ATLAS OF EEG.pdf

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Atlas of Pediatric
EEG
Pramote Laoprasert, MD
Assistant Professor
University of Colorado School of Medicine
Director of Surgical Epilepsy Program and Epilepsy Monitoring Unit
Department of Pediatric Neurology
The Children’s Hospital of Denver
Aurora, Colorado
New York Chicago San Francisco Lisbon London Madrid Mexico City
Milan New Delhi San Juan Seoul Singapore Sydney Toronto

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Dedicated to my wife Nan, my children Maddy and Rick, and my parents Saman and Vilai
For their unconditional love, enthusiastic support, encouragement,
and long-suﬀering tolerance during preparation of this book.
And to my patients and their families. Without them, this book would be impossible.

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vii
CONTENTS
Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix
Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xi
Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xii
1 Normal and Benign Variants . . . . . . . . . . . . . . . . . . . 1
2 Artifacts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125
3 Newborn . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201
4 Focal Nonepileptoform Activity. . . . . . . . . . . . . . 275
5 Generalized Nonepileptiform Activity. . . . . . . . 389
6 ICU. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 471
7 Epileptic Encephalopathy . . . . . . . . . . . . . . . . . . . 529
8 Generalized Epilepsy . . . . . . . . . . . . . . . . . . . . . . . . 613
9 Focal Epilepsy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 675
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 861

ix
FOREWORD
Epilepsy is a common and frequently disabling
disorder in children. Linking its clinical manifestations
to electrographic and imaging changes is essential to
correct diagnosis and management. This multimedia
work provides an accessible, comprehensive, and
timely tool for the child neurologist or epileptologist
in training or in practice to become familiar with the
extraordinary richness of the clinical and electrographic
manifestations of childhood epilepsy.
The text represents the distillation of an extraordinary
body of clinical experience and painstaking attention to
detail, which is characteristic of Dr. Laoprasert. I first had
the privilege of making his acquaintance two decades
ago, when he began his child neurology training at
Mayo Clinic. Since that time, he has established himself
as a first-class pediatric epileptologist and scholar. This
fine work is an appropriate testament to his diligence
and skill.
The text is laid out in a systematic and thoughtful
fashion, beginning with common and not-so-common
patterns and variants in the electroencephalogram,
which can be a source of confusion and diagnostic error
to the novice. Subsequently, pathological conditions
are explored in a similarly logical and comprehensive
fashion. Since most of us learn from our patients, I
predict that this case-based approach will be extremely
effective. I commend this work to anyone who wishes
to improve his or her grasp of epilepsy in childhood. It
will be essential reading for pediatric epilepsy trainees
but will also be a frequently consulted resource for
residents in training. By the same token, the child
neurologist who is not an expert in epilepsy, and even
experienced pediatric epileptologists, will find a great
deal of valuable material to enhance the care of their
patients. Whether read cover-to-cover, used to review
specific problems, or dipped into at random, this text
makes learning about epilepsy in children a pleasure
and will ultimately enhance the quality of their lives
and those of their families.
Marc C. Patterson, MD, FRACP, FAAN
Professor of Neurology, Pediatrics
and Medical Genetics
Chair, Division of Child and
Adolescent Neurology
Mayo Clinic
Rochester, Minnesota

xi
PREFACE
EEG presents a tremendous challenge to the neurologist.
Although EEG has been used for almost a century, it is
still and will continue to be one of the most important
diagnostic tools in neurology, especially in pediatric
neurology and epilepsy. The rapid advances in digital
and prolonged video-EEG as well as in epilepsy surgery
enhance the usage of the EEG to the higher level.
Atlas of Pediatric EEG presents both common and
uncommon EEG diagnoses in a case-study-oriented
manner. Unlike other EEG atlases that catalog only
the EEG patterns, this book stresses the viewpoint of
the practicing neurologists and neurophysiologists.
Integration of the EEG, clinical information, and
neuroimaging is the heart of this book and is
consistently presented throughout. Cited references for
further study are extensive and up to date. This will help
the readers to have a better understanding of the EEG
and its applications.
Atlas of Pediatric EEG is designed for the
electroencephalographer, child neurologist, EEG/
epilepsy fellow, neurology resident, pediatrician, and
EEG technologist with an interest in pediatric EEG. Other
healthcare providers, such as nurse practitioners and
physician assistants who care for children with neurologic
conditions, as well as medical students during the
pediatric neurology clerkship who want to learn about
the EEG in children, will also ﬁnd this atlas valuable.

xii
ACKNOWLEDGMENTS
I would like to acknowledge Dr. Marc Patterson for
his extraordinary mentoring and for a very kind and
thoughtful foreword. I thank Dr. Paul Moe and Dr. Andy
White for their critical review and proofreading. I also
thank my colleagues, epilepsy fellows, and neurology
residents at the Denver Children’s Hospital in the
preparation of this book.
I am also deeply grateful to the editorial staﬀ at
McGraw-Hill, especially to Anne Sydor, Christine
Diedrich, Sherri Souﬀrance and Priscilla Beer, as well as
Sandeep Pannu and Aakriti Kathuria of Thomson Digital,
for their generous support and competent assistance.

1
Normal and
BenignVariants
Alpha rhythm or posterior dominant
rhythm (Figures 1-1 to 1-5, 1-11, and 1-16)
Monomorphic either sinusoidal or having sharp
䡲
points at the top or bottom, 8–13 Hz in older children
and adults during relaxed wakefulness with eyes
closed.
Eye opening attenuates alpha rhythm (AR) and eye
䡲
closure accentuates AR.
AR also attenuates with:
䡲
Drowsiness
䊳
Concentration
䊳
Stimulation
䊳
Visual fixation
䊳
Anxiety
䊳
Eye closure with mental calculation
䊳
AR responsive to eye opening occurs in 75% of infants
䡲
between 3rd and 4th months.
Frequency
Mean AR frequency:
䡲
4 months – 4 Hz
䊳
12 months – 6 Hz
䊳
36 months – 8 Hz
䊳
9 years – 9 Hz
䊳
10 years – 10 Hz
䊳
Elderly – above 9 Hz
䊳
Abnormal AR:
䡲
1 year: <5 Hz
䊳
4 year: <6 Hz
䊳
5 year: <7 Hz
䊳
≥ 8 year: < 8 Hz (8.5 Hz by some authors)
䊳
Incidence of AR as slow as 8 Hz in adult is <1%;
䊳
therefore, consistent 8 Hz of AR is considered mild
abnormality by some authors.
Frequency of AR is constant throughout adult life, a
䊳
decline of ≥1 Hz is abnormal even if their absolute
frequency remains in the range ≥8 Hz.
Difference of AR frequency >1 Hz in the two
䊳
hemispheres.
Good AR is seen during crying and passive eye
䡲
closure.
Drowsiness must be considered if muscle artifact is
䡲
seen less than usual.
Fever and hypermetabolic states, including
䡲
hyperthyroidism and amphetamine intoxication, may
increase the AR’s frequency. High fever in children can
either increase or decrease the AR’s frequency.
Extreme upward gaze or lateral eye deviations may
䡲
facilitate AR frequency.
Voltage
Most adults have AR voltages of 15–45 μV; Children
䡲
(3–15 years) 50–60 μV; Children (6–9 years) 100 μV or
more.
6–7% of adults have voltage less than 15 μV.
䡲
Only 1.3% of children >12 years have AR voltage less
䡲
than 30 μV.
Low voltage (< 20 μV) EEG (electroencephalography)
䡲
is abnormal in children.
Low voltage (< 10 μV) EEG is more likely to be
䡲
abnormal in adult.
Very low voltage ≤ 2 μV EEG is seen in electrocerebral
䡲
inactivity and marked subdural fluid collection.
High-voltage AR alone should never be considered
䡲
abnormal.
Reduced voltage AR with advancing age is more
䡲
likely due to increased bone density and electrical
impedance of the intervening tissue rather than
decreased electrical brain activity.
Regulation
Sustained rhythm, in which the mean frequency does
䡲
not vary more than ± 0.5 Hz, and the smoothness of
the envelope of the waxing and waning of voltage.
Best regulation between 6 months and 3 years.
䡲
Poor regulation between 3 and 4 years (low voltage).
䡲
Affected by mental activity and anxiety.
䡲
1

1
2 Normal and Benign Variants
Distribution
AR is in occipital region in 65% of adults and 95% of
䡲
children.
Variant: central and temporal regions and widely
䡲
distributed AR.
Although slight AR in the frontal regions is occasionally
䡲
seen, prominent anterior alpha frequency rhythm is
considered abnormal.
Alpha frequency activity restricted to the frontopolar
䡲
electrodes is eyelid flutter until proven otherwise.
AR may be prominent in frontocentral region during
䡲
drowsiness.
Asymmetry
60% of adults and 95% of children, AR is higher
䡲
voltage in the right side with asymmetry less than
20%, regardless of handedness.
Most likely due to difference in skull thickness.
䡲
Asymmetry >20% is seen in 17% and >50% is seen
䡲
in 1.5% in all ages.
Voltage asymmetry >20% is seen in 5% of normal
䡲
children.
Persistent asymmetry of 50% or more is considered
䡲
abnormal.
Persistent asymmetry of 35–50% is considered
䡲
suspect if the lower voltage AR is on the right side.
Symmetry is best
䡲 measured in referential montage
to avoid phase cancellation.
The same rule is applied to mu and temporal theta
䡲
activity.
Squeak effect
Immediately after eye closure, alpha frequency may be
䡲
accelerated for 0.5–1 sec. Therefore, alpha frequency
assessment should not be done during this period.
Paradoxical AR
AR presents with eye opening if the environment
䡲
is devoid of light as the result of partial alerting.
Paradoxical AR is seen in drowsiness and sedation.
Beating or waxing and waning of the AR
Effect of two separate alpha frequencies.
䡲
Bancaud phenomenon
When unilateral cerebral lesions or transient
䡲
cerebral dysfunction (such as migraine or TIA) are
present in the occipital or, less commonly, parietal or
temporal lobes, the side of defective reactivity (eye
opening and alerting) occurs ipsilateral to the side of
the lesion. When both phenomena exist, the same
side of the brain is affected.
Beta activity
≥ 13 Hz; most common 18–25 Hz; less common
䡲
14–16 Hz; rare 35–40 Hz.
First develops between 6 months and 2 years
䡲
Distribution: frontocentral >widespread>posterior.
䡲
Voltage <20 μV in 98% and <10 in 70%
䡲
Voltage of >30 μV is rare but should generally not
䡲
be considered abnormal, although generalized but
anterior-predominant fast activity called“extreme
spindles”can be seen in mental retardation or
cerebral palsy as well as lissencephaly.
Drugs including barbiturates, benzodiazepine, and
䡲
chloral hydrate increase amplitude and amount of
beta activity.
Increase in amount and amplitude during drowsiness,
䡲
stage 2 sleep and rapid eye movement (REM);
decrease during deeper stages of sleep.
Consistently low voltage on one side >35% is
䡲
indicative of:
Cortical injury
䊳
Transient conditions such as postictal state
䊳
Subdural or epidural fluid collection
䊳
More sensitive than focal polymorphic delta
䊳
activity (PDA)
Amplitude asymmetry of >35% is considered
䡲
abnormal.
Focal
䡲 increased amplitude is seen in:
Skull defect (breach rhythm)
䊳
Focal structural abnormality, especially focal
䊳
cortical dysplasia
Presence of beta activity is almost always a good
䡲
prognostic sign.
Slow alpha variant (Figures 1-6 to 1-7)
A rare physiologic variant of AR (less than 1% of
䡲
normal adults), seen during relaxed wakefulness,
has a harmonic relationship and interspersed with
the normal AR, and shows similar distribution and
reactivity as a normal AR.
Usually alternates with AR.
䡲
Rhythmic sinusoidal, notched theta, or delta
䡲
activities that have a harmonic relationship with
the AR (one-third or, more commonly, one-half the
frequency).
Should not be misinterpreted as occipital
䡲
intermittent rhythmic delta (OIRDA) or theta
activity activities, and pathologic findings seen
in children and adults.
Slow alpha variant may be differentiated from
䡲
pathologic slow waves by:
Morphology (notched appearance)
䊳
Frequency (subharmonic of normal AR)
䊳
Reactivity to eye opening
䊳
Disappearance with sleep
䊳
Sometimes mimics rhythmic temporal theta bursts
䡲
of drowsiness (RTTD), except that it occurs only
over the posterior head regions.
Fast alpha variant pattern
(Figures 1-8 to 1-10)
Harmonic of the AR that has a frequency approximately
䡲
twice that of AR, usually within the range of 16–20 Hz,
with a voltage of 20–40 μV.
Usually intermingled with AR and shows reactivity
䡲
and a distribution similar to AR.

1 Normal and Benign Variants 3
Posterior slow waves of youth
(youth waves or polyphasic waves)
Physiologically high-voltage theta or delta waves
䡲
accompanied by the AR and creating spike wave-like
phenomenon
Most commonly seen in children aged 8–14 years
䡲
and are uncommon in children under 2 years.
A 15% incidence in healthy
䡲 individuals aged 16–20
years but rare in adults above 21 years of age.
Typically seen both unilaterally and bilaterally in a
䡲
single recording. They are always accompanied by
the AR, attenuated with eye opening, disappear with
the AR during drowsiness and light sleep, and may be
accentuated by hyperventilation and stress.
Characteristic ﬁndings:
䡲
Monorhythmic occipital rhythm attenuates with
䊳
eye opening
Normal slower waveforms rarely >1.5 times the
䊳
amplitude of AR.
Normal slower waveforms attenuate with AR
䊳
during alerting.
Slower
䊳 waveforms has the same asymmetry in the
ongoing AR
Index of abnormality of theta/delta slowing.
䡲
Complexity and variability of waveforms
䊳
Incidence (how often slow waves occur)
䊳
Voltage ratio (normal slow waves rarely >1.5 times
䊳
the amplitude of AR)
Persistence with eye opening
䊳
Symmetry (consistently predominant on one side).
䊳
Lambda waves (Figures 1-17 to 1-19)
Sharp transients of sawtooth shape (biphasic or
䡲
triphasic) occurring over the occipital region of
waking subjects during visual exploration (scanning
complex picture), mainly positive relative to other
areas and time locked to saccadic eye movements.
Amplitude varies, but is generally below 50 μV.
䡲
Duration is 100–250 msec except in 1–3 years that
can be up to 400 msec.
Resemble positive occipital sharp transients of sleep
䡲
(POSTS) and visual evoked potential. Subjects with
prominent lambda waves also have prominent
POSTS.
In children, highest amplitude and sharpest
䡲
component is surface negative in the occipital region.
Random and isolated waveforms but may be recur at
䡲
intervals of 200–500 msec.
Visual evoked
䡲 potentials occur in association with
saccadic eye movement.
Do not occur before 1 year of age.
䡲
Most common during the middle years of childhood.
䡲
The prevalence of lambda waves between 3 and 12
years of age is about 80%.
Lambda waves have been described as biphasic or
䡲
triphasic; their predominant positive component is
preceded and followed by a negative component.
Strictly bilateral synchronous although may be
䡲
asymmetrical on the two sides. Rarely present only
on one side.
Marked asymmetry indicates an abnormality on the
䡲
side of lower amplitude.
The most important precipitating factor is voluntary
䡲
scanning eye movements.
Lambda wave is attenuated by:
䡲
Darkening room
䊳
Staring at a blank card
䊳
Eye closure
䊳
Lambda waves usually occur as random and isolated
䡲
waveforms but may recur at intervals of 200–500 msec.
Accompanied by eye movement and eyeblink
䡲
artifacts.
Sometimes, especially when present unilaterally,
䡲
they may be mistaken for focal abnormalities, but the
distinction can be made by replacing the geometric
image with a blank surface.
Marked and persistent asymmetry indicates an
䡲
abnormality on the side of lower amplitude.
Positive occipital sharp transients
of Sleep (Figures 1-20 to 1-24)
Best seen at the age of 15–35 years and rarely
䡲
<3 years.
Seen in 50–80% of healthy adults.
䡲
Amplitude 20–75 μV; duration 80–200 msec.
䡲
Absent in individuals with poor
䡲 central vision.
Sharply-contoured
䡲 , surface positivity, occurring
in trains with a repetitive rate of 4–5 Hz, and
monophasic checkmark-like waveform seen
singularly or in clusters over the occipital regions.
Always bilaterally synchronous but are commonly
䡲
asymmetric on the two sides. Asymmetry of 50% is
normal.
POSTS occur during deep drowsiness and stage
䡲
2 sleep. Rare in REM sleep.
Posterior slow-wave transients
associated with eye movements
Seen in children age 6 months to 10 years, but most
䡲
commonly in children aged 2–3 years.
Consisting of a monophasic or biphasic slow transient
䡲
with a duration of 200–400 msec and a voltage of up
to 200 μV in the occipital regions.
A
䡲 latency of 100–500 msec is noted after the
eyeblinks or eye movements.
The initial component of the transient is surface
䡲
positive. The ascending phase is steeper than the
descending phase.
Occipital slow transients
Physiologic waves presenting during non-REM sleep,
䡲
especially a transition from light to deep sleep in
infancy until 5 years of age

1
Bilateral, isolated, medium- to high-amplitude,
䡲
monomorphic, triangular-shaped, delta waves with a
typical duration greater than 250 msec in the occipital
regions.
These waves vary from a
䡲 cone-shaped configuration
(cone waves or “O” waves) to a biphasic slow transient.
These transients occur every 3–6sec during light
sleep and more frequently during deeper stages
of sleep.
H-Response (Figures 1-32 to 1-34)
Prominent photic driving response at flash rates
䡲
beyond 20 Hz.
Sensitivity varied from 25% to 100%, and specificity
䡲
from 80% to 91%.
Although
䡲 there are relatively high sensitivities and
specificities of the H-response in distinguishing
migraine patients from controls and tension
headache, H-response is not more effective than the
history and examination in diagnosing headaches
and not recommended for use in clinical practice.
May be useful for clinical diagnosis in complicated
䡲
headache and help to monitor therapeutic response.
Needle-like spikes of the blind
(occipital spikes of blindness)
Occipital or parietal regions in most patients with
䡲
congenital blindness and retinopathy during early
infancy.
Prevalence of 75% in retrolental fibroplasia age
䡲
3–14 years and 35% in all causes of blindness.
Amplitude 50–250 μV.
䡲
Isolation or burst.
䡲
Activated by sleep.
䡲
Low amplitude at 10 months; typical features at
䡲
2.5 years; after-going slow waves in mid-childhood;
disappear by the end of adolescence.
Functional deafferentation of the visual cortex gives
䡲
rise to an increase in its irritability (denervation
hypersensitivity).
Not an epileptiform activity.
䡲
Seen more commonly in patients with mental
䡲
retardation and epilepsy.
Disappear during childhood or adolescence.
䡲
Sleep stages
Drowsiness (Figures 1-38 to 1-39)
Alpha dropout (earliest sign)
䡲
Increased beta activity over the frontocentral regions
䡲
Diffuse rhythmic theta activity with anterior
䡲
predominance
Slow eye movement
䡲
Mu rhythm, wicket wave, and 14 and 6 Hz positive
䡲
spikes can be seen.
Deep drowsiness is marked by the vertex waves
䡲
and POSTS that persist during light sleep and
deep sleep
Hypnagogic hypersynchrony in 3 months to 8 years.
䡲
Stage 2 sleep (Figures 1-40 to 1-41)
Symmetric, synchronous theta rhythms with posterior
䡲
predominance, 12–15/sec spindles, vertex sharp
waves, K-complexes, and POSTS.
Sleep spindles in the 12–15/sec range
䡲 are hallmark of
sleep onset.
Stage 3 sleep (Figure 1-42)
Delta frequencies in the 0.75–3/sec range are
䡲
prominent over the anterior regions.
Sleep spindle in the 10–12/sec and even in the 12–
䡲
14/sec ranges are still present but gradually become
less prominent.
Rhythmic activity of 5–9/sec is common.
䡲
Rhythmic and symmetrical delta activity is noted
䡲
between 20% and 50% of the recording
Stage 4 sleep (Figure 1-43)
Over 50% of the recording is delta rhythm.
䡲
Spindles are rare.
䡲
Arousal at this stage can be correlated with sleep
䡲
disorders (somnambulism, nocturnal terror, or
enuresis), and can cause confusion.
Occasionally, spikes in temporal lobe epilepsy will
䡲
only appear in stage 3 and 4 sleep.
REM sleep (Figure 1-44 and 2-1)
Low-voltage activity, polyrhythmic waves, and slower
䡲
alpha waves.
Short bursts of“saw-tooth waves”over the frontal or
䡲
vertex leads and quick lateral eye movements.
Appearance of REM sleep in routine EEG is seen in
䡲
narcolepsy and in patients who are withdrawn from
CNS depressants such as alcohol or phenobarbital.
K-Complex (Figures 1-45 to 1-48)
Contain 3 components including sharp, slow, and fast.
䡲
Seen in stage 2 sleep and arousal.
䡲
Largest in older children and adolescence. With
䡲
advanced age, the K-complexes show the decline in
voltage with tiny superimposed spindle-like waves.
First appears at 4 months of age. They have high
䡲
amplitude but their rise is not as abrupt and the
configuration is not as sharp as seen in older
children.
Sleep spindles (Figures 1-49 to 1-58)
Arise from synchronized activity in neuronal networks
䡲
linking the thalamus and the cortex. Spindles result
from rhythmic spike bursts in inhibitory (GABAergic)
thalamic reticular neurons that induce rhythmic
rebound bursting in cortical neurons resulting in
effective deafferentiation of the cerebral cortex. Cortical
neurons show enhanced synaptic plasticity that might
have a role in memory and learning processes.
First seen at 1.5–2 months with a frequency of 14/sec.
䡲
Throughout infancy, they are maximal over the
䡲
central and parietal areas with shifting asymmetry.
They usually are electronegative with rounded positive
component that is a typical hallmark of sleep spindles
in infancy. These surface-negative spindles with

wicket or comb-like shape can be erroneously
interpreted as 14/sec positive spikes
Between the ages of 3 and 6 months, sleep spindles
䡲
appear to be biphasic and as prolonged runs, up to 10–
15 sec. The prolonged run of spindles is a very useful
developmental marker and is rarely seen beyond this
age range.
Subharmonic or harmonic of sleep spindles with a
䡲
frequency approximately half or double that of sleep
spindles and notched appearance can be seen.
In the second half of the first year of life, the
䡲
spindles appear to be monophasic and are often
asynchronous between the two sides. The frequency
of spindles also changes, with 12/sec components
becoming more prominent.
Asynchronous spindles
䡲 may occasionally continue
from 1 to 2 year of age but rarely are seen after the age
of 2 years when interhemispheric synchrony of the
spindles appears.
Mitten patterns (Figures 1-59 to 1-62)
Consist of a sharp-contoured waveform on the slope
䡲
of a slow wave of the same polarity that resembles
a mitten, with a thumb of mitten formed by the last
wave of a spindle and the hand portion by the slower
wave component.
Maximal at the frontocentral vertex with spread into
䡲
parasagittal regions. The location is different from
K-complexes in that it is centered anterior to the
central vertex where K-complexes are maximal.
Variant of a vertex wave or K-complex and should not
䡲
be mistaken for a spike-and-wave discharge.
It is best seen in referential montage in stage
䡲
3 sleep.
Hypnagogic hypersynchrony
Seen in early drowsiness and arousal from deeper
䡲
sleep.
Characterized by bilateral synchronous, high voltage,
䡲
rhythmic 3–5 Hz activity.
The frequency of hypnagogic hypersynchrony is 3–4
䡲
Hz at the age of 2–3 months and increases to 4–5 Hz
in older children.
Asymmetric hypnagogic hypersynchrony with
䡲
shifting predominance can be seen and is not
considered abnormal.
At 2–3 months, first appears.
䡲
At 9 months, more prominent and continuous.
䡲
Between 4 months and 2 years, seen in almost all
䡲
infants.
Few infants do not show this pattern but show
䡲
occipital or widespread rhythmical and synchronous
4–5 Hz waves of low to medium amplitude.
At 4 years, shorter in duration and more paroxysmal.
䡲
At 9–11 years, it becomes rare (10%).
䡲
Although the presence of hypnagogic hypersynchrony
䡲
at age 12 years is considered abnormal by some
authors, it may be seen in normal children up to the
age of 12–13 years.
Occasionally, small sharp or spiky discharges may
䡲
be interspersed between the theta waves. These
discharges should not be interpreted as epileptiform
activity unless they are definitely distinct from
background activity and not only occur during
drowsiness or at the onset of sleep but persist into
deeper stages of sleep.
Hypnic myoclonia (hypnagogic jerks)
(Figures 1-67 and 1-70)
This wake-to-sleep transition event is characterized
䡲
by a sudden, single, brief muscular contraction
of the legs and occasionally the arms, head, and
postural muscles.
Sensory hallucinations (hypnagogic hallucinations)
䡲
often occur before the hypnic myoclonia.
Hypnic myoclonia occurs in 60–79% of normal
䡲
population. Although it may occur at any age,
90% of patients stop these movements by age
of 4 years.
They are more common in boys than girls by 4:1.
䡲
Midline theta rhythm (Figure 1-71)
Rare nonspecific finding of no clinical significance.
䡲
Rhythmic train of 5–7 Hz theta activity occurring
䡲
in the central vertex but may also be seen in the
frontal vertex.
Morphology includes sinusoidal, aciform, spiky, or
䡲
mu-like appearance.
Seen during wakefulness and drowsiness.
䡲
Variable reactivity to eye opening, alerting, and limb
䡲
movement. The rhythm usually lasts from 3 to 20 sec
and does not evolve.
Frontal arousal rhythm (FAR)
Rare nonspecific EEG pattern of no clinical
䡲
significance.
Frontal regions (F3 and F4 electrodes with minimal
䡲
spread to nearby scalp areas) during arousal from
sleep in children.
Characterized by 30–150 μV, predominantly
䡲
monophasic negative waves, occurring in bursts
or runs lasting up to 13 sec (usually 1–5 sec) with
a characteristic notching of the ascending or
descending phase of each wave that may represent
harmonics of the waveforms.
The waxing and waning of the amplitude often leads
䡲
to a spindle-like morphology.
70% of patients having epileptic seizures; a
䡲 reported
case in which FAR representing ictal electrographic
seizure activity.
Rhythmic temporal theta bursts of
drowsiness, rhythmic midtemporal
discharges (RMTD), psychomotor
variant (Figures 1-77 to 1-82)
Benign variant of no clinical significance.
䡲
Seen in 0.5–2.0% of normal adult population and
䡲
less common in adolescence. No prevalence in
childhood.

1
Bursts or runs of rhythmic, 5–7 Hz or 4–7 Hz (typically
䡲
5–5.5 Hz), theta activity with flat-topped, sharply
contoured, often notched appearance in the
temporal regions.
Maximally expressed in the mid- or anterior temporal
䡲
electrodes.
Monomorphic pattern with amplitude of 50–200 μV.
䡲
Duration: commonly 5–10 sec; vary from 1 to >60
䊳
sec with gradual onset and offset.
The sharper component of the wave usually has a
䊳
negative polarity in the anterior temporal region.
Unilaterally with shifting from side to side greater
䊳
than bisynchronous.
Differentiated from ictal epileptiform activity by
䊳
Monomorphic and monorhythmic (no evolution
앫
into other frequencies although amplitude
can vary)
No alteration of background activity
앫
Occurrence in relaxed wakefulness and
앫
drowsiness (most common) and disappearance
in deeper levels of sleep.
Although it has no clinical significance, it was
䡲
considered by some authors to be a pathologic
finding in selected cases.
Fourteen and six per second positive
spike discharge (Figures 1-83 to 1-92,
5-44 to 5-48, 6-44)
䡲
Bursts of arch-shaped waves at 13–17 Hz and/or
䡲
5–7 Hz, most commonly at 14 and/or 6 Hz. The 14 Hz
component is more commonly seen than 6 Hz.
Maximal
䡲 over the posterior temporal and adjacent
areas of one or both sides of the head.
Amplitude <75 μV.
䡲
Appearance in deep drowsiness and very
䡲
light sleep and disappearance in deeper levels
of sleep.
Electropositive of sharp component and
䡲
electronegative of smooth component.
Widespread field lasting for 0.5–1 sec.
䡲
Occurs in children after age 3 to young adult
䡲 but
more common between 12 and 20 years with a
peak at age 13–14 years.
Best seen in contralateral ear reference
䡲
montage.
Appearance in diffuse encephalopathy EEG pattern
䡲
in a wide variety of encephalopathies of childhood
suggesting that they are epiphenomena or a resilient
normal. Frequency is more variable and can be
elicited by alerting stimuli.
Small sharp spike (SSS) or benign
epileptiform transients of sleep (BETS)
䡲
20–25% of a normal adult population.
䡲
Appearance in deep drowsiness and very light sleep
䡲
and disappearance in deeper stages of sleep.
Usually low voltage, short duration, single
䡲
monophasic, or biphasic spike with an abrupt
ascending limb and a steep descending limb.
± After coming slow wave.
䡲
Either unilaterally or bilaterally.
䡲
Six-hertz spike-wave bursts (phantom
spike-wave) (Figures 1-97 to 1-98)
䡲
2.5% of both adolescents and young adults;
䡲
0.5–1% overall.
Appearance in relaxed wakefulness, drowsiness,
䡲
and light sleep and disappearance in deeper levels
of sleep.
Bursts of 1–2 sec duration diffuse, low voltage (<40
䡲
μV), short duration (<30 msec), 5–7 Hz, spike-and-
wave discharges, commonly bifrontal or occipital.
25% of phantom spike and wave have repetitive rate
䡲
of 4 Hz.
At times, spikes are difficult to see.
䡲
Six-hertz spikes with minimal or no associated
䡲
waves may represent a transitional pattern between
6-Hz spike-wave bursts and 14 and 6-Hz positive
bursts.
Waking, high-amplitude, anterior, male (WHAM) vs
䡲
female, occipital, low-amplitude, drowsy (FOLD).
WHAM is more likely to be associated with seizures
䡲
if the repetitive rate is <5 Hz or amplitude of spike
greater than slow wave.
Wicket waves (Figures 1-99, 1-101, 1-102)
One of the most common over-read EEG patterns
䡲
seen almost exclusively in adults, most commonly
>30 years of age and, usually, older than 50 years.
Benign variant pattern and is not associated with
䡲
epilepsy.
Rare waveform (0.9%).
䡲
It occurs in clusters or trains, but also as single sharp
䡲
transients, of 6- to 11-Hz negative sharp aciform
waves with amplitude of 60–200 μV.
Anterior or midtemporal regions.
䡲
Seen during relaxed wakefulness but facilitated by
䡲
drowsiness and may occur in light sleep. Recently
wicket waves have also been reported to occur
during REM sleep.
Unilaterally with a shifting asymmetry between the
䡲
two hemispheres.
During the wakefulness, wicket waves are often
䡲
masked by background EEG activity.
Cardinal feature is a changing mode of occurrence
䡲
through any single recording, from intermittent
trains of more or less sustained, aciform, discharges
resembling mu rhythm, to sporadic single spikes.
Amplitude may be high, but the transient arises out
䡲
of an ongoing rhythm and does not stand out.

When occurring singly, wicket waves can be
䡲
mistaken for anterior or middle temporal spikes.
Isolated wicket wave can be differentiated from
epileptiform discharge by the following criteria:
No slow wave component following the
䊳
wicket wave
Occurring in trains or in isolation and do not
䊳
disrupt the background
Similar morphology to the waveforms in the train
䊳
when occurring as a single spike
More commonly seen in patients with
䡲
cerebrovascular disease.
The age (younger than 30 years) and abnormal
䡲
background activity are strongly against the
diagnosis of wicket waves and supportive of
epileptiform activities.
Third rhythm (independent temporal
alphoid rhythm) (Figure 1-100)
Rhythmical activity in the alpha and upper theta
䡲
range over the midtemporal region.
Not seen in scalp EEG except the presence of skull
䡲
defect.
Physiologic rhythm that is clearly independent from
䡲
mu or AR.
It needs to be differentiated form the rhythmical
䡲
activity seen in anterior- and midtemporal
regions seen in patients with stroke.
Photomyogenic response
(Figures 1-103 to 1-106)
Occurs in 0.1% of the normal population and 1% of
䡲
patients with epilepsy.
Most prominent in the frontal regions as a
䡲
result of orbicularis oculi and frontalis muscle
twitching during eye closure and stops with flash.
Immediate cessation of the response at the end
䡲
of stimulation and prominent electromyographic
activity help to distinguish this photomyogenic
response from photoparoxysmal response.
Normal variant although it can coexist with
䡲
photoparoxysmal response or rarely progress
to generalized tonic-clonic seizures (GTCS).
Mu rhythm (Figures 1-107 to 1-115)
Physiologic EEG finding of no clinical significance.
䡲
Central rhythm of an alpha frequency band (8–10 Hz)
䡲
with an arciform configuration, intermix or alternate
with beta activity.
Occurs in less than 5% of children younger than
䡲
4 years of age and in 18–20% between the age
of 8 and 16 years.
Not blocked with eye opening, but blocked by touch,
䡲
movement of limbs (especially contralateral limbs) or
thought of movement.
Usually asymmetric, asynchronous and independent
䡲
in the two hemispheres.
Consistent asymmetry of amplitude or frequency
䡲
of mu suggests an abnormality on the side of lower
amplitude or frequency.
Believed to be the rhythm of the sensorimotor cortex
䡲
at rest.
Prominent in the patients with underneath skull
䡲
defect (breach rhythm).
Paradoxical mu rhythm – induced by contralateral
䡲
movement or touch after the mu rhythm has
dropped out in drowsiness. Paradoxical AR may
be induced at the same time.

1
FIGURE 11. Normal Alpha Rhythm and Squeak Eﬀect. An alpha rhythm appears immediately after eye closure and disappears with eye opening. Immediately after eye
closure, alpha frequency may be accelerated for 0.5–1 sec. Therefore, alpha frequency assessment should not be done during this period. This is called the“squeak eﬀect.”1

FIGURE 12. Alpha Rhythm in Subdural EEG. Subdural recording shows the alpha rhythm in the right occipital lobe with reaction to eye opening and eye closure. Harmonic
of the alpha rhythm is frequently seen in an intracranial EEG. In addition, alpha rhythms usually are sharper in morphology because the scalp and skull act as a high-frequency
ﬁlter and pass lower frequencies more eﬃciently than higher frequencies.2
All the normal EEG rhythms seen in the scalp EEG can be seen in the intracranial EEG.3

1
FIGURE 13. Beating (Waxing and Waning of Amplitude). The beating or waxing and waning of the alpha rhythm is the eﬀect of two separate alpha frequencies.

FIGURE 14. Alpha and Mu Rhythm. Eye opening (open arrow) attenuates the alpha rhythm but reveals a prominent mu rhythm (C3 and C4) at the same frequency (11 Hz).
Note lateral eye movement (X) after the eye opening.
Mu is an arc-like central rhythm with negative sharp component and positive slow component. The frequency is similar to alpha rhythm and it is intermixed with 20-Hz beta
activity. It is located at the C3, C4, and Cz electrodes. It is not blocked by eye opening but is attenuated by movement of extremities or thinking about moving with greater eﬀect
on opposite hand. The apiculate phase may resemble spikes.

1
FIGURE 15. Alpha and Mu Rhythm. Eye opening attenuates the alpha rhythm (open arrow), and eye closure accentuates the alpha rhythm. Eye opening or closure does not
aﬀect the mu rhythm (C3 and C4). Mu is an arc-like central rhythm with negative sharp component and positive slow component. The frequency is similar to alpha rhythm and it
is intermixed with 20-Hz beta activity. It is located at C3, C4, and Cz electrodes and is not blocked by eye opening but attenuated by movement of extremities or thinking about
moving with greater eﬀect on opposite hand. The apiculate phase may resemble spikes.

FIGURE 16. Slow Alpha Variant. Slow alpha variant (open arrow) is described as rhythmic sinusoidal, notched theta or delta activities, which have a harmonic relationship
with the alpha rhythm (one-third or, more commonly, one-half the frequency). Slow alpha variant is a rare physiologic variant of alpha rhythm (less than 1% of normal adults)
seen during relaxed wakefulness, has a harmonic relationship and is interspersed with the normal alpha rhythm, and shows similar distribution and reactivity as a normal alpha
rhythm.4, 5
It should not be misinterpreted as occipital intermittent rhythmic delta (OIRDA) or theta activity activities, pathologic ﬁndings seen in children and adults. Slow alpha
variant may be diﬀerentiated from pathologic slow waves by morphology (notched appearance), frequency (subharmonic of normal alpha rhythm), reactivity to eye opening,
and disappearance with sleep. It sometimes mimics RTTD, except that it occurs only over the posterior head regions.

1
FIGURE 17. Slow Alpha Variant. EEG of a 7-year-old boy with recurrent syncope showing semi-rhythmic notched theta activity, a subharmonic of the baseline alpha rhythm
at channels 4, 8, 14, and 18, which appears immediately following the eye blink. Slow alpha variant is a rare, benign EEG variant (less than 1% of normal adults), has a harmonic
relationship with the alpha rhythm, and shows similar distribution and reactivity as a normal alpha rhythm, reactivity to eye opening and eye closure (arrow), and disappearance
with sleep.4
It should not be misinterpreted as occipital intermittent rhythmic delta activity (OIRDA) or theta activity, pathologic ﬁndings seen in children and adults.

FIGURE 18. Fast Alpha Variant. The fast alpha variant pattern (arrow) is a harmonic of the alpha rhythm that has a frequency approximately twice that of alpha rhythm,
usually within the range of 16 to 20 Hz, with a voltage of 20-40 μV. It is usually intermingled with alpha rhythm and shows reactivity and a distribution similar to that of alpha
rhythm.

1
FIGURE 19. Fast Alpha Variant. The fast alpha variant pattern (within the rectangle) is a harmonic of the alpha rhythm that has a frequency approximately twice that of alpha
rhythm, usually in the range of 16 to 20 Hz, with a voltage of 20-40 μV. It is usually intermingled with alpha rhythm and shows reactivity and distribution similar to that of alpha
rhythm.

FIGURE 110. Fast Alpha Variant. The fast alpha variant pattern (box) is a harmonic of the alpha rhythm that has a frequency approximately twice that of alpha rhythm,
usually in the range of 16 to 20 Hz, with a voltage of 20-40 μV. It shows reactivity and a distribution similar to that of alpha rhythm.

1
FIGURE 111. Low-Voltage Background Activity. EEG of a 16-year-old-boy with recurrent syncope. Low-voltage EEG during wakefulness characterized by activity of voltage
≤ 20 μV over all head regions. With higher gain, a wide variety of different frequency waveforms are noted including beta, theta, and, to a lesser degree, delta waves with or
without a posterior alpha rhythm, over the posterior areas.6
Waves of higher amplitude can sometimes be activated by hyperventilation, photic stimulation, and sleep. Low
voltage EEG is a normal EEG variant and does not represent an abnormality unless the frequency band shows abnormal local or diffuse slowing, asymmetries, or paroxysmal
events. The prevalence of low-voltage EEG was 1% between ages 1 and 20 years, 7% between 20 and 39 years, and 11% between 40 and 69 years.7
The prevalence increases
sharply after the age 13.8
Low-voltage EEG in children below age 10 years is considered abnormal if neither hyperventilation nor non-REM sleep changes the low voltage
character. Low voltage EEG can be seen in adults with chronic vertebrobasilar artery insufficiency and chronic alcoholism.9

FIGURE 112. Posterior Slow Waves of Youth. EEG of a 9-year old boy with recurrent headaches and numbness shows bilateral occipital slow waves (Box) intermixed with
and brieﬂy interrupting the alpha rhythm.
“Posterior slow waves of youth”(youth waves or polyphasic waves) are physiologically high-voltage theta or delta waves accompanied by the alpha rhythm and creating
spike wave-like phenomenon. They are most commonly seen in children aged 8 to 14 years but are uncommon in children under 2 years. They have a 15% incidence in healthy
individuals aged 16 to 20 years but are rare in adults after age 21 years. They are typically seen both unilaterally and bilaterally in a single recording. They are always accompanied
by the alpha rhythm, attenuated with eye opening, disappear with the alpha rhythm during drowsiness and light sleep, and may be accentuated by hyperventilation.10–12

1
FIGURE 113. Posterior Slow Waves of Youth; Attenuated with Eye Opening. EEG of a 10-year-old boy with syncope showing occipital slow theta and delta waves (arrows)
mixed with and brieﬂy interrupting the alpha rhythm in both occipital regions but maximally expressed in the left hemisphere. These are so-called“posterior slow waves of youth,”
which are physiologic ﬁndings seen commonly in children aged 8 to 14 years. They are always accompanied by the alpha rhythm, are attenuated with eye opening (open arrow).
and disappear with the alpha rhythm during drowsiness and light sleep.10–12

FIGURE 114. Intermittent Right Occipital Delta Slowing; Simulating Posterior Slow Wave of Youth. An 8-year-old boy with autism and few generalized tonic-clonic
seizures. The 24-hour ambulatory EEG performed to rule out ESES persistently shows decreased alpha reactivity to eye closure (open arrow) and intermittent polymorphic delta
slowing (arrow head) in the right occipital region without shifting lateralization. This EEG can simulate“posterior slow waves of youth,”which is a physiologic ﬁnding. However,
persistent lateralization raises a concern of abnormality in the right posterior quadrant.

1
FIGURE 115. Asymmetric Alpha Rhythm. (same EEG recording as in Fig. 1-14) EEG shows a train of spikes in the right parietal region (open arrow) as well as theta and
polymorphic delta slowing in the right occipital region. Persistent lateralization of theta and delta slowing is a red ﬂag for posterior slow wave of youth and should raise the
concern of focal abnormality in that area.

FIGURE 116. Squeak Eﬀect. EEG of a healthy 10-year-old boy with migraine. Immediately after eye closure, the alpha frequency may be accelerated for 0.5–1 sec; therefore,
alpha frequency assessment should not be done during this period. This is called the“squeak eﬀect.”1

1
FIGURE 117. Lambda Waves. Lambda waves are“sharp transients occurring over the occipital region of the head of waking subjects during visual exploration, mainly positive
relative to other areas and time locked to saccadic eye movement. Amplitude varies, but is generally below 50 μV.”6
Lambda waves do not occur before 1 year of age and are
most common during the middle years of childhood. The prevalence of lambda waves between 3 and 12 years is about 80%. Lambda waves have been described as biphasic or
triphasic; their predominant positive component is preceded and followed by a negative component. They may be asymmetrical on the two sides or may be present only on one
side. Strictly speaking, they are bilaterally synchronous. The most important precipitating factor of lambda waves is voluntary scanning eye movements. Lambda waves usually
occur as random and isolated waveforms but may recur at intervals of 200–500 msec as in this EEG page.9
Sometimes, especially when present unilaterally, they may be mistaken
for focal abnormalities, but the distinction can be made by replacing the geometric image with a blank surface.13

FIGURE 118. Lambda Waves and Alpha Rhythm. Lambda waves (open arrow) are“sharp transients occurring over the occipital region of the head of waking subjects
during visual exploration,”mainly positive relative to other areas and time locked to saccadic eye movement. Amplitude varies, but is generally below 50 μV.6
Lambda waves have
been described as biphasic or triphasic; their predominant positive component is preceded and followed by a negative component. They are most commonly seen in children
aged 2–15 years. They may be asymmetrical, appearing bilaterally, or may be present only on one side. Strictly speaking, they are bilaterally synchronous. The most important
precipitating factor of lambda waves is voluntary scanning eye movements.9
Note alpha rhythm with eye closure (double arrows).

1
FIGURE 119. Lambda Waves. Lambda waves (A) are“sharp transients occurring over the occipital region of the head of waking subjects during visual exploration,”mainly
positive relative to other areas and time locked to saccadic eye movement. Amplitude varies, but is generally below 50 μV.6
Lambda waves have been described as biphasic or
triphasic; their predominant positive component is preceded and followed by a negative component. They are most commonly seen in children aged 2–15 years. They may
be asymmetrical on the two sides or may be present only on one side although are strictly bilateral synchronous. The most important precipitating factor of lambda waves is
voluntary scanning eye movements.9
POSTS (B, sample from the other EEG), also known as“lambdoid waves”are usually monophasic, sharply contoured electropositive waves
seen mainly during light to moderate levels of sleep.

FIGURE 120. Positive Occipital SharpTransients of Sleep (POSTs). EEG of a 4-year-old asymptomatic male during drowsiness. Characteristics of POSTS include
sharply-contoured, surface positive, occurring in trains with a repetitive rate of 4–5 Hz, and monophasic checkmark-like waveform seen singularly or in clusters over the occipital
regions. POSTS are always bilaterally synchronous but are commonly asymmetric on the two sides and should not be misinterpreted as epileptiform activity or focal nonepileptiform
activity.10,14
POSTS occur during drowsiness and stage 2 sleep.

1
FIGURE 121. Positive Occipital SharpTransients of Sleep (POSTs). EEG of a 3-year-old asymptomatic male during stage 2 sleep. Characteristics of POSTS are sharp-contoured,
surface positivity, occurring in trains with a repetitive rate of 4–5 Hz, and monophasic checkmark-like waveform seen in singly or in clusters over the occipital regions. POSTS are
always bilaterally synchronous but are commonly asymmetric on the two sides and should not be misinterpreted as epileptiform activity or focal nonepileptiform activity.10,14
POSTS occur during, drowsiness and stage 2 sleep.

FIGURE 122. Posterior Occipital Sharp Transients of Sleep (POSTS). POSTS (Box) can simulate epileptiform activity. Their triangular morphology, persistent lack of slow
wave following sharp transients, positive polarity, constant symmetry, and occurrence during sleep diﬀerentiate them from epileptiform activity.

1
FIGURE 123. Aymmetric Posterior Occipital Sharp Transient of Sleep (POSTS). A 7-year-old boy with recurring staring episodes and behavioral issues. The routine
EEG during sleep shows bilaterally synchronous but asymmetric POSTS. Characteristics of POSTS are surface positivity, occurring in trains with a repetitive rate of 4–5 Hz, and
monophasic checkmark-like waveforms. POSTS are always bilaterally synchronous but are commonly asymmetrical on the two sides and should not be misinterpreted as
epileptiform activity or focal nonepileptiform activity.10

FIGURE 124. Pathologically Asymmetry of Positive Occipital Sharp Transients of Sleep (POSTS). A 7-year-old girl born 24 weeks gestational age with grade 4
intraventricular hemorrhage (IVH). Subsequently, she developed spastic quadriparesis and global developmental delay. Cranial MRI showed periventricular leukomalacia with
bilateral white matter involvement, greater on the left. Prolonged 72-h-video-EEG demonstrates persistent suppression of POSTS and anterior beta activity in the left hemisphere
throughout the drowsy and sleep EEG recording. Although persistent asymmetric POSTS in this case are pathologic, physiologic POSTS can be quite asymmetric and may be
present on only one side in the routine EEG. Therefore, asymmetric POSTS without other associated abnormalities should not be misinterpreted as abnormal.

1
FIGURE 125. Posterior Slow-Wave Transients (Occipital Sharp Transients); Associated with Eye Movements. Posterior slow-wave transients associated with eye
movements is an EEG pattern consisting of a monophasic or biphasic slow transient with a duration of 200–400 msec and a voltage of up to 200 μV in the occipital regions (*).
The latency of 100–500 msec is noted after the eyeblinks or eye movements. The initial component of the transient is surface positive. The ascending phase is steeper than the
descending phase. This EEG pattern is seen in children age 6 months to 10 years, but seen most commonly in children aged 2–3 years. This EEG pattern is a normal phenomenon
but may be misinterpreted as epileptiform activity.9,10

movements is an EEG pattern consisting of a monophasic or biphasic slow transient with a duration of 200–400 msec and a voltage of up to 200 μV in the occipital regions
(open arrow). The latency of 100–500 msec is noted after the eyeblinks or eye movements. The initial component of the transient is surface positive. The ascending phase is
steeper than the descending phase. This EEG pattern is seen in children age 6 months to 10 years, but seen most commonly in children aged 2–3 years. This EEG pattern is a
normal phenomenon but may be misinterpreted as epileptiform activity.9,10

1
descending phase. This EEG pattern is seen in children age 6 months to 10 years, but seen most commonly in children aged 2–3 years. This EEG pattern is a normal phenomenon

descending phase. This EEG pattern is seen in children aged 6 months to 10 years, but seen most commonly in children aged 2–3 years. This EEG pattern is a normal phenomenon

1
FIGURE 129. Occipital Slow Transients; Cone Wave and Diphasic Slow Transient. In children, the transition from light to deep sleep may be associated with bilateral
high-voltage slow transients in the occipital regions. These waves vary from a cone-shaped conﬁguration (double arrows) to a biphasic slow transient (open arrow). These
transients occur every 3–6 sec during light sleep and more frequently during deeper stage of sleep.10

FIGURE 130. Occipital Slow Transients; Cone Waves. In children, the transition from light to deep sleep may be associated with bilateral high-voltage slow transients in the
occipital regions. These waves vary from a cone-shaped conﬁguration to a biphasic slow transient. These transients occur every 3–6 sec during light sleep and more frequently
during deeper stages of sleep.10
Cone waves or“O”waves (arrow) are physiologic waves presenting during non-REM sleep from infancy until 5 years of age. They are isolated,
medium- to high-amplitude, monomorphic, triangular shaped, delta waves with a typical duration greater than 250 msec that occur over the occipital region.15

1
FIGURE 131. Occipital Slow Transients; Cone Wave. In children, the transition from light to deep sleep may be associated with bilateral high-voltage slow transients in the
occipital regions. These waves vary from a cone-shaped conﬁguration to a biphasic slow transient. These transients occur every 3–6 sec during light sleep and more frequently
during deeper stage of sleep.10
Cone waves or“O”waves (arrow) are physiologic waves presenting during non-REM sleep from infancy until 5 years of age. They are isolated,
medium- to high-amplitude, monomorphic, triangular shaped, delta waves with a typical duration greater than 250 msec that occur over the occipital region.15

FIGURE 132. Excessive Photic Response at High Frequency Stimulation (H Response); Migraine. A 17-year-old with recurrent headaches after the epilepsy surgery
(resection of epileptogenic zone in the right frontal region). The patient had headache characteristics compatible with the common migraine, normal neurologic examination,
and a strong family history of migraines. His headaches resolved with amitryptylline. The neuroimaging was not performed. This EEG was performed as a routine postoperative
follow-up. The“H-response”is a prominent photic driving response at flash rates beyond 20 Hz. The sensitivity of the H-response varied from 25% to 100%, and the specificity
from 80% to 91%. Although the relatively high sensitivities and specificities of the H-response in distinguishing migraine patients from controls and tension headache patients,
the American Academy of Neurology concluded that the H-response was not more effective than history and examination in diagnosing headaches. They, therefore, did not
recommend its use in clinical practice. However, in the presence of complex or prolonged aura, visual hallucinations, disorders of consciousness, history of recent trauma, and
in infants with vomiting and ocular and head deviation, the EEG may be useful for clinical diagnosis and help to monitor therapeutic response.16,17

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FIGURE 133. Excessive Photic Response at High Frequency Stimulation (H Response) Migraine. The“H-response”is a prominent photic driving response at flash
rates beyond 20 Hz. In a critical review of the literature, the reported sensitivity of the H-response varied from 25% to 100%, and the specificity from 80% to 91%. Although the
relatively high sensitivities and specificities reported suggest that the H-response may be effective in distinguishing migraine patients from controls, and possibly migraineurs
from tension headache sufferers, the Quality Standards Subcommittee (QSS) of the American Academy of Neurology concluded that the H-response was not more effective than
the neurological history and examination in diagnosing headaches and not recommended in clinical practice. However, in the presence of complex or prolonged aura, visual
hallucinations, disorders of consciousness, history of recent trauma, and in infants with vomiting and ocular and head deviation, the EEG may be useful for clinical diagnosis and
help to monitor therapeutic response.16,17

FIGURE 134. Cyclic Vomiting; Migraine; Excessive Photic Response. A 2-year-old boy with cyclic vomiting who had normal extensive GI work-up. Cranial MRI was normal.
EEG shows excessive photic response intermixed with sharply-contoured waves. Very strong family history of migraines was noted. The patient was diagnosed with“cyclic
vomiting”caused by migraine. He showed dramatic improvement in vomiting after the treatment with cyproheptadine.
Photic driving responses in children <6 years are relatively small.18
Stimulus frequencies <3 Hz rarely produce a response. The maximal responses are obtained with stimulus
frequencies near the frequency of individual’s posterior dominant rhythm.15
Although excessive photic response can be seen in normal individuals, it is more commonly seen in
migraine patients. However, AAN concluded that the photic response was not more eﬀective than history and examination in diagnosing headaches and did not recommend its
use in clinical practice.16
In 2–4% of normal children, posteriorly predominant paroxysmal slow activity is sometimes associated with sharp components.11

1
FIGURE 135. Needle-Like Occipital Spikes of the Blind. A 4-year-old girl with congenital blindness due to congenital CMV infection who developed acute encephalopathy
due to enteroviral infection (hand-foot-mouth syndrome). This EEG was requested for altered mental status. EEG demonstrates diffuse delta slowing with occipital predominance
and frequent needle-like spikes in the occipital region. The patient regained her mental status completely 4 days later without treatment with anticonvulsant.
Needle-like spikes (*) develop in the occipital region in most patients with congenital blindness. Functional deafferentation of the visual cortex gives rise to an increase in its
irritability and this makes it fire off in this special manner. These spikes are not correlated with epileptic seizures. These discharges disappear during childhood or adolescence.19

FIGURE 136. Needle-Like Occipital Spikes of the Blind. A 7-month-old girl with congenital blindness due to septo-optic dysplasia and with pendular nystagmus.
This EEG was requested to evaluate for possible seizure as a cause of nystagmus. EEG demonstrates frequent low-amplitude and short-duration spikes in the occipital regions
(open arrows).
Needle-like spikes develop in the occipital region in most patients with congenital blindness. Functional deafferentations of the visual cortex give rise to an increase in its
irritability that make it fire off in this special manner. These spikes are not correlated with epileptic seizures. These discharges disappear during childhood or adolescence.19

1
FIGURE 137. Needle-Like Spikes of the Blind. A 25-month-old girl with congenital blindness and epilepsy due to congenital toxoplasmosis who has pendular nystagmus.
This EEG was requested to evaluate for epileptiform activity as a cause of her nystagmus. EEG demonstrates frequent low-amplitude and short-duration spikes in the occipital
regions (*).
Needle-like spikes develop in the occipital region in most patients with congenital blindness. Functional deafferentation of the visual cortex gives rise to an increase in its
irritability, which makes it fire off in this special manner. These spikes are not correlated with epileptic seizures. These discharges disappear during childhood or adolescence.19

FIGURE 138. Drowsiness; Older Children and Adults. In older children and adults, early drowsiness is associated with (1) alpha dropout (earliest sign); (2) increased beta
activity over the fronto-central regions; (3) diﬀuse rhythmic theta activity with anterior predominance; and (4) slow eye movement. Mu rhythm, wicket wave and 14- and 6 Hz
positive spikes can be seen during drowsiness. Drowsiness must be diﬀerentiated from increased alertness after eye opening or caused by emotional stress that can cause alpha
blocking. In such cases the slow frequency component is absent and beta frequency predominates. Deep drowsiness is marked by the appearance of vertex waves and POSTS
that persist during light sleep and deep sleep.20

1
FIGURE 139. Drowsiness; 14-and-6 Hertz Positive Bursts. In older children and adults, early drowsiness is associated with (1) alpha dropout (earliest sign); (2) increased
beta activity over the fronto-central regions (double arrows); (3) diﬀuse rhythmic theta activity with anterior predominance (open arrow); and (4) slow eye movement (double-
head arrow). Mu rhythm, wicket wave and 14- and 6 Hz positive spikes (*) can be seen during drowsiness. Drowsiness must be diﬀerentiated from increased alertness after eye
opening or caused by emotional stress that can cause alpha blocking. In such case slow frequency component is absent and beta frequency predominates. Deep drowsiness is
marked by the appearance of vertex waves and POSTS that persist during light sleep and deep sleep.20

FIGURE 140. Stage 2 (Light Sleep). Stage 2 sleep shows symmetric, synchronous theta rhythms with posterior predominance, 12–15/sec spindles, vertex sharp waves,
K-complex and POSTS. The appearance of sleep spindles in the 12–15/sec range is a hallmark of sleep onset.20

1
FIGURE 141. Sleep Spindles During Subdural EEG Recording. Subdural recording showing the sleep spindles in the parietal lobe during sleep. A harmonic of the sleep
spindles is more frequently seen in intracranial EEG. In addition, the sleep spindles usually appear sharper in morphology as the scalp and skull act as a high-frequency filter and
pass lower frequencies more efficiently than higher frequencies.2
Disappearance during wakefulness helps to differentiate the sleep spindles from low-voltage fast activity. All
normal EEG rhythms seen in the scalp EEG can be seen in the intracranial EEG.3

FIGURE 142. Stage 3 (Moderate Deep Sleep). Delta frequencies in the 0.75–3/sec range are prominent over the anterior regions. Sleep spindles in the 10–12/sec and even
in the 12–14/sec ranges are still present but gradually become less prominent. Rhythmic activity of 5–9/sec is common. Rhythmic and symmetrical delta activity occurs during
20% to 50% of the recording.20

1
FIGURE 143. Stage 4 (Very Deep Sleep). Over 50% of the recording is delta rhythm. Spindles are rare. Arousal at this stage can be correlated with sleep disorders
(somnambulism, nocturnal terror, or enuresis), and can cause confusion. Occasionally, spikes in temporal lobe epilepsy will only appear in stage 3 and 4 sleep.20

FIGURE 144. REM Sleep. EEG reveals low-voltage activity, polyrhythmic waves, slower alpha waves, and short bursts of“saw-tooth waves”over the frontal or vertex leads
(Box B), and quick lateral eye movement (Box A). Appearance of REM sleep in routine EEG is seen in narcolepsy and in patients who are withdrawn from CNS depressants such
as alcohol or phenobarbital.20,21

1
FIGURE 145. K Complexes. K complexes contain 3 components including sharp, slow, and fast. They are seen in stage 2 sleep and arousal. The K complexes are largest in
older children and adolescence. With increasing age, the K complexes show the decreasing voltage with tiny superimposed spindle-like waves.

FIGURE 146. Subdural EEG Monitoring; K-Complex During Arousal. Subdural recording showing a run of vertex waves and widely distributed K-complexes, maximally
expressed in the parietal lobe during arousal. Harmonic of the sleep spindles is frequently seen in intracranial EEGs. In addition, the sleep spindles usually are sharper in
morphology as the scalp and skull act as a high-frequency filter and pass lower frequencies more efficiently than higher frequencies.2
Disappearance during wakefulness
helps to differentiate the K-complexes from low-voltage fast activity.
All normal EEG rhythms in the scalp EEG can be seen in the intracranial EEG.3

1
FIGURE 147. Pathologic vs Physiologic Wave Forms in Intracranial EEG. The differentiation of physiologic waveforms and pathologic waveforms is extremely important
in intracranial EEG recording (open arrow-epileptiform in depth electrode; arrow-sleep spindles; double arrows-vertex waves). Harmonic and sharp morphology of the physiologic
waveforms in an intracranial EEG make distinguishing between nonepileptiform and epileptiform activities more difficult. Disappearance of spindles and vertex waves during
wakefulness, distribution, and morphology help to differentiate them from epileptiform activity, especially between sleep spindles and low-voltage fast epileptiform activity.

FIGURE 148. Early K-Complex (16 Week CA). K-complex ﬁrst appears at 4 months of age. They have high amplitude but their rise is not as abrupt and the conﬁguration is
not as sharp as one seen in older children.20

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FIGURE 149. Normal Sleep Spindles (2 Months); Definite 14/sec Spindles. Sleep spindles arise from synchronized activity in functionally important neuronal networks
linking the thalamus and the cortex. Spindles result from rhythmic spike bursts in inhibitory (GABAergic) thalamic reticular neurons that induce rhythmic rebound bursting in
cortical neurons. This process has been shown to result in effective deafferentiation of the cerebral cortex. Cortical neurons show enhanced responsiveness and properties of
synaptic plasticity that may have a role in memory and learning processes.22
At 1.5 to 2 months, 14/sec spindles are first seen.23

FIGURE 150. Normal Sleep Spindles (8 Weeks CA); Harmonic of Sleep Spindles. EEG of an 8-week-old full-term boy shows low-voltage 22–24 Hz biphasic beta activity
diﬀusely in the central vertex and bilateral central-parietal areas. This exceptional waveform most likely represents a harmonic of sleep spindles. More commonly spindles occur
independently from faster 18–25 Hz activity and both patterns may be seen at the same time.24

1
FIGURE 151. Normal Sleep Spindles (10 Weeks CA). Trace alternant disappears in the ﬁrst month of life. Sleep spindles usually appear in the second months of life with
frequency between 12 and 15/sec. Throughout infancy, they are maximal over the central and parietal areas with shifting asymmetry. They usually are electronegative with a
rounded positive component.20
A complete absence of spindles at age 3–8 months indicates a severe abnormality.25

FIGURE 152. Normal Sleep Spindles (3-6 Months CA); Prolonged Runs of Spindles. Between the ages of 3–6 months, sleep spindles appear to be biphasic and occur as
prolonged runs, up to 10–15 sec.22,23,26
The prolonged run of spindles is a very useful developmental marker and is rarely seen beyond this age range.

1
FIGURE 153. Prolonged Sleep Spindles (3-6 Months CA). Between the ages of 3–6 months, sleep spindles appear to be biphasic and occur as prolonged runs,
up to 10–15 sec.22,23,26
The prolonged run of spindles is a very useful developmental marker and is rarely seen beyond this age range.

FIGURE 154. Prolonged Sleep Spindles (3-6 Months CA). Between the ages of 3–6 months, sleep spindles appear to be biphasic and occur as prolonged runs, up to
10–15 sec.22,23,26
The prolonged run of spindles is a very useful developmental marker and rarely seen beyond this age range.

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FIGURE 155. Normal Sleep Spindles (16 Weeks CA). Between the ages of 3–6 months, sleep spindles appear to be biphasic and as prolonged runs, up to 10–15 sec.22,23,26
The prolonged run of spindles is a very useful developmental marker and rarely seen beyond this age range. Throughout infancy, sleep spindles are maximal over the central
and parietal areas with shifting asymmetry. They usually shows electronegative with rounded positive component that is a typical hallmark of sleep spindles in infancy.20,27
These surface-negative spindles with wicket or comb-like shape can be erroneously interpreted as 14/sec positive spikes (below).

FIGURE 156. Sleep Spindles with Subharmonic. Subharmonic of sleep spindles with a frequency approximately half that of sleep spindles with a notched appearance can
be seen. The subharmonic has the same reaction and distribution as sleep spindles.

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FIGURE 157. Normal Sleep Spindles (9 Months); Asynchronous Spindles. In the second half of the ﬁrst year of life, the spindles appear to be monophasic and are
often asynchronous between the two sides. Asynchronous spindles may occasionally continue from 1 to 2 years of age but rarely are seen after the age of 2 years when
interhemispheric synchrony of the spindles are.22,23

FIGURE 158. Normal Sleep Spindles (14 Months); Synchronous Spindles. After 1 year, interhemispheric synchrony of the spindles is seen although not constant until
the infant is nearly 2 years old. The frequency of spindles also changes, with 12/sec components becoming more prominent.22

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FIGURE 159. Mitten Pattern. Mitten patterns are seen during sleep and consist of a sharply-contoured waveform on the slope of a slow wave of the same polarity that
resemble a mitten, with the thumb of the mitten formed by the last wave of a spindle and the hand portion by the slower wave component. Mittens are a variant of a vertex
wave or K-complex and should not be mistaken for a spike-and-wave discharge.14
It is best seen in the referential montage and in stage 3 sleep.20

FIGURE 160. Mitten Pattern. Mitten patterns are seen during sleep and consist of a sharply-contoured waveform on the slope of a slow wave of the same polarity that
resemble a mitten, with the thumb of the mitten formed by the last wave of a spindle and the hand portion by the slower wave component. Mittens are a variant of a vertex
wave or K-complex and should not be mistaken for a spike-and-wave discharge.14

1
FIGURE 161. Mittens. Mitten patterns are seen during sleep and consist of a sharp-contoured waveform on the slope of a slow wave of the same polarity that resemble a
mitten, with a thumb of mitten formed by the last wave of a spindle and the hand portion by the slower wave component. Mittens are a variant of a vertex wave or K-complex
and should not be mistaken for a spike-and-wave discharge.14
It is best seen in referential montage and stage 3 sleep.20

FIGURE 162. Mittens. Mitten patterns are seen during sleep and consist of a sharply-contoured waveform on the slope of a slow wave of the same polarity that resemble
a mitten, with the thumb of the mitten formed by the last wave of a spindle and the hand portion by the slower wave component. Mittens are a variant of a vertex wave or
K-complex and should not be mistaken for a spike-and-wave discharge.14

1
FIGURE 163. Hypnagogic Hypersynchrony. Hypnagogic hypersynchrony is an activity seen in early drowsiness and in arousal from deeper sleep. It is characterized by
bilateral synchronous, high voltage, rhythmic 3-5 Hz activity. This activity ﬁrst appears at the age of 2 to 3 months and becomes prominent and continuous at 9 months. At age
4 years, it becomes shorter in duration and more paroxysmal in appearance. By age 9 to 11 years, it becomes rare. Although the presence of hypnagogic hypersynchrony at age
12 years is considered abnormal by some authors,21
it may be seen in normal children up to the age of 12-13 years.10
The frequency of hypnagogic hypersynchrony is 3-4 Hz at
the age of 2-3 months and increases to 4-5 Hz in older children. This EEG also shows slow eye movement (SEM), maximally seen at F7 and F8, which is also one of the signs of
drowsiness.

FIGURE 164. Hypnagogic Hypersynchrony. Nearly continuous hypnagogic hypersynchrony in a 22-month-old infant. Hypnagogic hypersynchrony appears at
approximately 3 months of age and is characterized by monorhythmic, slow generalized activity with the frequency of 3-4 Hz during drowsiness. It may be seen in older
children up to 12-13 years but is rare after 11 years (incidence of only 10%). The frequency increases to 4-5 Hz in older children.10

1
FIGURE 165. Asymmetric Hypnagogic Hypersynchrony. EEG of a 25-month-old boy with asymmetric hypnagogic hypersynchrony with shifting predominance. The
paroxysmal bursts of generalized high-voltage, rhythmically monotonous theta activity superimposed on low-voltage background activity, so-called“hypnagogic hypersynchrony,”
is the hallmark of drowsiness in early childhood. Occasionally, small sharp or spiky discharges may be interspersed between the theta waves. These discharges should not be
interpreted as epileptiform activity unless they are deﬁnitely distinct from background activity and not only occur during drowsiness or at the onset of sleep but also persist into
deeper stages of sleep. Asymmetric hypnagogic hypersynchrony with shifting predominance can be seen and is not considered abnormal.10,11,28,29

FIGURE 166. Hypnagogic Hypersynchrony. EEG of a 4-year-old boy with hypnagogic hypersynchrony. The paroxysmal bursts of generalized high-voltage, rhythmically
monotonous theta activity superimposed on low-voltage background activity, so-called“hypnagogic hypersynchrony”is the hallmark of drowsiness in early childhood.
Occasionally, small sharp or spiky discharges may be interspersed between the theta waves. These discharges should not be interpreted as epileptiform activity unless they
are deﬁnitely distinct from background activity and not only occur during drowsiness or at the onset of sleep but also persist into deeper stages of sleep.

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FIGURE 167. Hypnic Myoclonia (HM) (Sleep Starts or Hypnogogic Jerks). Video-EEG of a 5-year-old boy with well-controlled focal epilepsy shows a burst of high-voltage
3–4 Hz delta activity intermixed with low-amplitude spikes during chin quivering (*). This EEG pattern is compatible with hypnagogic hypersynchrony associated with HM.
This wake-to-sleep transition event is characterized by a sudden, single, brief muscular contraction of the legs and occasionally the arms, head, and postural muscles.30
Hypnagogic hallucinations often occur before the sleep starts, and the perception of falling may occur, ending with the myoclonic jerk. HM is a physiologic ﬁnding unless it is
frequent and results in sleep-onset insomnia. It also must be diﬀerentiated from seizure, especially if it occurs in patients with known epilepsy.31,32
HM occurs in 60–79% of normal
individuals. Ninety percent of patients stop these movements by age 4 years. It is more common in boys than in girls by 4:1.33
It may be frightening when observed by a parent,
especially if associated with a vocalization or cry. Injury from the massive movement is rare, but foot injuries secondary to kicking a bedpost or crib rail may occur.34

FIGURE 168. 14-and-6-Hertz Positive Spikes; Hypnagogic Hypersynchrony. EEG of a 5-year-old asymptomatic boy shows 14- and 6 Hz positive spikes (arrow head)
immediately after hypnagogic hypersynchrony (open arrow). Fourteen and six hertz positive spikes (arrow head) are commonly seen during drowsiness.35

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FIGURE 169. Asymptomatic Centro-Temporal Spikes; Hypnagogic Hypersynchrony. An 8-year-old boy with recurrent syncope without other associated symptoms
suspicious of seizures or other neurologic conditions except borderline ADHD. There was a history of GTCS in his 4-year-old brother. EEG during drowsiness shows hypnagogic
hypersynchrony and bilateral-independent centro-temporal spikes. Characteristic spikes over the rolandic area are regarded as neurobiological markers of BECTS. However,
rolandic (centro-temporal) spikes have been reported in normal children without clinical seizures or neurologic manifestations. They are seen in 1.2–3.5% of normal healthy
children in the community36,37
and 6–34% of siblings of patients aﬀected by BECTS.38,39
The risk of epilepsy is higher if rolandic spikes remain unilateral during sleep, rolandic
spikes continue during REM sleep, and if they occur in the presence of generalized spike-wave discharges.40
The frequency of rolandic spikes in children with ADHD (3–5.6%)
is signiﬁcantly higher than expected from epidemiologic studies although how ADHD symptoms are related to rolandic spikes is still unclear.41–44

FIGURE 170. Hypnic Myoclonia; Hypnagogic Hypersynchrony. Video-EEG of a 5-year-old boy with well-controlled focal epilepsy shows a burst of high-voltage 4 Hz delta
activity intermixed with low-amplitude spike-like during right arm jerks (arrow).This EEG pattern is compatible with hypnagogic hypersynchrony and the right arm jerking is most
likely to be hypnic myoclonia. Sleep starts (hypnic myoclonia) also have been termed“hypnagogic jerks”.This wake-to-sleep transition event is characterized by a sudden, single, brief
muscular contraction of the legs and occasionally the arms, head, and postural muscles.30
Sensory hallucinations (hypnagogic hallucinations) often occur before the sleep start, and
the subjective perception of falling may occur, ending with the myoclonic jerk. Sleep starts are common, occur in most individuals, and are not pathologic unless they are frequent and
result in sleep-onset insomnia.They also must be diﬀerentiated from seizure, especially if they occur in patients with known epilepsy.31
Hypnic myoclonia occurs in 60–79% of normal
individuals. Although it may occur at any age, 90% of patients stop these movements by age 4 years.They are more common in boys than girls by 4:1.33
It may be frightening when
observed by a parent, especially if associated with a vocalization or cry. Injury from the massive movement is rare, but foot injuries secondary to kicking a bedpost or crib rail may occur.34

1
FIGURE 171. Midline Theta Rhythm (Ciganek Rhythm). The midline theta rhythm is a rhythmic train of 5–7 Hz theta activity occurring in the central vertex but may also
be seen in the frontal vertex. The morphology includes sinusoidal, aciform, spiky, or mu-like appearance. The midline theta rhythm is seen during wakefulness and drowsiness
and shows variable reactivity to eye opening, alerting, and limb movement. The rhythm usually lasts from 3 to 20 sec and does not evolve. It is a nonspecific finding of no clinical
significance.35,45

FIGURE 172. Frontal Arousal Rhythm (FAR). Frontal arousal rhythm (FAR) is a rare EEG rhythm, seen in the frontal regions during arousal from sleep in children. The FAR is
characterized by 30–150 μV, predominantly monophasic negative waves, occurring in bursts or runs lasting up to 13 sec (usually 1–5 sec) with a characteristic notching of the
ascending or descending phase of each wave. The notched appearance may represent harmonics of the waveforms. The waxing and waning of the amplitude often leads to a
spindle-like morphology. The FAR appears at the F3 and F4 electrodes with minimal spread to nearby scalp areas.46
The incidence of the FAR in a normal population is unknown.
Although it was first reported in children with minimal cerebral dysfunction or a seizure disorder, it is later considered to be a nonspecific EEG pattern of no clinical significance.35

1
FIGURE 173. Frontal Arousal Rhythm (FAR). EEG of an 8-year-old girl with idiopathic generalized epilepsy. Frontal arousal rhythm (FAR) is a rare EEG rhythm, seen in the
frontal regions during arousal from sleep in children between ages 2 and 12 years, mainly 2 and 4 years. The FAR is characterized by 30–150 μV predominantly monophasic
negative waves, occurring in bursts or runs lasting up to 13 sec (usually 1–5 sec), maximally over the frontal midline, with a characteristic notching of the ascending or descending
phase of each wave. The notched appearance may represent harmonics of the waveforms. Waxing and waning of the amplitude often leads to a spindle-like morphology. The FAR
appears at the F3 and F4 electrodes with minimal spread to nearby scalp areas.46
The incidence of the FAR in the normal population is unknown. Although it was first reported in
children with minimal cerebral dysfunction or a seizure disorder, it is now considered to be a nonspecific EEG pattern of no clinical significance.35

FIGURE 174. Frontal Arousal Rhythm (FAR). An 8-year-old girl with a history of GTCS. EEG demonstrates trains of rhythmic 6-Hz sharp waves in bifrontal regions during
arousal state.
Frontal arousal rhythm (FAR) is a rare EEG rhythm, seen in the frontal regions during arousal from sleep in children. The FAR is characterized by 30–150 μV, predominantly
monophasic negative waves, occurring in bursts or runs lasting up to 13 sec (usually 1–5 sec) with a characteristic notching of the ascending or descending phase of each wave. The
notched appearance may represent harmonics of the waveforms. The waxing and waning of the amplitude often leads to a spindle-like morphology. The FAR appears at the F 3 and
F 4 electrodes with minimal spread to nearby scalp areas.46
The incidence of the FAR in a normal population is unknown. Although it was first reported in children with minimal
cerebral dysfunction or a seizure disorder, it is now considered to be a nonspecific EEG pattern of no clinical significance.35

1
FIGURE 175. Frontal Arousal Rhythm (FAR). EEG of a 10-year-old boy with idiopathic generalized epilepsy. Frontal arousal rhythm (FAR) is a rare EEG rhythm, seen in the
frontal regions during arousal from sleep in children between ages 2 and 12 years, mainly 2 and 4 years. The FAR is characterized by 30–150 μV predominantly monophasic
negative waves, occurring in bursts or runs lasting up to 13 sec (usually 1–5 sec), maximally over the frontal midline, with a characteristic notching of the ascending or descending
phase of each wave. The notched appearance may represent harmonics of the waveforms. Waxing and waning of the amplitude often leads to a spindle-like morphology. The FAR
appears at the F3 and F4 electrodes with minimal spread to nearby scalp areas.46
The incidence of the FAR in a normal population is unknown. Although it was first reported in
children with minimal cerebral dysfunction or a seizure disorder, it is now considered to be a nonspecific EEG pattern of no clinical significance.35

FIGURE 176. Frontal Arousal Rhythm (FAR). EEG of a 6-year-old boy with frontal lobe epilepsy during arousal from sleep. Frontal arousal rhythm (FAR) is a rare EEG rhythm,
seen in the frontal regions during arousal from sleep in children between ages 2 and 12 years, mainly 2 and 4 years. The FAR is characterized by 30–150 μV predominantly
monophasic negative waves, occurring in bursts or runs lasting up to 13 sec (usually 1–5 sec), maximally over the frontal midline, with a characteristic notching of the ascending
or descending phase of each wave. The notched appearance may represent harmonics of the waveforms. Waxing and waning of the amplitude often leads to a spindle-like
morphology. The FAR appears at the F3 and F4 electrodes with minimal spread to nearby scalp areas.46
The incidence of the FAR in a normal population is unknown. Although it
was first reported in children with minimal cerebral dysfunction or a seizure disorder, it is now considered to be a nonspecific EEG pattern of no clinical significance.35
Its mildly abnormal character is likely, but its clinical significance was thought to be debatable.47
Hughes found 70% of patients having epileptic seizures and demonstrated
a case in which FAR representing ictal electrographic seizure activity.48

1
FIGURE 177. Rhythmic Temporal Theta Bursts of Drowsiness (RTTD); Rhythmic Midtemporal Discharges (RMTD); (Psychomotor Variant). RTTD is seen in 0.5–2.0%
of normal adult population and less common in adolescence. It is described as bursts or runs of rhythmic, 5–7 Hz (typically 5–5.5 Hz), theta activity with flat-topped, sharply
contoured, often notched appearance in the temporal regions, maximally expressed in the midanterior temporal electrode. The sharper component of the wave usually has a
negative polarity in the anterior temporal region. It can occur unilaterally, bilaterally, or shifting from side to side with gradual onset and offset. The pattern is distinguished from
ictal epileptiform activity because it is monomorphic and monorhythmic (no evolution into other frequencies), does not alter background activity, occurs in relaxed wakefulness
and drowsiness (most common), and disappears in deeper levels of sleep. This pattern has no clinical significance35
. However, it was considered by some authors to be a
pathologic finding in selected cases.49
This pattern was previously called“psychomotor variant.”50,51
They are also now called“rhythmic midtemporal discharges (RMTDs).”52,53

FIGURE 178. Rhythmic Temporal Theta Bursts of Drowsiness (RTTD). A 15-year-old girl with recurrent passing out episodes. EEG during drowsiness shows rhythmic
5-6 Hz, theta activity with flat-topped, sharply contoured over the temporal regions with a phase reversal in the posterior temporal electrodes.
Rhythmic temporal theta waves of drowsiness (RTTD) is also called rhythmic midtemporal discharges (RMTDs) or psychomotor variant. RTTD is seen in adult and, less
commonly, in adolescent. This EEG pattern is distinguished from ictal epileptiform activity in that it is monomorphic and monorhythmic (no evolution), does not affect
background activity, and occurs in only in relaxed wakefulness and drowsiness. This EEG pattern is of uncertain significant 35.

1
FIGURE 179. Rhythmic Temporal Theta Bursts of Drowsiness (RTTD). A 16-year-old girl with recurrent vertigo who had been diagnosed with simple partial seizures
and was treated with carbamazepine. The treatment failed to stop the symptoms and caused side eﬀects. Brain MRI was unremarkable. EEGs were performed four times in
the past and were interpreted as epileptiform activity in the temporal regions. This EEG during drowsiness shows a burst of rhythmical 5.5 Hz theta activity in the left temporal
region (open arrow) with negative polarity of the sharper component of the burst in the midtemporal region. Note no disruption of alpha rhythm in the left occipital region
(arrow heads). The patient was completely normal throughout the discharge. This EEG pattern is compatible with RTTD and is considered a normal variant and has no clinical
signiﬁcance. The patient has done well since stopping carbamazepine.

FIGURE 180. Rhythmic Temporal Theta Bursts of Drowsiness (RTTD). A 17-year-old boy with recurrent headache and numbness of his right arm. EEG during resting
wakefulness shows bilateral-independent 5.5 Hz theta activity in the temporal regions in the 2 hemispheres. As the discharge proceeds, the morphology does not change
(monomorphic and monorhythmic). The discharge continues during drowsiness but disappears in stage 2 sleep. These diﬀerentiate the RTTD from focal ictal activity.

1
FIGURE 181. RhythmicTemporalTheta Bursts of Drowsiness (RTTD). A 17-year-old boy with a new-onset GTCS. EEG during drowsiness shows runs of bilateral-independent
5.5 Hz sharply-contoured theta activity in the midtemporal regions in the two hemispheres. As the discharge proceeds, the morphology does not change (monomorphic and
monorhythmic). The discharge continues during drowsiness but disappears in stage 2 sleep. These ﬁndings diﬀerentiate the RTTD from focal ictal activity.

FIGURE 182. Rhythmic Temporal Theta Bursts of Drowsiness (RTTD). EEG during drowsiness shows long runs of monomorphic and monorhythmic notched theta activity
that does not evolve into other frequencies or waveforms (same EEG tracing as in Figure 1-81). The patient was completely normal throughout the run of discharge. The discharge
disappears during deeper states of sleep. These ﬁndings diﬀerentiate RTTD from an electrographic seizure. Note an unusual morphology of the discharge that shows positive
polarity in the posterior temporal areas.

1
FIGURE 183. 14 and 6/sec Positive Spike Discharge. This EEG pattern is defined as bursts of arch shaped waves at 13–17 Hz and/or 5–7 Hz, most commonly at 14 and/or 6 Hz,
seen generally over the posterior temporal and adjacent areas of one or both sides of the head during deep drowsiness and very light sleep. The sharp peaks of its components are
electropositive compared to other regions. The bursts have a widespread field and last for 0.5–1 sec. This EEG pattern occurs in children from the age of 3 up to young adulthood but
more commonly occur between 12 and 20 years with a peak at age 13–14 years. It is best displayed in the contralateral ear reference montage. 14 and 6/sec positive spike discharge
is a benign variant of no clinical significance.6,54

FIGURE 184. 14 and 6/sec Positive Spike Discharge. Fourteen and six per second positive spike discharge shows mainly 13 Hz positive spikes (same EEG recording as in
Figure 1-83).

1
FIGURE 185. 14 and 6/sec Positive Spike Discharges; (Anterior-Posterior Bipolar). This EEG pattern is deﬁned as bursts of arch shaped waves at 13–17 Hz and/or 5–7 Hz,
most commonly at 14 and/or 6 Hz, seen generally over the posterior temporal and adjacent areas of one or both sides of the head during deep drowsiness and very light sleep
(arrow). The sharp peaks of its components are positive with respect to other regions. This pattern occurs in the children after age 3 to young adult with a peak at age 13–14 years.
This pattern is a benign variant of no clinical signiﬁcance.6,54

FIGURE 186. 14 and 6/sec Positive Spike Discharges; (Contralateral Ear Reference). The 14 and 6/sec positive spike discharges are best seen during a contralateral ear
reference run (same EEG page as in Figure 1-85).

1
FIGURE 187. 14-and-6-Hertz Positive Spikes; Diffuse Encephalopathy. A 12-year-old boy with symptomatic Lennox-Gastaut syndrome after the treatment of status
epilepticus with intravenous midazolam. EEG showed continuously diffuse polymorphic delta activity with superimposed“14-and-6-Hertz positive spikes.”
Although 14- and 6 Hz positive spikes in diffuse encephalopathy EEG pattern was once thought to be seen exclusively in coma due to Reye’s syndrome,55,56
it was later reported
in other encephalopathies of childhood as well57
suggesting that they are epiphenomena or a resilient normal. The 14- and 6 Hz positive spikes are best seen in contralateral ear
reference montage.

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