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DIAGNOSTIC TOOL

electromyograph
is a device that amplifies and converts the minute voltages recorded by a needle
electrodetypically a fi ne wire inserted within a 24-gauge hollow needleinserted
into muscle and expresses these currents by speaker or visually by a cathode ray
oscilloscope.
EMG is often performed when patients have unexplained motor weakness. EMG
helps to distinguish between muscle conditions in which the problem begins in the
muscle and muscle weakness resulting from nerve disorders. EMG can be used to
detect true weakness as opposed to weakness from reduced use because of pain or
lack of motivation. EMG can also be used to isolate the level of nerve irritation or
injury. EMG can detect disease involving the lower motor neuron from the anterior
horn cell to the neuromuscular junction, defects in transmission at the
neuromuscular junction, and primary muscle disease.
Ultrasound

Is specific and sensitive for compression of the median nerve at the wrist.
The test also can identify other structures that can complicate surgical procedures if not
appreciated early, such as persistent median artery within the carpal tunnel

Can help determine whether a cancer, another mass, or injury causing the plexus disorder.

Offer a larger field of view and opportunity to utilize intravenous contrast, but their value
is counter balanced by high cost and the extensive scan time needed to image a nerve
along its entire course.

CT Scan
MRI

Nerve Conduction Velocity


An electrical diagnostic test that provides information about abnormal conditions in the
nerves.
Nerves are stimulated with small electrical impulses by one electrode while other
electrode detects the electrical impulse down-stream from the first electrode.
Chest Radiographs
May show elevation of the diaphragm as a signature of phrenic nerve paralysis from
injury to the proximal upper cervical spinal nerves and roots.
Laboratory Screening Tests
Complete Blood Count

Th e CBC is an evaluation of components typically found in venous blood.


Th e components of the CBC include white blood cell (WBC) count, red blood cell
(RBC) count, hemoglobin (Hgb), hematocrit (Hct), and platelets
Basic Metabolic Panel
the constituents of the basic metabolic panel (BMP) are defined by Current
Procedure Terminology (CPT) codes.
Th e BMP is a group of eight tests and consists of serum concentrations of sodium,
potassium, chloride, calcium, blood urea nitrogen (BUN), creatinine, glucose, and
carbon dioxide. Venous blood samples obtained after a 10- to 12-hour fast are used
for assessment
Laboratory Diagnostic Testing
Hemostasis
Hemostasis, also called clotting studies and bleeding time, is used to determine the
bodys ability to initiate the clotting cascade and how rapidly the cascade occurs
and to diagnose specifi c primary clotting diagnoses such as hemophilia.
Inflammation
Th e presence and severity of infl ammation can be measured in a nonspecifi c
method using erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP).
ESR is the rate that RBCs settle by gravity in a given volume of unclotted plasma in
1 hour. Th e test is based on the premise that infl ammation and necrotic processes
lead to an alteration in blood cell proteins, resulting in an aggregation within the
RBCs making them denser than RBCs in individuals without infl ammation or
necrosis.
ESR may also be used to assess the eff ectiveness of medications given to decrease
infl ammation.
CRP was originally believed to quantify infl ammation specifi cally associated with
coronary artery disease, but subsequent studies have shown that acute and chronic
musculoskeletal conditions may also lead to an elevated CRP, reducing the
sensitivity of the test for coronary artery disease. 9

Cardiac Enzymes
Th e CK-MB is a particular CK enzyme found primarily in the heart. Th e CK-MB and
CK are measured in suspected cardiac injury, and if the CK-MB exceeds 5.0% of the
CK, there is a strong likelihood that cardiac injury has occurred.

Lactic acid dehydrogenase (LDH) is an extracellular enzyme distributed to most


internal organs.
Liver Enzymes
Liver tests are typically divided into two types: tests diagnostic of liver disease and
tests that measure a particular liver function.
An example of a test used to diagnose the cause of liver damage is the test for
gamma-glutamyltransferase (GGT). Th is test is a very sensitive indicator of
hepatobiliary tract disease. GGT is elevated after alcohol ingestion and in hepatitis,
primary or metastatic liver malignancy, and cirrhosis.
An example of a liver test measuring liver function is alanine aminotransferase
(ALT), which is a strong indicator of hepatocellular damage
Immunological Tests
Th ese tests are used in the diagnosis of immune disorders and allergic reactions,
infectious disease, rheumatological diagnoses, and neoplastic diseases.
Immunoglobulins, antibodies that are produced in response to antigens, are divided
into fi ve classes (IgG, IgA, IgM, IgD, and IgE)

PHARMACOLOGICAL MANAGEMENT
Medications Used to Treat Pain That Is Due to Peripheral
Neuropathy-delisa
Tricyclic antidepressants
Amitryptiline, imipramine, nortriptyline, desipramine
Anticonvulsants
Gabapentin, lamotrigine, phenytoin, carbamazepine, valproic
acid, topiramate
Antiarrhythmics
Topical agents
Capsaicin cream, lidocaine gel
Nonsteroidal antiinflammatory drugs
Antispasticity agents
Selective serotonin reuptake inhibtors
Tramadol
Clonidine
Stimulatory peptides
Neurotrophic factors
N-methyl-D-aspartate antagonists
Vitamin B
Biotin
Choline
Inositol
Thiamine
Gamma linolenic acid
Alpha-lipoic Acid
Mexilitine
Insulinlike growth factor1
Memantine
Dextromethorphan
Pain Management
1. Long-Acting Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
For patients with very mild pain
2. Anticonvulsants (Phenytoin, Gabapentin, Lamotrigine, Valproic acid, Topiramate)
Postulated to work by stabilizing the peripheral nerve membrane, suppressing ectopic or
ephaptic discharges, and modulating sodium channels.
3. Tricyclicanti Depressant
Nortriptyline or antiepileptic drugs such as gabapentin (Neurontin) and lamotrigine
(Lamictal).
4. Patients with severe neuropathic pain may require narcotic analgesia. Usually begins with
tramadol (Ultram). If becomes ineffective, oxycodone (OxyContin) is used with increasing doses.

The author uses fentanyl patches for patients who are allergic to codeine, morphine sulfate (MS
Contin) and methadone for patients with severe pain.
Others
1. Adjuvant Drugs
Medications that achieved initial Food and Drug Administration approval for indications
other than pain.
2. Gabapentin Monotherapy
For diabetic peripheral neuropathy can effectively reduce pain and improve sleep, and
has positive effects on mood and quality of life.
3. Stimulatory Peptides
Composed of short chains of amino acids and are derived from cytokine proteins or
growth factors.
These may work through membrane receptors to encourage remyelination, decrease and
reverse sensorimotor deficits, alleviate neuropathic pain, and prevent neuronal death.
4. Vitamin B, Biotin, Choline, Inositol, and Thiamine
Have been studied as possible treatments for diabetic and HIV-associated peripheral
neuropathies, with encouraging initial data.
5. Alpha-lipoic Acid
An antioxidant and may also prevent damage and inflammation of the peripheral nerve in
patients with diabetes.
6. Gabapentin
Used in treating neuropathic pain.
7. Carbamazepine
Work best for the prickling and tingling sensation, and also to some degree for the
burning discomfort.
8. Opiods (Oral Morphine, Methadone)
For patients who experience extremely severe pain.
SURGICAL MANAGEMENTS
1.

2.

Direct muscular neurotization


a.

Insert proximal nerve stump into affected muscle belly.

b.

Results in less than normal function but is indicated in certain cases.

Epineural Repair
a.

Primary repair of the epineurium in a tension free fashion.

b.

First resect proximal neuroma and distal glioma.

c.

It is critical to properly align nerve ends during repair to maximize potential of recovery.

3.

Fascicular Repair
Indications:
a. Median nerve in distal third of forearm
b. Ulnar nerve in distal third of forearm
c. Sciatic nerve in thigh
Technique:
Similar to epineural repair, but in addition repair the perineural sheaths
(individual fascicles are approximated under a microscope).
Outcomes:
No improved results have been demonstrated over epineural repair.

4.

Nerve Grafting
a.

Autologous Graft

Remains the gold standard of repair for segmental defects > 5cm is autologous
nerve grafting.

b. Allograft

The only synthetic graft which shows equal results to autologous nerve grafting
is a collagen conduit.

Collagen conduits allow for nutrient exchange and accessibility of neurotrophic


factors to the axonal growth zone during regeneration.

Rehabilitation
Intervention for Peripheral
Nerve Injury STEPHEN J. CARP, PT, PHD, GCSPG 177-179
Principle 1: Control Inflammation and the Downstream Components: Pain,
Scarring, Edema, Angiogenesis
High repetitionlow force and low repetitionhigh force injuries to soft tissue result in
an immediate migration of macrophages and monocytes to the site of injury. These
cells express proinflammatory cytokines that activate the inflammatory cascade.
Pain, edema (secondary to increased vascular permeability), angiogenesis, scarring,
and other healing activities develop at the injured site. Eventually,
antiinflammatory cytokines are expressed that turn off the inflammatory cascade.
If pathological activity and irritation continue at the injured site and the
inflammatory cascade is left unchecked, chronic pain and disability may result. The
rehabilitation therapist has many modalities available that control the downstream
effects of the proinflammatory cytokines. These are easily remembered with the

mnemonic PRICEMEM: protection, rest, ice, compression, elevation, manual therapy,


early motion, and medications.
Protection:
Protection is the removal of the off ending stimulus. If the off ending stimulus
is repetitive strain from keyboard typing, this is removed. If the off ending stimulus
is throwing a baseball, this is removed.
Rest:
Rest is the absence of an off ending stimulus and not the absence of
movement. Prolonged immobilization may have a deleterious impact on bone,
ligament, nerve, and muscle. Rest is the prescription of selective motions that will
not exacerbate the impairment but allow for normal, or as close to normal as
possible, functioning. Rest may be defi ned as bracing an injured area; wrapping to
control edema; nonweight-bearing to protect an injured bone; avoidance of lifting
to prevent back pain exacerbation; and avoidance of particular motions, such as
overhead shoulder elevation, in persons with venous thoracic outlet syndrome.
Ice:
Cold thermal therapies are an important adjunct to controlling the acute
inflammatory process and inflammation developed during the therapeutic
rehabilitation process.
Compression:
Compression, via wrapping, massage, positioning, or a pneumatic device,
helps prevent and alleviate edema associated with increased capillary permeability.
Elevation:
Used with ice and compression, elevation assists with decreasing edema
associated with inflammation. For elevation to be most effective, consider the heart
as the fulcrum for the fl ow of accumulated fluid. For elevation to be most successful
as a modality to decrease edema, the edematous part should be elevated above the
heart.
Manual therapy:
Manual therapy has many positive impacts on inflammation. Stimulation of
the large-fiber afferents assists with pain control. The mechanical effect of joint
movement assists with regaining joint motion. Prescribed forces and force vectors
assist with remodeling of connective tissue. Nerve glides and slides are an
important modality in assisting with preventing intraneural and extraneural scarring
commonly seen with inflamed peripheral nerves.

Early motion:
Early motion is helpful with reducing the muscle atrophy associated with rest,
assists with maintaining joint function, and assists with preventing ligamentous
creeping.
Medications:
Although not within the realm of physical therapy practices in most locations,
the judicious use of steroid and nonsteroidal medications assists with controlling
and limiting the inflammatory cascade.
Principle 2: Increase Flexibility
With the scarring that is a consequence of the inflammatory cascade, loss of
flexibilityarticular, single muscle, two joint muscle, and nerveis an expected
complication of injury. Posture and strength are dependent on proper joint
mechanics and range of motion. With a primary peripheral nerve injury, nerve glides
and slides within the symptom-free range are of tantamount importance in the
rehabilitation plan. Care must be taken when performing articular or muscle
stretching to avoid tension to injured neural tissue.
Principle 3: Correct Posture
With injury, the adaptive shortening and lengthening of tissues coupled with
protective and painful positioning leads to learning of abnormal, and, if untreated,
obligatory, posturing. Th e restoration of proper posture in standing, sitting, and
lying down assists with alleviating abnormal torque and joint positioning on the axial
and appendicular systems. Retraining correct posture can often be aided by
popular therapeutic techniques such as Alexander technique, yoga, Feldenkris,
Pilates, and Tai Chi Chuan.
Principle 4: Improve Movement Quality
Byl and Coq et al. showed that peripheral injury may result in alteration of the
central maintenance components of motor control leading to a loss of coordination
and function. As part of a coordinated plan of intervention, movement quality
cannot be ignored. Classic principles of motor acquisition, training, and learning
should be employed when there is identified loss of motor control.
Principle 5: Analyze and Integrate the Entire Kinetic Chain
The movement at one joint often depends on the quality of motion and the afferent
feedback of the large myelinated afferent sensory fibers from the distal and
proximal joints. A comprehensive rehabilitation plan encompassing all links along
the kinetic chain improves outcomes. Emerging research indicates improper

sequencing and activation of motor responses along the kinetic chain to


perturbation may be disease specific.
Principle 6: Incorporate Neuromuscular Rehabilitation
Neuromuscular rehabilitation is the method of training the enhancement of
subconscious motor responses to normal and aberrant perturbations by
simultaneously stimulating afferent signals and central mechanisms responsible for
dynamic and static motor control. The goal of this therapy is to improve the ability
of the central nervous system to sequence, control the amplitude of fi ring, and use
proper agonist/antagonist control of the muscle response to balance loss and
postural changes.
Principle 7: Improve Optimal Function
Short-term and long-term rehabilitation goals must be functional, objective, and
measurable. To meet this end, clinical interventions must be functionally directed.
This emphasis on function is an enhancement of past goals and plans that were
written solely to improve metrics such as manual muscle test grade or a degree
measurement of articular range of motion. All interventions should include a
therapeutic functional progression along with an exercise progression.
Principle 8: Maintain or Improve Overall Fitness and Health
Whenever possible, the treating therapist should address, along with the functional
limitation, the downstream impact of risk factors such as inactivity, improper
nutrition, tobacco usage, obesity, and an increased fall risk. As a result of the
paradigm shift from the Nagy model to the ICF, standards changes from Th e Joint
Commission, and amendments to state practice acts, the scope of rehabilitation
therapy services has expanded to include addressing risk factors and practices that
may affect health.
Principle 9: Provide Patient Education: Home Program, Risk Factor
Modification, Knowledge of Diagnosis, Pathology
Patient-therapist collaboration is the cornerstone of the therapeutic relationship.
The therapist and patient work together through the diagnostic journey, the
development of mutually agreed-on goals, the spectrum of the treatment plan, and
the schedule for reassessment. As part of the intervention, the therapist and patient
constantly discuss the path from impairment to health and from disability to
functional independence. The therapist helps mold the patient into an educated
consumer of health care, and the patient assists with educating the therapist about
the patients perceptions of illness and disability. The patient is taught to selfmanage his or her condition and how to prevent reoccurrences. The home program,
an extension of the clinical relationship, consists of the exercise prescription,

treatment goals and time frames, risk factor modification, and precautions. A
trusting therapeutic relationship promotes program adherence.
Principle 10: Incorporate Patient Self-Management
Many of the patients therapists treat have chronic or relapsing conditions. As part
of the therapeutic intervention, illness self-management skills are taught to the
patient. Self-management skills include disease specific knowledge of medication,
prevention, acute response to exacerbation, healthy lifestyle choices, and
intervention.
Principle 11: Ensure a Safe Return to a Maximum Level of Independent
Function
A focus of patient teaching is safety. The Joint Commission has taken the lead via
the National Patient Safety Goals encouraging the development of safety as a goal
for every patient in the United States. From hand washing to fall prevention to
documentation standards mandating the identification of at-risk suicidal patients,
the National Patient Safety Goals encourage therapists to promote a risk-free
assessment and intervention environment.
Principle 12: Coordination of Care
This is a general principle for all persons providing health care. All care, regardless
of the provider, must be communicated to the health care stakeholders of the
patient. These stakeholders vary by patient and episode of care. In most cases, the
primary care physician, as the gatekeeper of the patients care, should be informed
of all therapeutic interventions. In other instances, therapists may need to
communicate cogent fi ndings to nurses, specialists, social workers, case managers,
insurance companies, and other rehabilitation professionalsall within the scope of
patient privacy legislation.

The Role of Physical Agents in


Peripheral Nerve Injury
JAMES W. BELLEW, PT, EDD, AND EDWARD MAHONEY, PT, DPT, CWS

Physical Agents for Peripheral Nerve Injury

Electrical Stimulation
ES following PNI has long been considered to
promote nerve regeneration, decrease pain
associated with injury, and maintain denervated
skeletal muscle.
Regeneration of Nerve
low-frequency alternating current (AC) after
crush injury was reported to accelerate the
return of reflex foot withdrawal and contractile
force in reinnervated muscles.
ES has been associated with several fi ndings
indicative of nerve regeneration.
Modulation of Pain
Transcutaneous electrical nerve stimulation
(TENS) has been used in the management of
pain associated with peripheral neuropathy.
Prior studies of TENS on neuropathic pain are largely from populations with diabetic
peripheral neuropathy, with TENS reported to reduce pain in 50% to 75% of
patients.
Preservation of Denervated Muscle
Use of ES for increasing strength, volitional recruitment, re-education, and function
in normally innervated but weak skeletal muscle is well known and supported.
Ultrasound
Use of therapeutic US for PNI has been studied for two distinct eff ects: (1) reduction
of pain and improved function and (2) facilitation of nerve regeneration. Therapeutic
US is classifi ed as thermal or nonthermal. Th e physiological eff ects realized from
thermal or continuous US generally refl ect the thermal eff ects observed with other
thermal agents with two exceptions: (1) Th e depth of eff ect is greater with US than
other thermal agents except short wave diathermy, and (2) the eff ect is more
pronounced in tissues with higher collagen content because these tissues retain
more sound energy.
Laser
use of LLLT for tissue healing, based on the purported ability of LLLT to augment or
enhance the bodys natural processes of healing.

use of laser for PNI stems from observed responses in the metabolic activity of
tissues and cells, such as fi broblasts, endothelial cells, osteoclasts, and neurons,
exposed to laser energy in primarily animal models and in a few human studies.
Acute LLLT has shown decreased production of bradykinin, reduced levels of
prostaglandin E 2 , increased secretion of endogenous opioids, increased production
of serotonin and nitric oxide, and increased axonal sprouting and nerve cell
regeneration.
Laser energy, or photoenergy, emits packets of light energy, called photons,
that are absorbed by receptor chromophores within the mitochondria and cell
membrane of tissues irradiated with laser energy. Absorption of photoenergy
increases cellular metabolism and increases the oxidative production of adenosine
triphosphate (ATP)a process known as photobiomodulation. In the presence of
injury, ATP is used to synthesize DNA, RNA, proteins, and enzymes; facilitate cellular
mitosis; and increase synthesis of growth factors to repair compromised tissue.
LLLT for repair of incomplete PNI is proposed to (1) increase the rate of axonal
growth and myelination, (2) prevent or limit degeneration in the corresponding
motor neurons of the spinal cord, (3) off er immediate protective effects to increase
functional activity of the injured nerve, (4) maintain functional activity of injured
nerve over time, and (5) minimize scar formation.

Pulsed Electromagnetic Field


Pulsed electromagnetic field (PEMF) energy produced by diathermy devices passes
through bodily tissues with minimal refl ection at tissue interfaces or at bone,
whereby minimal traces of energy accumulate at these interfaces as it occurs with
US. Gradually, absorption of energy by deeper tissues causes increased cellular
activity. Biological eff ects of PEMF include increased microvascular perfusion,
changes in voltage-dependent ion-ligand binding, and alteration of cell membrane
function and cellular activity. 104109 PEMF therapy for 40 to 45 minutes and set to
600 pps has been shown to increase local blood fl ow signifi cantly in healthy
subjects without pathology and in patients with diabetic ulceration. Increased cell
mitosis and growth, expression of growth factors in fi broblasts and nerve cells,
activity of macrophages, and phosphorylation and protein synthesis have been
observed after PEMF therapy
Monochromatic Infrared Energy
Th e most widely used physical agent for the treatment of peripheral neuropathy at
the present time is infrared light. Monochromatic infrared energy (MIRE) is delivered
at a single wavelength (890 nm long, at a rate of 292 times per second) from a pad
containing 60 superluminous GaAlAs diodes by a therapeutic device manufactured
by Anodyne Th erapy, LLC (Tampa, Florida).

Use of MIRE for the restoration of impaired sensation in patients with peripheral
neuropathy

Rehabilitation Management of Peripheral Neuropathy- delisa


Problem
Functional Consequence
Rehabilitation
Intervention
Weakness Proximal
Rising from chair,
PREs
Distal
jumping stairs
Foot drop/slap, poor
AFO, UCBL, splint,
toe clearance
functional orthosis,
Ankle sprains, loss of
tool or equipment
dexterity and fine
modification
motor control
Generalized
weakness
and deconditioning
Distal sensory loss

Impaired
control
Autonomic
dysfunction

motor

Loss of endurance

Loss of
proprioception,
imbalance, impaired
fine motor control

As above

Abnormal sweating,
cold intolerance

Decreased activity

GCEs Education in
energy
conservation

Fine motor
exercises
Assistive device
(e.g., cane)

Pain

Educate regarding
gloves, clothing,
antiperspirant
Analgesics, TNS,
surgery

Deformity

Foot orthotics,
bracing, surgery

Recovery of Nerve Injuries


Management Guidelines Recovery from Peripheral Nerve Injury- kisner
Acute phase: Immediately after injury or surgery

Immobilization: time dictated by surgeon


Movement: amount and intensity dictated by type of injury and
surgical repair
Splinting or bracing: may be necessary to prevent deformities
Patient education: protection of the part

Recovery phase: signs of reinnervation (muscle contraction, increase


sensitivity
Motor retraining: muscle hold in the shortened position
Desensitization: multiple textures for sensory stimulation; vibration
Discriminative sensory reeducation: identification of objects with,
then without, visual cues
Chronic phase: reinnervation potential peaked with minimal or no signs of
neurological recovery
Compensatory function: compensatory function is minimized during
recovery phase but is emphasized when full neurological recovery
does not occur
Preventive care: emphasis on lifelong care to involved region
Patient Instruction for Preventive Care After Nerve Injury- kisner
While the nerve is regenerating, or if nerve recovery is incomplete
Inspect skin regularly; provide prompt treatment of wounds or
blisters
Compensate for dryness with massage creams or oils
In the upper extremity
Avoid handling hot, cold, sharp, or abrasive objects
Avoid sustained grasps; change use of tools frequently
Redistribute hand pressure by building up the size of the handles
Wear protective gloves
In the lower extremity
Wear protective shoes that fit properly
Inspect feet regularly for pressure points (reddened area) and
modify shoes or provide protection if they occur
Do not walk barefoot, especially in the dark or on rough surfaces
Shift weight frequently when standing for long periods

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