of their disease
and in those with only ocular symptoms. A group
of patients with autoantibody-negative myasthenia
gravis has been discovered. This small subset of pa-
tients has an antibody to muscle-specific kinase
(MuSK). The spectrum of clinical features in this
group is still being defined (35,36).
RNS remains a useful tool for the diagnosis of
patients with myasthenia gravis. It contributes to
the diagnostic yield and in the presence of suspi-
cious clinical symptoms of weakness and fatigabil-
ity may help to exclude a disorder of the NMJ.
Because of the variability of clinical weakness, the
evaluation of patients using RNS should always
387
include weak muscles. The abnormalities with
RNS are variable in each patient, so more than one
muscle should be studied; abnormalities should be
demonstrated in at least two muscles to make a di-
agnosis of myasthenia gravis based on the RNS
studies.
A reasonable approach to the evaluation of a
patient with suspected myasthenia gravis is to start
with a distal muscle—the abductor digiti minimi
muscle in ocular or generalized weakness, or the
tibialis anterior when the weakness involves only
the lower limb. These are technically easy muscles
to study and the least uncomfortable for the pa-
tient. However, the yield of abnormalities in
myasthenia gravis is low unless the disease is se-
vere. However, the motor nerve studies can help
to exclude other diagnoses under consideration.
Next, a more proximal muscle should be studied.
In the upper limb the largest decrement is often
seen in the deltoid muscle, but the study of this
nerve is technically more challenging. Finally, the
evaluation of a facial muscle, although technically
challenging, is useful in patients with either gen-
eralized or ocular symptoms.
The RNS should start with a routine motor
nerve conduction study to exclude other abnor-
malities of the nerve and muscle. RNS at 2 Hz,
collecting a train of four responses, should be per-
formed at rest and evaluated for decrement. If a
decrement is present, then a brief (15 seconds) pe-
riod of exercise should be performed. If there is no
decrement, then a 1-minute exercise period
should be done to accentuate a small or nonexist-
ent decrement that would be present during the
period of postexercise exhaustion. Following exer-
cise, the trains of four stimuli should be performed
immediately and then at 1-minute intervals for 4
minutes after exercise to identify decrement repair
and postexercise exhaustion. In infants or people
unable to cooperate, 50 Hz stimulation can be
used in place of exercise.
For a RNS to be abnormal and used to diag-
nose myasthenia gravis, the following criteria
should be met:
1. The decrement is greater than 10%, repairs
with exercise, and increases during the postac-
tivation exhaustion period.
2. The decrement is observed in more then one
muscle.
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388 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

3. The pattern of decrement is consistent with of in vitro electrophysiologic analysis of NMT,

that seen in myasthenia gravis (Fig. 15-7). The
expected pattern is seeing that the largest
decrement occurs between the first and second
responses. In generalized myasthenia gravis, if
multiple muscles are studied, an abnormality
will be seen in over 65% of the patients. Proxi-
mal muscles, such as the deltoid or trapezius,
are more likely to show abnormality than distal
muscles (20,32,37,38).
Congenital Myasthenic Syndromes
The congenital myasthenic syndromes are a het-
erogeneous group of inherited disorders of NMT
clinically presenting with weakness and fatiga-
bility with exertion (2,39,40). The identification
and classification of these syndromes have ex-
ploded in the past decade with the advancement
cytochemical and ultrastructural studies of the
NMJ, and the advances in identifying genetic ab-
normalities (3,4,39–41). The typical patient is a
young person with fluctuating weakness and
fatigability and no detectable autoantibodies to
the NMJ. Although evaluation and identification
of patients with congenital myasthenic syndrome
often require techniques not used in the clinical
neurophysiology laboratory, there still is a place
for routine and specialized studies for the identi-
fication of some forms of congenital myasthenic
syndrome, as well as to exclude the diagnosis in
some persons.
The congenital myasthenic syndromes are
classified as presynaptic, synaptic-based lamina-
associated defects and postsynaptic defects. The
majority of these types identified to date are the
result of postsynaptic defects (2) (Table 15-2). The

Figure 15-7 ● Two-Hz stimulation of the trapezius muscle in a 49-year-old woman with au-
toimmune myasthenia gravis. The baseline recording (A) was followed by 15 seconds of exercise, and
then the following responses were recorded: immediately after (B), 30 seconds (C), 1 minute (D), 2 minutes
(E), and 3 minutes (F) after exercise. The decrement is present at baseline (A), with partial repair of the
decrement (B) after exercise. The NMJ was severely affected and total repair of the decrement with postexer-
cise facilitation did not occur. (Sweep  5 ms, gain  2 mV.)
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CHAPTER 15 • NEUROMUSCULAR JUNCTION DISORDER 389

TABLE 15-2 Classification of Congenital Myasthenic Syndromes Based on the Site

of Abnormality in the Neuromuscular Junction

CLASSIFICATION OF CONGENITAL MYASTHENIC SYNDROMES

Presynaptic defects
Choline acetyltransferase deficiency
Paucity of synaptic vesicles and reduced quantal release
Lambert-Eaton syndrome-like
Other presynaptic defects
Synaptic basal lamina-associated defects
Endplate AChE deficiency
Postsynaptic defects
Primary kinetic abnormality of AChR with/without AChR deficiency
AChR deficiency with/without kinetic abnormality
AChR mutations with unclear effects
Rapsyn deficiency
MuSK deficiency
Na
channel myasthenia
Plectin deficiency
(Modified from Beeson D, Hantaï D, Lochmüller H, et al. 126th International Workshop: Congenital Myasthenic
Syndromes, Sept. 24–26, 2004, Naarden, The Netherlands. Neuromuscular Disorders 2004;15:498–512, with permission.)

abnormalities with RNS are also variable and de-
pend on the site of the abnormality.
The approach to a patient suspected of hav-
ing a congenital myasthenic syndrome is variable.
Routine motor and sensory nerve conduction
studies should be performed to exclude other dis-
orders. Muscles with demonstrated clinical weak-
ness should be studied with RNS. Prior to per-
forming repetitive stimulation, the CMAP should
be viewed after a single maximal stimulus to look
for repetitively occurring CMAP discharges. The
repetitive discharge is observed in patients with
the slow channel syndrome, and similar observa-
tions are seen in patients with high concentrations
of Mestinon. Two-Hz repetitive stimulation is
performed on clinically involved muscles. If a
decrement is found, then the muscle is exercised
and RNS is repeated, looking for facilitation, re-
pair of decrement, and postexercise exhaustion.
More rapid rates of stimulation (10 to 50 Hz) may
be needed when exercise is not possible. If there is
no decrement on RNS and there is a clinical suspi-
cion of an AChE deficiency disorder, then pro-
longed stimulation at 10 Hz should be considered.
The findings with repetitive stimulation re-
flect the areas of abnormality (42) in ways similar
to myasthenia gravis and Lambert-Eaton myas-
thenic syndrome. In a presynaptic congenital
myasthenic disorder there is likely to be a decre-
ment with slow and fast RNS, and varying de-
grees of facilitation with brief exercise. With
AChE deficiency there is likely to be repetitive
discharges with single stimuli and no decrement
or facilitation (Fig. 15-8). Also in postsynaptic dis-
orders, there may be decrement that is less likely
to repair with exercise in some disorders.
Lambert-Eaton Myasthenic Syndrome
The Lambert-Eaton myasthenic syndrome (43) is
an acquired autoimmune disorder characterized
clinically by fluctuating muscle weakness, fre-
quently affecting the lower limbs, that may im-
prove with exercise; depressed deep tendon re-
flexes; and autonomic changes (44–46). Although
most common in adults, and seen in men more
than women, it has been described in young chil-
dren. The safety margin for NMT is markedly
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390 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG

Figure 15-8 ● Single stimulus resulting in repetitive discharge following the CMAP in the
abductor digiti minimi in a patient taking pyridostigmine (top). The discharge disappears with
brief exercise (middle) and returns shortly after exercise is completed (bottom). The repetitive discharge is sim-
ilar to those seen in slow channel myasthenic syndrome.

reduced in these patients as a result of a reduction
of the net quantal content of the endplate potential
due to circulating antibodies to the presynaptic
voltage-gated calcium channels. The reduction in
calcium influx with the nerve terminal action po-
tential results in a reduction in the number of ACh
vesicles released, a reduction in the endplate poten-
tial, and little activation of the Nav1.4 channels (47).
The first result of these pathologic changes of
the NMJ are low CMAPs with routine nerve con-
duction studies. RNS at 2 Hz produces a low-
amplitude CMAP with a marked decrement. Brief
exercise produces marked facilitation and repair of
the decrement if the disorder is not severe. The
presence of facilitation of 200% or more in a muscle
in the proper clinical setting is virtually diagnostic
for Lambert-Eaton myasthenic syndrome (47,48).
The facilitation and decrement present after exer-
cise return to their pre-exercise condition within 30
seconds in most patients seen (Fig. 15-9).
Similar to other NMJ disorders, there is large
variation in the size of the decrement and postexer-
cise facilitation abnormalities in different muscles
in the same patient (48). At the same time that there
are marked abnormalities of RNS in one muscle,
another muscle may appear normal. The muscle
most likely to show the characteristic abnormalities
is the rectus femoris (personal observation).
Botulism
Botulism is an acquired disorder and the result of
toxins produced by the bacterium Clostridium bot-
ulinum. Botulism is categorized into two basic
types: infantile and adult. Although the sources of
the toxin producing the clinical symptoms and
electrophysiologic abnormalities in these types are
different, the observations with RNS are similar.
The salient clinical features are acute onset of con-
stipation, diplopia, and then progression of weak-
ness to the axial and appendicular muscles. Respi-
ratory failure is common, so inspiratory force
should be monitored.
With the exception of a low CMAP, the motor
and sensory nerve conduction studies are normal.
RNS at 2 Hz produces a decrement that may ap-
pear minimal, or even absent, if the CMAP is
markedly reduced. RNS with 50 Hz produces fa-
cilitation in 90% of infants and 60% of adults, but in
severe cases with denervation, facilitation may not
be present or it may require a prolonged
stimulation of up to 30 seconds to be observed. Un-
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CHAPTER 15 • NEUROMUSCULAR JUNCTION DISORDER
Figure 15-9 ● Two-Hz stimulation of the ab-
ductor pollicis brevis muscle in a 62-year-old
man with Lambert-Eaton myasthenic syn-
drome. The CMAP is reduced and there is a large
decrement at baseline (A). After 15 seconds of exer-
cise there is facilitation and repair of the decrement
(B), and after 30 seconds (D) it returns to baseline.
(Sweep  2 ms, gain  2 mV.)
like other presynaptic disorders of NMT, the dura-
tion of posttetanic facilitation is prolonged (49–51).
Other Neuromuscular Junction Disorders
Other disorders of NMT occur but are less com-
monly encountered. Drug-induced myasthenia
gravis, like the syndrome produced with D-
penicillamine, produces abnormalities similar to
autoimmune myasthenia gravis. Blockage of the
AChR postsynaptic receptors by snake toxins like
that from the cobra can produce symptoms and
signs resembling myasthenia gravis (52). The
391
Figure 15-10 ● RNS results in a patient
with a neuromyotonia. There is a severe decre-
ment with repetitive stimulation; the decrement re-
pairs with brief exercise and returns. The pattern of
the decrementing responses is different from that
seen in patients with myasthenia gravis, as shown in
Figure 15-7.
toxin from the black widow spider, on the other
hand, acts at the presynaptic junction and pro-
duces a rapid release of virtually all of the presy-
naptic vesicles (53,54).
Disorders That Produce Abnormalities on
Repetitive Nerve Stimulation with No
Neuromuscular Transmission Defect
Disorders of other components of the motor
unit may produce abnormalities on RNS or sin-
gle-fiber EMG. Decrements with repetitive
stimulation have been described in peripheral
neuropathies (particularly the distal form of
acute inflammatory polyradiculoneuropathy),
motor neuron diseases (7,55), neuromyotonic
disorders (Fig. 5-10), and primary muscle
disorders (56). In most cases the pattern of the
decrement abnormality is different from those
seen in primary disorders of the NMJ.
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392 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
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The Lambert-Eaton myasthenic syndrome: a re-
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Favourable prognosis in Lambert-Eaton myas-
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neuromuscular transmission in a patient with
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Electrodiagnosis of infantile botulism. J Child
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Miller Fisher anti-GQ1b antibodies: alpha-
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90749_ch16(395-416).ps 8/10/06 3:55 PM Page 395
CHAPTER 16
Pediatric Considerations
in Electromyography
Rosalind J. Batley
INTRODUCTION
Electrodiagnosis in the pediatric population differs
from that in adults with respect to the diagnoses,
clinical presentations, set-ups, and normal values.
In fact, it is probably easier to describe what is sim-
ilar between pediatric and adult studies than what
is different. The instruments and electrodes are
similar, but the latter are smaller than those used
with the adult. The underlying physiology is simi-
lar, but development of the myelin and motor unit
is incomplete in the pediatric patient. Due to the de-
veloping nervous system, normative data vary, as
do the presenting abnormalities. The pediatric
electromyographer must have an extensive knowl-
edge of growth and development and a familiarity
with pediatric differential diagnosis. The knowl-
edge of growth and development helps to narrow
down the differential. The pediatric examiner’s un-
derstanding of “primitive” reflexes can be used to
“trick” an infant into reflex movement, which will
allow more rapid analysis of the motor unit poten-
tials (MUPs). In keeping with this book’s title,
“Practical Electromyography,” this chapter will ap-
proach the practical aspects of the pediatric electro-
diagnostic medicine evaluation.
DEVELOPMENT OF THE MOTOR UNIT
The changes in the motor unit during growth are
the basis for the differences between pediatric and
adult normative data. Human fetal muscle devel-
opment was studied in the 1960s, and with the cur-
rent regulations regarding study of fetal tissue it is
not likely to be studied again in the near future.
Dubowitz found that muscle fiber diameters prior
to 6 months of gestation are 10 to 25
m, and after
6 months the diameter increases to 20 to 50
m. He
described three phases of muscle fiber development
in utero. During phase I, from 12 to 20 weeks of
gestation, the enzyme activity is equal in all fibers.
In phase II, from 20 to 26 weeks, differentiation be-
tween fiber types commences. However, only a
small number of type I fibers are present during
this period. In phase III, later than 30 weeks of ges-
tation, the fetus shows the same differentiation in
muscle fiber types as are found in adult muscle (1).
Evaluation of fetal tissue also revealed that
myelination of peripheral nerve axons begins to-
ward the end of the first trimester. Myelination
begins between weeks 10 and 15 and is completed
by 2 years of age (2). Nerve conduction velocities
(NCVs) increase with the diameter of the nerve
fibers and with the increases in the distances be-
tween the nodes of Ranvier. The internodal dis-
tances reach their maximum lengths by age 5 years
(2).
It is also important to be familiar with the
normal maturation of the MUP as seen with nee-
dle electromyography (EMG). Normal infant
MUPs are small in amplitude and duration,
making it a challenge to differentiate them from
potentials found in myopathies. Jablecki (3) and
395
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396 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
Sacco et al (4) reported that MUPs are similar in
appearance to adults but increase 20% in both am-
plitude and duration between age 3 months and
adulthood. The amplitudes of MUPs in nerve
studies in children have been well researched.
Nerve conduction velocities (NCV) increase 100

V to 700
V (5), with occasional units to 1,600

V (5,6). The MUP durations range from 2 to 10
ms (6). The electromyographer must have experi-
ence to differentiate between the small motor
units and fibrillations. One must focus on the ini-
tial deflection of the MUP and whether the poten-
tial is under voluntary control.
Many infants and children rapidly learn that
contracting a muscle causes pain when a needle
electrode is present in it. They will cease muscle
movement as soon as an electrode is inserted. This
further challenges the examiner, who must use
normal infantile reflexes (and sorcery) to induce
movement in the infant or child. Conversely, when
evaluating resting membrane potentials, the child
will frequently decide to move. Holding the joint in
such a position that the muscle is at its shortest
length is helpful in diminishing voluntary contrac-
tion (7).
Nerve conductions in children have been well
studied. Motor and sensory NCVs increase with
postconceptual age. Bougle reported that NCVs in
preterm infants (31 weeks of gestation at birth)
are about half that of adult normal values (usually
about 25 m/s) and that the lower levels of adult nor-
mal values are reached by age 4 years (8). Full-term
newborns have also been shown repeatedly to have
NCVs half the adult normal values, and the NCVs
also reach low adult normal values by age four
years (2,8–14). Premature infants have been shown
to have slower NCVs than full-term babies. The
motor velocities are correlated with postconceptual
age and are not affected by intrauterine growth re-
tardation (13). A small study suggests that sensory
NCVs are sensitive to growth retardation and can-
not be used to determine the postconceptual age,
which is possible with motor nerve conduction
studies (8,14). Thus, it is possible to determine the
postconceptual age of a small baby by motor nerve
conduction studies. Gestational age is estimated by
combining the velocities of the ulnar and posterior
tibial nerves, as this is thought to be more accurate
than that of a single nerve (8). Care in the position-
ing and measurement of the distances is critical.
Skin temperature must be controlled (8). The tech-
nique is rarely if ever used as it is expensive and
time-consuming. Alternative methods, such as the
Dubowitz maturity scale, have been adequate for
clinical purposes.
SETTING UP THE EMG LABORATORY
Once the physiology, growth, and development
are mastered, the pediatric electromyographer
must have appropriate space, instrumentation,
and personnel to make an accurate diagnosis. The
pediatric electromyographic laboratory should be
large enough to accommodate a standard wooden
plinth, electromyographic instrument, chairs, cab-
inets, warming lamps, sphygmomanometer, oxy-
gen saturation instrument, and a table. The space
must come equipped with a sink, suction, oxygen,
and a telephone. Electrical shielding is often not
necessary with modern instruments, but with the
small distances encountered in pediatric patients,
it is very helpful. Likewise, a telephone may not be
needed in an adult laboratory, but if the physician
is paged and is alone in the laboratory, he or she
cannot leave the child to answer.
The pediatric laboratory must have space and
seating for two or more parents or caregivers.
There must be room for a nurse to help sedate,
monitor, and distract the child. A resident or fel-
low will often be present as well. Additional room
for a crib or wheelchair will smooth patient flow
by preventing the need to move furniture. Blan-
kets and gowns for different age groups should be
stored close by. An otoscope, tongue blades, and
stethoscope must be available for pre-sedation ex-
aminations. Of course, some means of cleansing
toys and documenting this work must be devel-
oped. Scissors are needed to cut disposable elec-
trodes into infant or small child sizes. The
pediatric laboratory must have medicine cups and
oral syringes available to administer sedatives and
analgesics. Standard measuring devices and a cal-
culator (to adjust medication doses) must be pres-
ent as well. One must not forget a step-stool to
help children reach the plinth.
Cupboards for toy storage are helpful because
tubs of toys on the floor become cumbersome.
Toys are necessary for distraction during the his-
tory but are just as valuable during the physical
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CHAPTER 16 • PEDIATRIC CONSIDERATIONS IN ELECTROMYOGRAPHY 397

and the electrodiagnostic examination. A series of TECHNIQUES TO APPROACH

“cubbies” with toys for different ages would be
THE PEDIATRIC PATIENT
ideal. Bubbles make a mess but are good distrac-
tion for most young children. Contact your hospi-
The patient’s history, as with all medical evalua-
tal’s Child Life Department; their members will
tions, is critical. Physicians must ask about the
be very helpful, as one of their goals is to help chil-
birth history and development. Questions regard-
dren through difficult procedures. A TV and a ra-
ing whether a child is slowly progressing in devel-
dio are beneficial, especially if they use batteries, as
opment or actually regressing will often narrow
extra power cords create electrical noise. Older
the differential diagnosis. Age of presentation is
children and adolescents sometimes respond well
helpful, as well as the reason for the first physician
to music CDs with headphones.
visit. Slowly progressive, painless disorders are of-
To become more specific regarding equip-
ten picked up by teachers or coaches when the
ment, the pediatric EMG instrument must have
child cannot keep up with peers. Extended family
the ability to deliver 20, 30, and 50 Hertz repetitive
members who do not see the child except at holi-
stimulation, as the diagnosis of botulism is en-
days may also bring slowly progressive diseases to
countered routinely in most pediatric laboratories.
the parents’ attention.
Be wary of the sales representative or purchasing
Painful diseases are noticed immediately by
department who assume that because you are
parents. Questions regarding a child’s choice of
studying children you will not need the capability
activity after school can be helpful. Chronically
for sophisticated testing. The less expensive in-
weak children will not choose fatiguing activi-
struments may not offer rapid repetitive stimula-
ties. Parents may notice changes in their chil-
tion. The sales representative and the purchasing
dren’s choices, but this history is rarely offered
department will try to make the most economical
spontaneously. Specific questions must be used to
choice and during price negotiations may un-
elicit information regarding changes in a child’s
knowingly acquire an instrument that is inappro-
endurance and strength that parents may not be
priate for your needs.
aware of initially. Inability of the child to enjoy
Small, slender needles, 25 mm in length, are
field trips or visits to the mall is worrisome. Sub-
most frequently used, although the adult standard
acute presentations will be revealed in normally
lengths of 37 mm are routinely used with adoles-
athletic children having difficulty participating
cents. Both concentric and monopolar needles of
in their chosen sport. Congenital problems usu-
small gauges must be available. The laboratory
ally prevent children from choosing vigorous
must carry electroencephalograph abrasive paste
sports. Once again, this history can direct an ex-
and alcohol swabs for cleansing. Cleaning the skin
aminer toward a specific item in the differential
with the abrasive paste will decrease the imped-
diagnosis.
ance, which is helpful when dealing with the small
stimulator-to-electrode distances encountered
with pediatric patients. Disposable electrodes with PHYSICAL EXAMINATION
embedded gel are almost a necessity for a pediatric
laboratory. They are less likely to shift position The physical exam is a challenging portion of pe-
than do simple metal electrodes, which require diatric electrodiagnosis. Observing children in a
electrode gel and tape. Self-adhering electrodes parent’s lap and watching them play with toys is
are easier to use, so their use shortens the length of very helpful. I try to watch the child while getting
the examination, which secondarily allows the a history from the caregiver and then proceed with
child to tolerate a more thorough study. watching him or her crawl, walk, and run. Playing
In summary, a large space in an electrically with toys will allow examination of coordination
quiet room, but with a TV, telephone, and cup- and strength. Sometimes we are lucky enough to
board storage, is secondary only to the choice of be able to watch the child walk to the waiting room
appropriate instrument and electrodes. A skilled before he is even aware of us. Obtain as much of the
nurse is invaluable in teaching, sedating, and reas- physical examination as possible before touching a
suring patients and parents. pediatric patient, because from that point on, the
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398 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
examination may reveal only what can be obtained
from a crying and kicking child.
Observation of children’s movement patterns
is critical since it substitutes for the child cooperat-
ing with the examiner during the physical exami-
nation. Children move in specific patterns when
sitting down and arising from the floor normally,
and these patterns differ in the presence of weak-
ness. The most familiar example is the Gower’s
sign, when a child will walk his hands up his legs
when arising to stand. Though associated with
Duchenne muscular dystrophy, this phenomenon
occurs with any chronic proximal lower limb
weakness. A quarter-turn from a sit to a prone
four-point position is a more subtle hint and fre-
quently occurs prior to the development of a full
Gower’s sign. If you ask a chronically weak child
to stand up from the floor, he or she will crawl
over to a chair or a parent’s leg to pull up to stand
rather than fall. In contrast, a child with a new-on-
set weakness will fall. This is often helpful to de-
termine whether to proceed down a differential
diagnosis for acute-onset abnormalities versus
longstanding weakness that has just recently been
noticed.
Children with weak necks will prop their oc-
ciput upon their shoulders; they appear to have
lost their necks. This is seen in young children, as
their heads are bigger in proportion to the rest of
their body than are adult heads. Children will eas-
ily teach themselves to walk their fingers up a wall
to turn on a light switch when they have weak-
ened proximal upper limb strength. Children will
also accommodate for weakness by using “primi-
tive reflexes” in a functional manner. Children
learn to use an asymmetric tonic neck reflex to fa-
cilitate elbow flexion. When in a supine position a
child will reach out for a toy while looking toward
it, but will look toward the opposite shoulder
when raising the toy to his or her chest. Watching
a child sit up from a supine position is also helpful.
A weak child will rotate his body around so his
shoulders will come behind his pelvis for stability.
THE ELECTRODIAGNOSTIC EXAM
As with an adult examination, planning is critical
to efficient performance of the procedure. Seda-
tion is a controversial and important subject in this
planning. An examiner will develop a sense for
when distraction and verbal reassurance will be
sufficient or whether sedation will be necessary. If
sedation is going to be used, it is more effective to
use it from the outset than to start it after a child
has become agitated. It helps some children and
their parents tolerate a more detailed examination
than is possible without it. Parents know their
child’s ability to tolerate procedures and are often
the best source to consult if there is any question
regarding the use of sedation. A pediatric labora-
tory must have medicine cups and oral syringes
available to administer sedatives and analgesics. A
policy and procedure for sedative use must be de-
veloped and followed to ensure safety. New pedi-
atric electromyographers must become familiar
with the conscious sedation protocol for their hos-
pital and make sure that they have any certifica-
tions necessary. Some hospitals require pediatric
life support (PALS) training, and specific medical
staff privileges are necessary. Our pharmacy has
put together a “tackle box” with our medications
and documentation forms that our nurse signs out
prior to each EMG clinic.
Sedation has the unfortunate potential to
cause disinhibition and can occasionally make a
child more easily agitated. I have found this to be
more frequent with chloral hydrate (CH) than
some other medications. CH is a pure sedative
and in my experience does not offer relaxation:
the child either sleeps or not. I have found the
combination of lorazepam (0.07–0.1 mg/kg PO)
and acetaminophen with codeine (10 mg/kg of
acetaminophen and 1 mg/kg of codeine PO) in
liquid form to be the most helpful. It reduces
stranger anxiety, and children will often relax
during the set-ups between studies. Nasal mida-
zolam provides excellent anxiolysis for short
studies, but its duration of action is not long
enough to do a thorough study. The nasal ad-
ministration of midazolam causes nasal burning,
and rectal administration can be used as an alter-
native route with similar doses. The oral route is
also available.
Occasionally, general anesthesia is useful
when there is need for extensive nerve conduction
studies in cases of complicated peripheral injury or
when performing repetitive nerve stimulation.
Usually these children will have significant anxiety
when the physical examination is done. Obviously,
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CHAPTER 16 • PEDIATRIC CONSIDERATIONS IN ELECTROMYOGRAPHY
one cannot evaluate MUPs under general anesthe-
sia. Anesthesiologists will usually be willing to use
heavy conscious sedation for examination of MUPs
and then put the child under general anesthesia to
complete the nerve conduction studies. This tech-
nique is used infrequently, but occasional children
have an aversion to needles or have been so trau-
matized by frequent and painful procedures that
they cannot be studied while awake.
TECHNICAL CONSIDERATIONS
An electrically silent room, preferably with shield-
ing, is helpful. All accessory electrical equipment
should be unplugged and on a battery to prevent
60 Hz interference. If this is not possible, electrode
wires need to be as short as possible and shielded.
Needles can be monopolar or concentric. It is gen-
erally thought that monopolar needles are less
painful, but short concentric needles used for
small children are also very narrow in gauge. I do
not believe they are more uncomfortable than
monopolars, but this is a personal opinion based
upon trial and clinical experience. Concentric nee-
dles cause more bleeding, and some children are
very upset by the sight of blood, but the electrical
baseline is so much quieter with a concentric nee-
dle that the examination can frequently be accom-
plished in a much shorter time.
In an intensive care unit (ICU) setting, con-
centric needles are usually necessary. ICUs have
transport monitors available that run on batteries,
and these can be used to diminish electrical inter-
ference. Respiratory therapists can also be asked to
bag-ventilate a patient during an EMG. The ven-
tilator should be shut off and disconnected from
the AC source if interference continues to be a
problem despite the use of the 60 Hz notch filter.
Despite all these efforts, however, interference
from equipment in neighboring cubicles is often a
problem, and it is always easier to transport the
child to the EMG laboratory if the child is stable
enough.
INSTRUMENTATION AND SET-UPS
In young children, distances are shorter between
the reference and active electrodes than they are in
399
adults. This is also true for the distances between
the distal and proximal stimulation sites. Not only
does stimulator interference increase with shorter
distances, but shorter distances also introduce
greater measurement error. An error of 1 cm in
measuring an 8-cm latency introduces a 15% error
in the NCV (3).
Sensory nerve conduction set-ups in adults
are designed to have 4 cm between the reference
(E2) and active (E1) electrodes. The latency meas-
ured to the first take-off varies less than the peak
latency measured to the peak as the distance be-
tween the E1 and E2 electrodes narrows (15,16).
On infants and young children, it is often impossi-
ble to obtain a distance of 4 cm between the elec-
trodes; therefore, it is critical to evaluate the la-
tency to the take-off as well as the peak.
Sensory nerve conduction responses are more
easily obtained in children if the skin is prepared
prior to starting the procedure. Rubbing the skin
with a clean emery board or rubbing with EEG
paste and then cleaning the skin with alcohol to
remove oil and lotions increases the ability to
record reproducible sensory nerve action poten-
tials (SNAPs) by decreasing the skin impedance.
Another trick is to hold the foot or hand while
stimulating with the other hand. This enables the
examiner to determine when the child’s foot is re-
laxed so that the stimulation can be given when
there is less background electrical interference
from the patient’s voluntary activity. This takes
some practice to feel. An alternate approach is to
use the auditory feedback from the surface EMG
signal to determine the amount of voluntary mo-
tor unit activity.
TEMPERATURE
Attention to temperature is critical when exam-
ining children. Babies have a greater surface area
per kilogram than adults, which facilitates heat
loss. The room must be warm and the child must
be covered whenever possible. Heating lamps are
helpful to maintain body temperature in infants
as well as warming limbs of older children prior
to nerve conduction studies. Heating lamps must
be turned off and preferably unplugged during
the actual examination, however, as they cause a
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400 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
great deal of 60-Hz interference. Pressure-acti-
vated heating pads can be helpful for local
warming.
Control for skin temperature improves the
accuracy of motor and sensory latencies as well as
that of NCVs. Studies in adults have shown that
NCVs change from 1.4 to 2.4 m/s/°C in the upper
limbs and from 1.1 to 2.0 m/s/°C for the lower
limbs (16). One may assume that temperature will
affect the NCVs in young children, but the actual
amount is not known. It is therefore critical to
maintain a skin temperature close to the skin tem-
perature of the normal children studied when the
pediatric values were developed. Correction fac-
tors to adjust for skin temperature changes have
not been developed for young children.
Volume conduction must also be considered,
as it causes decreased latencies (16), which will af-
fect the NCV calculation. Care must be taken not to
overstimulate when trying to obtain a supramaxi-
mal compound motor action potential. The smaller
size of our patients makes this error an even greater
concern than it is in adults (see Fig. 3-22B).
Normative data are essential in interpreting
electrodiagnostic studies. It is difficult to collect
such data due to the reluctance of both parents and
physicians to cause discomfort to children. We
must thank investigators who have published the
data that they have collected. Careful attention to
their protocols regarding electrode set-up and dis-
tances used is necessary to use their data clinically.
It is best to refer to the original papers published to
ensure the closest reproduction of their techniques
possible (2,8,9,11,16–18). An invaluable reference
is the chapter entitled “Pediatric Electromyogra-
phy” in Neuromuscular Disorders of Infancy, Child-
hood, and Adolescence: A Clinician’s Approach (15),
in which the authors collected normative data for
children. From this list, the original articles can be
found to determine the specific protocols for the
normative data collected.
CLINICAL PROBLEMS
As in adult laboratories, there are groups of clini-
cal problems that arise frequently. Children are
frequently referred in the first year of life for eval-
uation of brachial plexus injuries, floppy tone, and
decreasing strength. Less frequently, a child will
be referred with regression of milestones in both
cognitive and motor spheres.
Brachial Plexus Injury
Babies with brachial plexus injuries are frequently
referred for evaluation during their second or
third week of life. Injuries occur perinatally and
are usually of the Erb type, an upper trunk injury
(19). In more severe injuries the entire plexus will
be involved. The classic Klumpke presentation of
a lower trunk injury is rarely seen. The majority
of Erb palsy injuries recover within the first 4
months (19,20), although Pondaag’s review (21)
has refuted this premise. All EMG laboratories are
referred a selected population of the more severe
injuries. Microsurgery continues to be controver-
sial, but children with the global brachial plexus
injuries and a group of the severe classic Erb
(C5–6  C7) will have a poor prognosis without
surgery (21–23). The electrodiagnostic studies will
be helpful to determine which babies are more
likely to have a spontaneous recovery. The par-
ents’ history of the child’s movement and clinical
observation are primary sources of information.
Use of the Moro reflex is very useful to activate the
muscles innervated by the upper trunk, including
the shoulder abductors, external shoulder rota-
tors, elbow flexors, and wrist extensors. If signifi-
cant motion is elicited, an electrodiagnostic study
may not be indicated, as spontaneous recovery
early frequently occurs. Heisse et al (24) recently
published a study that determined that the com-
pound muscle action potential (CMAP) ratio
(CMAP of the affected side as a percentage of the
CMAP on the unaffected side) was predictive of
motor prognosis.
The infant brachial plexus study starts with
evaluation of the amplitude of the CMAPs of the
axillary, radial, and suprascapular nerves. The
stimulations are done from a supraclavicular posi-
tion and responses are quite easy to elicit. If the
amplitudes are questionable, then the contralat-
eral side is stimulated for a comparison of ampli-
tude and latency. Normal values for amplitude
can vary up to 50% from side to side (24), but as
Heisse reports, other normal values are not read-
ily available (24). Sensory nerve conduction stud-
ies were previously thought to be necessary, as a
normal response was considered diagnostic of a
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CHAPTER 16 • PEDIATRIC CONSIDERATIONS IN ELECTROMYOGRAPHY
root avulsion. However, it has been found that
they are not always helpful, as their absence does
not exclude a root avulsion (23). A needle EMG is
also necessary to identify active MUAPs. The elec-
tromyogram for a brachial plexus study is started
within the sensory distribution of the axillary
nerve. Babies with a significant upper trunk lesion
cannot feel within the sensory distribution of the
axillary nerve, so examination of the deltoid can be
accomplished without discomfort to the child. It
is, in fact, a good clinical piece of information if
the child feels the electrode insertion, as it implies
a less severe injury. Once again, if the electromyo-
grapher has any question regarding the size and
recruitment of the MUAPs seen, then the child’s
contralateral arm can be used as a control. The cli-
nician should examine muscles that are obviously
weak. Those muscles that are questionably weak
will probably recovery spontaneously. The prog-
nosis and the discrimination among children who
may benefit from surgery and those that will not
are the goals of the study. Repeat studies can be
done to see whether reinnervation is occurring
electrically, if there is question left after the clini-
cal examination. The preoperative study will not
need to completely determine what surgical pro-
cedure is necessary, as an intraoperative study will
be done to direct the surgical decisions.
I have refused to do repeat electrodiagnostic
studies for medicolegal reasons, as I do not believe
it is ethical to hurt a child for that purpose. Pre-
diction of disability is based upon a clinical evalu-
ation of function rather than upon an electrical
analysis. Those examinations must wait until the
child’s neurologic function has had a chance to
stabilize.
The Hypotonic Infant
A frequent referral to a pediatric EMG laboratory
is a request to evaluate a “floppy infant.” Since
DNA testing is now available for many congenital
syndromes, the frequency of these referrals has
dropped.
Once again, a thorough history and physical
examination should direct the examination. Pri-
mary central nervous system dysfunction causes
80% of cases of newborn hypotonia (13,14,25). A
history of a difficult delivery frequently accompa-
401
nies these children. Knowledge of the normal pat-
terns of development is again necessary in the per-
formance of the physical examination. Examina-
tion of muscle stretch reflexes and of distal motor
control versus proximal motor control helps to
guide the electrical examination. Children with
central hypotonia almost invariably have muscle
stretch reflexes. A spontaneous and persistent
Babinski response is abnormal. All newborns have
a positive Babinski response unless they are under
influence of maternal sedation or they have severe
weakness secondary to a peripheral neuropathy or
another lower motor neuron lesion. Lower motor
neuron paraplegia is usually secondary to
myelomeningocele, but tumors are also possible.
Evaluate the alertness of the infant. Children
with central hypotonia are usually not as alert and
tend to have obligatory or persistent primitive re-
flexes. Distal strength is more difficult to appreci-
ate in infants than in older children, as distal hand
control does not develop until the latter half of the
first year. Distal ankle strength in children is usu-
ally examined during observation of gait, so spe-
cial care must be taken to look for it in an infant.
Most infants examined for a peripheral neuropa-
thy will have generalized weakness; the weakness
is just more profound distally than it is proxi-
mally.
Examination of the cranial nerves is critical in
the physical examination. Overall floppiness can
be impressive, and an examiner inexperienced in
examining young children may miss ptosis, facial
diplegia, or dysmorphic features. A good history
should direct the physical. Muscle stretch reflexes
are critical to evaluate, as their presence or absence
is a key factor in the decision algorithm of the dif-
ferential diagnosis, which leads to planning the
electrodiagnostic exam.
Next will be an overview of tone, followed by
a quick examination to look for cardiac dysfunc-
tion, hepatomegaly, and hernias. Following that,
joint range of motion is critical to examine. Con-
tractures are found in normal full-term infants; af-
ter all, they have been in cramped quarters for 9
months! Normal contractures will dissipate in the
upper limbs prior to the lower limbs, as a child is
born with a flexed position in all joints and will ex-
tend the upper limbs in a voluntary pattern earlier
than extension in the lower limbs occurs. The nor-
mal contractures will have a “give” or “softness” at
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402 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
the end point of range of motion, in contrast to the
contractures seen in children with congenital dys-
trophies or arthrogryposis.
As with any physical examination, approach
the pre-EMG physical examination in a systematic
manner. Clinical appreciation of distal weakness
will ensure that the electromyographer does not
miss a congenital peripheral neuropathy. The
electrodiagnostic procedure should also direct the
use of biopsies by identifying nerve versus muscle
problems and areas of greatest abnormality.
A rare group of diagnoses found in children
with floppy tone are the congenital myasthenic
syndromes. Congential myasthenia, which is
found when children receive the antibodies
transplacentally, is usually recognized since the
mothers have been previously diagnosed with
myasthenia gravis. Other congenital myasthenic
syndromes do not have acetylcholine receptor an-
tibodies and either are recognized in an infant or
present later in childhood (26–29).
Infants older than the newborn period may
present with a history of progressive weakness.
Poor head control may be noticed at a normal
well-baby check-up, initiating a referral. Some-
times a history of frequent, severe respiratory in-
fections will cause a referral from the pulmonary
consultant. Other children may present with rapid
decline, inability to feed, and severe floppiness and
dehydration and appear very ill. Differentiation
among acute, subacute and chronic weakness is
the first step in planning the electrical study.
Floppy infants may have weakness and spas-
ticity as well. It is critical to have a birth history, as
this will help to divide the children with cerebral
palsy from those with degenerative diseases. A
critical question to ask is whether the child has lost
any skills that he or she had acquired in the past. A
differential that takes into account the presence or
absence of muscle stretch reflexes must be consid-
ered. Systemically ill children with diseases such as
chronic infections or severe gastroesophageal re-
flux may have apparent regression in develop-
ment. These children usually progress in develop-
ment, just not as rapidly as healthy babies. A
careful history is necessary to determine whether
skills have actually been lost or if they have just
fallen behind. It is hoped that there will be other
clues to direct the diagnostic approach, but from a
practical point of view, conundrums will occasion-
ally appear in your office. Children with repeated
respiratory infections may be referred for possible
spinal muscular atrophy (SMA) when cystic fibro-
sis is the culprit, just as small children with SMA
have been referred to pulmonologists for evalua-
tion for cystic fibrosis. Cognitively impaired chil-
dren are often irritable, being unable to calm them-
selves. This history may be secondary to
gastroesophageal reflux disease or other causes of
pain, so one cannot assume that a history of irri-
tability implies central neurologic dysfunction.
Occasionally a child presents with hip and
knee flexion contractures without the characteris-
tic club foot deformities seen in arthrogryposis. If
the child is weak throughout, congenital muscular
dystrophy should be entertained as well as other
myopathies. Children with merosin deficiency
usually have large heads and leukodystrophy will
be seen on magnetic resonance imaging scans of
the brain. Their nerve conductions may be mildly
slowed (30). Their necks appear weak, and clini-
cally they may initially appear to have SMA. Chil-
dren with SMA do not usually present with
contractures, though they usually develop as the
disease processes. A child with congenital muscu-
lar dystrophy (CMD) will get stronger as he or she
grows, in contrast to a child with SMA, who will
become weaker. The EMG will identify CMD
rather than SMA as the diagnosis, since the
MUAPs will be small and there will be increased
recruitment.
CMDs are being studied to determine the
types of electrodiagnostic abnormalities (30).
Genetic studies have determined many of the
chromosomal locations for CMDs both with and
without central nervous system abnormalities.
The most common is the primary merosin defi-
ciency at 6q2.
Some floppy babies present in the newborn
nursery. The children with hypoxic ischemic
events will be ruled out by history. It is rare that a
neonatologist will refer such a patient for an elec-
trodiagnostic study; however, some children have
difficult perinatal courses because of their under-
lying disease. Neonatologists are skilled at identi-
fying babies with unusual facies, who have a
different differential diagnosis than children with
normal appearances.
Children with diagnoses such as the congeni-
tal myopathies often have a history of a difficult
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CHAPTER 16 • PEDIATRIC CONSIDERATIONS IN ELECTROMYOGRAPHY
perinatal course, but they will appear weak rather
than just floppy. Congenital myotonic dystrophy
is one of the most common entities. The face is not
as narrow as with some of the congenital my-
opathies; however, respiratory effort may be poor
and the infant may require intubation. Poor feed-
ing tolerance often presents due to smooth muscle
involvement. Facial diplegia shows with poor
mouth closure, described as a “tented mouth.”
The nasolabial folds are absent or diminished. It is
very helpful to examine the mother, as she may
have facial diplegia also. A high index of suspicion
is necessary: the weakness is not always obvious in
the mother, and if no formal examination is done,
myotonia could be missed. Myotonia may be ab-
sent in the infant, usually to appear by 3 to 5 years
of age. Needle EMG shows profuse fibrillation
potentials early on, and their appearance can be
the most prominent finding. Occasionally,
though, myotonia can be so severe that the new-
born’s hand will appear almost fisted. In that
instance, EMG is very helpful to differentiate my-
otonia from spastic hypertonicity (Fig. 16-1). The
electrodiagnostic study reveals normal NCV, but
the MUPs are small and recruit rapidly. Low-am-
plitude CMAPs may be present also. Myotonic
dystrophy is inherited in an autosomal recessive
manner with a trinucleotide repeat found on chro-
mosome 19 at q13.3 (31,32). The mother may be
unaware of her disease since there is anticipation
in this disease’s inheritance, with increasing
lengths of the trinucleotide repeat abnormality in
subsequent generations, resulting in increased
severity in future generations (31).
Myotonia congenita is the most common con-
dition mistaken for myotonic dystrophy. The
Figure 16-1 ● A portion of a train of myotonic potentials recorded with monopolar nee-
dle from the flexor carpi ulnaris muscle. A gradual increase in the frequency is seen during this time,
as is typical in this pathology.
403
myotonia is often so severe that it will cover up the
normal MUPs of myotonia congenita. Patience is
required to ensure that the MUP amplitudes and
durations are carefully evaluated.
Floppy infants with long narrow faces are
easy to recognize as having a neuromuscular dis-
ease. An X-linked recessive centronuclear myopa-
thy (32) will present with a very floppy infant with
a long narrow face. Intubation is usually necessary
and subsequent extubation is difficult. Long-term
ventilation may be necessary. Other congenital
myopathies do not have such poor prognoses. In-
fants with fiber-type disproportion have milder
weakness that may not be severe enough to pre-
vent the child from being discharged with the
mother prior to diagnosis. Children with nema-
line neuropathy have extremely long narrow
faces. There is obvious muscle atrophy noticed as
they get older, and their smile is horizontal. The
EMG can be abnormal in the newborn period,
with abundant fibrillation potentials and reduced
amplitude of the MUAPs (33–35).
Prader-Willi children will be profoundly hy-
potonic but have normal-shaped faces. They are
usually poor feeders. Children with normal faces
who have profound hypotonia, like a rag doll,
should have the FISH study done to include or ex-
clude the diagnosis of Prader-Willi. Most children
with congenital myopathies will have normal
EMG examinations, with the exception of cen-
tronuclear and nemaline myopathy (35). Congen-
ital myopathies may present later in the first year.
Children with central core disease may be weak
but are not usually identified in the newborn nurs-
ery. Their faces are usually normal and they do
not show the long, narrow faces typically seen in
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404 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
children with congenital myopathies. Needle
EMG and nerve conduction studies are usually
normal. These children may present with
developmental hip dysplasia or other skeletal de-
formities. They are at a high risk for malignant
hyperthermia when given halothane-type anes-
thetics. The complaint leading to presentation
varies considerably, and persons presenting at a
later age may have only exercise intolerance and
myalgias (35).
Hypomyelination (of the peripheral nerve)
syndrome usually presents at birth, and the chil-
dren affected frequently require ventilation. Oc-
casionally wrist and foot drop is profound, but the
level of alertness is not usually helpful, as these
children have a difficult early course and may be
on sedatives to ease ventilation. Electrodiagnosis is
critical in these circumstances. Both sensory and
motor nerve conduction studies are abnormal, and
sensory nerve potentials are usually absent. Motor
nerve conductions are very slow, reflecting the
poor myelin. Both muscle and nerve biopsies are
necessary to make the diagnosis. However, with-
out the conduction velocity information from the
electrodiagnostic studies, only a muscle biopsy
may be ordered. Therefore, performing the elec-
trodiagnostic study first may decrease the number
of anesthetics that the child must receive.
Other clinical problems will initiate referrals
from a newborn intensive care unit. A referral
may be received regarding an infant who is diffi-
cult to extubate, with the request to evaluate the
phrenic nerve and diaphragmatic function. Russel
et al (36) described a phrenic nerve technique in
babies. They described a set-up in which the
ground electrode is placed on the middle of the
sternum and the active electrode on the mid-axil-
lary line at the level of the seventh rib. The refer-
ence electrode is placed just below it, on the mid-
axillary line at the level of the eight intercostal
space. Stimulation is just behind the sternocleido-
mastoid muscle. Normal latencies range from 3.4
to 7.4 ms. Phrenic nerve palsies are most fre-
quently seen with severe upper trunk obstetric
palsies.
Arthrogryposis multiplex congenita presents
in the delivery room, but the neurologic work-up
can be delayed until the child is stable. Affected
children have more than one major joint with
congenital contracture (32), and the muscles are
atrophied. Dimples are characteristically found
over the joints. A recent paper (37) has reviewed
the accuracy of electrodiagnostic studies in com-
parison with muscle biopsies and has found that
the two studies together are far more accurate
than either alone. The authors also concluded that
a careful examination looking for an exogenous
sign (e.g., a midfacial superficial hemangioma) is
advantageous: if one is found, then both the elec-
trodiagnostic studies and the muscle biopsy may
be avoided (37).
The differential diagnosis changes after the
newborn period, and after 1 year of age it changes
again. Certainly some diagnoses are more likely to
be found in older school-aged children or in
adolescents. SMA can present at anytime, as can
Guillain-Barré syndrome (GBS). Few pediatric
electromyographers have seen GBS in patients
under 1 year of age.
Botulism
Infantile botulism is usually seen between 6 weeks
and 6 months of age and is a disease seen only by
electromyographers who evaluate children. Infan-
tile botulism will present as a somewhat more
acute illness than the previously described diseases
and will show in a previously normal child. These
children have normal birth histories and feed nor-
mally until the illness becomes apparent. Hypoto-
nia and poor feeding cause parents to consult a
physician. Parents usually complain that their
child is not feeding well and is having trouble with
drooling. Most will give a history of constipation if
it is asked for in a review of symptoms. The degree
of weakness also varies. In the most severe cases,
bilateral ptosis occurs and the pupils are pinpoint.
Weak facial muscles make the child appear dull
and sedated. The cry will be weak and pitiful,
causing the child to appear ill, in contrast to the
child with SMA, who is bright-eyed and interac-
tive. Classically the history of honey or corn syrup
intake is present, though many of the babies have
been fully breast-fed. The disease is more preva-
lent in certain areas, and it is believed that the
spores are airborne and can be encountered in
house dust.
The electrodiagnostic study should start with
nerve conduction studies, which should have nor-
mal to slightly slowed velocities. The child with
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CHAPTER 16 • PEDIATRIC CONSIDERATIONS IN ELECTROMYOGRAPHY
GBS would be expected to have slowed velocities
even at this age. Even if the NCVs are normal, if
the child has GBS, no facilitation to rapid repeti-
tive stimulation will be seen. The CMAPs will be
minute, sometimes only 50 to 100 microvolts in
size. Careful attention must be paid to the set-up,
since otherwise this small-amplitude response
may be lost within the background noise. Two-
Hertz repetitive stimulation will show a stable
amplitude. In the more severe cases, 20 Hz will be
sufficient to elicit the 150% to 500% increment
(Fig. 16-2), although with more questionable cases
50 Hz will be necessary (38–41). Prolonged postte-
tanic facilitation is also characteristic of infant bot-
ulism (39). Ten-second tetanizing stimulation is
very painful but is necessary for a complete evalu-
ation for botulism (37). Motor units seen in infan-
tile botulism can be so small that they appear to be
fibrillation potentials, except that they stop when
the child stops moving. The negative initial de-
flection can be difficult to appreciate with such
small MUAPs. There are often normal motor
units mixed in with the tiny ones, and this can also
be misleading, especially if the amplifier gain is set
too low (e.g., at 100
V/cm rather than 50 or even
20
V/cm).
Figure 16-2 ● Repetitive stimulation in a
child with botulism at 30 Hz demonstrates
an incrementing response from the exten-
sor digitorum brevis muscle over time,
with a more than 150% increase in ampli-
tude of the CMAP.
405
If the child is not intubated, the study may
stress the child enough to require intubation. If I
believe this may be the case, I will speak with the
primary care service and will decide either to
transfer the child to the ICU with an intensivist
standing by or to postpone the study until the clin-
ical situation is safer. The clinician must continu-
ally watch for evidence of respiratory compro-
mise, especially with inpatient consults, as
weakness of acute onset can be rapidly progressive
in infants. I prefer to do these studies in the ICU
with preparation for intubation clinically neces-
sary. Clinical criteria for ventilatory support must
be used to prevent the need for emergency intuba-
tion due to the stress of the study. Analgesia can be
used safely after intubation. Monitoring heart rate
and blood pressure is also used to determine pain
responses and the need for analgesia during the
study of a paralyzed child.
CASE 1
A 6-week-old infant boy presents to the emer-
gency department with a 2-day history of lethargy
and poor feeding. His parents state that he had a
normal birth history and has been gaining weight
well. He had started to smile. Tone had been ex-
cellent. Upon questioning, his parents indicate
that he had been constipated and does not seem to
be swallowing well.
The physical examination reveals a male in-
fant who appears ill. Temperature is 97°F. He is
lethargic and tone is poor. He is tachypneic and
breathing shallowly and appears to have bilateral
ptosis. His pupils are small. Muscle stretch reflexes
are absent.
A complete blood count, serum electrolytes,
and lumbar puncture are within normal limits.
Chest x-ray is normal. He is placed on antibiotics
for presumed sepsis and admitted to the PICU.
EMG Study
The nerve conduction study shows a peroneal mo-
tor amplitude of 100
V (reduced). The velocity is
normal at 27 m/s. Two-Hertz repetitive stimula-
tion shows no change in amplitude. Repetitive
stimulation for 10 s at 20 Hz shows no increase in
the amplitude. The stimulation rate is increased to
50 Hz and the amplitude gradually increases to
300
V. EMG shows very small, brief, simple
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406 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
MUAPs. At first the examiner feels that there are
4 fibrillation potentials, but she rapidly realizes
that the apparent fibrillation potentials are present
only when the child moves. The potentials are about
100
V in amplitude and about 2 ms in duration.
The diagnosis of infantile botulism is reported.
Supportive care is continued with mechanical ven-
tilation. Care is taken not to use any “mycin” antibi-
otics that can impair neuromuscular transmission.
No stool is available for 3 days despite enemas, but
within 1.5 weeks, the state health department labo-
ratory confirmed that botulism type B was the cul-
prit. The child recovered well.
Spinal Muscular Atrophy
With SMA, the younger the child presents with
weakness, the more severe the disease. Babies
generally have a normal birth history and appear
normal to both parents and physicians at first. Ex-
perienced parents will become aware of their
child’s weakness earlier, while in first children the
weakness is usually noticed by the pediatrician.
Children presenting prior to 6 months of age have
a poor prognosis for living beyond their second
birthday unless mechanical ventilation is given.
Babies have a frogleg posture and have no muscle
stretch reflexes. Normal NCVs are present, but
the amplitude of the CMAP is small. Sensory
nerve conductions are normal (42,43). If missing,
an electrical diagnosis cannot be definitive. The
sural nerve response is the easiest to obtain. The
child’s face is usually bright and alert. Fibrillation
potentials are present. MUAPs are usually high in
amplitude for age and have reduced recruitment.
However, in rapidly progressive disease no en-
largement of the MUAP will be seen, since disease
progression is faster than distal axonal sprouting.
In these children it is helpful to the neuropatholo-
gist if you call to discuss this possibility, since the
classical fiber-type grouping may be absent on
biopsy. The electrodiagnostic information will be
helpful to him or her in interpreting the muscle
biopsy. Blood testing for the survival motor neu-
ron (SMN) gene usually takes a week, and this is
too long in critical situations when end-of-life and
life-support decisions are necessary. Some physi-
cians wait for the SMN gene results instead of ask-
ing for an EMG, especially if the child is not in
critical condition. Parents are frequently anxious,
however, so we still are asked to do electrodiag-
nostic studies regularly.
Infants older than the newborn period who
have SMA will present with a history of progres
sive weakness. Poor head control may be noticed at
a routine well-baby check-up. A history of frequent
severe respiratory infections sometimes causes a re-
ferral to be placed to a pulmonologist. One child
was sent to me with the referring diagnosis of con-
stipation. Other children may present with rapid
decline, inability to feed, and severe floppiness and
dehydration. They may appear so ill that they are
admitted through an emergency department with
the diagnosis of presumed sepsis. Electrodiagnostic
studies are very helpful in this situation.
In the second 6 months, a child presenting
with SMA usually sits in some fashion, although
he or she has no reflexes. Once again he appears
bright-eyed and very alert. He has a normal per-
sonality and interacts with the examiner. The
physical signs previously described of “no neck” or
pseudoathetosis may be present.
The examiner should look for an age-appro-
priate grasp, because the distal development of
grasp is always further along than expected com-
pared to trunk control when a child has such pro-
found proximal weakness. Fine motor skills will
be symmetrical in the hands unless the child is
older than 1 year, since children do not display
hand preference until 1 year of age. Tongue fasci-
culations may be present, but crying children can-
not be examined for tongue fasciculations, as all
crying babies appear to have them.
NCVs are normal, though the amplitudes
may be diminished. MUAPs are larger and more
complex (polyphasic) than normal on EMG. Re-
cruitment shows the reduced interference pattern
seen with decreased numbers of motor unit poten-
tials. Fibrillation potentials are usually seen.
CASE 2
A 4-month-old girl presents in respiratory dis-
tress. She has a normal birth history, having been
born to a 19-year-old gravida 1, para 1 mother.
Her pediatrician had been a bit concerned regard-
ing her tone at her 2-month check-up, but she was
gaining weight well. Parents are chiefly concerned
about her constipation. She has been a very happy
baby but is not handling this “cold’ well. She is not
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CHAPTER 16 • PEDIATRIC CONSIDERATIONS IN ELECTROMYOGRAPHY
drinking well. The grandmother came to visit and
is very worried, as she thinks that the baby is “not
acting right.”
Physical examination shows a baby in mild
respiratory distress. She is breathing rapidly but is
not coughing. She looks at the examiner and is
alert but cranky. Abdominal breathing and nasal
retractions are present. It is difficult to determine
whether the tongue is fasciculating since she is
frequently crying. Neck weakness is shown, as
head lag is obvious. In a supine position her legs
assume a frogleg position. Muscle stretch reflexes
are absent. She is admitted for supportive therapy
and diagnostic evaluation. An SMN gene evalua-
tion was sent. Two days later her condition deteri-
orates. An EMG is requested for rapid diagnosis
to help with end-of-life issues. The nerve conduc-
tion studies reveal small-amplitude CMAPs and
the velocities are normal for age. Sural sensory
nerve responses are normal. EMG reveals large
polyphasic units about 1.5 mV in amplitude. Eval-
uation of recruitment reveals that MUAPs are
firing at 30 Hz in her legs and 20 Hz in her upper
limbs, with decreased numbers of motor units
recruited at all sites.
The primary team is told that her presenta-
tion and the electrodiagnostic study results sup-
port the diagnosis of SMA type I. Counseling is
offered to her parents. A muscle biopsy is re-
quested. The girl recovers from her respiratory ill-
ness before the results of the muscle biopsy and
SMN deletion study are available; both are indica-
tion of SMA. Ongoing support and management
of her disease are arranged.
Other First-Year Presentations
The first year of life has its own group of diseases,
which include Pompe’s disease, infantile acid mal-
tase deficiency (AMD), and several leukodystro-
phies. These children appear ill with generalized
weakness (35) and frequently have a large tongue.
They have the same frogleg posture as do children
with SMA, reflecting poor hip muscle strength.
The EMG may show myotonia as well as small,
brief MUAPs (27). Due to their cardiac involve-
ment, children with Pompe’s appear more system-
ically ill than children with myotonic dystrophy or
SMA. They may have mild hypertrophy of their
muscles in face of a severe hypotonia. Childhood-
407
onset AMD presents in a child with motor delay
and respiratory weakness. AMD is slowly and
steadily progressive. The electrodiagnostic exami-
nation is similar to that in the infantile form but
can be confined to the proximal muscles (35).
Pelizaeus-Merzbacher disease presents with
nystagmus and ataxia. Children may present with
floppiness, titubation, and nystagmus. Infants and
children may present with delayed milestones.
Eventually ataxia, choreoathetosis, and spasticity
ensue. The classic form is X-linked recessive and
the gene is located at Xq22 (32). NCVs may be
slowed. This disease is often categorized with the
leukodystrophies as the myelin is abnormal in both
the central and peripheral nervous systems (32).
Krabbe’s leukodystrophy usually presents af-
ter the newborn period but within the first few
months of life. The child appears irritable and
shows poor feeding and failure to thrive. Develop-
mental progress slows and then deterioration be-
comes apparent. On physical examination the
child feels spastic but characteristically has no
muscle stretch reflexes. NCVs are markedly
slowed due to the abnormal myelin. Biopsies show
reduced numbers of myelinated fibers and seg-
mental demyelination (44). The disorder is auto-
somal recessive and the gene is located at 14q24.3-
q32.1 (45). The disease can have a late onset that
begins in childhood or adolescence with optic at-
rophy, ataxia, gait abnormalities, and spasticity.
Leukocytes have the same deficiency as the infan-
tile form, a deficiency of galactocerebroside -
galactosidase (32).
Infants who present with rapid onset of
weakness and respiratory compromise may have
GBS. Diphtheria should also be considered, espe-
cially in children who have not been vaccinated.
Both diseases cause prolonged nerve conductions.
However, infantile botulism should remain at the
top of the differential diagnosis of rapid-onset
weakness and respiratory compromise, since it is
the most common cause of these findings and will
not be diagnosed unless rapid repetitive stimula-
tion is done (Fig. 16-2).
Presentation after 1 Year
When children over 1 year of age are evaluated,
knowledge of pediatric gait is necessary. Also im-
portant is familiarity with the usual changes in
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408 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
movement patterns assumed by weakened chil-
dren. When a child begins to stand, he or she will
pull up to a stand through a half-kneel. Mature
gait should be present by 10 months following ini-
tiation of independent gait. As a child’s gait ma-
tures, the stance will narrow and the toddler pat-
tern will smooth out. Knee flexion appears at
midstance. A child should be able to arise from the
floor without rotating into a four-point stance al-
most immediately after attaining the milestone of
being able to stand in the middle of the floor. Sen-
sory loss frequently appears as ataxia in young
children. Nerve conduction studies are very help-
ful to evaluate a possible peripheral neuropathy
presenting with ataxia.
Developmental knowledge is essential to the
pre-EMG physical examination. Weakness is eas-
ily missed, and the choice of muscles to be studied
by EMG depends upon the physical examination.
The pediatric electromyographer does not usually
have the ability to do studies on three limbs. Chil-
dren with deterioration of intellectual skills, de-
pressed or absent muscle stretch reflexes, and
spasticity may fall into the leukodystrophies if a
myelinopathy is present. Metachromatic leukody-
strophy (MLD) presents at about 2 years of age
and classic adrenoleukodystrophy (ALD) classi-
cally presents between 5 and 15 years (32). Late in-
fantile MLD presents with sensory ataxia. The
child has fairly normal intellectual function ini-
tially, but rapid cognitive deterioration occurs.
NCVs are severely slowed and have small-ampli-
tude responses. Juvenile MLD presents later, from
5 to 10 years of age. MLD is inherited in an auto-
somal recessive manner, with the gene located on
chromosome 22q 13q (32). Inadequate arylsulfa-
tase causes cerebroside sulfate to accumulate in the
myelin (32). ALD is inherited in a sex-linked re-
cessive manner, with the ABCD 1 gene located on
the q28 position on the X chromosome. Children
often present with intellectual deterioration and a
question of attention problems (32), but gait ataxia
rapidly becomes apparent. Mildly slowed motor
and sensory NCVs occur with evidence of “dener-
vation” on needle EMG (43). Families may recog-
nize the problem if other children in the family
have been affected, and EMG is not necessary in
that situation. Families are usually willing to
await the DNA test results.
Fairly acute weakness can present with der-
matomyositis, although this problem is unusual in
young children. A heliotrope rash alerts the exam-
iner to dermatomyositis. The course in dermato-
myositis is variable. NCVs are normal. Numerous
fibrillations are seen with needle study, along with
small-amplitude, brief, and complex MUPs. Chil-
dren presenting with acute-onset weakness usu-
ally demonstrate increased recruitment of motor
units at low strength. Chronic, severe cases of der-
matomyositis demonstrate many chronic myo-
pathic features, such as complex repetitive dis-
charges and reduced recruitment. Abnormalities
are more often found in proximal limb muscles
and are also seen in the paraspinal muscles (42).
Polymyositis is rare in children but can be seen,
and the electrodiagnostic findings are similar to
those seen in dermatomyositis.
Guillain-Barré Syndrome
GBS presents in children much the same as it does
in adults, with the exception of the ataxia. A sen-
sory level should not be present, but this is often
difficult to determine in young children. Dyses-
thesias are frequent in childhood GBS, so the sen-
sory examination is challenging. Irritability and a
high-pitched whine are clinical signs of pain in a
child with GBS. The dysesthesias of GBS particu-
larly seem to cause children to whine in a manner
that causes staff to believe that the child is spoiled
and demanding: the children do not seem to be in
pain, just obnoxious. The response of the staff is so
typical that it is actually helpful in making the di-
agnosis. It is estimated that pain is found in 50% to
80% of cases in childhood and adult GBS (46); our
clinical experience is consistent with the 80% inci-
dence. Gabapentin can be very useful in control of
this neuropathic pain, and “the whine” almost im-
mediately ceases.
Initial electrodiagnostic studies may be nor-
mal, but nerve conduction studies usually show
diminished amplitude and increased temporal
dispersion. Conduction block is usually present
early. NCVs are classically slow but are fre-
quently normal initially when the disease affects
proximal nerve segments. Conversely, distal la-
tencies can be prolonged, with the CMAP show-
ing low-amplitude and temporal dispersion de-
spite a normal NCV. F waves and H reflexes
should be tested if peripheral abnormalities are
not found, but these tests are not as helpful in
children as they are in adults (46). Multiple
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CHAPTER 16 • PEDIATRIC CONSIDERATIONS IN ELECTROMYOGRAPHY 409

nerves may need to be studied, since this is a mul-
tifocal disease. Needle EMG usually shows de-
creased recruitment of MUPs.
GBS is far more common than most of the di-
agnoses I have mentioned already. During the
past decade or so the syndrome has been looked at
critically and is now being divided into several cat-
egories that correlate with prognosis. Acute in-
flammatory demyelinating polyradiculopathy
(AIDP) is the most common form and involves
both sensory and motor nerves. AIDP presents
with acute or subacute history of weakness and
loss of tendon reflexes. The course can be as rapid
as a few hours or develop over a couple of weeks.
Nerve conduction studies may be normal early but
usually demonstrate slow velocities with evidence
of conduction block and temporal dispersion of
the CMAP (Fig. 16-3) (46). EMG usually shows
diminished recruitment with normal MUPs, but
no membrane irritability early in the course.
Nascent potentials and small complex MUPs are a
characteristic late finding.
Acute motor-sensory axonal polyradiculopa-
thy is an uncommon variation of GBS but clini-
cally appears to be the same as AIDP. The electro-
diagnostic studies show markedly diminished
amplitude of both CMAPs and SNAPs (46,47). If
they can be obtained, nerve conduction studies are
only mildly slowed, presumably due to the loss of
the faster-conducting fibers. EMG reveals
marked membrane abnormalities and decreased
recruitment.
Acute motor axonal neuropathy (AMAN)
also presents with a clinical picture similar to
AIDP. Sensory and motor NCVs are normal, but
the amplitude of CMAPs is diminished. SNAPs
continue to have normal amplitudes. EMG is typ-
ical of that seen with axonal neuropathies. Re-
cruitment is diminished, and membrane irritabil-
ity is absent initially but appears later, as would be

Figure 16-3 ● CMAP responses in a child with AIDP demonstrate severe delay in the dis-
tal latency (upper trace) as well as slowing of conduction velocity. These small-amplitude re-
sponses also demonstrate typical temporal dispersion seen in AIDP with prolonged duration times, more pro-
nounced with proximal stimulation (lower trace).
90749_ch16(395-416).ps 8/10/06 3:55 PM Page 410
410 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
expected of an acute-onset axonal neuropathy.
This syndrome is associated with Campylobacter
jejuni enteritis and was first described in China.
The prognosis is good in childhood (46,47).
The Fisher syndrome of ataxia, areflexia, and
ophthalmoparesis is seen occasionally in children
as a variant of GBS. The electrodiagnostic changes
can be purely sensory, or as the syndrome pro-
gresses the nerve conduction studies show changes
similar to those seen in AIDP. Prognosis is excel-
lent for full recovery in children (46).
Chronic inflammatory demyelinating poly-
radiculopathy (CIDP) can present in an acute
fashion similar to AIDP and then either relapse,
or fail to improve, as would be expected in AIDP.
CIDP can also present with a history of progres-
sive weakness over a period of months. I have seen
CIDP misdiagnosed as SMA type III in a girl who
was on a high-school swim team until she found
she did not have the strength to mount the diving
block. The history of a teenager being an athlete
is unusual with the diagnosis of SMA, as those
adolescents are usually not successful in physi-
cal endeavors. Careful NCVs revealed marked
differences in the conduction velocities of sim-
ilar nerves and conduction block with temporal
dispersion of the CMAP. Since CIDP is treat-
able, it is critical to pay attention to the history
and perform an adequate nerve conduction
study.
Occasionally a previously healthy adolescent
will be referred due to acute weakness and muscle
soreness. The primary care or urgent care physi-
cian may have ordered a creatinine kinase (CK)
level due to the significant weakness apparent on
the physical examination. The child is referred
when the CK level is reported to be significantly
above the upper limit of normal. The sedimenta-
tion rate may also be elevated. The family may
have been told that their child has muscular dys-
trophy or polymyositis, so they are usually very
anxious. The NCVs are normal, but the ampli-
tudes may be slightly diminished. The EMG is ab-
normal with positive waves, fibrillation potentials,
and small, brief MUPs. Recruitment is increased.
The history of a viral illness is usually present. A
rapid spontaneous decline in the CK confirms the
diagnosis of viral myositis (48). In fact, after seeing
several of these children, the electromyographer
may choose to recheck the CK before proceeding
to the EMG. If the CK has markedly diminished
since the referral, an EMG is not necessary (47).
Leukemia
Children may be referred for an EMG with the
appearance of proximal weakness when pain is ac-
tually causing the Trendelenburg gait pattern typ-
ically seen with bilateral gluteus medius weak-
ness. Experience in watching children will help to
determine children who “look sick” in contrast to
children with Duchenne muscular dystrophy,
who do not appear ill. The manual muscle testing
may appear normal, although a Gower’s sign and
a waddling gait may be present, but an antalgic
gait may appear as a “gluteus medius limp”
(49,50). The EMG in leukemia may show the
smaller-amplitude MUPs that are usually seen in
disuse atrophy. Thirty percent of children with
acute lymphocytic leukemia (ALL) present with
bone pain. A ventral polyradiculopathy has also
been reported in a 3-year-old with ALL 12 days
following intrathecal methotrexate, Ara-C, and
hydrocortisone administration during mainte-
nance chemotherapy (51).
Kocher-Debré-Sémélaigne
A very unusual referral is that of a girl with
pseudohypertrophy of the calves. Girls can present
with symptomatic weakness when they carry the
gene for Duchenne, but occasionally a hypothy-
roid myopathy presents in a similar manner.
Kocher-Debré-Sémélaigne syndrome’s actual
pathophysiology is unknown. Boys are reportedly
more likely to develop the pseudohypertrophy af-
ter a prolonged period of inadequate thyroid, but
I have seen it only in girls (52). EMG and NCVs
are normal.
Miscellaneous Diagnoses
Unusual presentations of pain, numbness, and
weakness in children or adults may be sent to the
EMG laboratory for evaluation. Younger children
may present with unusual pressure neuropathies
caused by deformities from congenital anomalies.
Mononeuropathies may be caused by exostoses.
Adolescents with anorexia nervosa may develop
peroneal palsies when they lose so much weight
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CHAPTER 16 • PEDIATRIC CONSIDERATIONS IN ELECTROMYOGRAPHY
that their nerves become vulnerable to pressure,
just as in adults who have rapid weight loss.
Carpal tunnel syndrome is rare in children but oc-
curs with myxedema and mucopolysaccharidoses
and in adolescents who crutch walk. Radicu-
lopathies are also unusual but appear in adoles-
cents with disc injury. Congential syndromes
must always be kept in the differential diagnosis
when evaluating children.
Children with diabetes may be referred for
evaluation if they are having symptoms of pain or
signs of weakness in their lower limbs. Kruger et al
studied a group of type 1 diabetics to compare the
femoral nerve to the peroneal nerve as a screening
test for diabetic neuropathy (53,54). They found
that the femoral nerve latency was not significantly
different between the diabetic children and the
controls. The peroneal nerve was more sensitive
for neuropathy: diabetic children had mean NCVs
of 50.2  6.9 m/s and control children had NCVs
of 54.1  3.5 m/s. Of interest, but not surprising,
was the finding that the NCV had an inverse cor-
relation with the HbA1c reading (54).
Another endocrine disorder that can mimic
Duchenne muscular dystrophy is Kocher-Debre-
Sémélaigne syndrome, which presents as general-
ized muscular hypertrophy secondary to hypothy-
roidism. Electrodiagnostic abnormalities show
low-amplitude and short motor units. The CK
level may be mildly elevated. The myopathy re-
solves with treatment of the hypothyroidism (53).
Traumatic peripheral nerve injuries will also
appear in a pediatric EMG clinic. The most com-
mon injury is a radial or ulnar neuropathy follow-
ing supracondylar humeral fractures; the median
nerve can also be affected. The nerve conduction
study will be helpful to the surgeon to determine
whether spontaneous recovery is occurring or
whether surgical exploration is necessary. Ante-
rior compartment syndromes may occur after se-
vere tibia and fibula fractures. I have also seen a se-
vere anterior compartment syndrome following
use of an umbilical catheter in the neonatal nurs-
ery. Penetrating injuries from sharp objects such as
broken windows are handled in children in a sim-
ilar manner as they are in adults, and other than the
possible need for sedation, the electrodiagnostic
studies are approached in a similar manner.
Peripheral nerve injuries can be the result of
postviral infection complications. The most
411
common is Bell’s palsy, which occurs in children
as well as adults, affecting the facial nerve. Very
young children do not do well with an electrode
stuck to their faces, nor do they tolerate sub-
mandibular stimulation. I would suggest stimu-
lating young, frightened children under deep con-
scious sedation or general anesthesia. Since
operating suites are very well electrically insu-
lated, you will encounter little electrical interfer-
ence. I have been amazed at how quickly the study
can be done with the child under anesthesia. If
surgery is being considered, an accurate study is
necessary; otherwise, the child and family receive
useless information.
Electromyographers working in a tertiary
pediatric hospital will encounter critical illness
neuropathy and steroid myopathies. Now that
these disease entities are well established, I am
not sure that an electrodiagnostic study is neces-
sary for diagnosis. EMG has rarely been helpful
to determine whether a child requires a tra-
cheotomy. Diagnosis of the cause of weakness
will not change the treatment, since there is no
specific treatment yet available for these prob-
lems. By the time the weakness is observed, extu-
bation is being considered, the need for high-dose
steroids is usually diminishing, and vecuronium
is no longer being used. Both parents and physi-
cians are reluctant to further traumatize a child
with electrical testing. In contrast to children
with diffuse severe weakness, children and ado-
lescents who are suspected of having a localized
phrenic nerve injury require an electrodiagnostic
study. It is much easier to stimulate a phrenic
nerve for a conduction study than to transport
the patient to fluoroscopy for examination of di-
aphragm motion. Fluoroscopy is more easily
done if the child is cooperative, whereas a
phrenic nerve study can easily be done under se-
dation when a child is ventilated and in the ICU.
A phrenic nerve study and diaphragmatic EMG
is a fairly short examination compared with the
time needed to determine the exact diagnosis of a
child with diffuse severe weakness following sep-
sis or acute respiratory distress syndrome (36). As
with any medical procedure, EMG should be
done only when the results are likely to direct
treatment.
Gradual onset of weakness and ataxia must
be evaluated by electrodiagnosis. A child thought
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412 SECTION III • SOLVING THE PROBLEMS IN CLINICAL EMG
to have ataxic cerebral palsy will be referred for
electrical evaluation when it is noted that his or
her condition is worsening. Absence of muscle
stretch reflexes with increased tone, a positive
Babinski response, and ataxia raise concerns of a
sensory neuropathy. Both Friedreich’s ataxia and
ataxia-telangiectasia show sensory neuropathy, so
the establishment by sensory nerve conduction
studies will guide the clinical investigation to dif-
ferentiate these from motor and sensory neu-
ropathies and central nervous system problems.
Friedreich’s ataxia is often suspected in a child
with previously diagnosed ataxic cerebral palsy
when it is noted that the child’s physical impair-
ments are progressing and no reflexes are present
on physical examination. Cavus feet may develop.
Cardiomyopathy with arrhythmias occurs fre-
quently (55). The child may present with cavus
feet, and there is an increased incidence of dia-
betes. Sensory nerve conductions have markedly
reduced or absent amplitude, and they have a
close-to-normal latency when present, suggesting
a primary loss of axons. Motor nerve conductions
are relatively spared, with almost normal NCVs
and normal CMAPs (55). The inheritance pattern
shows a homozygous X25 gene found on chromo-
some 9q13 (55).
Ataxia-telangiectasia presents with ataxic
gait and oculomotor apraxia, which begins at
about 2 years of age. The characteristic electrodi-
agnostic abnormalities are reduction in the ampli-
tude of the SNAP and a mild slowing in the distal
latency and NCV (43). Immunologic abnormali-
ties occur in serum and secretory IgA (53), as well
as abnormalities in IgG and IgE levels. Sinus and
pulmonary infections are frequent and are often
the clinical problems, along with the ataxia, that
prompt the diagnostic work-up. The genetic ab-
normality is found in the ATM gene on chromo-
some 11q22-q23. The characteristic telangiectasias
begin to appear at about 3 years of age, and the di-
agnosis is usually made prior to their appearance
(43,55,56).
Giant axonal neuropathy (GAN) presents in
early childhood with ataxia and nystagmus. A
progressive mixed motor and sensory axonal pe-
ripheral neuropathy is accompanied by degenera-
tion of the central white matter. Inherited in an
autosomal inheritance pattern, it produces an ab-
normal version of the protein giaxonin, which is
coded by the GAN gene at 16q24 (32,42).
Hereditary motor sensory neuropathies
(HSMN) usually present as a child having diffi-
culty with distal weakness, falls, tripping, and
handwriting problems; but without intellectual
deterioration. Also known as the Charcot-Marie-
Tooth (CMT) diseases, they are now specifically
diagnosed by genetic testing and nerve conduction
studies are rarely needed if there is a family his-
tory. Children with cavus feet who have no family
history will be referred to evaluate for a peripheral
neuropathy prior to surgery to rule out a neuro-
muscular etiology that could affect the outcome of
the surgery.
Type I and type II HSMN can be delineated
by NCVs, but genetic testing further categorizes
the disease into subgroups. Type I HSMN has a
myelinopathy with slowed NCVs but sparing of
amplitude. Type II has an axonal form that shows
reduced amplitudes but relatively spared NCVs.
Both types of HMSN are inherited in an autoso-
mal dominant manner (43,55). Type III HSMN,
Dejerine-Sottas syndrome, presents in infancy or
early childhood with severe weakness. Hy-
pomyelinization is present. Interestingly, the gene
locus is the same for this disease as it is for HSMN
type IA: 17p11.2 (32,43,55). Congenital hy-
pomyelinating neuropathy, which presents in a se-
verely floppy infant, represents severe Dejerine-
Sottas, HSMN III.
CONCLUSIONS
Electromyography is an important and useful ex-
tension of the history and physical when examin-
ing a child. The examination must be well
planned so that the critical information is obtained
first. This must be tempered with the plan to ac-
complish less painful studies first so that the most
complete examination possible can be done. If a
child cannot tolerate the study, then deep sedation
in an ICU setting or even general anesthesia may
be necessary. General anesthesia limits the study
of voluntary motor units and recruitment, but it
can be very helpful with repetitive stimulation
studies, or when multiple nerve conduction stud-
ies are necessary when studying a brachial plexus
or complicated peripheral nerve injury.
Personnel (with toys) to hold and help with
distraction are critical in a pediatric electromyog-
raphy laboratory. Some parents are excellent at
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CHAPTER 16 • PEDIATRIC CONSIDERATIONS IN ELECTROMYOGRAPHY
this job, but extra hands are necessary when this is
not the case. Appropriate-sized equipment must
be available. If conscious sedation is to be used, a
nurse will be necessary to monitor the patient’s
respirations and blood pressure. The pediatric
electromyographer should be comfortable with
parents or other caregivers in the room, as they are
almost invariably helpful in obtaining the best co-
operation possible from a child. Finally, although
some examiners are loath to use sedation, the
diminution of stranger anxiety has allowed me to
perform more extensive and focused examina-
tions, and I highly recommend its judicious use in
the pediatric population.
Pediatric EMG is a challenging procedure.
Skill in the area is critical to the evaluation and di-
agnosis of many pediatric diseases, and it is an in-
valuable service to offer a community. If the pedi-
atric EMG case volume is low in an area, then it
behooves an adult electromyographer to become
comfortable in studying children. It is far easier
for an adult electromyographer to become profi-
cient in pediatric EMG than it is for a pediatric
physiatrist or pediatric neurologist who does not
perform EMGs routinely to become proficient in
techniques. However, many adult electromyogra-
phers are uncomfortable examining children, and
it is not a skill that can be retained if the clinician
examines only one child a year. The child and
family rapidly realize when the examiner feels un-
comfortable, and that perception only makes the
study more difficult for all concerned. If one is un-
comfortable with handling children, then the
family and referring physician would appreciate it
if the adult electromyographer referred the pa-
tient to the nearest pediatric electromyographer to
perform the examination.
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IV
Appendices
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GLOSSARY OF TERMS
Stuart Reiner
Editors’ note: This Glossary of Terms, created by the
late Stuart Reiner, appeared in the first edition of
Practical Electromyography. The text was so well
composed, especially in defining technical terms of
instrumentation, that it continues to be of value.
It stands as a statement of and tribute to the brilliance
of this leader in the development of instrumentation
for electrodiagnostic medicine. The editors of this
edition have added and modified some items.
Action Potential. Membrane response in nerve or
muscle after reaching excitation threshold. The
complete response is the same regardless of the type
of stimulus and is referred to as an “all-or-none
response.”
Active Elements. The components of a circuit that
provide amplification or that control the direction of
current flow (e.g., diodes, transistors, and vacuum
tubes).
Address. In digital data storage systems, the
description of a location (stated in system notation)
where information is stored. Also, as a verb, to select
or to designate the location of information in a storage
system.
Alternating Current (AC). A flow of current in
which the direction of current flow reverses
periodically. When the reversal occurs cyclically, two
current reversals are termed one cycle. The number of
complete cycles per second is the frequency, and it is
stated in Hertz.
Amplifier. A device that multiplies its input voltage,
current, or power by a fixed or controllable factor,
usually without altering its waveform.
Amplifier, AC. This amplifier responds to alternating
current (AC) signals only and not to an input potential
that does not vary. This type of amplifier is used in
EMG apparatus. Sometimes termed resistance-
capacitance (RC)- or AC-coupled amplifier.
Amplifier, DC (or Direct Coupled). This amplifier
responds to direct current (DC) signals, pulsating DC
signals, and alternating current signals. This type of
amplifier is not used in clinical EMG. It is used in force
and tension measurements, as well as in the recording
of intracellular resting potentials in which fixed, slowly,
and rapidly changing phenomena are measured.
Amplifier, Differential. An amplifier used in EMG
preamplifiers. It has two recording electrode input
terminals (instead of the single input terminal of a
conventional amplifier) and a ground or zero-potential
terminal. It rejects unwanted potentials originating at
a distance and presenting at both input terminals
(common-mode or in-phase potentials).
Amplitude. The potential measured in volts for any
type of recorded response in electrodiagnostic testing.
Amplitude Modulation (AM). Systems of signal
transmission, recording, or processing that use an
alternating current carrier potential of peak amplitude
that varies proportionally with the instantaneous
amplitude of the signal.
Analog. A term applied to signals and devices capable
of accommodating continuous change and assuming
an infinite number of values with finite limits. An
analog signal may be a current or a voltage that varies
in time continuously, simulating and representing a
natural phenomenon.
Analog-to-Digital Converter (A/D Converter).
A device that converts an analog signal, usually a
varying voltage or current, to a digital output
(see “Digital System”).
Anode. A positive terminal. The terminal through
which “electron current” enters a device. “Conventional
current” flow, however, is said to be away from the
anode and toward the cathode (negative) terminal.
Antidromic. In nerve conduction testing, refers to a
test situation where the nerve action potential signal
propagates in the reverse of the normal physiologic
direction.
Artifact. All unwanted potentials that originate
outside the tissues examined. They are also called
“noise” when they appear in measurement. An artifact
may arise from biologic activity, the electrode or
apparatus used in the examination, the power line, or
the extrinsic electricity surrounding the apparatus or
patient (see “Noise”).
419
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420 SECTION IV • APPENDICES
Attenuator. In electrical circuits, an arrangement that
introduces a definite reduction in the magnitude of a
voltage current or power. Attenuators may be fixed or
adjustable either continuously or in steps.
Averager (Signal Averager). A signal-processing
method that aids in the recording of small-stimulus
evoked potentials that are obscured by noise or artifact.
The stimulus is repeated a number of times, and the
responses are subjected to a special summation
technique that causes the random noise portion of the
response to become smaller in proportion to the evoked
potentials that are coherent in time with each stimulus.
Axonotmesis. Nerve injury with loss of axon
membranes and myelin, preserving other support
structures.
Bandwidth. The amplifier frequency response limits,
defined by the high- and low-frequency filters, beyond
which the amplification falls to 70% of full power
(see “Frequency Response”).
Bias. A fixed electrical or mechanical input to a
device or a system that is distinct from the input
signal. The bias brings the system to a desired
operating range.
Binary Logic. A digital logic system that operates with
two distinct states, variously called “one and zero,”
“high and low,” and “on and off.”
Bit. A binary numeral, the “one and zero” or “high
and low,” and so on, of binary logic. A group of bits
make up a binary word or byte.
Blocking (Amplifier). An effect that results when a
large transient input potential is applied to an
amplifier, temporarily causing the disappearance or
severe distortion of the output signal.
Blocking (SFEMG). Intermittent loss of a component
of a single-fiber EMG recording.
Byte. A binary word containing a system-defined
number of bits.
Calibrator. A device that identifies units of
measurement by reference to a known standard.
Capacitance. A measure of electric charge that can be
stored within the insulation separating two conductors
when a given voltage is applied to the conductors.
A capacitor or a condenser uses conductors of large
surface area separated by air or by various insulators
(dielectrics) that enhance capacitative effects. The unit
capacitance is the farad. Direct current is not
conducted by capacitors; alternating current or
pulsating direct current signals are conducted to an
extent proportional to frequency.
Carrier. A potential, usually alternating current, of
sine or pulse waveform used in signal transmission,
recording, or processing systems that in itself carries
no information, but is modified most commonly in
amplitude (amplitude modulation), frequency
(frequency modulation), or timing by the signal.
The carrier is at least a number of times higher in
frequency than the highest-frequency component in
the signal.
Cathode. A negative terminal. The terminal through
which “electron current” leaves a device. Conventional
current flow is said to be toward the cathode or away
from the anode (positive) terminal.
Cathode Ray Tube (CRT). A vacuum tube used to
visualize electrical waveforms. It generates X-Y traces
on its screen by means of a moving fluorescent spot on
its screen.
Clipping (Limiting). This occurs when signals of
excessive amplitude are applied to an amplifier, with
a resultant waveform at the amplifier output that
faithfully reproduces the shape of the input waveform
only up to a level at which the signal becomes excessive
(clipping level). All portions of the waveform that
exceed the clipping level appear at the output at a fixed
level that does not vary with time and are therefore
seriously distorted.
Common Mode Rejection. An important property
of differential amplifiers that expresses their ability
to discriminate against artifact potentials that
appear equally at both amplifier input terminals
(common mode signals) and to amplify the desired
potentials (differential or series mode signals) that
appear as different signals at the two input
terminals.
Common Mode Rejection Ratio. A calculation
performed to measure the effectiveness of the
differential amplifier.
Commutation. A system that cyclically switches a
number of signals sequentially to a single device
amplifier, transmission, or recording channel.
Also termed multiplexing.
Complex Repetitive Discharge. High-frequency
recording in needle EMG, usually with abrupt onset
and ending.
Crosstalk. The incursion of information from one
channel into any other channel of a multichannel
information-handling system. The presence of
crosstalk in a multichannel EMG study can be
seriously misleading.
Cycle. A complete sequence of values of an alternating
quantity repeated as a unit. Cycles per second (CPS) is
also called Hertz.
Decibel (dB). A dimensionless unit for comparing the
ratio of signal levels on a logarithmic scale. Positive
90749_Glossary(417-426).ps 8/10/06 3:56 PM Page 421
decibel values represent a signal increase with respect
to a reference. Negative decibel values represent signal
decrement with respect to a reference signal.
Decrement. Diminished quality of response with
repeated identical stimulations.
Delay Line. A short-term electrical dynamic storage
device that delays potentials applied to its input so that
they appear at its output as if they had occurred (1 to
20 ms) later in time. This permits events preceding
action potentials to be seen on the monitor or CRT
screen when the sweeps are triggered by the potentials.
Differential Amplifier. See “Amplifier, Differential.”
Differentiator. A device or circuit with an output
waveform that is proportional to the rate of change
(e.g., speed, velocity) of the input waveform.
Digital System. A system or circuit for handing or
processing information in terms of numbers and
utilizing circuits that operate in the manner of
switches, having two (on–off) or more discrete
positions. The simplest and most common digital
system is the binary system.
Digital-to-Analog Converter (D/A Converter). A
circuit that accepts the discrete coded signal voltages of
a digital system and generates, at its output, voltages of
amplitudes analogous to the numbers represented by
the digital codes at its input. The analog output may
then be directly interpreted by viewing a CRT or
reading a meter or graphic recording.
Diode. A two-terminal device that permits the flow of
electric current in one direction only.
Direct Current (DC). A unidirectional current. An
intermittent or time-varying current that has a net
flow in one direction is called pulsating direct current
or direct current with an alternating current
component.
Duration. Length of time between onset and ending
of a response, usually in milliseconds in EMG.
Dynamic Range. The ratio of the maximum input
signal capability of a system without overloading to the
minimum usable signal (noise level).
Electrode. A conductor of electricity. In electro-
diagnostic medicine, it is generally a metal device that
introduces or picks up electricity from tissue.
Electrodes, Recording. Electrodes used to measure
electrical activity from tissue.
Bipolar or Bifilar Needle Electrodes. With these
electrodes, variations in voltage are measured
between the bared tips of two insulated wires
cemented side by side in a steel cannula. The bare
tips of the electrodes are flush with the bevel of the
cannula. The latter may be grounded.
GLOSSARY 421
Concentric or Coaxial Needle Electrode. With this
electrode, variations in voltage are measured
between the bare tip of an insulated wire, usually
stainless steel, silver, or platinum, and the bare shaft
of a steel cannula through which it is inserted. The
bare tip of the central wire (the exploring or
recording [E1] electrode) is flush with the bevel at
the end of the cannula (the reference electrode [E2]).
Macro EMG Electrode. A modified single-fiber
EMG needle exposing only a measured portion of its
cannula. A trigger potential from the single-fiber
electromyography (SFEMG) synchronizes the
acquisition by the cannula of a compound potential
arising from the other muscle fibers of its motor unit.
Monopolar Needle Electrode. A solid wire, usually
stainless steel, coated except at its tip with an
insulating varnish or plastic, such as Teflon.
Variations in voltage between the tip of the needle
(the exploring electrode) in the muscle and a metal
plate on the skin surface or bare needle in
subcutaneous tissue (the reference electrode) are
measured.
Multilead Electrode. Three or more insulated wires
inserted through a common steel cannula have their
bared tips arranged linearly at an aperture in the
wall of the cannula that is parallel with its axis. The
bare tips are flush with the outer circumference of
the cannula.
Single-Fiber EMG Electrode. A very small wire is
exposed through an aperture in the side of the
needle cannula. The bare tip is flush with the
surface and insulated from the cannula.
Surface Electrodes. Metal plate or conductive pad
electrodes placed on the skin surface. Various sizes,
shapes, and materials are used; they may be
self-adhesive or held with tape.
Endplate Activity. Signal recorded in needle
EMG from near the neuromuscular junctions
(endplate zone).
EMG Analyzer. A term applied to a wide range of
EMG computer-enhanced processing techniques that
attempt to display one or a number of attributes of the
EMG waveform in a more explicit manner than the
conventional voltage–time graph of the usual
EMG trace.
Ephaptic Transmission. Excitable membrane
activation produced by another cell without a synaptic
interaction.
Facilitation. Improved quality of response with
repeated identical stimulations.
Feedback. An effect that occurs when a portion of the
output of a system or a circuit is connected back to the
input. When the fed-back signal reinforces the original
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422 SECTION IV • APPENDICES
input, the feedback is positive; when the fed-back
signal tends to reduce the input signal, the feedback is
negative.
Negative feedback acts to stabilize the performance
of electronic instrument systems and to make the
operation and calibration of such systems stable and
independent of changes in many of the system
components.
Positive feedback appears in oscillating circuits.
Unintentional positive feedback occurs, for
example, when a microphone, which is the input to
an amplification systems, is brought too close to the
loudspeaker output. When this occurs, positive
feedback often produces an oscillatory howl. Similar
undesirable positive feedback may occur when the
input electrodes of an EMG system are brought too
close to the loudspeaker output or the CRT output
of an EMG system.
Fibrillation Potential. Spontaneous depolarization of a
single muscle fiber recorded in needle EMG.
Filter. In an EMG system, these are circuits, usually
comprising capacitors and resistors, that modify or
adjust the high- and low-frequency limits of the
amplifier’s frequency–response curve.
Frequency. The rate in cycles per second that an
alternating current signal alternates. The unit of
frequency is the Hertz.
Frequency Analyzer. This analyzes the EMG to
produce a spectrum of sine wave frequencies
(harmonics) that will uniquely describe the original
EMG waveform.
Frequency Modulation (FM). Systems of signal
transmission, recording, or processing that use a
constant amplitude carrier potential with an
instantaneous frequency proportional to the
instantaneous amplitude of the signal.
Frequency Response. Describes the speed range
(slowest to fastest) of potential waveform changes that
will be displayed by the EMG apparatus. Stated as a
range (band) of frequencies of sine wave test signals for
which the amplification will be uniform. Amplification
decreases progressively for sine wave test signals at
frequencies above and below the frequency response
band. The frequency between the lower and upper
frequency is called the bandwidth. The amplifier
frequency response bandwidth is often defined by two
frequencies, one at the low end and the other at the
high end, where the amplification falls to 70% of its
midband value.
Gain. The increase at the output of an amplifier in
voltage, current, or power of the signal applied to its
input is called the amplifier voltage, current or power
gain, or amplification.
Page 422
Gate. A circuit used in digital systems as a decision
element and having two or more inputs and one
output. The output depends upon the combination of
digital states of the signals at the input. A gate circuit
in an analog system acts like a switch that permits or
stops the flow of signals. The gate opens or closes in
response to a control voltage (or gating signal).
Graticule. The ruled scale on the monitor display or
face of the CRT. Time and voltage display calibrations
are usually adjusted with reference to the X and Y
rulings on the graticule.
Ground. The neutral electrical potential reference
terminal in a system. In power distribution systems, a
terminal that is usually physically connected to a
conductor in intimate contact with the earth.
Sometimes referred to as the earth terminal.
Frame and chassis portions of electrical systems are
almost always connected to ground to avoid the
possibility of their assuming other random potentials
that might either be dangerous or cause electrical
interference within the system.
Ground Loop. The condition that sometimes exists
when the ground connections of two interconnected
electronic instruments or circuits are not at the same
potential. This may result in power line interference.
Hertz (Hz). Cycles per second of a time-varying
signal.
High Pass Filter. A low-frequency filter that does not
significantly impede higher frequencies.
Impedance. The hindrance to electrical current flow
in an alternating current circuit; hence, it is
comparable in simplified terms to resistance in DC
circuits. It includes the effects of resistance,
capacitance, inductance, and frequency.
Integrated EMG. The integrated EMG is a time-
varying potential with instantaneous amplitude equal
to the total area (voltage
time) accumulated from a
designated start point under an EMG waveform.
It provides a measure of total electrical activity.
Interface. An expression or device that embodies all
technical considerations in interconnecting two
portions of a system, such as proper mating connectors,
shielding of connecting leads, establishment of
compatible voltage and impedance levels, and such
problems as ground loops.
Interference. A term generally applied to unwanted
signals outside the system. Power line frequency is
the most common form of interference (see
“Artifact”).
Linear Circuit. A circuit, the output of which is
congruent with its input, with the exception of possible
amplification or attenuation.
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Liquid Crystal Display (LCD). Display for signals
using points addressed by individual currents to produce
color or monochrome displays, in contrast to CRT
displays.
Low-Pass Filter. A high-frequency filter that does not
significantly impede lower frequencies.
Microphonics. An effect noted in sensitive electronic
systems and their connecting cables in which incidental
mechanical vibration applied to portions of the system
gives rise to spurious electrical outputs.
Monitor. A specialized CRT or LCD used with digital
displays for computers.
Motor Unit. The basic unit of peripheral motor
function; it includes the anterior horn cell and its axon,
the neuromuscular junctions, and the group of muscle
fibers with which it has synapses.
Multiplexing. See “Commutation.”
Myokymia. Clinically, a repeating undulating
movement of the skin due to spontaneous muscle
movement. Electrically, one observes repeating complex
waveforms that usually appear to be a collection of
motor unit potentials firing together in a rhythmic
pattern.
Myotonia. Clinically, delayed relaxation of muscle after
contraction. Electrically, a waxing and waning, high-
frequency signal recorded with intramuscular needle
EMG.
Neurapraxia. Reversible conduction block in an axon or
whole nerve, usually related to myelin disruption.
Neurotmesis. Disruption of the nerve supporting
structure, in addition to the axons and myelin (see
“Axonotmesis”).
Noise. Any potential other than that being measured.
Commonly applied to spurious potentials originating
within the apparatus of electrodes (see “Artifact,”
“Interference,” and “Root Mean Square Voltage or
Current”).
Off-Line. Any signal or data-processing function that
is deferred with respect to the original recording or
generation of signal or data.
On-Line. Any signal or data-processing function that
occurs simultaneously with the original recording or
generation of the signal or data.
Orthodromic. In nerve conduction testing, a test
situation where the nerve action potential signal
propagates in the normal physiologic direction.
Overload. A general condition in which the input to an
amplifier circuit is so large that it exceeds the capability
of the circuit to perform its intended function.
GLOSSARY 423
Parallel Circuit. Circuit elements connected in parallel
(as opposed to in series) all are subjected to the same
voltage. The current flow to elements connected in
parallel is inversely proportional to the impedance
(resistance) of the elements. The word “shunt” is
sometimes used to refer to parallel connections.
In digital systems, parallel refers to a technique of
transmission, storage, or logical operation on all bits of
binary data words simultaneously using separate
facilities (see “Serial”).
Parameter. Any specific characteristic of a device.
When considered together, all of the parameters of a
device describe its operation or its physical
characteristics.
Polarity Sense, Display. Many neurophysiologic
records are published with an upward deflection
denoting a negative potential on the active electrode.
Engineering convention dictates an upward deflection
for a positive potential.
Polarization. Electrolytic effects that occur at the
metal–tissue interface of electrodes that increase the
resistance of the junction and give rise to direct current
potentials (which may fluctuate) that can be many
times larger than EMG potentials.
Positive Sharp Wave. Biphasic potential from
intramuscular recording with a characteristic initial
spike followed by a slower negative phase. Suggests
instability of the muscle membrane that produces it.
Potential, Action. The voltage that results from
activity of a muscle or nerve. It can be spontaneous,
volitional, or evoked by stimulation. Action potentials
may be named for their appearance (high-frequency;
positive sharp; biphasic; monophasic; polyphasic;
tetraphasic; triphasic) or their origin (endplate;
fasciculation; fibrillation; motor unit; muscle; nerve).
The term “potential” also refers to an action potential.
Preamplifier. The first stage or stages of an EMG
amplifier system. It must have high input impedance
and common mode rejection, and low noise, as well as a
large dynamic range.
Pulse. A signal of very short duration. It can be
described according to its characteristic rise, duration,
and decay.
Raster. A predetermined pattern of lines generated on
a CRT display that provides uniform coverage of an
area. Also, the display on the CRT screen of an EMG
in which each successive sweep is displayed below or
above the previous sweep, thus permitting the observer
to see more information on the screen than is possible
when successive sweeps are superimposed (same
baseline). Also, a similar mode of graphic recording.
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424 SECTION IV • APPENDICES
Rectifier Circuit. A circuit using unidirectional
current flow properties of diodes that convert an
alternating current into a pulsating direct current.
Resistance. A property of matter that hinders the flow
of electric current. Resistance is expressed in ohms and
is derived by dividing the voltage impressed by the
current that flows. Resistance (R)  Voltage (E)
divided by the Current (I). R = E/I.
Ringing. A short-duration, transient, usually low-
amplitude, damped oscillation that occurs in the
output of certain electronic circuits, especially some
filters, wideband amplifiers, and certain delay lines,
immediately after the input wave suddenly changes
in amplitude.
Rise Time. A term used to describe rectangular pulses
and square waveforms or amplifiers or the circuits
transmitting them. Rise time is the elapsed interval
between the time at which the amplitude of the rapidly
changing transition part of the wave reaches specified
percentages of its lower and upper limits. The rise
time of an amplifier is a function of its high-frequency
response.
Root Mean Square Voltage or Current. The root
mean square value (RMS) is a means of stating
numerically the magnitude of an alternating voltage or
current. It equals a direct current that has the same
heating effect in a resistor as an alternating current of
the same RMS magnitude.
Semiconductor. A material that exhibits relatively high
resistance in a pure state but much lower resistance
when minute amounts of impurities are added.
Serial. A term applied to digital circuits in which each
bit is acted upon sequentially.
Series Circuit. Electrical components are in series
when they are connected so that a common current
flows through each of them (see “Parallel Circuit”).
Shield (Shielding). An electrostatic shield is an
electrically conductive sheath or an enclosure not in
contact with the circuit or device shielded. It comprises
electrically conductive material connected directly to
ground or by a low impedance to ground. It is used to
prevent undesirable capacitative coupling of external
voltages to the elements within the shield (or to
contain potentials within the shield).
Magnetic shielding requires an enclosure of iron or
other magnetically permeable alloys and provides
protection against interference from magnetic fields
that surround nearby current-carrying conductors
or permanent magnets.
Signal. Any potential, waveform, or intelligence that
is communicated, detected, transmitted, or processed
with a system. It is usually in the form of a voltage or
current within the system.
Solid State. Electronic devices using semiconductors.
Electric currents, as well as light, heat, and magnetic
fields, may interact in solid-state devices. The transistor,
integrated circuit, and microchip are solid-state devices.
Stabilized Current or Voltage Generator. A source of
direct current, alternating current, or voltage in which
the output current or voltage remains at a
predetermined, usually adjustable value independent of
wide variations of load resistance, impedance, or
variations of power supply voltages. The stabilized
current source exhibits wide fluctuations in output
voltage in response to changing load conditions,
whereas the stabilized voltage source exhibits wide
variations in output current in response to load changes.
Stimulator, Ground-Free (Isolated). Used in nerve
conduction studies to minimize stimulus artifact.
A ground-free stimulus output circuit has no connec-
tion to the common system ground, thereby removing
a possible path for injection of undesirable artifact via
the patient to the EMG amplifier input terminals.
Strain Gauge. An electrical transducer that generates
or modifies an electrical signal proportional to a
mechanical deformation owing to application of a
mechanical load.
Strain Relief. A mechanical restraint, usually applied
to the jacket of insulated cables where they join fixed
mechanical assemblies, connectors, or other
terminations, especially where the cable might be
subjected to repeated flexing or mechanical stress.
The purpose of the strain relief is to minimize the
possibility of failure of the electrical conductors that
are hidden within the cable or connector.
Supramaximal Stimulus. Stimulation of a nerve at a
level greater than that which results in a maximum
amplitude of the recorded signal, with the presumption
that all axons have reached their threshold of activation.
In a nerve conduction study the stimulus should be 10%
to 25% greater than one that exactly produces the
maximal response.
Sweep. The horizontal (X-axis) linear time axis of an
LCD or CRT display generated by the left-to-right
movement of the trace spot at constant preselected
speeds across the face of the CRT. Sweep velocities are
usually specified in reciprocals of speed: time per
division on the graticule.
Telemetry. The transmission of data, typically from
preamplifiers located on a subject (free to move about
the laboratory) via a radio link to a receiver, and then
to the remainder of the recording system.
90749_Glossary(417-426).ps 8/10/06 3:56 PM Page 425
Time Constant. A factor that is an index to a speed
with which voltage and currents respond to changes
in the input to resistor-capacitor (RC) circuits. This
term is used to describe the dynamic performance of
EMG amplifiers (which contain RC coupling
networks).
Time Scale, Electronic. A discontinuous waveform,
usually in short pulses, spaced in some convenient time
interval, such as 1 ms, or 0.1 ms.
Trace. The line of light on the face of a CRT that is
generated by the moving spot of light, which is
generated by the electron beam striking the phosphor-
coated screen. Used analogously for recordings on
modern LCD monitors.
GLOSSARY 425
Transducer. A device that changes the energy form
applied to its input to another form of energy at its
output, such that a proportionality exists between the
input and output. Transducers include loudspeakers,
microphones, strain gauges, and photocells.
Transistor. An active semiconductor device used as an
amplifier or switching device.
Trigger. A short pulse used to initiate some action
within an electronic system. Also used as a verb. The
nerve stimulator triggers the sweep to record the
response (see “Sweep”).
Wave (Waveform). A generic term loosely applied to
a time-varying voltage, current, or other quantity, the
amplitude of which varies with time.
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Abbreviations Commonly
Used in Electromyography
AAEE: American Association of Electromyogra-
phy and Electrodiagnosis (founded in 1953,
name changed to AAEM in 1989)
AAEM: American Association of Electrodiagnos-
tic Medicine (name changed to AANEM in
2004)
AANEM: American Association of Neuromuscu-
lar and Electrodiagnostic Medicine
ABEM: American Board of Electrodiagnostic
Medicine
ACh: acetylcholine
AChE: acetylcholinesterase
AChR: acetylcholine receptor
ADEMG: automated decomposition EMG
AEP: auditory evoked potential
CMAP: compound muscle action potential
CMRR: common-mode rejection ratio
CPS: cycles per second; preferred term is Hz
CRD: complex repetitive discharge
CRT: cathode ray tube
DSEP: dermatomal somatosensory evoked poten-
tial
E1: input 1 for amplifier; synonym is recording
electrode
E2: input 2 for amplifier; synonym is reference
electrode
EDX: electrodiagnosis or electrodiagnostic
EMG: electromyography or needle electromyog-
raphy
EMG examination: electrophysiologic studies that
could include needle EMG, nerve conduction
tests, or both
EPSP: excitatory postsynaptic potential
G1, G2: old term, grid, replaced by E1 and E2
Hz: hertz, unit of frequency in cycles per second
IPSP: inhibitory postsynaptic potential
LCD: liquid crystal display
MEP: motor evoked potential
MEPP: miniature endplate potential
MNAP: mixed nerve action potential
MNCV: motor nerve conduction velocity
MUAP: motor unit action potential
MUNE: motor unit number estimate
MUP: motor unit potential (same as MUAP)
NCS: nerve conduction study
NCV: nerve conduction velocity
NMJ: neuromuscular junction
PSW: positive sharp wave (also known as positive
wave)
QEMG: quantitative EMG
QSART: quantitative sudomotor axon reflex test
QST: quantitative sensory testing
R1, R2: measurements taken in the blink reflex
test
RMS: root mean square
RNS: repetitive nerve stimulation
SEP: somatosensory evoked potential
SFEMG: single-fiber EMG
SNAP: sensory nerve action potential
SSEP: short-latency somatosensory evoked poten-
tial
SSR: sympathetic skin response
TES: transcranial electrical stimulation
TMS: transcranial magnetic stimulation
VEP: visual evoked potential
427
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The Practical Exam in

Electromyography

Ernest W. Johnson and William S. Pease

429
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430 SECTION IV • APPENDICES

Each question refers to one figure. The figures are Bottom trace: stimulate radial nerve at wrist
from Dr. Johnson’s well-known slide collection What is your diagnosis?
gathered over the years from a variety of EMG A. Normal
instrument displays. Depending on your experi- B. Carpal tunnel syndrome
ence this will represent either a history lesson in C. Peripheral neuropathy, mild
instrument displays or memories. Abbreviations D. Both B and C
are defined in the appendix. Answers and com-
ments follow.

3. SNAP recorded from digit 1 (stimulate wrist

10 cm)
• Top trace: stimulate radial nerve at wrist 10 cm
1. Top trace: digit 3, wrist stimulation at 14 cm • Bottom trace: stimulate median nerve at wrist
Bottom trace: digit 3, midpalm stimulation at What is your diagnosis?
7 cm A. Carpal tunnel syndrome, mild
What is your conclusion? B. Normal
A. Carpal tunnel syndrome, mild C. Peripheral neuropathy, mild
B. Normal D. Cold hand
C. Cold hand
D. Technique error

4. SNAPs recorded from digit 4 stimulate at wrist 14

cm
• Top trace: ulnar nerve
sweep = 1ms, Gain = 20µV • Bottom trace: median nerve
What is your diagnosis?
2. SNAP recorded from digit 1 A. Carpal tunnel syndrome
Top trace: stimulate both median and radial B. Peripheral neuropathy, mild
nerves at wrist C. Cold hand
Middle trace: stimulate median nerve at wrist D. Both A and B
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THE PRACTICAL EXAM IN ELECTROMYOGRAPHY 431

7. Which nerve is compromised?

A. Anterior interosseus
B. Distal ulnar
5. CMAP recorded from abductor pollicis brevis C. Deep radial (post. interosseus)
(thenar) D. Proximal radial
Upper trace: stimulate wrist 8 cm
Lower trace: stimulate at thenar crease
What is your diagnosis?
A. Normal
B. Severe carpal tunnel syndrome
C. Mild carpal tunnel syndrome
D. Cold hand

8. Consider the polyphasic MUP at B.

Why does it have more phases than when it first
appears at A?
A. Unstable MUP
B. Two overlapping MUPs
C. Artifact of concentric needle EMG recording
D. Repetitive activation of one MUP
6. Needle in anterior tibialis muscle
In which condition was this recorded?
A. Crossed leg palsy s/p 5 months
B. Prior poliomyelitis
C. Acute L5 radiculopathy
D. Amyotrophic lateral sclerosis

9. Monopolar EMG needle in trapezius muscle

What is your diagnosis?
A. Reinnervation
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432 SECTION IV • APPENDICES

B. Proximal myopathy
C. Cranial nerve XII injury
D. Amyotrophic lateral sclerosis

12. What has changed from bottom to top trace?

A. Endplate area with MEPPs has been entered
B. Distant MUPs are now recorded
C. Noise level increased due to loss of reference
10. Monopolar EMG needle in frontalis muscle electrode (E2)
What is the complex potential seen? D. Poor contact of ground electrode (G)
A. Repetitive MUP firing
B. Reinnervation MUP
C. Grouped MUP discharges
D. Complex repetitive discharge

13. What procedure is being performed?

A. Facial nerve stimulation
B. Blink reflex stimulation
C. EMG of orbicularis oris
11. Median nerve sensory nerve recordings D. Nasalis CMAP recording
Upper trace (larger): digit 3 recording, midpalm
stimulation at 7 cm
Lower trace: digit 3 recording, wrist stimulation at
14 cm
What is your diagnosis?
A. Cold hand
B. Diabetic neuropathy
C. Carpal tunnel syndrome, severe
D. Carpal tunnel syndrome, mild

14. Monopolar EMG needle in peroneus longus

In what condition was this recorded?
A. Duchenne muscular dystrophy, age 24 months
B. Injury to sciatic nerve lateral division, s/p 4
month
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THE PRACTICAL EXAM IN ELECTROMYOGRAPHY 433

C. Crossed leg palsy of peroneal nerve, s/p 3 Lower trace: stimulate peroneal nerve at ankle
weeks What is your conclusion?
D. Injury to deep peroneal nerve, s/p 6 months
A. Normal motor nerve conduction study
B. Accessory peroneal nerve is present
C. Conduction block is shown at fibular head
D. Both B and C

15. SNAP recorded from digit 1

Top trace: stimulate radial nerve at wrist, 10 cm
17. Monopolar needle EMG recording in anterior tib-
Middle trace: stimulate median nerve at wrist,
ialis muscle
10 cm
Bottom trace: stimulate both median and radial What is potential at A, near the center of the trace?
nerves at wrist A. Artifact potential
What is your diagnosis? B. Endplate potential
C. Fibrillation potential
A. Normal
D. Fasciculation potential
B. Carpal tunnel syndrome
C. Mild peripheral neuropathy
D. Cold hand

18. Ring electrodes on long finger

Upper trace: median nerve stimulation at
midpalm, 7 cm
Middle trace: median nerve stimulation at wrist,
14 cm
Lower trace: median nerve stimulation at antecu-
bital crease, 34 cm
What is your diagnosis?
A. Nerve compromise in forearm
16. Record CMAP of extensor digitorum brevis B. Alteration due to cold hand
Top trace: stimulate peroneal nerve at popliteal C. Normal recordings
crease D. Possible mild carpal tunnel syndrome
Middle trace: stimulate peroneal nerve just below
fibular head
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434 SECTION IV • APPENDICES

19. Recordings from ulnar nerve stimulation

Top traces: CMAP recordings from abductor dig-
iti minimi
Lower traces: SNAP recordings from digit 5
Left traces: Stimulation at the wrist (W), 8 cm and
14 cm
Center traces: Stimulation just below the elbow
(BE)
Right traces: Stimulation above the elbow (AE)
22. CMAP response recorded from the abductor
What is/are your conclusion(s)?
pollicis brevis
A. Normal Top trace: median nerve wrist stimulation (W), 8
B. Sensory only block cm
C. Motor only block Bottom trace: median nerve elbow stimulation, 25
D. Both B and C cm from W
What is the calculated conduction velocity?
A. 60 m/s
B. 80 m/s
C. 40 m/s
D. 100 m/s

20. Figure shows a single-fiber EMG (SF EMG)

recording from the abductor digiti minimi muscle.
What would you expect to record on repetitive stimu-
lation (2 Hz) study of this muscle and its ulnar nerve?
A. Moderate decrement in responses
B. Moderate increment in responses
C. No change in amplitude of responses
D. No response (absent CMAP)

21. Refer to same figure as question 20. 23. What is the spinal cord (and nerve root innervation)
What is your diagnosis? level of motor nerve supply for the weak muscle exhib-
A. Myotonic dystrophy ited in the figure?
B. Acute radiculopathy A. C7
C. Reinnervation B. C6,7,8
D. Disuse atrophy C. C5,6
D. C2,3,4
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THE PRACTICAL EXAM IN ELECTROMYOGRAPHY 435

26. Extra credit

Name the animal (hint: the creature became more
popular when it came to share its name with a
common EMG procedure).
A. Llama
B. Asian camel
C. Arabian camel
D. Dromedary camel
24. Both traces are recordings of the SNAP of the
median nerve from digit 3 with stimulation at the
wrist, 14 cm. What are the temperatures (in Celsius)
likely to be recorded at the time of the two
stimulations?
A. Top 27°; bottom 22°
B. Top 32°; bottom 27°
C. Top 27°; bottom 32°
D. Top 34°; bottom 37°

25. Recordings made with median nerve study in an

85-year-old man
What is the diagnosis?
A. Normal study
B. Carpal tunnel syndrome, unknown severity
C. Carpal tunnel syndrome, mild
D. Carpal tunnel syndrome, severe
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The Practical Exam in Electromyography
ANSWERS AND COMMENTS
1. B Latencies and amplitudes are normal for this
technique. Amplitude change represents normal
temporal dispersion. See Figure 8-19.
2. D Radial response has a mildly prolonged latency,
with a long duration and low amplitude; this sug-
gests axonal neuropathy. Additional delay in latency
and reduction in amplitude of median response sug-
gest carpal tunnel syndrome in the setting of a vul-
nerable nerve in the face of neuropathy. The ratio of
median to radial SNAP amplitude is typically 2:1.
See Figure 9-20. The two-humped recording (top) is
termed the Bactrian sign.
3. B The latencies of the responses are within 0.1
ms, and the median SNAP shows an amplitude
four times that of the radial. Contrast with patho-
logic responses in question 2.
4. D Median latency is markedly prolonged at 6 ms,
and ulnar latency is also prolonged at 4.5 ms. Small
amplitudes of the responses argue against an error
due to cold temperature. See Figure 8-21.
5. C Wrist latency recording is abnormal at 5 ms,
with CMAP amplitude of only 3 mV. At first one
might think this a severe carpal tunnel syndrome
because of the small amplitude; however, the re-
sults of stimulation of the recurrent thenar branch
in the palm demonstrate that there is conduction
block, leading to a conclusion of mild carpal
tunnel syndrome. The prognosis for nerve recov-
ery is excellent in the situation of conduction block
(neurapraxia). See Figure 9-10.
6. C The rapid rate of motor unit potential (MUP)
firing (30 Hz) suggests neuropathy. The MUP is
within the normal range for amplitude, duration,
and phases, and these measurements make it un-
likely that the MUP was recorded from a chronic
neuropathic condition.
7. C The classic “hook ’em horns” sign of posterior
interosseus (deep radial) palsy is shown. All of the
finger extensors are weak from the injury, but the
force generated from both passive and active com-
ponents of the extensor digiti minimi and the ex-
tensor indicis is combined with that of the extensor
digitorum, resulting in slightly worse extension
force in the middle and ring fingers.
8. B Following the MUPs in time in these rastered
traces demonstrates the individual potentials over-
lapping and interfering to varying degrees. Some
of the potentials do appear polyphasic, and one
cannot be sure of stability of the MUPs.
9. A The MUP displayed (M) is the characteristic
small-amplitude, complex polyphasic potential
observed early in the course of reinnervation as
multiple nerve sprouts enter the muscle, but the
axon’s action potentials are poorly synchronized.
These potentials were previously known as nascent
potentials.
10. B Another example of the so-called nascent
potential as in question 9. Note that the maximum
amplitude is about 300
V, and several discrete
components are seen. Each component represents
an axon branch with innervation of one or a small
group of muscle fibers. Current naming conven-
tion is simply descriptive and refers to this as a
small complex polyphasic potential.
11. D Slowing of the distal latency and reduced
amplitude are seen with stimulation proximal to
the carpal tunnel. Stimulation distal to the site of
entrapment shows improved amplitude, suggest-
ing neurapraxia (conduction block) in the sensory
fibers. Neurapraxic injuries have a good prognosis
for recovery of function.
12. A Five- to ten-microvolt, randomly occurring
potentials are seen. These are typical of the end-
plate (neuromuscular junction) zone of the muscle.
The sound heard is often compared to that heard
when holding a large seashell near one’s ear.
13. B The supraorbital nerve is at the site of stimula-
tion to record the blink reflex. In this example only
unilateral recording is shown, but the test is usu-
ally performed with simultaneous recording of the
bilateral responses from the orbicularis oris mus-
cles. See Figure 9-2.
14. B The lateral division of the sciatic is also
known as the peroneal division and gives rise to
the common peroneal nerve. The MUPs recorded
in the figure are typical of polyphasic potentials
recorded during reinnervation. They would not be
expected in acute nerve compression. The per-
oneus longus is supplied by the superficial division
of the nerve.
15. C Both of the SNAPs have prolonged peak la-
tency values. The characteristic findings of distal,
axonal polyneuropathy are seen, including mildly
reduced amplitudes in proportion to the delay in
distal latency time. In contrast, if the hand were
cold, the SNAPs would increase in amplitude and
duration in proportion to the delay in latency time.
16. D Nearly complete conduction block is shown
with the two upper traces, produced by stimula-
tion proximal and distal to the head of the fibula.
Loss of the response’s amplitude with distal stimu-
lation can be explained only by either anatomic
variation in nerve supply or technical error. See
Figure 9-27.
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THE PRACTICAL EXAM IN ELECTROMYOGRAPHY
17. D Isolated motor unit and fasciculation poten-
tials cannot easily be differentiated. Contrast the
potential in question with the one of similar ampli-
tude at the left (B). The B potential has an initial
positive phase and brief duration typical of a fibril-
lation potential.
18. D Myelin damage to the median nerve in the
carpal tunnel typical of carpal tunnel syndrome is
shown, with identification of focal slowing and
conduction response (amplitude of the top trace is
almost double the size of middle trace). The
further reduction in amplitude seen when stimu-
lating at the elbow is the normal effect of the
temporal dispersion of a sensory nerve over a
long segment.
19. D Amplitude change in the CMAP between AE
and BE shows that the motor axons have conduc-
tion block, and the good amplitude with distal
stimulation suggests that little axon loss has
occurred. In the sensory responses there is dra-
matic loss of the response amplitude between AE
and BE (75%) that is more than would be expected
from temporal dispersion alone.
20. A The SF EMG recording demonstrates both
increased jitter in the varying interpotential
interval between the triggering first response and
its partner as well as blocking, as the second
response is occasionally absent. The effect of
blocking on the repetitive nerve stimulation
(RNS) test is to produce a decrementing series of
responses.
21. C One of the causes of the abnormal jitter and
blocking shown in the figure, as well as the decre-
menting response on repetitive nerve stimulation,
is the presence of immature neuromuscular junc-
tions during reinnervation.
437
22. D The upper trace reveals a prolonged distal la-
tency of 4.6 ms. Observe that the lower response
has an initial positive (downward) phase. The posi-
tive initial phase suggests that the recording is be-
ginning from a muscle whose motor point is not at
the recording electrode (E1) site. The common
cause of this is the presence of a Martin-Gruber
anastomosis (MGA) in a patient with carpal tunnel
syndrome. The initial deviation from baseline of
the lower trace represents the latency time for ax-
ons conducting through the wrist with the ulnar
nerve, which are not delayed in the carpal tunnel.
The nonphysiologic fast conduction velocity re-
sulting from the calculation is an artifact associated
with the MGA. See Chapter 1.
23. B The right scapula is displaced (winging) me-
dial and posterior to its normal location with the
load of forward flexion of the shoulder. This alter-
ation is caused by weakness of the serratus anterior
muscle. See also Chapter 1 and Figure 1-14.
24. C The lower trace is normal in all respects. The
upper trace has latency delayed by 1 ms, which is
consistent with 5 degrees of cooling. The upper
response also displays typical increases in ampli-
tude and duration, abnormalities that do not occur
together in any type of pathology.
25. B The traces shown in this set do not include
stimulation of the recurrent thenar motor branch
of the median nerve in the palm. Since this
response could be normal and result in a conclu-
sion of neurapraxia and good prognosis, we cannot
conclude the severity of the nerve injury using the
Sunderland grading system.
26. B Also known as the Bactrian camel, it has two
humps and was seen as similar to the combined
median and radial nerve responses shown in ques-
tion 2, which has been dubbed the Bactrian sign.
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INDEX

A Amplitude
Abductor digiti minimi, 181, 212 evoked potential recording, 46
spinal nerve stimulation, 57 fiber density and, 123f, 124
Abductor hallucis, 209 filtering, 47–48
Abductor pollicis brevis F wave, 51, 52
anatomy, 10, 166, 176 temperature effects, 45, 46
innervation, 166, 176 temporal dispersion effects, 39–40
needle placement, 166, 176 Amyloidosis, 324
Acetylcholine Amyotrophic lateral sclerosis
in axonal degeneration, 298 fasciculation potentials, 22f, 23f
conduction latency and, 50 macro EMG findings, 122–124
in myasthenia gravis, 387, 389 Anal sphincter
in neuromuscular junction, 70, 72–73, 378 anatomy, 187
transmission disorders, 113–114 innervation, 13–14, 187
Acid maltase deficiency, infantile, 407 needle placement, 13, 187
Action potential Anastomosis
current flows, 74 Riche-Cannieu, 14
electrophysiology, 32–34, 67–70 See also Martin-Gruber anastomosis
EMG measurement, 21–22 Anatomy
insertional activity, 23–26 intraneural, 41–42
nerve conduction studies, 22 knowledge requirements for electromyographers, 3
in volume conductor, 73–74 nerve root level innervations, 18t
waveform generation, 75–77 neuromuscular junction, 70, 71–72, 378
See also Motor unit potential peripheral nerve innervations, 19–20t
Active lead, 88 radial nerve, 277f
Acute inflammatory demyelinating radiculopathy findings, 333–334
polyradiculopathy, 409 ulnar nerve, 274
Acute motor axonal neuropathy, 409–410 Anconeus muscle, 163
Adductor longus, 188 Anode, electrical stimulator, 98
Adductor magnus, 189 Anorexia nervosa, 410–411
Adductor pollicis, 182 Anterior horn cell
Adenosine triphosphate, 31–32 F wave generation, 51
Adrenoleukodystrophy, 408 pathologies, 28
Age Anterior interosseous nerve syndrome, 281–284
jitter reference values, 110t Arsenic intoxication, 315–316
nerve conduction variation, 46–47 Arthrogryposis multiplex congenita, 404
See also Children Ataxia-telangiectasia, 412
Alcohol neuropathy, 260, 323–325 Atrophy, axonal, 298–299
Aliasing effects Audio
definition, 94 filter effects, 90
waveform, 94–96 maximal contraction, 27
American Association of Neuromuscular and Auricularis posterior, 146
Electrodiagnostic Medicine, 132, 336 Averaging, signal, 97–98
American Board of Electrodiagnostic Medicine, 132 Axillary nerve conduction studies, 218
Aminoglycoside toxicity, 363–364 Axolemma. See Membrane electrophysiology
critical illness neuromuscular disorder and, 365–366 Axon loss
Amiodarone-associated neuropathy, 310 atrophy, 298–299
Amplifier, EMG, 43, 88–90, 102 clinical course, 28
deterioration, 103 conduction block and, 36–37

439
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440 INDEX

Axon loss (continued) myokomic potentials in radiation-induced injury,

electrophysiology, 36–37 23f
in entrapment neuropathy, 261, 262 pediatric injuries, 61
nerve conduction study innervations, 3, 6t pediatric injury, 400–401
peripheral neuropathy evaluation, 301, 316–325 plexopathy, 264
Axonotmesis, 34 in radiculopathy, 333
in entrapment neuropathy, 262 Brachoradialis, 159
Axon(s)
classification of altered function, 34–35, 37 C
conduction block, 35–36, 37 Cables, EMG, 88, 102
conduction latency, 50, 51 Calcium metabolism
conduction slowing, 35 cell membrane electrophysiology, 30
damage endplate electrophysiology, 73
in critical illness motor neuromuscular disorders, neuromuscular junction, 378
370 Cannula signal, 127
in critical illness polyneuropathy, 369 Capacitance, 74
electrophysiology, 36–37 Carcinoma, 318
EMG findings, 22 Carpal tunnel syndrome
entrapment neuropathy assessment, 261 assessment and diagnosis, 263–267
partial nerve injury, 42 in children, 411
peripheral neuropathies, 28, 297–299, 304–305 Martin-Gruber anastomosis and, 14
regeneration potential, 37 median motor evoked response, 43f
death of, 36–37 pediatric, 61
evoked responses, 37–39 risk factors, 264
F wave generation, 51, 52f, 56–57 ulnar neuropathy at elbow and, 273
H reflex generation, 55f, 56–57 Catabolic myopathy, 372
loss Cathode, electrical stimulator, 98
aging and, 47 Cauda equina, 334
movement among fascicles, 41–42 Cerebral palsy evaluation, pediatric, 411–412
in nerve stimulation, 48 Certification and licensure, 132–133
rapid saltatory conduction, 51f Charcot–Marie–Tooth disease. See Hereditary motor
refractory period, 32–33 sensory neuropathy type I
salutatory conduction, 34 Chemical exposure. See Drug-induced disorders;
signal conduction, 30, 31, 32 Toxic substances
size of, and conduction velocity, 33–34 Children
spinal nerve stimulation, 56–57 acid maltase deficiency in, 407
Wallerian degeneration, 36–37 Babinski response, 401
botulism in, 383, 390–391, 404–407
B brachial plexus injury, 61, 400–401
Bell’s palsy, 411 chronic inflammatory demyelinating
Biceps brachii, 156 polyneuropathy in, 410
Biceps femoris clinician knowledge for pediatric practice, 395
long head, 205 critical illness neuromuscular disorders, 368, 411
short head, 197 dermatomyositis in, 408
Black widow spider, 391 diabetes in, 61
Bleeding complications, 133 diagnostic considerations, 61–62, 395, 412–413
Blink reflex, 214 diphtheria in, 407
Blocking agents, 365–366, 370 electrodiagnostic exam, 59, 60–61, 398–400, 413
Botulism case examples, 405–408
case examples, 405–406 EMG laboratory design for, 396–397
causes, 390 Erb’s point stimulation, 61
clinical features, 390, 404, 407 first year of life presentations, 407
definition, 390 focal neuropathy assessment, 61
nerve conduction studies, 404–405 gait assessment, 407–408
repetitive nerve stimulation studies, 390–391 Gower’s sign, 398, 410
Brachialis, 156 Guillain–Barré syndrome in, 404, 407, 408–410
Brachial plexus history taking, 397
anatomy, 6f hypotonia assessment, 401–404
lesion, 281 Kocher–Debré–Sémélaigne syndrome in, 410, 411
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INDEX 441

leukemia in, 410 pronator quadratus assessment, 10

leukodystrophies in, 407, 408 tarsal tunnel syndrome evaluation, 290
motor unit development, 395–396 temporal dispersion effects, 40–41, 78, 80f
needle selection, 399 Conduction block
nerve conduction in, 396 axon death and, 36–37
nerve conduction studies, 59–61 clinical features, 81
Pelizaeus–Merzbacher disease in, 407 electrophysiology, 35–36
physical examination, 397–398 in entrapment neuropathy, 262, 263
Pompe’s disease in, 407 motor fiber, waveform analysis, 81–83
sedation, 398–399, 412 myelin sheath lesions in, 299
shock artifacts in testing, 60 peripheral neuropathy evaluation, 307
spinal muscular atrophy in, 402, 406–407, 410 spinal, waveform analysis, 83–84
temperature control in assessment, 60, 399–400 in ulnar neuropathy at elbow, 270f
traumatic injury, 411 Conductivity in human body, 74
unusual diagnoses, 410–412 cell biology, 29
Chiralgia parasthetica, 281 pathophysiology, 34–41
Chloral hydrate, 398 temporal dispersion effects, 77–78
Chloride metabolism, 31, 67 Congenital hypomyelinating neuropathy, 310
Chronic ataxic neuropathy, ophthalmoplegia, IgM Connective tissue disease, 322
paraprotein, cold agglutinins, and Contraction
disialosyl antibodies, 321 endplate electrophysiology in, 73
Chronic inflammatory demyelinating polyneuropathy, maximal, 27
314 minimal, 26–27
pediatric, 410 motor unit potentials in myopathy, 361ff
Chronic obstructive pulmonary disease, 364 Coracobrachialis, 157
Cisplatin, 320–322 Corticosteroids, 370–371
Claims data, 138–140 CPT coding, 138–140
Closed fields, 74 Cranial nerve conduction studies, 213–214
CMAP. See Compound muscle action potential Creatinine kinase levels in viral myositis, 410
Coagulopathy, 133 Critical illness neuromuscular disorders
Colchicine, 324 classification, 366–368
Combined sensory index, 265–266 clinical conceptualization, 363–364
Common gain, 88 diagnosis, 364–365
Common mode rejection ratio, 88–89, 103 differentiating myopathic conditions and
Comorbid disorders. See Critical illness neuropathic conditions, 372–373
neuromuscular disorders drug-induced, 365–366, 370–371
Complex repetitive discharges, 23, 24ff etiology, 365–366, 368
Compound muscle action potential (CMAP) health system utilization, 363
age effects, 60 management, 373
in axonal degeneration, 298 myopathic conditions, 370–372
in critical illness neuromuscular disorders, 368–369, neuromuscular junction conditions, 373
370, 371, 372, 373 neuromyopathy, 373
decrement, 383 neuropathic conditions, 368–370
definition, 22 outcomes, 363, 369, 370, 371, 372, 373–374
electrode placement for recording, 43, 44 pediatric, 368, 411
electrophysiology, 37 treatment goals, 363
entrapment neuropathy assessment, 262, 263 ventilatory weaning and, 363, 365, 371
facial palsy assessment, 10 Current flow, 74–75
frequency settings, 90–91
in Lambert–Eaton myasthenic syndrome, 390
measurement technique, 22 D
motor unit calculations, 77 Dapsone, 317
myasthenia gravis evaluation, 389 Decomposition algorithms, 105–106
myopathy examination, 354 Decrement, 383
pediatric assessment Deep fibular nerve, 15, 16
brachial plexus injury, 400 Deep radial nerve, 8
Guillain–Barré syndrome, 534 Dejerine–Sottas disease, 310
peripheral neuropathy evaluation, 304, 307, Deltoid muscles, 158
314, 322 Demyelination, 35
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442 INDEX

Denervation leads, 88, 102

clinical course, 28 reusable, 88
fibrillation potential in, 23 types of, 106f
Depolarization See also Needle electromyography; Surface electrodes
in nerve stimulation, 48 Electrodiagnosis, 21
in salutatory conduction, 34 cell biology, 29
in signal conduction, 32, 33 claims data, 138–140
Dermatomal somatosensory evoked potential, critical illness neuromuscular disorders, 364–365,
radiculopathy examination, 338, 339 368–373
Dermatomyositis, 62, 408 doctor–patient relationship in, 134
Diabetes documentation, 134–142
electrodiagnosis case example, 325–327 medical consultation, 132–133
neuropathy, 259, 260, 299, 325 myopathy, 353–361
pediatric, 61, 411 organophosphate-induced delayed neurotoxicity,
spinal stenosis vs. polyneuropathy of, 347 320
Diaphragm pediatric considerations, 59, 60–61, 395, 398–400,
anatomy, 12f, 151 412–413
innervation, 151 peripheral neuropathy evaluation, 297–298,
needle placement, 10–13, 151 299–308, 327
phrenic nerve stimulation, 13 practitioner qualifications for, 132
surface electrode placement, 13 radiculopathy, 333–348
Differential amplifier, 88 Electromyography, generally
Digital converter, 92–96 ABCs, 28
Digital filters, 90 chronological considerations, 28
Diphasic action potential, 75 definition and scope, 21–22, 87
Diphtheria, 407 desynchronized impulses, 78–80
Direct muscle stimulation in critical illness electrophysiology, 67–70
neuromuscular disorder assessment, goals, 21
372–373 indications, 21, 28
Display, signal, 96–97 instrumentation and technique, 85–103
Disulfiram, 318, 319–320 knowledge requirements for, 3
Doctor–patient relationship, 134 program quality evaluation, 131–141
Documentation of care temporal dispersion effects, 77–78
claims and coding, 138–140 waveform generation, 75–77
content, 140–141 Electrophysiology
examples, 141 action potential generation and propagation, 68–70
good qualities, 134–138 axon movement, 41–42
potential errors in, 141–142 cell membrane, 29–34
reporting of findings, 59 conduction latency, 50–51
Dorsal ulnar cutaneous nerve, 238, 250, 253 conductivity in human body, 74
Drug-induced disorders current flow, 74–75
critical illness neuromuscular disorder, 363–364, individual development and maturation, 59–60
365–366, 370–371 intraneural anatomy, 41–42
myasthenia gravis, 391 nerve conduction velocity, 33–34
peripheral neuropathies, 310–311, 317–318, neuromuscular junction, 70–73
319–320, 321–322, 324–325 pathology, 34–41
Duchenne muscular dystrophy refractory period, 32–33
complex repetitive discharges in, 24f volume conductor, 73–74
pediatric assessment, 62 Embryologic patterns, 3
Dural sheath entrapment, 28 Endplate
anatomy, 71, 72–73
E electrophysiology, 73
Education and training of EMG professionals, 132 evaluation
Elbow, ulnar neuropathy at, 267–273 action potentials, 25
Electrode(s) EMG findings, 22
colors, 88 in myasthenia gravis, 113–114
for conventional EMG, 105–106 neuromuscular junction disease evaluation, 380
definition, 87 histology, 71–72
evoked potential recording, 42, 43 jitter during stimulation, 111
inspection and maintenance, 88, 102 End-stage renal disease, 327
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INDEX 443

Entrapment disorders Familial predisposition to pressure palsies, 260

anterior interosseous nerve syndrome, 281–284 Faraday cage, 103
demyelination in, 262 Fascicles, peripheral nerve, 41–42, 262–263
fibrillation in, 261 Fasciculation potentials, 23
fibular neuropathy, 286–289 Fatigue
history taking, 259–260 definition, 21
localization, 262–263 muscle fiber propagation velocity, 117
needle EMG, 261 myopathy examination, 353
nerve conduction studies, 58, 133, 261, 262, 263 Feet
neurapraxic, 262 innervation and anatomy, 209–212
pathophysiology, 261–262 needle EMG evaluations, 8, 209–212
physical examination, 260–261 Femoral motor nerve conduction studies, 239–240
prognosis, 262 Fetal development, 395
radial nerve lesions Fiber density, 118–119
deep, 279–281 development, 395
at spiral groove, 276–279 macro EMG amplitude and, 123f, 124
superficial, 281 myopathy findings, 122
reflexes in, 260 Fiber-type grouping, 105, 118
reinnervation, 261, 262 Fibrillation potential
sciatic nerve, 284–286 causes, 23
tarsal tunnel syndromes, 289–293 definition and characteristics, 23, 24f
timing of electrodiagnostic changes, 261 entrapment neuropathy assessment, 261
ulnar neuropathy Fibrosis, motor unit muscle fibers in, 105
at elbow, 267–273 Fibular nerve
at wrist, 273–276 entrapment localization in, 263
See also specific disorder entrapment neuropathy, 284
Erb’s point, pediatric studies, 61 at knee, 286–289
Evoked potentials See also Peroneal nerve
radiculopathy evaluation, 338–339 Filtering, 47–48
Evoked potential(s) frequency settings, 90–92
amplitude measurement, 39, 46 power line interference, 91
conduction block and, 39 types of, 90
definition, 37 Firing rate, 99–100
generation, 37 First dorsal interosseous muscle
impedance measurement, 87–88 manus, 183
overstimulation, 48 pedis, 210
recording, 43–48 First palmar interosseous, 182
shape determinants, 39 Fisher syndrome, 410
in spinal nerve stimulation, 56–57 Flexor carpi radialis, 171
temperature effects, 45–46 Flexor carpi ulnaris, 180, 262–263
temporal dispersion effects, 39–41 Flexor digitorum brevis, 212
Extensor carpi radialis, 160 Flexor digitorum longus, 207
Extensor carpi ulnaris, 165 Flexor digitorum profundus, 179
Extensor digitorum, 164 Flexor digitorum superficialis, 173
Extensor digitorum brevis, 202 Flexor hallucis brevis, 211
Extensor digitorum communis, jitter reference values, Flexor pollicis longus, 174
111. See also extensor digitorum Flick sign, 260–261, 264
Extensor digitorum longus, 199 Forearm
Extensor hallucis longus, 201 Martin-Gruber anastomosis, 14
Extensor indicis proprius, 169 surface electrode placement, 9
Extensor pollicis brevis, 168 Free-running signal display, 96
Extensor pollicis longus, 167 Frequency settings, 90–92
Friedrich’s ataxia, 321, 322
F pediatric, 412
Facial palsy Froment’s sign, 268
compound muscle action potential in, 10 Frontalis muscle, 147
nasalis muscle evaluation, 10 F wave
Facilitation age effects, 59
definition, 30 claims data, 138
in repetitive nerve stimulation, 383, 384f definition, 337
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444 INDEX

F wave (continued) source, 53

in diabetic neuropathy, 325 Humerus, 8f
diagnostic significance, 337 Hyperglycemia, 299, 327, 368
frequency settings, 91 Hypoalbuminemia, 368
H reflex and, 52, 55 Hypoglycemic neuropathy, 318–319
latency measurement, 52–53 Hypomyelination disorders, pediatric, 404
limitations, 56–57 Hypotonia assessment in infant, 401–404
lower body nerve conduction studies, 244–245
pediatric studies, 61 I
radiculopathy examination, 337–338, 347 Iliopsoas muscle, 190
source, 51 Impedance, 74
in upper extremity, 228 of dry skin, 44
variations in, 51–52 electrical stimulator technique, 98
input, 89
G recording goals, 87–88
Gain, signal, 88–89 reduction techniques, 87, 88, 102
Ganglionitis, 321 Inclusion body myositis, 356–357
Gastrocnemius, 208 Informed consent, 134
Gender differences, 47 Infraspinatus, 154
Gentamicin, 363 Injury potentials. See Insertional activity
Giant axonal neuropathy, 412 Insertional activity
Ginger, 320 causes, 24–25
Glucose metabolism, 299 definition, 23–24
impaired glucose tolerance, 326 technique, 26
See also Diabetes Instrumentation, EMG
Gluteus maximus, 194 amplifier, 88–90, 102
Gluteus medius, 196 analog to digital converter, 92–96
radiculopathy evaluation, 3 cables, 88, 102
Glycogen metabolism, muscle fiber distribution and, electrical stimulator, 98–99
125 electrodes, 87–88
Gower’s sign, 398 filters, 90–92
Gracilis muscle, 188 inspection and maintenance, 133
Grounding, power line, 60, 100–102 leads, 88, 102
Ground lead, 88 for pediatric practice, 396, 397, 399
Guillain–Barré syndrome, 51, 62, 311, 312, 315–316, safe use, 100–102, 133
318, 321, 322, 364 signal averaging, 97–98
pediatric, 404, 407, 408–410 signal display, 96–97
Intercostal muscles, 71–72, 186
H Interference, 87
Height, patient, 47 power line, 91
Hemorrhage, 133 reducing, 102–103
Hereditary motor sensory neuropathy type I Interosseous nerve lesions, posterior, 279–281
clinical features, 309 Interosseous nerve syndrome, anterior, 281–284
differential diagnosis, 310 Intramuscular stimulation
electrodiagnosis, 309–310 neuromuscular transmission studies, 115–116
pediatric, 412 technique, 108
pediatric assessment, 62 Ion physiology, 29–34, 67–68
Hereditary motor sensory neuropathy type II, 317 temperature effects, 45–46
pediatric, 412 Ischemia, jitter and, 111
N-Hexane, 311–312 Ithium, 324
Hip surgery, 285
H reflex J
F wave and, 52, 55 Jake paralysis, 320
latency, 53 Jitter
limitations, 56–57 abnormal findings, 111
lower body nerve conduction studies, 246 axonal stimulation, 111–112
measurement, 55 calculation, 108–109
nomogram, 53, 56f critical illness polyneuropathy manifestations, 369
pediatric studies, 61 definition, 108
radiculopathy examination, 336–337 in intramuscular stimulation, 108
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INDEX 445

ischemia effects, 111 stenosis, 347

neuromuscular junction disease evaluation, 386 Lumbricals, 177
in neuromuscular transmission disorders, 113–116 Lymphoma, 318
reference values, 110t, 111
single-fiber EMG studies, 111–113 M
during stimulation, 111 Macro EMG motor unit potential
voluntary activity, 108f, 109–111 clinical significance, 120
definition, 89
K
indications, 125
Kinesiology, knowledge requirements for
method, 120–121
electromyographers, 3
for motor unit estimation, 122
Knee, fibular entrapment, 286–289
myopathy findings, 122
Kocher–Debré–Sémélaigne syndrome, 410, 411
normal, 121–122
Krabbe’s leukodystrophy, 407
reinnervation findings, 122–125
L Magnetic resonance imaging, radiculopathy
Lambert–Eaton myasthenic syndrome evaluation, 338, 339, 348
clinical features, 389–390 Martin-Gruber anastomosis, 58, 267, 270–271, 282
compound muscle action potential, 390 anatomy, 14f
epidemiology, 389 carpal tunnel syndrome and, 14
nerve conduction studies, 354 epidemiology, 14
pathophysiology, 114 pathophysiology, 14
repetitive nerve stimulation in, 383 Masseter muscle, 145
single-fiber EMG, 386 Mean value of consecutive differences, 111
single fiber EMG findings, 114 Measurement, manual, 99–100
Latency Medial antebrachial cutaneous sensory nerve
of activation, 22, 50, 51 conduction study, 230
age effects, 59–60 Medial nerve lesion, 282
F wave, 52 Medial plantar motor nerve conduction studies, 242
in nerve conduction studies, 50–51 Median nerve
reporting of findings, 59 anastomosis, 14
Lateral antebrachial cutaneous sensory nerve anatomy, 15f
conduction study, 229 carpal tunnel assessment, 266–267
Lateral femoral cutaneous sensory nerve conduction nerve conduction studies, 8f
studies, 247 to abductor pollicis brevis, 221
Lateral plantar motor nerve conduction studies, 243 to fourth digit, 234
Late waves, 55–56 to pronator quadratus, 222
Latissimus dorsi, 157 to second and third digits, 231–232
Leads, EMG, 88 to thumb, 233
Leukemia, pediatric, 410 pediatric studies, 60–61
Leukodystrophies, 407, 408 Mees’ lines, 315–316
Levator labialis superioris, 10 Membrane electrophysiology, 29–34, 67–68
Levator scapulae, 152 action potential, 32–34
Lipoma, radial nerve, 279 membrane proteins, 30–31
Long thoracic nerve conduction studies, 216–217 resting potential, 31–32
Lorazepam, 398 Mentalis muscle, 148
Lower body nerve conduction studies Mercury, 324
F wave, 244–245 Merosin deficiency, 402
H reflex, 246 Metabolic disorders
motor nerves, 239–246 peripheral neuropathies and, 299
sensory nerves, 247–253 See also specific disorder
Lower limb Metachromatic leukodystrophy, 62, 310, 408
anatomic anomalies, 14 Methyl n-butyl ketone, 311–312
motor innervation, 4t Metronidazole, 322
nerve root level innervations, 18t Midazolam, 398
peripheral nerve innervations, 19–20t Miniature endplate potential, 72–73, 378–379
sensory innervation, 16t Motor nerves
Lumbar plexus anatomy, 7f anatomy, 3
Lumbar spine axonal loss evaluation, 6t
radiculopathy evaluation, 334, 335, 336–337, 338, nerve conduction studies
339, 341, 342–343, 348 lower body, 239–246
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446 INDEX

Motor nerves (continued) congenital syndromes, 388–389, 402

upper body, 215–228 definition, 387
pediatric electrodiagnosis, 60 drug-induced, 391
signal latency in nerve conduction studies, 50–51 incidence, 387
Motor neuron disease, 273 nerve conduction studies, 354, 387
Motor unit neuromuscular transmission in, 113–114
definition, 21 normal electrophysiologic findings in, 379–380
development, 395–396 pediatric, 62
EMG goals, 22 repetitive nerve stimulation evaluation, 387–388
estimation technique, 122 single-fiber EMG, 386
muscle fiber organization, 105, 125 single fiber EMG findings, 113–114
pathologies, 28 Myelin electrophysiology, 34, 35
structure, 21 conduction-slowing pathophysiology, 34
Motor unit potentials saltatory conduction, 34
contraction in myopathy, 361ff salutatory conduction, 34
conventional EMG recording, 105–106 Myelin sheath lesions, 299
in critical illness motor neuromuscular disorders, peripheral neuropathy evaluation, 301, 304,
371, 372 305–307, 314–315
definition, 21 Myokymic potential, definition and appearance, 23
EMG findings, 21–22 Myopathy assessment
entrapment neuropathy assessment, 261 acute necrotizing myopathy of intensive care, 371–372
filtering technique, 90, 92, 94–96 case examples, 355–361
firing rate, 99–100 catabolic myopathy, 372
in inclusion body myositis, 357 challenges, 353
macro EMG, 89 critical illness neuromuscular disorders, 370–372
in maximal contraction of muscle, 27 fiber density, 119, 355
in minimal contraction of muscle, 26 history taking, 353–354
in myopathy, 122, 355 inflammatory, 360–361
pediatric, 395–396 motor unit potentials, 355
polyphasic, 26, 106, 355 motor unit size, 122
early, 26 needle EMG, 354–355
recruitment patterns, 26–27 nerve conduction testing, 354
spike component, 90 noninflammatory, 359–360
stability, 26 pediatric, 402–403
Multi-MUP recording, 105–106 physical examination, 354
Muscle electrophysiology, 67–70 scanning EMG findings, 127
Muscle fibers thick filament myopathy, 370–371
conduction speed, 77 Myositis
density studies, 118–119 inclusion body, 356–357
development, 395 viral, 410
distribution assessment, 125 Myotonia congenita, 403
EMG findings, 22 Myotonic dystrophy, assessment and diagnosis,
endplates, 71 357–359
fiber-type grouping, 105, 118 pediatric, 402–403
local distribution, 107
motor unit organization, 105 N
in myopathy, 355 Nasalis muscle, 148
pathological arrangements, 105 anatomy, 10
propagation velocity, 116–118 Needle electromyography
scanning EMG studies, 125–127 anterior interosseous nerve syndrome, 283t, 284
Muscular dystrophy conduction block assessment, 39
macro EMG findings, 123f conventional recordings, 105–106
pediatric assessment, 402 critical illness motor neuromuscular disorder
Musculocutaneous nerve assessment, 370, 371, 372
nerve conduction studies, 218 distribution of sampling, 27
pediatric studies, 61 documentation, 138
M wave, 52, 55 electrode types, 106f
Myasthenia gravis, 353 entrapment neuropathy assessment, 261, 262
clinical features, 387 examination planning, 22–23
CMAP decrement, 383 fibular neuropathy evaluation, 287t, 289
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INDEX 447

frequency settings, 90–91 patient height considerations, 47

impedance reduction, 87, 90 pediatric, 59–61, 396
insertional activity, 23–26 brachial plexus injury assessment, 400–401
in maximal contraction, 27 Guillain–Barré syndrome assessment, 408
in minimal contraction, 26–27 peripheral neuropathy evaluation, 301–302, 316
myopathy examination, 354–355 polyphasic signals in, 44
case examples, 355–361 radial nerve lesion assessment, 277–279
neuromuscular junction disease evaluation, radiculopathy assessment, 336, 338
377–378, 385 reference values, 42–43
neuromuscular transmission studies reporting findings, 59
in disease, 113–116 sciatic neuropathy, 285t, 286
methods, 108–109 sensory, frequency settings, 90
normal, 109–113 signal deflection in, 43–44
pediatric brachial plexus injury assessment, 401 signal display, 96, 97
pediatric practice, 397 signal latency in, 50–51
peripheral neuropathy evaluation, 301, 302–303, sources of error in, 58
304, 315, 316–317 spinal nerve stimulation, 56–58
quiet muscle characteristics, 23 superficial radial nerve lesions, 280t
radial nerve lesions, 278t, 279, 281 tarsal tunnel syndrome evaluation, 290–292
radiculopathy assessment, 336, 339 technical basis, 22
response in critical illness neuromuscular disorders, temperature effects, 45–46, 58, 265
373 ulnar neuropathy at elbow, 268–272
safety considerations, 133 ulnar neuropathy at wrist, 274–276
sampling rate, 94 upper body
sciatic neuropathy, 285t, 286 F wave, 228
signal display, 96 motor nerves, 215–227
single-fiber recording, 106–107 sensory nerves, 229–238
steps, 23–27 Nerve conduction velocity
tarsal tunnel syndrome evaluation, 290, 292–293 age effects, 46–47, 59, 62
ulnar neuropathy assessment, 272–273, 275t, 276 axon size and, 33–34
waveform patterns, 76–77 in children, 396
See also Single-fiber EMG conduction slowing, 34
Nernst equation, 30–31 definition, 22
Nerve conduction studies electrophysiology, 33–34
anterior interosseous nerve syndrome, 283t, 284 in entrapment disorders, 263
application, 29 evoked potential shape and, 39
axonal loss evaluation, 6t measurement, 22
carpal tunnel assessment, 264–265 patient height and, 47
claims data, 138–140 peripheral neuropathy evaluation, 307
conceptual basis, 29 reference values, 42–43
cranial, 213–214 reporting of findings, 59
documentation, 138 saltatory conduction, 34
electrode placement, 43–45, 89 sensory latency and, 51
entrapment neuropathy assessment, 133, 261, 262, slowing in metabolic disorders, 299
263 temperature effects, 45
evoked potential recording, 43–48 ulnar neuropathy assessment, 271
fibular neuropathy evaluation, 287t, 288–289 Nerve root
latency measurement, 50–51 injuries, 28
late waves, 55–56 radiculopathy evaluation, 333–334
lower body innervations, 18t
motor nerves, 239–246 stimulation, 56–58
sensory nerves, 247–253 Neuralgic amyotrophy, 282, 283–284
Martin-Gruber anastomosis, 270–271 Neurapraxic injury, 34, 261, 262. See also Conduction
myasthenia gravis evaluation, 387 block
myopathy assessment, 354 Neurogenic disease, scanning EMG findings, 127
nerve stimulation, 48–50 Neurography, 22
neuromuscular junction disease, 377 Neuromuscular blockade
pathophysiology and, 34–42 blocking agents, 365–366, 370–371, 373
patient age considerations, 46–47 critical illness neuromuscular disorders, 373
patient discomfort in, 48–50 jitter and, 111
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448 INDEX

Neuromuscular junction Paraneoplastic syndromes, 321

anatomy and physiology, 70–73, 378–379 Paraspinal mapping, 341
postsynaptic cleft, 378 Paraspinal muscles
presynaptic terminal, 378 anatomy, 11f
synaptic cleft, 378 cervical, 184
Neuromuscular junction disease, 28 fibrillation, 341, 347
critical illness neuromuscular disorders, 373 lumbosacral, 185
current clinical understanding, 377 needle placement, 8
electrodiagnostic tests, 379–380 radiculopathy evaluation, 339–341, 342
EMG findings, 22 safety considerations in assessment, 133
endplate analysis, 380 Parenteral nutrition, 368
endplate profile in, 72 Paresthesias, EMG indications, 21
nasalis muscle evaluation, 10 Parsonage-Turner syndrome, 282
needle EMG evaluation, 377–378, 385 Patient comfort, 134
nerve conduction studies, 377 nerve stimulation studies, 48–50
pathophysiology, 377 Patient satisfaction, 131, 134
repetitive nerve stimulation evaluation, 377, 380–385 Pectineus muscle, 191
single-fiber EMG, 380, 385–386 Pectoralis major
See also specific disorder clavicular head, 155
Neuromuscular transmission sternocostal head, 178
assessment methods, 108–109, 111–113 Pectoralis minor, 178
in disease states, 113–116 Peer review, 132
in intramuscular nerve tree, 115–116 Pelizaeus–Merzbacher disease, 407
normal, 109–111 Penicillamine, 391
repetitive nerve stimulation abnormalities without Peripheral nerve(s)
deficit in, 391 anatomy, 41–42
single-fiber EMG studies, 107 conduction, 29
temperature effects, 384–385 innervations, 19–20t, 262–263
Neuromyopathy, critical illness, 373 Peripheral neuropathies, 28
Neuromyositis, 355 assessment and diagnosis, 133, 297–298, 299–308,
Neurotmesis, 34 327
in entrapment neuropathy, 262 differential diagnosis, 301
Nitrofurantoin, 318, 320 motor greater than sensory neuropathy with
Nodes of Ranvier, 34 mutlifocal conduction slowing, 312–316
Noise, defined, 87. See also Signal to noise ratio motor greater than sensory neuropathy with
Nomograms uniform conduction slowing, 309–312
F wave, 52, 53f motor or motor greater than sensory neuropathy
H reflex, 53, 56f and axonal loss, 316–320
Notch filter, 91 sensory greater than motor neuropathy with
axonal loss, 322–325
O sensory greater than motor neuropathy with
Occupational neuritis, 274 conduction slowing, 325–327
Open fields, 74 sensory neuropathy/neuronopathy, 320–322
Opponens digiti minimi, 181 axonal degeneration in, 298–299, 304–305
Opponens pollicis, 142 axonal loss in, 316–325
anatomy, 10, 176 chemical exposure-related, 311–312, 315–316
innervation, 176 classification, 308–309
needle placement, 176 distribution assessment, 307–308
Orbicularis oculi, 147 drug-related, 310–311, 317–318, 319–320, 324
Orbicularis oris, 149 epidemiology, 327
Organophosphates, 318, 320 metabolic disorders in, 299
myelin sheath lesions in, 299, 304, 305–307
P needle electromyography, 301, 302–303, 304
Paclitaxel, 322 nerve conduction studies, 301–302
Pain pathophysiology, 298–299
causes of, 21 rate of progression, 308
EMG indications, 21 severity, 308
Palmaris longus, 172 symmetry, 308–309
Pancuronium, 370 See also Entrapment disorders
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INDEX 449

Peroneal motor nerve surface electrode placement, 10

F wave, 244 Pronator syndrome, 264
nerve conduction studies, 241 Pronator teres, 170
pediatric studies, 60 Protein electrophysiology in cell membrane, 30–31
Peroneal nerve Puffer fish, 312
accessory, 14 Pyridoxine, 321
anatomy, 16f, 17f
Q
sensory nerve skin distribution, 15f
Quadratus femoris, 193
superficial branch, 17f
Quality improvement, 131–132
See also Fibular nerve
Quiet muscle electromyography, 23
Peroneus brevis, 203
Peroneus longus, 202 R
Peroneus tertius, 200 Radial nerve
Phalen’s test, 260, 264 anatomy, 8f, 277f
Phase cancellation, 39, 40f, 77–78, 79f, 80 deep lesions, 279–281
Phospholipids, in cell membrane, 29–30 lesions at spiral groove, 276–279
Phrenic nerve needle EMG, 278t, 279
nerve conduction studies, 215 nerve conduction studies, 277–279
pediatric injury, 61 to extensor digitorum, 223
Piriformis, 194 to extensor indicis proprius, 224
Piriformis syndrome, 286 to thumb, 233, 235–236
Plexopathies neuropathy, 268, 276, 277
nerve conduction studies, 338 superficial lesions, 281
vs. radiculopathy, 338 Radial tunnel syndrome, 279–281
vs. sciatic neuropathy, 286 Radiculopathies
Polio anatomic variations in, 333–334
macro EMG findings, 124 assessment
post-polio syndrome, 125 algorithm, 334, 335f
Polymyositis, 62, 355–356 goals, 333, 335–336, 348
pediatric, 408 guidelines, 336
Polyneuropathy C6, 281
assessment, 133, 260 C8, 267
F waves in, 337 causes, 333
nerve conduction studies, 338 cervical, 337, 338–339, 341, 342
pediatric assessment, 62 clinical course, 347
See also Critical illness neuromuscular disorders definition, 333
Pompe’s disease, 407 diabetes and, 347
Porphyrias, 317–318 differential diagnosis, 264
Positive wave discharges EMG diagnostic sensitivity, 340t
causes, 23 F wave in, 337–338, 347
endplate, 25ff H reflex in, 336–337
interpretation, 76–77 L5, 286
Posterior femoral cutaneous nerve conduction studies, limitations of EMG, 344–348
248 lumbosacral, 334, 335, 336–337, 338, 339, 341,
Posterior interosseous nerve lesions, 279–281. See also 342–343, 348
deep radial nerve magnetic resonance imaging, 338, 339, 348
Posterior tibialis muscle, 13 muscle selection for testing, 3–8, 341–344
Post-polio syndrome, 125 needle electromyography, 336, 339
Postsynaptic cleft, 378 nerve conduction studies, 336, 338
Potassium metabolism, 67–69 paraspinal muscle examination, 339–341, 342
cell membrane electrophysiology, 30, 31–32 pediatric, 411
endplate electrophysiology, 73 physical examination, 334–335
Power line grounding, 100–102 sensory nerve action potentials in, 333
Power line interference, 91 somatosensory evoked potentials in, 338–339
Prader–Willi disease, 403 treatment outcome prediction, 348
Presynaptic terminal, 378 vs. plexopathy, 336
Pronator quadratus, 175 Recruitment patterns
innervation, 10, 175 in maximal contraction, 27
needle placement, 10, 175 in minimal contraction, 26–27
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450 INDEX

Rectus abdominis, 186 normal, 127

Rectus femoris, 193 pathological findings, 127
Reference lead, 43, 88, 89 Schwann cells, 34
Reference values Sciatic nerve
jitter, 110t, 111 anatomy, 5f
nerve conduction, 42–43 entrapment localization in, 263
Refractory period, 32–33 entrapment neuropathy in, 284–286
Reinnervation nerve conduction studies, 51, 240
axonal lesions, 298 Scleroderma, myopathy in, 354
conduction slowing in, 35 Semimembranosus, 204
in entrapment neuropathy, 261, 262 Semispinalis muscles, 11f
macro EMG findings, 122–125 Semitendinosus, 203
neuromuscular transmission in, 114–115 Sensory nerve action potential
Remyelination, 35 age effects, 60
Renal failure, 327 in axonal degeneration, 298
Repetitive discharge polyphasic fasciculation axon calculations, 77
potentials, 23 conduction block waveforms, 82–83
Repetitive nerve stimulation in critical illness neuromuscular disorders, 369, 370,
abnormal findings, 382–383 371, 372, 373
without neuromuscular transmission deficit, 391 electrode placement for measuring, 44–45, 89
Botulism studies, 390–391 electrophysiology, 37–39
electrode placement, 383–384 entrapment neuropathy assessment, 261, 262, 263
facilitation, 383, 384f filtering technique, 90
Lambert–Eaton myasthenic syndrome studies, 390 in hereditary motor sensory neuropathy type II, 317
medication effects, 385 peripherial neuropathy evaluation, 304, 322
movement artifact in, 384 in radiculopathy, 333
myasthenia gravis evaluation, 387–388 signal averaging, 97
nerve and muscle selection, 380 superficial radial nerve lesion assessment, 281
neuromuscular junction disease evaluation, 377, temporal dispersion effects, 40–41, 77–78, 79f
380–385 ulnar neuropathy assessment, 271–272
patient preparation, 380 Sensory nerve action potentials (SNAPs), 22
protocols, 380–382 Sensory nerves
response in critical illness neuromuscular disorders, anatomy, 3
369, 370, 371, 372, 373 axonal loss evaluation, 6t
sources of error in, 383–385 entrapment neuropathy assessment, 260
temperature effects, 384–385 nerve conduction studies
Residual latency, 50 lower body, 247–253
Resistant tennis elbow, 279–281 upper body, 247–253
Resting potential, 31–32 pediatric electrodiagnosis, 60–61
Rheumatoid arthritis, 322 signal latency in nerve conduction studies, 51
Rhomboid major, 152 trunk and lower limb, 16t
Rhomboid minor, 153 Serratus anterior muscle, 153
Riche-Cannieu anastomosis, 14 axillary view, 13f
innervation, 153
S needle placement, 13, 153
Safe practice, 100–102, 133 surface electrode placement, 13
Saltatory conduction, 34 Shielded cable, 88, 90
Salutatory conduction, 34 Shock artifact, 44, 60
Sampling interval/rate, 92–96 Signal averaging, 97–98
Saphenous nerve Signal-processing algorithms, 90
anatomy, 10f Signal to noise ratio
sensory nerve conduction studies, 249 averaging, 97–98
Sarcoid myopathy, 360–361 differential amplification, 88–90
Sartorius muscle, 191 strategies for improving, 87, 88, 97, 102–103
Saturday night palsy, 277 Simple discharges, 23
Saxitoxin, 312 Single-fiber EMG
Scanning EMG application, 106–107, 119–120
indications, 125, 127 critical illness polyneuropathy manifestations, 369
method, 125–127 electrode maintenance, 88
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INDEX 451

fiber density studies, 118–119 Surgical complications

jitter studies, 111–113 sciatic neuropathy, 285
macro EMG motor unit potential, 89, 120–122 superficial radial nerve lesions, 281
motor unit estimation, 122–125 Synaptic gutter/cleft, 71–72, 378
neuromuscular junction disease evaluation, 380, Synaptic potential current flows, 74
385–386 Systemic inflammatory response syndrome, 365, 367f,
neuromuscular transmission findings in disease, 370
113–116
propagation velocity, 116–118 T
recording zone, 107 Tabes doralis, 321
scanning method, 125–127 Tacrolimus, 310
signal display, 97 Tarsal tunnel
waveforms, 76–77 anatomy, 4f
Sjögren’s syndrome, 321 syndromes, 289–293
Skin Temperature effects
electrode placement technique, 87–88 amplitude change, 45, 46
impedance, 44 on conduction velocity, 45
peroneal nerve sensory distribution, 15f controlling for, 46
temperature control in pediatric assessment, in nerve conduction studies, 45–46, 58, 265
399–400 pediatric electrodiagnosis, 60
Snake toxins, 391 in repetitive nerve stimulation, 384–385
SNAPs. See Sensory nerve action potentials Temporal dispersion effects, 39f, 77–78, 80
Sodium metabolism, 67–68 clinical significance, 39–41
cell membrane electrophysiology, 30, 32–33 definition, 39
endplate electrophysiology, 73 Temporalis, 146
neuropathy related to abnormalities of, Tensor fasciae latae
299, 312 anatomy, 195
Soleus muscle, 209 innervation, 195
Somatosensory evoked potential, radiculopathy needle placement, 195
examination, 338–339 radiculopathy evaluation, 3
Spider bite, 391 Teres major, 155
Spinal cord Teres minor, 158
anatomy, 7f Tetrodotoxon, 312
conduction block waveforms, 83–84 Thalidomide, 322
Spinal muscular atrophy, 402, 406–407, 410 Thick filament myopathy, 370–371
pediatric assessment, 62 Thoracic outlet syndrome, 51
Spinal nerve stimulation, 56–58 Thoracodorsal nerve conduction studies, 220
Spinal stenosis, 347 Tibialis anterior, 198
Spondylitic myelopathy, 263 Tibialis posterior, 206
Sternocleidomastoid muscle, 149 Tibial nerves, 242–246
Steroids, 365–366 anatomy, 4f, 5f
Stimulation, in nerve conduction studies, 48–50 F wave, 244
spinal nerve, 56–58 nerve conduction studies, 242–246, 251
Stimulator, electrical, 98–99 Tinel sign, 260, 264, 268
Superficial fibular nerve, 17 radial nerve lesion evaluations, 281
Superficial peroneal nerve conduction studies, 250 tarsal tunnel syndrome evaluation, 290
Supinator, 161 Tongue muscle, 150
Supramaximal stimulus, 48 electrode placement, 11f
Suprascapular nerve, 219 innervation, 150
Supraspinatus, 154 needle placement, 10, 150
Sural sensory nerve conduction studies, 252–253 Toxic substances
Suramin, 310–311 in critical illness neuromuscular disorder etiology,
Surface electrodes, generally 365–366
current flow recording, 74–75 peripheral neuropathy associated with exposure to,
evoked potential recording, 43, 44 311–312, 315–316, 320
leads and cables, 88 Transmembrane potential, 67–68, 75–76
nerve stimulation, 48 Trapezius muscle, 150
skin contact, 87 Triceps brachii, 162
temporal dispersion effects, 77–78 Triggered signal display, 96–97
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452 INDEX

Triorthocresyl-phosphate, 320 Vastus lateralis, 192

Triphasic waveforms, 76–77 Vastus medialis, 192
Trunk, sensory innervation, 16t Vecuronium, 370
Twisted pair leads, 88, 90 Velocity recovery function, 117–118
Vinca alkaloids, 318
U Vincristine, 318, 320
Ulnar dorsal cutaneous sensory nerve conduction Vitamin B12 deficiency, 324
study, 238 Vitamin E deficiency, 321
Ulnar nerve Vocal cords
anastomosis, 14 innervation, 10
anatomy, 274 needle placement, 10
elbow neuropathy, 267–273
entrapment localization in, 262–263 W
F wave latency in, 52–53 Wallerian degeneration, 28, 36–37
nerve conduction studies, 268–272, 274–276 in entrapment neuropathy, 261
to abductor digiti minimi, 225–226 Waveforms
to fifth digit, 237 aliasing effects, 94–96
to first dorsal interosseus, 227 clinical analysis, 80–84
to fourth digit, 234 conduction block evaluation, 81–83
pediatric studies, 60–61 desynchronized impulses, 78–80
wrist neuropathy, 272, 273–276 diphasic, 75–76
Upper body nerve conduction studies electrical device interference, 91
F wave, 228 fiber density studies, 118–119
motor nerves, 215–228 manual measurement, 99–100
sensory nerves, 229–238 rapid change in potential, 90
Upper limb signal display, 96–97
anatomic anomalies, 14 temporal dispersion, 77–78, 80
motor innervation, 4t triphasic, 76–77
nerve root level innervations, 18t Weakness
peripheral nerve innervations, 19t electrodiagnosis, 21
entrapment neuropathy assessment, 260
V myopathy examination, 353
Vagus nerve, vocal cord innervation, 10 West Nile virus, 319
Van der Waals bonding, 30 Wrist, ulnar neuropathy at, 273–276
Vasculitis neuropathy, 322