EEG and Epilepsy

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 EEG and Epilepsy
An Illustrative EEG Manual for Beginners, Pediatricians,
Physicians, Neurology Residents and Technicians

Series Editors
Anupam Sachdeva
Krishan Chugh
Ajay Gambhir
Satinder Aneja
AP Dubey
Shyam Kukreja

Guest Editors
Praveen Kumar
RK Sabharwal
Suvasini Sharma

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EEG and Epilepsy

First Edition: 2015

ISBN 978-93-5152-750-3

Printed at

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 Contributors

Praveen Kumar MD
Associate Consultant
Child Neurology and Epilepsy
Institute of Child Health
Sir Ganga Ram Hospital
New Delhi

RK Sabharwal MD DM
Senior Consultant and Chief
Child Neurology and Epilepsy
Institute of Child Health
Sir Ganga Ram Hospital
New Delhi

Suvasini Sharma MD DM
Assistant Professor
Pediatric Neurology
Kalawati Saran Children’s Hospital
Lady Hardinge Medical College
New Delhi

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 Preface

This EEG and Epilepsy manual has been prepared with an aim to give a basic
insight into pediatric EEGs to beginners. Technical aspects of EEG are covered
briefly. Normal and abnormal waveforms with common artifacts are shown.
Finally common epilepsies in children including non-convulsive seizures with
illustrative EEGs are discussed. Neonatal EEG in itself is a vast subject, normal
tracings in full-term neonate is dealt succinctly.
We are thankful to Dr Madhav Suri, Dr Derrick Chan, Dr Deepak Sachan,
Dr Suvasini Sharma for providing us with their EEG tracings. We are indeed
grateful to our children patients for giving us a valuable opportunity to learn
and our colleagues at Institute of Child Health, Sir Ganga Ram Hospital for
their valuable support. We would like to express our sincere appreciation to
Dr Anupam Sachdeva for his constant encouragement and stimulus to meet
the deadline for this publication. This manual would not have been possible
without Dr R K Sabharwal's constant guidance and persistent help including
EEG tracings. He repeatedly reviewed the chapters and incorporated valuable
changes which only he with his vast neurology experience and immense
knowledge could do.

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 Contents

1. Technique 1
2. Normal Waveforms 7
3. Abnormal Waveforms 15
4. Artifacts 18
5. EEG in Focal and Generalized Epilepsy 20
6. EEGs in Different Epileptic Syndromes of Childhood 27
7. EEG in Non-convulsive Electrographic Seizure,
Critically Ill Children, Coma and Brain Death 32
8. Neonatal EEG 38
9. Benign Patterns of Uncertain Clinical Significance 43

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 Introduction

EEG is an under-utilised and wrongly used investigation in clinical neurology.

In the management of epilepsy, often in our country MRI brain is done first and
EEG later. For the EEG to have an optimum diagnostic accuracy, it is important
that EEG machine be a good standard quality machine. Technician should be
a highly trained one who is aware of artifacts, adjusting sensitivity etc., and
should record them on the graph. Finally, the neurologist interpreting the EEG
should be an experienced one.
This introductory manual on EEG for the residents, pediatricians,
physicians with interest in neurology and EEG, has been brought out at a very
short notice. It has been a dedicated effort of my colleague Dr Praveen Kumar,
who has exceeded himself in giving birth to this simple, lucid and explanatory
handbook for the uninitiated. Majority of the tracings are from the Division
of Pediatric Neurology and Epilepsy, Institute of Child Health, Sir Ganga Ram
Hospital, New Delhi.
The material at hand was enormous, the desire to expand and make it
detailed, informative with the most recent classifications and theories was
very tempting. But that would have been more appropriate for a neurologist
audience. For his patience, zeal, enthusiasm and equanimity, Dr Praveen
Kumar deserves the title of "The Little Buddha".

RK Sabharwal
MBBS MD DM (Neurology)

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 Chapter

1 Technique

For the recording of EEG we need

1. Electrodes—To pick up the brain electrical wave activity and their attached
wire to connect with the EEG machines.
2. Amplifiers—To amplify these micro volts amplitude waves.
3. Filters—To filter out unwanted (artifacts) waves.
4. Writing units—To record these waves on paper.
Duration of EEG recording: EEG should be recorded for minimum of 30
minutes in normal routine hours and 60 minute for neonatal cases.
Electrodes usually consist of flat disc or cup (often gold or silver) connected
to silver wires. In modern digital EEG machine amplifiers, filters and writing
unit are within the computerised system.

Position of Electrodes
The 10–20 International System of Electrode Placement, where each electrode
is 10–20% away from a neighboring electrode, is mostly used.
By convention electrodes placed on the left side of cerebral hemisphere
are given odd numbers (e.g., Fp1, T3) while right sided electrodes have even
numbers (e.g., Fp2, T4). The name includes the first letter of the general area
of skull where electrode is placed and reveals lobe of the brain being recorded.
Fp1, 2—prefrontal
F3, 4—frontal
C3, 4—central
P3, 4—parietal
O1, 2—occipital
F7, 8—anterior temporal (records activity from anterior temporal region
but placed on frontal bone)
T3, 4—mid-temporal
T5, 6—posterior temporal
A1, 2—ear
Fz—front vertex
Cz—central vertex
Pz—parietal vertex
(z= zero)

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 2 EEG and Epilepsy

Measurement for International

10–20 System of Electrode Placement
Four skull landmarks are used in the 10-20 system. The nasion—a point just
above nasal bridge, inion—prominent part of occiput and right and left pre-
auricular points, indentations just above tragus (Figs 1.1A to D).

A B

C D

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 Technique 3

F
Neonatal EEG
Figs 1.1A to F

Neonatal Electrode Placement

11 channels due to small head size (Fig. 1.1F)
Frontal and parietal channels are usually omitted.

Montages
EEG records brain electrical potential by recording the difference between the
activity picked up by two electrodes. Montage refers to the different ways to
connect electrodes (Fig. 1.1E).
Commonly two types of montages are used:
1. Referential (monopolar)
2. Bipolar
Referential montage: Involves recording the difference between an active
electrode on the scalp and an inactive electrode placed over ear or nose or
chin (called reference electrodes).
Bipolar montage: Involves recording the difference between two active
scalp electrodes. Each channel of the EEG machine is connected to two
different electrodes and the difference in activity picked up by each of these
two electrodes is recorded on that one channel.
Montages should be arranged in an orderly sequence. Like for referential
montage, anteriorly placed electrodes are placed on the first channel and the
posteriorly placed electrodes on the later channel. Bipolar montages have
electrodes in chains usually from front to back (anteroposterior) or side to
side (transverse), from one electrode to its neighbour and then onto the next
one, etc.

Paper Speed
The paper speed generally adopted for EEG recording is 30 mm/sec (Figs 1.2
and 1.3).

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 4 EEG and Epilepsy

Fig. 1.2: EEG at paper speed of 30 mm/ sec

Fig. 1.3: Same EEG at paper speed of 60 mm/ sec reveals left hemispheric origin of
discharges

Slow paper speed of 15 mm/sec is used for monitoring repetitive/periodic

discharges as in SSPE.
• Periods of attenuation/ rhythmicity.
Faster paper speed of 60 mm/sec is used for study of asymmetrical onset of
seemingly synchronous activity.

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 Technique 5

Filters
A circuit which permits only the necessary signal to pass by varying the
frequency response of an electric current is called filter. It excludes very slow
and very fast activity and select the spectrum of frequencies which has the
greatest clinical significance. Filters should be used in such a way that they do
not eliminate spike/ sharp wave activity. It should not be used to clean up the
artifacts and produce a pretty record. Usually, a low frequency is set at 1 Hz
and high frequency filter at 70 Hz (so it does not allow waves below 1 Hz and
above 70 Hz to pass through it).

Sensitivity
Generally, sensitivity in pediatric EEG is kept at 7 microvolt/mm (7–10 uV/
mm). At this sensitivity, a voltage of 7 uV causes a pen deflection of 1 mm.The
sensitivity is adjusted to see appropriate waveforms (Figs 1.4 to 1.6). If waveforms
are of high amplitude, sensitivity should be kept at 10 uV/mm. Higher numeric
value of sensitivity mean lower sensitivity and vice versa.

Activation Procedures
Activation procedures are used to enhance epileptiform activity in recording
and thus improve diagnostic yield.
Hyperventilation—For 3–5 minutes are very important for provoking
epileptiform discharges in Idiopathic Generalized Epilepsy (IGE). It should not
be done in patients with significant cardiac and respiratory disease, suspected
cerebral aneurysm, raised intracranial pressure.

Fig. 1.4: Epileptic discharges at sensitivity of 7 uV/mm

Fig. 1.5: Epileptic discharges at sensitivity of 20 uV/ mm

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 6 EEG and Epilepsy

Fig. 1.6: Epileptic discharges at sensitivity of 15 uV/ mm

Photic stimulation—From 3 Hz to 24–30 Hz is used routinely to induce

photic sensitive discharges and for diagnosis of photosensitive epilepsy.
Sleep deprivation—Maximum sleep deprivation before EEG recording
is advised. It may be difficult in very young patients, but is very useful in
enhancing EEG abnormalities especially in focal seizures, rolandic epilepsy
and Juvenile Myoclonic Epilepsy. It also helps to induce sleep in children
without sedatives for sleep record in EEG. EEGs should have both sleep and
awake record. The diagnostic yields of sleep deprived EEG in patients with
normal awake EEG is enhanced to 40%.

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CHAPTER

2 Normal Waveforms

Electrical activity from the brain, waves, are named according to their
frequency in cycles per second (c/sec), also called Hertz (Hz.) (Figs 2.1 to 2.4).
Delta wave: frequency less than 4 Hz.
Theta wave: frequency is between 4–8 Hz.
Alpha wave: frequency is between 8–13 Hz.
Beta wave: frequency more than 13 Hz.
These different rhythms are found at different ages of the patient and also
under different states of sleep and wakefulness. The most prominent or obvious
frequency in record is called as “background rhythm”.
Background rhythm in awake:
in infants= 4–5 Hz
in children = 5–8 Hz
in adults = 8–10 Hz
Background rhythm in sleep: in light sleep = 5–6 Hz, in deep sleep = 2–3 Hz.
Beta waves are normally seen in three conditions:
1. In light sleep in the form of sleep spindles (discussed later)
2. Tense and anxious patients
3. Patients on certain drugs like benzodiazepines, barbiturates.

Fig. 2.1: Alpha wave in resting wakefulness

8 EEG and Epilepsy

Fig. 2.2: Beta wave in drowsy state

Fig. 2.3: Theta wave

Normal Sleep Rhythms

1. Vertex waves: are found in stage I of sleep. These are maximally seen
over central area (Fig. 2.5). They appear by 2 months of age and persists
throughout life.
 Normal Waveforms 9

2. Sleep spindles: are spindle like waves, 12–14 Hz in frequency, mostly

over central area (Fig. 2.6) They appear by 2 months of age, however, for
initial 12 months of age they may be asynchronous, thereafter it should be
synchronous.
3. K – complexes (Fig. 2.7): Typically, a high amplitude long- duration biphasic
waveform with overriding spindle. Its maximum voltage is in vertex and
frontal midline.

Fig. 2.4: Delta waves

Fig. 2.5: Vertex wave

10 EEG and Epilepsy

Fig. 2.6: Sleep spindles

Fig. 2.7: K-complexes

Physiological Waveforms that can be Mistaken for

Epileptiform Activities
Awake Drowsy Sleep
Mu Rhythm Hypnagogic Vertex transients of light sleep
Hypersynchrony
Lambda Waves Sleep spindles
Posterior Slow Waves of Youth (PSWY) K- complexes
Positive occipital sharp
transients of sleep (POSTs)
 Normal Waveforms 11

These are normal physiological activities found during EEG study in

wakefulness and in sleep. Proper identification of these physiological
waveforms are important to avoid misinterpretation. Sleep waveforms are
described earlier.

Mu Rhythm
Described by Henry Gastaut in 1952 as “Rhythme rolandique en arceau”. It
appears to be generated by “idling motor-sensory cortex in wakefulness”. It is
8–10 Hz rhythmic activity of arciform morphology at central or centro-parietal
area commonly seen in young adolescent females (Fig. 2.8).
It is present in relaxed motionless wakefulness with eyes open or closed
and attenuates with movement planning or execution or with somatosensory
stimuli (Fig. 2.8) (Blume et al, 2002).

Lambda Waves
First described by Yves Gastaut in 1951. These are probably visual evoked
potentials elicited by shifts of subject’s gaze. Waveforms are check—mark
or tick shaped and occur during eye opening and abolished by eye closure
especially in brightly illuminated rooms (Fig. 2.9). They may be surface positive
or negative and may occur symmetrically or asymmetrically over occipital
areas in both hemispheres. There is no prominent after following slow wave.

Posterior Slow Wave of Youth (PSWY)

It is slow activity over centro-occipital area superimposed over posterior
dominant rhythm. It is seen when awake with eyes closed and abolishes with

Fig. 2.8: Mu rhythm

12 EEG and Epilepsy

Fig. 2.9: Lambda waves

Fig. 2.10: PSWY

eye opening, drowsiness and sleep (Fig. 2.10). It may be activated by over
ventilation and stress. Maximally observed in children of 8-14 year age group
with a female preponderance.

Hypnagogic Hypersynchrony
These are paroxysmal bursts of high-amplitude sinusoidal waves of 3–5 Hz and
maximally seen over frontal- central area (Fig. 2.11). Sensitivity may need to
be altered to see true nature of these waveforms (Fig. 2.12). They are seen in
drowsiness and not seen during fully awake and sleep state. These are most
prominent in 1–5 year age group and are rarely seen after 15 year of age.
 Normal Waveforms 13

Fig. 2.11: Hypnagogic hypersynchrony

Fig. 2.12: Hypnagogic hypersynchrony

Positive Occipital Sharp Transients of Sleep

POSTs are 4–5 Hz surface positive sharp activity seen over occipital area in
light sleep or drowsiness especially during day time. POSTs are bilaterally
synchronous but may be asymmetrical (Figs 2.13 and 2.14).
14 EEG and Epilepsy

Fig. 2.13: POSTs showing surface positivity

Fig. 2.14: POSTs

 Chapter

3 Abnormal Waveforms

Epileptiform discharges stand out from surrounding activity. They tend to be

of high voltage, biphasic, asymmetrical with longer and larger second half and
can have an after going slow wave.
1. Spike wave—duration of less than 70 msec (Fig. 3.1).
2. Sharp wave—duration of 70–200 msec, so appear less sharp than spike
(Figs 3.2 and 3.3).

Fig. 3.1: Spike wave (note longer second phase and after coming slow wave)

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 16 EEG and Epilepsy

Fig. 3.2: Sharp wave discharges

Fig. 3.3: Sharp waves in hypnagogic hypersynchrony

3. Slow wave—in the range of delta and theta waveform and duration of >200
msec. It can be generalized slowing as seen in encephalopathy or focal
slowing suggestive of localised pathology or focal epilepsy (Fig. 3.4).
Spikes and sharp waves are mostly surface negative and generally have a
field of spread which includes more than one electrode.

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 Abnormal Waveforms 17

Fig. 3.4: Slow waves asymmetrically seen over left hemisphere

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 Chapter

4 Artifacts

EEG represents electrical activity of the brain, while artifacts are activity of
non-cerebral origin in the EEGs (Figs 4.1 and 4.2). Artifacts can arise from
diverse sources, e.g.:
1. EMG or muscle artifacts
2. Electrode artifacts
3. Ocular artifacts
4. Sweat artifacts
5. Cardiac artifacts.
Muscle artifacts are very common and usually arise from facial and scalp
muscles. EEG technician and interpreter need to be alert and aware of these
artifacts to avoid labeling it as an epileptiform activity.

Fig. 4.1: EMG artifacts at T3, ocular artifacts Fp1-Fp2

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 Artifacts 19

Fig. 4.2: Electrode pop artifact at T3

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 Chapter
EEG in Focal and
5 Generalized Epilepsy

Clinical history is of utmost importance and EEG is useful in differentiating

focal and generalized epilepsy.
Focal epilepsy may show localized epileptiform discharges in EEG (Fig.
5.1). At times focal seizures may have only focal slowing on EEG as postictal
phenomenon.
Generalized epilepsies have bilateral, synchronous, generalized
electrographic events without any detectable focal onset (Fig. 5.2).

Focal Epilepsy
Focal epilepsy can be Idiopathic/ Genetic or Symptomatic due to underlying
CNS pathology (Figs 5.3 to 5.7).

Idiopathic/Genetic
a. Rolandic Epilepsy (Benign Epilepsy of Childhood with Centrotemporal
Spikes—BECTS)

Fig. 5.1: Focal discharges on left hemisphere

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 EEG in Focal and Generalized Epilepsy 21

Fig. 5.2: Generalized discharges

Fig. 5.3: Right parietotemporal slowing in a child with NCC over right parietal region

Fig. 5.4: Right temporal discharges

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 22 EEG and Epilepsy

It occurs in neurologically normal

children between 4-12 years of age
and is characterized by nocturnal
focal and generalized seizures.
EEG typically has centrotemporal
spikes with frontal positivity which
are activated in sleep. Few reports
are available on the concomitance
of C AE (childhood absence
epilepsy) and BECTS in the same
patients or the later occurrence
of generalized epilepsy, Juvenile
myoclonic epilepsy, continuous
spike-and-waves during slow
sleep (CSWSS) in patients with a
history of partial epilepsy. We also
have few patients with BECTS,
later developing CAE (Figs 5.5
Fig. 5.5: BECTS
and 5.6). Recent observations in
animal models suggest that BECTS and CAE could be pathophysiologically
related and that genetic links could play a large role.

Fig. 5.6: BECTS to generalized discharges

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 EEG in Focal and Generalized Epilepsy 23

b. Benign Focal Epilepsy of Childhood with Occipital Spikes (Panayiotopoulos

Syndrome, Autonomic Epilepsy)
Commonly seen in children 1–12 years of age as infrequent nocturnal
seizures with predominant autonomic and behavioral symptoms including
nausea and vomiting. EEG reveals high amplitude sharp and slow wave
over occipital region. Prognosis is excellent.
Idiopathic Occipital Epilepsy of Gastaut: The typical clinical features
are visual seizures that typically consist of brief elementary visual
hallucinations, which are mainly multicolored and circular. Ictal blindness
and deviation of the eyes are also common symptoms. EEG shows occipital
spikes and often occipital paroxysms demonstrating fixation-off sensitivity.

Symptomatic Focal Epilepsy

Symptomatic focal epilepsy could be due to:
a. Congenital CNS malformation—Like focal cortical dysplasias presenting
with recurrent focal seizures and correlating MRI brain/ PET scan brain
abnormality.
b. Infections—Herpes encephalitis, cerebral abscess, neurocysticercosis (Fig.
5.3).
c. Vascular—Stroke, arteriovenous malformations.
d. Tumor/structural abnormality—Intracranial tumors can have focal slowing,
focal sharp slow wave discharges (Fig. 5.4).

Generalized Epilepsy
Generalized epilepsy is mostly genetic/idiopathic. It is also termed as primary
generalized epilepsy.
Secondary generalized epilepsy is when brain has some structural or
metabolic problem and child may have developmental delay, different seizure
types and an EEG suggestive of secondary generalized epilepsy.
At times generalized epilepsy may be secondarily generalized with focal
onset as partial seizure and a very rapid spread.
a. Childhood absence epilepsy (CAE): It typically occurs in neurologically
normal children of 4–10 years of age. Clinically frequent episodes of brief
loss of awareness/ day dreaming is described. The ictal and interictal EEG
shows classic 3Hz spike wave discharges with normal background (Fig.
5.8). Hyperventilation activates these discharges and may produce clinical
seizures.
b. Juvenile myoclonic epilepsy (JME): It is another common Idiopathic
Generalized Epilepsy with later age of onset than Childhood Absence
Epilepsy. Different seizure types as generalized tonic–clonic, absence
seizure and myoclonic seizures are present. Sleep deprivation is a common
trigger. Interictal EEG reveals generalized 4-5 Hz polyspikes and slow wave
complexes. Photosensitivity may be seen.

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 24 EEG and Epilepsy

Fig. 5.7: Left sided repetitive discharges

Fig. 5.8: 3 Hz spike and wave discharges

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 EEG in Focal and Generalized Epilepsy 25

c. Progressive myoclonic epilepsy (PME): It is rare with invariably poor

prognosis. Clinically progressive neurological deterioration is seen with
myoclonic seizures, generalized tonic-clonic seizures. EEG may show
fast irregular spike or poly spike and slow wave discharges with slow
background for age and photosensitivity. Detail neurological and genetic
evaluation is required.

Periodic Lateralized Epileptiform Discharges (PLEDs)

PLEDs are sharp waves or spikes which have a lateralized distribution and
appear in periodic or quasi periodic fashion (Fig. 5.9). They are seen in focal
destructive lesion or focal epileptogenic lesions like stroke, herpes simplex
encephalitis, glioblastoma multiforme, etc.
PLEDs may be generated independently over both hemisphere, bilateral
PLEDs (BIPLEDs), as seen in epileptic seizure, CNS infections or stroke.
Patients with PLEDs or BIPLEDs usually have poor outcome.

Subacute Sclerosing Panencephalitis (SSPE)

Clinically presents as progressive neurological deterioration with myoclonic
jerks in an apparently asymptomatic child with history of measles infection
or measles immunization. Characteristic EEG findings include periodic
discharges of polyphasic sharp and slow wave complexes of 0.5–2 sec duration
and recurring at 4–15 sec interval (Fig. 5.10). It is important to ask for slow paper
speed (of 15 mm/sec) to better delineate periodic complexes.
It is important to emphasize that absence of focal or generalized discharges
does not exclude epilepsy as epilepsy is still a clinical diagnosis.

Fig. 5.9: Right hemispheric PLEDs in a child with herpes encephalitis

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 26 EEG and Epilepsy

Fig. 5.10: Periodic discharges of SSPE at paper speed of 15 mm/sec

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 Chapter EEGs in Different
6 Epileptic Syndromes of
Childhood

In this chapter the EEG features of some common epilepsy syndromes of

infants and young children are discussed. Several epilepsy syndromes have
been described in children based on their electroclinical features (age of
onset, seizure type and EEG pattern). These include: Ohtahara syndrome, early
myoclonic encephalopathy, epilepsy of infancy with migrating focal seizures,
West syndrome, Dravet syndrome, Lennox-Gastaut syndrome and epilepsy
with myoclonic atonic seizures (Doose syndrome).
Other common patterns include CAE and JME.
1. Neonatal epileptic encephalopathy with suppression burst pattern: Typically
seen in Ohtahara syndrome and Early Myoclonic Encephalopathy (EME).
EEG shows paroxysmal burst of activity followed by suppression of the
background (Fig. 6.2). Structural brain malformation and inborn error of
metabolism should be excluded.
2. West syndrome: It is triad of infantile spasm, hypsarrhythmia on EEG and
developmental delay. Spasms usually occur in clusters comprising of tonic
contractions of limb and axial muscles, and may be flexor, extensor or
mixed. Hypsarrhythmia is an interictal finding and comprises high voltage
chaotic slow waves which are asynchronous and random (Fig. 6.1). There

Fig. 6.1: Hypsarrhythmia

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 28 EEG and Epilepsy

are intermixed spike and sharp wave discharges. More commonly variants
of hypsarrhythmia as modified hypsarrhythmia is seen which includes.
1. Increased interhemispheric synchronization.
2. Consistent voltage asymmetries.
• Consistent focus of abnormal discharge.
• Episodes of generalized/ regional or lateralized voltage attenuation.
• Primarily high voltage bilaterally asynchronous slow wave activity
with relatively little epileptiform abnormalities.
The most common pattern of the ictal EEG is a high voltage frontally dominant
slow wave followed by diffuse voltage attenuation (electrodecremental
event) (Fig. 6.2).
3. Lennox-Gastaut syndrome (Fig. 6.3): It comprises multiple seizure types
including tonic, atypical absence and atonic/myoclonic seizures. EEG
typically consists of 1–2.5 Hz slow spike-wave anterior dominant complexes
and can have 10–20 Hz faster activity in sleep. It can follow other epilepsy
syndrome like West syndrome and Doose syndrome.
4. Landau–Kleffner syndrome (Fig. 6.4): It is clinically characterized by
auditory agnosia and loss of speech in a child with appropriate previous
developmental history.
Sleep EEG is characterized by high frequency, sometimes continuous spikes
especially over posterior temporal region.
5. Continuous spike wave in slow sleep (CSWSS) (Fig. 6.5): Awake EEG has
infrequent focal discharges, while sleep EEG has continuous generalized
spike wave discharges. Relationship with Carbamazepine has been
reported.
Landau-Kleffner syndrome (LKS) and the syndrome of continuous
spikes-and-waves during slow sleep (CSWSS) are closely related epilepsy
syndromes. Both are characterized by seizures that are not very frequent

Fig. 6.2: Burst suppression

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 EEGs in Different Epileptic Syndromes of Childhood 29

Fig. 6.3: LGS

or difficult to control, but severe paroxysmal EEG abnormality, and

consequent language (LKS) and cognitive (CSWS) deterioration.
6. EEG in Angelman syndrome: The pattern most frequently observed is
prolonged runs of high amplitude rhythmic 2–3 Hz activity predominantly
over frontal region with superimposed interictal spikes (Fig. 6.6).
7. Rett syndrome: X-linked disease primarily affects females. Hallmark of
disease is period of normal development followed by regression and typical
hand stereotypy. EEG in sleep has slow spike-wave pattern as in lennox-
Gastaut syndrome (LGS) (Fig. 6.7).

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 30 EEG and Epilepsy

Fig. 6.4: LKS - runs of posterior temporal spike in sleep

Fig. 6.5: CSWSWS

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 EEGs in Different Epileptic Syndromes of Childhood 31

Fig. 6.6: Angelman syndrome—frontal rhythmic activity

Fig. 6.7: Rett syndrome—slow spike wave

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 Chapter
EEG in Non-convulsive
7 Electrographic Seizure,
Critically ill Children,
Coma and Brain Death

NCSE (non-convulsive status epilepticus) is defined as a change in behavior

and/or mental processes from baseline associated with continuous
epileptiform discharges in the electoencephalography (EEG).
Overall picture of the EEG discharge should be taken into account,
including its evolution in time and space. A clear incremental evolution of
regional or generalized rhythmic discharges and decremental features with
flat periods associated with clinical seizure activity strongly indicate NCSE.
A child who has not regained consciousness after an hour of generalized
seizure must be evaluated for NCSE.
Electrographic seizure may begin with focal ictal discharges and progress
to generalized spike wave or sharp and slow wave pattern (Figs 7.1 and 7.2).
Electrographic seizures have been reported in 10–40% of critically ill
children who undergo continuous electroencephalography (CEEG) monitoring
in pediatric intensive care units (ICUs) or emergency departments.

Fig. 7.1: Start of seizure—right hemisphere

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 EEG in Non-convulsive Electrographic Seizure 33

Fig. 7.2: Spread of seizure

Electrographic seizures may be subdivided into electroclinical seizures

(also referred to as convulsive seizures or clinically evident seizures) or non-
convulsive seizures (also referred to as EEG-only seizures).
The EEG may indicate that a diffuse central nervous system (CNS) disorder,
a focal process, or ongoing seizure activity, often without motor manifestations,
such as non-convulsive status epilepticus (NCSE), is responsible for the clinical
presentation. EEG findings in encephalopathies include diffuse slowing
of background rhythms (the most common finding), frontal intermittent
rhythmic delta activity (FIRDA), and triphasic waves (TWs), a pattern present
in a variety of metabolic encephalopathy, most commonly hepatic failure.
Other patterns include an alpha–theta coma pattern, a spindle coma pattern,
and periodic patterns, such as periodic epileptiform discharges (PEDs) that
can be lateralized or generalized, and a burst-suppression pattern. Findings,
such as focal polymorphic delta activity or localized attenuation of faster
frequencies suggest a focal lesion. EEG can be helpful in making a diagnosis,
contribute to an established diagnosis, as well as rule out a diagnosis. It can aid
in prognostication, particularly if the etiology is known, and in the treatment
of epileptic disorders (Table 7.1, Brenner, Epilepsia 2009).
The possibility of status epilepticus (SE), particularly non-convulsive status
epilepticus (NCSE), is the primary indication for an emergent or ‘‘stat’’ EEG.
These patients are often obtunded or comatose, and frequently there is no
clear etiology of coma or the mental state changes. Nonconvulsive seizures
may follow generalized convulsive seizures, and account for what is often
mistaken clinically for a prolonged “postictal state.” The EEG is the only reliable
means of detecting this phenomenon, and it is valuable diagnostically and
prognostically.

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 34 EEG and Epilepsy

Table 7.1: Etiologic factors and EEG pattern in generalized and lateralized
comatose NCSE
Etiology
Coma-GED Diffuse primary or secondary
brain distrubanes (anoxic,
toxic metabolic, infectious,
degenerative)
Space-occupying lesions
with brainstem compression
(direct or due to tentroiral
herniation)a
Coma-LED Focal brain lesions (in most
cases acutely acquired)
In rare cases diffuse
abnormalities (aminophyline
intoxication, some forms of
diabetic coma)
Known epilepsies?
Might also present as coma-LED
a
EEG pattern
Continuous generalized
spiking
Periodic spiking
Burst suppression pattern in
different variations
Other generalized periodic
abnormalities
Bilateral triphasic waves
Continuous focal spiking
PLEDs
Bi-PLEDs
Unilateral burst suppression
pattern
Unilateral triphasic waves

Abbreviation: Bi-PLED, bilateral periodic epileptiform discharges; GEDs, generalized epileptiform

discharges; LED, lateralized epileptiform discharges; PLED, periodic epileptiform discharges.

EEG is especially sensitive to the graded severity of brain dysfunction and

the direction of the process if serial tracings or continuous recordings are used.
Although rarely specific for the etiology of coma, the EEG may help determine
the class or general category of disease process (e.g. the differentiation of
seizures from metabolic or drug-induced coma). When the etiology of the
coma is known, the EEG can be very useful in determining the prognosis in
some conditions, especially when combined with the neurologic examination
(American Clinical Neurophysiology Society). It is valuable to assess EEG
reactivity after sensory stimulation in states of decreased consciousness. In
general, reactivity is a feature of lighter stages of coma. Reactivity may exist in a
variety of forms: an increase in amplitude, frequency, or even slowing (often as
bisynchronous rhythmic d-activity), or a decrease in amplitude of background
rhythms. In general, EEG responsiveness is associated with a greater chance
of recovery than the lack of reactivity. Hence reactivity should be tested in
all comatose patients unless unstable vitals or raised intracranial pressure
warrants its deferral. Passive eye opening is recommended in suspected alpha-
coma (no change in a) as well as a stimulus for reactivity.
The predictive value of EEG in comatose patients is greatly enhanced,
however, if serial or continuous EEGs are performed to monitor evolution,
reactivity, and variability and appearance of new findings.

EEG Frequency Patterns in Coma

Frequencies of background activity, such as alpha, beta, delta may predominate
in different encephalopathies, in coma, along with varying EEG background

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 EEG in Non-convulsive Electrographic Seizure 35

Fig. 7.3: Delta coma with superimposed faster activity in a child with encephalitis

reactivity to external noxious stimuli (Figs 7.3 and 7.4) (R Sutter, PW Kaplan
Epileptologie 2012;29).
• Beta coma—Generalized 12–16 Hz background activity is maximally seen
over the frontal regions in patients with beta coma. Reactivity to external
stimuli may vary. Common causes include drug overdosing, withdrawal
from sedating drugs, brain stem lesion.
• Alpha coma—Alpha activity of 8–13 Hz is mostly seen over frontal region
in a comatose patient. Posterior predominant activity is mostly seen with
brainstem lesions while diffuse pattern is observed with severe hypoxic
ischemic encephalopathy. Reactivity of pattern and underlying etiology
determines the prognosis.
• Theta coma—Theta coma refers to diffuse background activity of 4–7 Hz
in coma. There can be intermixed alpha or delta activity. It is seen with
mild-to-moderate encephalopathy.
• High voltage delta coma—It can be seen focally in focal subcortical
brain lesions. Diffuse pattern is seen mostly with advanced stage of
encephalopathy.
• Spindle coma—It is defined as predominant theta and delta background
activity with superimposed paroxysmal spindle-shaped bursts of around

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 36 EEG and Epilepsy

Fig. 7.4: High amplitude delta coma

14 Hz frequencies. Intermittent sleep features as K-complexes may

be triggered by noxious stimuli. It is seen in patients with injury
to pontomesencephalic junction below thalamus and in HIE, TBI,
intoxication, encephalitis etc. Prognosis depends on underlying cause.
• Burst suppression pattern—It consists of generalized, synchronous bursts
of high amplitude, irregular activity that interrupts EEG suppressed
background activity. With deeper coma, proportion of burst decreases
and of suppression increases. HIE, drug toxicity, anesthetics are common
causes for it.

Electrocerebral Inactivity (ECI)

It is also called as electrocerebral silence or flat EEG. It denotes severe
and widespread CNS dysfunction in which EEG activity is undetectable at
an sensitivity of 2 microvolt with conventional scalp electrodes placed at
double the routine international 10–20 electrode distance with body core
temperature of above 34 degrees centigrade and with at least 30 minute of
continuous recording. Various artefacts including ECG, respiration, ventilator,
IV drip must be excluded from true brain activity and the term should only

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 EEG in Non-convulsive Electrographic Seizure 37

be used in the global absence of electrical activity, even after intense sensory
stimulation. Diffuse hypoxic ischemic encephalopathy is the most common
etiology. Patients with ECI have grave prognosis, including death and persistent
vegetative state.
As per American Clinical Neurophysiology Society guidelines minimal
technical standards for EEG recording in suspected cerebral death includes:
• A full set of scalp electrodes should be utilized—The frontal, central,
occipital, temporal areas must be covered. Midline electrodes Fz, Cz, Pz
should be used for the detection of residual low voltage physiologic activity.
• Interelectrode impedances should be under 10,000 Ohms but over 100
Ohms- a test of inter-electrode impedances to assure that they are of
adequate magnitude should be performed during the recording.
• The integrity of entire recording system should be checked.
• Inter-electrode distance should be at least 10 Centimetres.
• Sensitivity must be increased from 7 microvolt/mm to 2 microvolt/mm for
at least 30 minutes of the recording.
• Filter setting should be appropriate for the assessment of ECI- In order to
avoid attenuation of low-voltage fast or slow activity, wherever possible,
high frequency filters should not be set below a high frequency setting of
30 Hz, and a low frequency filter should not be set above a low-frequency
setting of 1 Hz.
• Additional monitoring techniques should be employed when necessary
like ECG monitor.
• There should be no EEG reactivity to intense somatosensory, auditory, or
visual stimuli.
• Recording should be made only by a qualified technologist- Great skill
is essential in recording cases of suspected ECI. Elimination of most
artefacts and identification of all others can be accomplished by a qualified
technologist.
• A repeat EEG should be performed if there is doubt about ECI - In the event
that technical or other difficulties lead to uncertainty in the evaluation of
ECI, EEG should be repeated after an interval, for example after 6 hour.

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 Chapter

8 Neonatal EEG

EEG patterns of neonate depend upon conception age (CA=gestational age +

week since birth) and state of sleep. Distinct EEG patterns of active sleep (REM
sleep) and quiet sleep (NREM) are identified easily by 35 weeks. It is essential
to record both states of sleep and so neonatal EEG recording should be for an
hour. A full term neonate has waking and sleep behavioral states consisting of
wakefulness, active sleep (REM sleep) and quiet sleep (NREM sleep).
Details of neonatal EEG are beyond the scope of this manual.

In Full Term Neonate (38 to 42 weeks)(Figs 8.1 to 8.7)

• Active sleep has low-to-medium amplitude theta activity with superimposed
delta activity (2 to 4 Hz, less than100 mV), the latter appearing as continuous
activity or in short runs or bursts (Fig. 8.6).
• Diffuse continuous delta activity is seen in quiet sleep.
• Trace alterant is seen in quiet sleep (Fig. 8.1).
• Activite´moyenne is a continuous low amplitude activity (25 to 50 mV) at
1 to 10 Hz (predominantly 4 to 7 Hz) that characterizes wakefulness and
active sleep, particularly following a period of quiet sleep (Fig. 8.5).
• Delta brushes (Fig. 8.7) are rarely seen. These are hallmarks of premature
(32–35 weeks) and consists of short burst of faster rhythmic activity
superimposed over slow wave.

Fig. 8.1: Trace alternans

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 Neonatal EEG 39

Fig. 8.: Interburst interval (IBI)

Fig. 8.3: Encoches frontales

• Frontal sharp transients (Encoches frontales) (Fig. 8.3) are biphasic sharp
waves over frontal region. They appear at 35 weeks and persist till several
weeks post-term.

Abnormal Neonatal EEG may Contain (Fig. 8.4)

• Abnormal background pattern including BSP
• Dysmature pattern—if tracings are 2 week immature for CA
• Focal abnormalities
• Ictal EEG—sudden, repetitive, evolving stereotyped waveforms that have
a definite beginning—middle and end, and last a minimum of 10 seconds.

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 40 EEG and Epilepsy

Fig. 8.4: Right focal epileptiform discharges in a neonate with left clonic seizure

Fig. 8.5: Neonatal awake

Abnormal Neonatal EEG

Depressed Background
Suppression of the background activity may indicate encephalopathy of
unknown etiology. This may be seen in hypoxia-ischemic encephalopathy,
drug overdoses, meningitis, encephalitis, raised intracranial pressure,

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 Neonatal EEG 41

Fig. 8.6: Active sleep

Fig. 8.7: Delta brush

hypothermia etc. Serial EEG is required to see evolution of disease process

and prognosis.

Background with Suppression Burst Activity

It is characterized by an isoelectric background interrupted by bursts of
abnormal activity. Bursts are synchronous and contain no age appropriate
activity. In the severe form it is invariant and persists throughout waking
and sleep states. It is seen with severe brain insults as hypoxic-ischemic
encephalopathy (HIE), CNS infections and in drug induced coma. As discussed
earlier it is also seen in early-infantile epileptic encephalopathy (EIEE).
This abnormal pattern must be differentiated from normal trace discontinue
of preterm infants, which is mostly reactive to stimuli.

Background with Excessive Discontinuity

The background EEG is normally discontinuous in very preterm infants. With
maturation of brain, the duration of flat period, or interburst intervals (IBI)

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 42 EEG and Epilepsy

decreases, as the preterm infant approaches term. In a full-term neonate, the

IBI should not exceed 6 sec. Increased IBI indicates encephalopathy.

Background with Prolonged Interburst Intervals (IBI)

The longest duration of the IBI within a record that is acceptable within the
norm varies according to CA, and is state dependent. Acceptable duration of
the longest IBI according to CA include:
26 weeks = 46 sec
27 weeks = 36 sec
<30 weeks = 30–35 sec
31–33 weeks = 20 sec
34–36 weeks = 10 sec
37–40 weeks = 6 sec

Background with Excessive Interhemispheric Asynchrony

During quiet sleep, about 70% bursts are synchronous at CA of 31–32 weeks,
80% at 33–34 weeks, 85% during 35–36 weeks and almost 100% after 37 weeks.
Excessive interhemispheric asynchrony may be seen in HIE, callosal agenesis,
cerebral dysgenesis.

Neonatal Seizures and EEG Correlates

EEG is very useful in monitoring and evaluating different neonatal seizures
and differentiating from no-epileptic phenomenon like brainstem release
phenomenon, which is very common in this age group.
Ictal EEG activity: Repetitive, rhythmic activity on the EEG, with variable and
evolving morphology, lasting for longer than 10 sec is considered suggestive
of electrical seizure activity. During a seizure process there is a progressive
build-up of rhythmic activity. Neonatal seizures are generally focal in onset and
tend to spread as the seizure evolves, often to one hemisphere or may become
generalized. The morphology of the discharges can change during a seizure,
which helps to differentiate it from non-epileptic patterns. Multifocal seizures
are common in severe encephalopathies. Periodic lateralized epileptiform
discharges (PLEDs) may be seen in neonates with herpes simplex encephalitis,
focal ischemic strokes. Generalized ictal rhythms can be seen in EIEE.
Brief ictal rhythmic discharges (BIRD) are rhythmic ictal activity of
<10 sec duration. It has stronger correlation with epileptic process. Isolated
sharp waves in neonates do not correlate with epileptic process.
Electroclinical dissociation or decoupling characterizes absence of clinical
seizure activity while the electrical ictal rhythm continues. It may be seen after
administration of anticonvulsant drug to a seizing baby or in babies who are
paralyzed and are on mechanical ventilation.

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 Chapter
Benign Patterns of Uncertain
9 Clinical Significance

These are benign variants of EEG activity (BEVs). They denote waveforms
which are epileptiform in morphology, however, are not associated with
epilepsy. It is essential to correctly identify BEVs to avoid misinterpreting it as
epileptic discharges and thus to avoid unnecessary treatment and associated
complications and social implications of epilepsy.
1. Rhythmic Temporal Theta Bursts of Drowsiness (RTTD)
Psychomotor variant Pattern- It is rhythmic pattern over temporal region
resembling a “psychomotor” or temporal lobe seizure discharge. Bursts
or serial trains of rhythmic theta waves of 5–7 Hz with a flat topped, sharp
contoured, or notched appearance are seen maximum over mid temporal
with some spread to parasagittal region (Fig. 9.1). It waxes and wanes but
does not evolve in frequency or amplitude as seizure discharges. It arises
predominantly in drowsiness but may be seen in wakefulness.
2. Frontal Arousal Rhythm (FAR)
Trains of 7–20 Hz waveforms predominantly over frontal regions, occurs
in runs, lasting up to 20 seconds. It has varying harmonics giving pattern
a notched appearance. Occurs in children following arousal from sleep.
Disappears once child is awake (Fig. 9.2).
3. Fourteen- and Six-Hertz Positive Bursts
Gibbs and Gibbs (1952) first described it as 14 and 6 Hertz positive spikes. It
occurs predominantly during drowsiness and light sleep. Begins to appear
in children at 3–4 years of age, peak at 13–14 years, and then progressively
decrease in incidence with advancing age. Bursts occur at 14 Hz or 6-7 Hz.

Fig. 9.1: RTTD

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 44 EEG and Epilepsy

Fig. 9.2: FAR

Fig. 9.3: Fourteen- and six-hertz positive bursts

6 Hz rhythm is more frequent in young children, faster frequency is more

prevalent in older children. Maximal amplitude is over posterior temporal
region. It is best displayed on long distance or referential montage to ear
(Figs 9.3 and 9.4).
4. Breech Rhythm
High voltage activity that occurs in region of skull defect. Spiky, sharply
contoured arciform waveforms of 6–11 Hz. Most prominent when recorded

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 Benign Patterns of Uncertain Clinical Significance 45

Fig. 9.4: Fourteen- and six-hertz positive bursts

Fig. 9.5: Breech rhythm at C4

over central and temporal regions (Fig. 9.5). Absence of after coming slow-
wave and lack of spread to other areas differentiates it from true epileptic
activity.
5. Small Sharp Spikes (SSS): Benign sporadic sleep spikes/Benign epileptiform
transients of sleep
It is characterized by spikes of <50 microvolt amplitude and <50 msec
duration seen maximally over frontotemporal area. Its biphasic wave with
steep negative ascent and steeper declination seen predominantly in
drowsiness and in light sleep (Fig. 9.6).

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 46 EEG and Epilepsy

Fig. 9.6: Small sharp spikes (SSS)

     Benign EEGs variants (BEVs) can be mentioned on the body of EEG

report but should not be reported as an abnormality. Mostly these are
state dependent like present in drowsiness and light sleep with no after
coming slow wave and spread with normal background activities. Proper
identification will avoid misdiagnosis and unnecessary investigations.

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