Atlas of EEG, Seizure Semiology, and Management 2nd Ed

Atlas of EEG, Seizure Semiology,
and Management
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Atlas of EEG,
Seizure Semiology,
and Management
S E C O N D E D I T IO N
KARL E. MISULIS
VANDERBILT UNIVERSITY SCHOOL OF MEDICINE
NASHVILLE TENNESSEE
& WEST TENNESSEE HEALTHCARE
JACKSON, TENNESSEE
1
3
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Misulis, Karl E.
Atlas of EEG, Seizure Semiology, and Management / Karl E. Misulis.—2nd ed.
p. ; cm.
Rev. ed. of: Atlas of EEG & seizure semiology / Bassel Abou-Khalil, Karl E. Misulis. c2006.
Includes bibliographical references and index.
ISBN 978–0–19–998590–6 (alk. paper)—ISBN 978–0–19–998591–3 (alk. paper)—
ISBN 978–0–19–998592–0 (alk. paper)
I. Misulis, Karl E. Atlas of EEG & seizure semiology. III. Title.
[DNLM: 1. Electroencephalography—methods—Atlases. 2. Seizures—diagnosis—Atlases.
3. Seizures—therapy—Atlases. WL 17]
RC386.6.E43
616.8′047547—dc23
2013010299
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TABLE OF CONTENTS
Preface • vii
Acknowledgments • ix
1. Introduction to EEG • 1
2. Basic Science of EEG • 6
3. EEG Technology • 30
4. Clinical EEG • 80
5. Seizure Semiology • 235
6. Differential Diagnosis • 252
7. Seizure Management • 269
8. Samples and Case Discussions • 305
Appendix: References and Glossary • 353

Index • 363
v
PREFACE
It has been five years since the original edition of this book. Science and clinical practice have
moved on at a rapid pace, with advances in technology, clinical understanding, and diagnostic strat-
egies. In this second edition, Dr. Abou-Khalil and I have substantially expanded and updated the
material in the text, we have added a major section on seizure management, and we have expanded
the section on case studies. We recognize that the busy clinician not only wants a guide to evalu-
ation and diagnosis, but also a guide to medical and non-medical management of disorders. Note
that management strategies come and go and evolve, so this material must be supplemented by
current literature and scientific data.
This book covers the basics of EEG including basic science, technology, performance, interpre-
tation, seizure semiology, differential diagnosis, and seizure management. This book concentrates
on areas that are the specific domain of the authors, inpatient and outpatient EEG and epilepsy,
mainly in adults. While there is some discussion of pediatric EEG, intraoperative monitoring, and
advanced techniques, these sections are limited and are not the principal focus of this work.
The authors chose to adhere mainly to the older and more widely used seizure and epilepsy
classification schemes rather than the less widely used yet thoughtful schemes that are in develop-
ment. However, this edition includes presentation of the most recent recommended classification
schemes. It should be noted that these schemes are not fully developed and are not universally
accepted. In an effort to keep this work at a manageable size, the authors have had to be selective,
and as a result have omitted or limited discussion of some clinical and electrophysiological entities.
The information contained in this work is distilled from many years of clinical experience and
many scientific papers. In this concise text, it was impossible to list all of these valuable works.
vii
ACKNOWLEDGMENTS
The author would like to extend his sincere appreciation to technicians involved in the performance
of these studies. Also, numerous colleagues have provided material as well as feedback on the first
edition of this text. Special thanks are extended to my son, Karl C. Misulis for extensive work on
the digital imaging, and Riki Rager R. EEG T., B.S., FASET for help with the technical portions
of this text. The author would like to extend great appreciation to colleague, coauthor, and friend,
Dr. Bassel Abou-Khalil, who contributed substantially not only to his authored chapters but also to
much of the rest of the manuscript.
ix
1
INTRODUCTION TO EEG
Karl E Misulis
Electroencephalography (EEG) is an invaluable tool A recent proposal suggested that one unprovoked
for evaluating patients for suspected seizures and seizure is sufficient if there is also evidence of endur-
encephalopathy. While the study of EEG itself can be ing seizure tendency such as epileptiform activity on
exhaustive, as clinicians, we need to keep EEG in its the EEG (Fisher et al., 2005). This proposal has been
supportive role. As such, the study of EEG must nec- controversial and the authors favor the definition that
essarily be performed on a solid foundation of clinical requires at least two seizures.
neurology and basic neuroscience.
Classifications
SEIZURES AND EPILEPSY Before discussing the types of seizures, an introduc-

Definitions tion to seizure symptoms and signs is appropriate.
This is not a comprehensive glossary, as found else- Symptoms and Signs

where, but rather a summary of the important terms
for classification and definition of seizures (see • Prodrome is an abnormal sensation preceding
Table 1-1). the seizure in some patients, not associated with
The most critical distinction is between seizure and epileptiform discharge.
epilepsy. A seizure is a transient event that includes • Aura is a subjective sensation that can immedi-
symptoms and/or signs of abnormal excessive hyper- ately precede a seizure. This represents the initial
synchronous activity in the brain (Fisher et al., 2005), portion of the epileptiform discharge.
whereas epilepsy is a disorder in which the patient has • Clonic activity is episodic muscle contraction
recurrent unprovoked seizures. All patients with epi- associated with a seizure.
lepsy have seizures, whereas not all patients who have • Tonic activity is increased muscle tone during a
had a seizure have epilepsy. Recurrent seizures due to seizure, resulting in stiffening.
severe hyponatremia do not quality as epilepsy, since • Automatism is a stereotyped movement that
severe hyponatremia is known to provoke seizures. occurs as part of a seizure, such as lip smacking.
The traditional definition of epilepsy is that it takes • Postictal period is an episode of altered conscious-
at least two unprovoked seizures for the definition. ness or cognition following a seizure.
1
2 Atlas of EEG, Seizure Semiology, and Management
Table 1-1 Select Definitions Classification of Seizures and Epilepsies
Term Definition The 1981 international classification is still the most

Seizure Sudden attack that is usually commonly used seizure classification. It based on both
due to abnormal rhythmic EEG and clinical features of seizures (Commission on
discharge of neurons. Classification and Terminology, 1981). Classification
of seizures (Table 1-2) has two broad categories based
Epilepsy Recurrent episodes of seizure
on the onset being partial or generalized. Partial-onset
activity typically associated
seizures begin with a discharge in a focus, although
with abnormal EEG rhythms.
they then can spread to other parts of the brain.
Semiology Study of signs of seizures. Seizures that are generalized at onset, termed primary
Prodrome Change in mood or cognition generalized, start bilaterally in the brain. Generalized
prior to a seizure, but which is seizures may have some asymmetry, but that usually
not part of the seizure discharge. switches from side to side.
Aura Subjective sensation that Partial seizures are further subdivided into simple
precedes a seizure. partial and complex partial. Simple partial seizures do
Ictal discharge EEG discharge that is not disturb consciousness, whereas complex partial
associated with a seizure. seizures disturb consciousness. Complex partial sei-
zures were previously termed psychomotor because of
Interictal EEG discharge that is seen in
the cognitive disturbance. Partial-onset seizures can
discharge patients with seizures, yet the
spread to involve most of the brain, and this is termed
discharge is not itself a seizure.
secondary generalized seizure.
Postictal Episode of altered conscious- Other classification schemes have been suggested
period ness or cognition following a that could be helpful in specific circumstances. One
seizure. proposed seizure classification that has been used in
A complete glossary is provided in the Appendix.
the presurgical evaluation of epilepsy is purely semi-
ological, based solely on observed clinical features.
Table 1-2 Classification of Seizures

Major Classification Selected Seizure Types
Generalized Absence: Staring spells with decreased response, often associated with subtle
automatisms, lasting a few seconds, and with no postictal period.
Generalized tonic-clonic: Sudden loss of consciousness, tonic stiffening fol-
lowed by clonic movements of the body and/or extremities. Postictal period
subsequently.
Atonic: Sudden loss of tone which can be subtle (such as dropping of head), or
widespread resulting in fall.
Myoclonic: Brief seizures, lasting a fraction of a second. May be very focal and
subtle or widespread and severe.
Tonic: Sudden loss of consciousness with tonic posturing. Usually in neuro-
logically impaired individuals.
Partial Simple: Focal neurologic symptoms which can vary widely depending on loca-
tion of origin, but without disturbance of consciousness.
Complex: Focal neurologic symptoms including disturbance of consciousness.
Secondarily generalized partial onset: Partial seizure of either simple or complex
type which then spreads to become a generalized seizure.
Introduction to EEG 3
This classification includes somatotopic distribution meaning that they could be widely distributed in one
of the seizure manifestations and evolution of these hemisphere and possibly originating in subcortical
manifestations over the course of the seizure (Lüders structures. Generalized seizures were defined as “orig-
et al., 1998). This classification will not be used in inating at some point within, and rapidly engaging,
this book. bilaterally distributed networks,” which do not neces-
The International League Against Epilepsy (ILAE) sarily include the entire cortex (Berg et al., 2010a,b).
has classified epilepsy syndromes into types sum- Not included in this classification are non-epileptic
marized in Table 1-3. The classification of epilepsies seizures previously termed pseudoseizures. A major
still has two major subdivisions, localization-related task of the clinician and EEG-reader is the differentia-
(partial or focal being accepted synonyms), and gen- tion of epilepsy from non-epileptic events such as psy-
eralized. Most patients will have only partial-onset chogenic non-epileptic seizures, cardiac arrhythmia,
seizures or only generalized onset seizures, and be vasovagal syncope, orthostatic hypotension, transient
classified into one of these two categories. There is a ischemic attacks (TIA), and other conditions. This is
small group of patients with epilepsy who have both discussed in depth in Chapter 6.
partial-onset and generalized onset seizures. They are
classified in a third category of epilepsies and syn- Semiology
dromes undetermined as to whether they are focal or
generalized. Also classified into that category are sub- Semiology is a non-medical term meaning the study
jects who do not have enough evidence for the type of signs and symbols, which in our context means the
of seizure onset. symptoms and signs of seizures. The semiology of sei-
The classifications of seizures and epilepsies are zures of different localizations is discussed in detail in
evolving. The most recent revision of the seizure Chapter 5. A brief summary is provided in Tables 1-4
classification proposed by the International League and 1-5.
Against Epilepsy has maintained the major division of Semiology in these tables refers to primary gener-
seizures based on onset being generalized or partial, alized seizures (Table 1-4) and partial-onset seizures
but has recommended replacing the term “partial” without generalization (Table 1-5). Partial-onset sei-
with “focal”. Focal seizures were acknowledged to zures with secondary generalization are more com-
originate within networks limited to one hemisphere, plex and are discussed in Chapter 5.
Table 1-3 Classification of Epilepsies

Classification Types
Localization related (focal or Idiopathic (pure epilepsy not related to an underlying cause)
partial) Symptomatic (known etiology)
Cryptogenic (presumed to be symptomatic but cause is unknown)
Generalized Idiopathic
Cryptogenic
Symptomatic – can be nonspecific etiology or a specific etiology.
Undetermined as to whether With both generalized and focal seizures.
focal or generalized Without unequivocal generalized or focal features.
Special syndromes Include situation-related seizures – febrile convulsions, isolated seizures or
isolated status epilepticus, seizures only when there is an acute metabolic
or toxic event.
Adapted from the Commission on Classification and Terminology of the International League Against Epilepsy, 1989. Proposal for revised
classification of epilepsies and epileptic syndromes. Epilepsia 30, 389–399.
Table 1-4 Semiology of Generalized Seizures

Seizure Type Features
Absence Staring spells.
Automatisms that may be simple.
Loss of awareness.
Brief, usually less than 15 seconds.
Occasional motor manifestations.
Tonic-clonic Sudden loss of consciousness.
Generalized tonic and/or clonic movements.
Myoclonic Brief jerks that are variable in intensity, from small twitch to a massive jerk.
Usually bilateral but may be unilateral.
Often occur in clusters.
No disturbance of consciousness.
Atypical absence Loss of awareness.
Slower recovery than with absence.
Differentiated from absence mainly by EEG appearance.
ROLE OF EEG IN DIAGNOSIS AND Table 1-5 Semiology of Partial Seizures

MANAGEMENT
Seizure Features
Routine EEG
Type
Routine EEG is commonly performed in patients Temporal 90% have aura.
with episodic disorders in whom the differential diag- Most common aura is epigastric.
nosis includes seizures and in selected patients with Motor arrest, or
encephalopathy. Motionless staring, or
Automatisms that may be
Valid indications for EEG include:
oro-alimentary or extremity.
• Seizure or possible seizure;
Frontal Aura is uncommon.
• Well-controlled epilepsy to evaluate risk of recur-
May be epigastric sensation.
rence upon withdrawal of treatment
Focal clonic or tonic-clonic
• Syncope without definite cardiac or
seizures.
vascular cause;
• Loss of consciousness; Parietal Sensory aura, which may have march.
• Dementia when prion or virus is considered as an Can also have vertigo or focal
etiology; weakness.
• Encephalopathy without definite explanation; Staring, or
• Coma. Tonic posturing, or
Focal clonic activity, or
Not valid indications for EEG include: Head and eye deviation, or
• Headache; Immobility.
• Chronic behavioral disorder; Occipital Elementary visual aura, or
• Dizziness or vertigo; Visual hallucination.
Blinking, and/or
While the majority of patients who have EEGs per- Ictal blindness.
formed have suspected seizures, we will occasionally
Introduction to EEG 5
see patients in whom the documented reason for It is performed most commonly for the following
referral is dizziness or headache. Unless there is more indications:
to the story, these are inappropriate reasons for per- • Differentiation of epileptic seizures from
forming an EEG. non-epileptic seizures;
On the other hand, some epileptic syndromes • Classification of seizure type to assist treatment.
are likely under-diagnosed. Non-convulsive seizures, • Localization of the epileptogenic zone in the
including non-convulsive status epilepticus, may be presurgical evaluation of patients with drug-
incorrectly assumed to be metabolic encephalopathy, resistant seizures;
drug intoxication, or critical illness encephalopathy.
Similarly, episodic focal deficits may be assumed to Less common indications for video EEG include:
be transient ischemic attacks (TIA) yet are ultimately • Quantification of seizures, particularly when
diagnosed as partial seizures. In these patients a posi- seizures are very frequent and often missed by the
tive motor component may be subtle or the history patient.
merely incomplete. • Quantification of response to treatment.
• Studying seizure precipitants particularly in reflex
EEG-Video Monitoring epilepsy.
• Documentation of ictal and interictal discharges
EEG-video monitoring refers to prolonged EEG during circadian rhythms.
with simultaneous video recording, intended to cap- • Evaluating the clinical correlate of EEG dis-
ture clinical events. It allows the correlation of brain charges which are unclear as to whether they are
electrical activity with clinical manifestations. ictal or interictal.
2
BASIC SCIENCE OF EEG
Karl E Misulis
PHYSIOLOGY hydrophilic groups on the exterior of the membrane,

on the inner and outer surfaces of the cells.
Discussion of the physiology of EEG begins with the Complex proteins are inserted in and through the
foundations of neuronal function on a cellular level. membranes for a variety of functions, but the mem-
brane components of greatest importance to us are
Membrane Theory the ion channels and ion pumps. Normally, the hydro-
philic/hydrophobic arrangement of the membrane
Neuronal membranes are composed of lipid bilayers would make movement of many molecules across the
that have transmembrane proteins. These proteins membrane almost impossible, but with ion channels,
form the channels through which ions have differ- the movements of both cations (positively charged
ential permeability. Generally, potassium is seques- ions) and anions (negatively charged ions) can be
tered inside the cell, whereas sodium is excluded allowed and controlled.
from the cell. At rest, there is a greater permeability Depending on the ion channel, conductance can
to potassium than other ions. During an action poten- be dependent on membrane potential. For example,
tial, there is greater permeability to sodium. The some channels open only when a particular membrane
sodium-potassium pump uses energy to maintain the potential is reached (voltage gated). At rest the conduc-
ionic gradients, which are so important for intact neu- tance can be very low. When channels open, they often
ronal functions. This basic physiology is key to gen- are open only for a short and specific time, so that even
eration of EEG activity. if the membrane potential remains at a level that would
While the earliest membranes in evolution were activate the channels, they close after a specified time
likely composed of protein, membranes in all tissues (open time). Time sensitivity for channel closure is
now are composed of lipid bilayers (see Figure 2-1). particularly important for allowing the membrane to
The lipid bilayer is composed of long sheets of phos- be repolarized after a period of depolarization.
pholipids—substances with a hydrophilic end con- The sodium-potassium pump uses energy to
taining a phosphate group and chains of hydrophobic maintain the ionic gradients, which are responsible
lipid molecules. Because of the aqueous polarity, the for the diffusion potential and action potentials, pull-
stable configuration is for the hydrophobic ends to ing potassium inside the cell while expelling sodium
be together in the interior of the membrane with the from the cell.
6
Basic Science of EEG 7
a Extracellular Ion channel

Summation
Lipid bilayer
membrane
Summation of potentials is essential for central neu-
ral transmission. Often the depolarization associated
Intracellular
with a single synaptic event does not cause the release
b Na Na of sufficient transmitter to activate the subsequent
neuron. Therefore, the potential changes produced
Lipid bilayer
membrane by multiple incoming synaptic events are summed
so that depolarization of the next-order neuron can
K K
reach threshold.
Potassium Sodium Sodium-
channel channel potassium
Spatial summation is where potentials develop-
pump ing on different parts of the neuron sum to produce
a larger depolarization, more likely to activate the
Figure 2-1: Membrane Theory. next-order neuron.
a: Lipid bilayer membrane is impermeable to ions, but the Temporal summation is where repetitive activation
ion channels allow for and control ion flow. b: Simplified of a single input results in additive potential sufficient
diagram showing differential permeabilities of the sodium
to activate the next-order neuron. The first potential
and potassium channels and the sodium-potassium pump,
which maintains the chemical gradient required for resting has not completely decayed when the next potential
and action potentials. arrives. So there is summation of the depolarization
from the second potential on the first. With tempo-
ral summation, more than two potentials are usually
Diffusion Potential required. Also, for there to be summation, the fre-
quency of the potentials must be high enough and the
The diffusion potential is established by efflux of decay of potentials slow enough to allow for poten-
potassium, which travels down its chemical gradient tial summation. The decay rate is dependent on time
until the resulting electrical gradient opposes fur-
ther efflux of ions. The potential difference at which
there is electrochemical equilibrium is approximately a
Na+ Na+
75 mV for most neurons, with the inside negative.
Extracellular
The diffusion potential is essential for generation
of the depolarization, which will occur with electro-
tonic conduction and action potentials. Intracellular
Depolarization Electrotonic
Electrotonic Conduction from sodium depolarization
channel opening
Depolarization of a segment of membrane results in
activation of sodium channels. These allow the influx
of sodium down its electrical and chemical gradient. b
The influx continues until the channel closes in a
Potential
Electrotonic decay of
time-dependent manner. After the channel is closed, depolarization
it cannot be opened until a fixed period has elapsed
(i.e., the refractory period).
Depolarization of one segment of membrane Membrane distance
results in depolarization of adjacent membrane by elec-
trotonic conduction (see Figure 2-2). The depolarization Figure 2-2: Electrotonic Conduction.
spreads but decays along the length of the membrane. a: Lipid bilayer membrane with sodium channel that is
opened, resulting in depolarization not only at that site but
If the electrotonic depolarization of the membrane is
downstream by electrotonic conduction. b: Graph of expo-
sufficient, an action potential can develop at a locus nential decay in depolarization as a function of distance.
distant from the region of primary depolarization.
constant, which is a measure of how long it takes for Excitatory transmitters such as acetylcholine and
potentials to decay across a membrane; a longer time glutamate produce depolarization by opening of
constant results in longer duration of depolarizations. sodium and/or calcium channels. The depolarization
Time constant is dependent on a number of factors, can be recorded intracellularly as an excitatory post-
but a major factor is membrane conductance. synaptic potential (EPSP).
Inhibitory transmitters such as gamma-
Time Constant aminobutyric acid (GABA) produce opening of
potassium and/or chloride channels which results in
Time constant is a term used both in membrane physi- loss of excitability not so much by hyperpolarization
ology and in basic electronics. In electronics, time of the membrane, but rather by clamping of the mem-
constant describes the results of a step change in volt- brane potential near the equilibrium potential for
age input on an otherwise electrically stable system. these ions, which is far from threshold. For example,
This is discussed in detail later. In membrane physiol- the depolarization that would normally be produced
ogy, time constant is a measure of the decay of poten- by the opening of sodium channels is blunted by the
tial change of an otherwise stable resting membrane action of inhibitory transmitters essentially locking
potential. the membrane potential near the equilibrium poten-
For an RC circuit, or for a biological system mod- tial for potassium. The potential produced is the
eled as such, the time constant is the time to achieve inhibitory postsynaptic potential (IPSP).
1–1/e of the difference between the old and new
applied voltages, where e is the natural logarithm base. Action Potential
Since e is approximately 2.7, the value of this formula
is approximately 0.63 or 63%. So the time constant is The action potential is due to regenerative opening
the time to achieve approximately 63% of the differ- of sodium channels. The channel opening results in
ence between the new and old voltages.. depolarization of adjacent membrane, which then
The time constant is the product of the resistance causes sodium channels in these areas to open, thereby
and the capacitance across the membrane. perpetuating the depolarization. The channels close in
a time-dependent fashion.
TC = R × C The difference between an action potential and
an excitatory postsynaptic potential is that with an
where TC is time constant, R is resistance to charge action potential the opening of the sodium channels
flow, and C is capacitance of the membrane. results in further depolarization and thereby further
The resistance is the inverse of conductance, opening of more sodium channels, as a regenerative
where conductance is dependent on the number of cycle (see Figure 2-3). The process is regenerative
ion channels that are open. The number of ion chan- until terminated by time and changing conductance
nels is dependent on a number of factors, including to not only sodium but also other ions (e.g., potas-
numbers of channels, current membrane potential, sium and calcium)
and time. Most channels open at certain potential and
close after a certain time. More open channels and
longer open times make for increased conductance, ELECTRONICS
which by inverse is reduced resistance, which by for-
mula is reduced time constant. Basic science of electronics is important not only
for an understanding of how neurophysiological
Postsynaptic Potentials equipment works, but also for understanding how
the patient becomes an integral part of the circuitry.
Postsynaptic potentials are created by the release This understanding can help to minimize artifact and
of neurotransmitter onto the postsynaptic mem- improve the quality of studies.
brane. Transmitters modulate the conductance to The conceptual parallel between electrical circuits
ions on the postsynaptic membrane to produce and biologic circuits is of more than passing interest
their effects. to neurophysiologists. The general physical properties
Circuit Elements
The circuit elements are combined with conductors to

Action form complex circuits. Electronics has evolved from
potential tubes and solder to circuit boards at a microscopic level.
Traditional circuitry used boards to hold the elements
and wires to connect them. The next development
was the printed circuit board, where there were strips
of conductor painted onto the board to aid connect-
Sodium ing elements. Current design usually involves layers
conductance
of conducting, semi-conducting, and non-conducting
materials that are etched to form transistors, capacitors,
resistors, and conductors (see Table 2-1).
Potassium
conductance
Conductors and Non-conductors
Time Conductors are able to allow electrons to move
because they have unpaired electrons in their outer
Figure 2-3: Action Potential. electron orbitals. Some of these atoms can accept an
Sequence of changes in membrane conductance associated
“extra” electron, resulting in a net negative charge,
with an action potential. Potassium conductance predomi-
nates during rest. Sodium conduction predominates during but with atomic stability. The spot for this extra elec-
the action potential. tron is a hole. Other atoms can more easily donate
an unpaired electron, which results in a net positive
charge but is also atomically stable, since every orbital
of current flow in biologic tissues are comparable to is then full (Figure 2-4). During the process of con-
those in electrical devices, although the devices are duction, electrons move from hole to hole, driven by
far different. We will highlight some of these parallels a potential gradient that is established by the power
when appropriate. supply or biologic tissue (Figure 2-5).
Table 2-1 Circuit Elements

Element Features
Conductor Material that easily conducts current by allowing the flow of electrons.
This requires atomic structure conducive to mobilization of electrons.
Non-conductor Material that does not conduct current.
Semiconductor Material that conducts better than a non-conductor but less well than a
conductor. Used to make diodes and transistors.
Power supply Source for power that imparts energy to electrons, thereby causing them to move.
Resistor Element that opposes the flow of electrons, dissipating energy as heat.
Capacitor Element that stores energy in the form of separation of charge.
Inductor Element that stores energy in the form of magnetic field.
Diode Device made by layering two pieces of semiconductor. Conducts in only one
direction.
Transistor Device made by layering three pieces of semiconductor. Integral for amplifiers.
Amplifier Device to amplify signals. Semiconductors are integral components of amplifiers.
a – b
– – –
4+ 3+
– –
–
Electron Electron Electron Electron

gained lost gained lost
–
– –
– –
– –
4+ 4+ 3+ 3+
– – – – –
– –
Charge – 1 Charge + 1 Charge – 1 Charge + 1
Figure 2-4: Conductors and Non-conductors.

Atomic structure of the outer orbitals of some important elements. A would be a non-conductor, B would be a conductor.
a: The atom is electrically neutral and all orbitals are filled, so it unable to easily donate or receive an electron. An electron
donated to this atom would not be welcome, and formation of a new orbital does not occur. Losing an electron would require
a large amount of energy and would not occur in an electronic circuit. b: Electrically neutral but has one empty orbital spot.
Can easily receive an electron. Gaining an electron is favored since it fills the outer orbital, even though there is electrical
negative charge. Likewise, the single outer orbital electron can be donated easily.
Non-conductors do not have unpaired electrons that

a can be donated or holes to accept electrons. Therefore,
3+ 3+ 3+ electrons cannot pass through non-conductors, unless
there is such a large potential gradient across the mate-
3+ 3+ 3+
rial that electrons spark through the material. Contrary
to some popular belief, sparking can occur through
b c I non-conductors.
+
V R
– Resistors
e Resistors are composed of material that conducts less

well than conductors, but in this circumstance dissi-
Figure 2-5: Conductor Anatomy. pates some of the energy associated with the moving
a: Atomic structure of a conductor. Adjacent atoms share electrons as heat (see Figure 2-6).
electrons, shown as small gray circles. The small white cir-
cles are “holes,” which are unfilled portions of orbitals. Black Resistors are discussed further in the next section, par-
circles represent the path of an electron through the conduc- ticularly regarding:
tor. b: Less enlarged view of a conductor, showing electron
flow through the conductor. By convention, current flow • Ohm’s law;
is defined as the flow of positive charge, therefore, in the • Summation of resistors in series;
opposite direction to the flow of electrons. c: Simple circuit • Summation of resistors in parallel.
diagram of a conductor. The symbol for a battery “V” has the
positive terminal upward. Electrons flow from the negative Resistors are integral components of circuits since
terminal (bottom) through the conductor to the positive
terminal. Current flow is opposite to the flow of electrons.
they regulate current flow. Insertion of resistors
into a circuit reduces the rate of charge movement,
a I b I a
I
R
e
No resistance, resulting Energy dissipation
in high current, short across resistor, lower
circuit current. b c
– –
Figure 2-6: Resistors. –
a: A conductor connects the terminals of a battery. Current
will flow from the positive terminal to the negative terminal – – – – – – –
through the conductor. Electrons are flowing in the oppo- – –
site direction. The magnitude of current will quickly destroy
the battery. b: A resistor is inserted into the conductor cir-
cuit. This reduces the current flow by an amount that is pro- Figure 2-7: Capacitor.
portional to the resistance of the resistor. a: Simple circuit of a battery charging a capacitor. When the
battery is switched on, electrons flow from the negative ter-
minal and onto the lower plate of the capacitor. Electrons
or current. In addition to resistors as part of elec- leave the upper plate and travel through the conductor to
the positive terminal of the battery. The departure of the
tronic circuits, biologic tissues have a resistance to
electrons from the upper plate produces positive-charged
charge flow. holes. b: Close-up of the capacitor during the charging
When current flows through resistors, there is phase. Electrons accumulate on the lower plate and depart
a voltage drop across the resistor which refers to the from the upper plate. c: When the battery is switched off
energy dissipated. Some resistors are purely designed while the terminals of the capacitor are connected, electrons
flow off the lower plate and onto the upper plate. The moti-
for current regulation, whereas other circuit elements
vation for the electron movement is the charge separation
incorporate resistance as a mechanism to produce across the plates of the capacitor.
heat or light. For example, a modern incandescent
bulb uses a high resistance filament to generate light,
although only about 5% of the energy is dissipated as the capacitor is equal and opposite to that of the
light, the rest is dissipated as heat. power supply.
When the power supply is switched off, the only
Capacitors potential difference in the circuit is across the capaci-
tor. Electrons flow from the negative-charged plate
Capacitors are composed of plates of conducting through the connecting conductor and onto the
material separated by non-conducting material (see positive-charged plate, completing the circuit.
Figure 2-7). Therefore, current cannot flow directly Capacitors alter the frequency response of elec-
through a capacitor, although capacitive current can tronic circuits and additionally are used for a variety
flow. Capacitive current is virtual current through the of electronic applications requiring pulsed current—
capacitor. The capacity or capacitance is a measure of such as strobe lights and detonators. The former are
the ability of the capacitor to store energy by separa- used routinely in EEG labs, the latter are not.
tion of charge producing an electric field.
When the power supply is turned on, electrons Inductors
flow and build up on one plate of the capacitor.
Because of repulsive effect on electrons on the other Inductors are simply a coil of conducting wire (see
plate, electrons stream off this plate to the positive Figure 2-8). They capitalize on the general property
end of the power supply, leaving a positive charge. of conductors to build up a magnetic field around
Eventually, the potential developed across the capaci- them when current flows. As electrons flow through
tor is sufficient to oppose the flow of current, and net a straight conductor, a weak magnetic field is created.
electron flow stops. At this point, the charge across This field is large enough to be detected by sensitive
a Inductor circuit b Response graphs

Magnetic field lines
I
V
Induction
V
coil
e
S I
Figure 2-9: Inductor Theory.
Inductor leads
Axis of magnetic field a: Circuit diagram of a power supply (V), inductor, and
current (I) flowing through the circuit. Electrons flowing
through the inductor coil produce a magnetic field. b: Graph
Figure 2-8: Inductor. of the response to a step in voltage (V). The current builds up
Diagram of an inductor coil. The coil of wire results in the but more slowly than expected because some of the energy of
magnetic fields being in effectively the same direction, pro- the current flow is used to generate the magnetic field.
ducing summation of the fields. This makes for a powerful
field that is dependent on the amount of current flowing
through the coiled wire and the number of turns of the coil. Inductors are especially important for radios and a
variety of equipment in which flow of current through
a circuit needs to be controlled. But the biggest impli-
equipment but not typically enough to significantly cation of inductors for neurophysiology purposes is
influence the flow of current. However, when the con- stray inductance. This is unintentional inductance, due
ducting wire is coiled, the magnetic fields from mul- to the presence of wires all around us. While they may
tiple coils are summed, so the magnetic field can be not have all of the turns and tight structure of a com-
substantial. mercial inductor, they can produce sufficient induc-
One use of an inducting coil is as an electromag- tance to cause stray current flow and thereby noise in
net, where a constant current through the coil creates our sensitive neurophysiologic equipment. If all cur-
a stable magnetic field with north and south poles, rent was direct current (DC), so there was little or no
just like a permanent magnet. If there is an iron core change in voltage, this would not be a huge issue, but
in the middle of the coil, then the magnetic field is since line power is alternating current (AC), by defi-
even stronger. However, in the context of neurophysi- nition voltage is swinging from positive to negative
ological equipment, inductors are important for the and back at 50 or 60 Hz, depending on the frequency
effect this magnetic field has on the flowing current. of oscillation of line power. This means that the con-
Consider a power supply connected to an inductor stantly changing magnetic field is causing fluctuating
(Figure 2-9). When the power supply is switched on, current to be induced in conductors of your systems.
current begins to flow but there is a delay in develop- This might be in the microvolt range, but this is more
ment of maximal current. As the magnetic field builds than enough to cause artifact in electrode leads that
up, there is a lag in current until the field is maximally routinely measure these levels of electrical activity.
developed. At that point, the impedance abates and
current freely flows. This is because the energy is Semiconductors
taken from the system in creating the magnetic field.
The energy stored in the magnetic field is reclaimed Semiconductors are so called because they semi-
when the power supply is switched off. In this case, the conduct—they conduct better than non-conductors
current ceases to flow from the battery, and the mag- but less well than conductors. They are composed of
netic field begins to collapse, but this collapse in mag- a non-conducting material that has a few atoms of
netic field causes current to flow through the system, in conducting material intermixed. The base material is
the same direction as it initially did during the charg- usually silicon or germanium and the atoms inserted
ing phase (see Figure 2-9). The production of electric within the base material are often arsenic or gallium.
current by a changing magnetic field is induction. This is doping, and the type of the intermixed material
a Silicon or N-type P-type the concepts is appropriate considering the wide-

Germanium semiconductor semiconductor
spread use of semiconductors in our lives.
4+ 4+ 4+ 4+ 4+ 4+
4+ 4+ 5+ 4+ 3+ 4+ Diodes
Diodes are composed of two wafers of semiconduc-

b c tor, which are then joined. When the two are placed
together, electrons migrate from the N-side to the
– – – adjacent P-side, the electrons filling some of the
+ + +
available electron orbitals. This creates a junction
potential, which develops to the point that the charge
differential opposes the further flow of electrons.
Figure 2-10: Semiconductor. This is similar to the junction potential that develops
a: Atomic structure of semiconductor material. Pure silicon across biological membranes. Therefore, at rest, the
(left) is a non-conductor. Doping of this material with a junction between these materials is polarized with
conducting element results in either available electrons for a positive charge on the N-type side and a negative
flow (center, N-type), or available empty electron orbitals,
charge on the P-type side.
which can temporarily host a flowing electron (“hole” or
P-type). b: A piece of semiconductor material as part of a When a power supply is applied to deliver poten-
circuit can conduct electric current, though not as well as a tial difference across the diode, current can flow in
conductor. c: Two semiconductor pieces are placed together only one direction. If the negative side of the power
without a battery. Some of the spare electrons of the N-type supply is applied to the N-side, then the junction
semiconductor move to occupy partially filled orbitals of
potential is negated so current can flow. On the other
the P-type semiconductor. This is analogous to the diffusion
potential of biological membranes. hand, if the polarity is reversed, electrons delivered to
the P-side serve to augment the junction potential.
There are no “extra” electrons or “holes” available to
determines the type of semiconductor. Silicon and facilitate further current flow. Every atom on in the
germanium have 4 outer electrons, making them junction region has filled orbitals.
essentially non-conductors (see Figure 2-10). Arsenic There are diodes in electrophysiological equip-
has 5 outer electrons, so in a lattice with silicon, there ment, such as for rectifying AC voltage. However,
is tight binding of 4 of these and 1 is “spare” in that it the main purpose of semiconductors in our EEG
is not tightly bound and therefore can dissociate from
its nucleus and move fairly easily through the material
from arsenic atom to arsenic atom. This is an N-type a Forward biased b Reverse biased
semiconductor since it has spare electrons from an diode diode
orbital point of view though they are not spare in
terms of electrical neutrality. The term N-type means
P-type N-type
that it resembles a negative material in that it is happy + + + + +
to donate a negative-charged electron. Doping a semi- –
– – –
conductor with gallium, which has 3 outer electrons N-type P-type
and therefore an unfilled electron orbital, creates a

P-type semiconductor. The P-type indicates that the
semiconductor has properties of a positive material in Figure 2-11: Diode.
a: A battery is connected to the N-P semiconductor com-
that it likes to accept an electron. This naming can be plex. In this diagram, current can flow, since the junction
a little confusing in practice when N-type semicon- potential between the two materials is negated by the
ductors develop a positive charge and P-type semi- applied voltage. b: The position of the semiconductor mate-
conductors develop a negative charge when these rials is reversed so that the applied voltage serves to augment
materials are joined as layers. the junction potential. Current cannot flow. Since the N-P
semiconductor junction allows for current flow in only one
Mechanisms of action of semiconductors are not direction, this is a diode.
crucial to understanding devices, but understanding
equipment is for manufacture of transistors. The uni- voltage of the controlling side, so a small amount of
directional conduction used for diodes is the founda- voltage change in the controlling side alters the cur-
tion for transistor theory. rent flowing due to a much larger voltage on the
controlled side. For most transistors of this type, the
Transistors amplification is linear over a large range of input volt-
ages, and the set amplification for each amplifier stage
Transistors are typically composed of three layers of is about 9x.
semiconductors. One of the most common types is Amplifiers are created by using transistors in
the junction bipolar transistor, shown in Figure 2-12. series, to achieve the massive amplification needed to
With no applied voltage, junction potentials develop bring the electrophysiological signal into magnitude
at the NP junctions. The left side of the circuit is the at which it can be used by the attached electrophysi-
controlling side and the right side is the controlled ological equipment.
side. The left side may be the biological voltage of the
patient, and the right side is the rest of the amplifier
circuitry. Circuit Laws
The upper NP junction is reverse biased, and nor-
mally electrons would not flow. The lower PN junc- Overview
tion is forward biased, and current can flow on the
controlling side. When voltage is applied to the con- The basic laws that govern electric circuits are many, but
trolled side, this alters the potential developed at the the most important are:
upper PN junction, resulting in allowance of current • Ohm’s law;
flow. The voltage applied by the EEG machine’s power • Kirchhoff ’s current law;
supply to the controlled side is much larger than the • Kirchhoff ’s voltage law.
a collector In addition, there are a few basic additional formulae

that are important to remember.
N
base + • Summation of resistors in series;
P • Summation of resistors in parallel.
+
N
Table 2-2 presents a summary of these laws.
emitter
Ohm’s Law
b
Ohm’s law says that for any resistive circuit, the volt-
C
+ age is equal to the current times the resistance,
B
or:
+
E
V = I × R.
This is one of the intuitive laws of electronics. As

Figure 2-12: Transistor. the voltage increases across a fixed resistance, the cur-
a: A transistor is constructed from three layers of semicon- rent flow increases. On the other hand, as the resis-
ductor material. Voltage supplied on the left side of the cir- tance increases with a fixed voltage, the current drops
cuit controls the conductance across the entire transistor. (see Figure 2-13).
Therefore, a small amount of voltage on the controlling side
Ohm’s law is crucial for the development of other
governs current flowing on the controlled side. b: Circuit
diagram of the transistor shown above. circuit laws and theories. Permutations of Ohm’s law
apply and are useful in circuit theory.
Table 2-2 Summary of Important Circuit Laws

Law Features
Ohm’s law For a resistive circuit, the current flowing is equal to the applied voltage
divided by the resistance. Or:
I = V/R
Rearranged, this is V = I × R
Where V is applied voltage, I is current, and R is resistance.
Kirchhoff ’s current law For a node, or junction point of conductors, all of the current flowing into the
node must equal the current flowing out of the node. Since outward flow can
be considered the reverse of incoming, then:
Σ Ii = 0
where Ii represents the individual currents.
Kirchhoff ’s voltage law For a circuit loop, the sum of the voltage sources is equal to the voltage drops,
where voltage drop is dissipation across a resistance. Or:
Σ VS = Σ VR
Summation of resistors in For two or more resistors in series, the equivalent resistance is equal to the
series sum of the individual resistances. Or:
RT = Σ Ri
where RT is total resistance and Ri is resistance of the individual resistors.
Summation of resistors For two or more resistors in parallel, the reciprocal of the equivalent
in parallel resistance is equal to the sum of the reciprocals of the individual
resistances. Or:
1/RT = Σ (1/Ri)
Current of a resistive circuit is equal to the voltage

a I divided by the resistance, or:
Ohm’s law
V R V=I×R I = V/R
Similarly, resistance in a resistive circuit is equal to

the voltage divided by the current, or:
b c
I
R = V/I
I
V R Kirchhoff’s Current Law
Kirchhoff ’s current law is easy to conceptualize (see

Figure 2-13: Ohm’s Law.
a: Circuit diagram of a resistor-capacitor (RC) circuit. The Figure 2-14). The sum of the currents flowing into a
power supply provides a voltage (V), which drives electrons node, or connector in a circuit, is zero. In other words,
around the circuit in the opposite direction to positive cur- the sum of the current flowing into a node is equal to the
rent (I) through the resistor (R). b: Linear and positive sum of the current flowing out. This is evident since a
relationship between applied voltage and current. c: Linear
connector point has no ability to store or modify energy.
and inverse relationship between resistance of the resistor
and current flow. Higher resistance means less current.
Σ Ii = Σ Io
I1 Node I2 circuit loop, the sum of the voltage sources is equal

circuit circuit to the sum of the voltage drops. Voltage drop means
I3 dissipation of voltage across a circuit element, par-
ticularly in this case a resistor. Since voltage drops are
of opposite direction to voltage sources, the law really
circuit says that the sum of the voltages around a circuit loop
is zero.
Figure 2-14: Kirchhoff ’s Current Law. A circuit loop is any closed loop of connectors and
The sum of the currents flowing into and out of a node is their circuit elements. The figure shows both a simple
zero. The node cannot store or modify energy. single loop circuit and a more complex circuit with
three loops—the three loops of the circuit on the
right side of the image are, top, bottom, and the large
where Ii represents the incoming currents to the loop encompassing both power supplies and resistors,
node and Io represents the outgoing currents from without the central horizontal connector.
the node. Kirchhoff ’s voltage law is derived in part from
This indicates that the sum of the incoming cur- Ohm’s law. The voltage drop across a resistor is pro-
rents is equal to the outgoing currents. However, since portional to the current and to the applied voltage, so
outgoing currents are in the opposite direction from as the voltage of the power supply is increased, cur-
incoming currents, they can be considered negative rent increases so the voltage drop across the resistor
currents, though this means negative from a math- increases.
ematical point of view, not a charge point of view.
Therefore: Σ VS = Σ VR
Σ Ii = 0 where VS represents the individual voltage sources

such as batteries or biologic signals, VR is the voltage
where Ii in this formula represents all of the individual drop across each resistor.
currents.
Summation of Resistors in Series
Kirchhoff’s Voltage Law
Two or more resistors in series can be replaced con-
Kirchhoff ’s voltage law is somewhat more difficult to ceptually with a single resistor with a total equivalent
conceptualize (see Figure 2-15). It says that for any resistance (see Figure 2-16). The intuitive assumption
a b
I
R1 V R1 R1
V
V
R2 V R2
R2
e
Figure 2-15: Kirchhoff ’s Voltage Law.
a: The sum of the voltage sources and drops in a circuit loop
is zero. b: Kirchhoff ’s voltage law applies to all circuit loops, Figure 2-16: Resistors in Series.
including each of the smaller loops in this diagram and the The total resistance of two resistors in series is equal to the
large loop encompassing both batteries and both resistors. sum of the individual resistances.
is that the total equivalent resistance is the sum of the The greater the resistance, the less the conduc-
individual resistances, and this is correct. tance. If there are two or more routes of conductance,
Expressed mathematically: then each route increases the overall conductance.
The total conductance is equal to the sum of the indi-
RT = Σ Ri vidual conductances. Or:
where RT is the total equivalent resistance of the sys-

GT = Σ Gi
tem, and Ri is the resistance of the individual resistors.
This seems intuitive because the energy associ-
ated with the electrons comprising the current is dis- where GT is the total conductance and Gi is the con-
sipated across multiple resistors, resulting in greater ductance of the individual resistors.
overall resistance. If we then substitute 1/R for the conductances,
then we have the following formula:
Summation of Resistors in Parallel

1/RT = Σ (1/Ri)
Two or more resistors in parallel (see Figure 2-17) can
also be replaced conceptually by a single resistor with where RT is the total equivalent resistance of the resis-
a total equivalent resistance. However, many find that tors in parallel, and Ri is the resistance of the individ-
the fact that the total resistance is less than the resis- ual resistors.
tance of any of the resistors to be not intuitively obvi- This is essentially how parallel resistances sum. The
ous. This discrepancy is because although there may reciprocal of the equivalent resistance is equal to the
be two or more resistors, each resistor is a conduit sum of the reciprocals of the individual resistances.
for electron flow, so the more conduits in parallel, the
lower overall resistance. An analogy would be a reser-
voir being emptied by one narrow tube. Adding addi- Amplifiers
tional tubes, no matter how narrow, reduces the overall
resistance to flow. Each of these tubes can be consid- Overview
ered to have a resistance—meaning how much they Amplifiers are integral to all modern neurophysi-
impede fluid flow—but the reciprocal of resistance is ologic equipment. Biological potentials are of such
conductance—the capacity of the tube to allow flow. small magnitude that amplification is required in
Similarly, for electron flow, conductance is the order to handle and display the signals. The first
reciprocal of resistance. stage of amplification is commonly at the head-stage
of the device. This simple amplifier raises the magni-
G = 1/R
tude of the signal so that it far exceeds the magnitude
where G is conductance and R is resistance. of electrical noise. Noise already in the electrode
system will be amplified, however. Shielded cables
then lead to the EEG machine, which is nowadays
the combination of a computer and a display system.
The EEG machine further amplifies the raw signal,
which is then subject to either analog display or digi-
V R1 R2
tal display.
Analog display consists of using the massively
amplified signal voltage to drive pens on a paper
display or to deflect an electron beam on a cathode
ray tube. Digital display consists of analog-to-digital
Figure 2-17: Resistors in Parallel. conversion followed by mathematical manipulations
The reciprocal of the total resistance of two resistors in par- before digital video display and recording on some
allel is equal to the sum of the reciprocals of the individual
resistances.
sort of digital storage media. Details of some of these
steps are discussed below.
Amplifier Theory Transistors
Amplifiers do nothing other than increase the mag- Transistors are the most important implementation
nitude of an electric signal. When placed together of semiconductors. Almost all amplifiers use transis-
in various arrangements, transistors can produce tors as a foundation of amplification. Tubes are still
enhanced amplification or can alter the configuration used in some older equipment, but offer no significant
of the signal. advantages with many disadvantages.
The essentials of amplification with transistors
was described above. The biological signal is applied
Amplifier Circuits
to the controlling side and a higher-voltage repre-
Amplifier circuits have two ends, which can be sentation of the signal emanates from the controlled
termed input and output. Alternative names are con- side. Since the amplification needed for computer
trolling and controlled. The input side of the ampli- input is many orders of magnitude greater than
fier receives the biological signal. The output of the most biologic signals, multiple stages are required
amplifier is the enhanced representation of the sig- for amplification. For purposes of discussion, each
nal. This wording is chosen carefully, because it is amplifier stage provides approximately 10x amplifi-
not really just turning up the volume of the signal, cation so that a gain of 1000x requires 3 stages (10 ×
but rather measuring the signal, then using a power 10 × 10 = 103 = 1000). However, in reality, amplifica-
source to drive the output to look like the input tion is closer to 9x.
signal.
Amplifiers historically used tubes but currently Single-ended versus Differential Amplifiers
use transistors as their device for controlling and
multiplying signal. In either case, the device is a con- Single-ended amplifiers are the elementary ampli-
trolling device—the input signal controls passage of fying circuits created by the use of transistors (see
electricity through the unit. Figure 2-18). These consist of a transistor with the
a Single-ended amplifier
active 10x output
ref ref
b Differential amplifier
V1 10x
V2
–10x
V1-V2 difference
amplified
ref ref
Figure 2-18: Single-ended Versus Differential Amplifiers.

a: Single-ended amplifier: where the input and output are in reference to a common level so the amplified output is similar
to the input, just larger. b: Differential amplifier: where there is amplification, inversion, then addition so that the output is
the amplified difference between the two inputs.
controlling side of the circuit connected to the bio-

logic signal and the controlled side of the circuit pow-
Raw signal
ered by a substantial power supply. Small variations with digitized
in voltage on the controlling side affect the conduc- points
tance through the transistor, thereby altering current
flow through the controlled side. The output of a
Reconstructed
single-ended amplifier is a magnified representation signal from
of the input to the amplifier digital data
Differential amplifiers are composed of two ele-
mentary single-ended amplifiers plus a subtracting
circuit. Two input signals are used. Both are ampli-
fied by the single-ended amplifiers. Then, the ampli- Figure 2-19: Analog-to-digital Conversion.
fied output from one is subtracted from the amplified An analog (continuously variable) signal is essentially
placed on an X/Y grid where the X axis is time and samples
output of the other. This difference is displayed and
are taken at specific times. The Y axis is voltage with specific
represents the differential output. The output of a dif- voltage levels and the measurement is of the voltage level
ferential amplifier is the amplified difference between exceeded or met by the analog signal at each of the sample
the signal at two inputs. times. Then connecting the dots produces a digital represen-
Most amplifiers in routine electrophysiological tation of the analog signal.
equipment are differential amplifiers.
Signal Processing signal is processed, the data is displayed on a moni-

tor, just as any other graphical data. Power-spectral
Analog Devices analysis or other mathematical handling can also be
performed.
The first amplifier encountered by the biologic signal Analog-to-digital converters (ADC) effectively
is the preamplifier. The preamplifier raises the ampli- plot the raw signal on a discrete time/voltage grid.
tude of the signal so that it rises far above electrical They do this by sampling the voltage levels of the sig-
noise. Many devices have the first phase of amplifica- nal at specified intervals, so the time axis is not con-
tion in the head box. tinuous but at discrete times. Similarly, the voltage
The amplified signal is then large enough that levels that are discerned are discrete, with an interval
there is likely less further electrical contamination of that is defined by the gain used. Modern ADCs used
the signal. This signal is then passed through a series in EEG machines have a maximum time resolution of
of filters. The high-frequency filter and low-frequency about 4 μsec (250,000 samples/sec) and maximum
filter are in separate stages. The filtered signal is voltage resolution of about 15 μV. Front-end analog
then fed into a powerful driver amplifier. The poten- amplification further improves the voltage resolution.
tials required to move pens on a paper display are The very fast conversion rate allows for a single ADC
orders-of-magnitude greater than the potentials aris- to convert multiple channels.
ing from the brain.
Filters
Digital Devices
Overview
Digital signal processing begins with preamplifica-
tion of the raw signal, as described for analog signal Filters alter the frequency composition of EEG so
processing. Then, the amplified signal is fed to an that we can more easily see the frequencies of interest.
analog-to-digital converter (ADC). After the digital Raw EEG signal is composed of a broad range of fre-
conversion, the montages are generated by calcula- quencies, only some of which are relevant to routine
tions on the digital signal (see Figure 2-19). Filters interpretation. Frequencies slower than 0.5 Hz and
are also calculations on the digital data, and the type faster than 70 Hz are of little value and can obscure
of calculations differs between devices. Once the the other frequencies.
Filter action Physics of Filters
Frequency composition of the signal can be altered by There are three basic types of filters:
the three basic filter types: • Passive filters;
• High-frequency filter (HFF); • Active filters;
• Low-frequency filter (LFF); • Digital filters.
• 60-Hertz (or notch) filter.
Passive filters are described in detail because they
The HFF attenuates the higher frequencies, whereas show the mechanism of filters. However, most fil-
the LFF attenuates the lower frequencies. The 60-Hz ters in modern EEG equipment are active or digital.
filter attenuates frequencies around 60-Hz. The Passive filters are so called because they modify the
mechanism of this, however, is complicated. There is signal without use of an exogenous power source.
not a precise cut-off, but rather a decay in amplitude Active filters use transistors and a power supply to fil-
of these frequencies near the selected set frequency. ter the signal. Digital filters are calculations performed
This decay is called the roll-off. The signal drops off by on the digital data created from an analog signal.
a certain amount per octave of frequency, Therefore, The basic construction of the passive filter is the
the filter effect is described by the filter type, the RC circuit (resistor-capacitor circuit; see Figure 2-20).
cut-off frequency, and the roll-off. The RC circuit is a resistor and a capacitor in series
The 60-Hz filter is essentially an HFF and an LFF with a power supply. Current flows through the con-
combined, with a maximal attenuation at 60-Hz. ductor in the direction from the positive side of the
However, frequencies slightly faster and slower than power supply to the negative side. We are speaking of
60-Hz are also attenuated to a lesser extent, and there positive current, which is an electrical convention. In
may be some phase changes, though these changes are reality, current is electrons flowing from the negative
usually clinically insignificant. end of the power supply to the positive end. The effect
Filters are often used to remove artifacts from of the RC circuit can be best seen if meters are placed
EEG signals. Some artifacts have frequencies different across the resistor and capacitor and a measurement
from most EEG frequencies of interest. of current is made.
Meters applied to the circuit will show a potential
Common artifacts are: difference, which in the case of resistor is the voltage
• Electrical artifact; drop—a term which indicates that the applied voltage
• Cardiac (EKG); of the power supply is attenuated by passage through
• Muscle (EMG);
• Tongue movement (glossokinetic);
• Eye movement; I
• Sweat;
• Head movement; R1
• Respiratory movement.
The first three are high-frequency, and can be attenu- V

ated by HFF, but this may also attenuate important
fast activity, such as spikes and sharp waves. Therefore,
C
it is best if we can remove some of these electrical arti-
facts without filtering.
The slower artifacts can be attenuated by LFF, but
this also can attenuate some of the slower physiologi-
cal signals, such as frontal intermittent rhythmic delta Figure 2-20: RC Circuit.
Resistor-capacitor or RC circuit. Resistor (R) and capaci-
activity (FIRDA) or polymorphic delta, and can actu-
tor (C) are in series with a power supply (V). Current
ally change the morphology of some slow activity to (I) moved through the circuit.
appear as faster transients.
Am
VS
I
I I
R1
Vm VS
R1
C VR
V
VC
C Vm
Figure 2-22: Recordings from Elements of the RC

Circuit.
A step change in voltage, positive 1 volt, is applied and the
Figure 2-21: Voltage Differences in the RC Circuit. graphs show the changes in voltage difference and current
RC circuit as in Figure 2-20, but meters are placed to mea- with onset and offset of the step voltage. Current is initially
sure the voltage differences across the resistor and capacitor large, but as the capacitor is charged, that voltage opposes
and to measure the current. the supply voltage, and as the capacitor becomes fully
charged, current stops. When the applied voltage is zeroed,
the capacitor discharges with current moving in the oppo-
the resistor (see Figure 2-21). For the capacitor, the site direction. Voltage across the resistor varies directly with
measured voltage difference is the charge built up current, from Ohm’s law.
across the plates. Since electrons cannot jump from
plate to plate in the capacitor, as current flows, elec-
trons build up on one side of the capacitor and repel circuit, giving the high spike of current. With current
electrons on the opposite plate, making them flow off flow, there is buildup of charge across the capacitor,
through their conductor. This is capacitive current. and this potential difference opposes the further flow
The actual recordings that would be obtained of current, since it is in the opposite direction to the
are shown in Figure 2-22. For this illustration, a applied voltage. Therefore, the current is dependent
square-wave pulse is delivered by the power sup- on the difference in voltage of the power supply and
ply, equivalent to having a battery switched on for capacitor, giving the gradual decline. When the volt-
a second then switched off, yet leaving the connec- age across the plates of the capacitor is equal and
tors in place. A meter placed across the terminals of opposite to the voltage of the power supply, current
the power supply (V) shows the square-wave. The ceases.
voltage causes current to move through the circuit When the power supply voltage is switched off,
(I). Current charges the capacitor (C). The voltage the charged capacitor is now the only source of elec-
measured across the capacitor has a gradual increase tromotive force (EMF) in the circuit, so current flows
because it takes time for the capacitor to charge. The in the reverse direction to the initial current, hence
voltage plateaus because the maximum voltage that the negative current spike.
can develop across the capacitor is governed by the The voltage measured across the resistor looks
voltage of the power supply. When the voltage pulse exactly like the current measurements because the
is turned off, the voltage across the capacitor gradu- voltage drop across a resistor is equal to current mul-
ally decays because it takes time for the electrons dis- tiplied by resistance:
placed on either side of the capacitor plates to return
to their base state—equal electrons on both sides. Ohm’s law: V = I × R
The current flowing through the device (I) as
measured by the ammeter has a complex waveform Since resistance is a constant, the voltage drop across
because of the capacitor. When the voltage is first the resistor is directly proportional to the current, so
turned on, there is a lot of current flowing through the the relationship is linear.
What does this have to do with filters? The RC band of interest. For example, if the low-frequency
circuit is the simplest filter. Looking at the single step filter setting is high, then delta activity will not only
voltage just presented, the voltage measured across be reduced in amplitude, but differentiated, making a
the capacitor looks like the signal voltage but with faster component that was not in the original signal.
the high-frequency component filtered out—you can Similarly, if a high-frequency filter is set too low, spike
see what the signal voltage was, but not how fast it got activity will be blunted, perhaps giving the appear-
there. In contrast, the voltage measured across the resis- ance of a normal physiological potential of lower fre-
tor looks like a differential (dV/dt) of the signal voltage quency, again not part of the original biological signal.
(V). We can see the positive change in potential as the A 60-Hz filter can also attenuate spikes, though with
pulse starts and the negative change as the pulse stops, modern equipment, this is not as problematic as it
but we cannot see the plateau in voltage; essentially, the once was.
low frequency component has been filtered out. Phase shift occurs when a rhythm is passed
Rule: For the RC circuit, the voltage across the through a filter. The most common manifestation of
capacitor looks like a high-frequency filter signal and this is a phase lead; this is when the rhythm appears
the voltage across the resistor looks like a low-frequency to move ahead in time, due to a differentiating effect
filter signal. of the filter system. Consider a sine wave as shown in
This is a demonstration of passive filters, and the Figure 2-23.
simplest version—the RC circuit. Active and digital The original signal wave is shown on top, with
filters work in a similar fashion, but their physical peak positivity 1/4 cycle from the beginning (i.e.,
function is greatly different. 90 degrees). The wave is differentiated to filter out the
low frequencies. This is like the low-frequency filter.
Filters in Practice Every point of the lower wave is dV/dt, or the change
in voltage over time; dV/dt is most positive during
Passive filters, such as the RC circuit as just one exam- the rising phase of the native wave, most negative dur-
ple, have greater importance in generation of noise ing the falling phase of the native wave, and zero at
and distortion of signal than in equipment design. the flat points—peak positivity and negativity of the
The electrode leads have inherent resistance and native wave. When the points of peak positivity are
the proximity of the leads and other wires provides highlighted by dots to show a marker of the cycle of
capacitance. Therefore, unintentional RC circuits
can distort the signal voltage arising from the brain in
unpredictable and changing ways. Peak Peak
Active filters are circuits involving semicon-
ductors that amplify and attenuate the signal in a
frequency-dependent fashion. Though the exact Signal (V)
function is not presented here, suffice it to say that
frequency-dependent amplification involves feedback
Peak Peak
circuits that attenuate certain frequencies, and the
Filtered signal
active filters are not constrained by the high- versus (dV/dt)
low-frequency filtering function—specific frequency
bands can be accentuated or attenuated.
Digital filters are calculations performed on the
digitized data. The calculations can be of many types,
including smoothing across multiple data points, often Figure 2-23: Phase Shift.
with weighting, and attenuation of specific frequen- Filters not only alter the frequency response of the signal
cies. Digital filtering is performed on the digitized but can also produce a phase shift, where the peaks of the
data after analog amplification and analog-to-digital waves are not simultaneous with those of the input signal.
conversion. In this example, a filter has caused a phase-lead, where the
filtered signal is ¼ cycle or 90 degrees ahead of the native
Signal distortion occurs when the filtering process signal.
alters the appearance of signals within the frequency
the wave, you can see that the filtered wave is 1/4 cycle deviations in the quality or placement of electrodes
or 90 degrees ahead of the native wave. can greatly alter the recording. At times, electrodes
Phase shift is not important for most EEG appli- are considered to be mere junctures, connections in
cations. However, spikes may appear earlier because the circuit comprising the brain and EEG equipment.
of this phase-shifting effect, though this small effect However, the electrode and it’s interface with the
is not clinically important. Note that phase shift can scalp does have the ability to store and modify electri-
occur with digital filters as well as with analog filters. cal signal.
Filter Settings Electrode Basics
Filters are set to default values when the EEG Electrodes are connected to the scalp with a conduct-
machine is started. The most commonly used default ing gel, which serves a malleable extension of the elec-
values are: trode. Without this extension, any minor movement
of the head would result in mechanical disturbance
• Low-frequency filter = 1 Hz; of the electrode-scalp interface, producing electrical
• High-frequency filter = 70 Hz; artifact.
• 60-Hz filter = off. For most purposes, electrode basics are critical to
day-to-day performance of EEG.
The LFF may be decreased to better see some slow
Some important technical requirements of electrodes
activity, though most physiologic and pathologic slow
and electrode placement are as follows:
activity is seen well with default settings. The LFF is
increased if there is slow activity that at least partially • Electrodes of the same type and manufacturer;
obscures the recording, including specifically sweat • Equal lead length;
artifact. Unfortunately, increasing the LFF may also • Equal electrode impedances;
attenuate and thereby obscure some slow activity of • Leads are not in proximity to other devices;
clinical interest such as focal or generalized slowing. • Leads are not coiled.
The HFF is almost never increased. Reduction
of the HFF is usually done to attenuate fast activity, Electrodes should all be of good condition and be of
which can obscure the recording. This can include the same type and from the same manufacturer.
electrical artifact and muscle activity (EMG). The
former is best dealt with by the 60-Hz filter as well Electrode Theory
as improving the recording situation. Unfortunately,
lowering the HFF may attenuate and blunt some The electrode-amplifier interface is crucial to the
physiologic fast activity such as epileptiform dis- understanding of electrode theory. A circuit diagram
charges. This means that the epileptiform activity falls can be drawn that encompasses some of the essentials
into the noise of the recording. of the patient-electrode-amplifier interface.
The 60-Hz filter is most commonly needed when Referring to Figure 2-24, the signal voltage (Vs)
performing EEGs in the ICU or other portable is generated by the brain and conducted to the scalp.
position. In the office laboratory, this filter is rarely The electrode resistance (Re) is really impedance,
needed. In the hospital laboratory, the filter should which indicates frequency-dependent resistance.
not be needed, but this is not always realistic. The current flows from these electrodes through the
leads and to the input of the amplifier. The input
Electrodes of the amplifier is high-resistance, which results in
little charge being required in order to detect a volt-
Overview age. Therefore, the input resistance (Rin) should be
much larger than Re and the resistance of the body
Electrodes are often given an afterthought in the per- from which the recording is made. Again, while
formance of EEG, however, electrode properties are we are speaking of resistance, impedance is a more
a critical part of the EEG system, and even minor accurate term.
Re essentially conducting electric charge mainly in one

direction well, and the opposite direction less well.
A junction potential can be developed across inter-
faces, which can create electrode pops and distort the
VS Rin
frequency response of the recording system.
Needle Electrodes
Re
Needle electrodes are seldom used for EEG, being
used mainly for EMG. Fixation of scalp electrodes
VS is so good that needle electrodes for EEG are all but
C Rin
obsolete.
Intracerebral Electrodes
Figure 2-24: Electrode Theory. Subdural strips and depth electrodes are commonly
Top: Diagram of the electrode-amplifier interface. VS is the used for presurgical monitoring of patients with epi-
signal voltage from the body. Re is the electrode resistance. lepsy. Subdural strips are metallic electrodes that are
Rin is the input resistance of the amplifier. The signal voltage similar to those used for scalp recordings. The direct
is equal to the sum of voltages across the electrode (Re) and
the input resistance of the amplifier (Rin). Bottom: Same continuity of the electrode metal with the brain tis-
diagram as in A, but a small capacitance (C) is inserted into sue is less important than the field of recording. The
the circuit. This capacitance is created by proximity of the exposed area of metal is less than with scalp elec-
electrode leads and electrodes. trodes, so that the field of recording is more restricted.
Depth electrodes are inserted within the brain tis-
sue to a specified target. The exposed area on depth
In the second diagram, there is a small capaci- electrodes is extremely small, again restricting the
tor between the electrode leads. This is not a struc- recording field of view.
tural capacitor but rather is due to proximity of the
leads. This capacitance, along with the resistance of
the electrode-patient interface, creates an RC circuit Analog-to-Digital Conversion and
that can modify the recorded signal. The effect of this Digital Data Manipulation
capacitance is to distort the incoming signal, essen- The analog signal recorded from the brain is ampli-
tially acting as a filter. fied to increase the size of the signal so that there is
The signal seen by the amplifier is the most faithful sufficient signal to obscure noise introduced from the
representation of the input from the brain when all of conduction from head box to the analog-to-digital
the technical requirements for electrodes noted above converter. Subsequently, the analog signal is con-
are met and when the effects of noise-causing errors verted to digital format using an analog-to-digital
have been minimized. converter (ADC). The ADC performs analysis on the
analog signal, sampling the signal at specified times
Electrode Composition and making measurements. Analog-to-digital conver-
sion was discussed above, with Figure 2-19 illustrating
Electrodes are composed of a variety of metals. While the concept.
silver and gold have been traditionally used, a variety The frequency of sampling is dependent on the
of other metals are used. Electrodes are reversible or hardware, but generally, most electrophysiological
irreversible. Reversible electrodes include the typical equipment samples fast enough to have a good repre-
silver chloride electrodes. Reversible electrodes have sentation of time-dependent changes in the biologi-
easy bidirectional chemical reactions accounting for cal signal. The sample is taken in a microsecond, then
the movement of charge. Non-reversible electrodes the converter waits until it is time to sample again.
have difficulty with electron flow in one direction, Most ADC devices use the same converting circuitry
to sample more than one channel, so a sample is taken scratch, using assembly language. More commonly,
from channel 0, then channel 1, then channel 2, and so they are written in high-level languages that rely on
on. When the ADC has converted the complete list, it small sub-applications (applets) or runtime-routines
waits until the next time. The interval between samples for performance of the elementary processes of input
is the intersample interval, or ISI. This is sometimes and drawing, for example.
called the dwell time, although this is a misleading The displays required for the interpretation of
term and should be discarded. The number of samples EEG are generally higher resolution than most budget
per second is the sampling rate, not the sampling fre- displays. The reader is encouraged to spend the extra
quency, the latter being wrong because this is a descrip- money for larger and higher resolution displays. This
tion of amount per unit time and not frequency. greatly improves the ease and accuracy of interpretation.
In practice, the time resolution (sampling rate)
and voltage resolution (amplitude of voltage thresh- Standards
old levels) is so good that the reconstructed wave-
form would be virtually indistinguishable from the Overview
native waveform, and not a rough approximation as
in Figure 2-19. Standards for performance of EEG are established by
The digital data is able to be manipulated in a routine clinical practice and by published recommen-
way that is impossible with analog data. Filters have dations. Many of the technical aspects have already
already been discussed, and most of this discussion been discussed. Chapter 3 presents filter settings,
centered on analog filters. Digital filters are calcula- amplifier gain, display settings, performance of activa-
tions performed on the digital data. tion methods, documentation, and storage.
The calculations can accomplish various tasks,

including: Routine EEG
• Remove high frequencies; There are routine minimum standards that which
• Remove low frequencies; should be met and are outlined in Table 2-3. Special
• Remove specific frequencies, such as 60-Hz line comment about some of the elements is deserved.
power artifact; Duration of recording: While 20 minutes is the
• Identify amount of specific frequency bands minimum for most patients, diagnostic sensitivity is
(power spectral analysis); served by longer recordings, even of 30–60 minutes.
• Identify potentials that might be epileptiform Also, if a patient appears to be approaching some
activity (spike detection); event, then continued recording is certainly needed.
• Identifying sleep stages (particularly for sleep Technicians need to be sensitive to the clinical
studies, not discussed here). situation.
Activation methods: Photic stimulation is per-
These calculations are not perfect. Frequency and formed on most patients. Hyperventilation (HV) has
timing distortion can occur, including phase shifts. a number of contraindications discussed elsewhere,
but separate from that, HV is not performed on intu-
Digital Displays bated patients.
Filter and gain: Standard settings are used initially,
Computer displays are most commonly used. Paper but these may have to be adjusted to achieve a quality
records are considered obsolete and as such are not recording. In general, this is discouraged since adjust-
discussed in detail. Modern machines display the ing these may alter the recording so that an incorrect
EEG data on a computer screen. clinical interpretation is rendered.
The mechanisms to show data on the screen are Electrode impedance: A wide range of electrode
part of computer operating systems, and the pro- impedances is proposed, but in general the impedances
gramming consists of calculations then telling the should be as similar as possible. Similar impedances
computer what you want the picture on the screen are more important than low impedances. Similarly,
to look like. Few modern programs are written from it is not always possible to maintain impedances less
Table 2-3 Technical Requirements for Routine EEG

Standard Description
Routine EEG should met At lest 20 min of relatively artifact-free recording, 30 min for brain death
the following minimum studies.
standards Performance of activation methods when appropriate.
Use of standard filter and gain settings, modified as needed, depending on
the clinical situation and the appearance of the recorded EEG
Recordings must be performed by a qualified technician.
Recordings must be interpreted by a qualified physician.
Standard recording HFF = 70 Hz
parameters LFF = 1 Hz
Sensitivity at start = 7 μV/mm
Electrode impedance = 100–5,000 ohms
Standard recording montages
than 5 kohm, so in that circumstance at least we should as originating in defined nuclei, but in general, the
have the impedances approximately equal. electrical potentials represent the summed electrical
Qualified technologist and physician: What serves as activity from a substantial number of neurons.
qualified for technician and physician can be debated, EEG recorded from the scalp is generated by the
but comprehensive training and practical experience cerebral cortex, with the portion of the cortex adja-
are essential. The training and experience of the prac- cent to the skull being the greatest contributor.
titioner are more important than the paper board cer-
tification. One could pass neurophysiology boards by Cortical Potentials
reading texts, but this would not suffice as adequate
interactive training. Most cortical efferents are oriented perpendicular to
Standard montages are discussed in this text. Most the cortical surface. The gyration of the cortex results
digital machines allow for changing the montage dur- in only a fraction of the cortical efferents being ori-
ing review. ented perpendicular to the scalp. Therefore, those
Recording storage: The recordings are to be kept, but neurons would be expected to have a disparate contri-
most states do not give specific guidelines for mainte- bution to the surface-recorded EEG. Electrical activ-
nance of the records. Each lab should consult regula- ity at the large cortical neurons produces dipoles that
tions in effect at their locations. But in the absence of are summed to generate the scalp EEG. It is thought
defined regulations, the following would be reasonable: that summated excitatory postsynaptic potentials
(EPSPs) and inhibitory postsynaptic potentials
• Keep reports indefinitely; (IPSPs) are responsible for most of the EEG activity
• Keep digital recordings of adults for at least recorded at the scalp. Surprisingly, action potentials
10 years; probably have a lesser contribution to the EEG. The
• Keep digital recordings of children until they longer duration of postsynaptic potentials is more in
reach 21 years of age. line with the duration of most scalp recorded EEG
activity, while action potentials are too short.
GENERATORS OF EEG POTENTIALS Scalp Potentials
EEG activity is due to charge movement in neuronal Scalp electrodes are unable to see all of the elec-
membranes. It is attractive to think of EEG activity trical activity of the brain. Synchronous activity
of numerous neurons is required for there to be a GENERATION OF ABNORMAL EEG

recordable wave from the scalp leads. One estimate ACTIVITY
is that approximately 6 cm2 of cortical surface must
be synchronously activated in order for there to be a Abnormal EEG activity can be epileptiform or
potential recorded at the surface. Scalp potentials are non-epileptiform (see Table 2-4). The two most
volume conducted through the skull and scalp, which important types of abnormal EEG activity are slow-
results in considerable attenuation of the activity. ing and epileptiform activity. Slowing indicates disor-
There is greater attenuation of potentials that rise and dered function of the neurons, whereas epileptiform
fall rapidly (i.e., higher frequency potentials). activity indicates abnormal synchronous activity.
Table 2-4 Abnormal EEG Activity

Category Differentiation Description
Epileptiform Single vs. Single discharge is typically interictal, and there are usually mul-
repetitive tiple single discharges during an EEG recording
Repetitive discharges are usually at least 1/sec, usually faster, and
are commonly associated with clinical seizure activity
Focal vs. multifo- Focal epileptiform activity can be due to a local structural lesion
cal vs. generalized or associated with local circuit abnormality not due to an identifi-
able structural lesion
Multifocal epileptiform activity usually indicates a developmental
or multifocal process, sometimes metabolic.
Generalized epileptiform activity which is primary, i.e., not spread
from a focal onset, usually indicates a genetic or developmental
process.
Non- Attenuation or Attenuation is reduction in amplitude. With normal frequency
epileptiform suppression composition can be due to intracranial or extracranial fluid
collection. With loss of faster frequencies suggests focal structural
lesion, i.e., infarction.
Suppression is marked loss in amplitude and indicates severe
abnormality in cortical function from almost any cause. Focal
suggests localized damage, generalized is often seen with hypoxia
and other diffuse causes.
Slowing Focal slowing is usually due to a localized structural lesion.
Generalized bisynchronous slow activity is usually metabolic or
due to deep lesions.
Generalized asynchronous slow activity has the broadest differ-
ential diagnosis but is usually a diffuse, multifocal, or metabolic/
toxic process.
Abnormal Abnormal frequencies other than slowing include excessive fast
frequency activity especially in an unexpected distribution, e.g. Alpha from the
composition frontal lobes in a patient with hypoxic encephalopathy is abnormal;
Alpha from the occipital region of an awake patient is normal.
Abnormal A wide range of transients develop that are not strictly speaking epi-
transients leptiform but are abnormal. Frontal intermittent rhythmic delta activ-
ity and triphasic waves are examples of abnormal transient potentials.
Attenuation and Suppression circuit loops between the cortex and thalamus. This
type of abnormality is reported in conditions affecting
Attenuation and suppression are sometimes used both cortical and subcortical structures, as well as in a
interchangeably, but they are slightly different. number of toxic/metabolic encephalopathies, and in
Attenuation refers to reduction in the amplitude of deep midline lesions. In the latter situation, general-
the EEG; this says nothing about the frequency com- ized bisynchronous slow activity may be referred to
position. Suppression is also lower amplitude but is as a projected rhythm.
typically very low in amplitude and often is associated
with a loss of faster frequencies. Generalized Asynchronous Slow Activity
Focal Attenuation Generalized asynchronous slow activity has a broad

differential diagnosis, though it usually indicates
Focal attenuation usually indicates a cortical lesion or encephalopathy. Some of the possibilities include
reversible cortical dysfunction, since EEG activity is degenerative processes, encephalitis, extensive multi-
generated at the cortex. Focal attenuation could also focal vascular disease, and toxic and metabolic disor-
result from an increase in tissue between the cortex ders. This pattern is likely due to poor synchrony and
and the recording electrode. rhythmicity of regions of the cortex.
Since each EEG channel displays the potential dif-
ference between electrodes, attenuation will be seen if Epileptiform Activity
there is reduction in the potential difference between
electrodes in a channel. In bipolar recordings where each Epileptiform activity involves abnormal synchronous
channel displays the difference between adjacent elec- activation of many neurons. Corresponding to focal
trodes, attenuation will be seen if there is an electrical epileptiform activity at the cellular level is a wave of
shunt eliminating the potential difference. Such a shunt depolarization called the paroxysmal depolarization
can be due to smeared conductive electrode gel connect- shift (PDS).
ing the two electrodes, or a chronic subdural hematoma.
Paroxysmal Depolarization Shift
Generalized Attenuation
The PDS is the fundamental electrophysiological sub-
Generalized attenuation may suggest a generalized strate of focal epileptiform activity. The PDS cannot
cortical injury or transient dysfunction. However, an be recorded with scalp electrodes but requires cortical
attenuated EEG in adults could be a normal variant, as microelectrodes for detection.
long as the frequency composition is normal; a tense The PDS is an extracellular field potential where
individual may have a low-voltage fast background, not there is a wave of depolarization followed by a wave
showing the normal appearance of relaxed wakefulness. of repolarization. High-amplitude afferent input to
the cortex produces depolarization of cortical neu-
Slow Activity rons sufficient to trigger repetitive action potentials,
which in turn contribute to the potentials recorded
Focal Slow Activity at the surface. Repolarization due to inactivation
of interneurons is followed by a brief period of
Focal irregular slow activity is usually due to a local- hyperpolarization.
ized subcortical structural lesion (or dysfunction). Cyclic depolarization and repolarization are
Focal slow activity seems to be a result of deafferenta- believed to be the cortical counterpart to rhythmic
tion of the cortex from subcortical structures. spike-and-wave discharges seen sometimes in epi-
lepsy. The rhythmicity may be at least in part due to
Generalized Bisynchronous Slow Activity the inability of cortical neurons to sustain prolonged
high frequency discharges, but in addition is likely
Generalized bisynchronous slow activity can be inter- due to built-in circuitry to inhibit repetitive dis-
mittent or continuous. It may be due to disordered charges. The repetitive discharge is not terminated by
neuronal exhaustion but rather by this mechanism of Spikes and sharp waves are occasionally surface
inactivation. There may be membrane effects inde- positive. In neonates, positive spikes and sharp waves
pendent of active inhibition to terminate seizures, yet may have a particular significance due to association
the exact mechanisms of seizure termination are still with intraventricular hemorrhage.
under study.
Seizures
Spikes and Sharp Waves
There is a grey zone between interictal activity and
Sustained depolarization of a neuron can result in ictal activity. Repetitive discharge on the crest of
multiple action potentials on the crest of the depo- the PDS may be prolonged to produce a seizure. In
larization. If one neuron is activated by this burst, addition, a prolonged discharge of one neuron may
there will likely be no neurologic symptoms and the then entrain a group of adjacent neurons to depo-
discharge will not be recorded from scalp electrodes. larize and repetitively discharge, thereby producing
However, if there is synchronous activation of multi- expansion of the region of epileptogenic activity and
ple neurons, this can be recorded on scalp electrodes prolongation of the discharge to duration which is
as a surface negative spike or sharp wave. clearly ictal.
3
EEG TECHNOLOGY
Karl E Misulis
OVERVIEW In addition to extracranial electrodes, intracranial

electrodes are used for presurgical evaluation and can
EEG technology used in clinical and video EEG be of several types, with subdural strips and depth
recording are similar; in fact, most modern equipment electrodes being the most commonly used.
can serve both purposes, routine office EEG record-
ings and long-term video EEG recordings. This was Measuring the Head and Electrode
not true years ago. When acquiring equipment, we Positions
suggest that you make the modest extra investment
to have video capability. This is invaluable for evalua- “10-20” Electrode Placement System
tion of patients with spells of uncertain etiology, and
establishing the diagnosis is much easier with direct The 10-20 electrode placement system is a standard
correlation of behavioral with electrocerebral activity. for placement of scalp electrodes used by virtually all
neurophysiology laboratories. The 10-20 system uses a
systematic measurement process to create reproduc-
EEG METHODOLOGY ible electrode positions. Figure 3-1 shows a diagram
Electrode Placement of the electrode positions, and a variation of this dia-
gram appears as an option on some EEG software
The standard 10-20 electrode placement system is packages. Many readers prefer to have the head dia-
used by virtually all laboratories. Additional elec- gram on the screen, even though the individual chan-
trodes are also sometimes used including: nels are labeled.
Terminology for most electrodes is two charac-
• Sphenoidal; ters. The first character is the region and the second
• Nasopharyngeal; character is an element in that region. The regions are:
• Supraorbital;
• Nasoethmoidal; • Frontal (F);
• Eye-movement; • Central (C);
• Electromyogram (EMG); • Temporal (T);
• Electrocardiogram (EKG). • Parietal (P);
30
EEG Technology 31
a b
F3 C3 P3
Fp1 G Fp2
Fp1 F7 T3 T5 O1
F7 F3 Fz F4 F8
T3 C3 Cz C4 T4
T5 P3 Pz P4 T6
O1 O2
Figure 3-1: 10-20 Electrode Placement System.

The “10-20” electrode placement system is routinely used. The system is based on established measurements, as described in
the text. a: View from the top. b: View from the left side.
• Occipital (O); If F8 alone is involved, or if the field involves F8 and

• Auricular (A); Fp2 (Fp2 records frontopolar activity but could also
• Frontopolar (Fp). detect dipoles originating at the temporal tip), then
it is not clear if F8 is anterior temporal or inferior
In addition, there are electrode designations for naso- frontal, hence the name anterior sylvian (our preferred
pharyngeal, sphenoidal, depth, submental EMG, eye term) or frontotemporal. This uncertain status of F7/
movement, EKG, and other physiological recordings. F8 has resulted in the exploration of “true” anterior
temporal electrodes (discussed below).
The second character of most electrode position desig-
nations follows these rules: Other leads of interest include:
• Odd numbers are left-sided; • Ear (auricular) with left being A1 and right
• Even numbers are right-sided; being A2;
• Lower-case “z” is midline; • Ground (G) electrode.
• Lower numbers are more anterior and/or medial
to higher numbers; Measurement of the head:
• Not all numbered positions are used for
routine EEG. • Measure the distance from the nasion to inion
across the vertex. Mark a line at 50% of this dis-
Therefore, the left central electrode is C3, and the cor- tance at the top of the head.
responding position on the right is C4. Cz is in the • Measure the distance between the preauricular
midline. C1 and C2 are not used in routine recording. points, just in front of the ear. Mark a line at 50%
F7 is lateral to F3, and T4 is anterior to T6. of this distance at the top of the head. The inter-
The importance of accurate electrode placement section of this line with that of step 1 is Cz.
cannot be overemphasized. Sloppy electrode place- • Lay the measuring tape from nasion to inion
ment, based on estimates and “feel” result in inaccu- through Cz. Mark 10% of this distance above the
rate cortical localization. nasion for Fpz and above the inion for Oz. Fz is
Notice that F7 and F8 have several names, reflect- 20% of this distance above Fpz. Pz is 20% of this
ing that they can record both anterior temporal or distance above Oz.
inferior frontal activity (see Figure 3-2). Examining • Lay the tape between the preauricular points
the field of discharges can be essential to determin- through Cz. T3 is 10% of this distance above
ing the source of recorded activity (see Figure 3-3). the left preauricular point, and T4 is 10% of this
For example, if the field is F8 and T4, then F8 activ- distance above the right preauricular point. C3 is
ity is anterior temporal, while if the field is F4 and 20% of this distance above T3, and C4 is 20% of
F8, then F8 is likely recording inferior frontal activity. this distance above T4.
Figure 3-2: Additional Electrode Names.

These are additional electrodes occasionally used.
• Lay the tape from Fpz to Oz through T3. FP1 distance anterior to O1. Measure in the same
is 10% of this distance from Fpz, F7 is 20% of manner for Fp2, F8, O2, and T6 over the right
this distance posterior to Fp1. O1 is 10% of this hemisphere.
distance anterior to Oz, and T5 is 20% of this • Lay the tape from Fp1 to O1 through C3. F3 is half
the distance between Fp1 and C3. P3 is half the
distance between C3 and O1. Repeat for the right
side, with the tape from Fp2 to O2 through C4.
F4 is half the distance between Fp2 and C4, and
P4 is half the distance between C4 and O2.
• Lay the tape from F7 to F8 through Fz, F3, and F4
Anterior temporal to ensure that the distance between the electrodes is
Inferior frontal
equal. Then lay the tape from T5 to T6 through Pz,
P3, and P4 to ensure equal interelectrode distances.
Additional Electrodes Outside the 10-20 System
Additional leads are occasionally placed, although not

as part of routine EEG performance (see Figure 3-4).
These include:
• Silverman “true” anterior temporal (T1 and T2)

electrodes to monitor anterior temporal activity;
Figure 3-3: Potential Fields.
The left field suggests activity in an inferior frontal location, • Zygomatic electrodes and cheek electrodes
whereas on the right is an anterior temporal location.On the for monitoring of lateral-basal temporal lobe
left the field suggests that F8 is an inferior frontal electrodes, activity; and
whereas on the right the field suggests that it is an anterior • Supraorbital electrodes for monitoring anterior
temporal electrode.
orbitofrontal activity.
EEG Technology 33
T1 electrode placement: The distance from the audi-

tory canal to the outer canthus of the eye is measured
and divided in thirds. T1 will be one cm superior to
the mark closest to the ear canal.
1 cm “10-10” Electrode Placement System
The 10-10 electrode placement system is based on

the same landmarks as the 10-20 system, but involves
1/3 1/3 1/3 the addition of electrodes between 10-20 electrode
positions (see Figure 3-5). Although there have been
T1 - Silverman anterior temporal several nomenclatures for this system, the one rec-
electrode ommended by the American EEG Society (now
the American Clinical Neurophysiology Society),
is the modified combinatorial nomenclature. In this
nomenclature system, the letters identify the location,
particularly the coronal plane location, and the num-
Figure 3-4: T1 Electrode Placement. ber (or z) refers to the position relative to the mid-
Diagram of electrode placement for the T1 electrode. line. The odd numbers (1 to 9) belong on the left, the
even numbers (2 to 10) belong on the right, and z still
stands for the midline. The smaller numbers refer to
The reason for the T1/T2 electrodes is that F7/ positions close to the midline and the larger numbers
F8, which are the anterior temporal electrodes, are to positions farther away from the midline. In this
physically located over the lateral inferior-posterior new nomenclature, the 10-20 electrode names could
frontal region. They do record anterior temporal lobe be preserved, with the exception of T3/T4 and T5/
activity, but may also record frontal activity. To mon- T6. These electrodes lie in the same sagittal planes as
itor mesial-basal temporal activity, the most com- F7 and F8 and needed to have the same numbers. T3
monly used electrodes are sphenoidal electrodes. and T4 were therefore changed to T7 and T8. T5 and
Nasopharyngeal electrodes were frequently used in T6, the posterior temporal electrodes, are close to the
the past, but are rarely used now because they are temporo-parieto-occipital junction, and as they are
unstable, easily dislodged, and become more uncom- in the same coronal plane as P3 and P4, were named
fortable over time. Deep sphenoidal electrodes are P7 and P8. In this Atlas, both new and old names for
inserted just below the zygomatic arch, 2 cm ante- these electrodes are used.
rior to the line between the tragus and the condyle The additional coronal electrodes planes created
of the mandible. The needle is directed horizontally in the 10-10 system are AF for anterior frontal, FC and
and approximately 10 degrees posteriorly. The tip FT for frontocentral and frontotemporal plane, CP
should rest close to the foramen ovale (at a depth of and TP for centroparietal and temporoparietal plane,
4–5 cm). Although their insertion is painful, sphe- and PO for parieto-occipital plane. Additional elec-
noidal electrodes are well tolerated and stable, mak- trodes in the 10-10 system are rarely used in routine
ing them ideal for recording seizures with long-term EEG recording. Even in epilepsy monitoring, it would
monitoring. Mini-sphenoidal electrodes are inserted be very impractical to use all the 10-10 electrodes.
in the same location to a depth of only 1 cm. This However, when the field of certain activity has to be
makes them possible to insert by EEG technolo- clarified, selected additional electrodes can be used in
gists. Although they are not as good as sphenoidal a region of interest. For example, in suspected mesial
electrodes for detecting mesial-basal activity, their frontocentral foci, FC1, FCz, FC2, C1, C2, CP1, CPz,
ease of insertion makes them useful for short-term and CP2 could be added for best delineation of the
recordings. Note that any inserted electrodes should field. In left temporal lobe epilepsy, FT7, FT9, and T9
only be placed by physicians well trained in their could be added and may obviate the need for T1 and
placement. T2 electrodes.
Figure 3-5: 10-10 Electrode Placement.

The bold black electrodes are ones whose name was changed from the 10-20 system nomenclature.
The following are the new and old names for the • Clean dead skin and dirt from the region, using
revised 10-20 system: the cotton-tipped applicator and a skin-prep gel.
• T7 = T3; • Scoop some conductive gel into the electrode.
• T8 = T4; • Place the electrode in position over the skin.
• P7 = T5; • Put a 2"x2" gauze pad over the electrode and push
• P8 = T6. it firmly onto the head, providing a seal, which
prevents the electrode from falling off the scalp.
Applying Electrodes The electrodes are attached to the scalp using gel,
which is a malleable extension of the electrode. The
Which to Use: Gel or Collodion gel serves to maximize skin contact and allow for fixa-
tion on the skin, which minimizes the effect of small
Electrodes are placed by either paste or collodion.
amounts of movement. The gel lowers the impedance
Paste is commonly used for routine short-duration
of the electrode-skin interface.
EEG recordings. Collodion is also sometimes used
Removal of gel-fixed electrodes is easy. The gauze
for routine recording, but is more commonly used for
pads are pulled off, then the electrodes are gently pulled
long-term recordings such as inpatient and ambulatory
off, tilting them to release the vacuum effect. Then, the
monitoring and sleep studies. Collodion takes longer
gel left on the scalp can be largely removed by rubbing
to apply and remove, so that paste is preferentially
with a warm, wet washcloth. After the patient washes
used for routine recording. Before application of elec-
the hair that evening, all traces of the recording are gone.
trodes by either method, the skin must be prepared.
Application of Electrodes with Collodion
Application of Electrodes Using Gel • Prepare the head at the electrode positions as
• Locate the positions for electrodes using the mentioned for electrode gel.
10-20 electrode placement system. • Place the electrode on the scalp.
• Separate strands of hair over the electrode positions • Place a piece of gauze soaked with collodion over
using the wooden end of a cotton-tipped applicator. the electrode.
EEG Technology 35
• Use compressed air to dry the collodion. Special Electrodes

• Insert a blunt-tipped needle into the cup and
scrape the skin to lower electrode impedance. Special electrodes are helpful in a minority of patients,
• Inject electrolyte into the cup of the electrode especially for pre-surgical evaluation. Table 3-1 sum-
using the blunt-tipped needle. marizes some of the important special electrodes, and
the following text describes them in more detail.
Collodion is used preferentially for patients in inpa-
tient monitoring units and for ambulatory monitor- Sphenoidal Electrodes
ing. This is much more secure than paste for studies Sphenoidal electrodes are used to record activity
which are longer-term or where the patient is moving. from the temporal lobe, which would not show on
Removal of collodion-fixed electrodes is more scalp recordings. The electrodes are inserted percu-
difficult. First, the collodion is softened by use of a taneously adjacent to the zygoma until they reach
solvent, traditionally acetone but more gentle alterna- the base of the skull. Sphenoidal electrodes should
tives are available. Then the areas are cleaned as above. only be used by physicians trained in their insertion
The degree of washing required is greater both imme- and experienced in interpretation of the recorded
diately by the technician and later by the patient. potentials.
Table 3-1 Special and Invasive Electrodes

Electrode class Electrode type Description
Non-invasive Sphenoidal Inserted adjacent to the zygoma to the skull base. Used
especially when temporal location is suspected. Alternative is
mini-sphenoidal electrodes.
Nasopharyngeal Inserted through the nose to record especially mesial-basal
temporal discharges. Unstable and uncomfortable, so seldom
used and not for long-term recordings.
Supraorbital Applied over the orbit especially for orbitofrontal discharges.
Needle An alternative to disc electrodes for almost any scalp
location, but offer no advantage and seldom used.
Nasoethmoidal Applied by ENT physician for recording from the inferior
frontal region. Seldom used.
Invasive Foramen ovale Percutaneously inserted into the region of the foramen ovale
for recording from the medial and basal temporal lobe.
Subdural and epi- Placed through burr holes and under or over the dura on the
dural strips or cylin- region of the cortex targeted on the basis of imaging, scalp
drical electrodes EEG, and/or clinical suspicion. Our lab uses exclusively
subdural strips.
Subdural grid Implanted through craniotomy, of varying size up to
8x8 matrix. Placed over a region of interest to refine localiza-
tion of the epileptogenic zone as well as mapping cortical
functions with electrical stimulation.
Epidural peg Implanted through small burr hole so that the distal aspect of
electrodes the peg is touching the dura. Multiple pegs can be placed to
cover large regions. Muscle artifact is eliminated.
Depth electrodes Placed stereotactically through burr hole, targeted on the
basis of imaging, EEG, or clinical suspicion.
Nasopharyngeal Electrodes surgery through burr holes. The strips allow for a
To record from the mesial-basal temporal cortex, detailed map of the recorded electrical activity. The
nasopharyngeal electrodes were used in the past, but strips are typically in an array on a small sheet, so
are now much less frequently used. These electrodes there is spatial coverage over the cortical surface.
can be irritating and increasingly so with the passage of Subdural strip electrodes should only be used by
time. In addition, they are unstable and are likely to be physicians trained and experienced in placement and
dislodged with casual movement, as well as by move- interpretation, and only as part of a comprehensive
ment with a seizure. They are certainly not appropriate epilepsy intervention program.
for long-term monitoring beyond a few hours.
Depth Electrodes
Supraorbital Electrodes Depth electrodes are used to localize seizure foci
For patients with suspected orbitofrontal seizure ori- for surgery. A depth electrode consists of an array of
gin, supraorbital electrodes may enhance the record- electrodes on a single barrel that is inserted into the
ing of epileptiform activity and ictal onsets from the brain, usually in the temporal lobe. There are mul-
anterior orbitofrontal cortex. It should be noted, tiple electrode contacts on the side of the electrode
however, that supraorbital electrodes will frequently array, so superficial and deep electrical activity can be
record anterior temporal discharges. Therefore, the recorded. The electrodes are placed stereotactically
interpretation of activity originating in the supraor- on the basis of imaging, scalp, or subdural EEG data,
bital electrodes will depend on the field of this activity. and/or clinical suspicion.
Only trained and experienced epileptologists
Needle Electrodes should use depth electrodes, and these are used
Needle electrodes offer no advantages over conven- almost exclusively for preoperative evaluation.
tional surface electrodes and should not be used for
routine studies unless recording cannot be accom- Physiologic Monitoring
plished any other way. The risk of infection to the
patient and technician is unacceptably high. It is often important to monitor physiological param-
eters in conjunction with the EEG (see Table 3-2).
Nasoethmoidal Electrodes Electrocardiogram (EKG) is the most important and
Nasoethmoidal electrodes are impractical as they needs to be monitored in all patients. One reason is that
require placement by an ear, nose, and throat (ENT) EKG artifact often appears on EEGs and could result
specialist. They are seldom used in routine practice. in confusion regarding the origin of some sharp poten-
tials. Additional electrodes for physiological monitor-
Invasive Electrodes ing need to be used predominantly in neonatal EEGs,
in brain death recordings, and in select situations, par-
Invasive electrodes are used almost exclusively for ticularly for intensive care unit (ICU) recordings. They
presurgical evaluation. include, but are not restricted to the following:
Foramen Ovale Electrodes • Eye movement electrodes;

Electrodes are placed using an introducer into the • Infraorbital electrodes (these are placed imme-
region of the foramen ovale. These electrodes are used diately below each eye, for distinguishing verti-
mainly for evaluation of patients with seizure foci in cal eye movements from frontal EEG activity);
the medial basal temporal lobe. These electrodes • Electro-oculogram leads (both electrodes are
are available commercially from several sources, but lateral to the eyes, one above the right eye, and
should only be used by physicians well trained in their another electrode below the left eye). These leads
insertion, use, and EEG interpretation. record eye movements. They are used mainly for
neonatal EEG and for sleep recordings.
Subdural Strip Electrodes • Submental EMG electrodes;
Subdural strip electrodes are used to evaluate patients • Respiration monitor (to monitor respiratory effort);
for epilepsy surgery. The strips are placed during • Air flow monitor.
EEG Technology 37
Table 3-2 Physiological Monitoring

Parameter Recording method Clinical use
EKG Electrodes below the right clavicle EKG artifact commonly contaminates EEG
and left 5th intercostal space on recordings, and EKG monitoring is essential to
the mid-clavicular line. differentiate this from cortical sharp waves and
spikes.
Eye movements Electrodes placed above and to the Eye movements are seen on scalp EEG and can
side of the eyes in an array to map be misinterpreted as frontal EEG. Also used
eye movements. during some sleep studies.
EMG Disc electrode is placed usually on Recording muscle activity, especially in neo-
chin and/or arm or leg. nates during sleep. Of limited value in adults.
Respiratory Chest transducer or airflow Especially for polysomnography.
transducer.
Oximeter Especially for polysomnography.
EEG technologists should be encouraged to be pro- marker in the middle of the page is eye opening with
active and creative, adding electrodes as needed. For the expected attenuation of the background. Two sec-
example, if the patient has right arm jerks and EEG onds later, there is onset of eye blink.
potentials that may possibly be linked to these, the Movement of the globe creates slow activity that is
tech could add an electrode over the right arm, which easily identifiable as ocular in origin when eye blink is
would help the electroencephalographer in identify- vertical. However, lateral eye movements and roving
ing a consistent relationship between the two. gaze can easily be confused with pathologic frontal
slow activity (see Figure 3-8). Lateral and vertical con-
EKG Electrodes jugate eye movements produce disparate deflections
EKG electrodes are almost always placed for routine on the eye leads, so that slow activity on the EEG can
EEG, but especially are useful during long-term EEG definitively be determined to be cerebral or ocular.
monitoring and sleep studies. EKG monitoring is
particularly helpful for patients having routine EEG EMG Electrodes
when there are sharp transients that might be EKG EMG is a frequent contaminant of EEG recordings, espe-
or slow transients that may be pulse artifact (see cially in temporal leads. EMG artifact may be mistaken
Figure 3-6). Because of the common cardiac and vas-
cular contamination of the recordings, routine EKG Fp1-A1
lead placement is certainly reasonable, as long as ade-
quate channels remain available for EEG electrodes.
F3-A1
Eye Movement Electrodes
Eye movement artifact is common due to the polar-
C3-A1
ization of the globe. The globe can be considered to
be a dipole, with the corneal region positive com-
pared to the posterior retinal region. The recorded P3-A1
electrical activity is due to potential difference of the

retinal pigment epithelium.
The patient in the recording shown in Figure 3-7
Figure 3-6: EKG Artifact.
had rapid eye blinks that appeared after eye opening.
EKG artifact is best seen with ear-reference montages. EKG
On the left side of the figure is a normal background must be differentiated from electrocerebral discharge.
with posterior dominant rhythm (PDR). At the
Figure 3-7: Eye Blinks.

Repetitive potentials on the right side of the figure from the frontal region are eye blinks.
E2 for sharp activity. A noncephalic EMG electrode can be

a used for identification of adult EMG activity but has lim-
E1
ited use in most routine studies (see Figure 3-9).
E1 - A1 Down EMG monitoring is most commonly used for
determination of muscle tone in sleep recordings in
Up neonates. EMG monitoring is also performed during
E2- A2 some sleep studies for documentation of nocturnal
myoclonus or other limb movements during sleep.
Respiratory Monitoring
E3
Respiratory monitoring can be performed in a num-
E2 E1 ber of ways. One is by chest transducer, essentially a
b E4
strain gauge around the chest recording chest excur-
Right sions. Airflow can be measured by a detector near the
E1- E2 nares, but this has a greater possibility of disturbing
the patient. Airflow meters can be used on intubated
Down patients, but this is seldom clinically indicated.
E3 - E4
Up
Montages and Localization

Figure 3-8: Eye Movement Recording.
Potential eye lead placements are shown. a: Differentiates Overview
eye movement from frontal cerebral activity b: Differentiates
direction of eye movement EEG is performed in a variety of montages, so EEG
can be assessed with a spectrum of presentations. For
EEG Technology 39
Fp1-F3 zero-potential, and this is seldom the case. The deflec-

tion of the display is the relative difference in poten-
tial. For example, if input 1 has a negative signal, one
F3-C3 would expect a upward deflection, but if the field of
the potential is such that input 2 has an even greater
negative signal, then the deflection would be down-
C3-P3
ward since input 1 is relatively positive in comparison
to input 2.
P3-O1
So, the terms active and reference are really misno-
mers. For bipolar montages, adjacent electrodes are
usually connected in the two inputs. By convention,
for any electrode pair comprising an EEG channel,
Figure 3-9: Muscle Artifact. input 1 would be the electrode either anterior or on
This is the left parasagittal portion of the longitudinal bipo- the left of the electrode connected to input 2. From
lar montage. The prominent spiky activity is EMG, from this discussion, it should be evident that a positive sig-
frontal and temporal muscles. nal of 10 μV at input 1 would produce the same display
deflection as a negative signal of 10 μV at input 2. So,
the “reference” input can be just as active as the “active”
example, a spike may be more visible on one mon- input—positive 10 μV at the “reference” electrode will
tage than another. Modern digital machines have the give the same vertical deflection of the display as nega-
ability to change montage while displaying the same tive 10 μV at the “active” electrode. The recording is an
epoch, adding extra interpretive flexibility. arithmetic subtraction between the “active” and “ref-
erence” electrode potentials. In the remainder of this
Rules of Polarity book, we will use the terminology of input 1, or first
input, and input 2, or second input.
All EEG channels have two inputs. Each EEG chan-
nel represents the difference in potential between
Montages
two adjacent electrodes. In referential montages (see
discussion below), the active electrode is in the first Montages are created so that viewing the EEG gives
input and a presumably neutral reference is in the sec- the neurophysiologist a clear picture of the spatial dis-
ond input. Because of this relationship, the first input tribution of EEG across the cortex (see Figure 3-10).
has been called “active” input and second input “ref- Because of this, many neurophysiologists have their
erence” input. However, in bipolar montages (and in favorite montages, though they realize that they should
the instance of an active reference), both inputs are view multiple montages in a recording. A good mon-
active. By convention, a negative potential in the first tage is one that can be easily imagined and remem-
input is seen as an upward deflection, whereas a posi- bered. It should also have equal electrode distances
tive potential in the first input is seen as a downward within each chain (unless it includes electrodes out-
deflection. Potentials arising in the second input will side the 10-20 system, such as sphenoidal electrodes).
have the reverse appearance. The American Clinical Neurophysiology Society
(2006) has published extensive guidelines for perfor-
Polarity convention of EEG display is as follows:
mance of EEG. These will be called the Guidelines for
• Relative negativity at input 1—upward deflection; the rest of this text. The guidelines recommend the
• Relative negativity at input 2—downward following:
deflection;
• Relative positivity at input 1—downward • Record at least 16 channels.
deflection; • Use the full 21-electrode array of the 10-20 system.
• Relative positivity at input 2—upward deflection. • Both bipolar and referential montages should
be used.
However, this elementary localization only applies • Electrode connections for each channel should be
if a signal is at one electrode and the other is at clearly indicated.
a b
Fp1 G Fp2
9 13
1 5
F7 F3 Fz F4 F8
10 2 17 6 14
A1 T3 C3 Cz C4 T4 A2
11 3 18 7 15
T5 P3 Pz P4 T6
4 8
O1 O2 12 16
c d
1 1 2
2 3 4 5 11 3 4 12
6 7 8 9 10 11 6 14
13 5
12 13 14 15 15 7 8 16
16 9 10
Figure 3-10: Montages.
Common montages used in clinical practice: a: Electrode placement terminology, b: Longitudinal bipolar, c: Transverse
bipolar, d: Referential
• Pattern of electrode connections should be made Recommended montages for routine use in adults
as simple as possible and the montages easily and children after the neonatal period are shown in
comprehended. Table 3-3. Additional channels are used when avail-
• Bipolar electrode connections should run in a able and needed. The additional channels may be
straight unbroken line with equal interelectrode used for EKG, eye movements, respirations, or EMG.
distances. The ipsilateral ear reference (Ipsi) can be replaced
• Display of more anterior electrodes generally should with the linked reference (LE) if there is prominent
be placed above those of more posterior location. EKG artifact from one or both ear references. The
• At least some common montages should be used EKG artifact tends to be of opposite polarity on the
between studies for ease of comparison. two sides, and linking the ears will usually attenuate
it or eliminate it.
In addition, some recommendations that most labs
adhere to include:
Localization
• Display of left-sided electrodes generally
should be placed above those of right-sided Localization of an abnormal potential depends on
electrodes. spatial mapping using the electrode positions and
• Although 16 channels are considered minimum, applied montages discussed above. Here, we will
montages should be used employing the maxi- discuss montages and localization in more detail.
mum number of channels of the machine. Modern EEG equipment allows for changing of
• Three classes of montages should be used: montage on the fly, and allows for review of the same
• Longitudinal bipolar; epoch in multiple montages for comparison. This
• Transverse bipolar; is only part of the post-processing that can be per-
• Referential. formed on digital EEG recordings.
• If sufficient channels are available, polygraphic
channels are desirable. EKG is most commonly Referential Montages
recorded, but EMG and respiratory monitoring In referential montages, a single reference or two ref-
can be of value. erences (as in linked ear reference recordings) will
EEG Technology 41
Table 3-3 Montages in Routine EEG

Channel Longitudinal Transverse Average Reference Circumferential
bipolar (LB) bipolar (TB) (Ave) (Ref) (Circ)
1 Fp1–F3 Fp1–Fp2 Fp1–Ave Fp1–A1 T3–F7
2 F3–C3 F7–F3 Fp2–Ave Fp2–A2 F7–Fp1
3 C3–P3 F3–Fz F3–Ave F3–A1 Fp1–Fp2
4 C3–O1 Fz–F4 F4–Ave F4–A2 Fp2–F8
5 Fp2–F4 F4–F8 C3–Ave C3–A1 F8–T4
6 F4–C4 A1–T3 C4–Ave C4–A2 T3–T5
7 C4–P4 T3–C3 P3–Ave P3–A1 T5–O1
8 P4–O2 C3–Cz P4–Ave P4–A2 O1–O2
9 Fp1–F7 Cz–C4 O1–Ave O1–A1 O2–T6
10 F7–T3 C4–T4 O2–Ave O2–A2 T6–T4
11 T3–T5 T4–A2 F7–Ave F7–A1 Fp1–F3
12 T5–O1 T5–P3 F8–Ave F8–A2 F3–C3
13 Fp2–F8 P3–Pz T3–Ave T3–A1 C3–O1
14 F8–T4 Pz–P4 T4–Ave T4–A2 Fp2–F4
15 T4–T6 P4–T6 T5–Ave T5–A1 F4–C4
16 T6–O2 O1–O2 T6–Ave T6–A2 C4–O2
17 Fz–Pz Fz–Cz Fz–Ave Fz–A1 Fz–Cz
18 Cz–Pz Cz–Pz Cz–Ave Cz–A1 Cz–Pz
19 EKG EKG Pz–Ave Pz–A1 EKG
20 EKG EKG
be in the second input of each channel, while active contaminated. Therefore, the average reference is not
electrodes are in the first input. In the ideal situation ideal for examining generalized spike-and-wave dis-
where the reference is neutral, potentials of interest charges and other generalized abnormalities. The ipsi-
are compared by amplitude, the largest amplitude lateral ear reference, or linked ear reference, is optimal
reflecting the center of the field. However, references for evaluation of generalized discharges, which tend to
are frequently not neutral, hence the importance of have the lowest amplitude in the temporal periphery.
considering more suitable references. With digital The ear reference is not suitable for temporal lobe dis-
EEG recordings, this task is facilitated, as the same charges since the ear can be considered a lateral-basal
potential can be examined with a variety of refer- temporal electrode. It is frequently involved in tempo-
ences. Thoughtful consideration of the most appro- ral lobe discharges. The average reference will usually
priate reference is necessary. be a more appropriate reference for studying tempo-
The average reference is derived from averaging ral lobe activity. However, if the temporal lobe activ-
the activity of all electrodes (except frontopolar and ity has a wide field, the average reference could also
anterior temporal, which are subject to large eye become contaminated. Using the midline electrodes
movement artifacts). Assuming that no large field (Cz, Fz or Pz) is useful, particularly for evaluating
synchronous activity is present, there is cancella- ictal activity if the ictal discharge has not involved the
tion based on cerebral activity being out of phase in midline. In particular, if the discharge field is ante-
different channels. The average reference is ideal for rior, Pz could be sufficiently distant to be neutral. In
any focal abnormality. However, when discharges contrast, if the ictal discharge is predominately pos-
have a wide field, the average reference may become terior, then Fz would be more appropriate. In some
instances, the average reference can be manipulated to Localization of Potentials in a Bipolar Montage
become neutral by removing affected electrodes from In a bipolar montage, localization is accomplished by
the average reference. identification of reversal of polarity. Below are several
Laplacian referential montage is excellent for iden- situations and the expected pattern with each.
tifying focal gradients by using a unique reference for
each electrode, weighted by surrounding electrodes. • Potential is present in a single electrode: In this situ-
The Laplacian montage is excellent for pointing out ation, there will be reversal of polarity between
small focal potentials with a steep gradient, but is not the two channels that have this electrode in com-
appropriate for displaying generalized activity. mon. (see Figure 3-11)
• Two electrodes involved, both contained within a
Localization in a Referential Montage chain of electrodes, and not involving the ends of
Localization in a referential montage is dependent on the chain: The channel that compares the two
amplitude, assuming the presence of a neutral refer- affected electrodes would show cancellation.
ence. The channel containing the highest amplitude The reversal of polarity will be seen across that
will represent the location at the center of the field. channel. One can state that there is a reversal of
Unfortunately, there is no ideal reference that is polarity across a zone of equipotentiality between
always neutral. For very focal discharges, the average electrodes B and C. The two channels showing
reference is very suitable, because the contribution of a deflection will be mirror images of each other,
the focal discharge to the average is greatly diluted by again with equal amplitude of opposite polarity.
the uninvolved electrodes. (see Figure 3-12)
• Two electrodes, unequally involved, each contained
Bipolar Montages within the chain, with the ends of the chain not
Bipolar montages are composed of chains linking involved: There will be reversal of polarity seen
adjacent electrodes. These chains are either longitu- between the two channels that contain the most
dinal or transverse. They may also be in an arc, circle, affected electrode. The potential will also be
or semicircle. The longitudinal bipolar montage (also seen in the channel containing the less affected
called “double banana” because of the appearance on electrode and the unaffected electrode adjacent to
a montage diagram) can be organized in several ways. it. The amplitude in the channel with the largest
It is a general (but not universally followed) conven-
tion that anterior should be ahead of posterior and
A-ref
left ahead of right. Besides the example displayed in A-B
the table (see Table 3-3), one acceptable alternative
B-ref
arrangement is left temporal, left parasagittal, midline, B-C
right parasagittal, right temporal; another arrange- 100 100
C-ref
ment is left temporal, right temporal, left parasagittal, 100
right parasagittal, midline. There are relatively fewer C-D
potential permutations in the arrangement of trans- D-ref
verse bipolar montage. D-E
Localization of EEG activity in bipolar montages E-ref
is by reversal of polarity (see discussion below) and
is optimally accomplished when the center of the Figure 3-11: Referential Versus Bipolar
field is within the center of the chain. As a result, EEG Montages—Example A.
Referential recording on the left and corresponding bipolar
activity centered in the frontal or occipital pole is not recording on the right. Electrode C is the only electrode
optimally assessed by either the longitudinal bipolar affected by the discharge. The number is a measure of ampli-
or transverse bipolar montage. This is where a circum- tude. The bipolar recording shows reversal of polarity at C,
ferential montage may be useful. In a circumferential the electrode in common between the second and third
montage, the frontopolar and occipital electrodes are channels on the right. Note that the B-C and C-D are mirror
images, and the amplitude of the deflection is similar but of
at the center of the anterior and posterior semicircular opposite polarity.
chains.
EEG Technology 43
A-ref • The potential involves one end of the chain and

A-B the electrode adjacent to it, equally: There will be
100 100
B-ref cancellation in the channel that contains the two
B-C affected electrodes. The channel next to it will
100
C-ref show a deflection. There will be no deflection in
100 subsequent channels. There will be no reversal of
C-D
D-ref polarity. (see Figure 3-16)
D-E
E-ref Figures 3-11 through 3-16 show simulated record-
ings associated with the localization examples just
Figure 3-12: Referential Versus Bipolar discussed.
Montages—Example B. Every pattern in a bipolar montage has several
Since electrodes B and C are equally affected, the difference
potential solutions in a referential montage, assuming
between them is 0, hence the flat line. There is a reversal of
polarity across a zone of equipotentiality between B and a neutral reference. Usually, one solution is the most
C. B and C are equipotential, i.e., equally affected. likely.
Consider Figures 3-17 and 3-18 together. The
left side of each figure is a bipolar recording that is
deflection will be equal to the sum of the ampli-
tudes in the two channels with smaller deflec-
100
tions. From this, one can conclude that if there is A-ref
100
a reversal of polarity that is not a mirror image, it A-B
indicates that there is involvement of more than a B-ref
single electrode. (see Figure 3-13) B-C
• Potential is present at the end of the chain and not C-ref
involving any other electrode in the chain: In this C-D
instance there will be no reversal of polarity. D-ref
A deflection will be seen in the first (or last) chan- D-E
nel of the chain, where the potential is contained. E-ref
(see Figures 3-14 and 3-15)
Figure 3-14: Referential Versus Bipolar
Montages—Example D1.
End of chain phenomenon. The potential originates in the
anterior end of the chain.
A-ref
A-B
50 50
B-ref A-ref
B-C A-B
100 50 B-ref
C-ref
100 B-C
C-D
C-ref
D-ref
C-D
D-E
E-ref D-ref
100 D-E
E-ref 100
Figure 3-13: Referential Versus Bipolar
Montages—Example C.
This illustrates how EEG is an arithmetic operation. The Figure 3-15: End of Chain
reversal of polarity at C indicates that the highest voltage is Phenomenon—Example D2.
at C. The finding of a lower amplitude at B-C than C-D sug- End of chain phenomenon. The potential originates in the
gests that there is involvement of B. posterior end of the chain.
100 100 40
A-ref A1 A2
A-B 100 80
100 B1 B2
B-ref 100
B-C 100 40
C1 C2
C-ref 100
D1 D2
C-D
D-ref 100 E2
E1
D-E
E-ref
Figure 3-19: Localization With a Referential Montage.
Referential recording. To the left are left electrodes and to
Figure 3-16: End of Chain—Example E. the right are right-sided electrodes. Figure 3-20 is the bipolar
The source leads have equal potentials at the end of chain. recording corresponding to the above referential montage.
Therefore, the bipolar montage shows a response that might
not be obviously end-of-chain..
identical. The right is a potential referential recording
that could correspond to the bipolar recording.
Which of these two possibilities is most likely?
100 In these examples, the distribution shown in
A-ref
A-B
50 Figure 3-18 is less likely than that of Figure 3-17,
50 because the Figure 3-18 distribution assumes that
B-ref
B-C 50 three electrodes are all equally affected, an unlikely
distribution.
C-ref
Although a bipolar montage can be used to
C-D suspect asymmetries in widespread activity, these
D-ref asymmetries have to be confirmed in a referential
D-E montage. The main reason for this is that each bipo-
E-ref lar channel is an arithmetic subtraction of adjacent
active electrodes. There will be a low amplitude if
Figure 3-17: Localization. adjacent electrodes are equally affected. The pres-
Left: bipolar recording, Right: referential recording of same ence of a high amplitude signal depends on a sharp
potential.
gradient between adjacent electrodes. Fortunately,
most potentials have the highest gradients near the
center of the field, but this is not always the case. An
electrical bridge due to electrode paste smear will
A-ref
50 produce a very low amplitude that could be misin-
A-B
B-ref
terpreted as attenuation of activity in that region.
50 50 The examples in Figures 3-19, 3-20, and 3-21 illustrate
B-C
these concepts.
C-ref
100
C-D
Special Considerations
D-ref
100
D-E Average versus Ear Reference: Contamination of
E-ref 100 the Average
Many laboratories use average montages with few
ear-reference montages; however, there are some spe-
Figure 3-18: Localization. cial considerations when the average is contaminated
Left: bipolar recording.Right: referential recording of the
same potential. by activity prominent in the record. The example
in Figure 3-22 shows the posterior dominant alpha,
EEG Technology 45
A1-B1 A2-B2 40 Fp1 Fp1-F3

40
B1-C1 B2-C2
40
C1-D1 C2-D2
F3 F3-C3
D1-E1 D2-E2
Figure 3-20: Localization With a Bipolar Recording.

Compare with Figure 3-19. The bipolar derivations might C3 C3-P3
suggest that the discharge is not seen on the left. This shows
how asymmetries must be confirmed in a referential mon-
tage before definitive interpretation.
P3 P3-O1
Figure 3-21: Localization with Different Montages.

Left: A referential montage is used where the reference is
over an inactive area. The sharp wave has a maximum at
C3 but the field can be seen at F3 and P3. FP1 and O1 (not
which is clear in the right side of the figure in this ear shown) are not in the field of the sharp wave.Right: Bipolar
reference epoch. montage, the left parasagittal portion of the longitudinal
bipolar montage.
Figure 3-23 is of the same epoch but with an average
reference. The posterior dominant rhythm is evident,
but has a field that extends outside of the occipital End of Chain Phenomenon
area. This rhythm may not appear to be the PDR, but Bipolar montage may have difficulty in localizing
is so since the native rhythm contaminates the average. discharges at the end of the electrode chain, as was
Leads without the PDR show the rhythm well. illustrated in the diagrammatic examples above.
Figure 3-22: Ear Reference.

Prominent alpha especially seen on the right side of this figure.
Figure 3-23: Average Reference.

Same epoch as the above figure but with average reference, the field is more extensive than with the ear reference because the
posterior rhythm contaminates the average.
Figures 3-24 through 3-26 show this for a real patient. hospital records pertaining to the study, particularly
For the LB montage, this end of chain phenomenon the designation of indication.
is at the frontopolar and occipital regions. In the TB
So the technician needs to verify the following:
montage, the end of chain affects especially the tempo-
ral region. • Identity of the patient;
The patient recorded in Figure 3-24 has a right • Correctness of the study;
frontal discharge that is seen on LB montage, but pre- • Particulars of the study so that the clinical
cise localization is difficult. Ear-reference montage question can best be answered.
for the same epoch (Figure 3-25) shows better local-
ization. Bipolar montage across the frontal region On the recording as sent to the reading physician, the fol-
(Figure 3-26) is best able to localize the discharge. lowing information needs to be attached.
• Name;
Running the Test • Age;
• Identification number of the patient;
Initiation of the Test
• Index number of the recording;
Patient Identification and Study Verification • Time and date of the recording;
The patient is identified just as for any hospital or • Clinical reason for the study;
office procedure, using clinic or hospital documenta- • Time of the last seizure, if appropriate;
tion, arm-band if available, and check-in ID if not. • Ordering clinician;
The study is also verified, since it is possible that • Current medications;
the wrong study has been scheduled. The technician • Sedative medications used;
can verify the study intent by review of the office of • Name of the technician;
EEG Technology 47
Figure 3-24: LB Montage.
Right frontal discharge but precise localization is difficult.
Figure 3-25: Ear-Reference Montage.

Same discharge but better localization with an ear reference montage.
Figure 3-26: Bipolar Montage Across the Front.

Bipolar montage across the front is best able to map the discharge.
• Technical summary, including activation methods visualization of electrocerebral potentials. When two
and artifacts; electrodes are electrically connected by conductive
• Technician’s observations, including regions of gel/paste, they act as a single large electrode. Even in
particular interest. referential recordings they are a problem, limiting the
sharpness of localization.
Pretest Calibration and Testing
Pretest calibration and testing should be fairly stan- Square-wave Calibration
dard and includes the components discussed below. Square-wave calibration (see Figure 3-27) produces
The study reader should review the results of this cali- a typical appearance that can be compared visually
bration and testing since errors are not always noticed from channel to channel. One or more channels that
by the technician and errors can have significant have distorted waves from square-wave calibration are
effects on interpretation. an indication of either errant settings or equipment
failure. Square-wave calibration is performed before
Impedance Testing and after the study.
Electrode impedance should be at least 100 ohms and A square-wave pulse is delivered from a wave-
usually no more than 5 kohm. Sometimes, impedance form generator into each amplifier input. This pulse
cannot be kept within this window, so if the imped- is 50μV in amplitude and is alternated on and off at 1
ance has to be higher than 5 kohm, then the impedance second intervals. The wave does not appear precisely
should at least be approximately equal for the elec- square because of the effects of the preset default
trodes. Excessively high impedance indicates that there filters.
is a problem with the leads or fixation of the leads to the The low-frequency filter (LFF) transforms the
scalp. High electrode impedance increases noise. plateau of the signal pulse into an exponential decay.
Excessively low impedance usually indicates The rapidity of the decay depends on the filter setting.
smear between the electrodes, and would impair The lower frequency the setting, the slower the decay.
EEG Technology 49
Figure 3-27: Square-wave Calibration.

Square wave calibration performed prior to a study.
Higher settings of the LFF cause the decay to baseline Bio-calibration

to occur rapidly. Biological calibration (bio-calibration, or Biocal)
The high-frequency filter (HFF) rounds off the assesses response of the amplifiers and filters to a
top of the peak of the calibration recording. Lower complex biological signal, composed of a host of fre-
settings of the HFF cause the peak to be blunted and quencies. In the days of paper recordings, the mon-
of lower amplitude. Higher settings of the HFF cause tage Fp1-O2 was used for every channel, testing the
the peak to be sharper and of higher amplitude. integrity of the amplification system. Nowadays,
We recommend trying different filter settings while digital equipment provides each channel with its own
recording square-wave calibration. The experienced amplifier, so Biocal can be each electrode against a
neurophysiologist can determine an error in response common reference or the traditional Fp1-O2.
of the system by abnormalities in the square-wave cali- The technician and reader should review the
bration. Some of these abnormalities include: Biocal for unexpected differences in amplitudes or
frequency responses.
• Peak too rounded;
• Peak overshoot; Integrity of the System
• Incorrect rate of decay; Integrity of the system is checked especially for stud-
• Too low or too high amplitude of the signal. ies where there is such little signal that the recording
system error has to be considered. Brain death and
These determinations are made in comparison with severe encephalopathy can produce recordings that
other recordings and in comparison to the recordings are almost flat. So to test the integrity of the system,
from the other channels. the technician touches the electrodes and the artifact
Figure 3-28: Biocal.
Biocal performed prior to a study. Same patient as in Figure 3-27.
is readily visible. Representative electrodes need to be During recording, the technicians typically also
touched, not necessarily each one. select a variety of montages, except during prolonged
recordings, so they can identify potentials of interest
Montage Selection to bring to the attention of the readers.
Modern digital EEG allows for montage selection by Filters

the interpreting physician rather than use of prede-
termined montages during recording. This way, tech- Standard low-frequency filter (LFF) setting for rou-
nicians do not have to be as attentive to the specific tine EEG is 1 Hz. This corresponds to a time constant
wishes of the anticipated reader during acquisition. (TC) of 0.16 sec. If the LFF is set higher, there is distor-
Most of us use a combination of longitudinal bipolar, tion and attenuation of some slow waves. The waves
transverse bipolar, and referential montages during can have an increased number of phases and seem
reading. A particular wave of interest can be reviewed to be composed of faster frequencies. The techni-
in multiple montages, which can greatly help localiza- cians should be discouraged from turning up the LFF
tion, but we must not fall into the trap of believing when there is an abundance of slow activity. The low
that different visualizations of the same transient are frequency filter setting can be adjusted downward to
multiple occurrences of a transient. improve the identification of suspected slow activity.
Montages with vertex or ear reference are used less Standard high-frequency filter (HFF) setting for
than in the past, mostly because of prominent elec- routine EEG is 70 Hz. This is slightly higher than
trocerebral activity of these electrodes making them line power frequency. Therefore, turning the HFF to
imperfect references. a lower frequency will attenuate electrical artifact;
EEG Technology 51
however, this should be discouraged, because this will Digital displays depend on resolution of the monitors,
also attenuate physiological sharp activity. graphics cards, and acquisition and review software,
The 60-Hertz or “Notch” filter attenuates spe- but in general, the display time is adjusted so that the
cifically line power, 60-Hz in the United States and display looks roughly similar to a paper display. For
Canada and 50-Hz in the United Kingdom. The 60-Hz a typical 19" monitor, this means display of approxi-
filter is not needed for most patients in office practice, mately 10 seconds of EEG on one screen, with part of
because the office laboratories are electrically pro- the display taken up by other data elements. But since
tected. However, in a hospital or especially ICU set- display sizes are not standard, we cannot give fixed
ting, the filter may be required in order for line artifact recommendations on display time.
to not obscure the recording. The filter should not Display time may be altered in a few circum-
be used to correct focal 60-Hz artifact, which is most stances. Display time can be shortened substantially
likely related to focally increased electrode imped- if the reader is comparing timings with very short dif-
ance. Focal 60-Hz artifact should prompt the technol- ferences (e.g. spike onset from one hemisphere or the
ogist to perform an electrode impedance check and other). Display time can be lengthened if the reader
correct electrode impedances. is concentrating on EEG features such as sleep stage,
Digital filters accomplish the same tasks as analog where overview of much longer times is warranted.
filters, and are essentially calculations performed on Page rate is the rate at which the pages change. If
the arrays of data. we were to change pages at a rate concordant with
the number of seconds displayed on the screen, the
Sensitivities study would be reviewed at native speed. Reviewing
each EEG at acquisition real-time speed would be
Amplifier sensitivity is initially set to 7 μV/mm. impossible for most of us, so we page through digi-
Increased sensitivity is used with low-voltage record- tal EEGs faster than acquisition. Many readers review
ings, most common in elderly patients in the awake the EEGs at approximately twice acquisition speed.
state, and in pathological states of electrocerebral sup- Faster speeds than this may increase the risk of miss-
pression. The sensitivity is increased to 2 μV/mm for ing transients or other subtle abnormalities. We are
brain death studies. Reduced sensitivity is used for also commonly stepping back in study time to replay
patients with high-voltage EEGs, such as in children, an event or region of interest, often with a change in
especially in the sleeping state, and when there are montage and/or sensitivity.
high amplitude transients such as seizure discharges.
Sensitivities on reading need to be selected Annotation
with care. Reduction in sensitivity to better view a
high-amplitude event may make lower-amplitude Important events must be noted using annotations that
components invisible, such as a small spike compo- are available on all modern EEG devices. Technicians
nent or notch. This effect is especially notable with need to be familiar with how to create and edit annota-
seizure discharges—a reduction in sensitivity to view tions and must know the preferences on the part of the
the discharges may appear to accentuate postictal reading physicians for documentation of annotation.
suppression because the sensitivity is not returned to
Among the observations that should be noted are:
default levels.
• Apparent state changes;
Display Time and Page Rate • Beginning and ending of activation procedures
and comments about the performance, e.g. good
The concept of display time is new to digital record- effort on hyperventilation or not;
ings. Traditional paper EEG recordings used a paper • Clinical events that might be seizures. The techni-
speed of 30 mm/sec; this gave an x-axis resolution cian will likely note the beginning and ending and
that allowed for adequate visual interpretation of the later will have to create more detailed notes about
spectrum of frequencies of routine EEG, just as the the event, appearance, etc.
standard sensitivities gave a y-axis scale that allowed • Response to stimuli from the technician. Our
for detection of most of the range of EEG amplitudes. technicians usually assess responsiveness with a
spectrum of stimuli ranging from sternal rub to response from the stimulus might be misinterpreted
questions assessing mental status. as electro-cerebral response.
• EEG findings that the technician has noted and
wants to bring to particular attention of the read- Provocation of Seizures
ing physician. Provocation of seizures by means other than activa-
• Artifacts identified by the technician and noted at tion methods is controversial to some clinicians, since
least the first time or two, e.g. ventilator, IV pump, they might see this as intellectually dishonest when
or other artifact of the ICU. Similarly, electrical used to elicit non-epileptic seizures. However, this is
transients that are typical of a medical setting, an important tool to help diagnose epileptic as well
such as nearby machinery turning on and off, as non-epileptic events, and the diagnostic yield cer-
should be noted if visible to the technician on the tainly justifies the procedure in select circumstances.
record. The implications of event misdiagnosis can be much
more important.
Patient Behaviors during the Test Mechanisms to provoke seizures include:
As part of the annotation, patient behaviors are docu- • Asking the patient what provokes the event, then
mented, so even if the study does not include a video re-creating that as best as possible in the lab; for
component, the reading physician knows the clinical example, standing quickly, eating or drinking, and
observations. For example, a low voltage fast back- listening to particular music have been described
ground has different implications in an unresponsive by patients as evoking clinical seizures, and these
patient versus one who is awake. were all tested in our laboratory during EEG
Clinical seizures are described in detail in the recording.
annotations, including onset and offset. Not only • Induction techniques such as hyperventila-
is a description of the seizure itself important, but tion and photic stimulation, which can trigger
also the postictal period. This is of particular use in epileptic seizures, can also be used to trigger
differentiating epileptic seizures from non-epileptic non-epileptic events. Suggestion can also be used,
events. though deception should generally be avoided in
Movement artifact deserves a description in clinical practice.
the technician’s annotations (e.g., tremor or dys- • The technician might remark that signs of an
kinesias versus agitated delirium versus clinical impending seizure are appearing. While a clinical
seizures). event in response to suggestion does not rule out
genuine epileptic events, this does at least make
Testing Patients during Events the argument for a psychological component and
favor non-epileptic events. The use of suggestion
Stimulation is controversial.
Technicians assess the responsiveness and mental sta- • Some laboratories have used injections of
tus of the patient during the study. For awake patients, intravenous saline to induce clinical seizures, but
this usually includes noting the response to questions this is done rarely and then only under rigorous
such as name and location, and some additional cog- conditions. This should be used as a last resort for
nitive responses (e.g., “Name a red fruit”). diagnosis, if ever.
For encephalopathic patients, responses to verbal
stimuli are noted, as are responses to tactile stimu- Activation Procedures
lation if there is no response to verbal stimulation.
For severe encephalopathy and coma, response to Photic Stimulation
sternal rub or similar is essential. The annotation of Photic stimulation is produced by a bright strobe,
the stimulus not only allows the reading physician to which is placed in front of the patient with the eyes
know when an alerting response might happen but closed. The flashes are bright enough to illuminate the
also lessens the likelihood that the mechano-electric retina even through closed eye lids.
EEG Technology 53
The stimulation protocols are programmed into sleep deprivation is still considered a physiologic acti-
most modern EEG machines, but one typical proto- vation method.
col is the following:
Artifact Identification and Management
• Train duration of 10 seconds;
• Interval between trains of 10 seconds; Artifacts are discussed in detail, but in general, the
• Initial flash rate of 3/sec. technician should note not only epileptiform and
response events on the record but also sources of
Higher flash rates are subsequently delivered up to potential artifact. Some of the common artifacts that
30/sec. deserve annotation on the record include:
Abnormal EEG activity elicited by a specific fre-
quency should be identified by the technologist, and • Swallowing;
subsequently that particular frequency should be • Chewing;
repeated at the end of the photic stimulation session, • Talking;
to verify that the response was not coincidental. • IV pump;
For safety reasons, it is not advisable to precipi- • Ventilator;
tate a full-fledged generalized tonic-clonic seizure • Nurse working with patient;
with photic stimulation. If a clear photoparoxysmal • Tremor;
response appears, the technologist should abort the • Other patient movement.
stimulation train before a seizure develops. If a con-
sistent photoparoxysmal response is noted at two to This list is not comprehensive, but is representative of
three consecutive frequencies, then stimulation can be the types of artifacts the technician should note.
resumed from the highest frequency to establish the
upper limit of the photosensitivity frequency range. Termination of the Test
Hyperventilation Post-procedure Calibration

Hyperventilation is performed for 3 minutes on Calibration after the procedure is similar to the
routine testing, and should be performed for 5 min- pre-procedure calibration. This should be routine
utes if there is strong suspicion of absence epilepsy. and include all of the elements of pre-procedure
Hyperventilation is often not performed in elderly calibration.
patients for fear of resultant vasospasm and impaired
cerebral perfusion, but at the time of this writing, we Documentation
are unaware of good data proving high risk. The technician’s worksheet is paper or digital equiva-
The normal response to hyperventilation is diffuse lent and contains most of the information required for
slowing with the appearance of theta range activity. the reader to interpret the test. Limitations of these
The slowing is of higher amplitude in children than data makes the reader occasionally need to review the
adults. Hypoglycemia augments the slowing. electronic medical record, but good preparative data
Hyperventilation is used predominantly to active the should allow this to be minimized.
3-per-second spike-and-wave discharge of absence The physician’s report can be dictated or electroni-
epilepsy. In some patients, the discharges are only cally generated but should be created in a timely fash-
seen during hyperventilation. ion. We require outpatient studies to be read within
24 hours of completion, and inpatient recordings
Sleep Deprivation should be interpreted as soon as possible so that criti-
Sleep deprivation increases the possibility of see- cal abnormalities are addressed.
ing epileptiform activity, and therefore is used for
patients in whom routine EEG has not been able to Storage and Archive
identify interictal epileptiform activity. Although Modern digital EEGs are much easier to store than
sleep is attempted in most EEG studies for epilepsy, older paper records, which had to be microfilmed.
Figure 3-29: Rhythm of a Specified Frequency.

The background wave has a frequency as indicated by the vertical lines. Although there is variation in wave-period, there is
an average frequency that described this rhythm.
Storage is usually on optical disc for archive with • Look for changes in state.
recordings kept on the computers for a variable length • Synthesize an impression that places the EEG
of time. We recommend maintaining a record available findings in the context of the clinical snapshot.
for on-demand online viewing at least until the physi-
cians have reviewed the record and seen that patient. This section discusses some specifics of the basic
For hospitalized patients who may have a series of interpretation of EEG.
recordings, maintaining the recordings online for as
long as the patient is in the hospital is warranted. EEG Analysis
Archive is through a number of mechanisms, and
many facilities keep two copies, one local and one Terminology
remote. This is similar to data handling of patients’
Rhythmic: term used to describe ongoing EEG activ-
electronic medical records.
ity composed of recurring waves of equal duration.
The waves need not be identical, but they usually
resemble each other. Cerebral activity is never per-
ROUTINE EEG REVIEW fect, and slight variation should be allowed. For exam-
ple, the activity in Figure 3-29 is rhythmic, but some
Overview individual waves are slightly shorter or longer than
others, as demonstrated in Figure 3-30.
EEG performance and interpretation should be a system- Rhythm: EEG activity composed of recurring
atic process, with the following elements: waves of equal duration. A rhythm is often character-
• Understand the clinical snapshot of the patient, ized by its frequency.
including reason for the study, age, and condi- Frequency: the number of waves of a specified
tions that affect interpretation. rhythm per second, or 1/wavelength. Frequency is
• Review the study for background patterns in the measured in Hertz or Hz, meaning cycles per second.
context of state. Wavelength is measured in milliseconds or seconds.
• Look for transients and rhythms that may be Frequency can be applied to single waves as well as to a
abnormal. rhythm. If applied to a single wave, inferred frequency
• Assess response to stimulation and activation is 1/wavelength. Most digital EEG manufacturers will
methods. provide automatic calculation of frequency by marking
Figure 3-30: Regular Rhythm.

This rhythm is regular. Although there is some variation in amplitude and appearance, the rhythm has uniform period.
EEG Technology 55
Figure 3-31: Irregular Activity.

This rhythm is irregular. Although visual inspection shows a rhythm, the pattern is irregular and a uniform frequency cannot
be counted.
the margins of a wave. For a rhythm, the frequency will moderately frequent, very frequent, or almost con-
express how many waves will fit in one second. In the tinuous. However, it may be most useful to indicate
example, nine waves can be counted between the two the estimated percentage of time that the activity is
1-second lines (Figure 3-30). The frequency can also be present.
derived with the formula: frequency = 1/wavelength. Transient: a wave or combination of waves that
The duration of the average wave is 111 msec or 0.111 sec. stands out from the surrounding background. A tran-
The frequency is 1/0.111= 9 Hz. For frequency determi- sient can be normal or abnormal.
nation of fast activity, the measurement can be made Complex: combination of 2 or more waves.
more reliably by counting waves contained in one sec- This combination will usually be consistent when
ond, because of slight variation in wavelength duration. the complex recurs. Figures 3-33 and 3-34 show a
Regular: applies to activity that is uniform, with polyspike-and-wave complex that includes a series
individual waves having fairly consistent shape, in of 3 spikes followed by a high voltage slow wave.
addition to fairly consistent duration. Thus activity Figures 3-35 and 3-36 show a series of spike-and-wave
that is regular will also be rhythmic. Most rhythmic complexes, demonstrating that complexes look fairly
activity will also be regular. This is sometimes referred consistent when they recur.
to as “monomorphic.”
Irregular: activity that is not uniform (see
Figure 3-31). It is in theory possible for rhythmic
activity to be irregular, but that is uncommon.
Arrhythmic: term used to describe ongoing EEG
activity composed of waves of unequal duration.
Figure 3-32 shows an example of arrhythmic activity.
In this activity, individual wave components have dif-
fering wavelengths. Arrhythmic activity is also irregu-
lar. Note that individual waves not only have unequal
duration, but also unequal shape and unequal ampli-
tude. This is often called “polymorphic.”
Figure 3-33: Complex Rhythm.
Activity such as shown in Figure 3-32 can be
A complex is a combination of two or more waves, The fast
continuous or intermittent. If the activity is inter- polyspike complex has a following slow wave.
mittent, it can be described as rare, occasional,
Figure 3-32: Arrhythmic Activity.

Arrhythmic activity consists of activity that does not have an apparent rhythm.This differs from irregular in that there is no
apparent rhythm on visual inspection.
Periodic: term used to describe transients or

complexes that recur, but with intervening activity
between them. The rate of recurrence of periodic
transients is less than the “frequency” of this transient,
determined as 1/wavelength. Figure 3-37 demon-
strates the difference between rhythmic and periodic
discharges. The bottom line shows a single transient.
The top line shows the same transient recurring as a
periodic discharge. The middle line shows the same
transient recurring as a rhythmic train.
Differentiation of a periodic pattern from a rhythm.
The period is the time from the beginning of one dis-
charge to the beginning of the next. The wavelength is
Figure 3-34: Analysis of the Complex.
the duration of the discharge. A periodic pattern has
This is the same complex shown in Figure 3-33, but the com-
plex is divided by the vertical markers into fundamental a period longer than the wavelength. A rhythmic pat-
components. tern has a wavelength that is immediately followed by
the next wave.
Spatial distribution. The electrodes involved with
a discharge and the degree of their involvement
determines the field. Discharges can be described as
focal, regional, lateralized, or generalized. Focal dis-
charges are restricted to a few electrodes on one side.
The term regional can be applied to a discharge that
involves more than a few electrodes. If electrodes on
one side are all affected, the discharge can be con-
sidered lateralized. Generalized discharges affect all
electrodes, on both sides. It is almost never the case
Figure 3-35: Spike-and-wave Complex. that all electrodes are affected equally. Many general-
This is a classic appearance of a spike-and-wave complex, ized discharges have voltage predominance anteriorly,
Well-formed spikes and associated slow waves. but there can be voltage predominance in a variety of
regions. The terms diffuse and widespread are some-
times used synonymously with generalized, but gener-
ally indicate a less clearly generalized field. For focal
and regional discharges, a field can be designated with
isopotential lines that join equally affected regions.
Figure 3-38 shows an example of a field. The center
of the field is at F3, then C3 is a bit less involved, fol-
lowed by Fp1 and F7, then Fz and Cz.
When discharges are seen in several locations,
then the temporal relationship of the activity in
these different regions can be described with the
following terms:
Synchronous: occurring in two regions simultane-
ously. To indicate that a discharge is occurring on the
two sides simultaneously, the terms bisynchronous or
bilaterally synchronous are frequently used. Figure 3-39
Figure 3-36: Spike-and-wave-complex. shows a bilaterally synchronous spike-and-wave dis-
This is a less-typical spike-and-wave complex, The spike com-
ponent is small and riding on the end of the previous slow wave.
charge. It is easiest to see how the spikes are simulta-
neous on the two sides.
EEG Technology 57
wavelength
period
wavelength
Frequency = 1/wavelength (measured in seconds)
Periodicity = 1/period (measured in seconds)
wavelength
Figure 3-37: Periodic Pattern.
Asynchronous: describes transients or other activ- side. The tracing in Figure 3-41 shows both indepen-
ity that is seen in several regions, but not simultane- dent and bisynchronous discharges.
ously. Independent is often applied to a more extreme Synchronous activity can be in phase, indicating
situation where discharges occur at different times in a perfect correspondence in time, or out of phase,
two or more regions, or on the two sides. The circled indicating a small delay on one side in comparison
discharges in Figure 3-40 are occurring independently with the other. When there is a horizontal dipole,
on the two sides and in different regions on the same with negativity in one region and positivity in
another, the discharge is out of phase in these two
regions.
Basic EEG Analysis
EEG analysis consists of analysis of rhythms and

characterization of transients. EEG rhythms are
divided into four frequency bands for descriptive
purposes (see Table 3-4). Each rhythm is not spe-
cifically normal or abnormal, but the interpretation
depends on the context. For example, alpha activity
in the occipital region is normal in an awake patient
with eyes closed. The same frequency of activity is
very abnormal when diffusely distributed in a coma-
tose patient.
Transients can also be normal or abnormal
Figure 3-38: Spatial Distribution of a Potential. depending on character and context. For example,
Spatial distribution of a potential is represented on this multifocal sharp transients in a neonate can be nor-
computer presentation.This is a standard view of the scalp,
and the lines represent potential isobars.
mal but are distinctly abnormal in an older child
or adult.
Figure 3-39: Synchronous Spike-and-wave Discharge.

The 1st and 3rd lines are from the left hemisphere and the 2nd and 4th are from the right hemisphere. The spike-wave pattern
is synchronous.
Figure 3-40: Asynchronous Discharges.

This shows independent discharges from the left and right hemispheres, which are circled in red. Line 3 is from the left hemi-
sphere and line 4 is from the right hemisphere.
EEG Technology 59
F7-Ave
F8-Ave
T3-Ave
T4-Ave
T5-Ave
T6-Ave
Figure 3-41: Independent and Bisynchronous Discharges.

The left side shows independent discharges, whereas the right side shows bisynchronous discharges in the same patient.
Fundamental Frequency Bands rhythm is sometimes used for the posterior domi-

nant rhythm, but this is not preferred. Therefore,
Alpha one needs to keep in mind the potentially confusing
Alpha rhythm is 8–13 Hz. It is most commonly seen dual use of this term. There are other EEG activi-
in normal patients from the occipital regions in the ties in the alpha range: the mu rhythm, which is
awake state with eyes closed. When the eyes open, the resting rhythm of the rolandic region, and the
the alpha rhythm is attenuated. Because the occipi- third rhythm, which is seen at times in the temporal
tal rhythm is in the alpha range, the term alpha region.
Table 3-4 EEG Rhythms

Rhythm Frequency Features
Alpha 8–13 Hz Waking posterior rhythm in older children and adults. Mu rhythm.
Alpha coma. Seizure activity in the alpha range.
Beta > 13 Hz Drowsiness in children. Drug-induced. Breach rhythm over a skull
defect. Seizure onset in the beta range.
Theta 4–7 Hz Drowsiness, young children; temporal theta in the elderly.
Structural lesion. Encephalopathy.
Delta < 4 Hz Sleep, posterior slow waves of youth. Focal structural lesion.
Encephalopathy.
Beta referred to as interictal epileptiform discharges or activ-

Beta rhythm is greater than 13 Hz, and is most often ity. Spikes have a duration of less than 70 msec, and
seen in patients who have been sedated with benzodi- sharp waves have a duration of 70–200 msec, there-
azepines and barbiturates. The beta component of the fore appearing less sharp than spikes. Combinations
rhythm should be commented on during interpreta- of spikes, sharp waves, and slow waves are also epilep-
tion of the record, and an association with concurrent tiform discharges (see Table 3-5).
medications should be considered. However, beta can Spikes and sharp waves generated at the crown of
be abnormal, so the rhythm cannot be overlooked. a gyrus are usually surface negative, with the positive
end of the dipole deep to the cortex. However, some
Theta spike foci have a horizontal dipole, where both the
Theta rhythm is 4–7.9 Hz and is seen most commonly positive and negative poles are seen on surface record-
in normal drowsiness and in children. Theta in nor- ings. One notable example is Rolandic epilepsy, in
mal children makes determination of subtle encepha- which the positive end of the dipole can be seen ante-
lopathy difficult. Theta is most likely to be abnormal if riorly. This is discussed in greater detail in Chapter 4.
it is the posterior dominant rhythm in a waking adult, There are a number of features that distinguish
or if it is focal. spikes and sharp waves from non-epileptiform sharp
transients. Epileptiform discharges are different from
Delta the surrounding activity. They tend to be of high volt-
Delta activity is less than 4 Hz, and is most commonly age; they are usually asymmetrical with a longer and
seen in sleep. There is a gradual increase in the amount larger second half in comparison with the first half;
of delta activity as the patient progresses from stage 2 they tend to have more than one phase; and they tend
to stage 3 and stage 4 sleep. Focal delta activity devel- to have an after-going slow wave (see Figure 3-42).
ops in patients with focal structural lesions, and a In addition, epileptiform discharges are more con-
variable and unusual appearance is called polymorphic vincing if they arise from an abnormal background.
delta activity. Rhythmic anterior or posterior delta Epileptiform discharges should be different from nor-
activity can be seen in patients with diffuse or meta- mal sharp activity (such as vertex waves) in their fields
bolic disorders, as frontal intermittent rhythmic delta and in the states of arousal of the patient. The features
activity (FIRDA) or occipital intermittent rhythmic of the spike and slow wave are compared between dis-
delta activity (OIRDA). charges, as an aid to localization and characterization,
and clear differentiation from normal activity.
Figure 3-42 shows some of the elements of an
Transients
epileptiform discharge. These include high volt-
age, asymmetrical shape, more than one phase, and
Spikes and Sharp Waves after-going slow wave.
Spikes and sharp waves are the terms used when sharp Spike-like potentials that are normal are frequently
transients are determined to be abnormal and sug- a source of over-interpretation. Sharp potentials that are
gestive of epilepsy. Spikes and sharp waves are also often over-interpreted include sharp physiologic activity,
Table 3-5 Epileptiform Transients

Transient Duration Variants
Spike 25–70 msec Spike-and-wave complex
Polyspike complex
Polyspike-and-wave complex
Sharp wave 70–200 msec Sharp-and-slow wave complex
Sharply-contoured slow wave > 200 msec Can be isolated or with a triphasic
(strictly not epileptiform) appearance.
EEG Technology 61
Second phase-negativity Sharply Contoured Slow Waves

These are transients that could have been sharp waves
Aftergoing slow wave
had they not been longer that 200 msec. Such dis-
charges have a weaker association with epilepsy and
should not be called epileptiform.
Second half-
First half-
169 mcV
223 mcV
Slow Waves
Slow wave transients can be in the theta or delta range
and stand out from the background (see Table 3-5).
Focal slow transients can be a sign of focal central ner-
vous system (CNS) damage or reversible dysfunction
(see Chapter 1). Focal slow activity can occasionally
First phase- Third phase- be the only abnormality seen in association with focal
initial positivity positivity epilepsy.
Figure 3-42: Analysis of the Spike-wave Complex.

The features of the spike and slow wave are com- Clinical Analysis and Interpretation
pared between discharges, as an aid to localization and
characterization. Review of Routine EEG
Some neurophysiologists begin with review of the
EEG before any of the clinical information is reviewed.
such as is seen with skull defects, EMG potentials, and
However, most of us prefer to know the clinical details,
artifact. Differentiation of spikes and sharp waves from
including the age of the patient, reason for the study,
non-epileptiform potentials may also take into consid-
current medications, and technician’s impression of
eration the consistency of appearance of epileptiform
the state.
discharges. Figure 3-43 shows a non-epileptiform sharp
activity that looks symmetrical and is similar to sur- Review includes determination of the following:
rounding activity except for higher amplitude and sharp- • Background rhythm;
ness. Figure 3-44 demonstrates lateral rectus spikes, • Topographical organization of the background
EMG potentials from the lateral rectus that could be activities;
misinterpreted as epileptiform discharges. • Transients;
Epileptiform discharges do not consistently indi- • State changes;
cate epilepsy. Caution should be used in the interpre- • Response to activation methods;
tation of pediatric EEGs with occipital or rolandic
sharp waves. Caution should also be exercised in the Particular attention is paid to the following:
final interpretation if only a single spike is recorded • Ictal activity;
during the entire EEG. Figures 3-45 through 3-49 • Sharp waves or spikes;
show examples of spikes and sharp waves. • Focal and generalized slow activity;
Figure 3-43: Spike-like Potentials.

Non-epileptiform potentials resembling spikes.
Figure 3-44: Lateral-rectus Spikes.

Spikes from action of the lateral rectus resembling cerebral spikes.
• Inappropriate response to stimuli; marks all the seizures, as well as suspected ictal dis-
• EEG correlates to changes in state or behavior. charges. The electroencephalographer reviews these
segments first, analyzing both the EEG discharges
It is often best to proceed with one uninterrupted
and the clinical seizure semiology. In addition, the
rapid review of the recording before returning to it for
electroencephalographer will usually review the
a more detailed and in-depth assessment. The reason
spike detections and time samples.
for this is that there may be a prominent abnormality
later in the recording that would alter the approach to
Guidelines to Clinical Interpretation
the interpretation of the preceding part of the study.
Clinical interpretation of EEG should take into
account not only the EEG recording but also the clini-
Review of Video EEG
cal information that was provided. Unfortunately, this
Video EEG is initially reviewed by the technician.
information can be quite limited, thus restricting the
It is unrealistic for the neurophysiologist to review
utility of the interpretation. As with all neurophysio-
every second of the video EEG, but the epochs
logic interpretations, the EEG report represents a type
reviewed include the ones thought to be of interest
of consultation. Therefore, the impression should not
to the technician and ones that were noted by the
only be descriptive but also clinically useful.
event marker. In our institution, a spike and seizure
detection program identifies suspected seizures An EEG report impression could read:
as well as spikes and sharp waves. In addition, the
• “Abnormal study because of generalized asyn-
patient and patient’s family are instructed to push
chronous irregular theta and delta activity.”
an event marker button, which leaves a mark on the
EEG recording. The technologist reviews all the Such an interpretation may not be useful to the refer-
patient events and computer seizure detections, and ring clinician.
Figure 3-45: Spike Potential.

The fast polyspike complex has a following slow wave. The
duration of the above discharge is 69 milliseconds. It there-
fore qualifies as a spike. The dotted vertical lines are 200 mil- Figure 3-46: Sharp Wave.
lisecond lines. The duration of this wave is 95 msec, so this is a sharp wave.
EEG Technology 63
Figure 3-49: Polyspike-wave Complex.

Polyspike and wave complex.
Figure 3-47: Sharp Wave.
Sharp wave without an associated slow wave. Even though it
has small slow wave, it is not called a sharp-and-slow-wave state changes, and presence and absence of normal
complex unless the slow wave has a high amplitude (often and abnormal rhythms or transients. Any epilepti-
higher than the sharp wave). form and focal abnormalities, abnormal responses, or
absence of response should be described. The clinical
The impression should include a summary of the interpretation may need to be tailored to the question
key findings as well as a clinical interpretation. These asked. For example, if the clinical question is “rule out
could be divided into two paragraphs, as below status epilepticus,” it would be helpful for the clinical
interpretation to add “there was no seizure activity.”
• EEG Diagnosis: “Abnormal study because of gen- Epilepsy monitoring unit reports follow the same
eralized asynchronous irregular theta and delta guidelines. In our center, the report includes, in addi-
activity. No focal findings were seen.” tion to identifying information, the following:
• Clinical Interpretation: “This EEG consistent with
a generalized encephalopathy, but is not specific • A preamble summarizing the background infor-
as to etiology.” mation and the reason for the study;
• A description of the baseline EEG (this is like a stan-
The impression is not a substitute for a description dard EEG with hyperventilation and photic stimula-
of the record. The body of the report would include tion, performed within the first day of admission);
a description of the record, including background, • A daily description of clinical seizures and their
electrographic correlate;
• A daily description of the interictal abnormalities;
• EEG diagnosis summarizing the key abnormali-
ties, starting with ictal discharges (focusing on
localization at onset), then interictal discharges,
then non-epileptiform abnormalities;
• Clinical interpretation. In this section, the clinical
seizure description is provided first, with a state-
ment about the localizing and lateralizing value
of the seizure signs, then a statement about how
the semiology agrees (or not) with the EEG ictal
onset and other EEG abnormalities, and then a
summary synthesis of all the findings, to provide
a seizure diagnosis, classification, lateralization,
Figure 3-48: Spike-wave Complex.
Repetitive spike-wave complexes. and localization, together with the degree of
certainty of these determinations.
Activation Methods stimulus. It is seen mainly at flash frequencies of

5/sec and less.
Overview
Driving Response
Activation methods are routinely used for inducement The driving response appears with faster flash fre-
of epileptiform activity in patients with suspected sei- quencies, 7/sec and up. Unlike the evoked response,
zures. Activation methods include hyperventilation, it is time-locked to the stimulus.
photic stimulation, and sleep deprivation. Details of
the methods of hyperventilation and photic stimula- Photomyoclonic Response
tion were presented above. The photomyoclonic response is EMG activity in the
frontal scalp muscles induced by the flash. Only sus-
Hyperventilation ceptible individuals will show this rhythmic activity.
There is about 50–60 msec between the flash and the
Hyperventilation is used predominantly to activate EMG activity.
the 3-per-second spike and wave discharge of absence
epilepsy. In some patients, the discharges are only Photoparoxysmal Response
seen during hyperventilation. The photoparoxysmal or photoconvulsive response
The normal response to hyperventilation is dif- is uncommon but is a fairly good marker for seizure
fuse slowing with appearance of theta range activity. tendency. The discharge typically starts later than the
The slowing is higher in children than in adults and onset of the flash and does not terminate when the
patients with hypoglycemia. flash train does. Differentiation from non-paroxysmal
activity is discussed in Chapter 4.
Photic Stimulation
Photoelectric Artifact
Photic stimulation is especially helpful for the identi- The photoelectric artifact is produced by light from
fication of primary generalized epilepsies with motor the photic strobe interacting with the electrode-gel
symptoms. complex. This is a chemical charge movement and
not physiologic.
Responses to photic stimulation can be normal, It is non-cerebral and is not EMG. The potential is
abnormal, or artifactual. These are: generated by the electrode-gel complex.
• Normal:
• Visual evoked response; Sleep Deprivation
• Driving response.
• Abnormal: Sleep deprivation increases the possibility of see-
• Photoparoxysmal response. ing epileptiform activity, and therefore is used for
• Artifact: patients in whom routine EEG has not been able to
• Photoelectric artifact; identify interictal epileptiform activity. Although
• Photomyoclonic response. sleep is sought in most EEGs performed for suspected
epilepsy, sleep deprivation is still considered a physi-
Examples of responses to photic stimulation are pre- ologic activation method.
sented in Chapter 4 on Clinical EEG, and are summa-
rized in brief here.
VIDEO EEG AND LONG-TERM EEG
Visual Evoked Response (VER) MONITORING
The visual evoked response or photic evoked
response is the same potential that is recorded EEG monitoring includes video-EEG and prolonged
during flash evoked potentials. This has a major EEG recordings even without video recording,
positive component from the occipital leads, O1 but this monitoring is most effective when video is
and O2; it occurs approximately 100 msec after each included. These techniques were once the arena only
EEG Technology 65
of academic institutions, but with improvements in medication selection. However, when seizures do not
technology, video EEG is available in most hospitals respond to initial therapy, doubts arise regarding the
and in some office practices. certainty of the epilepsy diagnosis or the certainty
Brief video EEG is typically performed in the hos- of the epilepsy classification. The most solid clinical
pital or office for one or more hours, usually lasting up diagnosis requires the ability to witness and analyze
to a working day. The video is captured along with the a typical seizure and its EEG correlate. The technol-
EEG. We prefer to use two monitors, with video on ogy of video EEG allows the capturing of events and
one and EEG on the other, but this is not universally provides the ability to replay seizures an unlimited
available. Modern EEG software generally supports number of times for detailed analysis of the clinical
dual monitor display. signs and the corresponding EEG changes.
Long-term video EEG is typically performed in the
epilepsy monitoring unit (EMU). However, long-term The main indications for video EEG monitoring are:
EEG can also be performed in some sleep labs and is • Diagnosis of atypical seizures or spells of unknown
often performed in hospital rooms, or in the ICU. nature. The need for video EEG could arise
Long-term EEG recording without video is often per- because events are atypical for seizures, because
formed in office and hospitals that do not have video there has been absence of evidence for epilepsy
recording capability. While these studies are often by history and by tests, because there has been
helpful, video should be used if available, and the cost no response to antiepileptic drug (AED) therapy,
of acquisition of video capability is quite reasonable. or because a patient with known epilepsy started
Ambulatory EEG can be a good option for offices having new “different” spells.
that do not have easy access to long-term inpatient • Accurate classification of seizures for optimal choice of
monitoring or for patients who do not have seizures in medical therapy. This situation applies to individu-
the EMU but only in their normal outpatient environ- als with documented epilepsy in whom there may
ment. We have used ambulatory EEG for many years, be incomplete or contradictory clinical and EEG
but the lack of good clinical-EEG correlation afforded data for classification purposes. An example of this
by inpatient study makes the latter preferable. There would include an adolescent with staring spells and
are home video-EEG devices, but we have no experi- an EEG that shows both focal and generalized dis-
ence with these systems. charges. The seizures could represent generalized
absence seizures, in which case the most appropri-
Clinical Indications for Video EEG ate therapy could be ethosuximide or complex
partial seizures, in which case ethosuximide would
Video EEG is used for direct correlation of clini-
be ineffective and a medication more appropriate
cal events with EEG. This is especially of use when
for partial seizures could be best suited.
patients are having events that might be seizures. It is
• Localization of the epileptogenic focus for possible
also helpful for patients with abnormal EEG in whom
surgical resection. There is evidence to suggest
the electroencephalographer needs to visualize the
that after failure of two antiepileptic drugs, the
clinical appearance (i.e., does the patient have a clini-
chances of seizure freedom with another agent
cal correlate to a finding on EEG?).
decreases markedly. Patients refractory to medical
Prolonged video EEG monitoring was developed
therapy should be investigated for the presence of
for more direct evaluation of seizures. The 20-minute
a surgically remediable epileptic syndrome.
“routine” EEG is only an indirect assessment in
patients with seizures and spells of an unknown
nature. Aside from select syndromes, such as child- Additional indications for video EEG monitoring
hood absence epilepsy and benign epilepsy with cen- include:
trotemporal spikes, the interictal EEG is often normal • Quantification of seizures. Although this tends to
in patients with epilepsy. be a research application, it could be clinically
If the diagnosis of epilepsy was assured clini- useful in counting frequent seizures that can be
cally, treatment could proceed without the need for easily counted on EEG, for example generalized
EEG evidence, but the EEG is still of assistance in absence seizures.
• Quantification of response to treatment. This is also of epilepsy surgery. This is a definitive epilepsy diag-
frequently a research application, but has clinical nostic procedure for most patients with refractory
application for checking the efficacy of therapy of epilepsy. It is seldom needed for patients with pri-
absence seizures in childhood absence epilepsy. mary generalized epilepsy. The sensitivity of inpatient
In this syndrome, seizures are frequent, and monitoring is increased by longer term recordings—
the response can be quantified with a 24-hour up to several days—and by withdrawal of AEDs.
monitoring study. Withdrawal of especially levetiracetam and valproate
• Studying seizure precipitants described in the may reveal discharges that may not be seen otherwise.
history. Short-term video EEG is most appropriate for
• Reflex epilepsy: video EEG monitoring can easily patients with episodes that are frequent enough to
record seizures if the reflex precipitant can be have a reasonable expectation of being experienced
reproduced. during a recording of 8 hours or less. These are usually
• Self-induction: some patients have resistant patients admitted for spells of uncertain etiology.
seizures because of auto-induction. Video EEG Ambulatory EEG is most appropriate for patients
monitoring can document the occurrence of with episodes that may be induced by events in the
auto-induction in this situation. patient’s usual daily life. While some equipment does
• Situational factors: when situational factors are allow for a video component of the recording when
reported to precipitate seizures, they may poten- the patient is in bed or otherwise stationary, most
tially be reproduced in the setting of the epilepsy ambulatory EEG is electrocerebral-only. This means
monitoring unit. that the detailed character of the clinical event cannot
• Documentation of ictal and interictal discharges dur- be determined from the recording. Also, very subtle
ing circadian rhythms. This is frequently a research events can easily be missed, especially since much
application. sharp activity can be presumed to be artifact without
• Clinical correlate of EEG discharge. Some patients a clinical correlate.
have EEG discharges that could be ictal in nature.
The presence or absence of clinical changes may Methods
be necessary for counseling regarding driving or
other restrictions. Simultaneous video with the Inpatient Long-term EEG Monitoring
EEG allows testing and demonstration of changes
in responsiveness or cognitive functions in con- This is performed in a fixed epilepsy monitoring unit.
junction with the EEG discharge. In this setting, the most up-to-date equipment uses
• Transitory cognitive impairment. This is pre- cameras fixed in the patient rooms. Two cameras
dominantly a research application. Very sensitive with different angles and zoom settings are possible
testing has allowed the demonstration of subtle but not mandatory. The electrodes attached to the
dysfunction in association with interictal epilepti- patient’s head are connected to a head box. Signals are
form discharges. amplified and transmitted through a cable to a com-
• Finding interictal evidence for epilepsy. This application puter that records the digitized EEG signal. The video
does not necessarily require the video component. signal is similarly digitized and synchronized.
Most epilepsy monitoring units currently use
seizure and spike detection paradigms. These are
EEG Monitoring Choices extremely helpful for identifying seizures that
patients are not aware of, but they have a very high
Possible choices for video EEG monitoring include: false-positive detection rate so that every detection
• Inpatient long-term video EEG monitoring; has to be reviewed to determine its validity.
• Inpatient short-term video-EEG monitoring; Patients are typically admitted for several days. If
• Ambulatory EEG monitoring. they have been on anti-epileptic drugs, these drugs
are reduced or discontinued in order to facilitate
Inpatient long-term video EEG is most appropriate for the recording of seizures. Some medications have
patients who are being evaluated for the possibility to be withdrawn carefully, as they can be associated
EEG Technology 67
with particularly severe withdrawal seizures. This may be needed to resolve the conflict and to increase
in particular has been demonstrated for carbamaze- certainty.
pine. Identification of seizures can be performed in Some patients have independent left and right
several ways. temporal seizure onsets, and these patients may still
be candidates for surgery if more than 80% of seizures
Most video EEG units include:
arise in one focus, or if only clinically insignificant
• An event marker button that the patient or seizures arise on one side and all clinically significant
patient’s family can push in the event of a seizure; seizures arise on the other. In these more complicated
• Automatic seizure detection program; cases, a larger number of seizures may be needed for
• Seizure log/diary kept by the patient/family/ accurate classification.
caretaker; In some patients with independent interictal epi-
• Screening the EEG or video. leptiform discharges arising on both sides, a particular
cluster of seizures may come from one of the two foci.
Some manufacturers offer density spectral array dis- In these patients, seizures cannot be recorded solely
play that could identify periods in which changes are from a single cluster. Repeat monitoring at a different
suspicious and warrant review for possible seizures. point in time may be advisable to record a separate
This can markedly facilitate the review of EEG for cluster of seizures.
possible seizures.
Using a combination of all of the above, long-term Monitoring for Differentiation of Epileptic from
video EEG monitoring in the EMU is successful in Non-epileptic Spells
the vast majority of patients in recording epileptic sei-
zures for analysis. If the purpose of monitoring is to determine whether
a seizure is epileptic or non-epileptic, the recording of
Repeated Admissions a highly typical non-epileptic seizure could be suffi-
cient for the purposes of monitoring. However, there
Occasionally, admission has to be repeated. If a sec- are potential pitfalls, and one should be extremely
ond admission fails to record seizures, the approach careful in the analysis of data. For many patients,
to video EEG monitoring may have to be modified. recording additional seizures is advisable and con-
One of the factors that contributes to the failure of tinuing to record until anti-epileptic drugs have
video EEG monitoring is the elimination of daily life been cleared would provide further assurance. Some
stressors when the patients are admitted. These stress- patients may have had epilepsy but new spells may be
ors may be necessary to precipitate seizures. non-epileptic. The recording of a characteristic new
Some patients have cyclical seizure patterns and spell that is non-epileptic does not necessarily elimi-
the video EEG monitoring session would have the nate the possibility of persistent controlled epilepsy.
highest yield if scheduled at the next expected cycle. Non-epileptic seizures are often provoked early
This is most commonly encountered in women with with suggestion, whereas epileptic seizures will often
catamenial epilepsy in whom seizures are most likely appear at a latency, as anti-epileptic drugs are cleared.
just before or during the menstrual period. In other Some patients may erroneously identify an event as a
women, seizures are also more likely around the time typical seizure because they do not know what hap-
of ovulation. Even men may have cyclical seizure pre- pens during a typical event. Not only can some patients
cipitation, and the video EEG monitoring could have with epilepsy be suggested to have a non-epileptic
a higher yield taking these into consideration. event, but others may spontaneously have an atypical
psychogenic event in the charged environment. It is
Monitoring for Presurgical Localization essential for a patient’s family member to identify an
event as typical. If typical events are recorded and are
If video EEG monitoring is scheduled for the purpose deemed psychogenic and nothing different happens
of presurgical seizure localization, then recording of after anti-epileptic drugs have been essentially com-
three to six seizures is usually required. In the pres- pletely cleared, then the possibility of pure psychogenic
ence of conflicting data, a larger number of seizures seizures is most likely. One can be most secure in this
diagnosis when the onset of episodes is recent and it sleep deprivation may be less effective. In patients
can be clearly confirmed that no events other than typi- whose seizures are predominately in sleep, particularly
cal recorded ones have occurred in the past. The use of patients with frontal lobe epilepsy, sleep deprivation is
other suggestion techniques has been controversial. useful only in as far as making seizures more likely with
In particular, the element of deception that could be the next session of sleep. It is best in these instances to
involved has been deemed unethical by many. alternate sleep deprivation and full night’s sleep. Using
Also, caution should be exercised because some sleep deprivation on consecutive nights and days may
patients with epilepsy are suggestible and may be not be justified or fruitful. If an ictal single-photon
driven to have events that they don’t normally have. emission computed tomography (SPECT) is planned
Even patients with non-epileptic seizures may have during the session of video EEG monitoring, sleep
typical attacks with suggestion. Hence, the verifica- deprivation at night can be followed by allowing the
tion with family members that recorded attacks are patient to sleep during the daytime when the ictal
typical of historical ones is essential. SPECT injection is possible. This is most useful for
patients whose seizures typically occur in sleep.
Monitoring for Classification of Seizure Type If a patient or family has noted a possible provok-
ing experience, then this should be reproduced in the
If the purpose of the video EEG monitoring is to clas- EMU as much as possible. For example, rare patients
sify the seizure type, then recording of a single seizure have seizures induced by reading, music, smells, or
may be sufficient if that recorded seizure has a clear other experiences.
focal onset and seizure semiology that agrees with Withdrawal of AEDs is able to unmask some dis-
the EEG localization. In other instances, however, charges that would be not seen with certain AEDs
one cannot be so certain with a single recorded sei- (e.g. levetiracetam, valproate, and benzodiazepines).
zure. In some patients, the seizure onset may appear In addition, withdrawal of AEDs can result in a greater
generalized but the clinical seizure pattern may sug- tendency to have the seizure spread over the cortex,
gest a focal origin. In these instances, it may become making it easier to see on scalp EEG.
necessary to record more than one event, in addition
to interictal epileptiform activity. Observation during the Study
Baseline EEG Recording Technician observation during the study should be an

active encounter. There are events that might occur
Ideally, every session of video EEG monitoring during a study which deserve some intervention by
should be preceded by a baseline EEG. This baseline the technician. For example, if a seizure discharge is
EEG provides the opportunity to record clean activity noted during a recording, the technician should give
while the patient is relaxed and inactive. The posterior a command to the patient, or otherwise try to ascer-
background rhythm can be recorded and its reactivity tain responsiveness. One command might be “Hold
tested to eye opening and closure. Hyperventilation up two fingers” and note whether the patient makes a
and photic stimulation should be a component of that correct, incorrect, delayed, or no response.
baseline EEG if not contraindicated.
Testing Patients during Events
Provocation of Epileptic Seizures
In epilepsy monitoring units where patients are
Withdrawal of anti-epileptic drugs is the main method observed continuously and in any short-term video
of precipitation of epileptic seizures used in the moni- EEG monitoring where an EEG technologist is pres-
toring unit. However, other techniques can be added, ent, the testing of patients during events is of great
particularly sleep deprivation. This is most effective for clinical utility.
generalized epilepsy, particularly juvenile myoclonic
Testing is aimed at the following:
epilepsy. In that condition, seizures sometimes occur
only in the setting of sleep deprivation and usually after • Establish if the patient is unresponsive;
arousal from premature awakening. In partial epilepsy, • Determine if there is impairment in specific areas;
EEG Technology 69
• Determine if the patient has recollection for items During hyperventilation, a common EEG
given during the spell, or for events that occurred response is generalized bisynchronous delta activity
during the spell. that is totally normal, particularly for younger chil-
dren (Epstein et al., 1994; Lum et al., 2002). However,
The authors suggest that the patient’s ability to follow a rare pattern of absence seizures involve 3-Hz delta
commands and to name items be tested at baseline. activity without coexistent spikes. Because of this
Should a suspicious ictal EEG activity appear or any pattern, it is also advisable to test patients who have
behavioral changes occur that are suggestive of a sei- a sustained generalized 3-Hz delta activity during
zure, then the patient should be given a command, hyperventilation, to determine if responsiveness
the response to which can be assessed visually upon is altered. A definite diagnosis of absence seizures
video review. For example, the patient could be asked is not possible without demonstrating a clinical
to point to the ceiling, touch his/her nose, or clap alteration.
his/her hands. The patient can then be given items to
name and to remember.
One study used a sentence from the Boston End of the Study
Diagnostic Aphasic Battery, “I heard him speak over
When Should the Study End?
the radio last night,” to assess reading abilities postic-
The video EEG monitoring study ends once a suf-
tally (Privitera et al., 1991). Patients with left temporal
ficient number of seizures have been recorded and
seizures usually required more than one minute from
the patient has been stabilized. In patients who
the termination of the seizure to read the sentence
develop a cluster of seizures or who have generalized
correctly. Patients with right temporal lobe seizures
tonic-clonic seizures during the monitoring session,
were able to read the sentence within one minute
one day without seizures would be advisable before
from seizure termination.
discharge. Certainly, the safety of discharge also
When the patient has fully recovered, memory can
depends on many individual factors, such as whether
be tested by asking for items given during the seizure
the patient lives alone and how far the patient lives
as well as for events during a seizure. For example, it is
from the medical center or from an emergency depart-
not uncommon for patients with right temporal lobe
ment. A patient who lives alone requires a greater evi-
seizures to produce spontaneous sentences (often
dence of stability prior to discharge.
with a twinge of fear) and respond almost normally to
commands or other verbal stimuli. Once the seizure
is over, it is quite common for these patients not to Medications upon Discharge
remember the conversation. The admission to the epilepsy monitoring unit pres-
ents an opportunity to make medication changes for
Testing during Hyperventilation many patients. For patients with documented epi-
lepsy, the admission could be an opportunity to with-
Testing is sometimes useful to identify whether a draw a medication such as carbamazepine that would
seizure has occurred or the EEG discharge was sub- be difficult to withdraw on outpatient basis. The inpa-
clinical/asymptomatic. In patients with generalized tient setting allows a faster withdrawal and treatment
absence seizures, it is recognized that even a single of consequences with intravenous or p.o. medications
spike-and-wave discharge is usually associated with a on an as-needed basis.
neurological change when sufficiently sensitive test- For patients with non-epileptic psychogenic sei-
ing is used. However, the degree of gross alteration zures and no evidence of epilepsy, it is most appro-
of responsiveness and awareness varies tremendously priate to discontinue anti-epileptic drugs prior
between patients such that some patients have no to discharge. As a component of the treatment of
gross detectable change. Testing patients’ responsive- patients with non-epileptic seizures, withdrawal of
ness during generalized spike-and-wave discharges anti-epileptic drugs helps remove the ambiguity
should be routine when the EEG technologist is pres- about the diagnosis so that effective treatment can be
ent during the baseline EEG or a session of short-term pursued, with psychotherapy or psychiatric medica-
monitoring. tions as needed.
Short-term Video EEG Monitoring stressors. Most commonly, this technology is applied
without the video component. In the absence of
This form of video EEG monitoring is performed for video, interpretation of ambulatory EEG presents
2 to 8 hours on either outpatient or inpatient basis. many challenges. It is well-known that artifact can
This form of monitoring avoids the need for hospital imitate any EEG abnormality, and without knowing
admission. It is the preferred form of monitoring for the concomitant behavior one cannot exclude the
children and adults who have very frequent attacks or possibility that movement or other patterns of muscle
for patients in whom attacks can be reliably precipi- activity and behavior could be responsible. Similarly,
tated. For example, a variety of reflex epilepsies can be EEG discharge can be misread as movement or
diagnosed on outpatient video EEG. Examples could other artifact without video or other observational
include photosensitive epilepsy, startle epilepsy, correlate.
reading epilepsy, eating epilepsy, and musicogenic Ambulatory EEG alone would be most helpful
epilepsy. in major attacks that involve loss of consciousness
If the short-term video monitoring session fails to or complete loss of awareness. In these instances,
record an attack despite the use of appropriate activa- the persistence of a normal EEG strongly suggests a
tion techniques, then prolonged inpatient monitoring non-epileptic etiology. Ambulatory EEG becomes
could be performed. It is often impractical and inap- less appropriate for subtle events, in particular events
propriate to make medication changes in short-term that do not involve alteration of awareness.
video monitoring sessions. An exception could be The use of video in conjunction with ambulatory
the individual who reports that missing a single dose EEG is provided by some manufacturers. This con-
of medication reliably brings on attacks, or the indi- comitant video use is possible when the patient is
vidual who has only very mild events that would not stationary, for example working at a desk, sitting on
present a risk. a sofa, or sleeping.
Ambulatory EEG Monitoring Special Electrodes
Ambulatory EEG has the advantage of keeping the Clearly, diagnostic video EEG studies may not need
patient in an environment that includes the usual special electrode use. However, additional electrodes
Figure 3-50: EEG with DSA.

EEG Technology 71
Figure 3-51: Right Temporal Ictal Discharge.
besides the 10-20 system may be very useful for local- Technicians create the technical noted based on
ization purposes. Electrodes can be added from the this initial review. This is an aide to the reading phy-
10-10 system as needed, depending on the specific sician, guiding where to look in a long recording for
suspected localization. Methodology for special elec- abnormal electrocerebral activity or clinical events.
trodes was discussed previously, but the utility of The video is reviewed for every seizure starting
some of these is briefly reviewed here. approximately 30 seconds before the reported seizure
onset. The first clinical change is noted. The analysis
• Nasopharyngeal electrodes: Mostly to record from of the seizure should focus on early manifestations,
the medial-basal temporal cortex. particularly ones that have lateralizing or localizing
• Sphenoidal electrodes: Especially helpful for value. While the video is reviewed, a cursor points
temporal lobe foci that cannot be identified out the exact timing of every clinical feature in rela-
otherwise. Sometimes, sphenoidal are the only tion to the EEG (see Figure 3-52). The vertical line on
extracranial electrodes to show the discharge. the figure demonstrates the exact time on EEG cor-
• Supraorbital electrodes: For suspected orbitofron- responding to the video image.
tal seizure origin. Figure 3-53 provides an example of annotations
• Foramen ovale electrodes: For discharges from the entered on the EEG to describe clinical as well as
medial-basal temporal lobe. EEG features during a seizure. These annotations can
be exported to the EEG report with their correspond-
EEG Review by Technologist ing times.
Clinical annotations are entered at the cursor, mak-
Review by the technicians is performed daily on ing sure that the timing corresponds (see Figure 3-53).
patients admitted for prolonged monitoring. The The end of the clinical seizure is also annotated. In
review includes evaluation of burst detections. Any some cases, it is of value to review postictal manifesta-
potentially abnormal pages are reviewed for character- tions, particularly the presence of aphasia. After anno-
ization. Density spectral array (DSA) is reviewed for tating the clinical manifestations, the EEGer should
change in spectral power, which may suggest a seizure review the corresponding EEG, focusing on the initial
(Figures 3-50, 3-51). Clinical seizures as documented EEG changes. The EEG recording is annotated with
by staff, patient, and/or family are reviewed in detail. description of EEG features/patterns according to the
Figure 3-52: EEG with Video Inset.
Figure 3-53: EEG Annotations.

EEG Technology 73
time of occurrence of each feature. Annotation should recorded should be avoided. Of course, patient safety
include features of known clinical value, for example 5 is always a higher priority than an EMU recording.
Hz or faster rhythmic activity in a temporal electrode
within 30 seconds of seizure onset, which would favor Falls during seizures:
a mesial temporal origin. Seizure termination should Falls during seizures are uncommon, but significant
also be annotated. These annotations can be exported head or other bodily injury can occur (Noe and
to the report with their timing. Drazkowski, 2009). In addition, falls in the hospital
setting are a particular concern for patients’ safety. If
Safety in the Epilepsy the patient has significant ataxia or other issues that
Monitoring Unit predispose to falls, fall-prevention protocols are avail-
able in most hospitals.
Safety in the EMU is a major concern not only because
the patients are on the clinicians’ territory and under Postictal Psychosis
their personal care, but also because frequently Postictal psychosis is uncommon but is occasionally
patients are provoked to have seizures through activa- seen and has been an occasional cause of postictal
tion procedures and withdrawal of AEDs. In addition, injury (Kanemoto et al., 2012). Patients with epilepsy
some potential risks, such as falls, are of particular have an increased risk of psychological difficulties
sensitivity to health care institutions, so we must be even independent of the seizures themselves, but psy-
sensitive to the risks without being so overprotective chosis around the time of seizure is of particular con-
as to lower patient satisfaction or reduce the diagnos- cern. Medications such as olanzapine are used when
tic sensitivity of the study. needed, but the potential for exacerbation of seizures
Events can be separated into epileptic and with some of the neuroleptics has to be considered.
non-epileptic events. They are considered individually.
Ictal Cardiac Asystole
Epileptic Serious Events Cardiac arrhythmias and asystole can occur anywhere
in the hospital, including the epilepsy monitoring
Severe seizures: unit, but patients with epilepsy are more likely to have
Seizures are usually not associated with serious injury, sudden cardiac death. Arrhythmia including asystole
but they can be. After withdrawal of AEDs, seizures associated with a seizure—ictal cardiac asystole—is
are not only more frequent but are more likely to be uncommon but needs to be considered and evaluated
prolonged and more severe. by cardiac rhythm recording along with other physi-
ological monitoring. Incidence is far less than 1% of
Status epilepticus (SE): patients evaluated in the EMU (Marynissen et al.,
SE is more likely after withdrawal of AEDs, but 2012). Ictal asystole can occur not only with general-
is probably not increased by activation methods. ized seizures but also with partial seizures (Agostini
Standard therapy for status epilepticus should be et al., 2012).
available with rapid access to clinicians who can acti-
vate the protocols. Vanderbilt University Hospital Sudden Unexplained Death in Epilepsy (SUDEP)
has a protocol for SE that is reproduced in Chapter 7. SUDEP is sudden death in patients with epilepsy,
EMUs should have protocols for the management of which is felt to be usually related to a seizure but not
severe seizures and SE. always—the patient may have sudden death with-
out a clinical seizure. Cause is not entirely under-
Aspiration: stood and may be multifactorial. Cardiac arrhythmia
Aspiration is a common risk with seizures, especially and apnea are two prominent possibilities, along
generalized tonic-clonic seizures. Maintenance of with autonomic and other central causes (Moseley
adequate airway and suctioning as needed are war- et al., 2012).
ranted. However, if patients have partial seizures or While SUDEP is not preventable, therapeutic
other seizures for which aspiration risk is not high, treatment with AEDs is felt to reduce the risk (Surges
then manipulating the patient during a seizure being and Sander, 2012).
Non-epileptic Serious Events Clinical features to be assessed are:

• Time of occurrence;
Cardiac Arrhythmias • Activity the patient was engaged in;
Cardiac arrhythmias are more common in patients • Apparent precipitation;
with epilepsy. Autonomic changes are common, but • Time of first clinical change and the nature of the
occasionally atrial fibrillation or atrial flutter can first clinical change;
develop (Herskovitz and Schiller, 2012). This risk • Evolution of clinical activity and a description of
raises the possibility that if a patient with syncope is activity at each phase and its evolution;
found to have atrial fibrillation, the neurologist should • Apparent end of the clinical event;
at least consider the possibility that the arrhythmia • Duration of the clinical seizure, and the nature
was related to seizure disorder. of postictal behavior including interaction with
examiners;
Hypoglycemia • Time of return to normal functioning should be
Hypoglycemia is an occasional risk in the epilepsy recorded, if possible.
monitoring unit, especially if the patient is kept
without eating for a time after a clinical seizure.
Hypoglycemia can also trigger seizures and has even EEG features to be assessed are:
been reported to be a trigger of seizures otherwise felt • State of the patient at the time the event started
to be epileptic (Monami et al., 2005). (for example, waking versus sleep).
• First change in the EEG, including attenuation or
Hypotension disappearance of previous interictal epileptiform
Hypotension can occur during epilepsy monitor- activity and attenuation of previous background
ing as part of orthostasis and/or prolonged bed rest. activity. If the attenuation is focal, this can be a
In addition, hypotension can be an adverse effect of useful localizing finding.
treatment for seizures; the more meds are needed, the • First definite rhythmic activity and its localiza-
greater the chance of requiring blood pressure sup- tion, its evolution and pattern of spread, and the
port (Kowalski et al., 2012) time of its termination.
• It may be noted when ictal activity ends in one
Psychiatric Disease hemisphere or in the whole brain except one region.
Psychiatric disorders are higher in prevalence in • Time of complete termination of the ictal discharge.
patients with epilepsy than the general population. • Postictal EEG pattern (for example, generalized
Patients with epilepsy controlled have a much lower attenuation or lateralized or focal attenuation, or
rate of psychiatric disorders than those with incom- lateralized or focal irregular slow activity).
plete control (Kanemoto et al., 2012). In addition,
postictal psychosis is seen, especially in patients Filtering
with temporal lobe epilepsy (Sakakibara et al.,
2012). Comprehensive psychiatric management of The reviewer must look at the EEG unfiltered.
psychosis, depression, and even suicidal ideation Reviewing the ictal EEG in a filtered state first could
needs to be addressed for patients identified as result in misinterpretation of muscle and movement
at risk. artifact as cerebral in origin, because they have lost
some of their characteristic hallmarks as a result of
Clinical Interpretation the filtering. The pattern of muscle artifact during
a seizure can be greatly helpful. For example, gen-
Reviewing Studies eralized tonic and generalized clonic motor activ-
ity both produce typical myogenic patterns on the
In reviewing video EEG studies, the interpreter EEG. Subtle focal clonic activity in the face can be
places the greatest emphasis on ictal clinical events. recognized on EEG but not clinically, and chewing
There are clinical and EEG features to each of these and swallowing artifacts can also be recognized on
events. the EEG.
EEG Technology 75
Montages The rhythmic activity of epileptic seizures will

usually evolve or at least wax and wane in its fre-
For purposes of localization and classification, sei- quency, morphology, and amplitude. The rhythmic
zures may need to be viewed in more than one mon- activity associated with non-epileptic seizures is
tage. Using an initial bipolar montage, one can suspect either constant or includes irregularities that reflect
the center of the field based on reversal of polarity or on the EEG artifact. The occurrence of seizures
phase reversal. The seizure can then be viewed in a immediately out of sleep is strong evidence against
referential montage, choosing a reference that is least a psychogenic basis. Some patients with psychogenic
likely to be involved in the seizure activity. For exam- seizures report that attacks occur out of sleep, but the
ple, an anterior-inferomesial temporal seizure origin EEG will usually demonstrate a waking background
of the ipsilateral ear is an inappropriate reference. at onset.
The ear ipsilateral to the seizure origin is frequently
involved in the ictal discharge. The average reference Physician Interpretation and Reports
can be appropriate but may need to be manipulated
to exclude the most clearly involved electrodes. The video EEG report should start with identify-
Thoughtful consideration must be applied to select ing information, duration of study, a preamble that
the montage that likely provides the highest fidelity. includes the reason for the study and background
clinical information of relevance, medications, seizure
Video EEG Diagnosis of Psychogenic Seizures medication changes during the study, electrodes used
(for example 10-20 system, sphenoidal electrodes, T1/
The simplest diagnosis of psychogenic seizures occurs T2, etc.). Some centers produce a separate report for
in the absence of motor activity in patients who every day of recording. We prefer to have a unified
become unresponsive or who collapse and become report that includes a section for every day of record-
unresponsive. In these patients, the presence of a coming, identified by dates and times. Typically the first
pletely normal EEG background while the patient day includes a baseline EEG, which is a 20-minute
is totally unresponsive would be diagnostic of a recording that cycles through standard montages
non-organic psychogenic activity. (longitudinal bipolar average reference, ear reference,
A positive diagnosis of non-epileptic psychogenic transverse bipolar) and includes hyperventilation and
seizures becomes harder in the presence of associ- intermittent photic stimulation. For every day, the
ated motor activity. In many instances, movement and report should include a description of seizures, start-
muscle artifact can dominate the EEG, rendering its ing with clinical features by time of occurrence and
analysis impossible. In such instances, analysis of the then EEG features by time of occurrence, as well as
video component becomes the predominant basis for a description of interictal EEG including waking and
diagnosis. That could be potentially misleading, as epi- sleep patterns as well as epileptiform, slow wave, and
leptic seizures can be very bizarre in their manifesta- amplitude abnormalities. After the last day of record-
tions, with minimal associated EEG change when they ing, an EEG Diagnosis paragraph summarizes the key
arise from the mesial frontal or orbitofrontal region. EEG findings by number, starting with ictal discharges,
The video analysis of psychogenic seizures should then interictal epileptiform abnormalities, then slow
also take into consideration that no single feature or and amplitude abnormalities, and posterior rhythm.
even combination of features are totally specific. It is The final part of the report is Clinical Interpretation,
not uncommon for rhythmic movement to be asso- which is a synthesis of clinical and EEG data. We rec-
ciated with rhythmic motion artifact that could mis- ommend starting with a summary description of the
lead into a diagnosis of seizure activity. Clues to the clinical features of the seizures, their lateralizing and
diagnosis could come from brief quiet periods that localizing significance of the overall features, and how
still include unresponsiveness or from the immediate this is supported by ictal onset and interictal epilep-
postictal state when the patient is still unresponsive tiform and non-epileptiform abnormalities. There
but quiet, allowing for a perfectly normal EEG to follows a summary statement. Below are examples of
show through. When such periods are absent, the pat- EEG diagnosis and clinical interpretations based on a
tern of artifact can be helpful. variety of scenarios.
Scenario A: A patient with a psychogenic seizure not support an epileptic nature for these attacks.
and normal EEG However, since most simple partial seizures are not
associated with scalp EEG changes, the possibility of
EEG Diagnosis:
simple partial seizures is not ruled out.
• This EEG is normal in waking, drowsiness,
and sleep. Scenario D: No spells and normal EEG
• There is no EEG change in association with one EEG Diagnosis: This is a normal 3-day video EEG
typical spell, other than muscle and movement study
artifact. Clinical Interpretation: No events were recorded. This
normal study fails to provide support for the diagno-
Clinical Interpretation: This study recorded one of the sis of epilepsy but cannot rule it out, particularly in
patient’s typical spells. The main features were (men- the absence of recorded attacks.
tion the most prominent features, stressing the ones
that point to a psychogenic origin). There were no
Scenario E: No spells but with interictal epilepti-
associated EEG changes other than muscle and move-
form discharges and slow activity
ment artifact (if present). By both EEG and clinical
criteria this spell was non-epileptic, most probably EEG Diagnosis: This 4-hour video EEG study is
psychogenic in nature. In addition, due to the absence abnormal because of
of interictal EEG abnormalities, this study fails to pro- • Frequent left anterior temporal epileptiform
vide support for coexistent epilepsy. discharges;
• Left anterior temporal intermittent irregular delta
Scenario B: Psychogenic seizure plus epileptiform activity
abnormalities on the EEG
EEG Diagnosis: Clinical Interpretation: This study is most consistent
with the interictal expression of partial epilepsy with
• Frequent sharp waves recorded from the left a left anterior temporal potential epileptogenic zone.
temporal lobe.
• Intermittent irregular slow wave activity recorded
Scenario F: Examples of recorded seizures with
from the left temporal lobe.
totally congruent data.
• There were no EEG changes (other than muscle
and movement artifact) in association with one of EEG Diagnosis: This 7-day video EEG study recorded:
the patient’s typical spells. • Two ictal discharges associated with clinical
seizures. Both had a focal onset in the left infer-
Clinical Interpretation: This study recorded one of omesial temporal region.
the patient’s typical spells. Its main clinical features • Occasional left inferomesial temporal or left
were. . . . The EEG showed no change (other than inferomesial temporal predominant sharp waves,
muscle and movement artifact). By both clinical and which became extremely frequent during sleep.
EEG characteristics this spell was non-epileptic, and • Occasional left temporal intermittent rhythmic
most probably psychogenic in origin. delta activity (TIRDA).
On the other hand, the interictal EEG recorded • Intermittent left temporal irregular theta/delta
left temporal sharp waves and suggested potential epi- activity.
leptogenicity in the left temporal region.
Clinical Interpretation: This study recorded 2 complex
Scenario C: Predominantly subjective episodes or partial seizures. The clinical onset was with cessation
spells without definite altered awareness or respon- of normal activity, blank stare, chewing and swallow-
siveness with a normal EEG. ing movements, which favor a temporal involvement.
Clinical Interpretation: This study recorded two epi- Postictally after the first event, the patient was found
sodes that were predominantly subjective. There to be aphasic for almost 2–3 minutes, which favors
were no associated EEG changes. This study does a left temporal localization. This localization was
EEG Technology 77
supported by the ictal EEG onset and interictal epi- (F3>Fp1,F7,C3); 10 of the seizures started with
leptiform and slow activity that was left inferomesial transitional sharp waves.
temporal or inferomesial temporal predominant. • Frequent high frequency beta bursts recorded
In summary, this study is diagnostic of partial epi- from the same region as above.
lepsy with confident localization of the epileptogenic • Interictal epileptiform discharges from the left
zone to the left inferomesial temporal region with frontal or frontotemporal region.
excellent convergence of clinical seizure pattern, ictal • Irregular delta activity recorded from the left
EEG, interictal epileptiform activity, and slow wave frontal region.
activity.
Clinical Interpretation: This 4-day video EEG study
Scenario G: Example of fairly congruent data, less recorded 15 complex partial seizures, 6 secondarily
definitive generalized. The seizures included early head turn-
Example 1. Left lateral temporal ing to the left, hypermotor automatisms of the left
extremities, while the right side was motionless or
EEG Diagnosis: This 3-day video EEG monitoring is posturing, and, in transition to generalization, adver-
abnormal because of: sive head turning to the right, and asymmetrical tonic
• At least 16 ictal discharges with associated posturing (with figure of 4). The clinical features
clinical seizures. All ictal discharges started with strongly favor a left lateralization. The initial hyper-
theta activity in the left temporal region (at T7, motor activity may suggest frontal lobe involvement.
T1>P7, F7). A left frontal localization was supported by the ictal
• Bursts of left temporal rhythmic sharp activity in EEG onset and by the interictal epileptiform and slow
sleep (F7>T7>Fp1) lasting up to 10 seconds, with activity, which were consistently left frontal.
some evolution raising the possibility of subclini- In summary, this study is diagnostic of partial epi-
cal ictal discharges. lepsy, with strong evidence of a left frontal epilepto-
• Very frequent left temporal epileptiform dis- genic zone.
charges (T7 or F7 predominance).
• Left temporal intermittent irregular slow activity.
WHAT YOUR TECHNOLOGIST NEEDS
Clinical Interpretation: This 3-day video EEG study TO KNOW
recorded 16 of patient’s typical complex partial sei-
zures. Their main characteristics were sudden crying/ This discussion is not intended to be a comprehensive
moaning, appearing restless and scared, mild right technical manual but rather a guideline as to what the
facial twitching, head turn to the left, and bilateral EEG reader expects.
limb automatisms. The early head turning to the left
and right facial twitching at onset may favor a left Training and Expertise
lateral temporal localization. This localization is sup-
ported by the ictal onset and interictal epileptiform There is a national shortage of qualified EEG tech-
and slow activity. nologists and quite few training programs. Even the
In summary, this study is diagnostic of partial epi- programs that do exist produce small numbers of
lepsy with a probable left epileptogenic zone in the technologists. Therefore, many EEGs are performed
left lateral temporal region. by technicians who are at various stages of training
and experience, from novices to those eligible for
Example 2. Left frontal ABRET registry to those who are registered to those
who are qualified and experienced educators.
EEG Diagnosis: This 3-day video EEG study is abnormal EEG labs should be supervised by a registered EEG
because of: technologist, or at the very least an individual who is
• Fifteen ictal discharges associated with clinical eligible for ABRET certification. New technicians who
seizures, 6 of which secondary generalized. All have not gone through teaching programs should be
15 seizures started from the left frontal region supervised by a certified or eligible technologist.
Two organizations are integrally involved in further contaminated by secretions, especially

advocating quality training of technologists. The with prolonged recording. Depending on the type
American Society of Electroneurodiagnostic and level of contamination, cleaning may have to
Technologists (ASET) is involved in education of extend to wiping down the head box and possibly
technologists. The American Board of Registration other machinery with disinfectant. EEG electrodes
of Electroencephalographic and Evoked Potential used on patients with suspected Creutzfeldt-Jakob
Technologists (ABRET) has a comprehensive exam- disease (CJD), AIDS, hepatitis, and some other
ination that demonstrates competency in EEG, and infections may warrant additional antimicrobial
also has published pathways for achieving eligibility treatment.
for the examination. There are multiple pathways
to certification and these may be in flux. ABRET Red Flags
documentation should be consulted for current
information. The expectation is that technicians will EEG technicians should be expected to not only
proceed through one of these pathways to become place electrodes and run machinery, they should be
successfully registered. A significant pay differential expected to identify red flags during EEG perfor-
between registered and non-registered technicians mance. Some of these are potentially life threatening,
can be an incentive to complete the programs and while others should prompt the technician to alter the
take the exams. test procedures. Some examples follow:
Separately from the technicians, we are increas- Cardiac arrhythmia: Bradycardia or asystole or
ingly depending on nurses in the critical care units to other arrhythmia may produce symptoms that can
be able to perform clinically important interpretation be confused with seizure. Therefore, the technician
of bedside EEG monitoring. ASET has resources for should be attuned to development of any cardiac
information through meetings and publications, and irregularity.
more will be expected. Sleep apnea: Obstructive sleep apnea (OSA) is
As a separate issue from training, we expect that particularly common in our region (Tennessee), so it
the technicians will be skilled in more than merely is not uncommon for sleep apnea to be suspected on
applying the electrodes and piloting the machinery. the basis of the sleep phase of a routine or long-term
The technicians must know enough about EEG inter- EEG. If there are findings suggestive of OSA, then
pretation that they can identify common abnormali- respiratory monitoring should be considered if avail-
ties, especially if the interpretation would dictate a able. Alternatively, referral for sleep lab testing may be
change in the performance of the test or necessitate appropriate. STOP-BANG scores for assessing risk of
contact with a physician. Examples may include sleep apnea are now routinely performed in most hos-
end-of-chain localization where alternative montage pitals, including ours.
should be used, frequent seizure discharges, cardiac Spike-like potentials: Some non-epileptic
arrhythmia, or sleep apnea. spike-like potentials can be easily confused with
epileptiform activity. For some of these, such as
Infection Considerations 14 & 6 positive spikes, a change in montage to a con-
tralateral ear reference (not an active electrode for
Infections are a constant concern for office and hos- those potentials) can clarify the interpretation of the
pital EEG, but are of particular concern in patients in recording.
the ICU. Universal precautions are followed every-
where, and a major effort in hospitals is to ensure that Data Handling and Archive
proper hand hygiene, gowning, masks, and gloves are
used when appropriate. Technicians are relied on to correctly annotate the
EEG electrodes are not invasive, but the skin records, and should give a summary of their findings,
prep process makes them potentially contami- particularly drawing the attention of the reader to
nated by abraded skin or serum. Cleaning with regions of particular interest. These findings are not
disinfectant is routine, soaking often until the next for consumption as preliminary reports for clinicians,
study. EEG electrodes and their leads can become but can be of benefit to the reader.
EEG Technology 79
Digital EEGs are usually stored on central servers EEG machines and reading workstations are
and interpreted at workstations. Archiving the record- repositories and/or portals of personal medical
ings is performed in accordance with regulations. information. Therefore, standard security measures
Archiving is sometimes done by the technologists should be followed, just as for a workstation or
but sometimes by Information Systems (IS) or other device with an electronic medical record or PACS
support staff. system.
4
CLINICAL EEG
Karl E Misulis
TERMINOLOGY AND DEFINITIONS EEG can be abnormal in two ways. First, there are
some potentials that can be definitively abnormal.
Interpretation of clinical EEG begins with identifica- Second, some potentials are abnormal only in the
tion of the clinical state and events, and then identi- context of baseline EEG activity and patient charac-
fying the EEG correlates to those states and events. teristics and state.
For most patients, diagnosis can be accomplished by Non-epileptiform activity includes focal and
a routine EEG, but for some with uncommon events generalized slowing, and other abnormalities of
which need to be captured, prolonged recording is background activity. Interictal abnormalities include
needed. Table 4-1 describes some common clinical isolated spikes and sharp waves which also can be
states and events, and table 4-2 describes some com- focal or generalized. Ictal activity is associated with
mon EEG events. These and additional entities are clinical seizure activity and is usually repetitive spikes,
subsequently discussed in the text. again focal or generalized, although focal slowing or
suppression or focal rhythmic activity of almost any
frequency can be ictal activity.
NORMAL EEG The normal EEG is more difficult to specify than
the normal EMG or Nerve Conduction Study. There
Overview
are certainly specific rhythms that are expected at
Clinical EEG is performed in the office or hospital different ages and states of patients, but in addition,
setting, and is performed prior to long-term video there are specific patterns that are independent of
EEG monitoring. The recordings are of only a small quantitative frequency analysis.
epoch, 20 minutes or so, therefore, it is very possible
The normal EEG can be defined by:
to miss epileptiform abnormalities on a recording
of this duration. Encephalopathy is more difficult to • Frequency composition;
miss, unless the entirety of the recording was made in • Topographic organization of the activity—left/
the drowsy or sleeping state. right, front/back, asymmetry, interhemispheric
Normal EEG will be discussed first, followed synchrony;
by a discussion of artifacts and electrocerebral • State—including wake/sleep, tense/relaxed;
abnormalities. • Effect of activation methods on the EEG.
80
Clinical EEG 81
Table 4-1 Clinical Events
Term Definition
Epileptic seizure Episodes of change in neurologic behavior due to abnormal neuronal
activity in the brain
Psychogenic non-epileptic Episodic neurologic events that can resemble epileptic seizures but which
seizure are due to psychological issues rather than due to a change in neuronal
activity in the brain.
Non-epileptic event Episode of neurologic abnormality which can resemble epileptic seizure
but is not primarily due to epileptic discharge. E.g. clonic syncope.
The normal EEG across ages is typically symmetric, wakefulness and attenuates with eye opening and dis-
though not synchronous across the hemispheres, and appears as the patient falls into drowsiness and sleep.
has a spatial and frequency distribution that is appro-
priate for the patient’s age. Normal variants are often
Low Voltage Fast
age-dependent, as are some normal EEG patterns.
Some individuals have a very low-voltage posterior
rhythm that it is nearly invisible, and a low-voltage fast
Normal Adult EEG background is seen. Similarly, patients who have dif-
ficulty relaxing may never get into the relaxed wake-
Normal Waking Backgrounds fulness that allows for the posterior dominant alpha
rhythm. Absent of this posterior rhythm is not abnor-
A variety of background rhythms will be seen in EEGs,
mal unless unilateral.
many of which are distinctly abnormal. Sleep rhythms
will be discussed later. The following patterns can be
seen in the awake state and are distinctly normal. Sleep-wake Cycle
Waking State
Normal Posterior Dominant Rhythm Routine EEG (Figure 4-1) usually begins with the
The occipital leads show rhythm in the alpha range. patient awake with the eyes closed. The technician
Frontal and central leads show faster activity. The asks the patient to open and close the eyes to assess
posterior dominant alpha is present in relaxed the posterior background rhythm and its reactivity.
Table 4-2 EEG Events
Term Definition
Spike Sharp transient with a duration of 25–70 msec.
Sharp waive Sharp transient with a duration of 70–200 msec.
Slow wave Individual waves in the theta (4–13 Hz) or delta (< 4 Hz) range.
Sharply-contoured slow wave Sharp transient with a duration > 200 msec.
Epileptiform discharge Episodic waves or complexes that stand out from the background
and suggest predisposition to epilepsy.
Spike-wave complex Spike followed by a slow wave.
Posterior dominant rhythm A rhythm from the occipital region that is composed of one fairly
narrow band of dominant frequency. Waves of other frequencies
may be superimposed on this posterior rhythm
541 540
1 1
2 2
3 3
4 4
5 5
6 6
7 7
8 8
9 9
10 10
11 11
12 12
13 13
14 14
15 15
16 16
Figure 4-1: Normal Waking EEG. Figure 4-2: Normal Waking EEG with Eye Opening.
Normal waking EEG using the longitudinal bipolar (LB) There is attenuation of the posterior rhythm with eye open-
montage. Posterior-dominant alpha rhythm, with eye blinks ing. This is the same patient as in Figure 4-1.
anteriorly, is seen.
If activation methods are used, they are performed Drowsiness

during the initial segment of the EEG. Finally, the Patients progress from waking to drowsiness, during
patient is allowed to rest, progress into drowsiness, which time there are several changes, including pro-
and possibly fall asleep. Evaluation of encephalopathy gressive reduction of muscle artifact, a slight reduc-
does not typically require a sleeping study, but evalu- tion in the posterior rhythm frequency (usually not
ation for seizures is best if a sleep study is performed. more than 1 Hz), anterior widening of the field of
Adults with the eyes closed have a posterior domi- posterior dominant rhythm, and slow horizontal eye
nant rhythm of about 10 Hz. The minimum allowable movements. This is sleep stage 1A. With progression
frequency is 8.5 Hz, and 11 Hz is the upper end of the to stage 1B, there is attenuation then loss of posterior
range. Anterior cerebral EEG shows low-voltage fast dominant rhythm with the appearance of theta.
activity. Eye movement artifact is superimposed. Vertex waves may be seen in stage 1B, but this
A frontal-predominant beta activity is seen when is more of a characteristic of stage 2 sleep. Theta
patients are sedated with benzodiazepines or barbitu- becomes more prominent. Differentiation of stage
rates, but this is less prominent with chloral hydrate. 1A from 1B is not important for routine EEG, but is
Quantitative EEG analysis shows a small amount important in sleep studies, as 3 consecutive epochs
of theta and delta during the awake state, but this is (1 epoch = 30 seconds) of stage IB is considered the
not prominent with visual analysis. Older patients onset of sleep.
have less prominent posterior dominant alpha activ-
ity. Also, tense patients may have little or no visible Sleep
posterior dominant alpha-range activity. This should Sleep rhythms are described in Table 4-3. Composition
be commented on in the report, but not interpreted as of these features and background rhythms determines
an abnormality in the absence of other findings. the sleep stages, as described in Table 4-4.
Eye closure results in attenuation of the posterior Stage 2: Sleep is most easily recognized in stage 2. Stage
dominant rhythm, as shown in Figure 4-2. 2 sleep is heralded by the presence of sleep spindles,
Clinical EEG 83
Table 4-3 Sleep Rhythms

Component Features
Vertex wave Negative potentials with a maximum at Cz.
Prominent in stage 2 sleep and during arousal.
Sleep spindle 11–14 Hz waves of 1–2 sec duration.
Maximum at C3 and C4.
K complex Fusion of a vertex wave and a sleep spindle.
prominent in stage 2 sleep and partial arousal.
Positive sharp transients of sleep (POSTS) Positive potential with a maximum at O1 and O2.
more prominent vertex waves, and K-complexes, which of the record. Stage 3 sleep is not commonly seen in
are longer polyphasic vertex waves often associated with routine office EEG.
spindle activity. There is complete loss of the posterior Stage 4: Delta activity predominates in stage 4
dominant alpha rhythm. Since vertex waves may appear sleep, which now comprises more than 50% of the
in drowsiness and sleep stage 1B, the main differentiat- record. Vertex waves and sleep spindles are often
ing feature of stage 2 is the appearance of sleep spindles. absent. Stage 4 sleep is rarely seen on routine office
Delta begins to appear at this stage. EEG.
Figure 4-3 shows an example of stage 2 sleep from REM: Rapid eye movement sleep is characterized
the same patients as shown above for the waking by a low-voltage fast background. Superficially, this
records. pattern may resemble drowsiness, but is differenti-
Stage 3: Stage 3 sleep is characterized by more delta ated by rapid eye movements, hypotonia on sub-
and fewer faster frequencies. Delta comprises 20–50% mental EMG, and irregular respiratory rate.
Table 4-4 Sleep Stages
Stage Features
Wake Posterior dominant rhythm of 8.5–11 Hz.
Desynchronized background.
Stage 1a (drowsiness) Reduction in muscle artifact.
Anterior widening of the field of the posterior dominant rhythm.
Slow horizontal eye movements (SEM)
Stage 1b Attenuation of the PDR.
Appearance of theta activity.
Vertex waves may appear.
Stage 2 Loss of the PDR.
Sleep spindles.
Vertex waves and K-complexes.
Stage 3 More delta activity (20–50% of EEG).
Fewer vertex waves and spindles.
Spindles become more anterior and slower in frequency.
Stage 4 Prominent delta (>50% of EEG).
Vertex waves and spindles are few to none.
REM Low-voltage fast background.
Rapid eye movements.
1
649 patients may progress to stage 3 then 4. The progres-
sion to stage 4 does not occur with each cycle. There
2
are three to five cycles in a night’s sleep. REM sleep
3
occurs after at least one sleep cycle, and is of increased
4 duration with later cycles.
5
6
Activation Methods
7
8
Activation methodology and response is discussed
in Chapter 3 in the sections on EEG Methodology and
9
Routine EEG Review. The responses to these activa-
10
tion are revisited here.
11
12 Photic Stimulation
13 Responses to photic stimulation can be normal,
14
abnormal, or artifactual. Table 4-5 presents the photic
15
stimulation responses that may be encountered.
Not presented in Table 4-5 is induction of
16
non-epileptic seizures by photic stimulation. Photic
stimulation can induce both epileptic and non-epileptic
Figure 4-3: Stage 2 Sleep. seizures.
The background is composed of a mixture of frequen-
cies with sleep spindles and vertex waves. This is the same
patient as in the previous two figures. Referential montage. Visual Evoked Response
The visual evoked response is also sometimes termed
the photic evoked response and is a positive-predominant
Progression of sleep stages: Waking, drowsiness, wave seen from the occipital region approximately
and stage 2 sleep are commonly seen in routine 100 msec after each flash (see Figure 4-4). This is seen
office EEG. The progression is from waking to stage at slower flash frequencies, usually less than 5/sec.
1A to stage 1B to stage 2. With prolonged recordings, With increasing flash frequency, the VER disappears
Table 4-5 Photic Stimulation Responses

Type of response Response Description
Normal response Visual evoked Occipital positive-predominant wave which peaks
response approximately 100 msec after the stimulus. Seen
mainly at slow flash frequencies.
Driving response Occipital positive-predominant wave that is
time-locked to the photic stimulus. Seen mainly at
flash frequencies of 7/sec and greater.
Abnormal response Photoparoxysmal Discharge evoked by flash usually in a band of fre-
response quencies. Associated with generalized epilepsies.
Artifact Photoelectric artifact Electrical activity generated at the electrode-gel
interface by a flash stimulus. This is neither cerebral
or muscle but rather electrochemical.
Photomyoclonic Flash-induced electrical activity in the frontal
response muscles in response to a flash stimulus. Not a cerebral
potential.
Clinical EEG 85
Photic between VER and VEP is because of the method of

1 data display and the absence of averaging.
The absence of a VER is not abnormal unless uni-
F3-C3 lateral. Such asymmetry suggests abnormality in pro-
2 jections from one lateral geniculate to the cortex, or
the calcarine cortex, itself.
C3-P3
3 Driving Response
The driving response appears as the flash frequency
P3-01 accelerates beyond 7/sec, and the next evoked poten-
tial starts before the last evoked potential has ended.
4
It is created by the visual evoked responses merging
into each other. The driving response is usually most
prominent at the frequency of the posterior rhythm,
Figure 4-4: Photic Evoked Response.
or at multiples thereof (Figure 4-5).
Evoked response from the occipital region is seen approxi-
mately 100 msec after each flash. Photic driving response is time-locked to the stim-
ulus and appears at faster frequencies than the pho-
tic evoked response. The driving response is usually
and the driving response appears, with the transition seen, but absence is not interpreted as an abnormal-
complete by flash frequencies of 10/s. ity, unless unilateral or markedly asymmetric, in the
The VER is the same potential that is recorded absence of other abnormalities.
during visual evoked potential (VEP) testing, noting
that during diagnostic VEP testing, pattern-reversal Photomyoclonic Response
is the preferred mode of stimulus, and flash is used The photomyoclonic response (Figure 4-6) is not
when pattern-reversal does not produce a response cerebral in origin, but rather is electrical activity in
or cannot be done. The difference in appearance the frontal scalp muscles, which is induced by the
Photic
F3-C3
C3-P3
P3-O1
Figure 4-5: Photic Driving Response.

Driving response is seen from the occipital region time-locked to the flashes.
Figure 4-6: Photomyoclonic Response.

Muscle activity with photic stimulation. The activity is more temporal than usual.
flash stimulus in susceptible individuals. Repeated temporal lobe epilepsy). While some patients will
contraction of these muscles produces EMG activity have already noticed that there is photic trigger
that is time-locked to the stimulus, and recorded typi- of their seizures, this is not always the case. Some
cally from the frontal leads. patients with photosensitivity have never had a
The main issue with the photomyoclonic response spontaneous seizure.
is in differentiation of this from photoparoxysmal The discharge is usually activated by a band of
response. Some general guidelines are discussed in flash frequencies rather than by the entirety of the
Table 4-6. flash procedure. Identification of photoparoxysmal
response is generally by the following criteria:
Photoparoxysmal Response
The photoparoxysmal response (Figure 4-7) is • Activated by a band of flash rates;
a marker for seizure tendency, and most often • Does not begin with the first flash in the train;
noted with generalized epilepsies. Less commonly, • Frequency is not time-locked to the stimulus;
photosensitivity is noted with partial epilepsy • May outlast the photic stimulation train or stop
(occipital lobe epilepsy, and even less commonly before the end of the train.
Table 4-6 Differentiation of Photomyoclonic from Photoparoxysmal Responses

Feature Photomyoclonic Photoparoxysmal
Spatial distribution Anterior Posterior or generalized
Termination End of the stimulus May stop before the end or outlast the stimulus.
Rise time of the spike Fast (EMG) spike. Slower, spike-and-wave complexes most common
Frequency Same frequency as Frequency is independent of flash frequency, usually
the flash slower.
Clinical EEG 87
Figure 4-7: Photoparoxysmal Response.

Electrical discharge associated with photic stimulation.
The photoparoxysmal response is always interpreted from the retina. The ERG is often seen in the fronto-
as abnormal. It has been suggested that the best cor- polar electrodes as well, at high gains, when there is a
relation with epilepsy occurs if the discharge out- paucity of electrocerebral activity.
lasts the stimulus train, however this has not been
consistently noted. Hyperventilation
Hyperventilation is used predominantly to activate
Photoelectric Artifact the 3-per-second spike and wave discharge of absence
The photoelectric artifact is non-cerebral and not seizures. Patients with untreated childhood absence
EMG. The potential is generated by the electrode-gel epilepsy will almost always have these discharges with
complex. The artifact is often contaminating insecure hyperventilation. In some patients, the discharges are
leads with high impedance, so there is not equal rep- only seen during hyperventilation.
resentation across the forehead, and loss of common The normal response to hyperventilation is gener-
mode rejection. alized slow activity, both synchronous and asynchro-
Light produces changes in the electrode, which nous. In adults, there is mostly appearance of theta
disturb subtle junction potentials between the elec- range activity. The slow activity is more prominent in
trode and gel. This potential is detected mostly in the children than in adults and also more prominent and
frontal electrodes, which are directly illuminated and persistent in patients with hypoglycemia (Figure 4-8).
can be misinterpreted as a rhythmic spike potential Hyperventilation is performed for 3 minutes on
with a frequency equal to the frequency of photic routine testing, and should be performed for 5 min-
stimulation. utes if there is a strong suspicion of absence seizures.
With solid electrode placement and fixation this Hyperventilation is not performed in elderly patients
artifact is minimized. and in those with significant vascular disease, since
It may be difficult to distinguish from the electro- there may be resultant vasospasm and decreased cere-
retinogram (ERG) activity that records potentials bral perfusion.
Fp1-F3 method. It is often used for patients in whom routine

1 EEG has not been able to identify interictal epilep-
tiform activity. Sleep deprivation may be a particu-
F3-C3
larly potent activation method in patients with
2
juvenile myoclonic epilepsy. In these patients, the
C3-P3
highest yield is in recording most of the EEG after
3 arousal from a brief nap following sleep deprivation.
P3-01
Stimulus-Sensitive Epilepsies
4
Photic-induced epilepsy is not common but photic
stimulation is presented during almost all EEGs, perhaps
Fp1-F3 even during studies where this is not the clinical ques-
tion. However, there are other stimulus-sensitive epilep-
sies that which should be considered (see Table 4-7).
F3-C3 Musicogenic epilepsy is quite rare and likely
under-diagnosed, as are stimulus-sensitive epilepsies
C3-P3
in general (Maguire, 2012). The association with the
music stimulus is often not obvious and when the
P3-O2
diagnosis is made, there is usually a long history of
neurologic evaluation without the stimulus sensitiv-
ity being identified. If a patient reports possible musi-
cogenic epilepsy, the appropriate stimulus should be
Figure 4-8: Hyperventilation.
Top: Normal EEG epoch. Bottom: Hyperventilation, with used if needed (Kasteleijn-Nolst Trenité, 2012).
enhanced slow activity. Reading epilepsy is also rare but when suspected
should be tested in the lab. These patients often have
seizures when they are not reading and even sleep-
Sleep Deprivation ing, so the stimulus association is often not obvious.
Sleep deprivation increases the possibility of see- In this modern age of digital communication, cases
ing epileptiform activity in some patients, and also of reading epilepsy induced by the omnipresent text
increases the chance of obtaining sleep. Sleep depri- messaging may make this diagnosis more evident
vation increases the yield of epileptiform discharges (Watson et al., 2012).
beyond that expected from sleep alone, and there- Occasionally, patients with seizures may have
fore is considered a separate physiologic activation spikes triggered by auditory or tactile stimulation as
Table 4-7 Stimulus Sensitive Epilepsies

Type Features
Photic-induced epilepsy Most common stimulus-sensitive epilepsy. Associated with generalized
epilepsies especially and seen in people who have seizures even when the
photic stimulation is not presented.
Musicogenic epilepsy Uncommon and likely under-diagnosed epilepsy where seizures are trig-
gered by listening to or performing music.
Reading epilepsy Seizures precipitated by reading, likely rare yet under-diagnosed. Affected
patients have seizures independent of reading also.
Other sensory-evoked Simple sensory stimuli such as tactile, auditory, and visual stimuli can
seizures evoke seizures in selected individuals. Most commonly seen with anoxic
encephalopathy.
Clinical EEG 89
well as visual stimulation. This is particularly com- can be triggered, with non-epileptic events predom-
mon in patients who have anoxic encephalopathy but inating (Khan et al., 2009). Regardless of whether
can occur even if patients present with seizures not the events are non-epileptic or epileptic, there is
triggered by stimulus (Fernández-Torre et al., 2010). certainly diagnostic utility to having them revealed
Another example of sensory-sensitive epilepsy is on study.
associated with tooth brushing.
Effects of Aging
Reactivity to External Stimuli
Reactivity to external stimuli during EEG is used not Aging results in some defined changes in EEG activity:
only to induce seizures but in this context refers to deter-
• Decreased voltage of the posterior dominant
mining if the EEG exhibits reactivity separately from
rhythm;
epileptiform discharge. During routine EEG, patients
• Slight decrease in frequency of the posterior
are often asked questions to determine level of con-
dominant rhythm;
sciousness and roughly determine cognitive function. In
• Increased theta and delta on spectral analysis;
patients with hypoxic encephalopathy, lack of reactivity
• Increased beta activity;
of the EEG can be a poor prognostic sign in the appro-
• Decreased magnitude of the responses to photic
priate context—e.g., freedom from sedatives and time
stimulation;
from hypothermia (Rossetti et al., 2010; Rossetti et al.,
• Decreased slowing in response to
2012). Reactivity in a comatose patient is tested usually
hyperventilation.
by presenting an expectedly painful stimulus, speaking
to the patient even though a response is not expected, The PDR slows slightly with normal aging, but remains
and making a loud unexpected sound, e.g., clap. at least the minimum 8–8.5 Hz. Slowing to less than
Reactivity in other conditions is also tested if a this is abnormal and consistent with encephalopathy.
good waking record is not obtained, for the purpose The increased theta and delta with spectral analy-
of not only testing reactivity but also inducing a sis is difficult to see with visual inspection. A small
change of state of the sleep-wake cycle. amount of temporal theta is occasionally seen, and is
discussed in a subsequent page.
Placebo Infusion
Saline infusion during EEG has been used to both Normal Pediatric EEG
induce clinical events and to terminate documented
non-epileptic events. This was discussed in Chapter 3 Overview
in greater detail, but is seldom used in clinical practice
for ethical reasons. However, there is no doubt that this The EEG in children is superficially similar to that in
can be an effective technique and some clinicians use adults in that there is a posterior dominant rhythm
this as a technique of last resort (Wassmer et al., 2003). that is attenuated and eventually replaced by slower
activity in drowsiness and sleep. There are important
Suggestions to Induce Seizures differences, which are age and state dependent. Note
Suggestions to induce seizures are commonly used, that this book concentrates on adult EEG, which is
although some have objected to an air of deception the arena of the authors, so discussion of pediatric
that characterizes these suggestions. This was dis- EEG is limited and basic.
cussed in depth in Chapter 3. Technician suggestions
Among these differences are:
are effective but are sometimes complicated to inter-
pret; for example, patients without non-epileptic sei- • Frequency and appearance of the posterior domi-
zures might have one to suggestion even though they nant rhythm;
usually have epileptic events. • Posterior slow waves of youth;
Hypnosis had been studied in adults and chil- • Response to hyperventilation;
dren in the potential to induce seizures. With a hyp- • Vertex waves appear higher voltage and sharper;
notic suggestion to have a seizure during video EEG • Sleep spindles are often prolonged and higher
monitoring, both epileptic and non-epileptic events voltage.
Neonatal EEG Table 4-8 Neonatal Sleep Stages

Neonatal EEG is performed similarly to adult EEG, Stage Description
but the montages are somewhat different and there is Active Small eye and body movements
more physiologic monitoring. Common physiologic sleep (AS) with irregular respirations.
monitoring usually includes:
Quiet sleep Absence of eye movements and
(QS) regular respirations. One pattern
• Respirations;
has continuous slow wave sleep
• Eye movements;
with delta activity predominating
• Electrocardiogram (EKG);
with theta superimposed.
• Electromyogram (EMG).
Absence of eye movements and
regular respirations but with a
Respirations in adults are usually easily able to be dif-
discontinuous, trace alternant,
ferentiated from electrocerebral slow activity, but in
pattern with delta and some theta
neonates and young children, rapid respirations can
with superimposed bursts.
be mistaken for pathologic slow activity.
Neonatal EEG is so different from adult that expe-
rience and competence in interpretation of adult
studies does not assume competence in neonatal Active sleep (AS) is so termed because there are
studies; this field requires specific training. small eye and body movements. Respirations are
irregular. This is equivalent to a REM sleep later in
The following data need to be available for interpreta-
maturation. Theta predominates, with some delta and
tion of neonatal studies:
beta superimposed. The first AS epoch during sleep is
• Age, including conceptional age, gestational age, higher amplitude than later epochs. Later epochs have
postnatal age; not only lower amplitude but also more theta and less
• Clinical question; delta activity.
• Physiological state; Quiet sleep (QS) is so termed because there are
• Reactivity of the background. few to no eye and body movements. Respirations
are regular. This is equivalent to non-REM sleep
Conceptional age (CA) is the sum of gestational age at later in maturation. There are two patterns typically
the time of delivery plus postnatal age. This is important associated with QS. One is continuous slow activity
because some patterns continue to mature whether the predominantly in the delta range. The other is a dis-
maturation is intrauterine or post-delivery, in the case continuous pattern, trace alternant, with epochs of
of premature infants. alternating relative low-voltage activity punctuated
Physiological state refers to observations regard- by bursts of theta, which can be sharply contoured.
ing level of consciousness and the sleep-wake cycle This can occasionally look similar to a pathologic
(e.g., waking, sedated, or asleep). For sedated patients, burst-suppression pattern, but the interburst activity
it is helpful to know the agent used. with trace alternant is typically higher voltage and
Reactivity of the background refers to response to composed of a richer frequency of activities.
tactile and verbal stimuli, and is important not only
for neonates but for most routine and ICU EEGs.
Normal Neonatal EEG
Physiological State of Neonates The normal neonatal EEG is so dependent on concep-
Normal sleep-wake patterns evident in children and tional age that patterns need to be defined as typical of
adults are not seen early in premature infants. Normal individual epochs of pre-term development. The EEG
term-infant EEG patterns are not well-developed background typical of a term child is usually present
until 38–40 weeks conceptional age. At term, there by 38 weeks conceptional age.
are two sleep stages defined—active sleep and quiet EEG findings with different stages of development
sleep. These are summarized in Table 4-8. are presented in Table 4-9. To summarize, the youngest
Clinical EEG 91
Table 4-9 Neonatal EEG Patterns According to Conceptional Age

Conceptional age EEG patterns
22–29 weeks Discontinuous pattern with long intervals of low voltage activity up to 2 min
duration with brief high-voltage mixed-frequency bursts.
29–31 weeks Discontinuous pattern with shorter interburst intervals.
Delta brushes begin to appear.
32–34 weeks Discontinuous pattern in quiet and active sleep.
Multifocal sharp transients.
34–37 weeks Discontinuous pattern in quiet sleep but with progressively shorter interburst
intervals and increase in activity during the low voltage periods.
Active sleep (REM) is almost continuous.
Fewer multifocal sharp transients; more frontal sharp transients.
38–40 weeks Trace alternant pattern in non-REM sleep with approximately equal
bursts-interbursts.
May be a continuous slow wave pattern.
Fewer frontal sharp transients.
No delta brushes.
neonates commonly recorded (about 22 weeks) have The sharp contours of these bursts, along with
a very discontinuous pattern, meaning that there are the quite low voltage of the interburst epochs, can
alternating periods of low-voltage activity punctuated cause the appearance to resemble pathological
by bursts of high voltage mixed-frequency activity, burst-suppression. This is differentiated chiefly by
which commonly includes sharp waves. This can look knowledge of age of the patient and clinical condition.
similar to a burst-suppression pattern in an adult with
severe encephalopathy or sedation. 29–31 Weeks Conceptional Age
With maturation, the periods of low voltage The discontinuous pattern persists, but there are
activity become shorter and have greater activity changes, with the interburst intervals becoming
during this time. Therefore the bursts become more
Fp1-F3
frequent and the difference between the bursts and
interburst epochs are much less pronounced as the F3-C3
child approaches 38 weeks conceptional age—the
discontinuity is quite modest at that point. As the C3-P3
child approaches 38–40 weeks conceptional age,
P3-01
sleep-wake cycles become more obvious.
22–29 Weeks Conceptional Age Fp1-F3

EEG between 22 and 29 weeks CA consists of a dis-
continuous, mainly low-voltage mixed frequency F3-C3
activity with interspersed bursts of theta and faster
C3-P3
frequencies (see Figure 4-9). The interburst intervals
can be more than 1 minute, especially in very prema-
P3-O1
ture infants, although shorter intervals are typical.
The bursts exhibit poor inter-hemispheric synchrony
in very young prematures, but later in this age group
Figure 4-9: EEG of a Very Premature Infant.
there is better synchrony. The discontinuous pattern Low voltage activity with infrequent bursts.
is termed trace discontinu (TD).
shorter. The interburst intervals also are of higher

Fp1-T3
amplitude still, with a mixed-frequency background.
The sleep stages are now present with the TD pat- T3-O1
tern seen in quiet sleep.
Fp2-T4
Delta brushes are typical of this conceptional age
and are seen in active sleep. They have the appearance T4-O2
of a delta wave with superimposed fast activity in the 100 μV 1 sec
alpha or beta range. They can resemble sleep spindles,
but delta brushes are most prominent in the central
Figure 4-10: Term Infant EEG.
and occipital regions, whereas the later occurring Term infant shows a discontinuous pattern, less prominent
sleep spindles have a frontal predominance. Spindles than in the previous recording.
are not seen at this age, and waves with spindle
appearance could be epileptiform activity.
Non-REM sleep continues to show evolution
of the discontinuous pattern, with less differen-
32–34 Weeks Conceptional Age tiation of the burst from interburst appearance. The
Both active and quiet sleep remain discontinuous, burst-interburst ratio is now 1:1, and represents a
but the interburst intervals are of progressively higher mature trace alternant pattern. REM sleep shows a
amplitude and much shorter. mixed pattern of alpha, theta, and delta with frequent
Delta brushes are seen, with the fast-component eye movements and irregular respirations.
even faster in this conceptional age range. Delta activ- Frontal sharp transients are less prominent than
ity is more prominent from the occipital regions. in the younger age range, and abate totally after about
Multifocal sharp transients are seen both in the 2 months post-term. Delta brushes are absent in this
waking and sleep states. This can easily be mistaken age range.
for pathological sharp waves, but the multifocal
nature and the lack of repetitive discharge argues
Maturation of the Posterior Dominant Rhythm
against epileptiform activity.
The normal waking background of the child depends
34–37 Weeks Conceptional Age on age. The posterior dominant rhythm is approxi-
Active sleep is now virtually continuous, with irreg- mately 4 Hz in the infant and becomes faster through-
ular delta activity most prominent posteriorly and out childhood, reaching 8 Hz by age 3, and the average
theta and faster frequencies anteriorly. adult frequency of 10 Hz by 10 years of age. Figure 4-11
Quiet sleep shows a discontinuous pattern, but shows the maturation of the posterior dominant
with shorter interburst intervals and higher volt- rhythm. The amplitude tends to be higher than in
age activity during the interburst intervals. Burst- adults, in the range of 50–100 μV.
interburst rations are 1:2 to 1:3.
Frequency of posterior rhythm
12
EMG activity is a reliable indicator of state begin-
10
ning at this age range, whereas it was not in younger
9
prematures; low amplitude EMG is seen in REM
6
sleep. Multifocal sharp transients disappear and are
replaced with frontal sharp transients that are of 4
higher amplitude. 2
Reactivity of the EEG is more prominent than 0
0 2 4 6 8 10 12
in younger ages, with attenuation of the background Age (years)
with stimulation, and often a change of state.
Figure 4-11: Maturation of the Posterior Dominant
38–40 Weeks Conceptional Age Rhythm.
Change in the frequency of the posterior dominant rhythm
These are considered term infants, and the EEG pat- with age.
tern is considered normal term EEG (Figure 4-10).
Clinical EEG 93
Posterior Slow Waves of Youth Posterior slow waves of youth are augmented by
hyperventilation, as shown in Figure 4-13. This is from
There are slow waves superimposed on and inter- the same patients as Figure 4-12.
mixed with the normal posterior waking background, Posterior slow waves of youth are considered
referred to as slow waves of youth. These could poten- normal. They are differentiated from pathologic slow
tially be confused with abnormal slow potentials indi- waves by the following features:
cating encephalopathy, especially in the young child
with a posterior rhythm in the theta range. Posterior • Otherwise normal background;
slow waves may have an episodic occurrence or may • Appearance in wake and light sleep but disappear
be seen sequentially. They are usually notched, sug- later in sleep;
gesting that several alpha waves have merged to form • Reactivity to eye opening—attenuated.
them. They are not usually confused with epilepti-
form activity, although the sequence of an alpha wave They become less evident with growth, and are not
followed by a slow wave occasionally suggests a sharp seen after 30 years of age.
and slow wave complex.
In addition to posterior slow waves, there is Hyperventilation
more theta anteriorly in young children than in
adults, and this, also, should not be interpreted as Hyperventilation produces a greater reactive slow-
abnormal. ing in children than adults. In young children, the
Neurophysiologists who are not accustomed to inter- magnitude and synchronicity of the slowing can be
pretation of children’s EEGs often misinterpret normal mistaken for seizure activity (see Figure 4-14). This is
slow activity as pathological slow activity, indicative of particularly true if there is a notched appearance to the
encephalopathy. Therefore, consideration must be made rhythm, a common occurrence when the slow activity
to age as well as the state of the patient (Figure 4-12). is superimposed on faster underlying rhythms.
Figure 4-12: Posterior Slow Waves of Youth—Blocked by Eye Opening.

On eye opening the slow waves of youth are blocked.
Figure 4-13: Posterior Slow Waves of Youth—Increased by Hyperventilation.
Drowsiness Vertex Waves
Vertex waves (Figure 4-15) are not present at birth, but
One pattern of drowsiness seen in early childhood is that begin to appear at about 5 months of age. By 2 years of
of generalized bisynchronous high voltage slow waves, age they are prominent in stage 2 sleep, sharp in con-
often appearing abruptly. This pattern referred to a hyp- figuration, and high amplitude. They can be so promi-
nagogic hypersynchrony. It becomes less frequent with nent as to be confused with epileptiform activity.
advancing age, and is no longer seen by adolescence. While there is room for a lot of experience and
judgment in differentiation of juvenile vertex activity
Sleep Patterns from epileptiform activity, some general features of
vertex waves are:
Sleep should be obtained when the clinical question
is seizures, since interictal discharges (and sometimes • Prominence during sleep without any signs of
ictal discharges) are more common in sleep. For some abnormal vertex activity during the awake state;
patients, abnormal electrical activity is only seen in • Disappearance of the activity during deeper
sleep. There is effectively no difference between sedated stages of sleep;
sleep and natural sleep. Chloral hydrate a commonly • Association of the activity with spindles;
used sedative since it has a wide safety margin and this • K-complexes that have a vertex component simi-
agent does not produce the prominent drug-induced lar to the waves in question.
beta activity that is typical of benzodiazepines and bar-
biturates. However, this is considered conscious seda- Regarding these guidelines, prominence in sleep
tion and requires monitoring of vital signs. without a waking correlate is different from augmen-
The sleep records of children and adults are more tation during sleep. Occasionally, interictal or ictal
alike than the waking records. However, there are activity will appear during sleep when there is no sign
maturational changes in children. In addition, sleep during the awake state. However, total absence during
activity of children can be particularly sharp and high the awake state with prominence during light sleep is
in voltage. not impossible but is unexpected.
Clinical EEG 95
Figure 4-14: Hyperventilation in a Child.

Left side of the figure is before hyperventilation. Right side is with hyperventilation.
Figure 4-15: Vertex Waves with Prominence Around the Midline.

Disappearance during deeper sleep cannot be relied synchronous. By 2 years of age, the general appearance
on in most routine office studies, because sleep beyond of the sleep spindles is the same as in adults.
stage 2 is rarely obtained. Video-monitoring for longer
time would be required to capture all sleep stages. Cone Waves
Association with spindles is a good clue to the These high voltage occipital cone-shaped waves may
identity of vertex activity, although even this is imper- be seen in the occipital regions in infancy.
fect, since high-frequency rhythmic epileptiform
activity can occasionally be seen. This pattern is most
Variants and Transients
common in younger patients, so the chance occur-
rence of vertex epileptiform plus central alpha-range
Overview
rhythmic activity has to be quite uncommon.
K-complexes (Figure 4-16) are the fusion of a ver- Variants and normal transients are a frequent accompa-
tex with a sleep spindle. If K-complexes are seen and niment to an otherwise typical EEG (see Tables 4-10,
the vertex component has the same general appear- 4-11, and 4-12). Unfortunately, they can be confused with
ance as the midline waves under question, the activity epileptiform or other abnormal EEG activity. This sec-
is most likely to be vertex than epileptiform. tion describes some of the more important transients
and variants that are certainly not considered pathologic.
Sleep Spindles
Sleep spindles (Figure 4-17) are also not present at birth, 14 & 6 Positive Spikes
but begin to appear consistently at about 2 months. The
early sleep spindles are often prolonged and have an 14 & 6 positive spikes are sharply contoured positive
appearance different from adult spindles, in that that waveforms seen mainly in the posterior temporal region,
they have a sharp negative peak and rounded base. They but have a widespread distribution (see Figure 4-18).
are also frequently asynchronous or asymmetrical. After They appear predominantly in drowsiness and light
18 months of age, the majority of spindles should be sleep. The appearance is of a train of waves at about 14
Figure 4-16: K Complex is seen on the Left Side of the Image.

Clinical EEG 97
Figure 4-17: Sleep Spindles.

Prominent sleep spindles are seen in this patient (same patient as for the previous figure).
Table 4-10 Normal EEG Patterns and Variants: Rhythms

Pattern Description
Mu rhythm Negative arch-shaped rhythmic activity at about 8–10 Hz.
Attenuated by moving the contralateral arm.
Waking.
Third rhythm (temporal Alpha range activity in the temporal region.
alpha) Seen in waking state.
Recorded only in a minority of patients.
Not clear what influences its appearance other than skull defect.
Slow alpha variant Posterior rhythm of 4.5-5Hz, often notched.
A sub-harmonic of the posterior dominant alpha.
Seen in waking state, with eyes closed.
Fast alpha variant Posterior rhythm of 16-20 Hz
Seen in waking, with eyes closed.
SREDA Periodic sharp activity that evolves into a rhythmic theta pattern
Most often parietal in localization.
Seen in older patients in the waking state
Rhythmic midtemporal Sharply contoured theta trains in the temporal and central regions.
theta of drowsiness Seen in drowsiness or relaxed wakefulness
14 & 6 positive spikes Sharply contoured waves of these frequencies in brief trains.
Both frequencies may not be seen, but are sometimes seen together.
Posterior predominance.
Seen in drowsiness and light sleep
6 Hz (Phantom) Low voltage spike-wave complexes that are single or in brief bursts.
spike-and-wave Have a posterior and mid-parietal predominance.
Seen in drowsiness.
Table 4-11 Normal EEG Patterns and Variants: Transients

Transient Features
Mu—single transients Fragments of the Mu rhythm.
Most common in drowsiness.
Positive occipital sharp Irregular positive waves from the occipital region.
transients of sleep Have a similar appearance to lambda waves
(POSTS) Seen in sleep.
Lambda waves Positive occipital waves, look like POSTS.
Seen in waking, when viewing a scene or image.
Attenuated by eye closure.
Wicket spikes Sharply contoured waves from the temporal region.
May represent fragments of the third rhythm.
Seen in drowsiness and light sleep.
More common in older patients.
Phantom spike-waves Low-voltage spike-wave complexes that are single or in brief bursts.
Have a posterior and mid-parietal predominance.
Seen in drowsiness.
Benign sporadic sleep Small spike-like potentials in the fronto-temporal regions, typically shifting
spikes (BSSS) between the two sides.
Seen in drowsiness and light sleep.
Also known as small sharp spikes (SSS) and benign epileptiform transients
of sleep (BETS)
Frontal mittens Mitten-shaped complex formed from the fusion of a sharp alpha or theta
transient with a delta wave.
Seen in sleep, especially stage 2.
Table 4-12 Prevalence of Particular Patterns Depending on State.

State Patterns typical of this state
Waking and drowsiness Mu
Third rhythm
Slow alpha variant
Fast alpha variant
Rhythmic midtemporal theta of drowsiness
14 & 6 positive spikes
Lambda waves
Phantom spike-waves
SREDA
Sleep Mittens
POSTS
Wicket spikes
BSSS
Clinical EEG 99
or 6/sec, although both frequencies may not be seen in Figure 4-19). The duration is less than 50 msec with
the same recording epoch or in the same patient. A pro- an amplitude usually less than 50 μV (but they may
longed recording may be needed to see both frequencies. look larger in long-distance derivations). They may
The 6/sec pattern predominates in younger children, be monophasic, biphasic, and occasionally polypha-
whereas the 14/sec predominates in older children. sic. They may also have a small after-going slow wave.
Reports have associated the 14 & 6 pattern with BSSS are usually differentiated from epileptiform
a variety of pathologic conditions, but these associa- spikes by small amplitude, short duration, tendency to
tions are weak and the incidence is not clearly dif- shift from side to side, occasional oblique dipole with
ferent from the general population (Drury, 1989). negativity in one hemisphere and positivity in another
Therefore, this should be considered to be a normal hemisphere, and otherwise normal EEG background.
variant if the rest of the recording is otherwise nor- However, the most reliable distinguishing feature is
mal. Its presence should be mentioned in the body of disappearance in deep sleep, while true epileptiform
the report, and should probably be mentioned in the discharges are usually increased in deeper sleep. BSSS
impression for later consideration. is also called small sharp spikes (SSS) and benign epi-
Metabolic encephalopathies, such as hepatic fail- leptiform transients of sleep (BETS).
ure, may have an increased incidence of 14 & 6, but
the background is abnormal with slowing and often Lambda Waves
triphasic waves.
Lambda waves are positive waves that are pres-
BSSS (Benign Sporadic Sleep Spikes) ent when viewing a scene or complex image (see
Figure 4-20). The waves are blocked by eye closure.
Benign sporadic sleep spikes are very small spike-like These waves resemble POSTs. This pattern is seen in
potentials that occur in the temporal or frontotem- the waking state from the occipital region. The pat-
poral regions during drowsiness and light sleep (see tern is completely normal. The lambda waves may
Figure 4-18: 14 & 6 Positive Spikes.

Both 14 and 6 Hz positive spikes are seen in this recording.
Figure 4-19: Benign Sporadic Sleep Spikes.

This particular BSSS discharge had a dipole with negativity in the left frontotemporal region and positivity in the right tem-
poroparietal region.
Figure 4-20: Lambda waves.
Positive lambda-shaped waves are seen posteriorly.
Clinical EEG 101
be mistaken for occipital spikes; however, their posi- especially if the spindle component has a fast appear-
tive polarity and blocking with eye closure make this ance. Careful inspection of the record usually allows
clearly not epileptiform. the reader to dissect out the vertex and spindle com-
Lambda waves indicate visual exploration. Their ponents of the wave.
label comes from their resemblance to the Greek low-
ercase letter lambda (λ). Lambda waves are normal Mu
and should be commented on in the body of the report
but need not be mentioned in the interpretation. Mu rhythm (Figure 4-22) is seen in the waking state,
and is a negative arch-shaped rhythm of about 8–10
Mittens Hz. The potentials are most prominent at C3 and C4.
Mu activity is often sharp. Its sharpness and ampli-
Mittens are seen only in sleep and consist of a partially tude are increased in the presence of a skull defect
fused vertex wave and sleep spindle. The last wave of over the central region. In drowsiness, the Mu rhythm
the spindle is superimposed on the rising phase of the may be broken up into fragments that can easily be
vertex wave (see Figure 4-21). This voltage summation over-interpreted as abnormal epileptiform activity.
gives the last spindle wave a faster and higher ampli- Mu is very often asymmetric or even unilateral. The
tude appearance, which may simulate a spike. Mittens absence of Mu activity on one side is not abnormal,
are seen only in sleep. unless there is very frequent Mu activity on one side
The name comes from the appearance of a hand and none on the other side. The key to identification of
mitten, the thumb being the fused spindle wave and Mu rhythm is blocking by movement of the contralat-
the hand being the vertex wave. Mittens are nor- eral arm. Even contemplating movement can produce
mal, but can be confused with a spike-wave pattern, this change.
Figure 4-21: Mittens.
Typical mittens are seen near the middle of the tracing.
Figure 4-22: Mu Rhythm is seen on the right of the page.
Phantom Spike-Waves POSTS are not seen in every patient and have no
diagnostic significance, unless they appear only from
These low voltage 6 Hz spike-and-wave discharges one hemisphere. Even in this circumstance, asymmet-
can be single or in brief trains and occur typically in ric POSTS are unlikely to be the only abnormality on
drowsiness. The classical benign variant has biposte- the EEG.
rior predominance, particularly at Pz. They tend to
occur mostly in young women. Figure 4-23 shows
phantom spike-waves with reversal of polarity at Pz. Rhythmic Midtemporal Theta of Drowsiness
Positive Occipital Sharp Transients of Sleep Rhythmic midtemporal theta of drowsiness

(POSTS) (Figure 4-25) was once called psychomotor variant,
although this term has been discarded. This pattern
Positive occipital sharp transients of sleep (POSTS) consists of trains of sharply contoured notched waves
are surface positive potentials seen from the occipi- in the theta (6 Hz) range in the temporal region. The
tal region, maximal in derivations of O1 and O2 (see pattern may be bilateral, but most often seems to start
Figure 4-24). They look somewhat like lambda waves, on one side, then within a short time develops on the
but are present only in sleep, whereas lambda waves opposite side.
are only seen in the waking state with the eyes open. Rhythmic midtemporal theta of drowsiness can
POSTS are prominent through stage 2 sleep and dis- be distinguished from epileptiform activity by the
appear in deeper stages. POSTS can appear as single following:
waves or in trains.
POSTS are less commonly seen in patients who • Normal background before and after the rhythm;
are blind or who are severely visually impaired. One • Absence of a progressive change in frequency that
hypothesis is that POSTs represent replay of visual would be typical of epileptiform activity;
information. • Presence in drowsiness but not sleep.
Clinical EEG 103
Figure 4-23: Phantom Spike-Waves.

6-per-sec phantom spike-wave is seen.
This pattern is normal, but may be more likely in some is typically notched. The sub-harmonic can be mis-
patients with structural lesions. interpreted as a slow background in the theta range.
Differentiation of slow alpha variant (Figure 4-26)
from a pathologically slow background can be made
Slow Alpha Variant by the following features:
The posterior dominant rhythm in most adults is 8.5–
11 Hz. In some patients, there can be a sub-harmonic of • Notched appearance of the rhythm;
the posterior rhythm at 4–5 Hz. The slower frequency • Attenuation of the rhythm with eye opening.
• Stereotypic appearance of the background of
the slow alpha variant as opposed to polymor-
Fp1-F3 phic appearance of pathologic slow activity of
encephalopathy;
• Appearance of normal frequency of the posterior
F3-C3
dominant rhythm elsewhere in the recording,
sometimes intermixed with the slow variant.
C3-P3 • Normal frontal and cerebral activity with slow
alpha variant as opposed to slowing associated
with encephalopathy.
P3-01
Fast alpha variant

Figure 4-24: Positive Occipital Sharp Transients of
Sleep (POSTS). Fast alpha variant (Figure 4-27) is characterized by an
Positive transients are seen occipitally in sleep. otherwise-normal posterior dominant rhythm that
Fp1 - F3 appears as a harmonic of the native rhythm, appear-

F3 - C3
ing at twice the native frequency (16–20 Hz), which
C3 - P3
is in the beta range. The fast alpha variant is easy to
interpret as normal, since there is not the slowing that
P3 - O1
is more typical of pathology.
Fp2 - F4
F4 - C4
C4 - P4 SREDA
P4 - O2
Subclinical rhythmic electrographic discharge of
Fp1 - F7
adults (SREDA) is rhythmic sharp activity that
F7 - T3 appears in some older patients in the awake state
T3 - T5 (Figures 4-28a through 4-28d). Typically, periodic
T5 - O1 sharply contoured waves evolve into a rhythmic theta
Fp2 - F8 pattern.
F8 - T4
Although SREDA resembles an ictal discharge,
there is no clinical change during the discharge.
T4 - T6
T6 - O2 SREDA can be easily confused with seizure activity.

Some differentiating features are:
Figure 4-25: Rhythmic Midtemporal Theta of • Occurrence only in the waking and drowsy states;
Drowsiness. • Intact consciousness during the discharge,
The rhythmic theta is most evident on the lower part of the page.
• Abrupt onset and termination of the discharge.
Figure 4-26: Slow alpha variant.

The posterior rhythm is approximately 5 Hz, some of these have a notched appearance, revealing the faster native frequency.
Clinical EEG 105
Figure 4-27: Fast Alpha Variant.

The posterior rhythm is approximately twice the normal posterior alpha frequency.
Wicket Spikes and Third Rhythm • Normal background activity;

• Occurrence in a series of waves at 6–10 Hz.
Wicket spikes are sharply contoured waves that are
most prominent from temporal regions during drows- Wicket spikes are more common with increasing age.
iness and light sleep. Figure 4-29 shows also the so-called third rhythm.
This is a mid-temporal rhythmic activity that is
Wicket spikes can be differentiated from pathologic related to wicket spikes, but has an origin in asso-
spikes by: ciation with the posterior dominant alpha-range
• Absence of a following slow wave; activity and Mu rhythm. Third rhythm was thought
a Fp1-F3
F3-C3
C3-P3
P3-O1
Fz-Cz
Cz-Pz
Fp2-F4
F4-C4
C4-P4 50 μV
1 sec
P4-O2
Figure 4-28a: SREDA—1 of 4.
This sequence of images (4-28a–4-28d) shows evolution of SREDA.
b Fp1-F3
F3-C3
C3-P3
P3-O1
Fz-Cz
Cz-Pz 50 μV
1 sec
Fp2-F4
F4-C4
C4-P4
P4-O2
Figure 4-28b: SREDA—2 of 4.
c Fp1-F3
F3-C3
C3-P3
P3-O1
Fz-Cz
Cz-Pz 50 μV
1 sec
Fp2-F4
F4-C4
C4-P4
P4-O2
Figure 4-28c: SREDA—3 of 4.
d Fp1-F3
F3-C3
C3-P3
P3-O1
Fz-Cz
Cz-Pz
Fp2-F4 50 μV
1 sec
F4-C4
C4-P4
P4-O2
Figure 4-28d: SREDA—4 of 4.
Clinical EEG 107
Figure 4-29: Wicket Spikes and Third Rhythm.

Both wicket spikes and rhythmic temporal theta activity (third rhythm) are seen.
to be the third brain idling rhythm, besides these eye results in potentials that can be recorded from
other two. anterior leads. These potentials can occasionally be
mistaken for frontal lobe activity.
Non-cerebral Potentials Vertical eye movements: Downward gaze results
in the positive cornea moving away from the fron-
Artifacts can be biological or electrical. Unfortunately,
tal lobe, so negativity is seen in frontal leads. The
electrical artifacts can predispose to enhanced per-
reverse is true for upward gaze. Since the eyes move
ception of biological artifacts.
up and down together, the potentials from the
Biological two sides are synchronous. Of course, one must
remember the possibility of a prosthetic eye, pro-
Biological artifacts are generated by the body, but not ducing unilateral eye movement artifact. Certain
by the brain. They can be confused with electrocer- vertical eye movements have characteristic patterns,
ebral activity, and if so are frequently interpreted as including eye blinks, eye opening, eye closure, eye
slowing or spikes. fluttering.
Eye closures: Eye closure results in Bell’s phenom-
Eye Movement enon, an upward deviation of the eyes (Figure 4-30).
The eye is electrically charged with the cornea posi- This will be associated with a positive deflection in
tive relative to the fundus, so any movement of the the frontopolar electrodes. In addition, eye closure is
associated with appearance of the posterior dominant With eye blinks there is a negative potential that fol-
rhythm. lows the initial deep positive potential in the frontopolar
Eye blink: An eye blink causes the same positive electrodes. Eye blink can be more repetitive and have the
potential in the frontopolar regions, but the sub- appearance of frontal slow or sharp activity (Figure 4-32).
sequent eye opening causes a negative deflection Eye flutter can produce artifact that is even faster than
(Figure 4-31). The subsequent negative deflection dis- normal eye blink and can be mistaken for epileptiform
tinguishes an eye blink from mere eye closure. activity or for fast frontal beta activity (Figure 4-33).
Figure 4-30: Eye Closure.

With eye closure, there is a positive deflection at Fp1 and Fp1. The rate of return to baseline depends on the setting of the
low-frequency filter. Notice the appearance of posterior dominant rhythm in conjunction with eye closure.
Clinical EEG 109
Figure 4-31: Eye Blink.
Prominent eye blink potentials are of ocular origin, not cerebral.
1 of vertical eye movements, although the technician

2 should indicate this phenomenon along with other
3 patient movements. Eye closure results in restora-
4
tion of the posterior rhythm. The posterior dominant
frequency may be slightly faster immediately after
5
closure. Therefore that should be measured a few sec-
6
onds after eye closure.
7 Figure 4-34 shows a classic response to eye open-
8 ing. Figure 4-35 shows a much more subtle response
9 to eye opening.
10 Lateral eye movements: Lateral gaze results in the
11
positive cornea moving toward the temple to the
side of gaze (see Figure 4-36). For example, left gaze
12
results in positivity at the F7 electrode, whereas
13
there is negativity at the F8 electrode. The differ-
14
ential effect of lateral gaze on the two sides makes
15 for easy identification of this as a non-cerebral
16 potential.
Lateral eye movements (Figure 4-37) are often
associated with lateral rectus spikes. Typical, the spike
Figure 4-32: Repeated Eye Blinks Are Seen (LB
Montage). will be followed by a slower positive potential on the
side to which the eyes moved.
Differentiating eye movement from cerebral potentials

Figure 4-34 shows another example of eye flutter is based on some basic guidelines:
that occurs after the patient opens eyes, in the middle • Certain eye movements such as eye blinks have
of the recording epoch. a stereotypic appearance, different from frontal
Eye opening: Eye opening results in a negative slow activity.
potential in the frontopolar electrodes plus altera- • Vertical eye movements are generally restricted
tion in the posterior rhythm. The attenuation of the to, or at least markedly predominant, in the
posterior rhythm with eye opening and reappear- frontopolar electrodes. This has resulted in the
ance with eye closing are good clues to the presence principle that slow wave activity restricted to the
Figure 4-33: Eye Flutter produces rapid frontal electrical activity resembling beta. muscle artifact shows that
this is movement-related, however.
frontopolar electrodes is eye movement artifact seizing, or have other reasons for increased tone of
until proven otherwise. scalp muscles. EMG is often prominent from the
• Pathologic frontal slow activity tends to be associ- temporal leads. Frontal and occipital leads may also
ated with a slow background, with activity in the be prominently involved, whereas midline electrodes
theta and/or delta range. A normal background will usually be least affected. EMG artifact consists
will suggest that slow activity restricted to the of short needle-like spikes, which may occur in such
frontal region most likely represents eye move- frequency that they become confluent and give an
ment artifact. appearance that resembles noise.
• Patients with marked vertical eye movements will
often have prominent lateral eye movements as Some guidelines for differentiating EMG from epilep-
well, which can be easily recognized. tiform spikes are as follows:
• EMG is very fast, much faster than spikes.
Eye movement monitoring: Eye movement monitoring Activity recorded at the scalp that is shorter than
was discussed in detail in Chapter 3 can be facilitated 20 msec is highly unlikely to be epileptiform
by an arrangement similar to that shown in Figure 4-38. activity.
Figures 4-39 and 4-40 show the placement of leads • EMG spikes are not followed by a slow wave.
for differentiation of eye movements from frontal • EMG is prominent in the waking state, and disap-
cerebral activity: pears with sleep.
• EMG spikes recur at a rate that is much faster
Muscle Artifact than would be seen with repetitive spikes.
EMG activity frequently contaminates EEG record- • EMG is attenuated by asking the patient to relax
ings, and this is prominent when patients are tense, the jaw, open the mouth, or other maneuver.
Clinical EEG 111
Figure 4-34: Eye Flutter after Eye Opening.

LB montage. Left side shows waking record with eyes closed with normal posterior rhythm. This is attenuated with eye open-
ing. Right side shows repetitive eye blinks.
Figure 4-41 shows a typical appearance of muscle arti- • Glossokinetic artifact usually disappears in
fact. Occasionally, muscle artifact is more restricted, drowsiness and light sleep.
and may even arise from a single motor unit, particu- • Glossokinetic artifact is associated with activities
larly in the midtemporal region (see Figure 4-42). such as speaking, chewing, swallowing.
Although muscle artifact can be filtered using • Glossokinetic artifact is often concurrent with
the high-frequency filter, the unfiltered EEG should EMG artifact of the frontalis and temporalis
always be viewed first. The high-frequency filter may muscles
distort the appearance of muscle artifact such that it
starts to appear cerebral in origin. Figure 4-43 pro- If there is still doubt about identification, then elec-
vides an example. trodes can be placed below the eyes. The patient is
asked to make lingual movements such as “la la la”
Glossokinetic Artifact and the potentials observed, glossokinetic artifact
The tongue is polarized, with the tip negative in shows higher voltage at the infraorbital electrodes
comparison to the back. Movement of the tongue than at the frontopolar electrodes. Cerebral activity
is common in the waking state, and can occasion- will be higher in voltage in the frontopolar electrodes.
ally be mistaken for pathologic frontal slow activ- Identification of glossokinetic artifact is much better
ity. This is potentially even more problematic in a if the technician recognizes the problem and is able to
comatose patient who is having tongue movements. perform these maneuvers during the study.
Glossokinetic artifact can be differentiated from slow Combinations of muscle and glossokinetic arti-
activity in the following ways: fact produce very characteristic patterns. Some are
Figure 4-35: Eye Opening.

With eye opening there is a negative potential in the frontopolar electrodes and attenuation of the posterior dominant
rhythm
displayed in Figures 4-44, 4-45, and 4-46. The patient Mistaking this discharge for seizure would be
is a young woman who had episodes of tongue click- most likely if the behavior is not observed, as with
ing after arousal. The slow waves between the bursts long-term outpatient monitoring, where limited
are glossokinetic potentials. The EMG bursts are behavioral information is available.
related to temporalis muscle contraction. Figure 4-47
is the same epoch with different filter settings, and the EKG Artifact
non-epileptiform character is more evident. Electrocardiogram (EKG) artifact is seen mainly on
referential montages (see Figure 4-49). Increased
Toothbrush Artifact inter-electrode distance predisposes to EKG artifact.
During long-term monitoring a variety of artifacts are Differentiation from electrocerebral artifact is most
evident. When the patient is observed in the video unit, obvious if a special EKG channel is recorded, but
behavioral correlates are obvious. In the absence of obser- even in the absence of this, the regular nature of the
vation, the potentials shown in Figure 4-48 with brushing QRS complex and the distribution of the sharp activ-
of teeth could be misinterpreted as seizure activity. ity make the source evident.
Clinical EEG 113
Figure 4-36: Eye Movement.

This tracing indicates eye movement to the right then to the left.
Pulse Artifact this situation the background is usually abnormal,

Pulse artifact is due to movement of the electrode with slowing and disorganization. If there is still
leads overlying the scalp blood vessels. Pulsation of doubt, examination of the scalp by the technician can
a small artery results in movement of the electrode be revealing.
disc, which affects the electrode-gel connection
and, if large enough, can even move the electrode Electrical
leads. The appearance is an irregular delta wave that
is time-locked to EKG, except that there is a delay Electrical artifact includes potentials that do not orig-
between the QRS complex and the pulse. inate in the electrical activity of the body. Electrode
leads can be an origin of the artifact. In addition,
Pulse artifact can be differentiated from pathological induced electrical current in electrode leads by nearby
slow activity by the following features: electric lines is a major source of artifact.
• The artifact usually localizes over one electrode.
• The artifact is time-locked to the EKG but with Electrodes and Leads
a delay. Electrode leads can be a source of artifact especially
• The background is otherwise normal. if there is instability in fi xation of the electrode and
high impedance. Movement of the electrode results
Initial inspection could mistake pulse artifact in changes in the junction potential. The discharge
(Figure 4-50) for polymorphic delta activity, but in of the junction potential results in a potential that
Figure 4-37: Lateral Rectus Spikes.

Each lateral rectus spike is followed by a positive potential indicating eye deviation to the side of contraction.
E2
can be mistaken for a spike discharge and is termed
a an electrode pop (Figure 4-51). The appearance is of
E1
a brief spike, followed by a gradual decay to base-
E1 - A1 Down line. During the spike, the responsiveness of the
Up
E2 - A2 Fp2 Fp1
E3
E2 E1
b E4
Right
E1 - E2
E3 - E4 Down
Up
IO2 IO1
Figure 4-38: Eye Movement Monitoring.
Placement of eye leads can reveal not only eye movement Figure 4-39: Electrode Positions for Monitoring Eye
and differentiate from cerebral activity but also indicate Movements.
direction of movement. a: Vertical movement detection. Infraorbital (IO) electrodes in conjunction with frontopolar
b: Horizontal movement detection. (Fp) leads are helpful for characterization of eye movements.
Clinical EEG 115
a Fp1-ref amplifier can be briefly impaired, so the EEG back-

ground immediately following can be transiently
Fp2-ref suppressed.
Electrode pops are reduced by having good junc-
IO1-ref tion between the electrode and scalp with sufficient
gel. Also, stabilization of the electrode leads is helpful
IO2-ref
to minimize movement of the discs.
The example in Figure 4-52, obtained from the
b Fp1-ref same patient as in Figure 4-51, shows sharply con-
toured slow activity that has no field, restricted to C4.
Fp2-ref This makes it likely to be artifactual.
IO1-ref Machine Artifact

Machine artifact is especially prominent in the
IO2-ref
ICU. This is high-frequency stereotyped activity
that is seldom confused with cerebral activity. The
c Fp1-ref frequency can be the frequency of line power, but
also can be at faster or slower frequencies, since
Fp2-ref mechanical devices are not time-locked to line
power activity. Most mechanical devices are driven
IO1-ref by DC power, although the power comes from AC
power through a transformer; therefore, the artifact
IO2-ref
is the frequency of the motor, rather than the fre-
quency of line power. Motors are in ventilators, IV
Figure 4-40: Comparative Pattern of Activity pumps, hospital beds, and other electrical monitor-
Recorded from Different Sources with Frontopolar ing devices.
and Infraorbital Electrodes.
a: Activity related to vertical eye movements. This will be of Machine artifact can be reduced by:
opposite polarity in the infraorbital versus the frontopolar
• Minimizing electric equipment nearby the EEG
electrodes, b: Activity of cerebral origin. This has the same
polarity in the infraorbital and frontopolar electrodes, but laboratory;
has lower amplitude in the frontopolar electrodes, which are • Adequate grounding of the patient;
closer to the frontal cortex, c: Glossokinetic activity arising • Adequate grounding of the EEG machine.
in the tongue. This has the same polarity in the infraorbital
and the frontopolar electrodes, but has higher amplitude in
the infraorbital electrodes, which are closer to the tongue. 60-Hz Artifact (Line Power)
60-Hertz interference is a result of induction from
surrounding electronic circuits that are not directly
Fp1-F3
attached to the patient. Movement of current through
power lines produces a magnetic field that is created
F3-C3 around the line. This magnetic field causes current to
flow in electrode leads by induction, a fundamental
property of electronic devices. The induced current
C3-P3
flow will reverse at 60 Hz, since the magnetic field will
also reverse at 60 Hz. Therefore, there is 60 Hz con-
P3-O1 tamination in the electrode leads without any direct
connection between the power lines and the EEG
leads. This stray inductance is a major cause of electri-
cal interference. It is most likely to appear when there
Figure 4-41: Muscle Artifact in a Patient in the is impedance imbalance. It is also most problematic in
Waking State.
the ICU environment.
Figure 4-42: Muscle Artifact from a Single Motor Unit.

Muscle artifact arising from T7. As the patient relaxed more, this artifact became restricted to a single motor unit, with a
characteristic appearance in the lower figure.
Figure 4-53 shows the right parasagittal portion of attachment. However, movement sufficient to disturb
the longitudinal bipolar montage. Midway through this the connection results in charge movement between
epoch, the air bed is unplugged and the high-frequency the electrode and gel and scalp, which is recorded as
activity disappears. The focal nature of the 60 Hz arti- EEG (Figure 4-56). Differential amplification does
fact raises the possibility of high impedance at P4. not remove this artifact because the lead artifact
Focal 60 Hz artifact should always raise the pos- affects the recording from a single electrode.
sibility of focal high impedance (Figure 4-54). In this Movement artifact is also produced by movement
example the very fast activity at C4 without appearance of the leads. A small amount of current flows through
in other leads suggests that this is not electrocerebral. the electrode leads, and while this current is miniscule
compared to most electrical circuits, there is resis-
Phone Artifact
tance of the leads and capacitance between the leads.
Telephones commonly ring, especially when patients
Movement of the leads results in disturbance of the
are being monitored or examined. Figure 4-55 is an
capacitance. The built-up charge can dissipate with loss
example of the electrical artifact of the ringing of a
of the capacitance, and this too is recorded as EEG.
phone. The stereotypic rhythmic activity lasting just
a few seconds is the ringing of the phone.
How to Avoid Environmental and Machine
Movement Artifact Artifacts
Movement artifact is due to disturbance of the elec- Electrical artifact, including machine and 60-Hz poten-
trodes and/or leads. Electrode gel is a malleable tials, can be minimized by the following:
extension of the electrode, and minor head move- • Recording in an electrically quiet environment,
ment produces little effect on the electrode-gel-scalp certainly not possible for patients in the ICU;
Clinical EEG 117
Figure 4-43: Effect of High-Frequency Filter on Muscle Artifact.

The top segment has a high-frequency filter setting of 70 Hz, whereas the lower segment has a high-frequency setting of 15
Hz. Without looking at the unfiltered EEG, the muscle activity may be misinterpreted as beta activity.
• Avoidance of ground loops; first. Table 4-13 outlines some of the important

• Disconnection of all non-essential electronic non-epileptiform abnormalities.
equipment from the patient; The most common non-epileptiform abnormal-
• Minimizing the length of the exposed leads; ity is slowing. Generalized slowing is usually due to
• Turning off lights and other equipment in prox- diffuse encephalopathy, with a broad differential diag-
imity to the patient; nosis. Many patients have multifactorial etiology for
• Use of differential amplifiers (which is typical the encephalopathy. Focal slowing is usually due to a
with modern equipment) and equal electrode structural abnormality; features of the slowing can-
impedances; not distinguish between causes such as tumor, stroke,
• Use of the 60-Hz filter, as a last resort. mass lesion, and so on.
Amplitude abnormalities are less common
than slowing and can be focal or generalized.
ABNORMAL NON-EPILEPTIFORM EEG Generalized suppression indicates encephalopathy
and focal suppression indicates a focal structural
Overview lesion.
Periodic patterns are often non-epileptiform,
Abnormal EEG activity includes ictal and epilepti- although this is a controversial area in EEG. Some
form abnormalities and non-epileptiform abnormali- investigators believe that periodic patterns are all
ties. Non-epileptiform abnormalities will be discussed potentially epileptogenic, whereas others believe that
Figure 4-44: Chewing Artifact.

The high-voltage muscle potentials are related to temporalis muscle contraction. The slow potentials are glossokinetic,
related to tongue movement.
Figure 4-45: Glossokinetic Artifact.

Movement of the tongue produces a slow deflection on which is superimposed muscle artifact.
Clinical EEG 119

Chewing produces prominent muscle artifact, especially well seen from temporal leads.

Same recording as in Figure 4-46, but with filter settings to reduce much of the muscle artifact.
Figure 4-48: Toothbrush Artifact.

Rapid activity that is representative of approximately 7 Hz movement plus superimposed muscle activity.
the periodic patterns can indicate dysfunction of the

Fp1-A1 brain without necessarily being epileptogenic.
Slow Abnormalities
F3-A1
Overview
C3-A1
Slowing can be generalized or focal or regional. Focal
slowing is easier to identify than generalized slowing,
P3-A1 since comparison of the slowing with normal back-
ground facilitates recognition. Generalized slowing
must be distinguished from normal slow activity such
as drowsiness or sedation.
Focal slowing is most commonly seen with struc-
Artifact caused by cardiac electrical activity with an interval
of approximately 1/sec. tural lesions. Generalized slowing is most commonly
seen with encephalopathy.
Clinical EEG 121
Figure 4-50: Pulse Artifact, which is most Apparent in Channels 7 and 8. Note EKG at the Bottom of the Page.
Regional slowing is uncommon, and usually mani- hence the name polymorphic delta activity (PDA).
fests as intermittent rhythmic delta activity. Although In general, the area of the slow activity is overlying
this might be considered focal, it is bihemispheric, so the location of the structural lesion, but the anatomic
should be considered regional. correlation is not always exact.
The differential diagnosis of focal irregular slow activity

Focal Slow Activity is large, with some of the possibilities including:
Focal slow activity (Figure 4-57) usually indicates a • Tumor;
focal subcortical structural lesion. The slow activity • Stroke—ischemic or hemorrhagic;
typically has an irregular, polymorphic appearance, • Infection—abscess or encephalitis;
Figure 4-51: Electrode Pop.
This potential is focal at C4, with no involvement in any other electrode. Electrode impedance measurements obtained at the
beginning of the study indicate that C4 impedance was elevated at 9K.
Figure 4-52: Electrode Artifact.

The abnormality near the center of the recording is due to electrode artifact at C4 rather than due to cerebral abnormality.
• Trauma—contusion or hematoma;
Fp2-F4
• Epileptic focus—irregular slow activity may be
F4-C4 associated with an epileptic focus in the absence
of structural lesion;
C4-P4 • Transient focal abnormality may be seen in
migraine, ischemia, or postictal dysfunction after
P4-O2
a focal seizure.
70 μv 1 sec
Unfortunately, one cannot usually be definitive about
the etiology of the slow activity from the appearance.
Figure 4-53: 60 Hz Artifact.
While additional historical information may help the
The electric air pump on the bed was the source of this arti-
fact. When unplugged, the artifact disappeared. analysis, the diagnosis of focal structural lesions rests
largely with imaging studies.
Clinical EEG 123
Figure 4-54: Electrode Artifact with 60 Hz Signal.

Lower part of the recording shows 60 Hz artifact.
One form of focal slow activity, temporal intermit- predominantly in the theta or delta range. It usually
tent rhythmic delta activity (TIRDA), has a strong indicates encephalopathy. Slow activity in the theta
association with seizure activity (see Figure 4-58). range indicates mild or moderate encephalopathy,
whereas slow activity in the delta range means more
Generalized Asynchronous Slow Activity severe encephalopathy.
Expected normal background for age influences
Generalized asynchronous slow activity (Figures 4-59 the interpretation of the slow activity, since slow
and 4-60) is extremely non-specific. It can be activity is normally present in drowsiness and sleep
1 Fp1-F3
2 F3-C3
3 C3-P3
4 P3-01
5 Fp2-F4
6 F4-C4
7 C4-P4
8 P4-O2
9 Fp1-F7
10 F7-T3
11 T3-T5
12 T5-01
13 Fp2-F8
14 F8-T4
15 T4-T6
16 T6-O2
17 X3-X4
Figure 4-55: Phone Artifact.

Electrical artifact from ringing of a desktop phone.
Figure 4-56: Movement Artifact Related to Head Motion with Hyperventilation.

Movement artifact at P4, resembling focal slow wave activity.
Table 4-13 Abnormal Non-epileptiform EEG

Class Type Implication
Slow Focal slow activity Focal rhythm disturbance usually due to a focal structural lesion.
Generalized Generalized cerebral dysfunction, as in encephalopathy with a
asynchronous slow broad differential diagnosis
activity
Generalized or Usually due to encephalopathy, with typical manifestation being
regional bisynchro- frontal intermittent rhythmic delta activity (FIRDA) or occipital
nous slow activity intermittent rhythmic delta activity (OIRDA).
Attenuation Focal attenuation Due to either focal reduction in cortical activity or accumulation of
fluid over the cortex, e.g., subdural hematoma.
Generalized Global reduction in amplitude usually due to diffuse loss of cortical
attenuation activity. Bilateral fluid collection over the cortex is possible.
Increase Focal increase in Most common is skull defect that reduces the attenuation of faster
activity activity frequencies, a breach rhythm.
Generalized Usually due to encephalopathic disorders, especially excess diffuse
increase in activity beta activity most commonly seen with benzodiazepines.
Other Non-epileptiform Periodic lateralized epileptiform discharges (PLEDs) are often seen
abnormal periodic discharges in HSV encephalitis, and in this circumstance are either unilateral
patterns or independent bilateral. Hypoxic encephalopathy can produce
bilateral independent epileptiform discharges (BIPLEDs) or gener-
alized periodic epileptiform discharges (GPLEDs).
Alpha-theta coma Patients with coma from a variety of reasons can have alpha coma,
theta coma, or alpha-theta coma. The terms indicate the predomi-
nant frequencies and tend to portend a poor prognosis.
Spindle coma Appearance of spindles in coma, but these are different from sleep
spindles. Prognosis is less grave than some other patterns.
Burst suppression Severe encephalopathy often seen with hypoxic encephalopathy or
other severe cerebral damage or from deep sedation with certain meds.
Clinical EEG 125
Figure 4-57: Focal Slow Activity.

There is generalized (diffuse) slowing of the background with prominent focal slow activity over the right hemisphere. This
indicates a right hemisphere structural lesion in addition to a generalized encephalopathy.
Figure 4-58: Temporal Intermittent Rhythmic Delta Activity (TIRDA).

Rhythmic delta activity in a 48-year-old man with right temporal lobe epilepsy. This activity is present only intermittently.
Figure 4-59: Generalized Asynchronous Slow Activity.

The EEG shows mostly asynchronous generalized slow activity. Specific delta waves seen on one side not the other are
circled. The patient is a 74-year-old woman with anoxic brain injury.
Figure 4-60: Generalized Asynchronous Slow Activity.

In this example, the asynchronous slow activity is more pronounced.
Clinical EEG 127
at all ages and in the awake state in children. In these The differential diagnosis includes:
situations, there should be caution in interpretation • Metabolic encephalopathies;
of slow activity—we should only read it as abnormal • Degenerative disorders and other conditions
if the pattern is inconsistent with any normal stage of affecting cortical and subcortical gray matter;
the sleep-wake cycle. • Deep midline tumors;
• Normal.
Generalized or Regional Bisynchronous Slow
Activity FIRDA is normal in drowsiness and with hyperventi-
lation at any age and in waking in children.
Bisynchronous slow activity can be generalized or Children have intermittent rhythmic delta activ-
regional. Even when it is generalized, it usually predom- ity that tends to be centered over the occipital region
inates in one region of the brain. This type of activity is rather than the frontal region, hence occipital inter-
often, but not always, rhythmic and intermittent. The mittent rhythmic delta activity (OIRDA).
most important is frontal intermittent rhythmic delta Some neurophysiologists prefer the term PIRDA
activity (FIRDA) (Figure 4-61) and occipital intermit- for posterior-IRDA, finding the acronym OIRDA
tent rhythmic delta activity (OIRDA) (Figure 4-62). hard to pronounce. The clinical implications of
FIRDA is rhythmic activity in the delta range that OIRDA in children are considered identical to those
is synchronous on the two sides. This is either lim- of FIRDA in adults. However, OIRDA was reported
ited to the frontal region or generalized with frontal to be associated with epilepsy in children, particu-
predominance. The frequency is most often about larly generalized epilepsy. There may be subtle spikes
2.5–3 Hz. It can be seen in a wide variety of condi- embedded in the occipital rhythmic activity in chil-
tions, but more commonly is due to diffuse cerebral dren with childhood absence epilepsy. Generalized
dysfunction than due to deep structural lesions. absence and generalized tonic-clonic seizures were
Figure 4-61: Frontal Intermittent Delta Activity (FIRDA).

Frontal rhythmic delta is seen from both hemispheres.
Figure 4-62: Occipital Intermittent Rhythmic Delta Activity (OIRDA).

Occipital rhythmic delta is seen bilaterally in this child.
more likely in children with OIRDA than in control Slowing superimposed on an otherwise normal
subjects. background is a common finding and may be seen in
patients with mild cognitive changes and in vascular
Generalized Synchronous Slow Activity disease. However, this is not a specific pattern and
should not be interpreted as such.
Slowing of the waking posterior dominant rhythm Slowing of the background replacing normal back-
(Figure 4-63) is change of the posterior alpha-range ground activity suggests moderate encephalopathy.
activity to less than 8.5 Hz. Slowing to less than this The neurophysiologist must ensure that the patient is
level is almost always abnormal in adults. The most in the awake state, in this circumstance, to differenti-
common degree of slowing is in the theta range, with ate encephalopathy from a drowsy pattern. When the
slowing in the 6.5–8 Hz range. Slowing to less than technician knows that the clinical question is enceph-
this is associated with higher levels of disorganization alopathy, the patient should be stimulated to gain a
of the background. Interpretation is non-specific, but good waking record, if possible, and notation made if
generally is due to encephalopathy or dementia. this cannot be achieved.
Clinical EEG 129
Figure 4-63: Slowing of the Posterior Dominant Rhythm is Seen.
Interpretation of generalized slow activity (Figure 4-64): suppression or increase in amplitude. Generalized

amplitude abnormalities include global suppression
• Slowing of the posterior dominant rhythm is seen or increase in amplitude.
in dementia and in mild encephalopathy.
• Theta superimposed on an otherwise normal Attenuation/Suppression
background can indicate a mild encephalopathy
but is also seen in patients with vascular disease Focal Attenuation
without cognitive changes. The term attenuation indicates decreased amplitude
• Theta and delta slowing of the background are of one type of activity (such as activity in a cer-
suggestive of moderate encephalopathy. tain frequency) or of all activity. Focal attenuation
• Diffuse delta slowing is suggestive of severe (Figure 4-65) usually indicates a focal cortical lesion
encephalopathy. Triphasic waves seen with this (such as infarct) or dysfunction (such as ischemia or
background can be seen in hepatic encephalopa- postictal effect), but may also result from an increased
thy but are not specific for this, and can be seen distance between the cortex and the recording elec-
in other metabolic encephalopathies and hypoxic trode, such as may be seen from scalp edema, sub-
encephalopathy. dural hematoma, and occasionally from dural-based
tumors, such as meningiomas.
Amplitude Abnormalities The recording shown in Figure 4-66 is from a
patient with head injury and subsequent infarction.
Overview Focal suppression will usually involve multiple
electrodes. Focal suppression that is confined to one
Amplitude abnormalities can be focal or general- electrode is more likely to be due to smear of electrode
ized. Focal amplitude abnormalities include focal paste, or some other artifact that affects the recording
Figure 4-64: Generalized Slow Activity.

Slowing is diffuse and there is no posterior dominant rhythm.
Figure 4-65: Focal Attenuation of the Posterior Alpha Rhythm.

The posterior dominant rhythm is attenuated on the right side after a seizure.
Clinical EEG 131
Figure 4-66: Focal Suppression.

Generalized suppression with focality, worse on the left. Due to head injury with subsequent infarction and edema.
system. When this is ruled out, focal suppression is in amplitude but with a pattern that looks like the
usually due to one of the following: rest of the brain if the gain is increased.
• Cortical defects usually cause abnormalities
• Focal cortical dysfunction; in frequency of adjacent tissue, resulting in a
• Extracranial mass lesion; spread of suppression or slowing across adjacent
• Intracranial mass lesion. areas, whereas extra-cerebral lesions result in
normal potentials from cortex not underlying
Focal cortical dysfunction is the cause of prime
the defect.
importance to the neurologist; however, it may be
• Cortical defects are more likely to be associated
difficult to distinguish from loss of signal due to
with superimposed epileptiform abnormalities.
non-cerebral mass lesion. Extracranial mass lesion
such as scalp hematoma can result in attenuation
of the background. Similarly, intracranial hemato-
Generalized Attenuation/Suppression
mas such as subdural hematoma may also result in
The term suppression is a more severe attenuation,
attenuation of the background over the area of the
and is usually used to indicate complete or almost
cortex.
complete disappearance of EEG activity. Generalized
Differentiation of cortical from extra-cerebral
attenuation or suppression of the background can
suppression can be difficult, but some general
happen because of three reasons:
guidelines exist:
• Cortical defects result in disturbance of the • Decreased synchronicity of cortical activity;
background rhythms with a tendency to slowing, • Decreased cortical activity;
whereas extra-cerebral causes result in reduction • Excessive fluid or tissue overlying the cortex.
Decreased synchronicity of cortical activity may potential differences between electrodes and attenu-
occur in an awake, alert state, and is rarely abnormal; it ates the recorded potential at the scalp. The same
is often seen in anxious individuals. One normal vari- shunting of potential differences may occur with elec-
ant seen in a small proportion of adults is a low volt- trode gel smear on the scalp (often called salt bridge
age background that looks suppressed (Figure 4-67). or electrical bridge).
However, a low voltage EEG would be abnormal in
children and adolescents. Electrocerebral Inactivity (ECI)
Generalized decreased cortical activity can occur Electrocerebral inactivity (ECI) or isoelectric EEG rep-
with generalized cortical injury or transient dysfunc- resents absence of electrocerebral activity. The defini-
tion. Examples of generalized cortical injury include tion of ECI is one with no cerebral activity over 2 μV.
hypoxic-ischemic encephalopathy (HIE), or degen- This is often called electrocerebral silence (ECS) and
erative conditions such as advanced Huntington’s was so in the first edition of this text. In general ECI
disease; examples of transient dysfunction include is a better term because this indicates perceived lack
drug-induced coma or postictal state after a general- of electrical activity of the cerebral cortex. ECS uses
ized tonic-clonic seizure. Figure 4-68 shows marked the word silence which has an audio root, although
suppression from pentobarbital coma. Figure 4-69 the term silent sometimes means absence of motion.
shows marked suppression and periodic complexes Isoelectric has been widely used but brain death
due to hypoxic encephalopathy. recordings are never isoelectric (having no electrical
Excessive fluid or tissue overlying the cortex is charge or potential difference) and if they appeared
more likely an explanation for focal rather than gen- that way then there is something wrong with the
eralized attenuation. Examples include subdural recording system.
hematoma or scalp edema. With subdural hematoma,
The technical requirements of an ECI EEG are:
the attenuation is most pronounced with bipolar
recordings: there is cortical activity, but the conduct- • Electrodes >10 cm apart
ing ability of the subdural fluid results in reduction of • Electrode impedance >100Ω, <10,000Ω;
Figure 4-67: Attenuated EEG as a Normal Variant.

Low voltage EEG in an anxious 50-year-old woman. There is muscle activity from the left temporalis muscle.
Clinical EEG 133
Figure 4-68: Generalized Suppression from Induced Pentobarbital Coma.

Generalized attenuation of EEG activity due to pentobarbital coma. There is one brief burst of EEG activity in the right
temporal region.
Figure 4-69: General Suppression with Anoxic Encephalopathy.

Suppressed background with intermittent bursts. 76 year-old man with anoxic encephalopathy.
• Hypothermia, drug intoxication, shock must be However, a variety of rhythmic activities can be due
excluded; to machine artifact, movement artifact, or muscle
• Record should be >30 min long at a sensitivity of artifact. The EEG technologist may need to discon-
2μV/mm; nect non-essential equipment, reposition the patient,
• Physiological monitoring must include EKG. pad respirator tubes with towels, or move electrodes.
Other physiological monitoring such as respira- ECI not necessarily equivalent to brain death.
tion and EMG is very helpful. The criteria for determination of brain death include
EEG as a confirmatory test if the other criteria are met
(see Figure 4-70). An ECI EEG indicates neocortical
The background will look totally flat at a sensitivity of
death and is supportive of the diagnosis of brain death
7 μV/mm., except for artifact However, at a sensitivity
in conjunction with the appropriate exam findings, if
of 2 μV/mm, the recording is never perfectly flat, and
performed in accordance with accepted technical
if it appears to be, either the gain needs to be increased
guidelines in the appropriate clinical situation.
or there is an electrical problem in the recording sys-
tem. The residual activity more than 2 μV in the EEG
should be proven to be of artifactual origin. In fact, Increase in EEG Activity
artifacts are a major problem in interpretation. The
artifact most commonly encountered is EKG artifact, Focal Increase in EEG Activity
which may take on a variable appearance at the scalp. Focal increase in EEG activity is most often the result
Demonstrating perfect correlation with EKG channel of a skull defect (Figure 4-71). Since the skull filters
is usually sufficient to prove the activity is not cere- fast activity, the presence of a defect is most likely to
bral. The same is true for artifact due to respiration. cause increased fast beta activity, as well as increased
Figure 4-70: EEG Recording Meeting ECS Brain Death Criteria.

Clinical EEG 135
Figure 4-71: Increased EEG Activity Over a Skull Defect (Breach Rhythm).

Top segment shows increased beta activity over a right frontal skull defect. The bottom segment shows enhanced Mu and
beta activity over a left central skull defect (breach rhythm).
sharpness of less fast activity (sharpness represents frequency filter is used. This can be differentiated
a higher frequency component of that activity). from cerebral fast activity by asking the patient to
Specific rhythms can become more prominent with relax and open the mouth.
skull defects in specific regions. For example, if the Excessive beta activity should be interpreted as a
skull defect is over the central region, Mu activity minor abnormality, and the report should mention
may be exaggerated, and if the skull defect is over the that a common cause is sedative medication. The
temporal region, a third rhythm could become more neurophysiologists should not make this absolute
prominent. The EEG activity over skull defects in determination without full knowledge of the patient,
these areas is often referred to as a breach rhythm. It is of course.
not clear that this should necessarily be considered an The patient recorded in Figure 4-72 has been
abnormality. It is rather an expected effect of a skull treated with clonazepam and has some generalized
defect. slowing as well as excessive beta activity. Excess beta,
by itself, is commented on in the interpretation, but
Generalized Increase in EEG Activity is interpreted as a minor abnormality without other
Excessive Fast Activity pathologic implications. Excess beta in one region
Excessive fast activity is most commonly seen in usually means a skull defect and is interpreted as
patients receiving sedatives such as barbiturates or clearly abnormal.
benzodiazepines. Chloral hydrate usually produces
less excessive beta activity. Excessive Slow Activity
EMG activity from scalp muscles can appear as This has been discussed above in the section Slow
fast activity if its voltage is low, and when the high Abnormalities.
Figure 4-72: Excess Beta Activity.

This patient has been treated with clonazepam and has some generalized slowing as well as excessive beta activity.
Periodic Patterns periodic discharges. Lateralized periodic discharges

are often called periodic lateralized epileptiform dis-
Overview charges (PLEDs) even if the individual waveforms are
not epileptiform. Generalized periodic discharges can
Periodic discharges are repeated discharges with be classified as short-interval and long-interval peri-
other intervening activity between discharges. They odic discharges. Burst-suppression could also be con-
can be classified as lateralized or generalized/bilateral sidered a periodic pattern (see Table 4-14).
Table 4-14 Disorders with a Periodic Pattern

Disorder Pattern
Anoxia Generalized or bisynchronous periodic discharges.
Burst suppression pattern.
Herpes encephalitis Periodic lateralized epileptiform discharges.
Bihemispheric independent discharges are sometimes seen.
Creutzfeldt-Jakob disease Generalized periodic discharges are seen at some time during the course.
(CJD) Periodic discharges are not invariably seen, but typically develop within
three months from onset of symptoms.
Subacute sclerosing pan- Generalized periodic discharges, of longer interval than CJD.
encephalitis (SSPE) Differentiated by other historical features.
Clinical EEG 137
Periodic Lateralized Epileptiform Discharges metabolic disturbance who also have a chronic struc-
(PLEDs) tural lesion (especially in the setting of alcohol with-
drawal). PLEDs can also occur in the setting of chronic
PLEDs are periodic discharges that are lateralized epilepsy. Therefore, PLEDs are not specific for a partic-
to one hemisphere (Figure 4-73). This will include ular diagnosis. PLEDs in the temporal or frontotempo-
discharges that are focal, as well as others that affect ral area can be a sign of herpes encephalitis.
one whole hemisphere. Some involvement of the The majority of patients with PLEDs have clini-
other hemisphere is not unacceptable. Even though cal seizures. However, there is a controversy over
the term PLEDs excludes bihemispheric synchro- whether PLEDs themselves are ictal. The prevailing
nous periodic discharges, PLEDs can occur indepen- opinion is that PLEDs are not ictal, because more typ-
dently in the two hemispheres, in which case they are ical rhythmic ictal discharges are sometimes recorded
termed biPLEDs. PLEDs are usually high in ampli- in patients with PLEDs. However, there are patients
tude, at 100–300 μV. Lower voltage PLEDs can be with PLEDs who have myoclonic jerks synchronous
difficult to identify in the background. The discharge with the discharges, suggesting that they may be ictal
may be simple or complex, with additional sharp and in some instances (see Figure 4-74).
slow components superimposed on the waveform. In Some features have been suggested that, if present,
general, PLEDs are diagnosed only if they are present increase the odds that PLEDs are ictal. These features
throughout the routine 20-minute EEG recording. include:
PLEDs are most often the result of acute structural
lesion, such as stroke, acute infection, or rapidly growing • Fast rhythmic activity with the periodic complexes;
brain tumor (for example, glioblastoma multiforme). • Short interval between discharges; and
However, PLEDs can also occur in patients with acute • Absence of background between discharges.
Figure 4-73: Periodic Lateral Epileptiform Discharges (PLEDs).

Examples of PLEDs seen from the left hemisphere.There is a slight reflection of PLEDs in the right hemisphere, which is
not unusual. The patient developed confusion, aphasia, and witnessed focal motor seizure activity of the right arm and face,
10 days after a left carotid endarterectomy and was found to have a hyperperfusion syndrome.
Figure 4-74: Right Face Twitching in the Same Patient as in the Previous Figure.
Generalized Periodic Discharges recording. Stimuli can evoke the periodic discharges,
as in the recording in Figure 4-78 from the same
These are bilateral discharges that may be prevalent patient. Bursts are evoked by clapping.
in one part of the brain, usually anteriorly. They are
often classified as short-interval or long-interval peri- Subacute Sclerosing Panencephalitis (SSPE)
odic discharges. Short-interval periodic discharges Long-term periodic discharges have intervals of more
have a periodicity of 0.5–3 per second. They are than 4 seconds between discharges. They are more
more common and less specific than long-interval specific with respect to etiology, particularly when
discharges. The main underlying conditions include the clinical history is incorporated. Associated con-
metabolic disturbances (for example, triphasic ditions include some toxic encephalopathies, such as
waves with hepatic encephalopathy), anoxic injury, with baclofen overdose and PCP or ketamine effect,
toxic encephalopathy, Creutzfeld-Jakob disease, and anoxic injury, or subacute sclerosing panencephalitis
non-convulsive status epilepticus. Clinical correlation (SSPE). When long-interval periodic discharges are
is always required. seen in the setting of a dementing illness in a child
who also has myoclonic jerks, they are fairly specific
Creutzfeld-Jakob Disease for SSPE (Figures 4-79 and 4-80). In this condition,
In Creutzfeld-Jakob disease (CJD), the majority of the interval between complexes becomes progres-
patients will develop periodic discharges in the first sively shorter with disease progression.
3 months of the disease (Figure 4-75). Figure 4-76
shows a second case of CJD—a 69-year-old with Anoxic Encephalopathy
sporadic CJD. Anoxia can produce a variety of EEG features;
The periodic pattern is not always seen in the among these are periodic discharges, which in
patients, as shown for the same patient on the earlier this case are fairly synchronous between the
recording in Figure 4-77. The periodic discharges evi- hemispheres, although the slowing is markedly
dent later in the course are not obvious in this earlier asynchronous.
Clinical EEG 139
Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
70 μv
C4-P4 1 sec
P4-O2
FP1-F3
F3-C3
C3-P3
P3-O1
Fz-Cz 70 μv
1 sec
Cz-Pz
Fp2-F4
F4-C4
C4-P4
P4-O2
Figure 4-75: Generalized Periodic Discharges (CJD).

69-year-old patient with Creutzfeld-Jakob disease. The top tracing showed only subtle periodic discharges that are easy to
miss. The bottom tracing obtained 2 weeks later showed very clear periodic discharges with a periodicity of 1.2 per second
(Courtesy of Dr. Ivo Drury).
Figure 4-81 is from a 9-year-old male who had specific for any particular etiology. The most com-
anoxic encephalopathy due to choking on a ball. mon causes are hypoxic-ischemic encephalopathy
and medication-induced.
Burst-suppression Pattern The burst-suppression pattern (Figure 4-82)
consists of epochs of relative flattening of the
The burst-suppression pattern is sometimes called the background (suppression), alternating with
suppression-burst pattern since the duration of the epochs of mixed frequency EEG activity (bursts).
suppression is usually greater than the duration of The bursts usually have a polymorphic appear-
the burst. This pattern is seen mainly in patients with ance, but may contain high-voltage epileptiform
severe encephalopathy, although the pattern is not activity, especially in some patients who are placed
Fp1-F3 5
F3-C3 6
C3-P3 7
P3-O1 8
9
Fp2-F4
10
F4-C4
11
C4-P4
70 μv
12 1 sec
P4-O2
Figure 4-76: CJD, Case #2.

Sporadic CJD in a 69-year-old. This recording was performed 3 days before death.
Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4 70 μV
1 sec
C4-P4
P4-O2
Figure 4-77: CJD, Case #2, 3 Weeks Prior to the Recording Shown in Figure 4-76.
The periodic discharges evident later in the course are not obvious in this earlier recording.
in barbiturate coma because of refractory status • Anoxia;

epilepticus. • Drug intoxication;
Burst-suppression patterns can look similar, even • Encephalitis;
though the clinical correlation is very different. In • Stroke with resultant cerebral edema.
fact, this pattern resembles the discontinuous pattern
of a normal 19-week conceptional age child, suggest- Alpha Coma
ing that the burst-suppression pattern may represent The EEG is dominated by alpha activity, which is
a primitive pattern of neuronal activity. non-reactive in a patient in coma due to anoxia. Alpha
With drug-induced coma, the deeper the coma, the coma (Figure 4-84) is generally considered to indi-
shorter the bursts and the longer the periods of sup- cate poor prognosis, depending on etiology of the
pression. Eventually complete suppression is reached. coma and concurrent medications, which can affect
When seen in association with hypoxic-ischemic EEG background.
encephalopathy, the burst-suppression pattern is
indicative of a poor prognosis for neurological recov-
ery. In fact, any periodic pattern is a poor prognostic Spindle coma
indicator in this clinical setting (Figure 4-83). Spindle coma (Figure 4-85) was initially described
as an indicator of poor prognosis, but subsequently
Coma and Electrocerebral Silence the appearance of spindles has been seen in patients
who ultimately had good outcomes. If the spindles
Coma are seen with other sleep rhythms, including vertex
waves, then the spindles are supportive of a favorable
Coma is a state of complete unresponsiveness. The prognosis. The frontal spindles of encephalopathy
differential diagnosis of coma is huge, but some of the appear different from sleep spindles, so these should
most common causes are: be considered different processes.
Fp1-F3
F3-C3
C3-P3
P3-O1
Fz-Cz
Cz-Pz
Fp2-F4
F4-C4
C4-P4 70 μV
P4-O2 1 sec
Figure 4-78: CJD Case #2, Burst Evoked by Clapping.

Clinical EEG 141
Fp1-A1
Fp2-A2
F3-A1
F4-A2
C3-A1
C4-A2
P3-A1
P4-A2
O1-A1
70 μV
O2-A2 2 sec
Figure 4-79: SSPE.
Typical generalized periodic discharges in a child with SSPE. The interval between periodic complexes is 5–7 seconds
(Courtesy of Dr. Ivo Drury).
Electrocerebral Inactivity (ECI) Guidelines for Determination of Brain Death

ECI was discussed earlier in this chapter as an in Adults
extreme example of an amplitude abnormality. ECI The Medical Consultants on the Diagnosis of Death
means that there is no definite electrocerebral activ- to the President’s Commission for the Study of Ethical
ity recorded with scalp electrodes. ECS is supportive Problems in Medicine and Biomedical and Behavioral
of the diagnosis of brain death, which is discussed Research published guidelines for the determination
further below. of brain death in 1981. Guidelines were also published
by the American Academy of Neurology in 1995
Brain Death (AAN, 1995). An update was subsequently published
in 2010 (Wijdicks et al., 2010). Details of the criteria
Brain death (BD) criteria have been published for brain death are not within the scope of this text so
for adults and children, although there are no the reader is referred to especially the Wijdicks refer-
agreed-upon criteria for newborns. ence for guidance.
Determination of brain death is performed when Patients being evaluated for BD will frequently
a patient with intracranial catastrophe has complete be hypothermic and hypotensive; therefore, mainte-
lack of response on examination, despite the absence nance using warming blankets and pressors is often
of sedatives or neuromuscular blocking agents. required. Evidence against neuromuscular blockade
Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
C4-P4
70 μV
P4-O2 2 sec
Figure 4-80: SSPE, Case #2.

SSPE with periodic discharges.
Figure 4-81: Anoxic Encephalopathy.

This is from a 9-year-old male who had anoxic encephalopathy due to choking on a ball.
Figure 4-82: Burst-Suppression Pattern.

The lower segments show compressed pages with 60 seconds per page. They show the progression with deepening level
of coma.
Clinical EEG 143
Figure 4-83: Burst-Suppression Pattern after Anoxic Injury in a 76-Year-Old Man.

The bursts are generalized but parasagittaly predominant. There is suppression of all frequencies between bursts. The sup-
pression between bursts is variable but usually lasts around 1 second.
can be the presence of tendon reflexes, the presence with documentation of examinations for BD before
of primitive responses to nociceptive stimulation, or and after this period (see Table 4-15 for a summary of
the response of the muscle to electrical stimulation of the criteria, but this is not comprehensive).
motor nerves. Details of the determination of brain death are
The original guidelines for determination of BD best outlined as published by Wijdicks et al. (2010).
indicate that there should be a period of observation, This document is available from multiple sources
Figure 4-84: Alpha Coma.
The EEG is dominated by alpha activity, which is non-reactive in a patient in coma due to anoxia.
Figure 4-85: Spindle Coma.
The EEG in a comatose patient shows spindle-like activity.
including online. This publications even includes a evidence of cerebral or brainstem activity may have
helpful checklist. evidence of EEG activity but otherwise fulfill the clin-
BD should usually be established by clinical find- ical criteria for BD. The literature is not clear on what
ings alone, if possible. Some patients with no clinical to do in this situation.
Table 4-15 Procedures for Determination of Brain Death in Adults

Criterion Requirement to Meet Criterion
Steps for determina- Establish irreversible and proximate cause of coma.
tion of brain death Achieve normal core temperature
Achieve normal systolic blood pressure
Perform a neurologic exam for brain death.
Clinical examina- No responsiveness: Including no eye opening or movement to noxious stimuli.
tion for brain death Absence of brainstem reflexes: Pupil responses, oculocephalics, oculovestibular
reflex, corneal reflex, facial movement ot noxious stimuli, pharyngeal and tracheal
reflexeses.
Apnea: Absence of breathing drive.
Ancillary tests Use of ancillary tests is indicated especially if there is uncertainty about reliability
of certain parts of the examination or when apnea testing cannot be performed.
Depending on protocols, an ancillary test can reduce the period of observation
before determining brain death.
Preferred antillary tests include EEG, radionucleotide flow study, and angiography.
Extracted in part from Wijdicks et al., (2010)
Clinical EEG 145
Guidelines for Determination of Brain Death in protocol for the test differs from routine hospital or
Children even intensive care unit EEG (see Table 4-16).
The 1981 President’s Commission did not make specific
recommendations for the determination of BD in chil- Brain Death Studies in Adults
dren. The only specific comment recommended “cau- BD studies should be performed in the period of
tion in children under the age of five years.” The Task observation between two extensive neurologic exami-
Force for Brain Death in Children (1987) subsequently
nations. All of the above recommendations should be
provided recommendations that are increasingly used.
followed. All physiologic parameters set forth by the
In 2011, a successor to this task force published revised
guidelines (Nakagawa et al., 2011). These recommen- President’s Commission should be followed regard-
dations are too extensive to be repeated here and are ing temperature, blood pressure, and absence of seda-
not within the scope of this book, so the reader is tive and neuromuscular blockers (see Figure 4-86).
referred to these references for details. Suffice it to say
that the recommendations for children, especially the
very young, are more stringent than for adults. But the Brain Death Studies in Children
essentials of EEG performance are similar. BD studies in children are performed in the same
manner as BD studies in adults. More physiologic
EEG for Brain Death monitoring is often required in children’s stud-
ies, however. Because of small body size, respira-
EEG is one of the recognized confirmatory tests for tory movement artifact is relatively greater, and a
brain death in children and adults. However, the chest-wall sensor is desirable. An EKG channel is
Table 4-16 Technical Standards for Brain Death EEGs

Parameter Features
Number of electrodes Minimum of 8 covering all brain regions, usually a reduced version of the
10-20 electrode placement system. A full set of electrodes is preferred.
Usually Fp1, Fp2, C3, C4, O1, O2, T3, T4, as a minimum
Inter-electrode distances At least 10 cm, which is greater than normal distances. This allows for bet-
ter detection of low-amplitude EEG activity.
Inter-electrode impedances No greater than 10 kohm but no less than 100 ohms. Too low an imped-
ance suggests electrode paste smear. Amplitude of the recorded activity
will be excessively low if impedance is low.
Sensitivity 2 μV/mm during most of the recording
Low-frequency filter (LFF) not above 1 Hz
High-frequency filter (HFF) not below 30 Hz
Physiological monitoring EKG is routinely monitored since at high sensitivities EKG contamina-
tion of the EEG is common.
Chest wall motion if needed to determine if slow activity is respiratory.
Duration At least 30 min of relatively artifact-free recording.
Reactivity Test reactivity of the EEG to auditory, visual, and tactile stimuli.
Integrity Test the integrity of the system by touching the electrodes to evoke a
high-amplitude artifact. This ensures that a flat background is not due to
technical factors.
Telephone transmission EEG Telephone transmission EEGs cannot be used to support the diagnosis of
brain death.
Technologist Recording should be made by a qualified technologist.
Figure 4-86: Isoelectric EEG.
Sensitivity = 2 μV/mm
important for adult studies but is even more impor- 2013). In this same study, treatment of the seizures did
tant for BD studies in children; at high sensitivities, not improve outcome.
EKG artifact can be the predominant potential in
the record.
ABNORMAL EPILEPTIFORM EEG
EEG after Therapeutic Hypothermia Role and Diagnosis and Management
Years of study on prognostic significance of EEG, The EEG helps to provide support for the clinical diag-
clinical findings, and biomarkers have been com- nosis of epilepsy but should generally not be the basis
plicated by the increasingly widespread use of ther- for that diagnosis in the absence of clinical information.
apeutic hypothermia. The prognostic implications
The EEG has a role in all of the following:
after hypothermia do not necessarily still apply.
EEG is seldom performed during the cooled phase, • Help diagnose epilepsy;
but is done after rewarming; a richer background • Help diagnose status epilepticus;
and reactivity indicates a better prognosis (Kawai • Help classify the epilepsy and epileptic
et al., 2011). syndrome;
Continuous EEG recording in patients during and • Help localize the epileptogenic zone;
after therapeutic hypothermia showed that poor out- • Help predict seizure recurrence after a first
come was predicted by seizures, non-reactive back- unprovoked seizure or after anti-epileptic drug
ground, and epileptiform discharges (Crepeau et al., withdrawal;
Clinical EEG 147
• Help follow response to therapy in one specific look epileptiform but be normal for the conceptional
form of epilepsy, idiopathic generalized epilepsy age. Or, an apparent generalized seizure in an older
with absence seizures. In this situation, improve- adult may be associated with focal sharp waves, sug-
ment in seizure control is reflected with decreased gesting secondary generalization of a focal epilepsy
epileptiform discharges on EEG. due to a structural lesion.
• Infrequently, provide evidence for the etiology of
epilepsy. The EEG is generally non-specific with Discharges Associated with Epilepsy
respect to etiology.
In the routine 20- to 30-minute EEG, it is most likely
EEG Analysis in Patients with that only interictal abnormalities will be seen. These
Suspected Epilepsy are the abnormalities most often sought in routine
EEGs for epilepsy. Interictal abnormalities that are
When potentials are found that are suspicious for specific for epilepsy are termed epileptiform. It is gen-
interictal or ictal activity, there is a sequence of ques- erally suggested that the term epileptiform be reserved
tions to be considered in analysis: for interictal discharges associated with epilepsy,
while ictal EEG findings are termed seizure patterns or
• Is the discharge cerebral or artifactual? ictal patterns (see Table 4-17). Seizure patterns are only
• If the discharge is cerebral—is the discharge infrequently seen in the routine EEG. One notable
normal or abnormal? exception to that are ictal discharges associated with
• If the discharge is abnormal—is the discharge absence seizures. Absence seizures are almost reliably
specific for epilepsy, i.e., epileptiform? precipitated with hyperventilation in the untreated
• If the discharge is epileptiform—is the discharge child with childhood absence epilepsy.
focal or generalized? Focal spike or sharp waves without clinical sei-
• If the discharge is focal—what is the field of the zures is occasionally seen when an EEG is performed
discharge? for a non-epileptiform indication such as behavioral
disorder, developmental delay, or perhaps even an
This sequence of steps can seem simple, but when inappropriate indication (see Table 4-18). It is pos-
faced especially with a difficult interpretation, consid- sible that the patient may have seizures that are not
eration of basic analysis can be helpful. For example, noticed by observers, so evaluation in the epilepsy
multifocal sharp transients in a premature infant may monitoring unit (EMU) may be necessary. However,
Table 4-17 Discharges Associated with Epilepsy

Discharge Clinical Association
Focal spikes and sharp Suggest partial epilepsy with a focus at the locus of the spike, especially if
waves localization is consistent and persistent.
3 Hz generalized spike Suggest generalized epilepsy, most commonly typical absence epilepsy.
and wave
Slow spike and wave Generalizes spike-wave discharge of 2.5 Hz or less suggests symptomatic
generalized epilepsy, especially Lennox-Gastaut syndrome.
Fast spike and wave Discharges faster than 4 Hz suggest especially juvenile myoclonic epilepsy.
Focal ictal discharge Focal repetitive discharges with changing frequency, usually decreasing but
occasionally fluctuating or even increasing.
TIRDA (temporal inter- TIRDA is fairly specific for partial epilepsy of temporal lobe origin but is
mittent rhythmic delta not ictal. However, the strong correlation between this pattern and epilepsy
activity deserves mention in the interpretation.
Table 4-18 Spikes and Sharp Waves Not Associated with Epilepsy

Spikes and sharp waves Examples
Normal Vertex waves
Occipital lambda waves
14 and 6 Hz positive spikes
Wicket spikes
Benign epileptiform transients of sleep (BETS)
Positive occipital sharp transients of sleep (POSTS)
6-per-second (phantom) spike and wave
Abnormal Periodic lateralized epileptiform discharges (PLEDs)
Breach rhythm
Focal spike or sharp wave without clinical seizures.
we should avoid placing individuals on AEDs unless after-going slow wave. Spikes and sharp waves should
there is a clear indication, so we treat the patient, be differentiated from the background and not just
not the EEG. Report of such an EEG might read a higher voltage or sharper, but otherwise similar to
something like: surrounding rhythmic activity. The great majority of
sharp waves and spikes are surface negative. They gen-
Abnormal study because of epileptiform activ- erally have a field that includes more than one elec-
ity arising from the right temporal lobe. In the trode. They should be different from what is expected
appropriate clinical situation, this would be as physiologic activity in the particular field and state
supportive of a partial seizure disorder, how- of alertness. Not all the above features have to be
ever, the presence of this pattern does not present, however, the more features present, the more
mean that the patient is having seizures. confident one can be of the "epileptiform nature." (see
Figure 4-87).
Epileptiform Discharges Even though spikes and sharp waves usually have
after-going slow waves, the term spike-and-wave com-
These include spikes and sharp waves and combinations plex is usually reserved for the situation where the
of these with slow waves (see Chapter 3). By definition, slow wave is very prominent, often higher in voltage
spikes are shorter than 70 milliseconds, whereas sharp than the spike.
waves are 70–200 milliseconds in duration. Other epilep-
tiform discharges include spike-and-wave complexes, Ictal versus Interictal Epileptiform Discharges
slow spike-and-wave complexes, sharp-and-slow-wave Ictal discharges are usually not merely repetition of
complexes, multiple-spike complexes (or poly- interictal discharges and will generally have an appear-
spike complexes), multiple-spike-and-slow-wave ance different from multiple interictal discharges. One
complexes (or polyspike-and-slow-wave com- exception to this fairly clear differentiation between
plexes), multiple-sharp-wave complexes, and ictal and interictal discharges is generalized absence
multiple-sharp-and-slow-wave complexes. seizures. The distinction between interictal and ictal
Many EEG waves have a sharp appearance, but discharges is not always clear-cut. For example, in
they are only called spikes or sharp waves if they sat- patients with generalized absence seizures it has been
isfy a number of features, including a relatively high demonstrated that a subtle alteration of responsive-
voltage compared to the background, an asymmet- ness occurs even with a single spike-and-wave dis-
ric temporal appearance of the wave typically with a charge, if responsiveness is tested with sensitive tools.
shorter first half and a longer and higher voltage sec- On the other hand, generalized spike-and-wave dis-
ond half, a biphasic or polyphasic morphology, and charges that are shorter than 3 seconds are generally
Clinical EEG 149
a b c d
e f g
h i j
Figure 4-87: Epileptiform Discharges.

a- spike; b- sharp wave; c- spike-and-wave complexes; d- sharp-and-slow-wave complexes; e- slow-spike-and-slow-wave
complex; f- polyspike-and-wave complex; g- multiple-sharp-and-slow-wave complex; h- polyspike complex; i & j- multiple
sharp wave complexes.
not appreciated by family members, particularly in epilepsy, and consistent left occipital spikes suggest
the absence of motor accompaniments. Therefore, left occipital lobe epilepsy.
for practical purposes, one could state that bursts of Two independent spike or sharp wave foci still
generalized spike-and-wave discharges are ictal if they suggest partial epilepsy in most instances. However,
last more than 3 seconds, or if they are associated with if the discharges are frontal or central, they can be
clear clinical changes. consistent with generalized epilepsy. In generalized
Another pattern that can be ictal or “interictal” is epilepsy, “fragments” of generalized epileptiform dis-
that of paroxysmal fast activity noted in patients with charges could be noted, particularly in sleep, in the
symptomatic generalized epilepsy, particularly those frontal or central regions (see Figures 4-91 and 4-92).
with Lennox-Gastaut syndrome. In these patients, As a rule, patients with generalized epilepsy will have
the paroxysmal fast activity (or generalized polyspike generalized epileptiform discharges as well as these
activity) can be associated with generalized tonic sei- “fragments.”
zures or could be totally asymptomatic. Occasionally, When there are two or more independent foci,
such discharges cause arousal as their only clinical the localization of the epileptogenic focus becomes
manifestation. less certain. Many patients will still have a single ictal
Compare Figure 4-88 with the ictal discharge from focus, i.e., seizures may start in a single location even
the same patient in Figure 4-89. though interictal epileptiform activity is bilateral or
even multifocal (Figure 4-93). However, patients with
Types of Epilepsy Associated with Specific EEG independent foci are more likely to have independent
Patterns seizure onsets than those with single consistent foci
(Figure 4-94).
Focal Spikes and Sharp Waves
Focal spikes or sharp waves generally suggest focal 3Hz Generalized Spike-and-Wave Discharges
or partial epilepsy, particularly if there is a single and (range 2.5–4Hz)
consistent localization (Figure 4-90). For example, These discharges suggest generalized epilepsy. If they
consistent right anterior temporal spikes or sharp are noted in rhythmic, regular, synchronous, and sym-
waves suggest right anterior-mesial temporal lobe metrical trains, then they are strongly suggestive of the
Figure 4-88: Focal Epileptiform Discharge—A Sharp Wave.

Left temporal sharp wave in a 35-year-old woman with epilepsy and left hippocampal sclerosis. Compare with the figure
below of ictal discharge in the same patient.
presence of typical absence seizures. Typical absence based on the frequency of discharges in waking and
seizures generally correspond to normal intelligence not in sleep. Slow spike-and-wave discharges are sug-
and normal neurological status. As mentioned above, gestive of symptomatic generalized epilepsy such as
duration of 3 seconds or more is usually needed for Lennox-Gastaut syndrome. They are associated with
seizures to be noticed by observers. Occasionally, brain damage, and clinically correlated with atypical
however, the presence of motor manifestations in absence seizures. Atypical absence seizures are clini-
these seizures can make shorter discharges associated cally very similar to typical absence seizures except
with clinically detectable seizures. In sleep, general- that they may have a lesser alteration of conscious-
ized spike-and-wave discharges tend to become irreg- ness or responsiveness with them, may have a slower
ular and longer in duration. In addition, with sleep onset and a more gradual termination, as well as more
there is frequently a change in morphology to gener- prominent motor features. Slow spike-and-wave dis-
alized polyspike-and-wave discharges. Therefore, the charges are more often asymmetrical and may be asso-
appearance of these discharges in sleep cannot predict ciated with focal epileptiform and non-epileptiform
the appearance in waking (see Figures 4-95 and 4-96). abnormalities.
Slow Spike-and-Wave Discharges Fast Spike-and-Wave Discharges

A frequency of generalized spike-and-wave discharges Discharges that are faster than 4 Hz are called fast
below 2.5 Hz results in the term slow spike-and-wave or spike-and-wave discharges (Figure 4-98). These typi-
atypical spike-and-wave (Figure 4-97). This should be cally range from 4 to 7 Hz in frequency. They are
Clinical EEG 151
Figure 4-89: Focal Ictal Discharge.

Left temporal ictal discharge in the same patient as Figure 4-88.
Figure 4-90: Focal Sharp Wave.

Right temporal sharp wave in a patient with right temporal lobe epilepsy.
seen in association with juvenile myoclonic epilepsy, to termination. The end of the seizure is sometimes
but also with other generalized idiopathic epilep- clear-cut and at other times not. The postictal slow
sies, even in the absence of myoclonic seizures. Fast activity can occasionally be difficult to distinguish
spike-and-wave discharges tend to be irregular and from the rhythmic ictal activity towards the end of the
tend to occur in clusters. These clusters can be asso- seizure, which can also be in the delta range.
ciated with myoclonic seizures or could be subclini- Focal ictal discharges (Figures 4-99 and 4-100)
cal/interictal. In juvenile myoclonic epilepsy, they are may start with voltage attenuation. If this attenuation
most likely to be recorded after arousal, particularly is focal, it has a localizing value. At other times, the
following sleep deprivation. attenuation is diffuse and less useful. The presence
of high-frequency beta range activity at seizure onset
Focal Ictal Discharges suggests neocortical involvement.
Ictal discharges in association with partial epilepsy Hippocampal seizures will typically start in the
typically involve rhythmic activity that evolves in fre- theta range, and infrequently in the alpha range.
quency, morphology, voltage, and distribution, during Seizure onset in the delta range may suggest that
its course. Although it is most common for discharges the center of seizure activity is at some distance
to gradually decrease in frequency between their from where the delta activity is recorded. In the
onset and their termination, it is not at all uncom- case of temporal lobe epilepsy, a theta discharge in
mon for frequency to fluctuate, increasing and then the anterior-mesial temporal region should be seen
decreasing. However, toward the end of the seizure within 30 seconds of ictal onset. If not, the temporal
there is almost always a reduction in frequency prior localization is less than certain.
Clinical EEG 153
Figure 4-91: Fragments of Generalized Discharges.

Shifting left and right frontal epileptiform discharges in a patient with generalized epilepsy. These are termed fragments of
generalized discharges.
TIRDA (Temporal Intermittent Rhythmic Patterns of EEG Activity in Certain Forms of

Delta Activity) Epilepsy
This pattern is not ictal in nature, but it seems to be
quite specific for temporal lobe epilepsy. It is differ- Temporal Lobe Epilepsy
ent from intermittent irregular delta activity, which Temporal lobe epilepsy may be associated with a
is very non-specific in nature. Although TIRDA is normal first EEG in about 50% of instances. With
not yet considered epileptiform in most textbooks, repeated recordings, approximately 90% of patients
the EEG interpreter may comment that this pattern will demonstrate epileptiform abnormalities. There
is strongly associated with potential epileptogenicity will be approximately 10% of patients who will always
(Figure 4-101). have a normal EEG between seizures. Irregular delta
Figure 4-92: Shifting Asymmetries in Generalized Epilepsy.

Shifting asymmetries in an 18-year-old woman with idiopathic generalized epilepsy.
Figure 4-93: Independent Left and Right Temporal Sharp Waves, but a Single Ictal Focus.
Independent left and right temporal sharp waves (A & B) but consistent left temporal seizure onsets (C&D) in a 46-year-old
man with intractable complex partial seizures since age 5 and left hippocampal sclerosis.
Clinical EEG 155
Figure 4-94: Independent Left and Right Temporal Sharp Waves and Independent Left and Right Foci.
Independent left and right temporal sharp waves in a 34-year-old woman with intractable complex partial seizures proven to
start independently in the right and left temporal regions.
Figure 4-95: Generalized 3 Hz Spike-and-Wave.

Absence seizure in 9-year-old girl with spells of staring and unresponsiveness for one year. She averaged 2 to 3 attacks per day,
lasting seconds to 1 minute.
Figure 4-96: Regular Spike-and-Wave Activity in Waking with Irregular Polyspike-and-Wave Discharges in Sleep.
19-year-old with absence seizures since age 13. Spike-and-wave discharges were regular in waking but become irregular poly-
spike-and-wave discharges in sleep.
Figure 4-97: Slow Spike-and-Wave as can be seen in Lennox-Gastaut Syndrome.

Clinical EEG 157
Figure 4-98: Fast Spike-and-Wave Discharges.

The frequency of spike-and-wave discharges here is approximately 5 Hz.
Figure 4-99: Focal Ictal Discharge.

Three consecutive 10-second EEG segments showing onset and initial evolution of a right occipital ictal discharge. The evo-
lution included increase in voltage, decrease in frequency, and widening of the field.
'F3-AV SW
appearance of postictal slow activity as well as activa-
'F4-AV SW
tion of epileptiform discharges.
'F7-AV SW
'F8-AV SW In mesial temporal lobe epilepsy, spikes-and-sharp

'T7-AV SW
'T8-AV SW
waves will typically have a higher voltage anteriorly at
F7 or F8. If T1/T2 electrodes are used, they may have
the highest field or the highest amplitude. If sphenoidal
electrodes are used, they often have the highest ampli-
tude. There are some patients who have discharges only
recorded from the sphenoidal electrodes (Figure 4-102).
Approximately one-third of patients with tem-
poral lobe epilepsy have independent bitemporal
discharges, particularly in sleep. It is very common
that during sleep the field of epileptiform discharges
widens and mirror foci appear. If unilateral focal
spike activity is seen in waking and an independent
contralateral discharge is noted only in sleep, the wak-
ing activity is the most reliable for localization of the
seizure focus. In REM sleep there is also a narrowing
Figure 4-100: Focal Ictal Discharge. of the field and attenuation of mirror foci. Therefore,
Left fronto-temporal ictal discharge displayed on com- in patients with bilateral independent epileptiform
pressed EEG (60-second segments), showing evolution discharges, those interictal epileptiform discharges
with increasing amplitude, decreasing frequency, widening recorded in waking or REM sleep are the most reliable
field, and then abrupt termination (arrow). Postictal slow for localization. Most patients with bitemporal inde-
activity can be seen at F7 and T7.
pendent epileptiform discharges will still have unilat-
eral seizure onsets, but they have a higher chance of
activity may be the only EEG abnormality in some independent bitemporal seizure onsets than patients
patients with temporal lobe epilepsy. This is typi- with unilateral epileptiform discharges.
cally recorded from the anterior midtemporal region. If ictal discharges are unilateral, the side with the
TIRDA (see above) is strongly suggestive of temporal highest frequency of epileptiform discharges is typi-
potential epileptogenicity. Spikes-and-sharp waves cally the side of seizure onset. A small proportion of
are typically activated in drowsiness and sleep and patients may have generalized spike-and-wave dis-
also increase after the occurrence of seizures, particu- charges. This is not unexpected, as a high proportion
larly after the occurrence of secondarily generalized of patients may have a family history of epilepsy as
tonic-clonic seizures. As a result, in patients whose well as a history of febrile convulsions early in life. The
EEGs are repeatedly normal, one should try to obtain generalized spike-and-wave discharges are suspected
an EEG shortly after a seizure. This can help with the to be an inherited EEG trait.
Figure 4-101: Temporal Intermittent Rhythmic Delta Activity (TIRDA).

Right temporal rhythmic delta activity in a patient with right temporal lobe epilepsy
Clinical EEG 159
Figure 4-102: Focal Sharp Waves and Slow Activity in the Left Sphenoidal Electrode.
The focal epileptiform and slow activity is limited to the left sphenoidal electrode in a patient with left temporal lobe epilepsy.
Temporal simple partial seizures (Figure 4-103) onset (Figure 4-104). If sphenoidal electrodes are used,
are most often not associated with EEG changes. at least 5 Hz rhythmic activity noted in one sphenoidal
If they are, the EEG changes tend to be subtle and electrode within 30 seconds of seizure onset is strongly
quite focal. supportive of lateralization and localization. In second-
Complex partial seizures, on the other hand, are arily generalized tonic-clonic seizures of temporal lobe
almost always associated with a clear-cut ictal dis- origin, the same EEG changes are seen early on, but the
charge. In mesial temporal lobe epilepsy, the ictal dis- ictal discharge becomes generalized with extensive and
charge is in the theta range at onset or shortly after diffuse muscle artifact masking the EEG.
Figure 4-103: Simple Partial Seizures of Left Temporal Origin.

The ictal discharge is very focal, involving Sp1 and to a lesser extent Sp2. The subtle ictal discharge could have been missed
without the termination
Figure 4-104: Ictal Onset in a Patient with Right Hippocampal Sclerosis.

The ictal onset is with approximately 6–7 Hz rhythmic activity, predominant at Sp2 and F8.
It may be difficult to distinguish neocortical to extratemporal regions, and the discharge is

from mesial temporal lobe epilepsy. If sphenoidal more often bilateral from onset (see Figure 4-105).
electrodes are used, temporal lobe ictal activity not A high-frequency beta range activity at onset favors
represented in the sphenoidal electrode may favor a neocortical localization close to the recording elec-
a lateral temporal onset. With a neocortical origin, trode. However, a temporal beta frequency discharge
there may be more rapid spread of the ictal discharge could represent an extratemporal origin.
Figure 4-105: Interictal Sharp Wave (Top) and Ictal Discharge (Bottom) in a Patient with Lateral Temporal
Lobe Epilepsy with Auditory Aura.
Clinical EEG 161
Figure 4-106a: Posterior Temporal Lobe Epilepsy – MRI.

T2 - MRI brain slice showing lesion in the left posterior temporal region.
Figure 4-106b: Posterior Temporal Lobe Epilepsy – EEG.

EEG samples showing the discharge on both sphenoidal and scalp leads.
Posterior Temporal Lobe Epilepsy activity and ictal onset may be falsely localized. Some
In posterior temporal lobe epilepsy, the interictal epi- patients with posterior temporal lobe epilepsy may
leptiform discharges tend to have predominance in have only anterior-inferomesial temporal sharp waves,
the posterior or midtemporal electrodes, and not in or both posterior temporal and anterior-inferomesial
the anterior temporal region or the sphenoidal elec- temporal epileptiform activity. In these patients, ictal
trodes (see Figures 4-106a, 4-106b, and 4-107). The discharges may also appear to be anterior-mesial tem-
field may involve the parietal or occipital electrodes. poral. In patients with posterior temporal lesions, such
Ictal discharge onset also tends to predominate in false localization historically resulted in leaving the
the posterior temporal region and not involve the sphe- lesion and resecting the anterior temporal and hippo-
noidal electrodes. However, interictal epileptiform campal regions, with poor surgical results.
Figure 4-107: Falsely Localizing Ictal Discharge in Posterior Temporal Lobe Epilepsy.

Interictal epileptiform discharges in this patient included both anterior-inferomesial temporal sharp waves (Sp1 and F7) and
posterior-mid temporal spikes (P7 and T7).
The ictal onset appears to be typical of anterior- It is not uncommon for secondary bilateral syn-
inferomesial temporal lobe epilepsy. The patient in chrony to occur in frontal epilepsy. This is to be dis-
Figure 4-106 became seizure-free with lesionectomy, tinguished from primary bilateral synchrony seen in
without removal of the anterior and mesial temporal generalized epilepsy. Secondary bilateral synchrony
structures. is where focal spikes or sharp waves lead to bilateral
Frontal Lobe Epilepsy Fp1-3

The frontal lobe is the largest lobe and has surfaces
that are invisible or relatively invisible to EEG. F3-C3
Orbitofrontal onset seizures and mesial frontal onset
seizures may have essentially no surface EEG mani- C3-P3
festations. In orbitofrontal epilepsy, epileptiform
Fp2-F4
discharges may be recorded from the frontopolar elec-
trodes or from supraorbital electrodes (Figure 4-108). F4-C4
In mesial frontal lobe epilepsy, the midline electrodes
or parasagittal electrodes may record epileptiform C4-P4
discharges. On occasion, these discharges can be con-
fused with vertex waves in sleep (Figure 4-109). Their
occurrence in waking can help resolve this confusion. Figure 4-108: Frontal Lobe Discharges.
Anterior lateral frontal, dorsolateral frontal, and cen- Right frontal spike-and-wave discharges in a patient with a
right frontal convexity epileptogenic focus. There is reversal
tral foci can be associated with focal spike discharges
of polarity of discharges at F4.
in these regions (Figure 4-110).
Clinical EEG 163
Fp1-Av Frontal lobe seizures have a tendency to become

Fp2-Av rapidly generalized. Seizure spread is at times so fast
F3-Av that a focal onset could be hard to distinguish. The
F4-Av presence of high-frequency focal fast activity at sei-
C3-Av zure onset suggests good localization of the seizure
focus to the region of fast activity (Figure 4-112).
C4-Av
P3-Av
Occipital and Parietal Lobe Epilepsies
P4-Av
Occipital lobe epilepsy can be associated with focal
O1-Av
spike or spike-and-wave discharges in the occipital
O2-Av
region (Figure 4-113). It is not uncommon for dis-
F7-Av
charges to be bilateral, since volume conduction
F8-Av
occurs frequently at the occipital poles (as it does at
T3-Av
the frontal poles). Occipital lobe seizures can develop
T4-Av
focally or regionally, or can spread to frontal or tem-
T5-Av
poral lobe regions. Seizures starting above the calca-
T6-Av
rine fissure tend to spread to the frontal lobe, whereas
Fz-Av
seizures starting below the calcarine fissure tend to
Cz-Av spread to the temporal lobe. Occipital lobe seizures
Pz-Av
that remain regional have a tendency to develop very
slowly, starting with beta range activity that gradually
Figure 4-109: Sharp Wave Predominating at the Vertex evolves to alpha range and then theta range and then
in a Patient with Supplementary Motor Seizures. delta range, over several minutes. The progression of
The sharp waves are predominant at Cz. These are not vertex
the ictal discharge can be so slow that the seizure may
waves because the patient is awake.
not be appreciated until the EEG has changed quite
drastically.
synchronous discharges. This can be suspected when The EEG is often misleading in parietal lobe epi-
bilateral discharges have a consistent asymmetry or a lepsy. Only some patients have focal parietal interictal
consistent lead on one side, when some focal discharges epileptiform abnormalities and ictal discharges. Many
are seen only one side, or when a consistent focal slow patients have abnormalities in the temporal or frontal
abnormality is seen (see Figures 4-111a, 4-111b, 4-111c). regions, resulting in false localization.
Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
C4-P4
P4-O2
Fp1-F7
F7-T3
T3-T5
T5-O1
Fp2-F8
F8-T4
T4-T6
T6-O2
Figure 4-110: Supplementary Motor Seizures.

The ictal discharge could be easily missed. Definite EEG changes are noted toward the end of the discharge (indicated by
arrow).
a
Figure 4-111: Suspected Secondary Bilateral Synchrony.

There is a lead on the right in the discharge (a), a consistent asymmetry is noted with right predominance (a and b), and right
frontal slow activity is noted intermittently (c).
Clinical EEG 165
Figure 4-112: Right Frontal Fast Ictal Discharge.

The ictal activity is in the beta range at onset. The ictal discharge was associated with left arm twitching.
Figure 4-113: Posterior Quadrant Sharp Waves and Ictal Discharge.

Patient with a left posterior quadrant (predominantly occipito-temporal) seizure focus
Figure 4-114: Typical Interictal Epileptiform Activity in a Patient with Benign Rolandic Epilepsy.
The EEG was normal in waking (left), but very frequent independent left and right mid-posterior temporal sharp waves were
activated in sleep, with associated frontal positivity (arrow).
Benign Rolandic Epilepsy or Benign Epilepsy with be typical absence seizures. In such instances, it may
Centrotemporal Spikes (BECTS) be somewhat difficult to identify the specific clinical
In this condition, epileptiform discharges have a syndrome, as to whether it is benign rolandic epilepsy
typical appearance with broad blunt sharp waves or childhood absence epilepsy.
(Figure 4-114). The classical field is with negativity in
the central and mid-temporal regions and positivity Benign Epilepsy with Occipital Paroxysms
bifrontally. However, there are very frequent variants In benign epilepsy with occipital paroxysms, high
to this field distribution. The discharges are commonly voltage spike-and-wave discharges or sharp waves are
more posterior, involving posterior temporal and recorded over the occipital and posterior temporal
parietal regions. Some patients may have coexistent regions unilaterally or bilaterally, synchronously or
occipital lobe discharges. Marked activation of epilep- independently (Figure 4-116). They tend to occur in
tiform activity in sleep is typical. It is quite common repetitive trains at times. They are typically blocked
for discharges to be recorded independently on the by eye opening and enhanced by eye closure. They
two sides in sleep. Awake recordings may completely may coexist with centrotemporal or generalized
miss the epileptiform activity, hence sleep is essential. spike-and-wave discharges.
Ictal recordings are very rare in this condition. In fact,
seizures are often a rare occurrence despite the high Signs associated with Epileptiform Discharges
incidence of interictal epileptiform discharges.
In patients with benign rolandic epilepsy, there is The clinical signs associated with epileptiform dis-
an increased incidence of generalized spike-and-wave charges span a wide range (Table 4-19). Some of the
discharges. In fact, in some patients, there may even most common are discussed here:
Clinical EEG 167
Figure 4-115: Generalized Spike-and-Wave Discharge in a Patient with Benign Rolandic Epilepsy.

The first segment to the left shows typical discharges of benign rolandic epilepsy, with bifrontal positivity (arrowhead).
A generalized epileptiform discharge is seen to the right in the same patient.
Figure 4-116: Benign Occipital Lobe Epilepsy.

Eye opening blocked the left occipital discharges, while eye closure enhanced them.
Table 4-19 Clinical Correlates to Epileptiform Discharges

Type of Discharge Pattern Seizure types
Interictal discharges 3-per-second spike-wave pattern Absence seizures
Generalized tonic-clonic seizures
Fast spike-wave complex Generalized tonic-clonic seizures
Slow spike-wave complex Lennox-Gastaut syndrome
Hypsarrhythmia Infantile spasms
Focal discharge Temporal lobe focus Complex partial seizures
Frontal lobe focus Complex partial seizures and simple
partial seizures.
Parietal lobe focus Simple partial seizures especially with
sensory symptoms
Occipital lobe focus Simple partial seizures, especially with
visual symptoms
Focal motor activity: Simple partial seizures can Oroalimentary automatisms: Oral automatisms can
present with focal jerking, especially of face and/or include lip smacking and chewing.
arm. This is simple positive motor phenomena.
Adversive maneuvering is less common, but is charac- Generalized Seizure Activity
terized by turning to the side opposite the discharge.
Language disturbance: Speech arrest can occur, Seizure Patterns
with an abrupt loss of speech while talking. Other
movements can develop on top of this. Less common Generalized seizures have their origin in the circuits
is ictal jargon, where there is spontaneous speech that that are responsible for cortical-subcortical asso-
is unintelligible. ciations. A such, there is not a single focus, so these
Loss of responsiveness: Generalized and partial sei- seizures are unlikely to be due to a structural lesion.
zures can manifest as disturbance of responsiveness. These are primary-generalized seizures rather than
Absence epilepsy is the prototypic disorder with no secondarily generalized seizures.
response to command during a seizure but response
delayed until after the seizure. Generalized seizures come in several important types,
Fear and ictal language: Ictal fear can present with a including:
series of statements of alarm which, unlike jargon, are • Absence;
easily understandable. • Atypical absence;
Contralateral posturing: Posturing may be so sub- • Tonic-clonic;
tle as to be not noticed. The posturing can resemble • Myoclonic.
adversive maneuvering but with posturing of limbs
and head. Absence seizures are staring spells without loss of
Autonomic symptoms: Autonomic symptoms can postural tone. This is associated with the 3-per-second
accompany a seizure with motor manifestations or spike-wave pattern.
be isolated symptoms of seizures (Moseley et al., Atypical absence seizures include the
2012). Autonomic symptoms can be almost anything Lennox-Gastaut syndrome. There is loss of aware-
in the arena, but ones of greatest importance include ness. The differentiation from absence is mostly by
tachyarrhythmias, bradyarrhythmias, hyperventila- EEG where the discharge is slower, about 2.5/sec. In
tion, episodic abdominal pain, nausea, vomiting, contrast with absence, there is slower loss of aware-
flushing of the skin, and even sexual symptoms. ness and more gradual recovery.
Clinical EEG 169
Tonic-clonic seizures are one of a family of motor is maximal over the midline frontal region, and is
seizures that also includes tonic and clonic seizures. minimal in the temporal and occipital regions. The
EEG pattern is spike-wave of a variety of frequencies. individual waves consist of a spike, double spike, or
Myoclonic seizures include juvenile myoclonic polyspike component and a following slow wave.
epilepsy. In addition, there is benign myoclonus and Patients who show the polyspike complex are more
myoclonus associated with metabolic disorders. likely to exhibit myoclonus.
The EEG activity associated with generalized sei- Hyperventilation provokes the 3-per-second
zures comes in four common patterns, although some spike wave complex. If absence epilepsy is consid-
less common patterns do occur. ered, then hyperventilation should be performed for
5 minutes rather than the usual 3 minutes. Children
with absence epilepsy are typically identified by the
EEG Patterns observer as symptomatic if the discharge lasts longer
The common patterns are: than 5 seconds. The technician should ask a question
during the discharge and note the timing and type of
• 3-per-second spike-wave; subsequent response.
• Slow spike-wave (about 2.5/sec)
• Fast spike-wave (about 5/sec); Fast Spike-Wave Pattern
• Fast polyspike-wave (about 6-7/sec). The fast spike-wave complex is seen in primary gen-
eralized epilepsies and correlated with generalized
3-per-Second Spike-Wave Pattern tonic-clonic seizures with or without myoclonus (see
The 3-per-second spike-wave pattern (Figure 4-117) Figures 4-118 and 4-119). Absence seizures are rare.
is typically seen in patients with absence epilepsy,
although other seizure types may be seen, including Slow Spike-Wave Pattern
generalized tonic-clonic seizures. The discharge is The slow spike-wave complex (Figure 4-120) has a
synchronous from the two hemispheres and begins frequency of 2.5/sec or less. The morphology is less
with discharge at about 4/sec then slows to about 2.5 stereotyped than the 3-per-sec spike-wave complex.
during the duration of the discharge. The discharge The duration of the slow spike is usually more than
Figure 4-117: 3-per-Second Spike-Wave Complex.

Typical 3-per-second spike-and-wave discharge.
Figure 4-118: Fast Spike-Wave Pattern.

This discharge has a high frequency of approximately 5 Hz.
Figure 4-119: Fast Spike-Wave Pattern Evolving into a Generalized Tonic-Clonic Seizure.

The fast spike-wave complex has a frequency of 4–5/sec and has the appearance of slow waves with superimposed sharp
activity, rather than a distinct spike-wave complex. This pattern is less stereotyped than the 3-per-second spike-wave pattern,
with less synchrony.
Clinical EEG 171
Figure 4-120: Slow Spike-Wave Pattern with Atypical Absence Seizure.
70 msec, which technically makes it a sharp wave. The of LGS. Akinetic seizures show the slow spike-wave
complex is generalized and synchronous across both complex throughout the seizure. Tonic seizures occur
hemispheres, with the highest amplitude in the mid- in LGS and are characterized by rapid spike activity
line frontal region. During sleep, the slow spike-wave or desynchronization rather than the slow spike-wave
complex may be continuous, but this is thought to complex.
be activation of interictal activity during sleep rather
than status epilepticus. Hypsarrhythmia
The slow spike-wave complex is often associated Hypsarrhythmia is a pattern that is usually easily
with the Lennox-Gastaut syndrome (LGS). The term recognizable by the experienced neurophysiolo-
petit-mal variant is misleading and should not be used. gist (Figures 4-121, 4-122, and 4-123). The pattern
The slow-spike-wave pattern in LGS is often an inter- is characterized by high voltage bursts of theta and
ictal pattern but may be ictal. Since the patients have delta waves with multifocal sharp waves superim-
a mixed seizure disorder, ictal patterns may be other posed. The bursts are separated by periods of rela-
than the slow spike-wave complex. Atonic seizures tive suppression. In some circumstances, flattening
shows generalized spikes during the myoclonus, fol- of the EEG may be an ictal sign, indicating that
lowed by the slow spike-wave complex during the there has been sudden desynchronization of the
atonic phase. Atonic seizures are most characteristic record.
Figure 4-121: Hypsarrhythmia.
EEG shows high voltage slow disorganized background with multifocal spikes and periods of relative attenuation
Figure 4-122: Hypsarrhythmia, with a Spasm.

The period of attenuation corresponded to a clinical spasm.
Clinical EEG 173
Fp1-F7
F7-T3
T3-T5
T5-O1
Fp2-F8
F8-T4
T4-T6
T6-O2
150 μV
Figure 4-123: Hypsarrhythmia with Asynchronous Attenuation.

The periods of attenuation are asynchronous, suggesting Aicardi syndrome.
Hypsarrhythmia is seen particularly in patients The complex is composed of brief trains of small
with infantile spasms. Patients with symmetric spike-wave complexes, distributed evenly over both
hypsarrhythmia seldom have structural lesions, hemispheres, with either a frontal or occipital pre-
whereas patients with asymmetric or unilateral dominance, as described. They are most commonly
hypsarrhythmia are more likely to be associated with seen during the waking and drowsy states, and disap-
structural lesions. pear with sleep.
The sample shown in Figures 4-124 and 4-125 is
6-per-Second (Phantom) Spike-Wave from a 10-year-old female. The spikes reverse at Pz.
6 Hz spike-and-wave discharges recorded in the posterior
head region can be a normal variant, seen predominantly
Absence Seizures
in young women. This has been termed FOLD (referring
to preponderance in Females, Occipital predominance, Overview
Low-voltage, and occurrence in Drowsiness). Absence seizures are among the most common
6Hz spike-and-wave discharges that are anterior observed in clinical practice. Children may show these
in localization are more likely associated with epi- seizures on routine examination or during a routine
lepsy. These have been termed WHAM (referring to
Waking, High voltage, Anterior localization, and Male
predominance). T5 - P3
These acronyms were described by Hughes (1980). In

summary: P3 - Pz
• WHAM = Waking record, High amplitude,

Anterior, Males; Pz - P4
• FOLD = Females, Occipital, Low amplitude,
Drowsy. P4 - T6
WHAM is associated with seizures, but FOLD is not.

The seizures associated with the anterior/frontal dis- Figure 4-124: 6-per-Second Spike-Wave Pattern.
An entire page is shown below.
charge are generalized tonic-clonic.
EEG of Absence Seizure

Fp1 - A1 The recording in Figures 4-126 and 4-127 shows the
typical 3-per-second spike-wave pattern. The pattern is
Fp2 - A2
not as well developed at the beginning of the discharge,
F3 - A1
then becomes better developed through the duration.
F4 - A2 The 3-per-second spike-wave pattern is typically
C3 - A1 seen in patients with absence epilepsy, although other
C4 - A2
seizure types may be seen, including generalized
tonic-clonic seizures. The discharge is synchronous
P3 - A1
from the two hemispheres and begins with discharge
P4 - A2 at about 4/sec, then slows to about 2.5/sec by the end
O1 - A1 of the discharge. The discharge is maximal over the
O2 - A2 midline frontal region, and is minimal in the temporal
and occipital regions. The individual waves consist of
F7 - A1
a spike, double spike, or polyspike component and a
F8 - A2 following slow wave. Patients who show the polyspike
T3 - A1 complex are more likely to exhibit myoclonus.
T4 - A2 Hyperventilation provokes the 3per-seccond
spike-wave complex. If absence epilepsy is consid-
T5 - A1
ered, then hyperventilation should be performed for
T6 - A2
5 minutes rather than the usual 3 minutes. Children
with absence epilepsy are typically identified by the
Figure 4-125: 6-per-Second Spike-Wave. observer as symptomatic if the discharge lasts longer
than 3-5 seconds. The technician should ask a ques-
tion during the discharge and note the timing and
type of subsequent response.
EEG with hyperventilation. Typical of absence epi-
lepsy are the following features: Absence Without Spikes
Occasionally, absence seizures are seen without the
• Seizures characterized by loss of awareness with spike component visible on surface recordings (see
or without automatisms; Figure 4-128). There are no clinical implications. This
• Provocation of the seizures by hyperventilation; is a controversial area, but is rarely seen in routine
• No postictal confusion; recordings (Lee and Kirby, 1988).
• Normal examination;
• Normal EEG background, other than the Absence with Preserved Awareness
3-per-second spike-wave discharges. Patients with absence seizures may show preserved
awareness although responsiveness is impaired and
Seizures may be multiple during the day, and initially delayed.
passed off as inattention or daydreaming. Recognition Myoclonic Absence
of the automatisms may prompt the clinical suspicion Myoclonic absence is characterized by absence sei-
and diagnosis. EEG is usually abnormal, showing zures with a myoclonic component. This is more
brief 3-per-second discharges with an otherwise nor- prominent motor activity than is seen with the
mal background. automatisms associated with absence seizures.
Treatment is usually with ethosuximide, valpro-
ate, or lamotrigine. Patients often have total con- Absence with Self-induction
trol of their seizures with monotherapy. The EEG Absence can rarely be self-induced, such as by waving
usually dramatically improves with treatment, and the hand in front of the eyes while brightly illuminated
there may be no interictal discharge with patients on (Figure 4-129). This is the ultimate manifestation of
therapeutic AED levels, a feature not typical of many non-compliance, where the patient intentionally pro-
epilepsies. vokes a seizure for the experience.
Clinical EEG 175
Figure 4-126: Absence Seizure.

This shows the onset and early evolution of the 3-per-second spike-wave discharge.

This is a magnified portion of figure 4-126 to more clearly show the onset of the discharge. The EEG component of this
recording shows a rhythmic 3-per-second spike-wave pattern, which slows slightly during the recording. This slowing is
especially prominent with prolonged seizures. There is a rapid return to normal intellect following the seizure.
Figure 4-128: Absence without Spike.

The seizure shows a typical 3-per-second wave without the spike being apparent.
Atypical Absence Seizures atypical absence seizures is electrographic, as the lat-

ter have a slower frequency of less than 2.5 Hz. This
Overview is the slow spike-wave pattern. Clinical distinctive
Atypical absence seizures tend to occur in symptom- features reported are a slower loss of awareness and a
atic generalized epilepsy such as Lennox-Gastaut more gradual recovery, as well as perhaps more prom-
syndrome. The main distinction between typical and inent motor manifestations.
Clinical EEG 177
Figure 4-129: Absence Seizure due to Self-Induction.
The term petit-mal variant is misleading and complex. Atonic seizures show generalized spikes dur-
should not be used. ing the myoclonus, followed by the slow spike-wave
complex during the atonic phase. Atonic seizures are
Atypical Absence Seizure Presentation most characteristic of LGS. Akinetic seizures show
Atypical absence seizures usually begin in early child- the slow spike-wave complex throughout the seizure.
hood, under the age of 6 years, and continue into Tonic seizures occur in LGS and are characterized by
adult life. Not all patients have the Lennox-Gastaut rapid spike activity or desynchronization rather than
syndrome. Cause can be genetic or due to perinatal the slow spike-wave complex.
insult. The atypical absence seizures should be differ- Treatment is often difficult with incomplete
entiated from typical absence and from daydreaming response to monotherapy. AEDs most commonly used
and inattention. Other differential diagnoses include are valproate, lamotrigine, felbamate, and topiramate.
complex partial seizures, although these are unusual
to have onset in early childhood. EEG of Atypical Absence Seizures
Lennox-Gastaut syndrome (LGS) is a severe epi- The EEG in patients with atypical absence seizures is
lepsy characterized by mixed seizures including atypi- characterized by slow spike-wave pattern. The slow
cal absence, atonic, tonic, and myoclonic. Seizures have spike-wave complex has a frequency of 2.5/sec or less.
onset usually before the age of 4 years. Development The morphology is less stereotyped than the 3-per-sec
is usually abnormal, with intellectual impairment and spike-wave complex. The duration of the slow spike is
behavioral abnormalities. Cause can be genetic or due usually more than 70 msec, which technically makes
to a variety of perinatal insults. Seizures persist into it a sharp wave. The background is also often abnor-
adult life. The slow-spike-wave pattern in LGS is often mal, in contradistinction to absence, with slowing and
an interictal pattern but may be ictal. disorganization.
Since the patients have a mixed seizure disorder, The complex is generalized and synchronous
ictal patterns may be other than the slow spike-wave across both hemispheres, with the highest amplitude
in the midline frontal region. During sleep, the slow For example, Figure 4-133 shows the onset of a gen-
spike-wave complex may be continuous, but this is eralized tonic-clonic seizure in a patient with juvenile
thought to be activation of interictal activity during myoclonic epilepsy.
sleep rather than status epilepticus. In patients with generalized absence and general-
ized tonic-clonic seizures, absence seizures may sec-
Patient #1 ondarily evolve into tonic-clonic seizures.
Figure 4-130 shows the slow spike-wave pattern typi-
cal of atypical absence seizures. Figure 4-131 is a sec- Generalized Tonic-Clonic Seizure Presentation
ond epoch from the same patient. Generalized tonic-clonic seizures are characterized by
shaking and tonic contraction of the extremities. The
Patient #2 discharge is most commonly fast spike-wave, but can
The slow spike-wave pattern can look similar to the also be 3-per-second spike-wave or polyspike-wave.
3-per-second spike wave pattern, with the main differ- The generalized tonic-clonic seizure shown in these
entiating features being slower frequency, disorgani- Figures is primarily generalized, but tonic-clonic sei-
zation, and abnormal background, the latter of which zures can also be secondarily generalized from a par-
is the most helpful in clinical practice (Figure 4-132). tial seizure. In this circumstance, the focal onset may
or may not be seen clinically.
Generalized Tonic-Clonic Seizures
Overview EEG Appearance of Generalized Tonic-Clonic

Generalized tonic-clonic seizures may occur in many Seizure
generalized epileptic syndromes. The EEG appear- Figures 4-134 and 4-135 are from the same patient
ance at onset may vary with the specific syndrome. and show the beginning and peak-ictal period. While
Figure 4-130: Atypical Absence.

Slow spike-wave pattern with atypical absence seizure.
Clinical EEG 179

Second epoch from the same patient.
discharges are visible initially, with major motor common along with shoulder abduction and hip flex-
movements, the EEG can be obscured by EMG and ion. The seizure may start with a myoclonic jerk. They
movement. usually start in sleep and drowsiness.
Tonic seizures may be followed by atypical
absence, resulting in what appears to be a more
Evolution of a Tonic-Clonic Seizure
prolonged postictal state. This has been termed a
EEGs from three patients with generalized tonic
tonic-absence seizure.
clonic seizures are shown to demonstrate the initial
evolution of the discharge. The first (Figure 4-136a
EEG of Generalized Tonic Seizure
and 4-136b) is from a patient previously discussed
The EEG shows a fast spike pattern that shows evolu-
with JME. The other two are from different patients
tionary changes (Figures 4-139 and 4-140).
showing patterns of evolution (Figures 4-137
The EEG epoch in Figure 4-141 is not associated
and 4-138)
with overt clinical changes. This demonstrates slow
spike-and-wave activity. This is a characteristic find-
Generalized Tonic Seizures ing in the EEG of patients with Lennox-Gastaut
syndrome.
Generalized tonic seizures are brief episodes of
increase in tone, lasting only a few seconds to about Tonic-Absence Seizures
1 minute. The manifestation can be an increase in neck
tone or upward eye deviation, but may be more severe Tonic-absence seizures are characterized by tonic
with marked increase in tone of the axial and appen- activity followed by inattentiveness or impaired
dicular muscles. Neck and trunk flexion are most responsiveness. These usually occur in symptomatic
generalized epilepsy. Patients usually have tonic sei- tonic portion of the activity is longer and slower
zures without the prolonged absence. than myoclonus, with a contraction that is slightly
The patient is a 17-year-old with seizures since sustained.
infancy, following meningitis at 7 months of age. The epoch in Figure 4-142 was recorded using
The seizure is characterized by a brief tonic phase the longitudinal-bipolar montage; Figure 4-143 is the
followed immediately by the absence phase. The same epoch presented in an ear reference montage.
Clinical EEG 181
Figure 4-133: Onset of a Generalized Tonic-Clonic Seizure.
Figure 4-134: EEG of Generalized Tonic-Clonic Seizure.

Continuation of the seizure shown in Figure 4-133.
Figure 4-135: Generalized Tonic-Clonic Seizure—Continuation of the Seizure Shown in Figure 4-134.
Figure 4-136a: Evolution of a Tonic-Clonic Seizure—Beginning.

Clinical EEG 183
Figure 4-136b: Same Patient—Mid-Seizure.
Figure 4-137: Onset of Generalized Tonic Seizure (GTC) Seizure.

Figure 4-138: Onset of GTC Seizure.
Figure 4-139: Generalized Tonic Seizure.

The discharge as shown is fast with evolutionary changes in frequency.
Clinical EEG 185
Figure 4-140: Generalized Tonic Seizure.
Figure 4-141: Generalized Tonic Seizure—Interictal.

Figure 4-142: Tonic-Absence Seizure, LB Montage.
Figure 4-143: Tonic-Absence Seizure, Ear Reference.

Clinical EEG 187
Generalized Atonic Seizures Myoclonic Seizures
Atonic seizures are episodes of loss of tone. They Generalized myoclonic seizures last a fraction of a sec-
most commonly begin in childhood and continue ond. They vary in severity from mild with barely visible
into adult life. These seizures can vary in manifesta- twitch to severe with massive myoclonus associated
tion from subtle drooping of the head to a massive with falling. The myoclonic jerk may involve the whole
loss of tone with falling. They are more common in body, or the upper extremities, or the head alone.
children. They are associated with drop attacks. Drop Although they are usually bilateral, they could be uni-
attacks can be due to tonic seizures as well, and the lateral with shifting lateralization. Myoclonic seizures
distinction of the two can be difficult without direct are not associated with loss of consciousness because of
observation. their very brief duration. They often occur in clusters,
Myoclonic atonic seizures (Figure 4-144) have and patients occasionally report some disruption of
a brief myoclonic component to an atonic seizure. consciousness with a cluster of closely spaced seizures.
These seizures are commonly part of the syndrome of
myoclonic astatic epilepsy, also referred to as Doose’s Subsets of myoclonic seizures include:
syndrome. In these seizures, a myoclonic jerk precedes • Juvenile myoclonic epilepsy.
the loss of tone. The seizures are very brief with rapid • Myoclonic-atonic seizure..
recovery. However, injuries are not uncommon with a • Myoclonic seizures with developmental delay.
fall from loss of tone.
Atonic seizures can be induced by stimuli and The EEG in Figure 4-145 is of a 16-month-old patient
activities, such as eating. This is a form of reflex with developmental delay. The seizures are character-
epilepsy. ized by neck flexion and arm extension. The EEG of
Fp1 - F3
F3 - C3
C3 - P3
P3 - 01
Fp2 - F4
F4 - C4
C4 - P4
P4 - O2
Fp1 - F7
F7 - T3
T3 - T5
T5 - 01
Fp2 - F8
F8 - T4
T4 - T6
T6 - 02
Figure 4-144: Myoclonic Atonic Seizure.

Figure 4-145: Myoclonic Seizure.
this patient shows high-voltage discharges; note the The arms may sometimes elevate slightly during the
calibration signal, which indicates 200 μV. jerking (Bureau and Tassinari, 2005a,b).
Figure 4-146 is another discharge from the same The EEG in myoclonic-absence shows a 3-per-
patient. This is a longer duration discharge, again second spike-wave pattern, which may have a spike-
associated with myoclonus. wave or polyspike-wave appearance. The discharge
Primary reading epilepsy is characterized by sei- and the symptoms are usually symmetric. Motor
zures occurring exclusively in association with read- activity is synchronous with the discharge.
ing, as differentiated from secondary reading epilepsy, Consciousness is variably impaired, and some
where patients may have spontaneous seizures of dif- patients can retain the ability to continue some simple
fering types. This is shown in the section on Simple normal activities.
Partial Seizures. The seizures often are myoclonic Myoclonic absences are seen as an isolated entity
movements of the jaw. and also in association with developmental delay
The classification of seizures in primary reading and ataxia. The seizures are difficult to control.
epilepsy is uncertain, but the seizures in reading epi- Valproate and/or ethosuximide are commonly used.
lepsy seem to respond to the same agents effective in Alternatives include lamotrigine, levetiracetam, and
generalized myoclonic seizures. topiramate.
Myoclonic-Absence Seizures Epileptic Spasms and Infantile Spasms
Myoclonic-absence seizures are rare and mainly occur Epileptic spasms have a characteristic appearance.
in childhood, with a mean onset of about 7 years of They have gone by a number of names including
age. Episodes are characterized by rhythmic myo- infantile spasms. Epileptic spasms is presently a pre-
clonic jerks, most prominently of the upper arms and ferred term but historically referred to similar epi-
shoulders. The head and/or legs can also be involved. sodes outside the infantile age group.
Clinical EEG 189
Figure 4-146: Myoclonic Seizure.
West syndrome is the combination of infantile The child has subtle infantile spasms with movements
spasms and mental retardation. The term is some- including neck flexion and elevation of the arms.
times used as a synonym for infantile spasms itself. EEG prior to onset showed high-voltage slow
activity, with multifocal spikes. At seizure onset,
there is generalized attenuation with high-frequency
Case: Infantile Spasms in a Patient with
(beta-range) activity. After several seconds, the EEG
Lissencephaly
returns to the prior pattern.
These recordings (Figures 4-147 through 4-148d)
are all from the same patient in the same recording
session. This is a 2-year-old with lissencephaly and Focal Epileptiform Activity and
uncontrolled seizures. The baseline-interictal record- Partial-Onset Seizures
ing shows disorganized, high-voltage activity with
multifocal sharp waves and spikes, many followed by Overview
brief generalized attenuation.
The first frame (Figure 4-148a) shows disorga- Focal epileptiform discharges are the interictal hall-
nized high-voltage background with multifocal sharp mark of partial epilepsy. They include spikes, sharp
waves. A brief spasm is shown near the middle of the waves, and combinations of the above with slow
recording, with high-voltage, high-frequency activity waves. By definition, spikes last less than 70 msec,
followed by suppression. The background returns to whereas sharp waves last 70 msec to 200 msec. When
near baseline by the end of this frame (Figure 4-148d). recorded from the scalp, discharges shorter than
20 msec are unlikely to be cerebral or epileptiform.
A number of features help distinguish between epi-
Case: Child with Perinatal Asphyxia leptiform and non-epileptiform sharp activity. All
Figure 4-149 shows the EEG of a 9-month-old with a these features may not be present at once, but the
history of perinatal asphyxia and developmental delay. more features there are, the more confident one can
Figure 4-147: Interictal Background from the same Patient as in the subsequent figures.
Figure 4-148a: Infantile Spasms #1.

Clinical EEG 191
Figure 4-148b: Infantile Spasms #2.
Figure 4-148c: Infantile Spasms #3.

Figure 4-148d: Infantile Spasms #4.
Figure 4-149: Child with Subtle Infantile Spasms.

Clinical EEG 193
be of the epileptiform nature of the discharges. These it is still possible that there is a single seizure focus.
features include: For example, it is also not unusual for epileptiform
discharges to be bitemporal independent, while sei-
• A high-voltage, a biphasic or polyphasic morphol- zures arise only in one temporal lobe. The interictal
ogy with a primarily negative polarity, epileptiform discharge focus on the side opposite the
• An asymmetric appearance, typically with a seizure focus is frequently referred to as mirror focus.
steeper first phase, and an after-going slow wave. Although the side of greater epileptiform activity
generally turns out to be the seizure focus, there are
exceptions to this rule. At times, interictal epilepti-
In addition, epileptiform discharges usually: form discharges are temporal when the ictal seizure
• Arise from an abnormal background, focus is extratemporal. One potential explanation
• Stand out from normal rhythmic activity occur- may be that sharp waves arising in the seizure focus
ring in their area, and are invisible on EEG due to dipole orientation.
• Have a consistent identifiable field that cannot be Spikes and sharp waves may correspond to a focal
explained by artifact. structural lesion that could be evident on routine
imaging, or visible only on pathological examination.
A spike or sharp wave seen only from a single elec- However, they may also be seen without underlying
trode should be interpreted with caution. It is highly structural abnormality. This is particularly true for epi-
unusual for an epileptiform discharge to be noted in leptiform discharges arising outside the seizure focus.
a single electrode in an adult individual. If the field Truly epileptiform discharges may be seen in the
involves a neighboring electrode even slightly, there absence of epilepsy. This is most likely in children,
would be greater confidence in calling the epilepti- and is particularly true for occipital and rolandic
form discharge. spikes, as well as for generalized epileptiform activity.
With this in mind, a single spike or sharp wave in In addition, there are a number of benign variants that
a recording should not be reported as indicative of have a sharp configuration, but have no clinical signif-
epilepsy. If the conformation is worrisome, comment icance. These include physiologic activity with sharp
should be made in the interpretation, and re-study configuration (such as K-complexes, positive occipi-
should be considered. tal sharp transients of sleep, Mu activity), and benign
Interictal epileptiform discharges are recorded in variants such as sporadic spikes of sleep (also called
approximately 50% of first EEGs. However, the yield small sharp spikes [SSS] or benign epileptiform tran-
increases to approximately 90% with repeated or pro- sients of sleep [BETS]), 14- and 6-Hz positive spikes,
longed recordings in patients with well-documented and wicket spikes.
epilepsy. The likelihood of recording discharges The appearance of ictal discharges is dependent
varies with the epileptic syndrome and the seizure predominantly on the seizure type and on the seizure
type. In partial epilepsy, the location and orientation localization. Seizures of focal onset may be remain
of the cortex generating discharges is important in focal or may become widespread or secondarily gen-
determining whether discharges appear on record- eralized. At times, the initial focal onset is invisible,
ings. For example, discharges generated by medial because its localization makes it invisible to scalp elec-
frontal cortex may be invisible on EEG because the trodes and because secondary generalization occurs
dipole orientation is parallel to the surface. Other very quickly.
discharges partially generated in fissures may have Simple partial seizures can arise in any lobe.
such a dipole orientation that both negative and pos- However, due to the limited field of cortical involve-
itive ends of the dipole are seen. This is referred to ment in this seizure type, simple partial seizures
as a horizontal dipole. It is very common in benign are not associated with EEG changes in 60–80% of
rolandic epilepsy. instances. When EEG changes are seen, they may be
Interictal epileptiform discharges generally corre- focal rhythmic activity with a narrow field or peri-
spond well to the ictal seizure focus, particularly when odic sharp activity. Complex partial seizures are most
they have a single consistent field. When the interic- likely to arise in the temporal and frontal lobes, but
tal epileptiform discharges are bilateral or multifocal, may also arise in the parietal and occipital lobe.
Presented here are examples of seizures of differ- origin is most likely in the post-central primary sen-
ent focal origins. sory cortex. Less common symptoms include vertigo
and inability of localizing a limb in space. The seizure
Temporal Lobe Focus may be sensory, may progress to involve focal motor
Temporal lobe focus is the most common source of activity or tonic posturing, or may become complex
focal seizures. Patients with seizures of temporal lobe partial with immobile staring or automatisms. Parietal
origin often have auras that may be isolated (simple lobe seizures frequently spread to the temporal lobe
partial seizures) or may progress to complex partial or to the frontal lobe to produce manifestation typical
seizure. Just as isolated simple partial seizures often of these lobes.
have no EEG correlate, it is common for the first EEG
change to be seen late in the aura or in transition to Occipital Lobe Focus
the complex partial phase. Occipital foci usually produce a visual aura, which
Patients with a temporal lobe focus may have sim- may be an elementary visual sensation or com-
ple partial or complex partial seizures. These seizure plex hallucinations. Visual illusions may also be
types may coexist in the same patient. noted. Seizure progression will depend on seizure
spread. Ictal blindness may occur. Occipital lobe
Frontal Lobe Focus
seizures may spread to the temporal lobe or to the
Auras of frontal lobe origin are most commonly a
frontal lobe to produce manifestations typical of
non-specific cephalic sensation. Seizures may have a
these lobes.
variety of clinical features, depending on the site of
origin in the frontal lobe. Primary motor cortex focus
Case: Temporal Lobe Focus with Simple Partial and
results in simple partial seizures with focal clonic or
Complex Partial Seizures
tonic motor activity. Supplementary motor cortex
This patient is a 24-year-old female with intrac-
activity also produces simple partial seizures associ-
table simple partial and complex partial seizures.
ated with posturing. Cingulate and orbitofrontal foci
In childhood, she had been diagnosed as having
produce complex partial seizures.
meningitis and encephalitis on separate occa-
Parietal Lobe Focus sions. She became seizure-free after right tem-
The most common aura with a parietal lobe focus poral lobectomy, and is off AEDs. The EEG
is a sensory aura. If there is a march to the aura, the (Figure 4-150) shows right temporal lobe focus,
O1-P7
P7-T7
T7-F7
F7-SP1
SP1-SP2
SP2-F8
F8-T8
T8-P8
P8-O2
FP1-F3
F3-C3
C3-P3
FP2-F4
F4-C4
C4-P4
Figure 4-150: Complex Partial Seizure (CPS) and Simple Partial Seizure (SPS) with Right Temporal Focus.
Clinical EEG 195
01 - T5
T5 - T3
T3 - F7
F7 - Sp1
Sp1 - Sp2
Sp2 - F8
F8 - T4
T4 - T6
T6 - O2
Fp1 - F3
F3 - C3
C3 - P3
Fp2 - F4
F4 - C4
C4 - P4
Sp1 - Pz
Sp2 - Pz
Figure 4-151: Simple Partial Seizure.
which is seen best with special electrodes includ- Simple Partial Seizures
ing sphenoidal electrodes and additional temporal
scalp electrodes. Overview
The subsequent EEG (Figure 4-151) shows a Simple partial seizure is characterized by focal sharp
simple partial seizure. Note the restricted field of activity that is usually most prominent in the cen-
the discharge. The next EEG (Figure 4-152) shows tral region. Interictal abnormalities are common
a complex partial seizure in the same patient. and usually are sharp, although focal slowing can
Note the wider field of spread. MRI (Figure 4-153) occur, especially in patients with focal structural
shows prominent right hippocampal sclerosis lesions. Ictal discharge consists of repetitive spiking
with atrophy and increased signal intensity on this from the focus, although focal slowing can also be
T2-weighted image. seen. The sharp component of the discharge may be
O1 - T5
T5 - T3
T3 - F7
F7 - Sp1
Sp1 - Sp2
Sp2 - F8
F8 - T4
T4 - T6
T6 - O2
Fp1 - F3
F3 -C3
C3 - P3
Fp2 - F4
F4 - C4
C4 - P4
Sp1 - Pz
Sp2 - Pz
Figure 4-152: Complex Partial Seizure.

Figure 4-153: MRI from the Same Patient.
subtle or missing if the epileptiform activity is gen- Subjective Simple Partial Seizure
erated in a portion of the cortex deep to the scalp. Not all seizures are characterized by visible seizure
Partial seizures can spread throughout the activity.
hemispheres resulting in a generalized seizure.
Secondary-generalized seizures may have a focal Simple Partial Seizure in a 24-Year-Old with
onset that can be detected clinically, but this is not Hippocampal Sclerosis
always the case. The generalization may occur so In this example, the patient reports subjective symp-
quickly that the focal onset can only be determined toms. This is a 24-year-old female with seizures since
by EEG, and not by clinical appearance. age 7 years. This is the same patient described above
Clinical Appearance for complex partial seizures. The seizures begin with
Simple Partial Adversive Seizure an epigastric sensation of butterflies in the stomach.
An 18-year-old male with right occipito-parietal She has isolated subjective seizures. In addition, she
angiomatosis has simple partial adversive seizures. has complex partial seizures with staring, oroalimen-
He had previously had seizure surgery in this region tary automatisms, and right arm dystonic posturing.
12 years ago. He recently had recurrence of seizures. Figure 4-157 shows the interictal activity seen in this
EEG (Figure 4-154) shows prominent muscle patient. The EEG epoch in Figure 4-158 shows the
artifact in the left hemisphere and right frontal deriva- seizure onset. The MRI (Figure 4-159) shows another
tions. There is also rhythmic activity in the right fron- view of the right hippocampal sclerosis.
tocentral region. This first Figure is LB montage, but
the localization is easiest to see on the average deriva- Simple Partial Seizure with Clearly-Defined
tion shown after this. Focus at C3
Figure 4-155 is the Ave montage with the same This is a 6-year-old left-handed male with tuberous
EEG epoch. Localization is easier on this montage. sclerosis and seizures since 2 months of age. Seizures
Note that the artifact is more left-sided (frontotem- include flexion of the right arm with extension of the
poral), whereas the ictal discharge is predominantly fingers and sometimes fisting beside the ear.
right-sided. Figure 4-156 is the LB montage again, The EEG (Figure 4-160) shows a clearly defined
with a 20-second window rather than a 15 second win- focus maximal at C3. This would be a rolandic local-
dow, and is at a lower sensitivity. ization, although not benign rolandic epilepsy.
Clinical EEG 197
Figure 4-154: Simple Partial Adversive Seizure—LB Montage.
Figure 4-155: Simple Partial Adversive Seizure—Ave Montage.

Figure 4-156: LB Montage with a 20-Second Time Window.
Secondary Reading Epilepsy Three years following surgery, she noted that her
This is a 27-year-old female with a prior history of mouth jumped while she was reading, both aloud and
complex partial seizures of left temporal origin, which silently.
became controlled with left temporal lobectomy. EEG (Figures 4-161 and 4-162) shows subtle find-
Subsequently, she developed recurrence of rare com- ings of a discharge at about C3 in association with the
plex partial seizures that were controlled with AED. facial jerks.
01-P7
P7-T7
T7-F7
F7-Sp1
Sp1-Sp2
Sp2-F8
F8-T8
T8-P8
P8-02
Fp1-F3
F3-C3
C3-P3
Fp2-F4
F4-C4
C4-P4
Figure 4-157: Simple Partial Seizure with Subjective Symptoms.

Clinical EEG 199
01 - T5
T5 - T3
T3 - F7
F7 - Sp1
Sp1 - Sp2
Sp2 - F8
F8 - T4
T4 - T6
T6 - O2
Fp1 - F3
F3 - C3
C3 - P3
Fp2 - F4
F4 - C4
C4 - P4
Sp1 - Pz
Sp2 - Pz
Figure 4-158: Simple Partial Seizure with Subjective Symptoms, Seizure Onset.
These can exhibit secondary generalization with

tonic-clonic seizures.
Supplementary Motor Seizure
Supplementary motor seizures are a form of simple

partial seizure with the origin in the mesial frontal
lobe. Supplementary motor seizures may be unilat-
eral or bilateral. Interictal and ictal abnormalities
are seen near the midline in some patients, although
intracranial electrodes may be necessary to see the
discharge.
A 23-year-old female has had intractable partial
seizures since her teens. She was clinically thought
Figure 4-159: Simple Partial Seizure—MRI. to have non-epileptic seizures. She was found to
Right hippocampal sclerosis. have a left supplementary motor area (SMA) focus
with grid electrodes. Scalp EEG shows bilateral
parasagittal sharp waves at seizure onset, followed
Simple Partial Seizure with Midline Discharges by attenuation and muscle artifact (Figures 4-164a
Simple partial seizures can be produced by foci in through 4-164c). Two seconds before seizure termi-
various regions. Vertex spike activity is occasionally nation, a left parasagittal rhythmic theta discharge
seen. Figure 4-163 shows the interictal activity seen in is seen.
this patient.
Parietal Focus
Frontal Focus
Focal seizures in the parietal region are much less
Partial seizures with a frontal lobe focus can pro- common than frontal or temporal seizures. The exam-
duce a range of clinical manifestations. Among the ple in Figures 4-165a and 4-165b is from a patient with
most common are simple partial clonic movements. a mesial centro-parietal seizure focus.
Figure 4-160: Simple Partial Seizure.
discharges are independent, although findings from

Fp1-F3
both sides are usually seen during a routine recording.
F3-C3
Sleep augments the discharges. Earlier in this chapter
C3-P3 the clinical features were discussed in more detail and
P3-O1 in that section the title was benign epilepsy with cen-
trotemporal spikes (BECTS). Here is another clinical
example.
The sample EEG (Figure 4-167) shows a revers-
ing focus between the C4 and P4 electrodes on this
transverse bipolar montage. Relatives of patients with
Figure 4-161: Simple Partial Seizure—Reading Epilepsy. rolandic epilepsy may manifest the discharges with-
out clinical seizures.
Occipital Focus Complex Partial Seizures
This series of Figures (4-166a through 4-166k) is from Overview

a single patient with occipital discharge progression Complex partial seizures are associated with focal dis-
to secondarily generalized tonic-clonic seizure. charges that are usually in the temporal lobe but may
be in the frontal or other regions. The temporal lobe
Rolandic Epilepsy or BECTS focus is not always visible on routine surface EEG,
and may be missed without special electrodes or tech-
Rolandic epilepsy is a disorder of childhood, char- niques. Sphenoidal, nasopharyngeal, and depth elec-
acterized by discharges from the central regions, trodes can be used to identify the discharge. Interictal
especially the regions of C3 and C4. The interictal activity shows focal slowing or sharp activity in the
Clinical EEG 201
935 960
Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
C4-P4
P4-O2
Fp1-F7
F7-T7
T7-P7
P7-O1
Fp2-F8
F8-T8
T8-P8
P8-O2
Fz-Cz
Cz-Pz
Figure 4-162: Simple Partial Seizure—Reading Epilepsy.
Figure 4-163: Simple Partial Seizure with Midline Discharges.

a Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
C4-P4
P4-O2
Fp1-F7
F7-T3
T3-T5
T5-O1
Fp2-F8
F8-T4
T4-T6
T6-O2
Figure 4-164a: Supplementary Motor Seizure.
temporal region (or elsewhere). The interictal activity complex partial seizures. The Figures that follow show
is not associated with behavioral change, by definition. the results of focal seizures of varying localization.
Ictal discharge may be repetitive spike activity with
disturbance of the EEG background. Alternatively, Sphenoidal Electrodes
the spike component may not been seen in scalp elec- Sphenoidal electrodes are used for assessment of the
trodes, so there may be either no abnormal recording mesial temporal region. In Figure 4-168, the discharge
or repetitive slowing, associated with the seizure. is seen well on sphenoidal derivation; however, it is
virtually invisible with routine scalp electrodes.
Use of Special Electrodes for Complex Partial
Seizures Foramen Ovale Electrodes
Special electrodes are occasionally needed in order The example in Figure 4-169 is of a patient with
to precisely localize spike discharges in patients with complex partial seizures who has independent left
b Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
C4-P4
P4-O2
Fp1-F7
F7-T3
T3-T5
T5-O1
Fp2-F8
F8-T4
T4-T6
T6-O2
Figure 4-164b: Supplementary Motor Seizure.

Clinical EEG 203
c and right temporal sharp waves. The last lines of the

Fp1-Av EEG are made using electrodes in the proximity of
Fp2-Av foramen ovale.
F3-Av Localization of the discharge is important for
F4-Av identification of a site for surgical treatment. The
C3-Av recording shown in Figure 4-170 is of the beginning
C4-Av of a seizure, and shows activity in the foramen ovale
P3-Av leads several seconds prior to the discharges appear-
P4-Av ing on the cortex.
O1-Av
O2-Av Complex Partial Seizures with Left Temporal Focus
F7-Av Overview
F8-Av Left temporal lobe focus is commonly identified in
T3-Av video-EEG monitoring. This is usually the dominant
T4-Av hemisphere, so language difficulty is common. The
T5-Av language changes may be speech arrest or ictal jargon.
T6-Av The first example shows a patient with postictal apha-
Fz-Av sia. Later, there is ictal jargon.
Cz-Av
Pz-Av Case: Left Lateral Temporal Focus
This is a 43-year-old with intractable seizures since age
Figure 4-164c: Supplementary Motor Seizure.
3, starting with ringing in the ears, then trouble hear-
ing, and right-hand numbness.
Figure 4-165a: Mesial Centro-Parietal Seizure.

Figure 4-165b: Mesial Centro-Parietal Seizure—Zoomed Excerpt.
Figure 4-166a: Occipital Focus with Secondary Generalization.

Clinical EEG 205
Figure 4-166b: Occipital Focus with Secondary Generalization—Continuation.
Figure 4-166c: Occipital Focus with Secondary Generalization—Continuation.

Figure 4-166d: Occipital Focus with Secondary Generalization—Continuation.
Figure 4-166e: Occipital Focus with Secondary Generalization—Continuation.

Clinical EEG 207
Figure 4-166f: Occipital Focus with secondary Generalization—Continuation.
Figure 4-166g: Occipital Focus with Secondary Generalization—Continuation.

Figure 4-166h: Occipital Focus with Secondary Generalization—Continuation.
Figure 4-166i: Occipital Focus with Secondary Generalization—Continuation.

j
Figure 4-166j: Occipital Focus with Secondary Generalization—Continuation.
Figure 4-166k: Occipital Focus with Secondary Generalization—Continuation.

Figure 4-167: Rolandic Epilepsy.

Rolandic discharge, with reversal most prominent between the C4 and P4 electrodes. This location is in the right centro-
parietal region.
O1-P7
P7-T7
T7-F7
F7-SP1
SP1-SP2
SP2-F8
F8-T8
T8-P8
P8-O2
FP1-F3
F3-C3
C3-P3
FP2-F4
F4-C4
C4-P4
Figure 4-168: Complex Partial Seizures with Focus seen well on Sphenoidal Electrodes.
Clinical EEG 211
Figure 4-169: Complex Partial Seizures, Use of Foramen Ovale Electrodes.
Figure 4-170: Foreman Ovale Electrodes—Seizure Onset.

The EEG (Figure 4-171) shows a focus in the left repetitive activity and obscuration of the background
lateral temporal lobe. The same discharge evolves into (Figure 4-177b). The seizure continues with increased
sustained seizure activity (Figure 4-172). frequency of the repetitive activity (Figure 4-177c).
The seizure continues with slowing of the dis-
Complex Partial with Secondary Generalization charge with continued disorganization of the back-
This is a 26 year-old female with intractable seizures ground (4-177d). The termination of the seizure
since age 17 (Figures 7-173 through 4-175). The sei- and postictal period are characterized by slow-down
zures start with inability to understand language. The of the epileptiform activity and postictal slowing
CPS include early head turning to the left. There is (Figure 4-177e).
late head turning to the right with secondary general-
ization. She was found to have a left temporal cavern- Complex partial seizures with right temporal
ous angioma, as shown on the MRI slice. lobe focus.
The MRI (Figure 4-176) from this patient shows a Well-formed ictal language and partially preserved
cavernous angioma in the left temporal region, which responsiveness in the presence of oroalimentary
correlates well with the localization of the EEG. automatisms suggest non-dominant temporal lobe
origin. In this example, the patient appears to have
CPS with Postictal Aphasia preserved responsiveness, but has no memory of
This patient with complex partial seizures has a focus the event.
in the left temporal area. She loses awareness during This patient has a right temporal lobe focus and
the seizure and has decreased responsiveness. After the shows preserved responsiveness during the seizure
event, there is postictal aphasia (Figure 4-177a). The (Figure 4-178a). Figure 4-178b shows a continuation
seizure develops with increased frequency of the of the seizure activity.
Figure 4-171: Interictal EEG - Left Lateral Temporal Focus.

Clinical EEG 213
Figure 4-172: Seizure Onset - Left Lateral Temporal Focus.
Figure 4-173: EEG of Complex Partial Seizures (CPS) with Left Temporal Focus.

This EEG epoch shows rapid generalization of the focal discharge.
Figure 4-174: CPS with Secondary Generalization.

The left temporal sharp wave as a focus for the seizure is clearly seen on this recording, in the F7 and T7 electrodes.
Figure 4-175: CPS with Left Temporal Sharp waves.

Clinical EEG 215
Complex Partial Seizures with a Frontal Focus

Overview
Complex partial seizures (CPS) due to frontal lobe foci
are less common than temporal lobe foci. Clinical dif-
ferentiation from seizures of temporal origin is imper-
fect, but some general guidelines were discussed above.
CPS with Left Frontal Focus
This is a 38-year-old male who presented with seizures
since 5 years of age. The onset of the seizure appears
gradual, with clear global aphasia, while there is pres-
ervation of some responsiveness. Although unable to
speak, he retains the ability to smile.
The EEG shows interictal discharges which are most
prominent at F7, which could be interior frontal or ante-
rior temporal (Figure 4-179a). The MRI (Figure 4-179c)
gives the anatomic localization to the frontal region. The
discharge becomes more rapid and spreads with devel-
opment of the seizure (Figure 4-179b).
The MRI of this patient is shown in Figure 4-179c.
Figure 4-176: MRI Brain Showing Left Temporal On the basis of EEG appearance, differentiation
Cavernous Malformation.
between posterior frontal and anterior temporal was
not possible, but the lesion is in the frontal lobe.
Figure 4-177a: CPS with Postictal Aphasia.

Figure 4-177b: CPS with Postictal Aphasia.
Figure 4-177c: CPS with Postictal Aphasia.

Clinical EEG 217
Figure 4-177d: CPS with Postictal Aphasia.
Figure 4-177e: CPS with Postictal Aphasia.

Figure 4-178a: CPS with Preserved Responsiveness.
Figure 4-178b: CPS with Preserved Responsiveness—Continuation.

Clinical EEG 219
Figure 4-179a: CPS with Left Frontal Focus—Interictal.
Figure 4-179b: CPS with Left Frontal Focus.

c laughter is inappropriate. It can be seen in association

with partial, myoclonic, tonic, tonic-clonic, and even
absence seizures.
Differentiation from normal laughter is associated
ictal activity, prolonged duration, and absence of pro-
voking comedic stimulus.
Figues 4-180a and 4-180b show interictal discharges
in a patient with gelastic seizures. Figure 4-180c shows
ictal discharge in the same patient.
Partial-Onset Seizure with Secondary Generalized

Tonic-Clonic Seizure
This is the same patient as is shown in CPS with left

temporal focus with postictal aphasia (here). In this
seizure, the complex partial seizure becomes second-
arily generalized (Figures 4-181a through 4-181j).
Figure 4-179c: CPS with Frontal Foci—MRI.
ABNORMAL PEDIATRIC EEG
Gelastic Seizures
This section concentrates on findings that are spe-
Gelastic seizures are characterized by episodes of cific for children. Many of the abnormalities already
laughter, which can be very similar to spontane- described affect children as well as adults, but detailed
ous laughter. However, the timing and onset of the description will not be presented here.
Figure 4-180a: Gelastic Seizure, Interictal Discharge.

Clinical EEG 221
Figure 4-180b: Gelastic Seizure, Interictal Discharge.
Figure 4-180c: Gelastic Seizure, Ictal Discharge.

Figure 4-181a: CPS with Secondary Generalization.
Figure 4-181b: CPS with Secondary Generalization—Continuation.

Clinical EEG 223
Figure 4-181c: CPS with Secondary Generalization—Continuation.
Figure 4-181d: CPS with Secondary Generalization—Continuation.

Figure 4-181e: CPS with Secondary Generalization—Continuation.
Figure 4-181f: CPS with Secondary Generalization—Continuation.

Clinical EEG 225
Figure 4-181g: CPS with Secondary Generalization—Continuation.
Figure 4-181h: CPS with Secondary Generalization—Continuation.

Figure 4-181i: CPS with Secondary Generalization—Continuation.
Figure 4-181j: CPS with Secondary Generalization—Continuation.

Clinical EEG 227
Neonatal EEG Abnormalities For example, a discontinuous pattern with an inter-

burst interval of more than 1 minute would be normal
Neonatal EEG abnormalities usually fall into one of the at 26 weeks conceptional age but would be distinctly
following groups: abnormal at 34 weeks. A dysmature pattern is inter-
• Abnormality of maturation; preted as encephalopathy, but no specific etiology can
• Epileptiform activity; be inferred from these data.
• Background abnormality. Persistent dysmaturity is associated with poor
neurologic outcome, but transient dysmaturity can be
These are described in Table 4-20 and will be described associated with no neurologic sequelae.
subsequently in more detail.
Epileptiform Activity
Abnormality of Maturation Epileptiform abnormalities in neonates can have

markedly difference appearance from epileptiform
Dysmature pattern is typically an EEG appearance abnormalities in older children and adults. The abnor-
that is younger than expected for conceptional age. malities are usually focal or multifocal but seldom
Table 4-20 Neonatal EEG Abnormalities

Type Pattern Description
Abnormality Dysmature EEG background appears younger than conceptional
of maturation age. Suggests encephalopathy
Epileptiform Focal discharges Consistent localization of sharp waves, as opposed to
abnormality normal sharp transients. Often occur in trains.
Multifocal discharges Multifocal sharp waves or spikes with an abnormal
background, as opposed to normal multifocal transients.
Rhythmic activity Rhythmic activity in the alpha or theta range is typi-
cally abnormal and can be epileptiform even in the
absence of a sharp component.
Pseudo-beta-alpha-theta-delta Ictal discharge beginning in the beta range and slow-
ing to the delta range.
Background Excessive slow activity Excessive slow activity can be difficult to diagnose
abnormality with already prominent delta. Pathologic delta is
more widespread and lacks reactivity.
Low voltage background Low voltage suggests global cortical dysfunction.
At the extreme of this, the isoelectric EEG can be a
confirmatory test for brain death.
Burst suppression pattern Burst suppression can be difficulty to differentiate
from discontinuous pattern, but when seen indicates
serious cerebral functional disturbance.
Asymmetric background Asymmetry in background suggests a functional or
structural lesion usually affecting the side with the
lower and less rich activity. Amplitude asymmetries
are usually only significant for a difference of 50% or
more. Intracranial and extracranial fluid collections
are a common cause.
generalized since pathways facilitating generalization the frequency slows to 0.5–3/sec. The appearance can
are not fully developed. be smooth or sharp. Associated seizures are clonic,
Focal discharges are usually central, right or left. myoclonic, or subtle, and as such this is an ictal pat-
Differentiation from normal sharp transients is usu- tern. The most common cause is perinatal asphyxia,
ally by a consistent localization of pathologic sharp often with a poor prognosis. The decrease in frequency
waves and occurrence of abnormal sharp activity in can have the appearance of dropping to a harmonic of
trains; normal sharp transients do not occur in trains. an original frequency.
Trains of discharges can have an unimpressive sharp Seizures in neonates, as in older patients, occa-
component so that they appear like a run of fast activ- sionally are associated with no EEG abnormality on
ity in the alpha or theta range, but rhythmic activity scalp recording. In these circumstances, the genera-
in neonates is not normal, helping with differentiation tor is likely subcortical or at least not involving cortex
from normal activity. Differentiation of rhythmic fast close to the scalp where the electrodes are. Seizures of
activity from a normal delta brush is by absence of subcortical origin in neonates usually indicate severe
the underlying delta wave and longer duration of the damage with the failure of cortical projection being a
rhythmic train with seizure activity (Figure 4-182). manifestation of this damage.
Focal discharges often correlate with focal sei-
zures, but the correlation between discharge loca- Background Abnormality
tion and clinical motor manifestation is not as good
as in older children and adults. Also, focal discharges State changes might not be seen during the 20 minutes
in neonates do not have as strong a correlation with of a routine EEG, but in long-duration recordings, if
focal structural lesion as in older individuals. Most there are not changes in state, then this is abnormal.
epileptiform discharges are surface-negative, as in Excessive slow activity is difficult to identify in
older individuals. Surface-positive discharges are seen neonates since delta is such a prominent part of the
in some infants with intracerebral hemorrhage, but record. Abnormal delta tends to be unilateral or dif-
this correlation is far from highly sensitive or specific. fuse whereas normal delta is symmetrically regional
Multifocal discharges are differentiated from (e.g., anterior). Abnormal delta tends to not respond
normal multifocal sharp transients by an otherwise to stimulation with attenuation, but this lack of reac-
abnormal background, occurrence of the discharges tivity is normal in very young prematures.
in trains, and associated clinical seizures. The seizures Amplitude asymmetries are abnormal if at least
may be subtle but are usually clonic. 50% and consistent. Usually there are differences in
Pseudo-beta-alpha-theta-delta is descriptive pattern frequency composition associated with amplitude
of a discharge that starts at high frequency and slows. asymmetry as well. Note that both intracranial and
Beginning frequency is usually at least 8–12/sec and extracranial pathology can result in amplitude asym-
metry; for example, subdural hematoma and scalp
hematoma can both produce attenuation of EEG over
the affected area.
Fp1-C3
A low-voltage EEG is usually abnormal in
non-REM sleep and usually indicates a global abnor-
C3-O1 mality in cortical function. Note that REM sleep
might be associated with a low-voltage background,
so recording of non-REM sleep is important. Also,
Fp2-C4
bilateral subdural hematomas can produce symmetric
attenuation, and therefore may be missed on EEG.
C4-O2 Isoelectric EEG can be a confirmatory test for
brain death in neonates, but there are special consid-
erations concerning diagnosis of brain death in neo-
nates, as discussed above.
Figure 4-182: Rhythmic Discharge in a Neonate. Burst-suppression can be difficult to differentiate
from a normal discontinuous pattern. Implication is
Clinical EEG 229
usually a global cerebral process such as anoxia. Burst these on EEG bases alone difficult if not impossible in
suppression is differentiated from a normal discontin- some circumstances (Dan and Boyd, 2006).
uous pattern, usually by knowledge of conceptional
age with an expectation of the degree of discontinu- Epileptic Encephalopathies
ity, reactivity of the background if the patient is old
enough, and clinical information. Young children may develop progressive encepha-
We frequently observe a disconnect in appear- lopathies associated with epileptic and/or myoclonic
ance of the EEG and clinical appearance of prema- seizures. These have been classified by ILAE as epi-
ture infants. Pre-term infants can manifest markedly leptic encephalopathies (Khan and Al Baradie, 2012).
abnormal neurologic exam with little or no abnormal- In general, they tend to be refractory to many AEDs.
ity in EEG and vice versa. Suffice it to say that the EEG Some of the most important types are discussed in
and the examination are evaluated independently and Table 4-21.
then interpreted in concert.
Pediatric EEG Abnormalities INDETERMINATE EEG PATTERNS
Many of the abnormalities seen in the pediatric Overview

population are discussed in the broad presentation
of epileptiform and non-epileptiform abnormali- Some seizures cannot be clearly characterized as par-
ties. Some findings are shared between children and tial or generalized in onset.
adults (e.g., focal and generalized spikes or slowing).
But some are specific to a pediatric population (e.g., Generalized Clonic versus Frontal
hypsarrhythmia). Lobe Origin Seizure
Abnormalities Dependent on Maturation This patient shows clonic activity typical of frontal
lobe focal seizure activity. Figure 4-183 shows the
Maturation of the EEG requires that the EEG reader’s EEG. In this case, it is difficult to determine whether
expectation of background change commensurate this is generalized or focal in onset since the initial dis-
with the age of the patient. Posterior slow waves of charge seems bilateral.
youth are normal in a child through early adult life,
but similar waves in middle or advanced age are likely Frontal Absence
physiologically different and pathologic. A discon-
tinuous pattern is still seen in a normal term infant, to Absence seizures have occasionally been demon-
a certain extent, but would be distinctly abnormal at strated to originate in the frontal lobe, as determined
6 months of age. by depth EEG or other methods while the EEG was
Certain EEG rhythms can look remarkably simi- indistinguishable from generalized-onset absence sei-
lar yet be of totally different implication depending zures (Figure 4-184a).
on age. Sleep spindles in young children can be pro- The example is from a 8-year-old female with a
longed yet are normal when they first appear. Almost history of prematurity with congenital left hemipare-
identical patterns in pre-term infants are not sleep sis, as well as seizures. The seizures are characterized
spindles and can represent an ictal pattern. by altered responsiveness, decreased tone, and head
A markedly discontinuous pattern is normal nodding and blinking for a few seconds. The EEG
in a very premature infant but in an older child was usually consistent with generalized absence sei-
or adult an almost identical appearance can be a zures; however, MRI (Figure 4-184b) showed a dys-
burst-suppression pattern, indicative of severe cere- plastic right hemisphere. Ictal PET (Figure 4-184c)
bral dysfunction. Similarly, this burst suppression pat- revealed right frontal hypermetabolism, suggesting
tern can be due to cerebral destructive process or to that the seizure originated in the abnormal right
medication-induced coma, with distinction between frontal lobe.
Table 4-21 Epileptic Encephalopathies

Disorder Clinical EEG
Early infantile epileptic Early seizures, even in utero. Tonic Burst suppression in waking and
encephalopathy (EIEE) spasms especially but also tonic-clonic, sleep states, often asymmetric.
or Ohtahara syndrome clonic, myoclonic, atonic, absence,
complex partial. May progress to West
or Lennox-Gastaut syndrome.
Early myoclonic Myoclonus that can be subtle or Burst suppression, often
encephalopathy pronounced, often shifting in location. asymmetric. Eventually
Onset in first months. May have subtle hypsarrhythmia.
partial seizures, tonic seizures. Epileptic
spasms may develop. Developmental
delay.
Infantile spasms and West West syndrome is triad of infantile Hypsarrhythmia
syndrome spasms, developmental delay, and
hypsarrhythmia.
Severe myoclonic epi- Initially clonic seizures with fever in the Normal early, later polyspike
lepsy of infancy (SMEI or first year. Often focal but may be gen- and spike-wave discharges, focal
Dravet syndrome) eralized. Later afebrile, with myoclonic or generalized. Some show a
seizures and photosensitivity. Often photoparoxysmal response.
developmental slowing with worsening
seizures.
Childhood epileptic Multiple seizure types with develop- Slow spike-and-wave discharges
encephalopathy mental regression. May have especially at 1.5–2 Hz. Slow background in
(Lennox-Gastaut syn- tonic, atonic, and/or absence seizures. most, becoming more disorga-
drome or LGS) May also have myoclonic, generalized nized in sleep.
tonic-clonic, or partial-onset seizures.
Acquired epileptic Progressive regression of language func- Spike-and-wave discharges
aphasia (AEA, Landau- tion in previously normal children, usu- of high amplitude, especially
Kleffner syndrome) ally both receptive and expressive but temporal bilaterally, but also may
one may predominate. Seizures in most, be multifocal or generalized,
especially complex partial with atypical especially in non-REM sleep.
absence appearance or generalized.
ADVANCED TECHNIQUES or supplemental electrodes to provide better

localization.
Electrocorticography (ECoG) When ECoG is used during resection, a record-
ing is usually made before and after the resection. If
Electrocorticography (ECoG) is performed at the patient already had subdural strip electrodes, then
the time of surgery for electrode placement or these provide the pre-op recording, and the ECoG
resection. When used at the time of electrode electrodes are placed for post-op recording, usually at
placement, ECoG is an aid to determine proper the margins of the resection. Frequent discharges near
location of the electrodes. For example, if ECoG the margins are often an indication for further surgery.
shows that discharges are near the margin of a grid, Discharges that are infrequent or distant from the
then the coverage area may be revised by moved margin do not necessarily warrant additional surgery.
Clinical EEG 231
Figure 4-183: Generalized Clonic Versus Frontal Lobe Seizure.
Critical Care Monitoring Data have indicated some prognostic factors that have
been relied on for years. However, with the advent
Continuous critical care monitoring is increasingly and widespread use of therapeutic hypothermia, the
used for a variety of indications. The most com- specificity of some of these indicators has been ques-
mon are post-CPR encephalopathy and seizure tioned. EEG is part of the neurological evaluation,
monitoring. which certainly includes detailed examination and
Post-CPR encephalopathy: Encephalopathy after sometimes additional labs, such as neuron specific
CPR is a common reason for neurologic consultation. enolase. While routine EEG can be helpful, bedside
a Fp1 - F3
F3 - C3
C3 - P3
P3 - O1
Fp2 - F4
F4 - C4
C4 - P4
P4 - O2
Figure 4-184a: Frontal Absence—EEG.

b EEG monitoring is often used to allow for continu-

ous evaluation of brain activity as sedatives are with-
drawn, as well as for the identification of seizures or
periodic discharges.
Seizure monitoring: Patients admitted with sta-
tus epilepticus often benefit from EEG monitoring,
which can be done in two ways. One is continuous
recording using a portable EEG machine. The other
is bedside monitoring, usually limited to 2 channels.
Both of these can be helpful. We find the video com-
ponent of the portable device particularly helpful for
atypical events.
Hospital encephalopathy: An increasing propor-
tion of patients with marked encephalopathy associ-
ated with hospitalization, especially sepsis-associated
encephalopathy, are found to have seizures (Iacobone
et al., 2009; Kaplan and Rossetti, 2011). The diagnosis
Figure 4-184b: Frontal Absence—MRI
Figure 4-184c: Frontal Absence—PET.

Clinical EEG 233
Table 4-22 Clinical Correlates to EEG Findings with Critical Illness

Finding Clinical correlate
Generalized slowing Almost any encephalopathy, including renal, hepatic, toxic, sepsis, hypoxic,
endocrine.
Triphasic waves Hepatic, renal, some toxicities including lithium and baclofen.
Periodic discharges Symmetric—hypoxic, seizures.
Asymmetric or unilateral—HSV encephalitis, other focal destructive lesion
such as stroke.
Beta activity Patients with coma with prominent beta are most often due to intoxication,
especially benzodiazepines, but this has also been seen with other condi-
tions, especially hypoxic encephalopathy.
Normal background Psychogenic unresponsiveness is the most common cause of coma with
normal EEG. Locked-in syndrome should be considered and repeat neuro
exam performed for this possibility.
of these non-convulsive seizures in this population called. The dependence of non-EEG lab staff for
is facilitated by longer recordings, and bedside EEG critical care monitoring, especially outside academic
monitoring can be particularly helpful for this. We medical centers, creates the need for training for
believe that non-convulsive seizures in the hospital these individuals.
are significantly under-diagnosed. EEG findings in some of the common disor-
Role of non-EEG staff in critical care monitor- ders seen with critical monitoring are discussed in
ing: Continuous critical care EEG monitoring usu- Tables 4-22 and 4-23.
ally depends on critical care nursing to maintain the
electrodes during ICU care and even to perform a Intra-operative Monitoring
provisional interpretation of the recordings. If there
are abnormalities that deserve further review, than Intra-operative monitoring is not a focus of this
a physician trained in EEG interpretation must be text but is used by our institutions especially
Table 4-23 EEG Findings with Specific Critical Illnesses

Disorder EEG finding
Sepsis-associated Slowing, sometimes seizures.
encephalopathy
Hepatic encephalopathy Generalized slowing. Triphasic waves.
Renal encephalopathy Generalized slowing. Sometimes triphasic waves and seizure activity.
Herpes encephalitis Slowing most prominent over the temporal region. Periodic lateralized
epileptiform discharges are typical but not always seen; repeat study may be
needed.
Hypoxic encephalopathy Generalized slowing and suppression
Psychogenic Normal EEG. Sometimes excess beta because patient might have received
unresponsiveness benzodiazepine for non-epileptic seizures.
Stroke of one hemisphere Focal polymorphic slowing over the region of the stroke. Sometimes peri-
odic discharges. Sometimes seizures.
during seizure surgery. So part of the discussion surgical margins for determination of recommended
on invasive electrodes pertains to intra-operative extent of resection to optimize se 4-180c izure control.
monitoring. EEG monitoring during carotid surgery has been
Mapping of epileptic foci is the most common used to determine the effectiveness of blood flow and
intraoperative monitoring performed by our insti- hence maintenance of cerebral circulation during
tutions. This includes assessment of EEG near the clamping and shunting for carotid surgery.
5
SEIZURE SEMIOLOGY
Bassel Abou-Khalil & Karl E Misulis
OVERVIEW Elementary motor manifestations include:

• Tonic activity: sustained muscle contraction;
Much of seizure semiology was discussed in Chapter 4 • May result in a posture (usually involving
on Clinical EEG. Details of semiology are discussed in contraction of several muscles).
this section with a minimum of figures. This chapter is • Versive: sustained deviation of the eyes or the
organized starting with definition and description of head to one side.
the individual signs and symptoms then seizure clas- • Dystonic: abnormal posture with a rotatory
sification and seizure types then clustering of signs and motion.
symptoms in relation to localization and lateralization • Epileptic spasms: proximal and truncal tonic
of the epileptogenic zone. activity more sustained than a myoclonic jerk but
yet very short in duration.
SEIZURE TERMINOLOGY • Myoclonic: very brief contraction usually lasting
less than 100 msec.
Many of the definitions below are derived from the
• Negative myoclonic: interruption of muscle tone
glossary of descriptive terminology for ictal semiol-
for a fraction of a second.
ogy, reported by the International League Against
• Clonic activity: sustained rhythmic jerking.
Epilepsy (ILAE) task force on classification and ter-
• Without a march: remains in the same
minology (Blume et al., 2001). Ictal semiology refers
body part.
to the signs and symptoms associated with seizures.
• With Jacksonian march: spreads unilaterally to
adjacent body parts as a result of the spread of
Motor manifestations
seizure activity along the motor strip.
Motor manifestations are most often positive, with • Tonic-clonic activity: initial tonic posturing that
a muscle contraction that produces a movement. evolves to clonic activity.
Negative motor manifestations, with a decrease in • Atonic: decreased muscle tone usually lasting
muscle contraction, are less common. more than 1 second.
235
Automatisms • Complex sensory manifestations: seeing people or

hearing music.
Automatisms are repetitive coordinated motor activ- • Sensory illusions: alteration/distortion of perception.
ity that is not purposeful, though it may look volun-
tary. Automatisms are usually associated with altered Experiential phenomena
sensorium and amnesia.
Experiential phenomena include:
• Perseverative automatisms involve continuation • Affective experiences such as fear, euphoria, sadness.
of pre-ictal activity. • Dysmnesic phenomena: déjà vu (inappropriate
• De novo automatisms start after seizure onset. feeling of familiarity); jamais vu (inappropriate
• Oro-alimentary automatisms: lip smacking, feeling of unfamiliarity).
chewing, swallowing, lip licking. • Dyscognitive: altered cognition, such as altered
• Manual automatisms: involving the hand. perception, memory, or executive function.
• Reactive or manipulative automatisms imply
interaction with nearby objects, for example pick- Autonomic phenomena
ing on bedsheets or fumbling with an object.
• Non-manipulative automatisms: rhythmic move- Autonomic phenomena May be subjective (most com-
ments that are independent of environment. If mon is epigastric sensation, nausea, feeling hot) or objec-
involving the hand they are referred to by the tive (pallor, flushing, goosebumps, vomiting, flatulence).
acronym RINCH (rhythmic ictal nonclonic
hand) movements. SEIZURE CLASSIFICATION
• Gestural automatisms: movements commonly
used to enhance speech. The international classification of seizures divides sei-
• Pedal automatisms: involving the feet. zures into two major groups, partial (or focal or local)
• Hyperkinetic automatisms imply a rapid and generalized (Commission on Classification and
sequence of movements with frenetic character. Terminology, 1981). The subdivision is dependent on
Examples are thrashing, kicking, pelvic thrusting, whether the onset is in one part of one hemisphere or
body rocking, bicycling motions. in both hemispheres simultaneously. Partial seizures are
• Gelastic: involuntary laughter. further subdivided into simple partial, complex partial,
• Dacrystic: involuntary crying. and partial becoming secondarily generalized. Simple
partial seizures do not affect awareness or responsive-
ness, whereas complex partial seizures are associated
Sensory phenomena
with impairment or complete loss of awareness or
Sensory phenomena may involve any sensory modality. responsiveness. Partial seizures vary remarkably in their
manifestations, depending on where they originate,
• Elementary sensory manifestation: unformed
where they spread, and how fast they spread. Generalized
sensations involving a single primary sensory
seizure types include absence (typical or atypical), myo-
modality, including:
clonic, clonic, tonic, tonic-clonic, and atonic seizures.
• Flickering or flashing lights, simple patterns,
Generalized seizure types are more homogeneous in
spots, visual loss.
their clinical manifestations, though they have a wide
• Single tones or buzzing, humming, or ringing
spectrum of severity. Partial seizure semiology will be
sounds; loss of hearing.
discussed first, based on the lobe of origin.
• Tingling, numbness, pain, or a sense of move-
The 1981 International League Against Epilepsy
ment; may have a Jacksonian march with
(ILAE) Classification of Epileptic Seizures (the most
sensation moving to adjacent body parts,
commonly used classification):
reflecting spread of electrical activity over the
sensory strip. I. Partial (Focal, Local) Seizures
• Olfactory hallucinations, most often unpleasant. A. Simple partial seizures (consciousness not
• Gustatory hallucinations, most commonly impaired)
metallic taste. 1. With motor symptoms
Seizure Semiology 237
2. With somatosensory or special sensory When simple partial seizures are purely subjective
symptoms they may be called isolated auras. The new ILAE pro-
3. With autonomic symptoms posal suggested dividing these seizures as either having
4. With psychic symptoms observable motor or autonomic components or only
B. Complex partial seizures (with impairment involving subjective sensory or psychic phenomena.
of consciousness) The clinical manifestations of simple partial sei-
1. With simple partial onset followed by zures depend on the brain region involved in the ictal
impairment of consciousness discharge. This brain region may or may not be the
2. With impairment of consciousness epileptogenic zone; at times the clinical manifesta-
at onset tions reflect seizure spread to adjacent or even distant
C. Partial seizures evolving to secondarily regions. Despite that, seizure manifestations may
generalized seizures have important lateralizing and localizing value. Focal
1. Simple partial seizures evolving to gener- clonic or tonic motor activity, somatosensory experi-
alized seizures ences, visual auras, and auditory auras have value in
2. Complex partial seizures evolving to localization and lateralization of the epileptogenic
generalized seizures zone. However, some auras such as odd feeling in the
3. Simple partial seizures evolving to head or generalized body tingling are non-specific
complex partial seizures evolving to with respect to localization.
generalized seizures
II. Generalized Seizures (Convulsive or
Complex Partial Seizures
Non-convulsive)
A. Absence seizures Complex partial seizures involve altered conscious-
1. Typical absence seizures ness during the seizure, ranging from subtle confu-
2. Atypical absence seizures sion to complete loss of contact. There may be some
B. Myoclonic seizures recollection of events or total amnesia. Complex par-
C. Clonic seizures tial seizures may start with loss of awareness, or may
D. Tonic seizures have a simple partial onset. The most recent ILAE rec-
E. Tonic-clonic seizures ommended revisions suggest replacing the term com-
F. Atonic seizures plex partial seizure with focal seizure with impairment of
III. Unclassified Epileptic Seizures consciousness or awareness (Berg et al, 2010). However,
the term complex partial seizure is still widely used.
PARTIAL It is not always possible to tell if a seizure is simple
partial or complex partial, since decreased ability to
Simple Partial Seizures respond verbally may be due to aphasia or motor inhi-
These are associated with preserved consciousness bition, as well as altered awareness. Complex partial
throughout the seizure. The most recent recom- seizures may manifest only with altered awareness/ con-
mendations of the International League Against fusion, or may include motor activity, most commonly
Epilepsy (ILAE) Commission on Classification and automatisms. Complex partial seizures may arise from
Terminology suggest replacing the term simple partial any brain region, but they most often originate in the
seizure with focal seizures without impairment of con- temporal lobe, followed by the frontal lobe. The manifes-
sciousness or awareness (Berg et al, 2010). However, the tations of complex partial seizures can vary with lobe of
term "simple partial" is still widely used. origin, as will be discussed later.
Simple partial seizures may have:

Partial Seizures Evolving to Generalized
• Motor signs; Tonic-Clonic Activity (Secondarily Generalized
• Somatosensory or special sensory symptoms; Tonic-Clonic Seizures)
• Autonomic symptoms or signs;
• Psychic symptoms; Secondarily generalized tonic-clonic seizures may
• Combination of the above. evolve directly from simple partial onset, directly
from a complex partial onset, or may evolve from • Parietal;

simple partial to complex partial to generalized • Occipital;
tonic-clonic. The transition to secondary general- • Insular.
ization usually involves some lateralizing features,
the most important of which is versive head turn- Of the partial seizures, temporal origin is the most
ing opposite the side of seizure onset. There may common, with frontal origin next in frequency, fol-
also be contralateral tonic or clonic motor activity. lowed by parietal, occipital, and insular origin (see
During generalized tonic contraction, there may be also Table 5-1).
an asymmetry with arm extension contralateral and
arm flexion ipsilateral to the seizure focus phase. This Frontal
is designated figure-of-4 posturing. The clonic activity
may be symmetrical and synchronous, or may have The frontal lobe is the second most common source
some asymmetry and asynchrony. The clonic activ- of seizures after the temporal lobe. A great variety of
ity may be more pronounced on the side of seizure seizure manifestations can be related to frontal lobe
onset, but may also become more prominent on the origin.
ipsilateral side late in the seizure. The clonic activity Aura: An aura is less common with frontal lobe
may even stop earlier on one side of the body. Late origin than with temporal lobe origin. There is only
ipsilateral head deviation may be seen in some indi- a limited specificity in auras. Autonomic auras with
viduals. Asynchrony may produce some relatively abdominal sensation are more likely to be of tem-
low-amplitude side-to-side head jerking. Clonic poral lobe origin. However, frontal lobe limbic sei-
activity usually decreases in frequency progressively, zures may have the same autonomic auras, including
such that longer pauses develop between seizures epigastric sensation. These autonomic auras have
over time. The generalized tonic-clonic phase rarely been ascribed to the orbitofrontal and the cingulate
lasts more than 2 minutes. Following the end of the regions.
clonic activity, it is common to observe stertorous Somatosensory auras are generally ascribed to
respiration (deep loud snoring respiration). The activation of the primary sensory cortex. However,
speed of recovery from a secondarily generalized frontal lobe seizures originating in the supplementary
seizure depends to a large extent on seizure duration sensorimotor area are frequently associated with a
and severity. Tongue biting is common, most often sensory aura due to activation of the supplementary
involving the side of the tongue. Incontinence of sensory area. The sensory auras related to supplemen-
urine and less often of stools may also occur. After tary motor seizures generally do not have a march,
awakening, patients commonly report headache and are more often proximal, and may be bilateral in dis-
generalized muscle soreness. tribution, although a contralateral occurrence is most
likely. Forced thinking may be seen with dorsolateral
Partial Seizure Semiology by frontal lobe origin.
Localization Perhaps the most common aura in frontal lobe sei-
zures is the non-specific cephalic sensation, which has
Symptoms and signs of partial-onset seizures can, to a no localizing value. It has been suggested that isolated
certain extent, help to localize the site of origin of the auras are a common feature of temporal lobe but not
discharge to one of the following lobes. Simple partial frontal lobe epilepsy. Thus, many patients with frontal
seizures do not produce alteration of consciousness, lobe epilepsy deny auras that do not progress further.
and tend to have an extratemporal focus. Complex Motor manifestations: Activation of the primary
partial seizures commonly have a temporal lobe focus motor cortex is well-known to be associated with
and do produce alteration of consciousness. In addi- clonic activity. Focal clonic or tonic-clonic seizures
tion to subdivision into simple and complex, seizures therefore are most likely originating in the primary
are classified according to site of origin: motor cortex. Focal cortical myoclonus is another
manifestation of primary motor cortex epileptoge-
• Temporal; nicity. In general, consciousness is preserved unless
• Frontal; there has been spread of seizure activity to the
Table 5-1 Semiology of Partial Seizures

Seizure type Semiology
Temporal lobe Mesial temporal:
Subjective: epigastric sensation (butterflies, nausea, pain, etc.), especially rising;
déjà-vu, jamais-vu; fear; olfactory or gustatory hallucination
Objective: motor arrest and staring, often with oro-alimentary and extremity
automatisms. Combination of ipsilateral manipulative automatisms and contra-
lateral dystonic posturing is common in mesial temporal lobe onset.
Lateral temporal:
Subjective: auditory aura; vertigo
Objective: early facial twitching; absence of oro-alimentary automatisms or pat-
tern of contralateral dystonic posturing and ipsilateral extremity automatisms.
Language manifestations may include speech arrest (non-specific), ictal
aphasia, ictal jargon (dominant left temporal), well-formed ictal language
(non-dominant temporal).
Frontal lobe Subjective: cephalic aura; forced thought; sensory aura without a march (most
often contralateral) may occur with supplementary sensorimotor seizures
Motor cortex involvement—focal clonic or tonic-clonic activity.
Supplementary sensorimotor area—posturing, especially proximally.
Cingulate and orbitofrontal—CPS with gestural automatisms.
Parietal lobe Subjective: marching somatosensory experience, sensation of movement in an
extremity, feeling of body motion, or feeling of absence of an extremity; vertigo
Objective (usually reflecting spread to temporal or frontal region): contra-
lateral posturing, clonic activity, head and eye deviation, immobility, staring,
oro-alimentary automatisms.
Occipital lobe Subjective: elementary visual hallucinations.
Objective: bilateral blinking, eye deviation, usually contralateral; temporal or
frontal seizure patterns with spread outside the occipital lobe.
Insular lobe Subjective: laryngeal discomfort, shortness of breath, and perioral paresthesias.
Objective: dysarthria, dysphonia, hypersalivation
contralateral hemisphere. If motor activity involves be accompanied by loss of consciousness. These sei-
the lower extremity, this suggests mesial localiza- zures tend to be brief in duration, tend to cluster,
tion, while facial involvement suggests inferior frontal and tend to be predominantly nocturnal, arising out
localization. of sleep. The posturing of the extremities is predom-
Seizures originating in the supplementary sen- inantly proximal, while the hands and fingers or feet
sorimotor area tend to be asymmetrical tonic or and toes seem to be free. Patients will frequently
postural seizures. They are characterized by postur- wiggle the distal extremities. There is often a vocal-
ing that can affect one limb, two limbs, or all four ization of moaning or groaning and the patient
extremities. If the seizure origin is in the supple- reports being unable to breathe. Supplementary
mentary motor area, they will usually be simple sensorimotor seizures are occasionally precipitated
partial seizures, with no alteration of consciousness. by startle, most commonly by unexpected auditory
Supplementary motor seizures are a notable excep- stimuli, less often by unexpected somatosensory
tion to the rule that bilateral seizure activity should stimuli.
Seizures originating in the supplementary senso- gelastic seizures are usually not associated with emo-
rimotor area may occasionally manifest with inhibition, while temporal gelastic seizures seem to be. The
tion of movement. There may be ictal paralysis or gelastic seizures of frontal cingulate and hypothalamic
just inhibition of motion without paralysis, with loss origin may have preserved awareness, while those of
of ability to move or speak. These seizures are usually temporal origin are associated with altered awareness
simple partial or may start as simple partial seizures after the initial sense of mirth. Frontal gelastic seizures
with later altered awareness. The ictal paralysis may be may be accompanied by hypermotor manifestations
followed by positive motor (tonic or clonic) activity in or tonic posturing.
the same affected extremity, or may be accompanied Seizures originating in the anterior-mesial frontal
by positive motor activity in a different body part on region at times imitate absence seizures through rapid
the same side. The ictal inhibition is presumed second- secondary bilateral synchrony. These seizures are fre-
ary to seizure activity in a negative motor area, often quently referred to as frontal absences. They can clini-
seen adjacent to the supplementary sensorimotor area. cally be characterized by altered responsiveness and
Since the seizure origin is in the mesial frontal cor- arrest of activity for a few seconds with rapid return to
tex, there is often no recorded interictal or ictal EEG baseline, with minimal postictal manifestations. Such
activity due to the unfavorable dipole orientation. seizures can be totally indistinguishable from gener-
These seizures are frequently misdiagnosed as psycho- alized absence seizures, except for the presence of a
genic. The correct diagnosis is reached upon observa- frontal lesion, and at times the presence of consistent
tion of evolution to secondary generalized tonic-clonic asymmetry on EEG. Frontal lobe origin seizures can
seizure activity after the withdrawal of anti-epileptic imitate a variety of other generalized seizure types,
drug therapy in the epilepsy monitoring unit. including generalized tonic, generalized atonic, and
Bizarre complex partial seizures have been ascribed generalized tonic-clonic seizures. Frontal lobe sei-
to seizure origin in the cingulate gyrus or orbitofrontal zures are recognized to have a more rapid spread to
region, but they may also arise in other regions of the the contralateral hemisphere. This is partly why fall-
frontal lobe and even outside the frontal lobe, usually ing (drop attacks) and incontinence seem more likely
manifesting after spread to the cingulate gyrus or orbi- with frontal lobe seizures.
tofrontal region. Such seizures are frequently character- Seizures originating in the frontal operculum are
ized by frenetic gestural automatisms (also referred to characterized by hypersalivation, oral-facial apraxia,
as hypermotor behavior) that are often bilateral, unless and at times facial clonic activity.
there is associated contralateral posturing. These Seizures originating in the dorsolateral frontal lobe
automatisms can be bizarre and can be associated with may manifest with tonic posturing of the extremities
bizarre vocalizations and verbalizations, including and versive eye and head deviation. The head devia-
expletives. These seizures tend to be short and associ- tion preceding secondary generalization is contralat-
ated with only brief postictal manifestations, unless eral, but early head turning can be in either direction.
there is spread to the temporal lobe. The presence of The lateralizing value of signs in frontal lobe sei-
unilateral posturing and rotation along the body axis, zures may be less than with temporal lobe seizures,
such as with turning prone, favor a mesial frontal ori- due to the propensity for rapid contralateral spread
gin, while severe agitation favors an orbitofrontal local- and contralateral hemisphere activation.
ization. Again, the clinical features and the frequent It is important to recognize that seizures originat-
absence of interictal epileptiform activity, as well as ing in the frontal lobe, particularly in the orbitofrontal
absence or artifact masking of rhythmic ictal EEG region, may manifest after propagating to the tempo-
activity, have frequently resulted in the misdiagnosis of ral lobe, with semiology typical of mesial temporal
psychogenic seizure events. lobe seizures.
Gelastic seizures, which are short seizures char-
acterized by sudden unprovoked laughter, are best Temporal
known as a seizure type originating from hypo-
thalamic hamartomas. However, they may also be Temporal lobe epilepsy (TLE) is the most common
seen with frontal cingulate as well as mesial-basal symptomatic/cryptogenic partial epilepsy. The charac-
temporal seizure origin. Frontal and hypothalamic teristic manifestations of temporal lobe seizures have
long been recognized. However, the advent of video aura are more likely with right temporal foci, but this
EEG monitoring and its use in presurgical evaluation is only a trend. Whereas viscerosensory auras are gen-
have had a great impact on the understanding of tem- erally more common in mesial TLE associated with
poral lobe seizure semiology. Temporal lobe epilepsy hippocampal sclerosis, experiential auras and deja vu
is often refractory to medical therapy, and is often ame- in particular are more common in the benign familial
nable to surgical treatment. The surgical outcome is temporal lobe epilepsy syndrome.
dependent on accurate localization of the epileptogenic Multiple sequential auras in the same seizure
zone. The analysis of clinical semiology in patients who suggest a non-dominant localization most often
were seizure-free after temporal lobectomy versus those temporal. Chills and goosebumps are more com-
still experiencing seizures has helped to identify mani- mon with left temporal foci, and if they are unilat-
festations characteristic of temporal lobe origin, and eral, they are usually ipsilateral to the seizure focus.
those that suggest extratemporal localization. In addi- Olfactory and gustatory auras are uncommon
tion, specific seizure manifestations were analyzed for mesial temporal lobe epilepsy auras. They are asso-
their lateralizing and localizing value within the tempo- ciated with mesial temporal tumors. An auditory
ral lobe (see Figure 5-1). aura is very suggestive of lateral temporal origin.
This can be a positive (buzzing or ringing sound)
Seizure Aura or negative symptom (loss of hearing). The audi-
Most patients with TLE report a seizure aura. This is tory aura is a hallmark of an autosomal dominant
particularly true in mesial TLE, by far the largest TLE form of temporal lobe epilepsy. Cephalic auras
group. In a selected patient group with proven mesial (non-specific sensation in the head) are more likely
temporal lobe origin, more than 90% of patients extratemporal. The same is true of somatosensory
reported an aura. The most common was an epigastric and visual auras. Absence of an aura is more likely
aura. Although no aura is totally specific for temporal with bitemporal epilepsy.
lobe seizures, some are very strongly associated with
a temporal lobe origin, particularly viscerosensory Motor Manifestations
(such as epigastric sensation) and experiential or psy- The complex partial phase of mesial temporal lobe
chic auras (such as “deja-vu”). Both of these types of seizures usually starts with motor arrest or motionless
Figure 5-1: Left temporal sharp waves in a patient with temporal lobe epilepsy.

staring, oro-alimentary automatisms, or non-specific ictal activation in the contralateral putamen. There is
extremity automatisms. evidence that there is a spectrum of posturing, with
Oro-alimentary automatisms, mainly lip smack- classical dystonic posturing at one extreme, and sim-
ing, chewing, and swallowing movements, are sug- ple immobility of an extremity at the other, including
gestive of temporal lobe involvement. However, they subtle posturing without a clear demonstrated rota-
are not specific for temporal lobe epilepsy. They may tory component in between. Dystonic posturing has
reflect the spread of seizure activity to the temporal a strong lateralizing value in temporal lobe epilepsy.
lobe from other locations, and can also be seen in a However, as with any other manifestations, late occur-
more subtle form in absence seizures, or postictally in rence could represent activation of the contralateral
a variety of seizure types. side and may therefore have a lesser value.
Spitting and drinking automatisms suggest right Head turning in temporal lobe epilepsy has been
temporal localization. the subject of great controversy. Current evidence sug-
Automatisms with preserved responsiveness also gests that early head turning, particularly that associ-
favor right temporal localization. ated with dystonic posturing, tends to be ipsilateral to
Extremity automatisms are less specific and can the focus. Its mechanism is not well defined. Some have
be seen in temporal as well as extratemporal epi- suggested it could represent neglect of the contralateral
lepsy. However, the progression of these automa- hemisphere. However, in many instances the early head
tisms is more gradual in temporal lobe epilepsy. In turning is of a tonic nature, which raises the possibility
extratemporal epilepsy, they tend to have an abrupt of a motor drive, possibly from the basal ganglia. In one
bilateral onset and a frenzied character. The most study, the occurrence of head turning within 30 seconds
common upper extremity automatisms are manipu- of seizure onset, in association with dystonic postur-
lative, involving interaction with the environment, ing and not leading to secondarily generalization, has
for example picking on clothing or bedsheets or been strictly ipsilateral to the temporal seizure focus
fumbling with objects. Manipulative automatisms (Fakhoury and Abou-Khalil, 1995). Late head turning,
in of themselves have no lateralizing value. However, on the other hand, is more likely to be contralateral.
the extremity contralateral to the side of the focus Head turning that leads to secondary generalization can
is often involved in dystonic posturing or immo- have a tonic or clonic character and has been termed
bility and may therefore not demonstrate automa- “versive” or “adversive”. Versive head turning is almost
tisms. In this instance, manipulative automatisms always contralateral to the seizure focus. However, an
will predominate in the extremity ipsilateral to the ipsilateral versive head turn has been noted towards the
seizure focus. This may lead to confusion for the end of secondarily generalized tonic-clonic seizures in
inexperienced observer, who may interpret repeti- some patients (Wyllie et al., 1986).
tive automatisms as clonic activity. The less common
non-manipulative upper extremity automatisms Language Manifestations
involve rhythmic repetitive motions that are either Language manifestations are potentially very valu-
distal (milking, pill rolling, grasping, fist clenching, able in lateralizing temporal lobe seizure origin (Gabr
or opening–closing motions) or proximal (often with et al., 1989).
a circulatory character like waving or stirring). These Ictal speech arrest does not seem to have lateral-
automatisms tend to be contralateral and often pre- izing value. It may be due to disruption of language
cede dystonic posturing (Lee et al., 2006; Kelemen mechanisms, to loss of awareness/responsiveness, or
et al., 2010). to a positive or negative motor effect. There is a sug-
Seizures originating in the temporal pole often gestion, however, that in temporal simple partial sei-
manifest with hypermotor activity, similar to what is zures a speech arrest could represent aphasia and may
seen in orbitofrontal complex partial seizures. This is thus be lateralizing to the dominant temporal lobe.
related to seizure spread to the orbitofrontal region Well-formed ictal language strongly suggests a
(Wang et al., 2008; Vaugier et al., 2009). non-dominant right temporal lobe focus. This is not
Defined in the strictest manner, dystonic posturing true, however, of single words or non-verbal vocaliza-
is an unnatural position that includes a rotatory com- tions. The well-formed ictal language in some patients
ponent. Dystonic posturing has been associated with with right temporal lobe seizures has a tinge of fear.
For example, it is not uncommon for patients to utter and clonic activity are most often contralateral to
“I’m sick, I’m sick,” or “I’m going to die, don’t let me seizure origin. Occasionally, however, they can be
die.” In most instances, however, the patient does not falsely lateralizing if there is contralateral seizure
remember these utterances, and fear may not be a spread prior to generalization.
known component of the semiology.
Ictal jargon is rare but has been associated with Postictal manifestations:
dominant temporal lobe foci. It may reflect a par- • Postictal cough has been found predominantly
tial disruption of language mechanisms, as seen in following right temporal seizures.
chronic Wernicke’s aphasia. • Postictal nose wiping tends to be performed with
Global aphasia may occur in association with local- the hand ipsilateral to the seizure focus.
ized simple partial seizures restricted in the tempo- • Postictal urinary urgency suggests a right tempo-
ral lobe, including the basal temporal language area. ral localization.
Chronic temporal lobe lesions do not produce global
aphasia. However, acute electrical stimulation of
None of the above signs is sufficient in isolation.
Wernicke’s area and basal temporal language area does
However, the combination of several signs and
produce global aphasia, perhaps because compensatory
symptoms can be a powerful tool in localizing
mechanisms have not had the chance to be activated.
and lateralizing temporal lobe epilepsy. The addi-
Global aphasia in simple partial seizures therefore
tion of semiological information unquestionably
could be consistent with a temporal localization.
enhances the localizing ability of the presurgical
Postictal aphasia is strongly associated with a left
evaluation.
dominant temporal localization. In one study, all
patients with right temporal seizures were able to cor-
rectly read a test sentence within one minute of sei- Parietal
zure termination, while patients with dominant left
temporal foci had disruption of reading for more than The parietal lobe is the next most likely source of sei-
one minute. In patients with atypical language rep- zures after the temporal and frontal lobe.
resentation, the lateralizing significance of language Aura: The best recognized manifestation of pari-
dysfunction has to be reinterpreted. etal lobe origin is a sensory aura, particularly if there is
an associated march. The sensation can be described
Other manifestations as numbness, tingling, pins and needles, burning, or
pain. It can also be nondescript.
A variety of other ictal manifestations may have Sensory march is strongly suggestive of a post-central,
lateralizing value: primary sensory cortex involvement. This is lateralized
• Ictal vomiting has been associated with contralaterally to the ictal discharge.
right-sided foci. However, this is not uniform, Sensory aura without march can originate in
and vomiting may also be a manifestation of the second sensory area, which is located over the
extratemporal foci. parietal operculum. The sensory manifestations
• Ictal spitting, ictal flatulence, and ictal drinking from the second sensory area are most often con-
are more common with right temporal foci. tralateral, but they are occasionally ipsilateral or
• Unilateral eye blinking tends to be ipsilateral to bilateral.
seizure origin. Ictal vocalization has limited speci- Vertigo, difficulty localizing body position in
ficity with respect to localization or lateralization. space, sensation that a body part is moving, or that
• Focal facial motor activity early in the seizure an extremity is absent are other less common sensory
favors a lateral neocortical origin (Foldvary auras that suggest a parietal lobe origin.
et al, 1997). Focal weakness has also been described with
• Transition to secondary generalization. The parietal foci. Seizures with focal weakness have been
motor manifestations during transition to sec- referred to as focal inhibitory motor seizures or focal
ondary generalization can be very valuable in lat- atonic seizures (Abou-Khalil et al., 1995). They fre-
eralization. Versive head turning, tonic posturing, quently have a preceding sensory aura.
Seizures without parietal lobe symptoms: Most progression of ictal manifestations. For example, the
patients with parietal lobe epilepsy have no pari- eye deviation that is seen with occipital lobe origin
etal lobe symptoms, but rather manifestations tends to be much slower than that noted with frontal
resulting from spread to occipital, temporal, or lobe origin.
frontal lobe. Some studies suggest that manifestations of
seizures originating in the occipital lobe are most
Common manifestations with frontal lobe propaga- commonly related to seizure spread to the tem-
tion include: poral or frontal lobe. Seizure spread to the tempo-
• Contralateral tonic posturing; ral lobe commonly manifests with oroalimentary
• Focal clonic activity; automatisms, while seizure spread to the frontal
• Generalized asymmetrical tonic posturing; lobe may produce asymmetrical tonic posturing.
• Head and eye deviation, described in almost 50% Secondary generalization is common with frontal
of patients. lobe propagation.
When there is propagation to the temporal lobe, com- Insular

plex partial seizures can be characterized by:
Insular epilepsy cannot be analyzed with scalp video
• Staring;
EEG studies since it is not possible to record from the
• Relative immobility with minimal automatisms;
insula with scalp electrodes. The semiology of insu-
• Oro-alimentary automatisms.
lar epilepsy was elucidated only with analysis of sei-
zures recorded with depth electrodes implanted in the
Occipital insula (Isnard et al., 2004).
Aura: The most common subjective manifesta-
Aura: Sensory symptoms suggesting occipital origin are:
tions of seizure activity in the insula are laryngeal dis-
• Visual aura is the key manifestation that suggests comfort, shortness of breath, and paresthesias around
occipital lobe origin. the mouth. Sensory manifestations may also involve
• Elementary visual hallucinations strongly other body parts contralaterally. Autonomic manifes-
suggest involvement of primary visual cortex. tations are common, with visceral sensations in the
These hallucinations may be black or white or chest or abdomen.
colored. They can be flashing or steady. They Motor: Dysarthria or dysphonia may occur, at
can be stationary or moving. There may be times extreme with resultant muteness. Hyper-
distortion of vision, and there may also be a loss salivation is very common. Seizure propagation to
of vision. The ictal blindness can be a blackout the frontal lobe may manifest with tonic spasm of the
or a whiteout. If this is in one field, it strongly contralateral face and upper extremity, and contralat-
suggests seizure activity contralateral to that eral head and eye deviation. There may be hypermo-
field. More complex visual hallucinations, such tor manifestations mimicking frontal lobe complex
as ones involving scenes, suggest involvement of partial seizures (Ryvlin et al, 2006). There may also
the occipitotemporal junction. be typical temporal semiology with spread to the
• Auditory hallucinations, vertigo, and focal sensory temporal lobe.
experiences may also be seen, but suggest seizure
spread to the lateral temporal or parietal regions.
Other
Motor symptoms suggesting occipital origin include: Seizures very rarely start in subcortical regions. The
• Bilateral blinking; best recognized are hypothalamic seizures from hypo-
• Nystagmoid eye movements; thalamic hamartomas. The most typical seizure type
• Eye deviation, usually contralateral. is gelastic seizures (seizures with laughter), and some
of these patients may also have dacrystic seizures
One distinctive feature of occipital lobe seizures (seizures with crying). However, patients with hypo-
that develop and propagate posteriorly is the slow thalamic hamartomas may also have other seizure
types that seem to develop over time, including so mild in clinical manifestations is that they involve a
complex partial seizures, non-gelastic simple partial restricted bilateral frontoreticular network.
seizures, generalized tonic-clonic seizures, and some
other generalized seizure types, such as atonic and Generalized Absence Seizures
tonic seizures and epileptic spasms.
There are also rare reports of seizures starting in These seizures can occur in a variety of epileptic
cerebellar gangliogliomas, usually in infants (Harvey syndromes, particularly childhood absence epi-
et al, 1996; Chae et al., 2001). These seizures are char- lepsy and juvenile absence epilepsy (Hirsch and
acterized by hemifacial twitching ipsilateral to the Panayiotopoulos, 2005). These seizures are character-
lesion, and at times contralateral head and eye devia- ized by sudden onset without any aura, brief duration,
tion or contralateral nystagmus. typically less than 15 seconds, and sudden termina-
tion without any postictal state. Typical generalized
absence seizures are associated with generalized
GENERALIZED 2.5–4 Hz spike-and-wave activity (see Figure 5-2).
Typically, there is suspension of awareness and
Generalized-onset seizures start simultaneously in arrest of activity during the episodes, but some motor
both hemispheres. They vary considerably in sever- manifestations are quite common. Absence seizures
ity of clinical manifestations (see Table 5-2). At one with altered awareness or responsiveness only are
extreme are generalized tonic-clonic seizures, and at sometimes called simple absence seizures. When there
the other are generalized absence seizures. The reason is associated motor activity or autonomic manifesta-
that generalized absence seizures are generalized yet tions, absence seizures are sometimes referred to as
Table 5-2 Semiology of Generalized Seizures

Seizure type Semiology
Generalized absence Sudden behavior arrest and loss of awareness. Simple automatisms;
subtle twitching or change in tone.
Atypical absence Sudden loss of awareness but with slower recovery and more
prominent motor symptoms such as myoclonic, tonic or atonic
components.
Generalized absence with Eyelid myoclonia occurs in addition to absence symptomatology
eyelid myoclonia
Myoclonic absence Absence but with prominent myoclonic activity at the same
frequency as the spike-and-wave discharge.
Myoclonic seizures Brief myoclonic jerks (fraction of a second) too short for clear
alteration in consciousness
Generalized tonic-clonic seizures Initial tonic phase followed by clonic phase with prominent
postictal period.
Generalized tonic seizures Sudden loss of consciousness with generalized tonic posturing.
Usually in neurologically impaired individuals.
Generalized atonic seizures Sudden loss of tone either restricted (e.g., head) or whole body. One
cause of drop attacks.
Epileptic spasms Sudden flexion (or extension) of trunk with arm abduction
Myoclonic-atonic seizures Myoclonic jerk precedes the atonic phase.
Negative epileptic myoclonus Loss of tone for a fraction of a second without disturbance of
consciousness.
Figure 5-2: Typical Generalized Absence Seizure.
complex absence seizures (to be distinguished from When there is some preservation of awareness but
complex partial seizures). loss of responsiveness, patients may describe some
Simple automatisms are the most common, par- subjective experiences that could erroneously suggest
ticularly perseverative automatisms. Automatisms an aura. For example, lightheadedness or spaciness
may include fumbling with an object that the patient may be reported. In addition, some patients report
was holding, rubbing a body part, or mouth move- confusion after the seizure. This usually reflects the
ments such as licking lips. Automatisms are more effect of missing parts of a conversation rather than
likely with longer duration of absence seizure activity. true confusion.
Myoclonus is the next most common motor mani-
festation. This includes blinking and subtle twitching Atypical Absence Seizures
of fingers.
Tonic features may occur, with up-rolling of the This variant of generalized absence seizures
eyes and slight stiffening of the neck with neck exten- tends to occur in symptomatic generalized epi-
sion, though this is mild. lepsy, such as Lennox-Gastaut syndrome. The
Atonic components can also be seen, with slight main distinction between typical and atypical
decrease of tone and slumping, again to a mild degree. absence seizures is electrographic, as the latter
Autonomic manifestations may occur, includ- have a slower frequency of less than 2.5 Hz (see
ing pupillary dilation, piloerection, and infrequently, Figure 5-3). Clinical distinctive features reported
incontinence. At times, consciousness is partially pre- are a slower loss of awareness and a more gradual
served. This is more likely to occur in adults who have recovery, as well as perhaps more prominent motor
had persistent absence seizures from childhood. manifestations.
Figure 5-3: Atypical Absence Seizure.
Generalized Absence Seizures with Eyelid they could be unilateral with shifting lateralization.
Myoclonia Myoclonic seizures are not associated with loss of
consciousness because of their very brief duration.
These seizures occur predominantly in women, as They often occur in clusters, and patients occasionally
part of an epileptic syndrome. In this syndrome, report some disruption of consciousness with a clus-
eyelid myoclonia may occur with or without associ- ter of closely spaced seizures.
ated spike-and-wave activity (Caraballo et al., 2009). Generalized myoclonic seizures are to be distin-
Women with this condition are usually photosensi- guished from non-epileptic myoclonus, which can
tive and also have eye closure sensitivity. originate at any level of the central nervous system.
Myoclonic Absences Generalized Clonic Seizures
These seizures associated with the typical 2.5–3.5 Hz These seizures, characterized by rhythmic clonic
spike-and-wave discharge differ from absence seizures jerking, start with loss of consciousness. They are
by the presence of a very prominent clonic activity at the infrequent. They are seen in children with severe
same frequency as the spike-and-wave discharges. The myoclonic epilepsy of infancy (Dravet syndrome)
seizures in this syndrome tend to be harder to control. and patients with progressive myoclonic epilepsies.
Generalized Myoclonic Seizures Generalized Tonic-Clonic Seizures
Generalized myoclonic seizures last a fraction of a Generalized-onset tonic-clonic seizures do not have an
second (see Figure 5-4). They vary in severity from aura, although they may be preceded by a prodrome
mild with barely visible twitch to severe with massive (sometimes prolonged feeling of being seizure-prone).
myoclonus associated with falling. The myoclonic jerk The onset is abrupt, with loss of consciousness, then
may involve the whole body, or the upper extremities generalized tonic contraction. In patients with juve-
or the head alone. Although they are usually bilateral, nile myoclonic epilepsy, it is common for generalized
Figure 5-4: Generalized spike-and-wave activity in a patient with Juvenile Myoclonic Epilepsy. The reference
is linked ears.
tonic-clonic seizures to start with repetitive myoclonic with stertorous respiration. Postictal confusion and sleep
jerks (then called clonic-tonic-clonic seizures). Generalized are common. The postictal manifestations are similar to
tonic-clonic seizures may also evolve from generalized what is noted with secondarily generalized seizures. See
absence seizures. The tonic phase may be symmetrical, Figures 5-5a through 5-5d for the EEG appearance of a
but asymmetries may be seen. In particular, versive head generalized tonic-clonic seizure.
turning is common, and may change direction from one The duration of the postictal period can be from
seizure to the other. Versive head turning alone does not minutes to hours; however, a postictal period of days
mean that the seizure onset was focal (Niaz et al, 1999; is not expected and other pathology has to be con-
Chin and Miller, 2004). The tonic phase may show evo- sidered. Prolonged generalized tonic-clonic seizures,
lution from flexion to extension. The eyes are usually half even if masked by paralytics, can cause neuronal dam-
open and the mouth is open. A loud vocalization may age, so failure to improve following a prolonged sei-
result from contraction of the diaphragm and contracted zure can be of concern for sustained damage.
glottis. Cyanosis is most likely to occur during the tonic
phase of the seizure. Clonic activity evolves from the Generalized Tonic Seizures
tonic phase, initially with high frequency, but progress-
ing to lower frequency and larger amplitude. After the These seizures occur most often in neurologically
jerking stops, the individual is limp and unresponsive, impaired individuals. They are more likely to occur
Figure 5-5a: Generalized Tonic-Clonic Seizure (generalized EEG onset).
Figure 5-5b: Generalized Tonic-Clonic Seizure (onset of tonic phase).

Figure 5-5c: Generalized Tonic-Clonic Seizure (tonic phase evolving to clonic activity with pauses in muscle
activity).
Figure 5-5d: Generalized Tonic-Clonic Seizure (end with postictal attenuation).

out of sleep. They are characterized by sudden loss Generalized Atonic Seizures
of consciousness with generalized tonic posturing
that may be asymmetric, with turning to one side. These seizures can vary in manifestation from subtle
The pattern of muscle involvement may evolve, drooping of the head to a massive loss of tone with
producing a change in body and limb position falling. They are more common in children. They are
over the course of the seizure. The tonic contrac- associated with drop attacks. Drop attacks can be due
tion may end with one or more pauses that result to tonic seizures as well, and the distinction of the two
in a few clonic jerks. The posturing/stiffening can be difficult without direct observation.
can be generalized and massive or minimal, mani- Generalized atonic seizures are associated with
festing only with eye opening or with slight neck brief loss of consciousness. The duration is usually
extension. not more than a few seconds. More prolonged atonic
Tonic seizures can be abrupt or can manifest with seizures are seen in association with Lennox-Gastaut
slow posturing. The most common pattern of gener- syndrome and related epilepsies.
alized tonic seizure posturing involves flexion of the
trunk and extension of the extremities with abduction Myoclonic-Atonic Seizures
at the shoulders. There may be associated vocaliza-
tion, particularly with the massive and abrupt gener- These seizures are commonly part of the syndrome of
alized tonic seizures. myoclonic astatic epilepsy, also referred to as Doose’s
Generalized tonic seizures are typically quite syndrome. In these seizures, a myoclonic jerk pre-
brief but may have a postictal state with a duration cedes the loss of tone. The seizures are very brief with
and severity that are disproportionate to their dura- rapid recovery. However, injuries are not uncommon
tion. This may be because tonic seizures may be fol- with a fall from loss of tone.
lowed by atypical absence, referred to as tonic-absence
seizures (Shih and Hirsch, 2003). Negative Epileptic Myoclonus
These seizures can be difficult to distinguish from
partial-onset seizures of frontal or parietal origin. Just as asterixis resembles non-epileptic myoclonus,
but with momentary loss of tone rather than momen-
Epileptic Spasms tary contraction, negative epileptic myoclonus is
associated with very brief loss of tone that may not
Epileptic spasms is the term now recommended to be appreciated unless the affected extremities are
replace infantile spasms, because these seizures may elevated or engaged in other activity.
occur after infancy (Goldstein and Slomski, 2008;
Ramgopal et al., 2012). Epileptic spasms are shorter Generalized-Onset Seizures with Focal
than generalized tonic seizures but longer than gen- Evolution
eralized myoclonic seizures. The intensity of con-
traction is greater in the middle of the spasm than Just as focal onset seizures may secondarily generalize,
at onset or termination, while the contraction seen generalized-onset seizures rarely evolve to become
with tonic seizures is more likely to be sustained. focal (Williamson et al., 2009). This focal evolution
The classic epileptic spasm involves flexion of the can occur with generalized myoclonic or generalized
neck and trunk with arm abduction. These seizures absence seizures. Such seizures most often manifest
typically occur in clusters, with a seizure every few with prolonged staring and arrest of activity, at times
seconds to a minute, and demonstrate increasing with subtle automatisms. Focal clonic activity may
then decreasing intensity over the course of the also occur. Postictal confusion is common and results
cluster. in misdiagnosis as complex partial seizures.
6
DIFFERENTIAL DIAGNOSIS
OVERVIEW Psychogenic nonepileptic events is even more specific,

since the term nonepileptic seizures could potentially
The differential diagnosis of seizures includes a host of include other disorders for which this term is cer-
non-epileptic events. The most common conditions in tainly not intended. The incidence of PNES in the
the differential diagnosis vary somewhat with age. For general population can reach up to 5 per 100,000 per-
example, transient ischemic attacks (TIAs) and tran- sons per year. There is a higher prevalence in women
sient global amnesia are important conditions in the who represent 70-80% of those affected.
differential diagnosis in old age, but not in younger indi- Some patients have both epileptic seizures and
viduals. Psychogenic nonepileptic seizures, syncope, nonepileptic seizures, perhaps 10-15% of patients
and some sleep disorders imitate epilepsy through with PNES (Benbadis et al., 2001; Lesser et al., 1983;
much of the lifespan. Most of these are nonepileptic Martin et al., 2003). Distinguishing the two can be
neurologic, cardiac, vascular, or psychiatric in origin. difficult. We often have to teach the patient or family
Table 6-1 lists some common disorders that can be how to distinguish the two and ask for the frequency
mistaken for seizures. of each type of event separately.
Clinical Presentations
PSYCHOGENIC NONEPILEPTIC
SEIZURES (PNES) A major role of epilepsy monitoring units is the dif-
ferentiation of epileptic seizures from PNES, and
PNES are emotionally-triggered attacks that resemble video-EEG monitoring has helped analyze the semi-
seizures, but are not associated with epileptic seizure ology of nonepileptic seizures. The spectrum of clini-
activity. Approximately 20% of patients present- cal presentations of non-epileptic seizures is almost as
ing to an epilepsy center with intractable epilepsy broad as that of epileptic seizures. PNES semiology can
are found to have nonepileptic seizures. The term be classified in three categories: PNES with generalized
nonepileptic seizures is preferable to the term pseudo- shaking, PNES with minor motor activity, PNES with
seizures. Psychogenic nonepileptic seizures (PNES) or motionless unresponsiveness or collapse (Groppel
252
Differential Diagnosis 253
Table 6-1 Disorders Often Mistaken for Seizures

Disorder Features
Psychogenic Psychogenic event that resembles a clinical seizure but is not due to abnor-
non-epileptic seizure mal electrical discharge and not associated with ictal abnormalities on EEG.
Psychological disorder.
Syncope Episodic loss of consciousness due to hypo-perfusion of the brain.
Wide variety of causes including arrhythmia, vasovagal syncope, orthostasis.
Breath-holding spells Children may hold their breath until they lose consciousness.
Subsets include pallid and cyanotic breath-holding spells.
Cough syncope Loss of consciousness associated with decreased cerebral perfusion.
Most often seen in individuals with COPD, asthma, or other causes of
chronic cough.
Sleep myoclonus Periodic jerks of the extremities during sleep.
Interferes with quality of sleep.
Parasomnia Include night terrors, sleep walking, and some cases of nocturnal bed-wetting.
Can be mistaken for seizure or postictal effect.
Chorea Irregular stereotypic movements of the extremities.
Due to disorder of the basal ganglia.
Sandifer syndrome Torsional dystonia mainly involving the neck and shoulders.
(reflux) Associated with hiatal hernia and esophageal reflux.
Non-epileptic myoclonus Myoclonus during the day but not associated with EEG changes.
Startle Startle-induced seizures can be seen in patients with certain types of
epilepsy, but excessive startle alone is usually not epileptic
Transient peak toxic- Patients taking AEDs may misinterpret symptoms of peak level toxicity
ity and drug-induced as seizures. The key distinguishing features are duration (usually longer
encephalopathy than 10 minutes), type of manifestations, and relationship to AED intake.
Tiagabine may be associated with prolonged episodes of altered aware-
ness and responsiveness which may be a type of encephalopathy or
tagabine-induced absence status epilepticus.
Transient ischemic attacks Usually present with episodic loss of function due to focal ischemia
Transient global amnesia Episodes of memory loss without other cognitive disturbance
Panic attacks These can resemble some seizure manifestations of temporal lobe epilepsy
Behavioral abnormalities Repetitive movements in children with mental retardation.
in children and adults Can resemble seizure activity because of repetitive stereotypic movements.
with mental retardation
Rage attacks and violence Rage attacks and directed violence are almost never epileptic.
Non-directed violence can be epileptic, but usually is not.
et al., 2000; Meierkord et al., 1991; Selwa et al., 2000). was the most common pattern (Kramer et al., 1995).
Generalized shaking is the most common manifesta- Although there are many features that PNES have in
tion of PNES in adults and adolescents. Staring spells common with epileptic seizures, there are some dif-
can occur as well, with clinical features that could be ferentiating features (Szabó et al., 2012; DeToledo and
mistaken for absence or complex partial seizures. In Ramsay, 1996; Gates et al., 1985; Avbersek and Sisodiya,
children, prolonged staring and unresponsiveness 2010; Chung et al., 2006; Azar et al., 2008).
Clinical features that may suggest PNES as opposed of how epileptic seizures and nonepileptic seizures
to generalized tonic-clonic seizure include: can manifest. Vagal nerve stimulation (VNS) has
• Responsiveness during a generalized convulsive even been placed in patients in whom PNES was ulti-
seizure; mately documented (Arain et al., 2011). Video-EEG
• Seizure usually precipitated by suggestion; monitoring with recording of typical attacks is cru-
• Forward pelvic thrusting; cial for the definitive diagnosis of PNES.
• Large amplitude side-to-side head movements. Suggestion may help trigger PNES; hyperventi-
• Asynchronous or alternating jerking of the two lation and photic stimulation are preferred sugges-
sides (as opposed to synchronous jerking); tion techniques, since they are usually standard for
• Absence of whole-body rigidity before general- all patients. If other suggestion methods are used,
ized jerking. they should not involve patient deception. It is also
• Seizure can be terminated by the examiner by important to keep in mind that some individuals are
non-pharmacological means such as suggestion suggestible and suggestion may precipitate atypical
• Abrupt termination of the seizure, without a events. Family members have to view the recorded
postictal period; events and verify that they are typical for recorded
• Eyes closed during an event, particularly if there attacks.
is reistance to eye opening (DeToledo and It is important to keep in mind that some epileptic
Ramsay, 1996). seizures may have no scalp EEG correlate; examples
• Shallow rapid respiration (as opposed to sterto- include cingulate or orbitofrontal complex partial
rous respiration) seizures, supplementary motor seizures, and motor
simple partial seizures. It is often necessary to record
No single clinical feature is sufficient for diagnosis; multiple attacks to evaluate if events are stereotyped.
combination of features increases their value. Many of Frontal lobe seizures tend to be very stereotyped. In
the above clinical features are reported in frontal lobe addition, they may demonstrate increased severity in
complex partial seizures; PNES tend to be prolonged association with AED withdrawal. Secondary gen-
in duration, while frontal complex partial seizures are eralization is usually definitive proof that the initial
short in duration (Saygi et al., 1992). manifestations are epileptic.
PNES usually do not start out of sleep. Seizures Urinary incontinence has been considered by
that clearly arise out of sleep are usually epilep- some to be a differentiating feature between epilep-
tic. However, PNES may arise out of a waking state tic and non-epileptic events, but this is not the case
by EEG while the patient clinically appears asleep if one depends on history; urinary incontinence has
(pseudosleep). no significant differentiating value between epileptic,
nonepileptic, and syncopal events (Brigo et al., 2013;
Peguero et al., 1995 ).
Other features that favor PNES include: Tongue biting occurs more commonly with
• Discontinuous clinical seizure activity. epileptic generalized tonic-clonic seizures, but is
• Prolonged seizure duration (pseudostatus epilep- also frequently reported by patients with PNES
ticus is common in patients with PNES) (Peguero et al., 1995). Epileptic seizures are associ-
• Eye fluttering ated with biting the side of the tongue, while PNES
• Dramatic vocalizations of choking, gagging or are more likely to be associated with biting the tip
gasping of the tongue or the lip (DeToledo and Ramsay,
• Stuttering 1996).
• Weeping and other emotional display
• Excessive variability in seizure manifestations
EEG Manifestations
Despite these general guidelines, experienced neu- EEG during nonepileptic seizure is normal, although
rophysiologists are commonly wrong in clinical muscle and movement artifact may obscure the
diagnosis of seizures because of the broad spectrum recording. Evaluation of the recording may depend
Figure 6-1: EEG with a Non-Epileptic Seizure. Top shows baseline EEG, Bottom shows EEG during non-
epileptic seizure.
on observing the EEG background immediately Evolution of EEGs of Nonepileptic Seizure

before and after the clinical seizure. Epileptic sei- with Tremor
zures have a slow and/or suppressed background
after the seizure, whereas non-epileptic seizure Figures 6-4 through 6-7 are the recordings of a
shows an EEG background that returns to normal 26-year-old female with recurrent psychogenic
immediately after the seizure artifact subsides (see non-epileptic seizures. The rhythmic activity repre-
Figure 6-1). sents artifact due to rhythmic coarse tremor.
This patient shows movement and muscle Figure 6-4 shows rhythmic activity associ-
artifact, but there is no electrocerebral discharge ated with clinical seizure activity, which could
associated with the clinical seizure activity. easily be confused with epileptiform activity. The
Movement during an epileptic or non-epileptic sei- normal background is replaced by growing artifact
zure can obscure the EEG, so that visualization or from movements. There are no spikes in associa-
non-visualization of electrographic seizure activ- tion with the slow activity. In addition, the fre-
ity is not possible. The EEG activity immediately quency does not evolve during the course of the
before and after the clinical seizure activity is eval- activity.
uated to determine whether there is an abnormal- The page shown in Figure 6-5 directly follows the
ity that makes it more or less likely to be epileptic. page shown in Figure 6-4. The repetitive slow activity
This differentiation is described in Table 6-2 (see continues at a constant frequency, without evolution
also Figures 6-2 and 6-3). in appearance of rhythm.
Table 6-2 Differentiation of Epileptic from Non-epileptic Events

Feature Epileptic event Non-epileptic event
EEG before event May be normal or show focal or general- Normal EEG
ized discharges prior to the clinical seizure
EEG during event Electrocerebral discharge during the No electrocerebral discharge during
seizure the episode.
Muscle and movement artifact may
obscure the recording.
EEG after event May show slowed activity or attenuation Normal, no postictal slowing or
after the seizure attenuation.
Figure 6-2: Normal EEG Prior to a Non-Epileptic Seizure.
The last epoch of EEG (Figure 6-6) shows the end Termination of the seizure is associated with restora-
of the seizure, where the amplitude of the activity tion of the normal background.
reduces until normal background returns. There is not Observation of the same seizure at a slower time
background slowing or attenuation, although reduc- base (Figure 6-7) shows the monorhythmic charac-
tion in amplitude results in appearance of attenuation, ter of the clinical seizure, quite different from the
especially if gain was reduced during the episode. appearance of an epileptic seizure.
Figure 6-3: Non-Epileptic Seizure (Same Patient as in Figure 6-2).
Figure 6-4: Evolution of a Non-Epileptic Seizure—Beginning of the Seizure.

Figure 6-5: Continuation of a Non-Epileptic Seizure. Monorhythmic Electrical Activity with the Tremor.

The background is obscured.
Figure 6-6: Continuation of a Non-Epileptic Seizure. Termination of the Clinical Seizure Activity.

Figure 6-7: Non-Epileptic Seizure at Slower Time Base.
SYNCOPE with no preceding lightheadedness. Among the car-

diac causes are both brady- and tachy-arrhythmias.
Overview
Orthostatic hypotension is characterized by light-
Episodic disturbance of consciousness includes not headedness and syncope when the patient arises to
only seizure activity but also syncope. Syncope is a stand (Carreño, 2008; Crompton and Berkovic,
transient loss of consciousness due to loss of brain 2009). Basilar migraine is commonly associated with
perfusion, but the differential diagnosis of this final dizziness that is more akin to true vertigo than presyn-
common path is wide. copal sensation. Migraine, in general, can be associ-
ated with syncope due to autonomic instability (Thijs
et al., 2006) Likewise, vertebrobasilar insufficiency
Causes of Syncope can be associated with syncope as a component of the
symptoms, but dizziness and ataxia are more com-
The causes of syncope are multiple, some of which include: mon symptoms.
• Cardiac arrhythmia;
• Orthostatic hypotension;
Differentiation of Syncope from
• Vasovagal (“neurocardiogenic”) syncope;
Seizure Activity
• Orthostatic hypotension;
• Migraine; Differentiation of syncope from seizures is often a
• Vertebrobasilar insufficiency. focus of neurologic consultation. While syncope is
best recognized by loss of consciousness, loss of tone
Most causes of syncope are preceded by a sensation of and loss of posture, most individuals will have brief
light-headedness. However, the duration of this may multifocal arrhythmic myoclonus, which is a com-
not be long enough for it to be remembered. Syncope mon source of misdiagnosis of epileptic seizures
due to cardiac arrhythmia may also be more abrupt (Lempert et al., 1994). Syncope with myoclonus has
been called “convulsive syncope”, but the myoclonus even to experienced clinicians. EEG can help dif-
is of brainstem origin, not cortical in origin. In addi- ferentiation. In both types of spells, the EEG
tion to myoclonus, patients with syncope may have becomes suppressed and, depending on duration,
posturing, head turning, lateral or upward eye devia- virtually flat.
tion, or oral automatisms.
Some differentiating features are: Cough Syncope
• Syncope can be triggered by certain activities, During prolonged coughing, intrathoracic and
unexpected with seizures. Examples include intra-abdominal pressures are transmitted via the
intense pain, intense emotion, standing for great veins to the intracranial compartment, causing
prolonged periods of time in hot crowded places, transient elevated intracranial pressure. The resulting
sudden standing from sitting or lying position, reduction of cerebral perfusion pressure may cause a
urination, defecation, cough. In addition, pres- critical impairment of cerebral blood flow (CBF).
ence of dehydration, known heart disease and During coughing, patients show a transient cere-
prior syncope should favor syncope. bral circulatory arrest, which coincides with loss of
• Syncope often has warning presyncopal sensa- consciousness. EEG shows slowing and attenuation
tion, such as nausea, cold sweat, lightheadedness, (see Figure 6-8).
graying of vision, sounds becoming more distant, Obstructive airway disease seems to be a prerequi-
different from common seizure auras. site to build up the intrathoracic and intracranial pres-
• The myoclonus associated with syncope is of much sures to a degree sufficient to compromise CBF and
shorter duration (usually less than 15 seconds) than cause cough syncope.
tonic-clonic activity (usually longer than 15 seconds)
• Prominent pallor described by witnesses favors
syncope although it may also be an autonomic OTHER DISORDERS MISTAKEN FOR
manifestation of some seizures. SEIZURES
• Seizures result in postictal confusion or lethargy, Movement Disorders
not expected with syncope. However, if the fall
from syncope results in concussion, there could Some movement disorders can have sufficient fast
be more confusion than expected. components that they might be confused with seizure
• Recollection of loss of consciousness favors activity. This is especially true for myoclonus but also
syncope (Crompton and Berkovic, 2009). for others including dyskinesias and hemiballismus.
Breath-holding Spells Nonepileptic Myoclonus
Breath-holding spells can be frightening to parents, Myoclonic seizures, seen in a number of epilep-
and can be mistaken for seizures or even cardiac tic syndromes, particularly juvenile myoclonic
arrest. There are two types of breath-holding: cya- epilepsy ( JME), are generated in the cortex, and
notic and pallid. usually associated with an electrical discharge at
Cyanotic breath-holding spells are characterized the scalp. However, myoclonus can also be non-
by a brief cry, followed by apnea in end-expiration. epileptic, and can be generated at any level of the
The child becomes cyanotic and unconscious central nervous system. Essential myoclonus is epi-
because of hypoxia. A few minutes later, the child sodic jerking not associated with other epileptic or
awakens. degenerative disease. There are either no other neu-
Pallid breath-holding spells are characterized by rologic signs, or there may be dystonia or tremor.
little or no cry, followed by asystole, resulting in the Inheritance can be dominant or sporadic. The dom-
pallid appearance. The child is pale and lifeless. The inant essential myoclonus usually presents before
child becomes awake and normal color in minutes. the age of 20 years. The movements disappear in
Diagnosis of breath-holding spells depends sleep. Treatment of benign myoclonus is usually not
on observation, and the spells can be frightening, needed.
Figure 6-8: Cough Syncope.
Nocturnal Myoclonus • Chorea is not associated with postictal weakness.

• Chorea is not associated with cognitive changes.
Nocturnal myoclonus is a normal phenomenon.
However, if excessive, it may interfere with the qual- When chorea is paroxysmal, it is more likely to be con-
ity of sleep. fused as epileptic. Paroxysmal dyskinesia is characterized
Nocturnal myoclonus is commonly seen as a pri- by combinations of chorea, athetosis, ballism, and a dys-
mary disorder or with restless legs syndrome (RLS), tonic posture, occurring in attacks. It is classified into two
but can also be secondary to a variety of other medical broad categories: kinesigenic and non-kinesigenic (Fahn
and neurologic conditions. and Frucht, 2008). Both conditions are usually familial.
Kinesigenic dyskinesia: The attacks of paroxys-
mal kinesigenic dyskinesia are very brief, lasting
Chorea and paroxysmal dyskinesia
seconds, and are brought on by a sudden move-
Chorea can occasionally be confused with seizure ment, particularly after inactivity. The movements
activity because of repetitive and stereotyped writh- may or may not be stereotyped, and can be bilateral
ing, twisting movements. or alternate sides. This is helpful in distinguishing
them from epileptic seizures which tend to consis-
Differentiation of chorea from seizure is aided by the
tently affect the same side. As with other movement
following features:
disorders, consciousness is always preserved, and
• Chorea is associated with maintained ability to there is no postictal change. However, the condition
move the limbs, even during the episode of invol- responds very well to antiepileptic drugs which are
untary limb movement. effective in preventing recurrence of attacks.
• Chorea is present only in the waking state and Nonkinesigenic dyskinesia: The attacks in par-
disappears during sleep. oxysmal nonkinesigenic dyskinesia are longer,
lasting minutes to hours. They are not precipitated Paroxysmal nocturnal dystonia
by movement, but can be brought on by a variety of
factors such as stress, fatigue, excitement, alcohol, or Paroxysmal nocturnal dystonia is episodic abnormal
caffeine. This condition does not usually respond to movements and postures in sleep. These were thought
antiepileptic drugs. to be a movement disorder as they were not associ-
ated with scalp EEG changes. However, investigation
Hemiballismus with intracranial electrodes has indicated that these
are indeed mesial frontal seizures.
Hemiballismus is violent movements of one side of
the body. The movements are most marked in the Sleep disorders
proximal muscles. The flailing of the limbs can result
in injury to the patient. Parasomnias
Hemiballismus is due to damage to the subthalamic
nucleus, with stroke being the most common cause. Parasomnias are disorders of sleep characterized by
Hemiballismus can be mistaken for seizure activ- “undesirable physical events or experiences that occur
ity, but can be differentiated by preservation of con- during entry into sleep, within sleep, or during arous-
sciousness and movement of the affected side, normal als from sleep”. [Thorpy, 2012; American Academy of
EEG during the movement, and irregular appearance Sleep Medicine, 2005.] They can be subdivided into
of the movements. disorders of arousal from non-REM sleep, parasom-
nias associated with REM sleep, and other parasom-
Hyperekplexia nias. (see Table 6-3).
In general, parasomnias tend to occur in younger
Hyperekplexia is characterized by exaggeration of star- patients, children and young adults. Some have a
tle reflexes (Crompton and Berkovic, 2009). The exag- familial basis. Parasomnias can be mistaken for sei-
gerated startle can be mistaken for a startle-evoked zures, particularly frontal lobe seizures which often
seizure. Hyperekplexia is an inherited disorder, most arise out of sleep. Differentiation depends on careful
often with an autosomal dominant transmission. history and observation. Video EEG monitoring can
Table 6-3 Sleep disorders that could be mistaken for seizures.

Disorder Features
Restless legs syndrome Motor restlessness associated with discomfort or pain and urge to move.
Sleep myoclonus Jerking of the legs, which can cause arousal. Differentiated from seizure in
part by occurrence of single jerk and arousal.
Hypnic jerks Brief jerks at sleep inception. Differentiated from seizures in part because
they are single jerks and not seen in deep sleep.
Rhythmic movement Rocking of the head or body, especially in young children, often misinter-
disorder preted as seizure activity. Head banging is the most common type.
Sleep walking Occasionally confused with seizure because the patient may appear
confused as if postictal.
Sleep talking Seldom confused with seizures in the absence of other symptoms.
Sleep terrors and Abrupt awakening with fright; sleep terrors are from non-REM sleep,
nightmares nightmares are from REM sleep.
REM behavior disorder Motor activity during dreaming can be vigorous and even violent, but
differs from stereotyped movements of nocturnal seizures.
Enuresis Losing control of bladder at night can suggest seizure, but this would sel-
dom be the only sign.
aid in the differential diagnosis, although this is sel- are frightening dreams, the details of which are
dom needed. recalled, an important distinguishing feature from
Arousal parasomnias: Sleep walking, sleep terror, sleep terror. Nightmares often result in awakening
and confusional arousals are arousal parasomnias from sleep with anxiety. Upon awakening there is
that occur with partial awakening out of slow wave full alertness, with no confusion or disorientation,
sleep, the deepest non-REM sleep, usually within 1 unlike the case with night terrors. While single
to 3 hours after sleep onset. With all arousal parasom- nightmares are common in normal individuals,
nias, the child usually has no memory of the events. recurrent nightmares represent a disorder. REM
These parasomnias cause concern in family members. behavior disorder is motor activity during dream-
With sleep walking, patients are found to be walking ing. The physiology is thought to be pathological
around or standing. The eyes are open and there may absence of normal sleep paralysis that should be
be partial responsiveness. When the patient is stimu- present during REM. The behavior can be quite
lated, arousal is often accompanied by confusion violent, including punching, kicking, and running
and disorientation for a brief time. With confusional movements. REM behavior disorder is more likely
arousals the child may be found seated in bed with in the second half of the night when REM is more
eyes open, appearing alert, but unresponsive. Again, if prevalent. It is more common after age 50 years, with
awakened, the child will be confused and frightened. strong male predominance. It may be seen in some
Sleep terrors have more extreme manifestations, with normal patients, particularly as a transient effect of
screaming, crying, facial expression of terror, agita- some medications or medication withdrawal. When
tion, and thrashing. There is often associated sweat- it is a chronic disorder it is more common in some
ing, tachycardia and tachypnea. The duration is a few neurologic disorders, particularly Dementia with
minutes, and the patient then goes back to sleep. Sleep Lewy Bodies and Parkinson’s disease.
terrors are more common in children, and become
less prevalent with increasing age. The distinction of REM behavior disorder from fron-
tal lobe seizures is based on the following features:
The distinction between arousal parasomnias and • The age at onset of REM behavior disorder is usu-
nocturnal frontal lobe seizures is based on the follow- ally over 50, later than usual for nocturnal frontal
ing clinical features (Tinuper et al., 2012): lobe epilepsy
• Arousal parasomnias tend to have an earlier age • The REM behavior disorder episodes occur in
at onset than nocturnal frontal lobe seizures, and association with dreams, usually in the second
tend to resolve with increasing age, unlike frontal half of the night. Frontal lobe seizures occur at
lobe seizures. any time during sleep.
• Arousal parasomnias typically occur once in a • The patients remember their dreams, and the
night, infrequently, while frontal lobe seizures are behaviors in sleep are consistent with dream
more frequent, often with several in one night. content.
• Arousal parasomnias last several minutes, while • After arousal from REM behavior disorder, the
frontal lobe seizures usually last less than one patient is lucid and oriented.
minute.
• Episodes in arousal disorders can vary in clinical Sleep talking is a common disorder which affects
manifestations, while frontal lobe seizures are normal people and is increased in incidence with cer-
very stereotyped. tain disorders. In older adults, dementia is commonly
• Posturing is not usually present in arousal para- associated with development of sleep talking. Sleep
somnias, while common in nocturnal frontal lobe talking occurs most frequently in Dementia with
complex partial seizures. Lewy Bodies, where it also tends to be loud (Honda
et al., 2013). Sleep talking is seldom confused with sei-
REM parasomnias arise out of REM sleep zure activity in the absence of other symptoms.
and include nightmares and REM behavior dis- Other parasomnias include a large number of
order. These are more likely in the last half of the conditions only some of which are potentially con-
night when REM sleep predominates. Nightmares fused with seizures. Enuresis is seldom confused
with seizure activity, although this, along with find- Migraine and Migraine Equivalent
ing blood on a pillow, make the thoughtful patients
or parents have concern over unobserved nocturnal Migraine can rarely cause episodic symptoms that
seizure activity. These findings are not commonly due can be mistaken for seizure activity (Carreño, 2008;
to seizure in the absence of other manifestations. Kossoff and Andermann, 2010).
The types of migraine most likely to be confused with

Sleep related movement disorders
seizure activity are:
Restless legs syndrome: RLS is motor restless of the legs • Classical migraine with visual aura. Migraine with
which can affect patients day or night, but is worse in visual aura can be difficult to distinguish from
the evening or night. The main criterion for diagnosis occipital lobe seizures, which may be followed by
is an urge to move the legs caused by uncomfortable a migraine-like headache. Distinguishing features
sensations. The manifestations worsen or start dur- include
ing inactivity and are relieved by movement. In the • The migraine aura is longer than visual seizures
differential diagnosis of seizure, patients may report (5 to 60 minutes as compared to less than 30
twitching of the legs and may emphasize violent jerk- seconds).
ing which could suggest seizure activity. Sleep myoc- • The visual aura in migraine is most commonly
lonus is often seen in patients with RLS. a fortification spectrum or scintillating sco-
Sleep myoclonus: Sleep myoclonus is episodic jerking toma, whereas the most occipital lobe seizure
of lower leg muscles. The jerks can interfere with not aura is colored circles.
only the sleep of the patient but also with sleep of the • Classical migraine with sensory aura. Both
spouse. Sleep myoclonus is often familial and often seen sensory seizure and migraine can have a sensory
in patients with RLS, as discussed below. Sleep myoclo- march, but the sensory march is much shorter in
nus is differentiated from seizure by the occurrence only duration in sensory seizures.
during sleep, single and irregular nature of the jerks, and • Acute confusional migraine.
absence of ictal or interictal abnormalities on EEG. • Migraine without headache, or migraine
Hypnic jerks: Hypnic jerks are the brief jerks which equivalent.
interfere with descent into sleep. They may involve a • Basilar migraine.
single limb or the entire body. They are differentiated
Episodic vertigo and syncope can be a sign of basilar
from seizure activity by the single nature of the jerks,
migraine. One example is a 9-year-old female with epi-
absence of occurrence in awake state or deep sleep. This
sodes that occur about every other day. She becomes
is a common condition which is considered normal.
irritable and whiny, and this is followed by develop-
Sleep-related rhythmic movement disorder: this is
ment of ataxia. She used to become unresponsive, but
a stereotyped rhythmic movement disorder affect-
treatment with levetiracetam has resulted in improve-
ing the head, body or extremities, which can occur
ment in this manifestation. Duration is 30–45 minutes.
with the patient either supine or prone or even on
The first sample, shown in Figure 6-9, is the base-
hands and knees. The rocking can cause movement of
line normal EEG. This is followed by high-voltage
the bed or actual banging of the head into the head-
bursts of delta activity (Figure 6-10). Note the sensi-
board, which may be mistaken for seizure activity.
tivity of 30 μV/mm.
The behaviors may result in injury. Young children
are most commonly affected. Head banging and other Reflux
sleep-related rhythmic movement disorder may occur
during any stage of sleep. Parents may have difficulty Sandifer syndrome is torsional dystonia of the neck
awakening the children, solidifying their concern over and upper arms. This is due to reflux, although the
seizure activity. The behavior usually lasts less than 15 exact pathophysiology is not known. Children with
minutes at a time, but may repeat through the night. reflux can present with apnea, with or without motor
Differentiation from seizure activity is mainly by activity that can suggest seizure activity. This, however,
description of the activity. Video-EEG monitoring or is an atypical presentation of reflux; episodic vomit-
polysomnography are rarely necessary for diagnosis. ing, poor feeding, and weight loss are more common.
Figure 6-9: Confusional Migraine—Between Episodes.
Figure 6-10: Confusional Migraine—During an Episode.

Diagnosis of reflux often depends on coopera- Episodic dyscontrol or intermittent

tive consultation of neurology and gastroenterology. explosive disorder
Observation during an episode is key to the diagnosis.
These are so common that observations are multiple. This is characterized by recurrent bursts of uncontrol-
lable rage with minimal provocation. The disorder
Behavioral Disorders affects children and adults. While this rage can result
in violence, it does not have to. Tension and fear as well
Behavioral disorders can be mistaken for seizure activity. as other symptoms may precede the outbursts. The
This activity can include: subject may report no memory of the events, which
• Panic attacks can raise the possibility of seizures. Seizure activity is
• Episodic dyscontrol not the cause of rage attacks, although organic brain
• Directed violence disease such as traumatic brain injury may predispose
• Non-directed violence to the disorder (Gordon, 1999; McTague et al, 2010).
• Stereotypic behaviors in cognitively impaired
individuals Directed Violence
Seizure activity has been used as a legal defense

Panic attacks for directed violence. Most physicians believe that
directed violence does not occur as a result of sei-
A panic attack is defined by the DSM-IV (Craske, zure activity. Plotting, traveling to a crime scene, and
2010) as a “discrete period of intense fear or discom- attacking an individual are highly unlikely to be due to
fort, in which four or more of the following symp- epileptic seizure activity.
toms develop abruptly and reach a peak within 10
min:
Non-directed Violence
• Palpitations, pounding heart, or accelerated heart
rate Non-directed violence can be occasionally seen as a
• Sweating component of seizure activity. Motor activity associ-
• Trembling or shaking ated with complex partial seizures may appear violent.
• Feeling of choking Biting, hitting, kicking, and scratching are uncom-
• Chest pain or discomfort mon with epileptic seizures, and when present, are
• Nausea or abdominal distress non-directed, affecting only those restraining the
• Feeling dizzy, unsteady, lightheaded, or faint patient or in proximity.
• Derealization (feelings of unreality) or deperson- Postictal states can be associated with agitation
alization (being detached from oneself) and confusion, resulting in non-directed violence,
• Fear of losing control or going crazy again especially when trying to fight restraints.
• Fear of dying
• Paresthesias (numbness or tingling sensations) Behavioral abnormalities in associa-
• Chills or hot flushes tion with mental retardation
Panic disorder is characterized by recurrent unex-
Children and adults with mental retardation may have
pected panic attacks at least one of which is followed
repetitive stereotypic movements that can resemble
by persistent concern over additional attacks, worry
seizure activity. These behaviors may provide sensory
about the implications and consequences of the
stimulation or may help alleviate anxiety. Video-EEG
attacks, or change in behavior related to the attacks.
may be necessary to evaluate the nature of the behaviors.
Some of the above manifestations of panic attacks
may be seen with epilepsy, particularly temporal lobe
epilepsy. If panic attacks are associated with altered Startle
consciousness, then epileptic seizures have to be con- All of us normally have alerting reactions in response
sidered as a more likely alternative. to stimuli that we consider to be novel and important.
In startle syndrome, the alerting response is enhanced. but it is unlikely that this could be confused with
This can be present in some patients for unknown rea- seizure activity.
sons, can be inherited, or can be acquired due to CNS Tiagabine is an uncommonly used AED, espe-
disease. cially for partial seizures. Some patients treated with
Hyperekplexia was discussed briefly above and tiagabine may develop episodes of altered respon-
is an inherited disorder in which there is exagger- siveness and awareness, lasting up to hours. It is not
ated startle. An unexpected even relatively minor totally clear if this is an encephalopathy or a type
stimulus results in transient stiffness followed by of nonconvulsive status epilepticus of the absence
a fall. Hyperekplexia has to be distinguished from variety. Recent reports have shown generalized slow
epilepsy. activity in association with the encephalopathy.
Startle-induced seizures occur in some epilepsies, Reduction in dose of the tiagabine results in disap-
particularly frontal lobe epilepsy originating in the pearance or decreased severity of the episodes (Azar
supplementary motor area. Stimulation induces sei- et al., 2013).
zure activity with a startle-like stiffening of the body.
In contrast to other startle conditions, there is an elec- Transient ischemic attacks
trographic discharge evident with this (Dreissen and
Tijssen, 2012). Transient ischemic attacks (TIAs) are a result of
focal transient cerebral ischemia. The main features
that help distinguish them from seizures are:
Peak toxicity of AEDs
• Chorea is associated with maintained ability to
Patients taking AEDs may misinterpret symptoms of move the limbs, even during the episode of invol-
peak level toxicity as seizures. This is more likely with untary limb movement.
some AEDs, particularly those acting on the sodium • TIAs usually manifest with loss of function,
channel. Symptoms may include blurred vision, while seizures usually manifest with positive
double vision, dizziness, unsteadiness, and confu- manifestations. For example, TIAs involving
sion. These manifestations can be distinguished from motor cortex or motor pathways usually mani-
seizures by fest with weakness, while seizures involving
motor cortex most often manifest with tonic,
• Longer duration (usually longer than 10 clonic, or myoclonic activity. Rarely, TIAs
minutes). with high-grade stenosis or occlusion of the
• Manifestations of blurred vision or double vision internal carotid artery present with limb shak-
unlikely during seizures. ing (Persoon et al, 2010). One feature that could
• The symptoms are temporally related to AED distinguish “limb shaking TIAs from seizures is
intake. precipitation by changing to upright position or
• The symptoms are more likely with taking the by exercise. On the other hand, rarely seizures
AED on an empty stomach and less likely if the also may manifest with focal weakness or
AED is taken with food. paralysis (Abou-Khalil et al, 1995).
• The symptoms subside with reducing or dividing • Somatosensory TIAs are more likely to mani-
the dose, or after switching to an extended release fest with sensory loss, while somatosensory
preparation. seizures are more likely to cause paresthesias,
burning or pain. A sensory Jacksonian march
Drug-induced Encephalopathy is suggestive of seizure activity, although
s sensory march may also be seen with
Encephalopathy is the most common cause for migraine. The sensory march of migraine is
neurological consultations in most hospitals. much slower
Patients have confusion, memory loss, or other • TIAs usually last longer than seizures. Most
cognitive deficits. Occasional patients may have seizures last less than 2 minutes, while most TIAs
myoclonic activity and others may have tremor, are longer than 5 minutes.
Transient global amnesia lasts hours, but recovers within 24 hours of onset.
Older individuals are more likely to be affected.
Transient global amnesia is an episode of memory Single isolated attacks occur in most instances, but
loss without impairment of other cognitive func- attacks may repeat in a minority of individuals. The
tion. Affected subjects do not forget their identity pathophysiology of transient global amnesia is not
and are still able to engage in complex activities totally clear and may be different in different indi-
during the attacks. Transient global amnesia usually viduals (Hunter, 2011).
7
SEIZURE MANAGEMENT
MEDICAL may be warranted in such cases, provided a seizure

recurrence does not involve undue risk to the patient
or to the patient’s career.
Initiation of Therapy
Single provoked seizure due to metabolic derange-
ment/toxic exposure, acute head injury, or other
If and When to Initiate Therapy
limited central nervous system (CNS) insult does
Anti-epileptic drugs (AEDs) are prescribed for most not necessarily demand AED therapy. If the seizures
but not all patients with seizures. Some of the clini- recur, then initiation of therapy appropriate to the sei-
cal scenarios that may not require medical treatment zure type is warranted. The duration of treatment is
include: dependent on how quickly the provoking factor can
be reversed. It can be for only a few days. If the pro-
• Single unprovoked seizure; voking factor cannot be immediately reversed, such as
• Provoked seizure(s); the case with an inflammatory process, the duration
• Benign epilepsy of childhood with centrotempo- of treatment may be as long as several months. Febrile
ral spikes (BECTS) with infrequent seizures; seizures usually do not need long-term seizure medi-
• Juvenile myoclonic epilepsy ( JME) with myo- cine. The risk of recurrence is 30–40% but multiple
clonic seizures only. recurrences are infrequent. Children with frequent
recurrences can be treated with oral or rectal diaz-
A single unprovoked seizure has a relatively low risk epam at the time of illness.
of recurrence with a normal neurologic exam, nor- Benign epilepsy with centrotemporal spikes
mal MRI, and normal EEG (see Figure 7-1). Risk of (BECTS) may manifest with seizures that are infre-
recurrence after a single unprovoked seizure is about quent, occur mainly at night, and spontaneously
40–50% overall at 2 years. However, patients with remit before driving is an issue, so treatment is not
normal neurological examination, normal imaging, always necessary.
and normal EEG have a significantly lower rate of JME in selected patients might be relatively mild,
approximately 25%. Observation without treatment manifesting with only myoclonic seizures. It may be
269
First Seizure Therapy

First seizure provoked
No Yes
Normal MRI and EEG; no Provoking factor

risk factors for recurrence; resolved or can be
seizure was not severe rapidly resolved?
False True False True

Seizure recurrence
unlikely to have
Treatment x2
major psychosocial Short-term No treatment
yrs
consequences treatment until
provoking factor If MRI or EEG
is resolved are abnormal,
False True
consider an
AED
Treatment x2 (provocation
yrs No treatment may have been
apparent, not
real)
Figure 7-1: First Seizure Therapy Algorithm.
managed by self-help guidelines (e.g., avoid sleep this guideline in patients with infrequent seizures.
deprivation, alcohol binges, and certain medications). For these patients it is best for the initial target dose
In these patients AEDs may not be needed. However, to be a “middle of the road” dose. Below are the rec-
unlike with BECTS, this is a relatively small propor- ommended initial treatment options, depending on
tion of the JME patient population. seizure classification.
Recurrent Unprovoked Seizures Partial

Recurrent unprovoked seizures usually deserve AED
therapy. With more than one unprovoked seizure, the Partial-onset seizures have traditionally been treated
risk of recurrence is much more likely than not. More with carbamazepine or phenytoin. However, these
than two-thirds of individuals will have a seizure older agents have been largely replaced by some of
recurrence. Treatment is usually initiated with a single the newer AEDs, which have pharmacokinetic and
AED. It is preferable to start at a low dose and titrate tolerability advantages (see Table 7-1). Among the
slowly, unless there is a reason for urgency. For many new AEDs, FDA approval has been given for oxcar-
AEDs, the starting dose can be even lower than rec- bazepine and topiramate as first-line treatments.
ommended in the prescribing information. The initial However, good clinical evidence supports the effec-
target dose is usually the smallest dose found effectiveness of lamotrigine, levetiracetam, and gabapen-
tive in clinical trials. However, for some AEDs an even tin. Lamotrigine seems to be particularly attractive
smaller dose has been found effective after marketing. due to favorable tolerability (particularly less effect
For example, lamotrigine 125–200 mg per day was suf- on cognition and alertness) but the slow titration is
ficient for seizure control in most patients with new a limiting factor when rapid onset of action is needed.
onset epilepsy, while the smallest dose found effec- However, even in this situation, it is worthy of con-
tive in add-on trials was 300 mg per day (Kwan and sideration for later transition. The large Standard and
Brodie, 2001). If the initial target dose is not sufficient New Antiepileptic Drug (SANAD) trial compar-
to control seizures, the dose can then be increased ing lamotrigine, carbamazepine, gabapentin, oxcar-
gradually until seizure control is achieved or adverse bazepine, and topiramate in partial epilepsy favored
effects appear. There is an important exception to lamotrigine for the primary outcome measure,
Seizure Management 271
Table 7-1 Anti-epileptic Drugs
Drug Clinical use
Carbamazepine Partial-onset, generalized tonic-clonic (may aggrevate myoclonic and absence
(Tegretol) seizures),
Clobazam (Onfi) Lennox-Gastaut syndrome.
Clonazepam (Klonopin) Lennox-Gastaut (absence type, atonic, and myoclonic seizures) as adjunctive
or monotherapy.
Ethosuximide Absence
(Zarontin)
Ezogabine (Potiga) Partial-onset seizures in adults as adjunctive therapy.
Felbamate (Felbatol) Partial-onset seizures in adults.
Only for highly refractory cases.
Adjunctive therapy for generalized seizures in children with Lennox-Gastaut
Gabapentin (Neurontin) Adjunctive therapy for partial-onset seizures.
Lacosamide (Vimpat) Adjunctive therapy for partial-onset seizures.
Lamotrigine (Lamictal) Adjunctive therapy for partial-onset, primary generalized tonic-clonic, gener-
alized seizures of Lennox-Gastaut.
Monotherapy for partial-onset seizures.
Levetiracetam (Keppra) Adjunctive therapy for partial-onset seizures, myoclonic seizures of JME,
primary generalized tonic-clonic seizures in patients with idiopathic general-
ized epilepsy.
Initial monotherapy for partial-onset and primary generalized tonic-clonic
seizures.
Methsuximide Absence seizures refractory to other AEDs.
(Celontin) May be used as adjunctive therapy for partial-onset seizures resistant to other
AEDs.
Oxcarbazepine Partial seizures as monotherapy or adjunctive therapy in adults and children.
(Trileptal)
Phenobarbital Broad range of seizures except absence.
(Luminal)
Phenytoin (Dilantin) Tonic-clonic, partial-onset, post-operative seizures (May aggravate myoclonic
and absence seizures).
Primidone (Mysoline) Broad range of seizures including primary generalized tonic-clonic,
partial-onset seizures. Used alone or in combination.
May also be effective for myoclonic seizures.
Pregabalin (Lyrica) Partial-onset seizures in adults as adjunctive therapy.
Rufinamide (Banzel) Lennox-Gastaut
Tiagabine (Gabitril) Partial-onset seizures as adjunctive therapy
Topiramate (Topamax) Adjunctive therapy or initial monotherapy for partial-onset or primary gener-
alized tonic clonic seizures.
Adjunctive therapy for seizures associated with Lennox-Gastaut syndrome
Valproate (Depakote, Broad range of seizures including partial-onset seizures as well as
Depakene, Depacon iv) generalized-onset seizures (including absence).
Vigabatrin (Sabril) Adjunctive therapy for adults with refractory partial-onset seizures, who have
tried several alternatives and in whom the potential benefits outweigh the
potential loss of peripheral vision.
Zonisamide (Zonegran) Partial-onset and generalized-onset seizures in adults as adjunctive therapy.
Monotherapy fo partial-onset seizures supported by recent study.
balancing efficacy and tolerability (Marson et al., 2 years old. Also more common in children are rash
2007). Topiramate also requires a slow titration, and it from lamotrigine, and behavioral effects of some
has important cognitive potential adverse effects. As a medications such as phenobarbital and levetiracetam.
result, it is usually not a first-choice treatment, unless On the other hand, children under 13 do not seem at
there is comorbidity such as migraine and obesity. risk of aplastic anemia from felbamate.
When rapid onset of action is needed, the new AEDs Older age predisposes to hyponatremia from
to be considered as first-line treatment are levetirace- carbamazepine and particularly oxcarbazepine.
tam and oxcarbazepine. Seniors also are more likely to experience the com-
mon adverse effects of somnolence and ataxia. Also,
Generalized seniors are more likely to be on multiple drugs,
hence a predisposition to drug-drug interactions.
Absence seizures: Ethosuximide is the drug of choice Lastly, seniors are more likely to have reduced
for initiating therapy in most patients with general- hepatic and renal clearance, requiring consideration
ized absence seizures. If the patient has coexistent in dosing. In general, lamotrigine and gabapentin
generalized tonic-clonic or myoclonic seizures, then are better tolerated in the elderly than carbamaze-
valproate is a better choice. Lamotrigine was found pine (Rowan et al., 2005). However, administering
to be less effective than ethosuximide and valpro- carbamazepine in an extended release preparation
ate for absence seizures in a large comparative trial improves its tolerability.
(Glauser et al., 2010). Nevertheless, it is an impor-
tant option in a woman of childbearing potential Pregnancy and Childbearing Potential
(due to valproate teratogenicity) or in a man with
comorbidities that prohibit the use of valproate Many patients taking anti-epileptic drugs are women
(such as obesity). of childbearing age. While many of these are taking
Idiopathic generalized epilepsy with generalized the medications for epileptic indications, a consider-
tonic-clonic seizures: Valproate appears to be the most able number are taking them for other uses, includ-
effective agent and is the drug of choice for men, but ing migraine prophylaxis and psychiatric indications.
because of the risk of birth defects and other develop- When a woman considers pregnancy or becomes
mental abnormalities, lamotrigine and levetiracetam pregnant, cessation of medications is considered, but
are preferable first-choice options for women with this is potentially unsafe when AEDs are given for
childbearing potential. epilepsy; there are considerable risks to the mother
Generalized myoclonic seizures: Valproate is as well as potential deleterious effects of uncontrolled
likely the most effective agent as monotherapy. seizures to the fetus. In addition, by the time the
Levetiracetam is approved for adjunctive therapy but patient is found to be pregnant, much of the terato-
may also be effective in monotherapy. Other agents genicity on major organs has already taken effect, so
have weaker evidence for efficacy and no FDA indi- cessation of the AED at that point does not protect
cation. Lamotrigine may be effective in some indi- against major organ birth defects.
viduals, but may also exacerbate myoclonic seizures To lower the incidence of birth defects in women
in others. Topiramate, zonisamide and benzodiaz- with epilepsy and to optimize pregnancy outcome,
epines may also be effective in some individuals (see it is essential to have a discussion of changes in AED
Table 7-2). therapy prior to planned pregnancy. While there is
debate about which AEDs are safest, there are AEDs
Considerations in Therapy to be avoided. The FDA has a classification that pro-
vides a general guideline regarding safety in preg-
Age nancy (see Table 7-3).
Age plays a complex role in drug selection, mainly FDA pregnancy classification:
in relation to medication tolerability and safety. The • Category A: Safe in humans—studies have failed
best-known age-related association is hepatic fail- to demonstrate a risk to the fetus in the first
ure with valproate, most common in children under trimester of pregnancy.
Table 7-2 Spectrum of Efficacy

Anti-epileptic Seizure type indication
drug
Partial Generalized Generalized Generalized Tonic/atonic in the
tonic-clonic Absence Myoclonic setting of Lennox-
Gastaut syndrome
Phenobarbital FDA – – –
Primidone FDA – + –
Phenytoin FDA – – –
Methsuximide + – FDA – –
Ethosuximide – – FDA – –
Clonazepam + + FDA-A FDA-A FDA-A
Carbamazepine FDA – – –
Valproate FDA-M ++ FDA-M ++ ++
Vigabatrin* FDA-A – – – –
Felbamate FDA- A/MC + – – FDA- A
Gabapentin FDA- A – – – –
Lamotrigine FDA- MC/A FDA- A + +/– FDA- A
++ MI
Topiramate FDA- MI/A FDA- A +/– + FDA- A
Tiagabine FDA- A – – – –
Levetiracetam FDA- A FDA- A + FDA-A +/–
++ MI
Oxcarbazepine FDA- MI/A – – – –
Zonisamide FDA- A + + + +
++ MI
Pregabalin FDA- A – – – –
Lacosamide FDA- A – – – –
Rufinamide + – – – FDA– A
Clobazam + + + + FDA– A
Ezogabine FDA- A – – – –
Perampanel FDA- A – – – –
FDA = FDA-approved indication without specification as to adjunctive versus monotherapy indication.
FDA-A = FDA-approved indication for adjunctive therapy
FDA-MI = FDA-approved indication for initial monotherapy
FDA-MC = FDA-approved indication for monotherapy conversion
FDA-M = FDA-approved indication for monotherapy without specification as to initial monotherapy or conversion to monotherapy
++ = class 1–3 evidence of efficacy
++ MI = class 1–3 evidence of efficacy as initial monotherapy
+ class 4 evidence of efficacy
+/– inconsistent evidence of efficacy (some reports suggests lack of efficacy or exacerbation)
* Also approved for infantile spasms
• Category B: Safe in animals—unknown in • Category D: Adverse effect on the human

humans or adverse effect in animals, but human fetus; potential benefits may warrant use in
studies suggest it is safe. pregnancy.
• Category C: Adverse effect in animals, not enough • Category X: Adverse effect on human fetus; risks
data in humans; potential benefits may warrant clearly outweigh potential benefits in pregnancy.
use in pregnancy. • Category N: FDA has not classified this drug.
Table 7-3 AED use in renal impairment
Dose change with renal impairment Replacement after dialysis

Phenobarbital Reduce slightly based on level Supplement based on level
Primidone Reduce slightly based on level Supplement based on level
Phenytoin * No change No change
Methsuximide No change **
Ethosuximide No change Supplement one dose
Clonazepam No change No change
Carbamazepine No change No change
Valproate * No change No change
Felbamate Reduce dose by 50% **
Gabapentin Reduce dose by 50–90% Supplement one dose
Lamotrigine Reduce by 0–20% Supplement 20% of dose
Topiramate Reduce by 50% Supplement ?% of dose
Tiagabine No change No change
Levetiracetam Reduce dose by 50–70% Supplement one dose
Oxcarbazepine Reduce dose by 0–50% No change ?
Zonisamide Reduce by up to 35% Supplement ?% of dose
Pregabalin Reduce dose by 50–85% Supplement one dose
Lacosamide Reduce dose by 0–30% Supplement 50% of dose
Rufinamide Not affected Supplement 30% of dose
Vigabatrin Reduce dose by 25–75% Supplement half dose
Ezogabine Reduce dose by 0–50% **
Perampanel Not recommended with several renal **
impairment
Clobazam No change **
* Low protein state associated with renal impairment requires monitoring of protein free serum level.
** No recommendations on the basis of available data.
Most but not all AEDs are assigned a pregnancy cat- trimester and safe for use later in pregnancy, once
egory. Some of the older drugs do not have catego- major organs have formed, but more recent data dem-
ries assigned by the FDA because of differences in onstrate adverse cognitive and behavioral adverse
the approval process. Some have been stated to have effects, and support avoiding valproate at all stages of
a pregnancy category by investigators on the basis of pregnancy if possible (Meador et al., 2013).
recent findings, but these categories will typically not The North American AED Pregnancy Registry
be found on published prescribing information. Note organized through Massachusetts General Hospital
that all AEDs with a pregnancy category are in either (MGH) is a massive database of patients exposed to
category C or D. AEDs for seizures as well as non-epileptic indications.
No drug is without risk during pregnancy, and no Patients continue to be enrolled, so physicians of all
drug consistently provides perfect seizure control. specialties using these drugs on women of childbear-
But in general the authors prefer to use lamotrigine, ing potential should advise patients to enroll in the
levetiracetam, or oxcarbazepine during pregnancy. registry if they become pregnant. Recent data just
Valproate is associated with a dose-dependent released from the registry compares AEDs for risk
increased risk of birth defects. It was once believed of birth defects (Hernández-Díaz et al., 2012). Note
that valproate was problematic mainly during the first that many AEDs have very limited experience in
monotherapy, so that their safety in pregnancy cannot supplementation at prenatal doses for women with
yet be concluded. For example, there were no malfor- any reasonable risk of pregnancy, particularly those
mations in the zonisamide monotherapy group, but who are actively trying to get pregnant.
there were only 90 pregnancies on zonisamide mono-
therapy at the time of reporting. During Pregnancy
Management is much more complex when the patient
Before Pregnancy presents after she is already pregnant. All of the same
Managing AEDs in a woman with childbearing poten- factors discussed above will be considered, but there
tial should be proactive when at all possible, and is a sense of concern that a substantial portion of
there should be counseling prior to pregnancy. There the risk of major malformations has already been
should be discussion as to which medications are the experienced, so while medications may need to be
most appropriate for the seizure type, which AEDs changed, in some respects damage has already been
place the fetus at higher risk for defects, and what the done. In addition, a trial off AEDs during pregnancy
risk of seizures is for the fetus. Because of the imper- is riskier than before pregnancy. Simplification of
fect data and complexity of the decision-making AED polytherapy would still be appropriate. In addi-
process, each case must be individualized, and the tion, patients who become pregnant on valproate
ultimate decision is made by the patient and physician should be changed to an alternative agent if possible.
together. There should certainly be an effort to reduce Although exposure to valproate in the beginning of
the medication load in women taking multiple AEDs. pregnancy is associated with risk of major malforma-
If the patient has pure absence or pure subjective sim- tion, later exposure also can result in lower IQ and
ple partial seizures, withdrawal of seizure medications other developmental abnormalities (Meador et al.,
can be considered. If a patient is on valproate, then a 2012; Meador et al., 2013).
change to an alternative, such as lamotrigine, should All patients who are pregnant should be on mul-
be considered. tivitamin supplementation, including prenatal doses
of folate.
Some examples follow: AED blood levels have to be monitored more
• A 19-year-old woman with absence epilepsy has closely during pregnancy than before, because of
been seizure-free on ethosuximide for two years. changes in metabolism and volume of distribu-
She has never had another type of seizure besides tion. In particular, lamotrigine level is lowered by
generalized absence. After discussion with the estrogen in the second trimester, with a higher risk
physician, she decides to discontinue ethosuxi- of breakthrough seizures, so the dose usually has to
mide before pregnancy. She is not expected to be increased. Following delivery, the dose has to be
develop any seizures that would be dangerous to decreased. It is recommended that the dose is brought
the child. She decided to remain off the drug even back to what it was before pregnancy in two steps: half
if absence seizures recur. the reduction the day of delivery and the other half
• A 25-year-old woman with generalized after one week.
tonic-clonic seizures is well controlled on
valproate, given for both seizures and migraines. Comorbid Conditions
Considering the high risk of birth defects and
cognitive as well as developmental risks of Numerous comorbid conditions alter potential AED
valproate, it was recommended that she should selection and dose management. Some comorbid
switch to another AED. After discussion with conditions are effectively treated with certain AEDs,
the physician, she transitions off valproate to which makes these AEDs preferable. AEDs with
lamotrigine. FDA-approved non-epileptic indications include:
Folate and multivitamin supplementation reduce • Topiramate for migraine prophylaxis;

the incidence of birth defects associated with AEDs. • Valproate for migraine prophylaxis and acute
Folate use is also associated with higher IQ in chil- treatment and maintenance for mania/bipolar
dren exposed to AEDs in utero. We recommend disorder;
• Lamotrigine for maintenance for bipolar the efficacy of treatment or makes the cost of therapy
disorder; substantially higher.
• Clonazepam for panic attacks;
• Carbamazepine for trigeminal neuralgia; Epileptic Syndrome and Genetics
• Gabapentin for postherpetic neuralgia and rest-
less leg syndrome (for gabapentin enacarbil); At present, the seizure type is the main predictor of
• Pregabalin for diabetic peripheral neuropathy, response, and epileptic syndrome plays limited role.
postherpetic neuralgia, and fibromyalgia. There are only rare exceptions. For example, autoso-
mal dominant nocturnal frontal lobe epilepsy responds
In addition, several AEDs are used without official particularly well to carbamazepine and oxcarbazepine.
FDA indication in the treatment of headaches (par- However, there are also instances where the epileptic syn-
ticularly gabapentin), insomnia (gabapentin and drome diagnosis makes a particular AED undesirable. For
pregabalin), restless leg syndrome (gabapentin and example, lamotrigine and other sodium channel-blocking
pregabalin), and essential tremor (primidone and AEDs are known to aggravate severe myoclonic epilepsy
topiramate). On the other hand, some comorbid con- of infancy (Dravet syndrome). Phenytoin is contrain-
ditions can be exacerbated by certain AEDs, which dicated in progressive myoclonic epilepsies because it
makes them less desirable. For example, patients with can worsen progressive ataxia and cause dementia. It is
obesity should avoid valproate, carbamazepine, and expected that genetics and syndrome diagnosis will have
pregabalin, which can cause weight gain. Topiramate a greater role in medication selection in the future, as the
and zonisamide, which can cause weight loss, could pathophysiology of epilepsy is better understood.
then be favored. Topiramate and zonisamide are
relatively contraindicated in individuals with kidney Adverse Effects
stones. Patients with psychosis should avoid topira-
mate, zonisamide, and levetiracetam. While we can- Adverse effects can be easily accessed by online refer-
not be complete in this discussion, below are some ences. These include dailymed.nlm.nih.gov as well as
general guidelines. product-specific websites. Note that there are some
Migraine: the coexistence of epilepsy and migraine common reported adverse effects, including dizziness,
is common. Topiramate and valproate both have FDA gait difficulty, nausea, headache, rash, and somnolence.
indications for migraine and could be considered if Comparing the frequency of these symptoms in patients
the frequency of migraine attacks justifies prophylac- treated with active drug compared with patients treated
tic therapy. with placebo can give us a good indication of how often
Bipolar disorder: valproate and lamotrigine have these can be attributed to the drug. In addition, there are
FDA indications for bipolar disorder. The former often numerous adverse effects listed for which there is
would be favored for predominant mania and the no clear cause-and-effect relationship with the AED.
latter for predominant depression. Carbamazepine,
oxcarbazepine, and topiramate have also been used
off-label for bipolar disorder. Dosing for First-line Therapy
Hepatic insufficiency: Valproate and other agents
The dosing for first-line therapy is described for most
with principal hepatic metabolism should be avoided
common used AEDs in Figures 7-12 to 7-19. It is essen-
if possible. If used, dose adjustment is needed.
tial to be familiar with the pharmacokinetics of AEDs
Renal insufficiency: Renal insufficiency reduces
for best use, and particularly for dosing schedule
the clearance of many drugs with renal elimination,
(see Table 7-4).
so that lower doses have to be used. In addition,
patients on hemodialysis may need to be redosed
after dialysis. Drug-Level Monitoring
Chemotherapy and immune modulators: Some che-
motherapeutic agents and anti-rejection medications AED levels are measureable for most AEDs. AED
have their metabolism altered by enzyme-inducing serum levels should only assist in clinical decision
AEDs. For some of these medications, this reduces making, and should not be the primary basis for
Table 7-4 Pharmacokinetic Properties of AEDs Appropriate as Initial Monotherapy

AED Oral absorption/ Half-life Extended Intravenous Metabolism
bioavailability (hours) release preparation + <50%
High: ≥90 % Short: ≤10 preparation ++ >50%
Intermediate: Intermediate: – <90%
≥70%–<90% >10–30< +++ >90%
Low: <70% Long: ≥30
Phenobarbital High Long – Yes ++ Liver
Phenytoin High Intermediate Yes Yes +++Liver
Ethosuximide High Long – – ++Liver
Carbamazepine Intermediate Intermediate Yes –** +++Liver
Valproate High Intermediate Yes Yes +++Liver
Gabapentin Low Short –* – None
Lamotrigine High Intermediate Yes – +++Liver
Topiramate Intermediate Intermediate –** – +Liver
Levetiracetam High Short Yes Yes +Blood
Oxcarbazepine High Intermediate¶ –** – +++Liver
Zonisamide High Long – – ++Liver
* Not approved for epilepsy ** In development
¶ Combination of parent drug and active metabolite monohydroxyderivative
dosing decisions. A “therapeutic range” has been sug- • Verifying stability of AED level for phenytoin,
gested for some AEDs. This is best established for the which has non-linear kinetics. The phenytoin
old AEDs phenytoin, carbamazepine, and valproate, level can fluctuate widely with a small change in
and is also helpful for lamotrigine and oxcarbazepine. dose or small change in absorption.
The range is only a useful guide, and a value outside • After a breakthrough seizure occurs, to determine
the range should not be the only reason to change the if the breakthrough seizure was related to a drop
dose. Routine AED levels are not necessary. in the serum level.
• To help explain lack of AED efficacy at what appears
to be a high dose. A low level despite a high dose
AED levels are most helpful in the following situations: may indicate that the patient is a high metabolizer
• As a reference value once a clinically effective or is not compliant. A low level may encourage
dose has been reached. repeating the measurements to verify stability. Large
• Verifying that the AED level is within the effective variability may suggest inconsistent compliance. If
range for a patient with infrequent seizures, for the patient is compliant, a low level indicates room
whom ascertainment of effective seizure control for further increases in dosing if needed for seizure
may take a very long time. In this case, the neurolo- control, even at the maximal dose recommended
gist would aim for a level in the middle of the range. in the prescribing information. Undetectable levels
• Monitoring phenytoin level during titration in a despite a high dose suggest non-compliance.
patient with difficult to control seizures. Because • To help explain appearance of adverse effects at a
of non-linear kinetics, the level may increase relatively low dose. A high level may suggest that
excessively with a small increment in the dose. the patient is a slow metabolizer and a lower dose
The level may need to be checked intermittently may be indicated.
during the process of titration. At a serum level • To watch for pharmacokinetic interactions after
near 20 mcg/ml, additional titration may result in introduction of another medication that may
toxicity. affect the baseline AED.
• To monitor AED level during pregnancy, which is with very infrequent seizures. In such a case, it may
known to reduce some AED levels. take a very long time to determine if the treatment has
• To monitor stability of AED level when switching been successful. It is then recommended to titrate to a
to a different formulation or a different brand. middle-range dose or a middle-range level.
If the seizures are not controlled on what would nor-
For highly protein-bound AEDs such as phenytoin mally be a reasonable target dose, then measurement
and valproate, the protein-free portion is respon- of the level can determine whether there is room to
sible for efficacy and toxicity. When these AEDs are increase the dose further. Toxicity is usually determined
used in monotherapy in an otherwise healthy indi- by clinical symptoms rather than levels. However, if
vidual, the total serum level is a good predictor of the the drug level is significantly higher than the published
protein-free level. However, measuring protein-free upper limit of “therapeutic range,” then further increase
levels will be important in states that may change in dose is likely not warranted. On the other hand, if
the proportion of binding, such that the total level is good seizure control is achieved by a level that is some-
no longer a predictor of the protein-free level. These what higher than the “therapeutic range” yet there are
clinical situations include low protein states such as no symptoms or signs of toxicity, then the dose should
renal failure, hepatic failure, malnutrition, and old usually not be reduced despite the high level.
age, pregnancy, or concomitant use of phenytoin If a patient has loss of seizure control, one of the
and valproate, with resultant competition for protein possible reasons is reduction in blood level, either due
binding. Phenytoin and valproate are both approxi- to missing doses or change in metabolism. Missing
mately 90% protein-bound. Protein-binding of val- doses is a major cause of reduced drug level. Altered
proate can be saturated at high doses, at which point metabolism can be from exposure to a new drug (e.g.,
the free level may be much higher than predicted by antibiotic) or alcohol.
the total serum level. Some drugs have non-linear kinetics, so small
AED levels should generally assist therapy rather changes in dose can produce large changes in levels.
than direct it. With some exceptions, it is generally Phenytoin is currently the only AED with non-linear
not appropriate to drive the AED dose to achieve a kinetics. At low levels, small dose changes produce
level in the “therapeutic range,” because the definition small changes in level, whereas at higher levels (e.g.,
of the therapeutic range is arbitrary to a certain extent. mid-to-high therapeutic) small dose changes can
If there is a good clinical response, then measurement produce large changes in level. As phenytoin is being
of the level can show what an effective level is for that pushed to maximal therapeutic levels, careful moni-
patient. One exception to the above rule is the patient toring of the level is warranted (see Table 7-5).
Table 7-5 Anti-epileptic Drug Levels

AED Lower end of range (mcg/ml) Higher end of range (mcg/ml)
Breakthrough seizures more Toxicity more likely above this
likely below this value value
Phenytoin Total level: 10 Total level: 20
Free level: 1 Free level: 2
Carbamazepine 4 12
Valproate Total level: 50 Total level: 100
Free level: 5 Free level: 10
Lamotrigine 2 20
Oxcarbazepine (level measures 10 35
MHD metabolite)
Most useful AED serum level range; note that these value are merely statistical, suggesting increased risk of seizures below the lower end of range
and increased risk of toxicity above the upper end of the range.
Second-line Therapy with another medication (Beghi et al., 2003; Kwan
and Brodie, 2000b). From a commonsense perspec-
If an AED is not tolerated, it should be replaced with tive, replacement monotherapy is the best choice if
another. However, if an AED trial fails due to lack of the first AED was completely ineffective. However, if
efficacy, there are more options. Before an AED trial the first AED was partially effective, adding a second
has been declared a failure, it is important to review a AED may be a better consideration. Replacing the
number of questions: first AED usually requires first adding the new AED
before withdrawing the old one. It is acceptable and
• Has the medication been titrated to the maxi- sometimes advantageous to reduce the dose of the first
mum tolerated dose? AED as the new AED is titrated. An overnight switch
• Has the patient been compliant with the is possible for some AEDs, provided the doses are not
medication? high. An overnight switch has been well tested for car-
• Are the breakthrough seizures provoked by factors bamazepine to oxcarbazepine conversion using a 2 to
that can be corrected, such as sleep deprivation, 3 dose ratio, provided the dose of carbamazepine is
alcohol or drug abuse, or concomitant use of a 800 mg or less. Based on some similarity in properties
medication known to reduce the seizure threshold? and mechanism (but without supportive published
evidence), one of the authors also switches gabapen-
If it is determined that the AED has truly failed due tin to pregabalin using a 6 to 1 ratio (if the gabapentin
to lack of efficacy, the physician can choose to replace dose is 1800 mg or less), and topiramate to zonisamide
it with another AED in monotherapy or add another (using a 1 to 1 ratio for a dose of 200 mg or less).
AED. Studies do not show a difference in efficacy All AEDs are FDA approved for adjunctive ther-
and side effects between these two options, although apy. Table 7-6 outlines the pharmacokinetic proper-
there is a slight trend favoring adjunctive therapy ties of AEDs that are not candidates for initial therapy.
Table 7-6 Pharmacokinetic Properties of AEDs Not Appropriate as Initial Monotherapy

AED Oral absorption/ Half-life Extended Intravenous Metabolism
bioavailability (hours) release preparation + <50% ++
High: ≥90 % Short: ≤10 preparation (USA) >50%– <90%
Intermediate: Intermediate: >90%
≥70%–<90% >10–30<
Low: <70% Long: ≥30
Primidone High Intermediate* – – ++Liver
Clonazepam High Long – – ++Liver
Methsuximide** High Long – – +Liver
Felbamate High Intermediate – – ++Liver
Tiagabine High Short – – +++Liver
Pregabalin High Short – – None
Lacosamide High Intermediate – Yes +Liver
Rufinamide Intermediate Short – – +++Liver
Vigabatrin High Short¶ – – None
Ezogabine Low Short – – ++Liver
Clobazam High Long – – +++Liver
Perampanel High Long – – +++Liver
* Long for the metabolite phenobarbital ** applies to active metabolite desmethylmethsuximide
¶ The duration of effect is longer than expected from T1/2 because the drug works through irreversible inhibition of GABA transaminase enzyme.
Adding a new AED to an old one should consider affect valproate or warfarin levels, which are markedly
interactions between the two AEDs. The interaction affected by carbamazepine.
can be pharmacokinetic (for example, a change in the Valproate is a hepatic enzyme inhibitor and mark-
serum level of the old drug as the new one is added) edly reduces the metabolism of lamotrigine and
or pharmacodynamic (no change in the level of the rufinamide, so that titration rates and target dose
old AED, but increased toxicity because of additive of these latter medications is considerably reduced
adverse experiences, for example). Some pharma- in the presence of valproate. If valproate is added to
codynamic interactions are favorable, with evidence lamotrigine or rufinamide, the doses of these medi-
of synergy. Such beneficial additive effects are best cations have to be reduced by at least 50% to prevent
demonstrated for the combination of lamotrigine toxicity. Felbamate is also an important inhibitor of
and valproate. Another combination that seems to liver enzymes, so that doses of several AEDs have to
be particularly helpful is that of lamotrigine and leve- be reduced in conjunction with its addition. Valproate
tiracetam, but it has less support in the literature. In and felbamate both inhibit the clearance and cause
general, there is a suggestion that an AED combina- accumulation of carbamazepine epoxide, which is a
tion with different mechanisms may be more effica- metabolite of carbamazepine responsible for some
cious than a combination of two AEDs with the same important carbamazepine toxic adverse effects.
mechanism (see Table 7-7). For the recommended Awareness of this interaction is important since toxic-
AEDs as second- and third-line therapy, please refer ity may occur in the presence of low carbamazepine
to Table 7-8. levels. Carbamazepine epoxide levels must be mea-
sured upon request and sent to a central laboratory.
Drug Interactions Several AEDs are selective inhibitors of specific liver
enzymes. For example, oxcarbazepine can inhibit the
Pharmacokinetic interaction implies that the addition liver enzyme responsible for phenytoin metabolism
of an AED to another results in a change in serum and can produce an elevation of phenytoin level.
level. Factors that make a drug more likely to interact Another type of interaction is competition for pro-
are enzyme induction or inhibition, liver metabolism, tein binding, which can play a role in AEDs that are
and high protein binding. Table 7-9 shows the poten- highly protein bound. In particular, the competition
tial of AEDs to interact based on these properties. of phenytoin and valproate for protein binding is clini-
The most common pharmacokinetic interactions cally relevant because therapeutic decisions are often
are a result of enzyme induction resulting in increased made based on total serum levels, when it is the free
clearance and lower serum level, or enzyme inhibition levels that determine efficacy and toxicity. For example,
resulting in decreased clearance with resulting accu- in the presence of valproate competing for protein
mulation and increased serum level. binding, the protein-free portion of phenytoin may rise
Some AEDs such as carbamazepine, phenytoin, from 10% to 30%. A phenytoin total level of 15 mcg/ml
and phenobarbital produce profound and wide- may be associated with severe toxicity because the
spread enzyme induction and result in reduced levels free level is 4.5 mcg/ml, equivalent to a total level of
of other AEDs that are metabolized by the liver. The 45 mcg/ml in an individual with the expected 10%
greater the liver metabolism of an AED, the more it unbound fraction. Thus when valproate and pheny-
is affected by enzyme inducers. This is why it can be toin are used together, free levels should be measured
very difficult to achieve a therapeutic level of valpro- if needed for therapeutic decisions. Tiagabine is also
ate in the presence of carbamazepine or phenytoin. highly protein bound, but because of its low dose and
The increased metabolism can also increase the pro- small concentration, it is less likely to affect phenytoin
duction of toxic metabolites that mediate some types or valproate protein binding. In addition, tiagabine dos-
of valproate toxicity. Other AEDs have more modest ing is almost never based on its serum level.
and more selective enzyme induction. For example, Pharmacodynamic interactions do not involve
oxcarbazepine enzyme induction is more specific a change in serum concentration of involved AEDs.
for hepatic enzymes responsible for the metabolism They are most often related to the additive toxicity
of some calcium antagonists, oral contraceptives, of AEDs that have the same mechanism of action.
and cyclosporin. However, oxcarbazepine does not Pharmacodynamic interactions are often seen when
Table 7-7 Key Known AED Mechanisms of Action
Sodium channel blocking
Potassium channel opening
Blocking high voltage activated

Enhancing GABA
Glutamate receptor antagonism
Blocking T- calcium channels
voltage-activated calcium channels
Binding SV2A
Comment
calcium channels
Binding Alpha-2-delta subunit of

AED
Phenobarbital X X X
Primidone X X
Phenytoin X
Methsuximide X? X
Ethosuximide X
Clonazepam X
and clobazam
Carbamazepine X
Valproate X X X
Felbamate X X X X NMDA receptor
antagonism
Gabapentin X
Lamotrigine X X
Topiramate X X X Kainate and AMPA
Receptor antagonism
Tiagabine X Inhibition of GABA
reuptake
Levetiracetam X
Oxcarbazepine X
Zonisamide X X X
Pregabalin X
Lacosamide X Selective enhancing
of slow inactivation of
voltage-gated sodium
channels
Rufinamide X
Vigabatrin X Irreversible inhibition of
GABA transaminase
Ezogabine X
Perampanel X Selective noncompetitive
antagonism of the AMPA
receptor
Table 7-8 AEDs for First Through Later Lines of Therapy

First-line, second-line, third-line, and late consideration AEDs (listed in general order of
consideration). First-line agents are always considerations for second- and third-line therapy. The
table does not follow FDA indications.
Partial-onset Primary general- Generalized Generalized Generalized
ized tonic-clonic absence myoclonic tonic-atonic
in LGS
First-line Lamotrigine Valproate Ethosuximide Valproate Valproate
Levetiracetam Lamotrigine Valproate Levetiracetam
Oxcarbazepine Levetiracetam Lamotrigine
Topiramate Topiramate
Zonisamide
Carbamazepine
Phenytoin
Valproate
Phenobarbital
Gabapentin
Second- and All above All above All above All above Rufinamide
third-line Pregabalin Zonisamide Levetiracetam Zonisamide Lamotrigine
Lacosamide Clonazepam Zonisamide Topiramate Topiramate
Ezogabine Lacosamide Clonazepam Lamotrigine* Clobazam
Tiagabine Rufinamide Clobazam Clonazepam Clonazepam
Clobazam Clonazepam Methsuximide Clobazam
Perampanel Clobazam
Methsuximide
Clonazepam
Late Vigabatrin Phenytoin** Topiramate*** Primidone Zonisamide
consideration Felbamate Carbamazepine** Felbamate Felbamate Levetiracetam
Primidone Phenobarbital Lacosamide
Primidone Felbamate
Methsuximide
Felbamate
* May worsen myoclonic seizures in some patients
** May activate myoclonic and absence seizures in some patients
*** Ineffective in one controlled trial
combining AEDs that act on the sodium channel. with the oldest AEDs. The enzyme-inducing AEDs
For example, dizziness, blurred vision, diplopia, may reduce the efficacy of many medications metabo-
and unsteadiness are often seen when combining lized by the liver, such as warfarin, oral contraceptives,
lamotrigine, lacosamide, carbamazepine, or oxcar- many chemotherapeutic agents, etc. Similarly, AED
bazepine. Thus mechanism of action is currently more levels are affected by inducers or inhibitors of their
relevant to tolerability than to efficacy of AEDs. metabolism. Carbamazepine and phenytoin levels can
be elevated by many non-AED medications. The long
AED–non-AED Interactions list of agents that inhibit carbamazepine metabolism
and result in carbamazepine accumulation includes
Interactions between AED and non-AED medica- cimetidine, diltiazem, erythromycin, clarithromycin,
tions are potentially bidirectional and are most likely fluoxetine, isoniazid, propoxyphene, ketoconazole
Table 7-9 Pharmacokinetic Interactions

Anti-epileptic Hepatic Autoinduction Hepatic Affected Affected Protein
drug enzyme enzyme by by binding
induction inhibition enzyme enzyme
inducers inhibitors
+ minimal (usually selective) + affected High ≥85%

++ intermediate – not affected Low<85%
+++ pronounced
– absent
Phenobarbital +++ – – + + Low
Primidone +++ – – + + Low
Phenytoin +++ – – + + High
Methsuximide + – – + – Low
Ethosuximide – – – + – Low
Clonazepam – – – – – High
Carbamazepine +++ +++ – + + Low
Valproate – – +++ + + High
Felbamate + – ++ + + Low
Gabapentin – – – – – None
Lamotrigine + + – + + None
Topiramate +¶ – +¶ + – Low
Tiagabine – – – + – High
Levetiracetam – – – +/– – Low
Oxcarbazepine ++ ** – +** + + Low
Zonisamide – – – + + Low
Pregabalin – – – – – None
Lacosamide – – – + – Low
Rufinamvide + – + + + Low
Vigabatrin + – – – – None
Clobazam + – + – + Intermediate
Ezogabine – – – + – Low
Perampanel + – + + + High
¶applies to dose ≥ 200 mg
** applies to dose ≥ 900 mg
(and related agents), verapamil, and grapefruit juice. Success of AED Therapy
Oxcarbazepine, which is related to carbamazepine, is
not subject to this type of interaction. Effectiveness of medical therapy is strongly depen-
One important interaction is between estrogen, dent on epilepsy syndrome and underlying pathol-
an inducer of glucuronidation, and AEDs that are ogy. Patients with idiopathic generalized epilepsy are
metabolized by glucuronidation. Lamotrigine is the much more likely to have complete seizure control
most susceptible, but valproate and oxcarbazepine are than patients with partial epilepsy or symptomatic
also affected to a lesser degree. Estrogen-containing generalized epilepsy. For those with partial epilepsy,
oral contraceptives can reduce the lamotrigine serum specific lesions such as hippocampal sclerosis or dual
level considerably, with associated increase in seizure pathology are associated with a lower chance of sei-
frequency. zure control.
Drug-resistant Epilepsy seizure freedom. Examples of “surgically remediable

syndromes” include epilepsy with unilateral hippo-
Despite the proliferation of AEDs, approximately campal sclerosis and epilepsy with a well-defined
one-third of patients with epilepsy have persistent small epileptogenic lesion such as cavernous mal-
seizures (Kwan and Brodie, 2000a). Early response formation or benign tumor. For these patients, the
to treatment is an important predictor of drug resis- chances of seizure freedom with epilepsy surgery
tance. Patients started on a first monotherapy trial are approximately 70%, which is much better than
have a roughly 50% chance of seizure freedom. If the could be expected with any subsequent planned
first AED is failed due to side effects, the chance of medication trial.
seizure freedom with next monotherapy remains Patients who do not have a surgically remedi-
roughly 50%. However, if the first drug is failed due to able syndrome should have trials of additional AEDs,
lack of efficacy, the chance of the second drug achiev- most probably combination therapies. However,
ing total seizure control becomes much less, approxi- dietary therapy and vagus nerve stimulation can
mately 11%. After failure of two AEDs, few patients be considered in individuals who are tired of inef-
become seizure-free in the long term, whether with fective AED therapies or are experiencing adverse
a third monotherapy or with combination therapy. effects from ineffective therapies. Vagal nerve stimu-
One study that related the chances of seizure con- lation (VNS) should not be implanted without first
trol to the number of failed AEDs found 0% of sei- confirming the diagnosis of epilepsy; a considerable
zure control after failure of 6 or 7 AEDs (Schiller and number of patients subjected to this procedure have
Najjar, 2008). non-epileptic events, and we must be extra vigilant to
confirm the epilepsy diagnosis.
If a patient is not an optimal candidate for epi-
Definition of Drug-resistance lepsy surgery, trials of additional AEDs alone or in
combination are appropriate before consideration of
What failed treatment is sufficient for the patient to
a surgical procedure that has a lower yield or that is
qualify as drug-resistant? The International League
palliative. An algorithm for identifying and managing
Against Epilepsy (ILAE) defined drug resistance as
drug-resistant epilepsy is provided in Figure 7-2.
“failure of adequate trials of two tolerated, appro-
priately chosen and used anti-epileptic drug sched-
ules (whether as monotherapy or in combination) Discontinuation of Medical Therapy
to achieve sustained seizure freedom” (Kwan et al.,
When patients enter into long-term remission, dis-
2010). Failure of an AED must be because of lack of
continuation of AED therapy may be considered
efficacy and not intolerance. Epilepsy cannot be con-
in some individuals. However, it is not possible to
sidered drug resistant if the AED is under-dosed or
determine if the remission will persist after medica-
inappropriate for seizure type, or if the diagnosis of
tion withdrawal. While there are indicators to help
epilepsy is wrong (e.g., non-epileptic events).
predict successful AED withdrawal, there is no way to
be absolutely sure that seizures will not recur. When
Management Options for Drug-Resistant Epilepsy deciding to withdraw medications, one must consider
both the consequences of seizure recurrence (loss
Patients with drug-resistant epilepsy should have of driving privileges, risk to employment, possibility
a reevaluation of the diagnosis. As always, the pos- that seizures may be harder to control after recur-
sibility of a diagnosis other than epilepsy should be rence) and the benefit of eliminating medication side
considered when seizures do not respond to appro- effects and medication cost.
priate medications. The most common alternative Children have a lower risk of seizure recurrence
diagnoses are psychogenic non-epileptic events and than adults, in general, although it depends on sei-
syncope. If the diagnosis of epilepsy is confirmed, zure type and etiology. This means that a trial of
evaluation for epilepsy surgery is warranted. Epilepsy AED withdrawal can be considered sooner in chil-
surgery is appropriate if the patient has a surgically dren (1–2 years of seizure freedom) than in adults
remediable syndrome with a high chance of complete (4–5 years of seizure freedom).
First monotherapy
Second monotherapy or
adjunctive therapy
Reassess diagnosis; video- Not epilepsy-revise

EEG monitoring therapy
Consider/evaluate for
epilepsy surgery for TLE
with hippocampal sclerosis Yes, proceed with epilepsy
or lesional partial epilepsy surgery after presurgical
with well-defined and evaluation
resectable epileptogenic
lesion
No, continue trials of Dietary therapy may be

medical therapy: third, considered in motivated
fourth, fifth, sixth AED individuals or those that
regimens are tube-fed
VNS can be considered
In event of persistent AED

failure (whether due to lack
of efficacy or poor
tolerability), re-evaluate for Good candidate-proceed
epilepsy surgery, including with epilepsy surgery
invasive EEG-video
monitoring if appropriate
Not a surgical candidate

consider VNS, dietary
therapy, palliative epilepsy
surgery, or additional AED
trials
Figure 7-2: Algorithm for Identifying and Managing Drug-Resistant Epilepsy.
AED withdrawal is more likely to be successful in: • Patients with a normal EEG as compared to those
• Patients with idiopathic epilepsy as compared to with abnormal EEG;
those with symptomatic epilepsy; • Patients with partial seizures who became
• Patients with epilepsy onset in adolescence as seizure-free quickly as compared to those who
compared to epilepsy starting in childhood; needed more than 5 years to become seizure-free;
• Adults with shorter duration of active epilepsy for epilepsy surgery evaluation. Evaluation for epi-
and a longer duration of seizure remission as lepsy surgery is not appropriate for patients who are
opposed to adults with longer duration of active non-compliant with medications and have not truly
epilepsy and shorter seizure remission; failed medical therapy. Evaluation for epilepsy surgery
• Patients with normal psychiatric examination as should only be for patients with disabling seizures; it
compared to those with abnormal psychiatric should not be pursued in patients who have subjective
examination; simple partial seizures as their only seizure type.
• Patients with normal IQ as compared to those
with IQ less than 70; Presurgical Evaluation and Planning
• Patients with normal MRI as compared to patients
with MRI showing hippocampal sclerosis. Detailed presurgical evaluation should be per-
formed in specialized epilepsy centers with trained
Abrupt discontinuation of AEDs is never a good idea. personnel, equipment, and experience in epilepsy
Severe seizures may occur during withdrawal of some surgery. Good results are largely the product of
AEDs, particularly benzodiazepines, carbamazepine, good subject selection. The best candidates for
and oxcarbazepine. It is generally best to withdraw epilepsy surgery are subjects with temporal lobe
medications slowly. epilepsy due to hippocampal sclerosis and patients
with partial epilepsy and an underlying focal epilep-
togenic lesion.
NON-MEDICAL TREATMENT OPTIONS FOR
EPILEPSY The presurgical evaluation aims to:
• Localize the epileptogenic zone. The epilepto-
Partial epilepsies are much more likely than general- genic zone is defined as the zone whose resection
ized epilepsies to be drug-resistant. These patients is necessary and sufficient to eliminate seizures. It
are the most likely to benefit from surgical therapy. cannot be directly measured. Much of the exten-
Surgical approaches include temporal lobectomy, sive presurgical evaluation is an attempt to make
selective amygdalohippocampectomy, lesionectomy, the best estimate of this zone. The tests available
hemispherectomy, multiple subpial transection, and to us in the presurgical evaluation measure other
corpus callosotomy. “zones” that can help estimate the epileptogenic
Patients with generalized epilepsy are usually not zone (see Table 7-10)
candidates for resective (curative) surgical therapy. • Determine if surgery puts any cerebral functions
However, some non-pharmacological treatments can at risk.
be helpful. Dietary therapy is an effective treatment • Identify patients who need additional testing,
for patients able to comply with this therapy. Vagal including invasive EEG, either because the
nerve stimulation (VNS) has been used mainly for epileptogenic zone is not well-defined or because
partial onset seizures, but there is evidence to suggest eloquent cortex may be at risk from surgery.
that VNS can be helpful for idiopathic and symptom-
atic generalized epilepsies. The presurgical evaluation always includes video EEG
monitoring (which records interictal and ictal EEG
Surgical Treatment of Epilepsy and video of clinical seizures) and magnetic reso-
nance imaging (MRI). MRI cannot be performed on
When to Do Surgery patients with some implanted devices such as auto-
mated implantable cardioverter-defibrillator (AICD)
Failure of medical therapy is an indication for con- and pacemakers. If MRI cannot be done, state-of-
sideration of epilepsy surgery. Generally, medical the-art brain CT (computed tomography) can show
therapy is considered to have failed if there is no sei- most large structural lesions. However, brain CT usu-
zure control by two appropriate and tolerated drugs ally misses important lesions such as hippocampal
used at therapeutic doses. In actuality, most patients sclerosis, cortical dysplasia, and small basal temporal
have failed many more AEDs by the time they present mass lesions (due to bone streak artifact).
Table 7-10 Terms for Regions Pertaining to Localization of the Epileptogenic Zone, and Tests
That Help Identify These Regions
Zone Significance Tests that define zone
Ictal onset zone or Zone in which seizures are originating. This Ictal EEG onset; ictal SPECT
pacemaker zone zone is always contained in the epileptogenic
zone, but may be smaller than the epilepto-
genic zone.
Epileptogenic Lesion causing epilepsy; some lesions are MRI; etiologic factors, age at risk
lesion unlikely to be epileptogenic (for example, factor/injury may suggest associa-
arachnoid cyst or venous angioma). Lesions tion with specific pathology
may be multiple.
Irritative zone Zone in which interictal epileptiform Interictal epileptiform discharges
discharges originate. This is often larger than on EEG or MEG
the epileptogenic zone
Symptomatogenic Zone that produces the first ictal clinical Seizure description; analysis of sei-
zone manifestations. This may be within or outside zure semiology recorded on video
the first brain region along the path of seizure
propagation to produce signs and symptoms.
Functional deficit Zone responsible for functional deficits. Physical examination; interictal
zone Functional deficit can vary depending on test slow activity or attenuation on
used. Using certain tests such as FDG, it can EEG; PET; neuropsychological
be much larger than the epileptogenic zone. testing; Wada test
Other tests that are commonly included in (during awake surgery) or extraoperative (involving
the presurgical evaluation are positron emission electrical stimulation and evoked potential recordings
tomography (PET) with fluorodeoxyglucose from implanted subdural electrodes).
(FDG) and neuropsychological testing. A Wada After the epileptogenic zone has been localized,
test is indicated for patients with temporal lobe the appropriate surgery depends on its location,
epilepsy who may require resection of the hippo- relationship to eloquent cortex, and the presumed
campus. The Wada test may be skipped if there underlying pathology (see Figure 7-9). Invasive
is right hippocampal sclerosis. In complex cases EEG recordings may be needed when the localiza-
where localization is not clear, additional testing tion of the epileptogenic zone is not confident after
may include ictal single photon emission com- non-invasive evaluation. This can be pursued only if
puted tomography (SPECT), magnetoencephalog- there is a hypothesis regarding the localization.
raphy (MEG), and invasive EEG with implanted
intracranial electrodes (see Figure 7-3). Figures 7-4 Surgical Procedures
though 7-8 identify the elements of the presurgical
evaluation in a few scenarios. Surgical procedures are summarized in Table 7-12.
When eloquent cortex may be at risk from epi-
lepsy surgery, localization of cortical functions is indi- Outcomes of Surgery
cated (see Table 7-11). Non-invasive testing should
be obtained first, and may be sufficient. However, The outcome of epilepsy surgery depends on careful
Wada test may be needed if localization of memory selection of patients and thoughtful localization of
is indicated, and electrical stimulation mapping may the epileptogenic zone. Epilepsy surgery can be very
be necessary if it seems that eloquent cortex is at risk. effective in certain groups of patients. Patients with
Electrical stimulation mapping can be intraoperative mesial temporal lobe epilepsy generally fare better
Epilepsy Surgery Evaluation-Phase 1-

noninvasive
Essential-universal
Video-EEG monitoring in the EMU to record 3-6 seizures (3 seizures may
be sufficient if there is an epileptogenic MRI lesion or hippocampal
sclerosis)
Brain MRI using chronic epilepsy protocol
Important, but not universal-could be omitted in certain circumstances

Brain PET scan (most important in the absence of structural brain
abnormalities)
Neuropsychological testing
Wada test (can be skipped for patient with right hippocampal sclerosis
pursuing selective amygdalohippocampectomy, lesional epilepsy pursuing
lesionectomy or extratemporal epilepsy)
Visual fields (can be skipped if visual pathways are not at risk)
Test can be added to resolve conflicting or unclear data

Ictal SPECT-must be combined with interictal SPECT scan (and possibly
subtracted) for best interpretation-not useful to resolve bilateral
independent foci, since one ictal SPECT reflects one seizure.
MEG/MSI-most useful to resolve localization of epileptiform discharges
with complex but consistent field.
MRS-can help identify dysfunction in certain brain regions.
Tests that can localize cortical functions and may replace the Wada test
for determination of language dominance
fMRI-this is most widely available, but not feasible or less useful in
individuals who are claustrophobic, have vascular malformations, or have
sources of MRI artifact
MEG-less widely available than fMRI, equally useful to localize cortical
functions.
Figure 7-3: Epilepsy Surgery Evaluation—Phase 1, Non-Invasive.
than patients with neocortical foci, and patients with be simplified and dose could be reduced in seizure-free
small well-defined epileptogenic lesions fare better patients. However, there is a risk of seizure recurrence
than those without lesion. Up to two-thirds of patients after AED withdrawal. Such recurrence is less com-
with mesial temporal lobe epilepsy are seizure-free at mon after temporal lobe surgery for mesial temporal
2 years [Spencer et al., 2005]. While neocortical epi- lobe epilepsy than surgery for neocortical epilepsy. It
lepsy has a lower response rate, it is still about 50% is also less common in children than adults. In fact,
(Cascino et al., 1993). Other improvements besides recurrence is predicted by older age at surgery and
seizure control include improved quality of life. longer duration of epilepsy before surgery. Recurrent
However, epilepsy surgery also has risks, particularly seizures may be harder to control in patients taken
verbal memory loss after dominant temporal lobe epi- off AEDs after neocortical epilepsy surgery than after
lepsy surgery. mesial temporal lobe epilepsy surgery.
AED Management after Surgery Vagus Nerve Stimulation (VNS)
AED therapy is usually continued for at least 1 to VNS is approved for adjunctive therapy for partial
2 years after surgery. However, the AED regimen can onset seizures in adults and adolescents 12 years of
Scenario of a single discrete structural lesion with known

epileptogenic potential such as cavernous malformation
Presurgical evaluation includes
Brain MRI using chronic epilepsy protocol has demonstrated single
epileptogenic lesion. It is important to verify that there are no other
lesions (cavernous malformations may be multiple)
Video-EEG monitoring in the EMU to record 2-3 seizures, to verify that
the ictal onset zone corresponds to the lesion.
Visual fields only if lesion is close to visual pathways
fMRI (or MEG) of language or other function if lesion is close to
functional cortex
Wada test only if the lesion involves the left hippocampus.
Surgery (lesionectomy with margin) could be pursued directly if

the ictal and interictal EEG/video are congruent
Additional tests can be added to resolve conflicting or unclear data

(incongruence between EEG and MRI)
Repeat video-EEG monitoring to record more seizures
PET, ictal SPECT, MEG) may be needed if there is incongruence between
EEG and MRI.
Invasive EEG needed if conflict cannot be resolved.

Invasive EEG to record from lesion or around lesion as well as apparent
ictal onset zone.
Note that posterior temporal lesions may have an ictal EEG onset that
appears anterior temporal. It may be acceptable to perform a
lesionectomy first and consider invasive evaluation later if surgery fails B
Figure 7-4: Scenario of a Single Discrete Structural Lesion with known Epileptic Potential.
age and older (VNS Study Group, 1995). In addition, the greater chance of seizure freedom with epilepsy
there is more recent approval for selected patients surgery, patients are advised to consider it first if they
with refractory depression. Improvement in sei- are felt to be good candidates. There are reports of
zure control with VNS seems to increase over time. VNS being helpful in patients with refractory gener-
However, less than 10% are seizure-free. Because of alized epilepsy, although this is not an FDA-approved
Scenario of temporal lobe epilepsy with right

hippocampal sclerosis
Video-EEG monitoring in the EMU to record ~3 seizures, to verify
that the ictal onset zone is right temporal.
Brain MRI using chronic epilepsy protocol has demonstrated right
hippocampal sclerosis.
Brain FDG PET scan (optional)
Visual fields
Consider language fMRI if there is any concern over dominance
(for Example left handedness, Etc..)
Surgery (right selective amygdalohippocampectomy or right
temporal lobectomy) could be pursued directly if the ictal and
interictal EEG/video are congruent
Figure 7-5: Scenario of Temporal Lobe Epilepsy with Right Hippocampal Sclerosois.

Scenario of temporal lobe epilepsy with left

hippocampal sclerosis

Video-EEG monitoring in the EMU to record ~3 seizures, to verify that
the ictal onset zone is left temporal.
Brain MRI using chronic epilepsy protocol has demonstrated left
hippocampal sclerosis.
Brain FDG PET scan (optional)
Wada test
Visual fields
Consider language fMRI to avoid language areas during surgery
Surgery (left selective amygdalohippocampectomy) could be

pursued directly if the ictal and interictal EEG/video are
congruent and Wada test indicates no undue risk to memory
function
Figure 7-6: Scenario of Temporal Lobe Epilepsy with left Hippocampal Sclerosis.
indication. As with many epilepsy therapies, VNS was beneath the left clavicle. The stimulator settings are
tested in and approved for partial-onset seizures, but adjusted as needed based on seizure control and
its clinical utility extends beyond FDA indications. adverse effects. The default stimulation cycle is stim-
The electrodes are placed on the left vagus nerve ulation for 30 seconds followed by 5 minutes of no
and the stimulator is usually placed subcutaneously stimulation. Adjustment usually involves increasing
Scenario of nonlesional temporal lobe epilepsy

Video-EEG monitoring in the EMU to record ~6 seizures.

Brain FDG PET scan
Wada test
Visual fields
Consider language fMRI if left temporal
Surgery (temporal lobectomy) could be pursed directly if the

ictal and interictal EEG/video are congruent with PET scan,
Pointing to a single nondominant right remporal epileptogenic
zone and the wada test indicates no undue risk to memory
Function.
Invasive EEG with subdural grids is usually considered for a
dominant left temporal epileptogenic zone, in order to localize
language functions and spare eloquent cortex before surgery.
Additional noninvasive testing such as ictal/interictal SPECT and
magnetoencephalography can be considered if there is concern over
localization due to normal PET or inconguent EEG data
Invasive EEG with subdural grids is usually considered if the
epileptogenic zone is suspected to be neocortical, for better
definition of the epileptogenic zone.
Figure 7-7: Scenario of Non-Lesional Temporal Lobe Epilepsy.

Scenario of case with misleading information –what the current intensity, but other parameters can also
to do when presurgical tests disagree be adjusted (see Figure 7-10).
Presurgical evaluation includes In addition to cyclical stimulation, single VNS
Video-EEG monitoring in the EMU to record at least 6 seizures. stimulation cycles can be generated on demand with
Brain FDG PET scan
magnet activation. The magnet-activated current
Neuropsychological testing can be programmed with different parameters from
Wada test if temporal localization is possible
Consider Visual fields only if considering resection that includes
the recurrent output current. Patients can initiate
visual pathways on-demand stimulation with the magnet if they expe-
Consider language fMRI if may be dominant
Additional noninvasive testing such as ictal/interictal SPECT and
rience an aura, or a family member or caregiver can
magnetoencephalography are usually considered to resolve initiate the on-demand stimulation at the beginning
incongruent data
of a seizure. Magnet activation is more likely to be
Invasive EEG with subdural grids is considered only if the helpful at the onset of a seizure and less likely to help
epileptogenic zone is well lateralized but insufficiently
localized. Depth electrodes if there is evidence
after the seizure has progressed. In addition, the mag-
that the epileptogenic zone may invole deep structures that net can turn the stimulator off by holding it or taping
cannot be covered with subdural grid electrodes. it over the stimulator.
One VNS side effect to be expected is voice change
Figure 7-8: Scenario of Case with Misleading or hoarseness. This improves over time. Individuals
Information—What to do when presurgical Tests
who sing or speak in public may want to turn off the
Disagree.
Table 7-11 Most Commonly Used Localization Techniques

Technique Cortical functions Advantages Disadvantages
reliably tested
fMRI Motor Widely available Indirect assessment of hemodynamic
Sensory Non-invasive, safe effect of activation (may be misleading
Language in the presence of an arteriovenous
malformation)
Difficult to dissociate true activations
from spurious ones
Identifies areas activated by task, not
areas necessary for task
Not possible in patients who are claus-
trophobic, restless, have metal in head
MEG Motor Direct assessment of Not widely available
Sensory physiologic effect of Expensive
Language activation
Non-invasive, safe
Wada test Language Identifies dominance Test of lateralization, not localization
Memory for language and risks Invasive; has risks and discomforts
to memory function
Extra-operative Motor Identifies regions Invasive
electrical Sensory necessary for Requires additional surgery for
stimulation Language function implantation
Unlimited time
Intraoperative Motor Identifies regions Discomfort
electrical Sensory necessary for certain Limited time and repertoire in operat-
stimulation Language functions ing room
Epilepsy Surgery Evaluation-Phase 2-invasive should be considered in the armamentarium of the

Requirements neurologist. Young children are more likely to benefit
Invasive testing with implanted electrodes requires evidence based than older children and adults, partly because of bet-
hypothesis regarding the probable localization of the epileptogenic zone ter compliance.
Electrode options The ketogenic diet can be used for patients with
Subdural grids-require craniotomy
Subdural strips, epidural strips- can inserted through burr holes refractory seizures of almost any type, especially if
Foraman ovale electrodes-inserted through foramen ovale there is difficulty with tolerating seizure medications.
Depth electrodes- can be inserted through burr holes
Epidural PEG electrodes Particular types of epilepsy that may respond better
Indications for specific invasive electrodes than others include epilepsy due to glucose trans-
Subdural grid- assumes a strong hypothesis regarding the lateralization of porter deficiency or pyruvate dehydrogenase defi-
the epileptogenic zone-most useful for refining a broad laocalization and
for localizing cortical functions with electrical stimulation
ciency, myoclonic-astatic epilepsy, tuberous sclerosis,
Subdural strips- useful to sample various brain regions with wide or infantile spasms. Ketogenic diet should not be used
coverage
Foramen ovale electrodes- useful to resolve lateralization in patients with in patients with mitochondrial disorders, pyruvate
apparent bitemporal independent seizure onsets on scalp EEG-assumes
that seizures are mesial temporal in origin
carboxylase deficiency, and β-oxidation defects.
Depth electrodes –useful for recording from deep difficult to access Difficulty maintaining compliance is the main lim-
regions, such as insula, depth of sulci, heterotopias, hippocampi,
amygdala, mesial frontal region itation of the ketogenic diet. Hence it is most useful
Epidural PEG electrodes- can be used as “seni-invasive” electrodes to in individuals for whom compliance is not an issue,
explore EEG from a wide distribution, without the interference of muscle
artifact for example tube-fed subjects or infants receiving
Combinations of above- the most common are combinations of subdural
grids and strips. formula. Other diets have been explored to improve
Intraoperative electrocorticorapy (ECoG) compliance with dietary therapy.
Intraoperative electrocorticograpy (ECoG) can be used in the place of

Invasive EEG, but only if the localization question can be answered Modified Atkins Diet
satisfactorily with interictal epileptiform discharges. The modified Atkins diet is a response to difficulty
tolerating the ketogenic diet. The diet is also low car-
Figure 7-9: Epilepsy Surgery Evaluation—Phase 2, bohydrate, but with no restriction in proteins, fats, or
Invasive. calories.
This diet has been used for a variety of epilepsies
with reported success in children not very different
stimulator temporarily during performances (by tap- from the ketogenic diet (Chen and Kossoff, 2012).
ing a magnet over it). This is better tolerated and with less adverse effects
than the ketogenic diet and may be considered as an
alternative for select patients, particularly adults.
Dietary Treatment of Epilepsy
Dietary therapy, which was popular many years ago, Low Glycemic Index Diet
was often forgotten during the explosion of newer The low glycemic index diet is another low-
AEDs, but has regained some interest with the real- carbohydrate diet that is a bit more permissive, in
ization that the new AEDs are not the miracle drugs that it allows carbohydrates with low glycemic index
we might have hoped for. (meaning they will not raise blood glucose). It has
also shown seizure reduction in children with refrac-
tory seizures (Muzykewicz et al., 2009).
Ketogenic Diet
Ketogenic diet is a high-fat low-carbohydrate diet with
some sustained caloric restriction. It is often initiated Immune Therapies Directed to the
with fasting. This diet has been shown to be effective Underlying Pathology
for a substantial minority of patients, with about 10% There is increasing recognition that some forms of
seizure-free and 40–50% or greater reduction in sei- epilepsy are immune in nature, and immunological
zure frequency (Vining et al., 1998). These results are therapy may be effective in these disorders. Steroids
remarkable since this diet is tried in patients who have may be particularly effective in epilepsy associated
failed most available therapies, and the ketogenic diet with Hashimotos’s encephalopathy, also referred to as
Table 7-12 Modalities of Surgical Therapy and Their Indications

Modality Indication
Lesionectomy Focal lesion associated with single epileptogenic zone; in some cases
the resection must include surrounding brain tissue (for example
hemosiderin-stained tissue surrounding a cavernous malformation)
Temporal lobectomy Well-localized temporal lobe focus, particularly non-dominant. This is
most appropriate for non-lesional temporal lobe epilepsy when it is not
known if the epileptogenic zone is mesial or lateral temporal
Selective Well-localized mesial temporal focus, particularly if associated with
amygdalohippocampectomy hippocampal sclerosis
This was reserved for dominant foci, but no longer so
Tailored neocortical resection Localized neocortical epileptogenic zone
Multilobar resection Epileptogenic zone involves more than one lobe in one hemisphere
Hemispherectomy, Well-lateralized widespread epileptogenic zone and severe associated
hemispherotomy or anticipated motor deficit (ex: Rasmussen syndrome); if there are
no independent finger movements, no significant worsening in motor
function will be expected in the long term
Multiple subpial transections Neocortical epileptogenic zone well-localized over functional (elo-
quent) cortex
Most often used with motor, sensory or language cortex
May be combined with resection
Corpus callosotomy Palliative surgery that can be useful if the dominant seizure manifesta-
tions require rapid spread to the opposite hemisphere (for example,
drop attacks). This surgery does not usually eliminate seizures, but may
eliminate some debilitating manifestations such as falls.
steroid-responsive encephalopathy with anti-thyroid QUALITY OF CARE STANDARDS AND

antibodies (Castillo et al., 2006). Steroid pulse ther- COUNSELING
apy (intravenous methylprednisolone 0.5–1 gram per
day for 3–5 days) is effective in eliminating seizures The American Academy of Neurology has established
in patients with limbic encephalitis and antibodies quality standards for evaluation and management of
against voltage-gated potassium channels- LGI1 com- epilepsy. The standards are summarized in Table 7-14.
plex (Malter et al., 2010). There is a suggestion that For each of these standards, it is important to
inflammation may play a role in chronic epilepsy, document consideration and discussion. The qual-
even when the initial underlying cause is not autoim- ity standards are particularly relevant to patients with
mune, and immune therapies are in early testing for drug-resistant epilepsy. They ascertain that the treating
drug-resistant epilepsy. physician will reconsider the epilepsy diagnosis and
will attend to new features that might alter treatment.
Investigational Approaches to Discussion with the patient should include suf-
Management ficient feedback to ensure that the patient or care-
giver understands the issues. All questions are ideally
New approaches are needed to further improve sei- answered. Documentation of these discussions is key.
zure control for patients with refractory epilepsy. Not only does this ensure that we are reminded in
Investigational approaches are both medical and sur- future visits when the issues were discussed, but good
gical. Table 7-13 lists some of the promising therapies. documentation affords some liability protection.
VNS management algorithm
Initial output settings:

Intensity: 0.25mA Titrate output current
Frequency: 30 Hz intensity by 0.25 mA Start reducing the time
Pulse width: 250 μsec every 2 weeks to 3 off by one decrement
Time on: 30 sec months as needed, upto every 1-3 months
Time off: 5 min 1.5-2 mA
Increase pulse width to Switch to rapid cycling

Reduce frequency to 20 500 μsec if well- paradigm, (7 sec on and
Hz if sleep apnea is tolerated 0.2 min off)
suspected
Initial magnet current Titrate magnet current

settings: intensity by 0.25 mA
Intensity: 0.25 mA every 2 weeks to 3
pulse width: 500 μsec months as needed to
successfully abort
Time on: 60 sec
seizures
Figure 7-10: VNS Management Algorithm.
Counseling long auras that allow them time to get off the road
before the altered awareness. These leniencies are not
Counseling for patients with epilepsy is complex, without risk and merit careful discussion between
with specific recommendations depending on the clinician and patient and total awareness of the
specific clinical issue. laws in their locale. The pattern of purely nocturnal
sleep-related seizures or pure simple partial seizures
Driving and Other Safety Issues must have been established for at least 6 months in
order to remove restrictions.
Common sense dictates that patients who have sei- Recreational activities such as swimming, hik-
zures, arrhythmia with syncope, and other medical ing, and climbing have risks to both people with epi-
conditions that interfere with mental activities and lepsy and those without. In general, risky activities
neurologic functioning should not be driving, work- become riskier in the presence of epilepsy. A deci-
ing with heavy moving machinery, working at unpro- sion has to be made individually, considering a num-
tected heights, or performing other risky duties. ber of factors including patient age, type of seizures,
Driving is only one part of the discussion of safety. frequency of seizures, and neurologic functioning.
The period of seizure-freedom before a patient can
drive varies between states, from 3 months to 1 year. Sudden Unexplained Death in Epilepsy (SUDEP)
Also, there are differences between states concern-
ing whether the patient must surrender the driver’s The risk of sudden unexplained death is increased in
license or just not drive, and whether the physician epilepsy, more than 20 times that of controls when con-
must report patients with uncontrolled seizures to the sidering the age group of 20–40 years. SUDEP is most
state. So physicians must be familiar with laws in their often in the setting of a seizure, usually a generalized
state. In addition, some businesses have restrictions tonic-clonic seizure. There is evidence that complete
on activities that are more stringent than the state law seizure control essentially eliminates the risk of SUDEP.
for driving. Breakthrough seizures related to poor compliance are a
Some states allow exceptions to the driving restric- risk factor for SUDEP. Most neurologists do not discuss
tion for people with purely nocturnal seizures, or sim- SUDEP with their patients so as not to cause undue
ple partial seizures that do not interfere with ability anxiety. However, bereaved family members feel that
to drive (for example, isolated auras) or patients with patients should have been counseled about SUDEP
Table 7-13 Select Investigational Therapies for Epilepsy

Therapeutic approach Description
Thalamic stimulation Bilateral stimulation of the anterior thalamus may be promising with more
than half the patients experiencing at least a 50% seizure reduction (Fisher
et al., 2010; Jobst et al., 2010a). This stimulation is performed in steady state
with settings adjusted to achieve optimal control. If FDA-approved, this treat-
ment will most likely be used for patients who are not candidates for epilepsy
surgery and have failed most commercially available therapies including VNS.
Responsive cortical This treatment modality is based on the finding that an electrical stimulus
stimulation can abort a seizure if delivered very shortly after onset. Responsive cortical
stimulation requires prior localization of the epileptogenic zone or zones.
Candidates for this type of stimulation most probably will have bilateral inde-
pendent seizure foci or an epileptogenic zone that overlaps with eloquent
cortex, thus precluding surgical therapy. The stimulating device also records.
Stimulation is delivered on demand through implanted depth or subdural
strip electrodes when an electrographic seizure onset is first detected. In
the pivotal clinical trial more than 40% of patients had at least 50% seizure
reduction (Morrell MJ; RNS System in Epilepsy Study Group. Responsive
cortical stimulation for the treatment of medically intractable partial epilepsy.
Neurology. 2011;77:1295–304).
Trigeminal nerve In this non-invasive treatment modality, ophthalmic and supratrochlear
stimulation branches of the trigeminal nerve are stimulated bilaterally transcutaneously.
A recent study provided evidence of efficacy and safety in drug-resistant
partial epilepsy (Degiorgio et al., 2013)
Radiosurgery Radiosurgery involves radiation beams precisely directed to a target from
different angles with the help of a stereotactic frame that immobilizes the
head. It is a useful treatment modality for epilepsy associated with small
hypothalamic hamartomas (which can be difficult to access surgically). It
is also being explored for mesial temporal lobe epilepsy with hippocampal
sclerosis. Studies indicate that it is an effective treatment, with more than
three-quarters of patients becoming seizure-free after a latency of 1 to 2 years
(Barbaro et al., 2009). If FDA approved for mesial temporal lobe epilepsy,
this procedure may be useful for individuals with hippocampal sclerosis who
are not willing to have standard open surgery.
risk, and that fear of SUDEP would have improved com- few forms of epilepsy. While there are few instances
pliance. Physicians should consider counseling select where epilepsy genetics predict AED efficacy, obtain-
patients who are at high risk of SUDEP due to frequent ing a genetic diagnosis can be very valuable for clo-
uncontrolled generalized tonic-clonic seizures. Patients sure and to avoid unnecessary continued search for
with mild seizures and patients with well-controlled epi- an etiology. An underlying genetic etiology is often
lepsy need not be educated about SUDEP. evident without specific genetic testing. Most com-
monly, patients are interested to know the risk of
Inheritance epilepsy in their children, or parents may want to
know the risk of having another affected child. Most
Many epilepsies have a genetic basis or a genetic genetic epilepsy syndromes, such as juvenile myo-
component. Genetic tests are available for only a clonic epilepsy, are polygenic and the risk of epilepsy
Table 7-14 Recommended Quality Measures for Epilepsy Care

Quality measure Where applicable Description
Seizure types All patients Document seizure types and current seizure fre-
Current seizure All visits quency for each type
frequency
Etiology of epi- All patients Document etiology of epilepsy or epilepsy syndrome
lepsy or epilepsy All visits (or specify as unknown)
syndrome
EEG results All patients Document results of at least one EEG reviewed or
All initial evaluations requested or order EEG if not previously performed
Brain MRI (or CT) All patients Document result of at least one MRI scan reviewed
results All initial evaluations or requested or order MRI scan if not previously
obtained. CT is acceptable though MRI preferred
AED side effects All patients Document inquiry into and counseling about AED
All visits side effects
Surgical therapy Patients with Document that surgical therapy was considered
consideration or drug-resistant epilepsy (and referral made) in patients with drug-resistant
referral At least every 3 years epilepsy or why it is not appropriate
Counseling about All patients Document counseling about epilepsy-specific safety
safety issues At least once a year issues relevant to age, seizure type, occupation and
leisure activities (e.g., injury prevention, burns, driv-
ing restrictions, or bathing)
Counseling for Female patients of child- Document counseling about how epilepsy treat-
women of childbearing potential ments may affect contraception, pregnancy, and the
bearing potential At least once a year fetus
in a child is less than 6–7%. However, epilepsy is 2 minutes. For complex partial seizures, treatment
monogenic in some families, with higher associated should start after 10–15 minutes.
risk in offspring. Convulsive status epilepticus includes status epi-
lepticus with tonic or clonic motor manifestations,
whether generalized or focal. Non-convulsive status
STATUS EPILEPTICUS epilepticus includes complex partial status epilepticus
without tonic-clonic motor activity and absence status
Status epilepticus is commonly encountered in a busy epilepticus. Subjective simple partial status epilepticus
emergency room or neurology practice and treatment is usually considered separately and is often referred
should be rapid and aggressive. Status epilepticus is to as aura continua. Generalized convulsive status epi-
defined as seizure activity continuing for 30 minutes or lepticus is a medical emergency requiring immediate
recurrent seizures without recovery between events. treatment. While non-convulsive status epilepticus is
However, since there is risk of neuronal damage with a lesser emergency, it also requires prompt therapy.
increasing seizure duration, aggressive treatment is
warranted and should not wait for the 30-minute Diagnosis
definition. Acute therapy of generalized convulsive
seizure activity should start within 5 minutes, based EEG is performed as soon as possible on patients
on the finding that generalized tonic-clonic activ- with suspected status epilepticus. This is for confir-
ity that stops spontaneously rarely lasts longer than mation of the diagnosis, characterization of the ictal
discharge pattern, and monitoring of response to (Alldredge et al., 2001; Silbergleit et al., 2012). This
treatment. Confirmation of the diagnosis is particu- can stop the seizure activity in more than half of
larly important since it is common for psychogenic patients. Alternatively, if the patient has a history of
non-epileptic events to present as clinical status prolonged seizures, the caregivers may administer
epilepticus. rectal diazepam, which can be helpful even though it
Continuous EEG monitoring of patients with sta- is FDA approved for seizure clusters rather than status
tus epilepticus should be performed when possible. epilepticus. Use of rectal diazepam before emergency
The possibility of persistent electrical seizure activity room arrival was associated with shorter duration
should always be considered in a patient with con- of status epilepticus, even if status was still ongoing
vulsive status epilepticus who does not wake up after upon arrival.
motor activity stops. Figures 7-11a through 7-11c show suggested pro-
In a patient without prior known epilepsy, iden- tocols for treatment of status epilepticus, based on
tification of the cause of the status epilepticus usu- Vanderbilt protocols. As shown in the figures, ben-
ally requires imaging with MRI or CT, blood tests zodiazepines and fosphenytoin are cornerstones
(glucose and electrolytes), and sometimes lumbar for treatment of generalized tonic clonic status
puncture (LP) for possibility of CNS infection. epilepticus.
However, imaging and LP should be performed Complex partial status epilepticus can be treated
only after convulsive status epilepticus has been with the same initial medications (but a lower dose
controlled. of lorazepam), but if additional therapy is needed,
non-sedating intravenous AEDs should be used
Treatment preferentially.
Generalized absence status epilepticus can be
Treatment of the status epilepticus can begin before treated with IV lorazepam and valproate.
hospitalization, with paramedics administering loraz- Generalized myoclonic status epilepticus can be
epam 2–4 mg IV or midazolam 10 mg IM (dosing treated with IV lorazepam, IV valproate, and/or IV
for adults and children weighing more than 40 kg) levetiracetam.
a Treatment of Generalized Convulsive Status Epilepticus

0-15 minutes
IV: draw blood for studies; normal saline at TKO

If blood glucose low: 1 amp D50 (50 mL IV) and start second IV with D5NS
Thiamine 100 mg IVP if given D50 or if malnourished or alcoholic
If actively seizing:
Lorazepam IV, 10 mg at <2 mg/min
Fosphenytoin, total dose 20 mg/kg; max. delivery rate = 150 mg/min (slower if there is
AV block or hypotension)
• Do not use if status is due to a metabolic cause unlikely to respond to phenytoin
(such as cocaine intoxication)
• Current treatment with phenytoin is not a contraindication
15-60 minutes
For patients with decreasing seizures after fosphenytoin load:

Addtional 10 mg/kg of fosphenytoin
For patients continuing to seize who require intubation:
Thiopental ± succinylcholine (avoid succinylcholine if possible)
Consider additional dose of fosphenytoin 10 mg/kg)
For continuing seizures post intubation:
Midazolam: 0.3 mg/kg by slow IV injection, may repeat at 5-min intervals x3.
Midazolam infusion: 2 μg/kg/min; increase by 1 μg/kg/min every 15 min until
seizure activity stops
or:
Protofol: 1-2 mg/kg, then 2-10 mg/kg/h
or:
Pentobarbital: 5 mg/kg loading dose (to achieve burst-supression pattern on EEG
with interburst intervals of approx. 7 sec); repeat load as necessary to max. of 15
mg/kg, then 1-3 mg/kg/h maintenance dose ×6-12 h; reevaluate patient
or:
Phenobarbital: 20 mg/kg at <100 mg/min
After 60 minutes
EEG in progress if patient has not woken up
Identify etiology of status (CT or MRI +/– LP if indicated) and develop appropriate
treatment plan
Treat hyperthermia if present
Beside glucose for patients still seizing
Check phenytoin level
Maintenance AEDs if indicated
Figure 7-11a: Suggested Protocol for Treatment of Generalized Convulsive Status Epilepticus.

b Treatment of Complex Partial Status Epilepticus

0-15 minutes
IV: normal saline at TKO
Continuous EEG in progress
Lorazepam IV, 1-2 mg at <2 mg/min
Fosphenytoin, 20 mg/kg IV-max delivery rate 150 mg/min
or
Levetiracetam 20 mg/Kg IV
or
Valproate 20 mg/Kg IV
or
Lacosamide 400 mg IV
15-60 minutes
If seizure activity continues, cross over to another agent
Fosphenytoin 20 mg/kg IV
or
Levetiracetam 20 mg/Kg IV
or
or
Lacosamide 400 mg IV
Late treatment
Continue to sequence nonsedating AEDs, avoiding excessive sedation

Avoid general anesthesia as long as possible
Figure 7-11b: Suggested Protocol for Treatment of Complex Partial Status Epilepticus.
c Treatment of Generalized Absence Status Epilepticus
IV: normal saline at TKO

Continuous EEG in progress
Lorazepam IV, 1-2 mg at <2 mg/min
If seizure activity continues,

Levetiracetam 20 mg/kg IV (limited data for efficacy)
Figure 7-11c: Suggested Protocol for Treatment of Generalized Absence Status Epilepticus.

Table 7-15 Anti-epileptic drugs: How supplied.

Generic name Brand name How supplied
Carbamazepine Tegretol 100 mg chewable
200 mg tablets
100 mg/5 ml suspension
Tegretol-XR 100 mg, 200 mg, 400 mg tablets
Carbatrol 100 mg, 200 mg, 300 mg capsules
Generic All of the above
Clonazepam Klonopin 0.5 mg, 1 mg or 2 mg tablets
(Generic is same) 0.125 mg, 0.25 mg, 0.5 mg, 1 mg or 2 mg orally disintegrating tablets
Divalproex Depakote 125 mg, 250 mg, 500 mg tablets
125 mg sprinkle capsules
Depakote ER 250 mg, 500 mg tablets
Generic All the above
Ethosuximide Zarontin 250 mg capsules
(Generic is same) 250 mg/5 ml oral solution
Felbamate Felbatol 400 mg and 600 mg tablets
(Generic is same) 600 mg/5 ml oral Suspension
Gabapentin Neurontin 100 mg, 300 mg, 400 mg capsules
(Generic is same) 600 mg, 800 mg tablets
Lamotrigine Lamictal 25 mg, 100 mg, 150 mg, 200 mg tablets
(Generic is same) 2 mg, 5 mg, and 25 mg chewable dispersible tablets
25 mg, 50 mg, 100 mg, 200 mg orally disintegrating tablets
Lamictal XR 25 mg, 50 mg, 100 mg, 200 mg, 250 mg, 300 mg tablets
Levetiracetam Keppra 250 mg, 500 mg, 750 mg, 1000 mg tablets
(Generic is same)
Keppra XR 500 mg, 750 mg tablets
Methsuximide Celontin 150 mg, 300 mg capsules *
Oxcarbazepine Trileptal 150 mg, 300 mg, 600 mg tablets
(Generic is same)) 300 mg/5 ml oral suspension
Phenobarbital – 15 mg, 16.2 mg, 30 mg, 32.4 mg, 60 mg, 64.8 mg, 97.2 mg, 100 mg
tablets
20 mg/5 ml elixir.
Phenytoin Dilantin 100 mg and 30 mg capsules of phenytoin sodium
50 mg tablets of phenytoin (infatab)
125 mg/5ml suspension
Phenytek 200 mg, 300 mg capsules
Generic 100 mg, 200 mg, 300 mg capsules, 125 mg/5ml suspension
Primidone Mysoline 50 mg and 250 mg tablets
(Generic is same)
Tiagabine Gabitril 2 mg, 4 mg, 12 mg, 16 mg tablets
Topiramate Topamax 25 mg, 50 mg, 100 mg, 200 mg tablets
(Generic is same) 15 mg, 25 mg sprinkle capsules
Valproic acid Depakene 250 mg capsules
250 mg/ 5ml syrup
Zonisamide Zonegran 25 mg, 100 mg capsules
Generic 25 mg, 50 mg, 100 mg capsules
Carbamazepine titration & dosing

Initiation Titration Optimization
-Extended release
preparations provide
Increase to 200 mg bid x steadier levels
100 mg bid for immediate 3 days then 300 mg bid as -Use bid dosing
release or 200 mg Qhs for initial target dose. The -Consider tid dosing for
extended release dose can be increased by immediate release
preparation 100-200 mg every 3 days preparations
as needed - Little therapeutic
benefits, toxicity expected
after a level of 12 mcg/ml
Figure 7-12: Carbamazepine Dosing.
Lacosamide titration & dosing

-Lacosamide is better
tolerated and doses
higher than 400 mg per
Increase by 100 mg every day are more likely to be
one to two weeks as successful when used in
50 mg bid or 100 mg Qhs needed until seizures are conjuction with non-
x 1 week controlled, adverse sodium-channel AEDs
then 100 mg bid effects appear, or a dose -Tolerability may be
of 600 mg per day is helped by TID dosing and
reached. by removal of sodium
channel AEDs when
higher doses are needed
for seizure control.
Figure 7-13: Lacosamide Dosing.

Lamotrigine titration & dosing Levetiracetam titration & dosing

Initial monotherapy or Initial Initial Titration
Combination with valproate Combination with enzyme-
adjunctive to non-enzyme-
(regardless of other drugs) inducing AEDs Using extended Increase by 500 mg per
inducing AEDs Using immediate
release preparation week as needed until
Orange starter kit Blue starter kit Green starter kit release preparation
seizures are controlled,
25 mg every other am × 2
25 mg Qam × 2 weeks 50 mg Qam × 2 weeks 500 mg Qhs × 1 week adverse effects appear,
weeks 250 mg bid × 1 week
50 mg Qam × 2 weeks
25 mg Qam × 2 weeks
100 mg Qam × 2 weeks then 1000 mg Qhs or no further benefit is
100 mg Qam × 1 weeks 200 mg Qam × 1 week then 500 mg bid
50 mg Qam × 1 week noted after the last
May start at 1000 mg increase beyond 2000
Commericial starter kit for extended release (XR) preparation- if not using extended
Qhs if rapid onset of May start at 500 mg
release product, split into bid dosing as feasible, Administer with meals. bid if rapid onset of mg per day.
Avoid late dosing due to possible insomnia. action is needed and
there is no concern action is needed and Suggested titration
Further titration Further titration Further titration for behavioral there is no concern steps
adverse effects for behavioral (Qhs or am-pm):
100 mg Qam × 1 week 50 mg Qam × 1 week 200 mg Qam + 100 Qpm
Then 200 mg Qam Then 100 mg Qam × 1 week adverse effects 1500 mg or 500-1000
Then 200 mg bid Start at 250 mg Qhs 2000 mg or 1000-1000
Increase by 100 mg every Increase by 50 mg every Increase by 100 mg every (immediate release) Start at 250 mg Qhs
2500 mg or 1000-1500
two weeks as needed until two weeks as needed until two weeks as needed until if there is concern for if there is concern for
seizures are controlled,
3000 mg or 1500-1500
seizures are controlled seizures are controlled
behavioral adverse behavioral adverse
adverse effects appear, or a adverse effects appear, or a adverse effects appear, or 3500 mg or 1500-2000
effects effects
serum level of 20 mcg/ml serum level of 20 mcg/ml an AED level of 20 mcg/ml 4000 mg or 2000-2000
has been reached has been reached has been reached
Administer bid if not using extended-release (XR) preparation or if seizures persist Optimization
-The maximum dose approved by the FDA is 3000 mg per day, but doses
Optimization up to 4000 mg per day were tested in trials. Doses higher than 4000 mg
• The maximum dose is lowest for use with valporate per day should be avoided unless serum level is low despite adequate
• While lamotrigine doses greater than 500 mg per day are not FDA approved, compliance
higher doses may be necessary in drug-resistant patients, particularly in -Levetiracetam therapy may be associated with paradoxical increase in
combination with enzyme inducing drugs. seizures at higher doses
• The maximum doses is not known. Serum level may be more useful than -TID dosing with immediate release preparation or bid dosing with
dose to identify the point at which there the risk-benefit balance becomes
unfavorable for additional titration. Little benefit and greater risk of adverse extended release preparation may improve tolerability-efficacy at doses
effects are expected after a serum level of 20 mcg/ml. higher than 2000 mg per day
-Levetiracetam serum level is not particularly useful to identify toxic dose.
The upper limit is not known. The dose should not be reduced just because
of a serum level that exceeds the upper limit in the “therapeutic range”.
Figure 7-14: Lamotrigine Dosing. However, a low level (for example below 10-15 mcg/ml) despite
compliance may encourage a higher dose if there are no adverse effects
and seizures are not controlled
Figure 7-15: Levetiracetam Dosing.
Oxcarbazepine titration & dosing

Initial Titration Optimization
Increase by 300 mg every The maximum dose

150 mg bid × 1 week week as neede until used in trials was 1200
then 300 mg bid seizures are controlled, mg PO bid
adverse effects appear, or a
May start at 300 mg bid
serum level of 35-40 mcg/
in a young individual if TID dosing may improve
ml has been reached
rapid onset of action is tolerability at doses
important higher than 1200 mg
Suggested titration steps
(am-pm or am-noon-pm): per day
Would start at 150 mg 300-600
Qhs × 1 week in an old If used concomitantly
600-600
individual at risk of with another sodium
600-900 or 600-300-600
hyponatremia or with channel blocker,
900-900 or 600-600-600
other concern for tolerability may be
900-1200 or 600-600-900
tolerability improved by a 2-hour
1200-1200 or 900-600-900
interval between the
doses of the two AEDs
Figure 7-16: Oxcarbazepine Dosing.

Phenytoin titration & dosing

Titration should be –When possible, use

primarily based on extended release
clinical response, phenytoin sodium
secondarily on serum capsules (30 and 100 mg)
levels. rather than immediate
200-400 mg per day, in view of 0 order release phenytoin
initially given as one dose kinetics, smaller tablets.
at bedtime increments should be
– Use bid or even tid
–200 mg per day is used when in the
dosing if needed when
preferable for the elderly therapeutic range. Rough
seizures are drug-
and for individuals with guide to titration :
resistant
impaired liver funtion –increase by 100 mg if the
– For fine tuning,
level is <8 mcg/ml
combinations of 30 and
–increase by 60 mg if the
100 mg can be used for
level is 8-12 mcg/ml
10 mg increments or
–increase by 30 mg if the
decrements
level is 12-15 mcg/ml
Figure 7-17: Phenytoin Dosing.
Topiramate titration & dosing

Initial titration
25 mg Qhs × 1 week Optimization
50 mg Qhs × 1 week
75 mg Qhs × 1 week – The maximum dose
100 mg mg Qhs approved by FDA is 400 mg
per day, but higher doses
Further titration were used in trials and could
If 100 mg is not enough If 300 mg is not enough be considered if there is
for seizure control for seizure control, add incremental benefit with
125 mg Qhs × 1 week 25 mg × 1 week increasing doses
150 mg Qhs × 1 week 50 mg × 1 week – Topiramate serum level is
175 mg Qhs × 1 week 75 mg × 1 week not particularly useful to
200 mg Qhs 100 mg for a total of identify toxic dose. However,
400 mg per day a low level despite
If 200 mg is not enough
(100-300 or 200 mg bid) compliance may encourage a
for seizure control, add
higher dose if there are no
25 mg Qam × 1 week
adverse effects and seizures
50 mg Qam × 1 week
are not controlled
75 mg Qam × 1 week
100 mg Qam
Figure 7-18: Topiramate Dosing.

Divalproex titration & dosing

–Extended release
preparation provide
steadier levels
–Use bid dosing to
–Increase by 250 mg as optimize seizure control
500 mg Qhs using the
needed. in drug-resistant patients
extended release
–Avoid a dose higher than –Consider tid dosing for
preparation or 250 mg
1000 mg per day in a delayed release
bid for the delayed
woman of childbearing preparation
release preparation
potential. –Little benefit and
increased risk of toxicity
is expected beyond a
serum level of 100 mcg/
ml
Figure 7-19: Valproate (Divalproex) Dosing.

8
SAMPLES AND CASE DISCUSSIONS
Karl E Misulis
EEG STILLS Absence Seizure

14 & 6 Positive Spikes—14 Hz
Predominant 10-year-old with episodes of spacing out and staring
(Figure 8-4). He was previously diagnosed with atten-
54-year-old male with altered mental status tion deficit hyperactivity disorder.
(Figure 8-1). The 14 Hz positive bursts are best appre-
ciated with the linked ear or contralateral ear refer-
Absence Without Spike
ence. This benign variant is reported with increased
incidence in Reye syndrome, but also other encepha- 7-year-old girl with staring spells (Figure 8-5). The
lopathies (Yamada et al., 1977). EEG showed a burst of generalized 2.5–2 Hz delta
activity associated with a delayed response to a
14 & 6 Positive Spikes—6 Hz Predominant command. This may be consistent with an absence
seizure. Bursts of rhythmic delta activity without
74-year-old with generalized epilepsy (Figure 8-2). spikes have been described as a rare ictal pattern in
The recording shows 6 Hz intermittent notched absence seizures. However, there is a debate about
rhythmic activity in both temporal regions. Elsewhere the nature of such discharges brought on with
the EEG recorded occasional generalized 3–4.5 Hz hyperventilation.
spike-and-wave discharges.
Alpha Coma
60 Hz Electrical Artifact
14-year-old who had a cardiac arrest (Figure 8-6). He
60 Hz artifact at Fp1, reflecting increased impedance was on propofol and fentanyl. Diffuse alpha-range
at that electrode (Figure 8-3). activity is clearly abnormal.
305
Figure 8-1: 14 & 6 Positive Spikes—14 Hz Predominant.
Figure 8-2: 14 & 6 Positive Spikes—6 Hz Predominant.

Figure 8-3: 60 Hz Electrical Artifact.

Figure 8-5: Absence Without Spike.
Figure 8-6: Alpha Coma.
Samples and Case Discussions 309
Figure 8-7: Alpha-theta Coma.
Alpha-theta coma with bifrontal ictal activity. Note the onset of the eye
blinks after eye opening with dramatic attenuation of
38-year-old who had a cardiac arrest (Figure 8-7). He the posterior dominant rhythm.
was unresponsive to voice but had spontaneous eye
opening. He had extensor posturing to stimulation. The Generalized Polyspike-and-Wave
EEG shows generalized frontally dominant alpha-theta
activity, not reactive to passive eye opening and closure. 38-year-old male with past epilepsy, extensive burn
injuries, and recurrent seizures in the hospital
Periodic Discharges with Anoxia (Figures 8-10a and 8-10 b). EEG showed frequent gen-
eralized polyspike-and-wave discharges consistent
56-year-old with witnessed tonic-clonic jerking with generalized epilepsy.
after cardiac arrest (see the series of EEGs shown in
Figures 8-8a through 8-8d). The EEG showed con- Rhythmic Midtemporal Theta of Drowsiness
tinuously evolving pattern and frequency, with abrupt
termination of rhythmic EEG activity with attenu- Rhythmic midtemporal theta of drowsiness is seen in
ation followed by periodic activity. The evolution is this otherwise normal EEG (Figure 8-11). This can be
consistent with an ictal pattern. However, the anoxic easily misread as pathological, especially with unilat-
etiology implies a poor prognosis. eral appearance especially at onset.
Eye Blinks Hepatic Encephalopathy
17-year-old with anger outbursts (Figure 8-9). 44-year-old woman with cirrhosis with hepatic failure,
Repetitive eye blinks and eye flutter may be confused and declining mental status (Figures 8-12a through
Figure 8-8: Periodic Discharges with Anoxia.

Figure 8-8: (Continued)
8-12c). The semi-periodic triphasic waves had a shift- Hyperventilation Artifact

ing anterior-posterior predominance. Stimulation
seemed to activate the discharges. Ammonia was 103 29-year-old female with staring spells (Figures 8-14a
(normal range 11–35 mcmol/L). through 8-14c). The patient was lying over the left
side. Readjustment of head position largely elimi-
nated the left occipital artifact (Figure 8-14c). The
HSV Encephalitis
EEG was normal.
94-year-old female with HSV encephalitis. She had
been having episodes of eye twitching, which in Hypsarrhythmia
retrospect may have been small seizures, for sev-
eral days. Then she had a decline in level of activity 9-month-old male with prematurity and one month
progressing to nonverbal. She was in stupor at the of epileptic spasms (Figures 8-15a and 8-15b). MRI
time of the EEG (Figure 8-13a), which shows a dis- was normal. The study recorded 3 clusters of infantile
organized and slow background with left temporal spasms. The associated EEG changes were high volt-
periodic discharges. MRI (Figure 8-13b) showed age slow waves with superimposed fast activity fol-
a T2 hyperintense lesion of the left anterior and lowed by 1–2 seconds of generalized attenuation. The
lateral>medial temporal lobe. She had a positive interictal EEG showed multifocal epileptiform dis-
CSF test for HSV-1. charges, most often right parietal, and a chaotic high
Figure 8-10: Generalized Polyspike-and-wave.

Figure 8-11: Rhythmic Midtemporal Theta of Drowsiness.
Figure 8-12: Hepatic Encephalopathy.

Figure 8-13: HSV Encephalitis.
amplitude disorganized slow background with no video EEG monitoring. Her EEG was previously
posterior rhythm, consistent with hypsarrhythmia. interpreted by a general neurologist as showing right
and left midtemporal spikes and an electrographic sei-
Wicket Spikes zure from the left temporal area. The EEG recording
in Figure 8-16 shows wicket patterns from both tem-
75-year-old woman with spells that were determined poral regions, but predominant on the left. The higher
to be non-epileptic when evaluated with inpatient voltage sharply contoured waves are components of
Figure 8-14: Hyperventilation Artifact.

Figure 8-16: Wicket Spikes.

Figure 8-17: Breach Rhythm.

Referential montage.
a monorhythmic activity that waxes and wanes in its EEG showed increased beta activity and fragments of
voltage, but does not evolve in frequency. mu rhythm at C3, suggesting breach rhythm. The CT
scan confirmed the presence of a skull defect. There had
Breach Rhythm been no mention of craniotomy in his hospital notes,
but a search of the records determined that he had had
77-year-old man with altered mental status (Figures 8-17a craniotomy for placement of cortical stimulating elec-
through 8-17c). He had old right thalamic stroke. The trode to relieve thalamic pain syndrome.
Figure 8-17b: Breach Rhythm.

Bipolar Montage.
Figure 8-17c: Breach Rhythm.

CT brain Showing the Left-sided Skull Defect.
Generalized Tonic-clonic Seizures activated with arousal and stimulation. The MRI
shows typical increased left posterior and right frontal
21-year-old man with juvenile myoclonic epilepsy has cortical ribbon signal on diffusion MRI images. The
generalized tonic-clonic seizures with no aura; he may finding is absent in the FLAIR MRI. The autopsy con-
stare before the motor activity (Figures 8-18a and 8-18b). firmed the diagnosis of prion disease with the charac-
He also has myoclonic jerks, mostly in the am. The gen- teristics of sporadic Creutzfeldt-Jakob disease.
eralized tonic-clonic seizure started with generalized,
frontally dominant, polyspikes and spike-and-wave dis- Cough Syncope
charge initially at 9 Hz then 3–6 Hz. The activity evolved
to approximately 10 Hz rhythmic activity in transition to 48-year-old man with obesity and spells of unclear
the generalized tonic-clonic seizure. nature that were determined to be non-epileptic
(Figures 8-21a and 8-21b). He had an episode of brief
Burst Suppression multifocal myoclonus and altered responsiveness
after persistent cough in the setting of hyperventila-
36-year-old woman with severe closed head injury in tion. The EEG showed generalized slow activity then
pentobarbital coma for increased intracranial pressure generalized attenuation, followed by slow activity
(Figure 8-19). CT showed multiple areas of intracranial then recovery of normal EEG rhythms. The findings
hemorrhage with increasing surrounding edema. EEG represent an episode of cough syncope.
showed a burst suppression pattern. The bursts consisted
of generalized irregular theta and delta activity lasting Pentobarbital Coma
2 to 4 seconds. Suppression periods ranged between
30 seconds to 4.5 minutes by the end of the recording. 24-year-old male with severe traumatic brain injury
from motorcycle accident (Figures 8-22a and 8-22b).
Creutzfeldt-Jakob Disease CT showed right frontal intraparenchymal hemor-
rhage, diffuse subarachnoid hemorrhage, subdural
74-year-old man with rapidly progressive demen- hematoma along the falx, extensive intraventricular
tia (Figures 8-20a through 8-20c). The EEG showed hemorrhage predominantly on the left, right to left
intermittent left hemisphere periodic discharges midline shift, and uncal herniation. He was placed in
Figure 8-18: Generalized Tonic-clonic Seizures.

Figure 8-19: Burst Suppression.
Figure 8-20: Creutzfeldt-Jakob Disease.

pentobarbital coma for treatment of increased intra- through 8-23c). He has left hemiplegia, can only use
cranial pressure. The EEG segments show the effect of the right arm. CT shows right frontal and right tem-
deepening pentobarbital coma, with increasing dura- poral encephalomalacia, diffuse enlargement of the
tion of interburst intervals, until complete suppression. ventricular system, and a ventriculoperitoneal shunt
entering from a left parietal approach.
Polymorphic Delta Activity The EEG shows polymorphic delta activity as
well as a sharp wave in the right posterior quadrant,
19-year-old man with severe traumatic brain injury, the presumed epileptogenic zone. In this case the
daily complex partial seizures, and occasional second- polymorphic delta activity is more related to func-
arily generalized tonic-conic seizures (Figures 8-23a tional (focal epilepsy) than structural lesion.
Figure 8-21: Cough Syncope.

Figure 8-22: Pentobarbital Coma.
EKG Artifact ear reference recording and longitudinal bipolar

recordings.
38-year-old obese man with hypertension and hyper-
glycemia (Figures 8-24a and 8-24b). EKG artifact is Parkinsonism with Tremor
most prominent with ipsilateral ear reference. It will
be noted that the artifact is of opposite polarity on 84-year-old man with advanced Parkinson’s disease
the two sides. It became less prominent with linked complicated by anxiety and dementia (Figures 8-25a
and 8-25b). Examination showed bilateral resting and Attenuation with Subdural Hematoma
postural tremor, worse with stressful discussions. He
also had a mild head tremor and chin tremor. EEG Patient with subdural hematoma with signs on CT of
was obtained because of episodes of unresponsive- acute and chronic blood (Figures 8-26a and 8-26b).
ness. The EEG above shows tremor artifact in the left The EEG shows attenuation over the left hemisphere.
posterior head region. The loss of faster frequencies is evident on this side.
Figure 8-23: Polymorphic Delta Activity.

c

Figure 8-25: Parkinsonism with Tremor.

Figure 8-26: Attenuation with Subdural Hematoma.
Photic Driving Response Polymorphic Delta Activity
The patient is being evaluated for epilepsy This is a 42-year-old woman with seizures since
(Figure 8-27). During photic stimulation, a promi- age 15 (Figure 8-28a). The EEG was done one day
nent photic driving response is seen. Because of the after the police found her wandering the street
very regular activity that is time-locked to the stimu- in complex partial status epilepticus or postictal
lus, and the abrupt termination at the end of photic confusion. The EEG showed irregular delta-theta
stimulation, this should not be confused with epilep- activity in the right hemisphere, with midtemporal
tiform discharge. and posterior temporal predominance. There was
Figure 8-27: Photic Driving Response.
Figure 8-28: Polymorphic Delta Activity.

also attenuation of posterior dominant rhythm on She is described as being in the awake but confused
the right. state, so she is not deeply asleep. This pattern is too
CT brain shows right temporal encephalomalacia slow for simple drowsiness. Slowing of the back-
(Figure 8-28b). The slowing on the EEG is likely a com- ground can be seen in patients with infections and
bination of this structural lesion plus postictal slowing. multiple metabolic abnormalities, however, the
findings are not specific. The interpretation of the
Excess Beta Activity recording should reflect the non-specific nature of
the results.
An adult female is being evaluated for syncope
(Figure 8-29). This patient has excessive beta activity, PLEDs
which in this case was due to clonazepam, a benzodi-
azepine. Barbiturates also typically produce excessive An adult female is being evaluated for mental sta-
beta activity. This is commented on in the report, but tus changes associated with fever and seizures
not interpreted as a specific abnormality. (Figure 8-31). This EEG shows periodic lateralized
epileptiform discharges (PLEDs). These are typi-
Encephalopathy cally seen in patients with herpes encephalitis, as
in this patient. However, they can also be seen with
An adult female is being evaluated for mental sta- stroke and other destructive lesions. The etiology
tus changes (Figure 8-30). The pattern shows of PLEDs cannot be determined without clinical
symmetric slowing consistent with encephalopathy. information.
Figure 8-29: Excess Beta Activity.

Figure 8-30: Nonspecific Encephalopathy.
Figure 8-31: PLEDs.
Eye Blink The background is disorganized and there are

high-voltage, polymorphic discharges. This is char-
A patient being evaluated for seizures has the follow- acteristic of hypsarrhythmia. Patients with hypsar-
ing EEG (Figure 8-32). The patient is awake. Eyes rhythmia are more likely to have seizures including
open at the midpoint of the recording, as indicated by infantile spasms. West syndrome is the triad of infan-
the technician’s comment. tile spasms, hypsarrhythmia, and mental retardation,
Eye blink artifact is shown on the right side of although not all three of the triad have to be present
the recording. The activity is coming from the fron- for diagnosis.
tal electrode leads. The activity is more stereotyped
than would be seen with FIRDA. The patient is in the
Absence Seizure
awake state and the localization of the activity takes
it out of the realm of vertex activity. Frontal arousal A 10-year-old boy is being evaluated for seizures
rhythm is an unusual rhythmic activity seen in young (Figure 8-34). He has episodes of unresponsiveness
children awakening from sleep, and has a different without focal motor activity and without loss of pos-
appearance. ture. He has a normal examination. The following
epoch is from his recording. The technician did not
Hypsarrhythmia notice any behavioral correlate to the repetitive activ-
ity noted in this epoch.
A 3-year-old male is being evaluated for seizures and This patient has a 3-per-second spike-wave pat-
developmental delay (Figure 8-33). The following tern. This is typical of primary generalized epilepsy.
EEG is recorded. Without a behavioral correlate, one could only


speculate as to the type of seizure, however, with there Focal Attenuation in a Patient with
being no motor activity associated with this discharge, Right Hemisphere Stroke
absence seizure is the clinical interpretation. Drowsy
burst should not have the sharp component and does This patient has had a large right hemisphere
not grow as this discharge does. Non-epileptic seizure infarction and subsequently had seizures. EEG
is behavioral symptoms without EEG correlate, dif- (Figure 8-36a) shows signs of the focal damage
ferent from this presentation. Non-epileptic seizures while the MRI (Figure 8-36b) shows typical signs of
may have movement artifact, but the appearance acute-subacute infarction. Review of the EEG shows
and distribution of this discharge indicates that it is frontal activity that is attenuated over the right hemi-
electrocerebral. sphere. However, it would be easy to assume that
the left side with the higher amplitude slowing is the
more abnormal side.
OIRDA
Figure 8-35 shows the EEG of a child with moderate

encephalopathy. He has a history of medulloblastoma SURGICAL CASES
status post chemotherapy and radiotherapy. He pres- Scenario A: Single Discrete Structural
ents with sepsis and lethargy. A portion of the EEG is Lesion with Congruous EEG
shown. This patient has occipital intermittent rhyth- Localization
mic delta activity (OIRDA). This is a counterpart to
FIRDA, and is seen mainly in children. The etiology This is a patient with a single discrete structural lesion
is thought to be a disconnection syndrome between with known epileptogenic potential and congruous
cortical and subcortical centers. The finding is clearly EEG data—the EEG localization fits the structural
abnormal, but not specific for a single etiology. lesion location.
Figure 8-35: OIRDA.
Figure 8-36: Focal Attenuation.
This is a 26-year-old left handed/ambidex- EEG (Figure 8-38a) showed rhythmic dis-
trous man who had seizure onset at 24 years with charge seen best on sphenoidal electrode on the
complex partial seizures. Seizures are described left, indicating inferomesial temporal region discharge.
as hot flash, staring, lip smacking, clenching of Consecutive EEG page (Figure 8-38b) shows spread
the fist. Duration is 15–30 sec. Seizure frequency of the seizure activity in the left temporal region to
is about one per week. He had failed gabapentin, involve T1, F7, and T7. But the discharge maintains
oxcarbazepine, oxcarbazepine + levetiracetam predominance at Sp1.
combination. Neuropsychological testing: low average intel-
EMU seizure description is of a motionless stare lectual range, consistent with educational attain-
followed by lip smacking and right finger extension ment and demographic history. Verbal IQ was 80
movements. (9th percentile), and performance IQ was 88 (21st
MRI (Figures 8-37a and 8-37b) showed a cavern- percentile). He had low performance on language
ous malformation in the left temporal region seen skills overall. Testing showed bilateral prefron-
well on coronal and axial T2 sequences. tal weaknesses with weaknesses in visuospatial
b
a
Figure 8-37a: Focal Structural Lesion—MRI.

Coronal T2 MRI showing cavernous malformation in the
Figure 8-37b: Focal Structural Lesion—MRI.
left mesial temporal region.
Same patient, axial image.
processing. Wada test results were left hemisphere Scenario B: Single Discrete Structural
dominance for language, bilateral memory (passed Lesion with Incongruous EEG Results
memory testing with left and right amobarbital
injections). This patient has a discrepancy between location of
Stereotactic resection through a transcortical the structural lesion on MRI and the EEG localiza-
approach was successful. MRI (Figure 8-39) shows tion. MRI shows a posterior temporal region of
surgical results. He was seizure-free off AEDs at abnormality but EEG suggests anterior temporal
2.5 years follow-up. ictal onset.
Figure 8-38a: EEG: Left Sphenoidal Discharge.

Seizure onset with an alpha-range rhythmic discharge at Sp1, recording from the left inferomesial temporal region.
Figure 8-38b: EEG: Spread of Seizure.

Subsequent page to the previous figure, demonstrating spread of seizure activity in the left temporal region to involve T1, F7,
T7. Discharge maintains prominence at Sp1.
A 42-year-old right-handed man presents with sei-

zures since 10 years of age. The seizures are described
as feeling like a pop in his head, then stares, smacks
lips, repeats the word “what,” and has manual pick-
ing automatisms. Seizures last 20 seconds and he has
word-finding difficulty after the events. Seizure fre-
quency is about 3 per month. He has failed gabapen-
tin, oxcarbazepine, oxcarbazepine + levetiracetam
combination.
EMU seizure description was fumbling with the
left hand followed by right arm dystonic posturing of
the right arm, lip smacking and chewing, versive head
turning and eye deviation to the right in transition to
generalization.
MRI (Figures 8-40a and 8-40b) showed cavernous
malformation in the mid-posterior lateral temporal
region.
EEG (Figures 8-41a and 8-41b) shows ictal onset
with 7-8 Hz rhythmic activity at Sp1 more than
F7 more than T7.
Figure 8-39: Post-operative MRI.
Interictal activity was prominent in the left infer-
Post-operative changes are seen in the left temporal region
on this T2 weighted image. omesial temporal region, Sp1 more than F7, and poste-
rior temporal region, P7 more than T7 (Figure 8-41c).
Figure 8-40a: MRI Brain—Sagittal T1. Figure 8-40b: MRI Brain—Axial T2.

Left mid-posterior lateral temporal lesion. Left mid-posterior lateral temporal lesion.
Figure 8-41a: EEG ictal Onset Sp1.

Ictal onset with rhythmic 7-8 Hz activity starting at Sp1.
Figure 8-41b: EEG Ictal Onset Sp1—Second Example.

Another ictal onset example from the same patient showing predominant inferomesial-anterior temporal region discharge,
Sp1 > F7 > T7.
Figure 8-41c: EEG Interictal Activity.

Same patient, interactivity in the left inferomesial temporal region (Sp1 > F7) and posterior temporal region (F7 > T7).
loud). Duration is usually less than 30 sec, followed by

few minutes of postictal confusion.
EMU recorded seizures that were described as a
funny feeling of flushing and shakiness, with a brief
motionless stare and fluent speech. Simple partial sei-
zures were about one per day, complex partial seizures
were once every two days.
Treatment had been with lamotrigine up to 700
mg/day and levetiracetam up to 3000 mg/day. She
had failed phenytoin, valproate, carbamazepine,
lamotrigine monotherapy and combinations.
EEG (Figure 8-43a) showed ictal onset in the right
temporal region with right inferomesial temporal pre-
Figure 8-42: MRI Post-operative—Sagittal T1
dominance, most prominent at Sp2 with lesser dem-
Sagittal T1-weighted MRI showing successful resection of
the malformation with good clinical result. onstration at F8 and T8.
Interictal EEG (Figure 8-43b) shows discharge in
the right temporal region with right inferomesial tem-
Neuropsychological testing showed borderline poral predominance.
abilities, significantly stronger aptitude for nonverbal In addition to the interictal discharge was
than verbal skills, and stronger memory from visual irregular slow activity in the right temporal region
material than verbal material. (Figure 8-43c).
Wada test results were left hemisphere domi- MRI brain (Figure 8-44a) showed marked atrophy
nance for language, bilateral memory (passed of the right hippocampus.
memory testing with left and right amobarbital FDG-PET (Figure 8-44b) showed decreased
injections). FDG uptake in the right mesial temporal region, as
The cavernous malformation was resected and note in the figure by arrows.
the surgical result is shown in the MRI (Figure 8-42). Right transcortical selective amygdalohippocam-
Clinical outcome was excellent with the patient free pectomy was performed with good surgical result, as
of complex seizures at 7 years follow-up, but he still shown on MRI (Figure 8-44c).
has isolated auras. Clinical outcome was excellent with patient free
of complex partial seizures and auras at 6 years of
Scenario C: Right TLE with Right follow-up. She had two complex partial seizures
Hippocampal Sclerosis and several isolated auras during lamotrigine taper,
but these came under control as the dose was
This is a case of right temporal lobe epilepsy with increased.
right hippocampal sclerosis.
She was a 49-year-old woman with epilepsy since Scenario D: TLE with Left
the age of 15 years but was only diagnosed at 32 years. Hippocampal Sclerosis
The seizures had been attributed to head trauma with
loss of consciousness at age 1 year. This is a case of a patient with left temporal lobe epi-
She had both simple partial and complex partial lepsy due to hippocampal sclerosis.
seizures. The simple partial seizures started with a The patient was a 39-year-old right-handed
feeling of tingling starting around the abdomen and woman with epilepsy since age 10 years. She
rising to the neck and head. She also had a taste in had an antecedent complex febrile seizure at age
her mouth. 18 months.
She also had complex partial seizures described as She had both simple partial and complex partial
80% preceded by an aura progressing to spacing out, seizures. The simple partial seizures started with a
lip smacking, extremity automatisms (ex: swinging of feeling that is hard to explain. She used to have tin-
the right foot), and verbal automatisms (may pray out gling on the left side.
Figure 8-43a: EEG—Ictal Onset.
Ictal onset discharge was in the right temporal region with right inferomesial temporal predominance, Sp2 > F8 > T8.
Complex partial seizures usually had no aura; sei- EMU recording showed seizures characterized
zures mostly started with loss of awareness, a deep by motionless staring, early head turning to the left,
stare, and automatisms including rubbing of the legs right arm dystonic posturing, automatisms of the
and smacking of the lips. left arm, occasional oro-alimentary automatisms,
Figure 8-43b: EEG: Interictal—Right Temporal Discharge.

Interictal EEG shows discharge in the right temporal region with right inferomesial temporal predominance.
Figure 8-43c: EEG: Interictal—Right Temporal Slow Activity.

Interictal activity included irregular slow activity in the right temporal region.
and postictal aphasia. She also had versive head carbamazepine withdrawal, but there was no recur-
deviation to the right in transition to secondary rence after the dose was increased.
generalization.
Frequency of the simple partial seizures was once
Scenario E: Temporal Lobe Epilepsy Without a
every 2–3 days, frequency of the complex partial sei-
Defined Structural Lesion
zures was one every 1.5 weeks. Secondary generalized
seizures were rare, with the last one more than a year This is a 25-year-old right-handed woman with epi-
prior to evaluation. lepsy since age 5 years.
She was on carbamazepine, zonisamide, and pre-
gabalin. She had failed phenytoin, phenobarbital, a
primidone, valproate, gabapentin, levetiracetam, topi-
ramate, lamotrigine, and clonazepam.
EEG (Figure 8-45a) showed ictal discharge in the
left temporal region with left inferomesial temporal pre-
dominance. The ictal field widened during the course.
Interictal activity was sharp waves in the left tem-
poral region with greatest prominence in the region of
Sp1 and lesser in F7 and T7 (Figure 8-45b).
MRI brain (Figure 8-46a) showed atrophy and
increased T2 signal in the left hippocampus.
FDG-PET (Figure 8-46b) showed left temporal
hypometabolism, greatest in the left mesial-basal tem-
poral region.
Operative result was excellent. MRI (Figure 8-46c)
showed the region of the transcortical left selec-
tive amygdalohippocampectomy. Patient was free
Figure 8-44a: MRI Brain—Coronal T2.
of complex partial seizures and auras at 5 years of
MRI brain showed marked atrophy of the right hippocampus.
follow-up. She had one complex partial seizure during
Figure 8-44b: FDG-PET Brain.
FDG-PET showed decreased FDG uptake in the right mesial temporal region (arrows).
She had complex partial seizures described as hav- without focal postictal deficits. Has no recollection of
ing no warning, characterized by gagging, picking these events. Duration less than 1 minute.
with right arm, able to speak in sentences although EMU recorded seizures showed key features
usually inappropriate. Afterward has brief confusion including bilateral paddling movement of the lower
extremities and left gaze deviation, along with
arrhythmic arm shaking and a motionless stare. May
c
have well-formed verbal automatisms (would say “I
am fine, I am fine”).
Seizure frequency for complex partial seizures was
about 6 per month; secondarily generalized seizures
had only occurred twice in her life.. Medical therapy
at the time of presentation was levetiracetam, topira-
mate, and pregabalin. She had previously failed val-
proate and gabapentin.
Interictal EEG (Figure 8-47a) shows sharp waves
in the right frontotemporal region, greatest around F8
and Fp2 and less at T8 and P8.
EEG at ictal onset (Figure 8-47b) is character-
Figure 8-44c: MRI Brain Post-operative. ized by voltage attenuation immediately after a
Right transcortical selective amygdalohippocampectomy
was performed with good surgical result as shown on MRI.
high voltage sharp wave that resembles interictal
sharp waves.
Figure 8-45a: Ictal Discharge.
Figure 8-45b: Interictal Discharge.

Figure 8-46a: MRI Brain—coronal T2. Figure 8-46c: MRI Brain—post-operative.
Figure 8-46b: FDG-PET.
Figure 8-47a: EEG—Interictal.
Interictal sharp waves are right frontotemporal, F8, Fp2 > T8 > P8. There is irregular slow activity in the same distribution.
Figure 8-47b: EEG—Ictal.
EEG at ictal onset is characterized by voltage attenuation immediately after a high voltage sharp wave that resembles inter-
ictal sharp waves.
a MRI brain (Figure 8-48a) showed no lesion, par-

ticularly no hippocampal atrophy.
FDG-PET (Figure 8-48b) showed no
asymmetry.
Ictal SPECT (Figure 8-48c) showed right lateral
temporal increased blood flow, different from the
interictal baseline (arrow on image).
Magnetoencephalography (MEG) (Figure 8-48d)
showed epileptiform activity sources centered pre-
dominantly over the mid-posterior lateral temporal
region.
Wada test showed good memory with injection of
either side.
Subdural grid electrodes showed a defined field
Figure 8-48a: MRI Brain—Coronal T2. of the ictal discharge. In Figure 8-48e, the black circle
MRI brain showed no lesion, particularly no hippocampal
atrophy.
Figure 8-48b: FDG-PET.
FDG-PET showed no asymmetry.
Figure 8-48c: Ictal SPECT.
Ictal SPECT showed right lateral temporal increased blood flow, different from the interictal baseline.
shows the ictal center, whereas the white line sur- Clinical outcome was excellent with her free of com-
rounds the next most affected electrodes. plex partial seizures at 5 years follow-up. She remains on
Right temporal lobectomy was performed with seizure medications, not being willing to take the risk of
good surgical results (Figure 8-48f). seizure recurrence with AED withdrawal.
Figure 8-48d: Magnetoencephalography
Magnetoencephalography (MEG) showed epileptiform activity sources centered predominantly over the mid-posterior
lateral temporal region.
e f
Figure 8-48e: Skull X-ray with Implanted Grids and

Figure 8-48f: MRI Brain—Post-operative. Sagittal T1.
Ictal Map.
Right temporal lobectomy was performed with good surgi-
Subdural grid electrodes showed a defined field of the ictal
cal results.
discharge. In the figure, the black circle shows the ictal cen-
ter whereas the white line surrounds the next most affected
electrodes.
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Glossary potential connections and loops in the circuit.
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temporal region, especially in drowsiness and light shaking.
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Absence: Seizure characterized by a brief lapse of conscious- associated with loss of awareness. As opposed to
ness without major motor activity. Associated with simple partial seizure.
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Hz. normal when a posterior rhythm in a waking material to allow the flow of electrons. In the case of
state. Abnormal when seen anteriorly in a coma. biologic membranes, conductance indicated by the
Amplifier: Electronic device that increases the amplitude of ability of ions to pass through the membrane.
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Analog: Data as a continuously variable value, as opposed structure to mobilization of electrons.
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Analog-to-digital converter: Electronic device that converts infants.
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a digital signal (sequence of data bits representing direction of current is in the flow of positive charge,
the data). but since current is carried by negatively charged
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composed of waves of unequal duration. electrons.
Asynchronous: Describes transients or other activity that is Delta rhythm: EEG rhythm of less than 4 Hz. Seen normally
seen in several regions, but not simultaneously. in sleep but can also be seen with encephalopathy,
Atonic: Loss of tone. Atonic seizures are associated with focal structural lesion, and in children.
loss of tone rather than muscle contraction. Digital: Data as an array of digits, regardless of base. While
Aura: Subjective sensation that precedes a seizure. we display data in base 10, computers fundamentally
Benign epilepsy with centrotemporal spikes (BECTS): operate in base 2, with combinations to create longer
Another term for Rolandic epilepsy. digital words.
Diode: Device made by layering two pieces of semiconduc- Lennox-Gastaut syndrome: Severe epilepsy with mixed
tor. Conducts in one direction. seizures.
Discharge: Electrical potential burst recorded on EEG. Mitten: EEG potential formed from partial fusion of a ver-
Dravet syndrome: Eponymic name for severe myoclonic tex wave and spindle wave. The thumb of the mitten is
epilepsy of infancy. a spindle wave and the hand is the vertex wave.
Epileptic seizure: Episode of change in neurologic behavior Mu rhythm: Normal negative rhythmic potentials.
due to abnormal neuronal activity in the brain. Myoclonic: Sudden positive or negative motor symptoms,
Epilepsy: Recurrent episodes of seizure activity typically such as a brief jerk of a muscle.
associated with abnormal EEG rhythms. Narcolepsy: Disorder of recurrent attacks of daytime
Epileptiform discharge: Episodic waves or complexes that sleep attacks, often also with episodes of paralysis
stand out from the background and suggest a predis- (cataplexy).
position to epilepsy. Non-conductor: Material that does not conduct current. Has
Fast alpha variant: Posterior rhythm that is 16–20 Hz rather atomic structure that does not allow for free flow of
than 8.5–10 Hz, essentially a harmonic of the normal electrons from atom to atom.
posterior dominant rhythm. Notch filter: Archaic term for a 60 Hz filter—refers to a
Frequency: The number of waves of a specified rhythm per “notch” seen in the power spectrum produced by the
second, or 1/wavelength. Frequency is measured in filter.
Hertz or Hz, meaning cycles per second. Wavelength Obstructive sleep apnea: Disorder that produces periods of
is measured in milliseconds or seconds. apnea because of failure to maintain a patent airway
Frontal intermittent rhythmic delta activity (FIRDA): when asleep
Rhythmic delta from the anterior regions, especially Occipital intermittent rhythmic delta activity (OIRDA):
in patients with diffuse or metabolic disorders. Abnormal episodic delta activity seen especially in
Ictal discharge: EEG discharge that is associated with a children from the posterior regions. Usually seen
seizure. with diffuse and metabolic conditions. Childhood
Impedance: Measure of the effective resistance of a circuit correlate of FIRDA.
where voltages are changing. While typically used to Ohm’s law: For any resistive circuit, current is positively
describe AC circuits, it also applies to other chang- correlated with voltage and negatively correlated
ing voltages. Due to resistance of the elements plus with resistance. Or voltage is equal to current times
effects of inductance and capacitance on current flow. resistance.
Inductance: Measure of the induction capacity of an Open time: The time that an ion channel stays open after
inductor. being activated. Ion channels generally close after a
Induction: Production of current in a conductor by a chang- brief time, regardless of what happens to the mem-
ing magnetic field. brane potential.
Inductor: Circuit element composed of a wire winding so Periodic: Term used to describe transients or complexes
that the magnetic fields from movement of current that recur, but with intervening activity between
flow sum to form larger magnetic field. them.
Interictal: Between seizures. Used to describe a pattern on Periodic lateral epileptiform discharges (PLEDs): Discharges
EEG that is seen between clinical seizures. from one hemisphere or locus at a rhythm that is
Interictal discharge: EEG discharge that is seen in patients often about 1/sec. Seen especially with destructive
with seizures, yet the discharge it not, itself, a seizure. lesions.
Irregular rhythm: Activity that is not uniform. It is in theory Photoconvulsive response: Electrical seizure activity pro-
possible for rhythmic activity to be irregular, but that duced by photic stimulation.
is uncommon. Photoelectric artifact: Artifact seen during photic stimula-
K-complex: Fusion of a vertex wave with a sleep spindle. tion where the electrodes are directly activated by the
Seen mainly in stage 2 sleep and with partial arousal. light flashes.
Kirchhoff ’s current law: For any node, the sum of the cur- Photomyoclonic response: Electrical manifestation of an
rents flowing into the node is equal to the currents involuntary contraction of frontal muscles during
flowing out. photic stimulation.
Kirchhoff ’s voltage law: For any resistive circuit loop, the Positive sharp transients of sleep (POSTS): Positive potential
sum of the voltage sources is equal to the sum of with a maximum at O1 and O2, seen during light sleep.
voltage drops. Posterior dominant rhythm: Rhythm from the occipital
Lambda wave: Occipital positive waves created by visual region that is composed of a narrow band of a domi-
exploration. nant frequency, usually in the alpha range in adults.
Posterior slow wave of youth: Slow waves in the occipital Sharply contoured slow wave: Transient that has a duration
region in waking state, mainly of young children. longer than a sharp wave but has a subjectively sharp
Postictal: Referring to the time after a seizure, such as post- appearance and stands out from the background.
ictal EEG appearance or clinical state. Simple partial seizure: Partial (focal) seizure with no
Power: A measure of the ability to do work, for example, the disturbance of consciousness, as opposed to complex
energy of a power supply or of brain electrical activity. partial seizure.
Power spectrum: Distribution of energy across different Sleep spindle: Brief run of repetitive waves in the 11–14 Hz
frequent components. range. Are usually of 1–2 sec duration. Seen in light
Power supply: Circuit element that imparts energy to elec- sleep.
trons, causing them to move down a potential gradient. Slow alpha variant: Posterior alpha rhythm in waking state
Primary generalized seizure: Seizure that is generalized from which is a sub-harmonic of the normal posterior
the onset, as opposed to secondarily generalized alpha.
seizure. Spatial distribution. The electrodes involved with a
Psychogenic non-epileptic seizure: Episodic neurologic events discharge and the degree of their involvement deter-
that can resemble epileptic seizures but that are due mines the field.
to psychological issues rather than due to a change in Spike: Transient with a duration of 25–70 mg that is often
neuronal activity in the brain. epileptiform. Not all spikes are epileptiform, and
Rectifier: Device that converts AC into DC current. some are normal. Spikes must stand out from the
Rectify: Convert AC into DC current. Most modern circuits background to be interpreted. Not all potentials with
may use AC line power but many of the electronics this duration are spikes.
are powered by DC. Spike-wave complex: Spike followed by a slow wave.
Regular rhythm: Applies to activity that is uniform, with Startle: Jerking body movements due to a stimulus.
individual waves having fairly consistent shape, in Stevens-Johnson syndrome: Skin and mucous membrane
addition to fairly consistent duration. necrosis that can develop from some medications.
Resistance: The degree to which a material opposes the Synchronous: Occurring in two regions simultaneously.
passage of electric current. Dissipates the energy in Syncope: Loss of consciousness due to insufficient cerebral
another form, usually heat. blood flow.
Resistor: Circuit element that opposes the passage of Theta rhythm: EEG rhythm in the 4–7 Hz range. Normal
current, dissipates the energy usually in the form of in drowsiness at all ages and waking in young
heat. children. Also seen in encephalopathy, focal
Rhythm: EEG activity composed of recurring waves of structural lesion.
equal duration. A rhythm is often characterized by its Third rhythm: Rhythmic temporal activity in the waking
frequency. state. Normal.
Rhythmic: Term used to describe ongoing EEG activity Tonic: Increase in tone, in context of a seizure, steady
composed of recurring waves of equal duration. contraction.
Rhythmic midtemporal theta of drowsiness: Trains of Transient: A wave or combination of waves that stands out
charply-contoured waves in the theta range from the from the surrounding background.
temporal region in the drowsy state. Transistor: Semiconductor device that is able to amplify or
Rolandic epilepsy: Disorder of children with epilepsy with a rectify electrical current.
focus in the centro-temporal region. Vertex wave: Negative potential with a maximum near Cz.
Secondarily generalized seizure: Generalized seizure that has Occurs in stage 2 sleep and during arousal.
a focal onset. Voltage: Potential difference that is an electromotive force
Seizure: Sudden attack that is usually due to abnormal for circuits.
rhythmic discharge of neurons. Voltage drop: Reduction in voltage across a resistor or other
Semiconductor: Material that has conductivity better than a circuit element. This indicates the reduction in energy
non-conductor but less than a conductor. A key ele- associated with the electrons across this element.
ment to diodes and transistors. Voltage-gated: Voltage-gated ion channels open in response
Semiology: Study of signs of seizures. to a change in transmembrane voltage of the cell.
Sharp wave: Transient with a duration of 70–200 mg that West syndrome: Infantile spasms plus mental retardation.
is often epileptiform, although some sharp waves are Wicket spikes: Sharply contoured waves from the temporal
normal or if abnormal are not epileptiform. Must region during drowsiness and light sleep.
stand out from the background; not every wave of
this window of duration is a sharp wave.
INDEX
absence seizures 169, 173–76 amplitude abnormalities 28, 117

atypical 4, 150, 168, 176–78, 246 electrocerebral inactivity 132–34
EEG patterns 150, 166, 174, 177–78, 305, 334–36 focal attenuation/suppression 28, 129–31, 327, 336
frontal absences 229, 240 focal increase 134–35
hyperventilation and 53, 69, 87, 169 generalized attenuation/suppression 28, 131–32
ictal vs interictal discharges 148–49 generalized increase 135
management 66, 174, 177, 272, 275, 282 in neonates 228
myoclonic-absence 174, 188, 247 analog signal processing 19, 51
semiology 4, 174, 245–47 analog-to-digital conversion 24–25
status epilepticus 299 analysis and review of data 54–63
tonic-absence 179–80, 251 video-EEG 62–63, 71–73, 74–77
acquired epileptic aphasia 230 annotations 51–52, 71–73
action potential 8 anoxia
activation methods 25, 52–53, 64, 68, 84–88, 330 coma 140
in children 93–94 encephalopathy 89, 133, 138–39, 143, 309
“active” input (input 1) 39 perinatal 189, 228
adversive seizures 166–68, 196 periodic discharges 138, 309
see also versive head turning see also breath-holding spells
AEDs see anti-epileptic drugs anterior-mesial frontal lobe 240
affective symptoms 168, 236, 241 anterior-mesial temporal lobe 152
age anterior sylvian (F8) electrode position 31
AEDs and 272 anterior temporal electrodes (Silverman, T1/T2) 33
hyperventilation and 87 anti-epileptic drugs (AEDs) 269–86
normal EEG changes 89, 90–92 absence seizures 174, 177, 272, 275, 282
alpha coma 140, 305 adverse effects 272–75, 276
alpha rhythm 59 age and 272
see also posterior dominant rhythm comorbidities and 275–76
alpha-theta coma 309 dosing protocols 301–4
ambulatory EEG 65, 66, 70 drug–drug interactions 280–83
American Clinical Neurophysiology Society efficacy/effectiveness 273, 283–84
EEG guidelines 39–40 first-line treatment 270–72, 277
amplifiers 14, 17–19 formulations 300
sensitivity settings 51 generalized seizures 272, 282
363
364 Index
anti-epileptic drugs (AEDs) (Cont.) parietal lobe 194, 243

initiation of therapy 269–70 temporal lobe 160, 194, 241
mechanisms of action 281 auto-induction of seizures 66, 174
monitoring 275, 276–78 automatisms 1, 168, 236
myoclonic-absence seizures 188 absence seizures 246
partial-onset seizures 270–72, 282 orbitofrontal/cingulate gyrus seizures 240
pharmacogenetics 276 temporal lobe seizures 242, 243, 244
pregnancy and 272–75 autonomic symptoms 168, 236, 238, 246
resistance to 284 average references/montages 41–42, 44–45
second-line therapy 279–80 awake normal EEGs 81–82
status epilepticus 297, 298–99 children 92–93
after surgery 288 variants/transients 98, 99–101, 101, 103–5, 105–7
toxicity 269
withdrawal due to remission 284–86 baseline EEGs 68
withdrawal prior to video-EEG 66–67, 68, 69 bedwetting 264
anxiety 132 behavioral disorders 266
aphasia 168 benign epilepsy with occipital paroxysms 166
acquired epileptic aphasia 230 benign rolandic epilepsy (benign epilepsy with
postictal (temporal lobe epilepsy) 69, 203, 212, 243 centrotemporal spikes) 60, 166, 200, 269
archiving 26, 53–54, 79 benign sporadic sleep spikes (BSSS) 99, 193
arousal parasomnias 263 benzodiazepines 271, 297
arrhythmia, cardiac 73, 74, 78, 259 increased beta activity 60, 82, 135, 332
arrhythmic activity on EEG 55 beta rhythm 60
artifacts 53 focal increases in skull defects 134–35, 320
in ECI 134 generalized increase and sedatives 82, 135, 332
EKG 37, 40, 112, 134, 326 ictal discharges 152, 160
electrical 12, 52, 113–17, 305 bio-calibration 49
eye movements 37, 107–10, 117 bipolar disorder 276
filters and 20, 22–23, 51, 74, 111 bipolar montages 39, 42–43
glossokinetic 111–12, 117 end of chain phenomenon 45–46
hyperventilation 312 birth defects, AEDs and 272–75
muscle (EMG) 37–38, 60, 74, 110–11, 135 bisynchronous discharges 56, 59
in non-epileptic seizures 254–59 bisynchronous slow activity 28, 127–28
photoelectric 64, 87 blinking 108, 243, 309, 334
photomyoclonic response 64, 85–86 blood pressure, low 74
pulse 113 orthostatic hypotension 259
toothbrush 112 brain death 134, 141–46
aspiration during seizures 73 in neonates 228
asynchronous discharges 57 breach rhythm 134–35, 320
generalized asynchronous slow activity 28, 123–27 breath-holding spells 260
asystole 73 burst-suppression pattern 139–40, 229, 321
Atkins diet 292 in neonates 228–29
atonic seizures 2, 171, 177, 187, 251
attenuation 27, 28 calibration 48–49, 53
focal 129, 327, 336 capacitors 11, 24
generalized 131–32 RC circuits 20–22
atypical absence seizures 4, 150, 168, 176–78, 246 carbamazepine 270, 271, 272, 276, 278
auditory auras 160, 241 dosing protocols 301
aura continua 296 drug–drug interactions 280, 282–83
auras 1 withdrawal 67
frontal lobe 194, 238 cardiac arrhythmias 73, 74, 78, 259
insular cortex 244 cardiac monitoring (EKG artifact) 37, 40, 112, 134, 326
occipital lobe 194, 244 catamenial epilepsy 67
Index 365
cavernous malformations 212, 289, 337, 339 left temporal focus 77, 203–12, 220, 243
cephalic auras 194, 238, 241 right temporal focus 212
cerebellar seizures 245 secondary generalization 204–9, 212,
chemotherapy 276 222–26
chewing artifact 118, 119 semiology 237
children status epilepticus 296, 299
absence epilepsy see absence seizures surgery 230, 286–88, 336–51
AEDs 272, 276 vagus nerve stimulation 284, 288–92
age-related changes 99, 229 computed tomography (CT) 286
brain death 145–46 conceptional age 90–92, 227
breath-holding 260 conductance/conductors 8, 9–10, 17
epileptic encephalopathies 229 cone waves 96
epileptic (infantile) spasms 173, 188–89 confusion 237, 246, 248, 251, 260, 263
febrile seizures 269 consciousness, decreased
hypsarrhythmia 171–73, 312, 334 simple vs complex partial seizures 2, 237
juvenile myoclonic epilepsy 88, 152, 247–48, syncope 259–60
269–70 see also absence seizures
Lennox-Gastaut syndrome see Lennox-Gastaut corpus callosotomy 293
syndrome (LGS) cortical dysfunction 131, 132
neonates 29, 90–92, 227–29 see also encephalopathy
normal rhythms 89–96 cortical potentials 26
OIRDA 127–28, 336 cortical stimulation 295
remission 284 corticosteroids 292–93
rolandic epilepsy 60, 166, 200, 269 cough syncope 260, 321
Sandifer syndrome 264–65 counseling 275, 294–96
sleep disorders 262, 263, 264 Creutzfeld-Jakob disease (CJD) 138
sleep patterns 94–96 critical care monitoring 231–33
SSPE 138 cyanotic breath-holding spells 260
chloral hydrate 94 cyclical seizure patterns 67
chorea 261
cingulate gyrus 240 dacrystic seizures 244
circumferential montages 41, 42 data protection 79
classification of seizures 2–3, 236–37 data storage 26, 54, 79
clinical governance 293 death
clinical signs and symptoms see semiology brain death 134, 141–46, 228
clonic activity 1, 235, 237 SUDEP 73, 294–95
clonic seizures 247 déjà vu 236, 241
see also tonic-clonic seizures delta brushes 92
clonic-tonic-clonic seizures 248 delta rhythm 60, 83
collodion used in electrode placement 34–35 FIRDA 127
coma 140 focal slowing (polymorphic delta) 28, 121–23,
EEG patterns 133, 140, 305, 309, 321–24 324, 330–32
reactivity testing 89 generalized slowing 123, 129
complex absence seizures 245–46 ictal discharges 152
see also absence seizures in neonates 228
complex activity 55 OIRDA 127–28, 336
complex partial seizures (psychomotor seizures) TIRDA 123, 153
AEDs 270–72, 282 dementia 129, 138, 263, 321
case reports 194–95, 336–51 density spectral array 71
classification 2, 237 depolarization
EEG patterns 159, 195, 200–203 of cell membranes 6–8
encephalopathy following 231–32 paroxysmal depolarization shift 28–29
frontal focus 194, 215 depth electrodes 24, 36
366 Index
diagnosis electrode lead artifacts 12, 116

differentials (non-epileptic conditions) 121–22, 127, electrodes 23–24
252–69 artifacts 113–15, 116
EEG in routine use 4–5, 146–47 in complex partial seizures 202–3
epileptic vs non-epileptic seizures 67–68, 75 impedance 23, 25–26, 48
status epilepticus 296–97 placement/nomenclature 30–38, 39, 114, 230
video-EEG 65, 67–68, 70 in video-EEG 70–71
diazepam 297 electromyelogram (EMG) artifact 37–38, 60, 74,
diet 275, 292 110–11, 135
diffusion potential 7 electronic circuits 8–19
digital signal processing 19, 24–25, 51 electronic signal processing 19–23, 24–25, 51
diodes 13–14 electrotonic conduction 7
discharge (from long-term EEG monitoring) 69 EMG artifact 37–38, 60, 74, 110–11, 135
displaying the data 25, 39–46, 51 employment issues 294
documentation 53 encephalitis
archiving 26, 53–54, 79 herpes 124, 136, 233, 312, 332
doctor–patient discussions 293 SSPE 138
pre-test checks 46 encephalopathy
report annotations 51–52, 71–73, 78 anoxic 89, 133, 138–39, 143, 309
report structure 62–63, 75–77 after complex partial seizures 231–32
Doose’s syndrome (myoclonic astatic epilepsy) 187, 251 drug-induced 269
dorsolateral frontal lobe 240 epileptic encephalopathies in children 229
Dravet syndrome 230, 276 hepatic 129, 309
drinking automatisms 243 hospital-related 232–33
driving a motor vehicle 294 periodic patterns 138–40, 309
driving response 64, 85, 330 reactivity testing 52, 89
drop attacks 187, 251 slow activity 117, 123, 128–29, 332
drowsiness 82, 94, 98 end of chain phenomenon 45–46
normal variants and transients 96, 102, 102–3 epigastric auras 236, 241
drug-induced coma 133, 140, 321–24 epilepsy
drug-resistant epilepsy 284 classification 3
drugs see anti-epileptic drugs definition 1
duration of the EEG 25 epileptic spasms (infantile spasms) 188–89, 251
dyskinesia 261–62 hypsarrhythmia 171–73, 312, 334
dysmaturity in neonates 227 epileptiform activity 27, 28–29, 60–61, 147–48
dystonic posturing 235, 242 in the absence of epilepsy 193
paroxysmal nocturnal dystonia 262 clinical signs 166–68
compared with non-epileptiform 60–61, 189–93
early infantile epileptic encephalopathy 230 focal (partial) 149, 158–66, 189–220, 228
early myoclonic encephalopathy 230 generalized 149–52, 169–73, 309
ear reference electrodes 40, 41, 44–45 ictal vs interictal 148–49, 193
ECI see electrocerebral inactivity neonatal 227–28
education see also specific patterns/types
patient counseling 275, 294–96 epileptogenic zone localization 36, 286–87
staff training 26, 77–78 estrogen 283
EKG artifact 37, 40, 112, 134, 326 ethosuximide 272, 275
elderly patients 87, 89, 272 experiential symptoms 168, 236, 241
electrical artifacts 12, 52, 113–17, 305 eyelid myoclonia 247
electrocardiogram (EKG) artifact 37, 40, 112, 134, 326 eye movement
electrocerebral inactivity (ECI) (electrocerebral silence) artifact 37, 107–10, 117
132–34, 141–46 blinking 108, 243, 309, 334
in neonates 228 opening/closure 82, 107–8, 109
electrocorticography (ECoG) 230 ezogabine 271
Index 367
facial symptoms gabapentin 271, 272, 276

frontal lobe seizures 239, 240 gastrointestinal reflux 264–65
temporal lobe seizures 243 gaze, eye movement artifact 37, 107–10, 117
falls during seizures 73 gelastic seizures 220, 240, 244
fast alpha variant 103–4 gel used in electrode placement 34
fast spike-and-wave discharges 150–52, 169, 178, 179 generalized discharges 56
fear 168 referential montages 41
febrile seizures 269 generalized non-epileptiform activity
felbamate 271, 272, 280 amplitude changes 28, 131–32, 134–35
figure-of-4 posturing 238 asynchronous slow 28, 123–27
filters 19–23, 25 bisynchronous slow 28, 127–28
artifacts and 20, 22–23, 51, 74, 111 periodic 138–39
digital 25 synchronous slow 128–29
settings 50–51 generalized seizures 168–69
square-wave calibration 48–49 absence see absence seizures
FIRDA (frontal intermittent rhythmic delta activity) 127 atonic 2, 171, 177, 187, 251
fluttering of the eyelids classification 2, 3, 237
EEG artifact 108–9 clonic 247
eyelid myoclonia 247 EEG patterns 149–52, 169–73, 309
focal discharge localization epileptic (infantile) spasms 173, 188–89, 251
montages 40–46 focal evolution 251
presurgical evaluation 36, 65, 66, 67, 286–87 fragments of generalized discharges 149
focal epileptiform activity 149, 158–66, 189–220, 228 ictal vs interictal discharges 148–49
see also specific types of seizure indeterminate 229
focal ictal discharges 152, 159, 160, 193 management 272, 282, 292
focal motor activity 168 myoclonic see myoclonic seizures
focal non-epileptiform activity 117, 120 secondary generalized see secondary generalized seizures
amplitude changes 28, 129–31, 134–35, 327, 336 semiology 4, 168, 245–51
slowing 28, 121–23, 324, 330–32 status epilepticus 296, 298
focal seizures see complex partial seizures; partial-onset tonic 2, 171, 177, 179, 248–51
seizures; simple partial seizures tonic-absence 179–80, 251
focal weakness 243 tonic-clonic see tonic-clonic seizures
folate supplements 275 generalized spike-and-wave discharges 149–52,
FOLD 6-Hz spike-and-wave discharges 173 169–73, 309
foramen ovale electrodes 36, 202–3 absence seizures 174, 177–78, 307, 334–36
fosphenytoin 297 benign rolandic epilepsy 166
14 & 6 positive spikes 96–99, 305 temporal lobe epilepsy 158
frequency (Hz) 54–55 genetics 295–96
frontal intermittent rhythmic delta activity (FIRDA) 127 AEDs and 276
frontal lobe seizures global aphasia 243
absences 229, 240 glossokinetic artifact 111–12, 117
complex partial seizures 194, 215
EEG patterns 162–63 hand automatisms 236, 242
generalized or focal? 163, 229 headaches (migraine) 259, 264, 276
nocturnal seizures compared with parasomnias 262, 263 head injuries 131, 133, 327
orbitofrontal 36, 162, 240 head measurement 31–32
paroxysmal nocturnal dystonia 262 head turning
PNES compared with 254 frontal lobe seizures 240
propagation from parietal lobe 244 temporal lobe seizures 242
semiology 4, 199, 238–40 tonic-clonic seizures 238, 248
simple partial seizures 194, 199 heart
supplementary motor seizures 163, 199, 238, arrhythmias 73, 74, 78, 259
239–40, 269 EKG artifact 37, 40, 112, 134, 326
368 Index
hematoma 131, 133, 327 interpretation of EEGs 54–63

hemiballismus 262 video-EEG 62–63, 71–73, 74–77
hemispherectomy/hemispherotomy 293 intra-operative monitoring 230, 233–34
hepatic encephalopathy 129, 309 ion channels/pumps 6–7
hepatic metabolism of AEDs 272, 276, 280, 282–83 irregular activity 55
herpes encephalitis 124, 136, 233, 312, 332 isoelectric EEG 132–34, 141–46
high-frequency filters (HFF) 20, 23, 49, 50–51, 111 in neonates 228
hippocampal sclerosis 160, 196, 287, 289, 290, 342–44
hippocampal seizures 152 Jacksonian march 235
horizontal dipoles 60, 193 jerks (clonic activity) 1, 235
hospitalized patients with critical illnesses 232–33 juvenile myoclonic epilepsy 88, 152, 247–48
hyperekplexia 262, 269 management 269–70
hypermotor behavior 240, 242
hyperventilation 25, 53, 64, 69, 87 K complexes 83, 96
artifact 312 ketogenic diet 292
in children 93, 169 kidney impairment, AEDs and 274, 276
hypnic jerks 264 kinesigenic dyskinesia 261–62
hypnosis 89 Kirchhoff ’s current law 15–16
hypoglycemia 74 Kirchhoff ’s voltage law 16
hyponatremia 272
hypotension 74 lacosamide 271, 301
orthostatic 259 lambda waves 99–101
hypothalamic seizures 240, 244–45 lamotrigine 270, 271, 272, 276, 278, 280, 283
hypothermia, therapeutic 146 dosing protocols 302
hypoxia, breath-holding spells 260 in pregnancy 274, 275
see also anoxia Landau-Kleffner syndrome 230
hypsarrhythmia 171–73, 312, 334 language disturbance 168
acquired epileptic aphasia 230
ictal cardiac asystole 73 postictal aphasia 69, 203, 212, 243
ictal discharges 2, 29, 80, 147, 148–49 in temporal lobe epilepsy 203, 212, 242–43
focal 152, 159, 160, 193 Laplacian referential montages 42
ictal fear 168 lateral rectus spikes 61, 109
ictal jargon 168, 203, 243 laughter, inappropriate (gelastic seizures) 220, 240, 244
ictal paralysis 240 legal issues 266, 294
imaging, presurgical 286–87, 291 Lennox-Gastaut syndrome (LGS) 177, 230, 246
immunosuppressant drugs 276 management 177, 282
immunotherapy 292–93 paroxysmal fast activity 149
impedance 23, 25–26, 48 slow spike-and wave pattern 150, 156, 171
incontinence 238, 254 levetiracetam 271, 272, 274, 280, 302
independent discharges 57 lipid bilayer in cell membranes 6
indications for use of EEG 4–5 lip-smacking automatisms 168, 236, 242
video EEG 65–66 lissencephaly 189
inductors/inductance 11–12, 115 liver
infantile spasms (epileptic spasms) 188–89, 251 hepatic encephalopathy 129, 309
hypsarrhythmia 171–73, 312, 334 metabolism of AEDs 272, 276, 280, 282–83
infection control 78 localization of abnormalities
input channels 39 montages 40–46
insular epilepsy 244 presurgical evaluation 36, 65, 66, 67, 286–87
integrity testing 49–50 localization-related epilepsy see complex partial seizures;
interictal discharges 2 partial-onset seizures; simple partial seizures
see also epileptiform activity longitudinal bipolar (LP) montages 40, 41, 42
International League Against Epilepsy (ILAE) long-term EEG monitoring 66–69, 71–73
on classification 3 lorazepam 297
on drug resistance 284 low-frequency filters (LFF) 20, 23, 48–49, 50
Index 369
low glycemic index diet 292 muscle artifact (EMG artifact) 37–38, 61, 74, 110–11, 135
low-voltage EEG 132 muscular signs and symptoms see motor signs and
fast rhythm 81 symptoms
in neonates 228 musicogenic epilepsy 88
myoclonic activity 235, 246
machine artifact 52, 115 eyelid myoclonia 247
magnetic resonance imaging (MRI) 286, 291 myoclonic encephalopathy 230
magnetoencephalography (MEG) 291 myoclonic epilepsy of infancy (Dravet syndrome) 230, 276
management myoclonic seizures 187–88
case reports 336–51 juvenile myoclonic epilepsy 88, 152, 247–48, 269–70
counseling 275, 294–96 management 272, 276, 282
diet 292 myoclonic-absence 174, 188, 247
immunotherapy 292–93 myoclonic-atonic 187, 251
investigational therapies 295 negative epileptic myoclonus 251
role of video-EEG 65, 66 semiology 4, 247, 251
vagus nerve stimulation 284, 288–92 status epilepticus 297
see also anti-epileptic drugs; surgery myoclonus, non-epileptic 260
manipulative automatisms 236, 242 nocturnal 261, 264
membrane theory 6–8 in syncope 259–61
memory testing
postictal 69 nasoethmoidal electrodes 36
presurgical 287, 291 nasopharyngeal electrodes 33, 36
mesial centro-parietal seizures 203–4 needle electrodes 24, 36
mesial frontal lobe seizures (supplementary motor negative epileptic myoclonus 251
seizures) 162, 199, 238, 239–40, 269 neocortical epilepsy 160
mesial temporal lobe epilepsy 158, 159, 241 surgery 287–88, 293
methods see test procedures neonates 29, 90–92, 227–29
methsuximide 271 neurotransmitters 8
midazolam 297 nightmares 263
midline discharges 199 nocturnal enuresis 263–64
migraine 259, 264, 276 nocturnal myoclonus 261, 264
mirror focus 193 non-conductors 10
mittens 101 non-epileptic seizures 3, 81, 252–69
monitoring epilepsy misdiagnosed as 240
AED levels 275, 276–78 provocation by suggestion 52, 67–68, 89, 254
during EEG 36–38, 90 video-EEG 75, 76
intra-operative 230, 233–34 withdrawal of AEDs 69
see also video monitoring non-epileptiform activity 27–28, 117, 254–59
montages 38–40, 50, 75 amplitude changes 28, 129–35, 327, 336
localization of abnormalities 40–46 in coma 133, 140, 305, 309, 321–24
motor signs and symptoms 1, 235 compared with epileptiform 60–61, 189–93
absence seizures 245–46 in ECI/brain death 132–34, 141–46
frontal lobe seizures 238–40 generalized 28, 123–29, 131–33, 134–35
generalized seizures 247–51 in neonates 228–29
insular seizures 244 periodic patterns 136–40
occipital lobe seizures 244 slowing 27, 28, 117, 120–29, 228
parietal lobe seizures 243 spikes and sharp waves 60–61, 148, 193
partial seizures 168 non-kinesigenic dyskinesia 261
secondarily generalized tonic-clonic seizures 238 normal EEGs 80–81
temporal lobe seizures 241–42, 243 adult 81–85, 87
movement artifact (lead movement) 116 age-related changes 89
movement disorders 260–62, 264, 326–27 awake rhythms 81–82, 92–93
movement during dreaming (REM behavior disorder) 262 children 89–96
mu rhythm 59, 101 sleep rhythms 82–84, 90–92, 94–96
370 Index
normal EEGs (Cont.) patient monitoring see monitoring

variants and transients 96–107, 132 PDA (polymorphic delta activity) (focal slow activity) 28,
see also artifacts 121–23, 324, 330–32
notch filters (60-Hz) 20, 23, 51 pediatrics see children
nurses 78 pentobarbital coma 133, 140, 321–24
nutrition 275, 292 periodic lateralized epileptiform discharges (PLEDs)
137, 332
obesity 276 periodic patterns 56, 117, 136–40, 309
occipital intermittent rhythmic delta activity (OIRDA) burst-suppression pattern 139–40, 228–29, 321
127–28, 336 petit-mal variant 171
occipital lobe seizures 163 see also Lennox-Gastaut syndrome
secondary generalized 204–9 phantom spike-waves 102, 173
semiology 4, 194, 244 pharmacodynamics 280, 278–82
occipital rhythms see posterior dominant rhythm pharmacogenetics 276
Ohm’s law 14–15 pharmacokinetics 276, 277, 278, 279
Ohtahara syndrome 230 drug–drug interactions 280
OIRDA (occipital intermittent rhythmic delta activity) phase shift 22–23
127–28, 336 phenobarbital 271, 280, 300
operculum, frontal 240 phenytoin 270, 271, 276, 277, 278, 280
oral contraceptives 283 dosing protocols 303
oral/oro-alimentary automatisms 168, 236, 242 phone artifact 116
orbitofrontal seizures 36, 162, 240 photic stimulation 52–53, 64, 84–87, 330
orthostatic hypotension 259 photoelectric artifact 64, 87
oxcarbazepine 270, 271, 272, 274, 276, 278, 280 photomyoclonic response 64, 85–86
dosing protocols 302 photoparoxysmal response 64, 86–87
PNES see psychogenic non-epileptic seizures
page rate 51 polarity of EEG channels 39
pallid breath-holding spells 260 reversal in bipolar montages 42–43
pallor 260 polymorphic delta activity (PDA) (focal slow activity) 28,
paralysis, ictal 240 121–23, 324, 330–32
parasomnias 262–64 polyspike-and-wave complexes 55–56, 156, 169, 309
parasthesia (sensory aura) 236, 243 positive sharp transients of sleep (POSTS) 102
parietal lobe seizures 163, 194, 199 posterior dominant rhythm 81, 82, 89
semiology 4, 194, 243–44 in children 92
Parkinson’s disease 326–27 fast variant 103–4
paroxysmal depolarization shift 28–29 slowing (abnormal) 128
paroxysmal dyskinesia 261 slow variant (normal) 103
paroxysmal fast activity 149 posterior slow waves of youth 93
paroxysmal nocturnal dystonia 262 posterior temporal lobe epilepsy 161–62
partial-onset seizures (localization-related epilepsy) postictal manifestations 1, 212
AEDs 270–72, 282 aphasia 69, 158, 212, 243
case reports 336–51 confusion 246, 248, 251, 260, 260
classification 2, 3, 236–37 EEG patterns 74, 212
EEG patterns 149, 158–66, 189–220, 228 psychosis 73
evolution from generalized seizures 251 temporal lobe epilepsy (other than aphasia) 243
ictal discharges (focal) 152, 159, 160, 193 tonic-clonic seizures 248
indeterminate 229 tonic seizures 251
semiology 4, 166–68, 194, 236–45 postsynaptic potentials 8, 26
surgery 230, 286–88, 336–51 posttest procedures 53–54, 69
vagal nerve stimulation 284, 288–92 posturing see tonic activity
video-EEG reports 76–77 potassium ions (sodium-potassium ion pump) 6–7, 8
see also complex partial seizures preamplifiers 19
patient behavior (during the test) 52–53 pregabalin 271, 276
patient identification (before the test) 46 pregnancy, AEDs 272–75
Index 371
premature infants 91–92, 229 normal variants 97

presyncope 260 in sleep 82–84
primary generalized seizures see generalized seizures rhythmic midtemporal theta of drowsiness 102–3, 309
primidone 271 rolandic epilepsy 60, 166, 200, 269
prodrome 1 rufinamide 271, 280
provocation of seizures 25, 52–53, 64, 68, 84–88, 330
in children 93–94 safety issues 73–74, 78, 294–95
pseudo-beta-alpha-theta-delta pattern 228 saline injections 52, 89
pseudoseizures see non-epileptic seizures Sandifer syndrome 264
psychiatric disorders scalp electrodes 23–24, 30–35
comorbid 74 scalp potentials 26–27
postictal psychosis 73 secondary generalized seizures 2, 196
psychogenic non-epileptic seizures (PNES) 81, 252–59 occipital lobe 204–9
epilepsy misdiagnosed as 240 semiology 237–38, 243
provocation by suggestion 52, 67–68, 89, 254 temporal lobe 159, 212, 222–26, 243
video-EEG 75, 76 tonic-clonic 159, 178, 222–26, 237–38
withdrawal of AEDs 69 sedatives 271, 297
psychomotor seizures see complex partial seizures increased beta activity 60, 82, 135, 332
psychomotor variant (rhythmic midtemporal theta of seizures
drowsiness) 102–3, 309 classification and definitions 1–3
pulse artifact 113 EEG patterns see ictal discharges
self-induction of seizures 66, 174
quality of care 293 semiconductors 12–13
semiology 4–5, 166–68, 235–36
radiosurgery 295 absence seizures 4, 174, 245–47
rapid eye movement (REM) sleep 83, 158, 262, 263 atonic seizures 187, 251
RC circuits (passive filters) 20–22 clonic seizures 247
reactivity testing 52, 89 in differential diagnosis 252–69
reading epilepsy 88 epileptic (infantile) spasms 251
primary 188 frontal lobe seizures 4, 199, 238–40
secondary 198 generalized seizures 4, 168, 245–51
record-keeping see documentation insular cortex seizures 244
recurrence of seizures myoclonic seizures 4, 247, 251
initiating AEDs 269, 270 occipital lobe seizures 4, 194, 244
after surgery 288 parietal lobe seizures 4, 194, 243–44
reference input (input 2) 39 partial seizures 4, 168, 194, 236–45
referential montages 40–42 PNES 252–54
reflex epilepsy 66, 187 secondary generalization 237–38, 243
regional discharges 56 temporal lobe seizures 4, 194, 240–43
regional slowing 121, 127 tonic-clonic seizures 4, 237–38, 247–48
regular activity 55 tonic seizures 179
see also rhythmic activity sensory-sensitive epilepsy 86, 88–89
remission 284–86 reading epilepsy 88, 188, 198
REM sleep 83, 158, 262, 263 sensory symptoms/auras 194, 236, 238, 241, 243, 244
renal impairment, AEDs and 274, 276 SE (status epilepticus) 73, 232, 296–97, 298–99
resistance/resistors 8, 10–11, 14–17, 23 severe myoclonic epilepsy of infancy (Dravet syndrome)
respiratory monitoring 38, 90 230, 276
responsive cortical stimulation 295 sharply contoured slow waves 61
restless legs syndrome 264 sharp waves
rhythmic activity 54, 56, 57, 59–60 epileptiform 29, 60–61, 148
intermittent rhythmic delta activity (FIRDA/OIRDA/ non-epileptiform 61, 147–48
TIRDA) 123, 127–28, 153, 336 see also spike-and-wave patterns
in neonates 228 short-term video-EEG monitoring 70
normal adults 81–84 signal processing 19–23, 24–25, 51
372 Index
signs and symptoms see semiology frontal lobe seizures 162–63

Silverman anterior temporal electrodes (T1/T2) 33 generalized 149–52, 169–73, 309
simple absence seizures 245 in neonates 228
vagus nerve stimulation 284, 288–92 non-epileptiform 60–61, 148, 193
see also absence seizures occipital lobe seizures 163
simple partial seizures phantoms 102, 172
AEDs 270–72, 282 temporal lobe epilepsy 158
classification 2, 236–37 tonic-clonic seizures 178
EEG patterns 159, 193, 194–200 tonic seizures 179
semiology 166, 237 spindle coma 140
6-Hz (phantom) spike-waves 102, 173 square-wave calibration 48–49
60-Hz artifact 115–16, 305 staffing issues
60-Hz filters 20, 23, 51 non-EEG staff in critical care facilities 233
skull defects (breach rhythm) 134–35, 320 technicians’ roles and responsibilities 46–48, 51–52, 53,
sleep 63, 78
benign rolandic epilepsy 166 training 26, 77–78
generalized spike-and-wave discharges 150 standards for EEG recordings 25–26
movement disorders 260, 262, 264 staring spells 4, 253
neonates 90–92 startle reaction 262, 266–69
normal adult rhythms 82–84 status epilepticus (SE) 73, 232, 296–97, 298–99
normal childhood rhythms 94–96 steroids
normal variants and transients 98, 99, 101, 102, 105, 193 anti-inflammatory 292–93
parasomnias 262–64 in oral contraceptives 283
PNES 254 stray inductance 12, 115
temporal lobe epilepsy 158 stroke 233, 336
sleep apnea 78 subacute sclerosing panencephalitis (SSPE) 138
sleep deprivation 53, 64, 68, 88 subclinical rhythmic electrographic discharge of adults
sleep-related rhythmic movement disorder 264 (SREDA) 104
sleep spindles 83, 96, 229 subcortical structural lesions 28, 121–22, 324, 330–32
sleep talking 263–64 subdural hematoma 131, 133, 327
sleep terrors 263 subdural strip electrodes 24, 36
sleep walking 263 subjective symptoms
slow activity, non-epileptiform 27, 28, 117, 120–29 absence seizures 246
bisynchronous 28, 127–28 simple partial seizures 196, 237
focal (polymorphic delta) 28, 121–23, 324, 330–32 sudden unexplained death in epilepsy (SUDEP)
generalized asynchronous 28, 123–27 73, 294–95
generalized synchronous 128–29 suggestion, seizure provocation by 52, 67–68, 89, 254
in neonates 228 summation of membrane potentials 7–8
slow alpha variant 103 summation of resistors 16–17
slow spike-and-wave discharges 150, 169–71, 177–78 supplementary motor seizures (mesial frontal lobe) 163,
slow transients 61 199, 238, 239–40, 269
slow waves of youth 93 suppression 27
small sharp spikes (benign sporadic sleep spikes) 99, 193 focal 129–31
sodium-potassium ion pump/channels 6–7, 8 generalized 131–32
spatial distribution 56 suppression-burst pattern 139–40, 229, 321
spatial summation of potentials 7 in neonates 228–29
speech disturbance see language disturbance supraorbital electrodes 36
sphenoidal electrodes 33, 35 surgery 286–88
temporal lobe seizures 158, 159, 160, 202 case reports 336–51
spike-and-wave patterns 29, 55–56, 60–61, 148 electrocorticography 230
absence seizures 174, 177–78, 307, 334–36 indications 284, 286
benign epilepsy with occipital paroxysms 166 intra-operative monitoring 230, 233–34
benign rolandic epilepsy 60, 166 presurgical evaluation 36, 65, 66, 67, 286–87
focal 149, 158–66, 189–95, 228 symptoms see semiology
Index 373
synchronous discharges 56, 57, 128–29, 163 management 272, 275, 282
syncope 259–60 secondary generalized 159, 178, 222–26, 237–38
cough syncope 260, 321 semiology 4, 237–38, 247–48
tonic seizures 2, 171, 177, 179, 248–51
technical staff toothbrush artifact 112
roles and responsibilities 46–48, 51–52, 53, 63, 78 topiramate 270, 271, 272, 276
training 26, 77–78 dosing protocols 303
telephone artifact 116 trace discontinu 91
temporal intermittent rhythmic delta activity (TIRDA) training of staff 26, 77–78
123, 153 transients 55, 57, 60–61, 98
temporal lobe electrodes 33, 35–36, 158, 159, 160, 202–3 see also individual patterns
temporal lobe epilepsy 194 transistors 13, 18
case reports 336–51 transverse bipolar (TB) montages 40, 41
EEG patterns 152–62, 194–95, 200–12 treatment see management
left lobe focus 77, 203–12, 220, 243 tremor 255–59, 326–27
propagation from parietal lobe 244 trigeminal nerve stimulation 295
reference electrodes 41
right lobe focus 212 unresponsiveness 168
secondary generalization 159, 212, 222–26, 243 see also absence seizures
semiology 4, 194, 240–43
surgery 287–88, 289, 290, 293 vagus nerve stimulation (VNS) 284, 288–92
temporal relationships of discharge activity 56–57 valproate 271, 272, 276, 278, 280
temporal summation of potentials 7–8 dosing protocols 303
10–10 electrode placement system 33 in pregnancy 274, 275
10–20 electrode placement system 30–32, 34 versive head turning
teratogenicity of AEDs 272–75 frontal lobe seizures 240
test procedures 51–53 temporal lobe seizures 242
long-term video-EEG 66–69 tonic-clonic seizures 238, 248
short-term video EEG 70 vertebrobasilar insufficiency 259
see also analysis and review of data; posttest procedures vertex waves 83, 94–96
thalamic stimulation 295 video monitoring (EEG-video) 5, 64–73, 286
therapeutic drug monitoring 275, 276–78 analysis 62–63, 71–73, 74–77
theta rhythm 60, 90 safety in the EMU 73–74
ictal discharges 152 vigabatrin 271
rhythmic midtemporal theta of drowsiness 102–3, 309 violence 266
slowing 123, 129 visual auras 194, 244
third rhythm 59, 105–7 visual evoked potential (VEP) testing 85
3Hz generalized spike-and-wave patterns 149–50, 169, 174 visual evoked response (VER) 64, 84–85
tiagabine 269, 271, 280 voltage-gated ion channels 6
time constant 8 vomiting 243
TIRDA (temporal intermittent rhythmic delta activity)
123, 153 Wada testing 287, 291
tongue biting 238, 254 wakefulness, normal 81–82
tongue movement artifact 111–12, 117 in children 92–93
tonic-absence seizures 179–80, 251 variants/transients 98, 99–101, 101, 103–5, 105–7
tonic activity 1, 235 West syndrome 189, 230
absence seizures 246 WHAM 6-Hz spike-and-wave discharges 173
frontal lobe seizures 238–39 wicket spikes 105, 316
partial seizures 168 women
secondary generalized tonic-clonic seizures 238 catamenial epilepsy 67
temporal lobe seizures 242 pregnancy and AEDs 272–75
tonic-clonic seizures 2, 168, 169
EEG patterns 170, 178–79, 222–26, 321 zonisamide 271, 272, 276

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Appendix: References and Glossary • 353

SEIZURES AND EPILEPSY Before discussing the types of seizures, an introduc-

This is not a comprehensive glossary, as found else- Symptoms and Signs

Table 1-1 Select Deﬁnitions Classiﬁcation of Seizures and Epilepsies

Term Definition The 1981 international classification is still the most

Table 1-2 Classiﬁcation of Seizures

Table 1-3 Classiﬁcation of Epilepsies

Table 1-4 Semiology of Generalized Seizures

ROLE OF EEG IN DIAGNOSIS AND Table 1-5 Semiology of Partial Seizures

PHYSIOLOGY hydrophilic groups on the exterior of the membrane,

a Extracellular Ion channel

The circuit elements are combined with conductors to

Table 2-1 Circuit Elements

Electron Electron Electron Electron

Charge – 1 Charge + 1 Charge – 1 Charge + 1

Figure 2-4: Conductors and Non-conductors.

Non-conductors do not have unpaired electrons that

e Resistors are composed of material that conducts less

a Inductor circuit b Response graphs

a Silicon or N-type P-type the concepts is appropriate considering the wide-

Diodes are composed of two wafers of semiconduc-

and therefore an unfilled electron orbital, creates a

a collector In addition, there are a few basic additional formulae

This is one of the intuitive laws of electronics. As

Table 2-2 Summary of Important Circuit Laws

Current of a resistive circuit is equal to the voltage

Similarly, resistance in a resistive circuit is equal to

Kirchhoff ’s current law is easy to conceptualize (see

I1 Node I2 circuit loop, the sum of the voltage sources is equal

Σ Ii = 0 where VS represents the individual voltage sources

where RT is the total equivalent resistance of the sys-

Summation of Resistors in Parallel

active 10x output

Figure 2-18: Single-ended Versus Differential Amplifiers.

controlling side of the circuit connected to the bio-

Signal Processing signal is processed, the data is displayed on a moni-

Filter action Physics of Filters

The first three are high-frequency, and can be attenu- V

Figure 2-22: Recordings from Elements of the RC

Filter Settings Electrode Basics

Re essentially conducting electric charge mainly in one

The calculations can accomplish various tasks,

Table 2-3 Technical Requirements for Routine EEG

GENERATORS OF EEG POTENTIALS Scalp Potentials

of numerous neurons is required for there to be a GENERATION OF ABNORMAL EEG

Table 2-4 Abnormal EEG Activity

Focal Attenuation Generalized asynchronous slow activity has a broad

OVERVIEW In addition to extracranial electrodes, intracranial

Figure 3-1: 10-20 Electrode Placement System.

• Occipital (O); If F8 alone is involved, or if the field involves F8 and

Figure 3-2: Additional Electrode Names.

Additional Electrodes Outside the 10-20 System