Review Article

EEG and Epilepsy

Address correspondence to
Dr Paul Rutecki, University of
Wisconsin, Department of
Neurology, 1685 Highland
Avenue, Madison, WI 53705,
rutecki@neurology.wisc.edu.
Relationship Disclosure:
Monitoring
Dr Maganti serves on the Rama K. Maganti, MD; Paul Rutecki, MD
speakers bureaus of
GlaxoSmithKline and UCB
and served as a consultant for
Lundbeck. Dr Rutecki holds ABSTRACT
stock valued at more than
$10,000 in Cyberonics, Inc; Purpose of Review: This article reviews the utility of EEG and prolonged video-
receives research support EEG telemetry in the diagnosis and management of a patient with epilepsy.
for a clinical trial from Recent Findings: The EEG can be the most helpful test to determine a diagnosis of
NeuroPace, Inc; and receives
a grant support from the epilepsy; it can also distinguish focal and generalized neurophysiologic correlates of
Epilepsy Foundation epilepsy. Furthermore, when paired with video monitoring, EEG can not only define
of America. epileptic and nonepileptic events but also aid in localization of seizures in patients
Unlabeled Use of
Products/Investigational
with epilepsy. Finally, when history and other imaging modalities are considered
Use Disclosure: with the EEG, the epileptic syndrome can usually be defined and the treatment can
Drs Maganti and Rutecki be focused. In critically ill patients, continuous EEG monitoring can define sub-
report no disclosures.
clinical seizures, although a variety of periodic patterns may also be identified.
* 2013, American Academy
of Neurology. Summary: EEG is an invaluable tool in the diagnosis and management of a patient
with epilepsy, and continuous EEG monitoring is useful in identifying subclinical
seizures and nonconvulsive status epilepticus in critically ill patients.

Continuum (Minneap Minn) 2013;19(3):598–622.

INTRODUCTION the physiologic basis for interictal and

The EEG is the defining study for epi- ictal EEG patterns provides insight to
lepsy and is used to support the diagnosis the pathophysiology and treatment
of epilepsy and the epilepsy syndrome. approach used for the different epi-
The first human EEG was recorded by lepsies. The two main EEG hallmarks
Hans Berger in 1924 and demonstrated of epilepsy are the interictal spike or
the occipital dominant alpha wave pat- sharp wave in focal epilepsies and the
tern associated with eye closure. The frontocentral spike-wave discharges in
patterns of generalized spike-and-wave the generalized epilepsies.
activity and focal spikes or sharp waves The EEG signal is produced by
were defined as markers of epilepsy by current flow carried by ion movement
Gibbs, Lennox, and Jasper in the 1930s. across the membrane of neurons and
Since then the EEG has been invaluable glia.1 The direction of current flow is
to the study of epilepsy. This article will defined by the movement of positive
review the basis for the EEG, discuss charge; areas where positive current
the use of the EEG in diagnosing epi- flows into a cell are referred to as
lepsy, and provide a framework for how sinks, and positive flow out of a cell is
the EEG can be used to provide appro- termed a source. The sink produces a
priate treatment choices. negative potential recorded extracellu-
larly. Interictal focal spikes and sharp
PHYSIOLOGIC BASIS FOR waves are negative and represent a
INTERICAL EEG PATTERNS large sink near the surface of a gyrus
The EEG offers high temporal resolu- (Figure 2-1). The sink is produced by
tion of brain activity. Understanding excitatory synaptic and intrinsic inward

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FIGURE 2-1 Schematic demonstrating a radial dipole typical of a focal interictal spike.
The population of neurons that generate the dipole is depicted as a single
pyramidal neuron. A large inward current in the apical dendrite generates a
surface-negative potential, maximal at T4 (by convention, EEG depicts negative as an upward
deflection). Following the spike is a negative, slower wave that is also surface-negative because
of a similar dipole produced by potassium ions leaving the soma and chloride entering the
soma, producing outward current at the soma. The traces on the right show a bipolar recording
of the spike wave and show phase reversal at T4 localizing the surface negativity to the T4
electrode.

currents in the apical dendrites of a trode referred to a reference electrode

large number of cortical neurons. Often can be used to map out the dipole.
following excitation of a large number Electroencephalographers use bipolar
of neurons, a recurrent inhibitory po- montages that compare the potential
tential produced by +-aminobutyric acid measured at each electrode, and local-
(GABA) and after-hyperpolarizations ization of a sharp wave occurs when
produced by potassium currents result there is a phase reversal associated with
in a source at the neuron soma that an electrode (Figure 2-1).
produces a surface negative slow wave Generalized spike-wave activity as-
that follows the interictal spike. This sociated with generalized epilepsies in-
slow wave helps to define epileptiform volves widespread neural circuits that
sharp waves and may distinguish them represent interplay of abnormal synchro-
from other sharp, rhythmic activity that nization of the thalamus (both cortical
occurs in the EEG. projecting nuclei and the reticular nu-
At least 6 cm2 of gyral cortex is cleus of the thalamus) and the cortex.
required to produce a spike or sharp The spike component appears to repre-
wave at the scalp2; therefore, absence sent a barrage of thalamic synaptic input
of interictal spikes in an EEG does not to the cortex, and the wave component
rule out epilepsy, and more often corresponds to a large synchronous in-
than not there is not an EEG signature hibitory component.4 For absence sei-
for focal seizures that activate a small zures, 3-Hz spike-wave oscillations
area of cortex.3 Localization of a focal are largely driven by the propensity
interictal sharp wave or spike can be of the thalamic relay neurons to fire
defined by the EEG. The dipole pro- bursts driven by low-threshold calcium
duced by current flow creates a voltage currents. These currents are reduced by
that has a vector associated with it. The ethosuximide, an antiepileptic drug that
amplitude of the voltage at each elec- is most effective in absence epilepsy.

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 EEG and Epilepsy Monitoring

KEY POINTS
h Yield of an outpatient For many years, EEGs were re- Sensitivity and Specificity
EEG may be low even in corded with analog recordings that The sensitivity of EEG in various stud-
patients with known then were charted on paper. The ies had ranged from 29% to 55%, with
epilepsy. amplifiers and the frequency response studies showing an average of one-third
h Repeat EEGs over time of the EEG pens limited the ability to of initial EEGs being abnormal.12,13
or sleep deprivation may record higher-frequency activity. More However, the sensitivity improves to
increase the yield. recently, recordings have been digital about 80% to 90% if EEGs are re-
h With an epileptiform
and able to display high frequencies peated over time.14 Timing of EEG is
abnormality on EEG,
when digitized at a high enough rate important, with studies showing 51%
chances of recurrence (at least twice as high as the frequency of EEGs being abnormal if done within
of seizures are high, and that one is interested in). Using a fast 24 hours of a seizure compared to
treatment decisions may sampling rate (2000 Hz) has defined 34% demonstrating abnormalities in
be made even after activity known as fast ripples that occur later EEGs.10
first-time seizures. in the 250- to 600-Hz frequency range Specificity of EEG for diagnosis of
and are more clearly defined when re- epilepsy is fairly high in most studies.
corded intracranially. High-frequency Interictal epileptiform discharges are
oscillations appear to be a biomarker seen rarely in normal adults or chil-
for epileptogenic tissue and in the fu- dren (0.2% to 3%).15 Occipital spikes
ture may be useful to define areas to re- have been reported in normal blind
sect in patients with intractable epilepsy.5 people, and generalized spikes have
been reported in first-degree relatives
USE OF ROUTINE OUTPATIENT of patients with idiopathic generalized
EEG IN DIAGNOSIS OF EPILEPSY epilepsies. Moreover, patients with
EEG is an important diagnostic tool in epilepsies may have normal EEGs.
epilepsy. While clinical history generally Even in those with epileptiform ab-
provides adequate information regard- normalities, localization on an EEG
ing the diagnosis of epilepsy, history may not accurately denote the epi-
may not always aid in establishing an lepsy syndrome. Examples of this are
epilepsy syndrome. Outpatient EEG is the presence of generalized spike-
an important tool along with imaging wave discharges in a small proportion
studies that aid in establishing an of children with benign epilepsy with
epilepsy syndrome.6 Both American centrotemporal spikes, and the pres-
Academy of Neurology and Interna- ence of focal epileptiform discharges
tional League Against Epilepsy guide- (fragmented generalized spike-wave)
lines recommend EEG in diagnosing among patients with generalized epi-
epilepsy in adults and children, with lepsy (Figure 2-2). These findings may
inclusion of photic stimulation, hyper- lead to erroneous diagnosis as far as
ventilation, and sleep deprivation in the epilepsy syndrome is concerned.
adults as part of the protocol.7,8 An Interictal spikes or epileptiform ab-
epileptiform pattern seen on EEG af- normalities may be seen as a result of
ter a first-time seizure often predicts drugs such as cefepime, bupropion,
recurrence of seizures based on stud- lithium, tramadol, and clozapine. Fo-
ies in both adults and children, with cal, multifocal, and diffuse epilepti-
recurrence rates that range from 30% form abnormalities have also been
to 70% in the first year.9Y11 Therefore, reported in metabolic disorders such
when the EEG is epileptiform after a as uremia and thyrotoxicosis and in
first-time seizure, treatment may be con- autoimmune encephalopathies such
sidered even before a diagnosis of epi- as Hashimoto encephalopathy. There-
lepsy is established. fore, the presence of an ‘‘epileptiform
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FIGURE 2-2 EEG from a patient with juvenile myoclonic epilepsy with more focal frontal spike-wave activity (A) that may also be
seen as more generalized occurring at a frequency of 3 Hz (B).

abnormality’’ does not always mean are most often seen in generalized
epilepsy, and EEG findings should be epilepsiesVespecially childhood ab-
interpreted in the clinical context, sence epilepsy with or without eyelid
albeit with caution. myoclonia, juvenile absence, and myo-
clonic epilepsyVand very rarely in pa-
Photic Stimulation and tients without epilepsy.17
Hyperventilation Hyperventilation is another pro-
Photic stimulation is a useful method cedure that can activate epileptiform
of activating epileptiform discharges abnormalities. Typically, absence sei-
primarily in patients with idiopathic zures are activated with hyperventila-
generalized epilepsy, but also those tion, although epileptiform discharges
with partial epilepsy. Photic driving of in focal epilepsies may be activated
a posterior rhythm is a normal re- as well.18
sponse, and a photomyogenic response
that consists of brief repetitive muscle Sleep Deprivation
activity such as eye blinks seen in Sleep deprivation is an important tool
anterior electrodes that increase in when EEGs are unyielding in provid-
amplitude with flash frequency and ing diagnostic information. In a review
cease when stimulation stops is a of all earlier studies, Ellingson and
normal variant. A photoparoxysmal re- colleagues19 concluded that sleep
sponse (Figure 2-3) that consists of deprivation increases the chances of
generalized spike-wave or polyspike- finding interictal epileptiform dis-
and-wave discharges, which may be charges on an EEG in 30% to 70% of
anterior or posterior dominant, and cases. Similarly, Fountain and col-
that may or may not be associated leagues20 reported an activation rate
with loss of awareness or myoclonic of 52% with sleep deprivation when
jerks, is an abnormal response often baseline EEGs are normal. Further-
associated with epilepsy, especially if it more, activation by sleep deprivation
outlasts duration of the photic stimu- is more common in younger patients
lation, and is often termed photocon- and those with primary generalized
vulsive.16 Photoparoxysmal responses epilepsy syndromes.16,21

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 EEG and Epilepsy Monitoring

FIGURE 2-3 EEG of photoparoxysmal response. Note that the patient is undergoing photic stimulation at 15 Hz (denoted by
Ph at the bottom of the page), during which the patient is initially noted to have a posterior driving response
(higher amplitude beta range activity at the beginning of the page) followed by a generalized spike-wave discharge
that is anteriorly dominant.

KEY POINT Sources of Error ABNORMAL EEG

h Several nonspecific Abnormal Nonepileptic
Sources of error may come when EEGs
patterns may be seen in
are normal in patients with spells whose Patterns That Are Nonspecific
patients with epilepsy.
diagnosis is uncertain. Errors can also but May Be Seen in Epilepsy
occur in patients with nonepileptic The patterns often seen in patients with
paroxysmal neurologic disorders when epilepsy but also with other etiologies
focal abnormalities are noted or when (Table 2-1) include focal slow activity;
benign patterns are seen and misin- focal voltage attenuation; diffuse slow-
terpreted as epileptiform activity. Lastly, ing; frontal intermittent rhythmic delta
patients may be misdiagnosed as having activity (FIRDA) (Figure 2-4); and
epilepsy when epileptiform activity is triphasic waves (Figure 2-5). Most
due to drugs or metabolic disorders. common and least specific of these is
Therefore, the EEG should always be diffuse slow activity. All of these pat-
correlated with the clinical history and terns may be seen postictally as well.
imaging studies. Of these, FIRDA may be confused with

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TABLE 2-1 Abnormal EEG Findings That Are Not Epileptiform But May Be Seen in
Patients with Epilepsy

Abnormal Findings Possible Etiologies

Focal slow activity Transient or permanent lesions of brain: multiple sclerosis, dementia,
traumatic brain injury, migraines, ischemia, and postictal states
Focal voltage attenuation Decrease: Acute infarct, subdural hematoma or hygroma, skull
or asymmetry hyperostosis, and Sturge-Weber syndrome
Increase: Skull defects
Diffuse slow activity Acutely with traumatic brain injury, subarachnoid hemorrhage, and
toxic or metabolic encephalopathy
Chronically seen in epileptic encephalopathies such as West syndrome
or Lennox-Gastaut syndrome
Frontal intermittent Seen with hyperventilation, during sleep, with deep midline or diffuse
rhythmic delta activity subcortical lesions, raised intracranial pressure, and metabolic abnormalities
Triphasic waves Metabolic encephalopathy, diffuse cerebral process such as an infection

FIGURE 2-4 EEG showing frontal intermittent rhythmic delta activity in a 70-year-old patient admitted with mental status
changes. Note the rhythmic high-amplitude delta that waxes and wanes.

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 EEG and Epilepsy Monitoring

FIGURE 2-5 EEG showing triphasic waves in a 48-year-old patient with renal failure and obtundation. Note that the EEG shows
triphasic waveforms that have maximal amplitude anteriorly and an anteroposterior lag.

KEY POINT ictal discharges (bilaterally synchro- Abnormal Epileptic Patterns

h Abnormal epileptic nous frontal spikes) when they are Abnormal epileptic patterns may in-
patterns can be notched. Triphasic waves can have a clude spikes or sharp waves. De-
syndrome-specific periodic or pseudoperiodic pattern pending on the epilepsy syndrome,
and if seen on an EEG
and may be confused with epilepti- they may be focal, multifocal, or gener-
can readily provide
syndromic diagnosis.
form activity. The general features of alized and with or without associated
triphasic waves are that the waveforms background EEG abnormalities. The
have three phases lasting 250 to 500 location of spikes may aid in localiza-
milliseconds, anterior or posterior tion as well as in defining the epilepsy
dominance, and a lag anteropos- syndrome.
teriorly. However, when they are phase Focal spikes or sharp waves. Focal
reversing focally, if they are unilateral, spikes or sharp waves (Figure 2-6) are
and when there is less generalized typically asymmetric and only occasion-
background slowing, they may rep- ally are bilaterally synchronous, often
resent an epileptiform pattern. 22 followed by a slow wave. Spikes are
Triphasic waves are suppressed by ben- defined as having a duration of less
zodiazepines and sleep but activated than 70 milliseconds, with sharp waves
by stimulation.23 having durations between 80 and 500

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FIGURE 2-6 EEG showing centrotemporal spikes in a patient with benign rolandic epilepsy. Note that the spikes are seen on the
left side and have maximal amplitude and phase reverse in the temporal and central leads on the left (T3 and C3).

milliseconds. They generally have a Generalized spikes: 2 to 3 Hz; 3 to

radial dipole (formed when current 4 Hz; polyspike and wave. General-
flow is perpendicular to the scalp) ized spike-wave discharges have a
except in cases of benign rolandic symmetrical distribution and ampli-
epilepsy where they have a tangential tude with a similar configuration in a
or horizontal dipole (when current given record (Case 2-1) (Figure 2-7).
flow is tangential to the scalp). The They can repeat at regular rates and
field of distribution on a scalp record- usually have an anterior predominance
ing depends on the location of the and occasionally a posterior predomi-
cortical zone of irritability. They occur nance. Three-Hz spikes and waves are
singly but in some cases can be focal seen in absence epilepsy; 4- to 6-Hz
polyspikes, and the state during which anteriorly dominant spikes and poly-
they appear (ie, awake or sleep) can spikes are seen in juvenile myoclonic
vary with the epilepsy syndrome. epilepsy. Generalized spikes of 2 to
Multifocal spikes may arise indepen- 2.5 Hz are seen in atypical absence
dently from multiple foci, phase revers- epilepsy. Atypical absences are differ-
ing in different regions at different ent from typical absences in that they
times. occur in children with developmental

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 EEG and Epilepsy Monitoring

Case 2-1
A 38-year-old, right-handed man presented with a history of generalized tonic-clonic seizures since
age 12. The seizures occurred relatively rarely, but frequently enough (every 3 to 6 months) to
make it difficult for the patient to obtain a driver’s license; they occurred more often in the context
of sleep deprivation or alcohol use. In addition, the patient described brief episodes of impaired
thought or concentration associated with twitching of one or both sides of his mouth. In some cases
he had a cluster of these before having a generalized tonic-clonic seizure. He used diazepam as
needed to try to abort them and the generalized tonic-clonic seizures. These smaller seizures and
his tonic-clonic seizures had not been controlled despite trials of phenobarbital, phenytoin,
carbamazepine, lamotrigine, valproate, and levetiracetam. It was unclear whether he had frontal
lobe seizures with generalization or a primary generalized epilepsy.
At the time of evaluation, his family history was negative for epilepsy, and a prior EEG had shown
an isolated left frontal sharp wave.
The brief seizures with facial twitching were fairly common and often occurred at night before
sleep or early in the morning.
He was evaluated with continuous video-EEG monitoring and several of his typical smaller
seizures were captured. They were associated with brief (4- to 5-second) episodes of generalized
spike-and-wave discharges occurring at 4 to 5 Hz associated with subtle upper lip twitching
(Figure 2-7). This was diagnostic of absence seizures with perioral myoclonia. He was started on

FIGURE 2-7 EEG recording from the patient described in Case 2-1. The patient felt a brief lapse and twitch
of his jaw. The EEG correlate demonstrated generalized spike-wave activity occurring at 3 to
4 Hz. Note that the patient pushes an event button that identifies he had a seizure.

Continued on page 607

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 Continued from page 606
valproate and 1 year later remained free of generalized tonic-clonic seizures; his briefer seizures still
occurred at times but were not disabling. He was reluctant to try other medications because of
cognitive side effects. The patient’s 3-year-old son began to have similar brief absence seizures with
facial myoclonia and rarer generalized seizures.
Comment. This patient’s epilepsy was not correctly diagnosed until he underwent video-EEG
monitoring. The monitoring study changed his therapy and improved seizure control. Valproate
appeared to be a better treatment. The patient had been on valproate for 1 month in the past but
had a seizure and was placed on another medication. Patients with generalized epilepsy may have
multiple seizure types, including briefer absence seizures that culminate in a generalized tonic
clonic seizure when they recur repetitively. Generalized tonic-clonic seizures can be associated with
myoclonic seizures, as occurs in juvenile myoclonic epilepsy, or with absence seizures and more limited
myoclonia, as in this case.

delays, often last longer than typical EEG in epileptic encephalopa- KEY POINT
absences with gradual onset and offset, thies. EEG patterns seen in epileptic h Many normal variants
and may be associated with atonia, encephalopathies that deserve special can lead to erroneous
diagnosis of epilepsy,
with EEG showing diffuse background mention include hypsarrhythmia seen
such as wicket spikes,
slowing and 2- to 2.5-Hz generalized in West syndrome, slow spike and
small sharp spikes, and
spikes, unlike the 3-Hz spikes seen in wave and paroxysmal fast activity seen 14 and 6 positive spikes.
typical absence epilepsy. Fragments of in Lennox-Gastaut syndrome, continuous
generalized spikes may appear focally spike and wave during slow-wave sleep
within the same record showing gener- seen in Landau-Kleffner syndrome,
alized spikes16 (Figure 2-2). The 3-Hz burst-suppression seen in Ohtahara
spike-wave discharges of childhood ab- syndrome, and polyspike-and-wave
sence epilepsy can be associated with discharges of 3 to 6 Hz with slow
occipital intermittent rhythmic delta background and photosensitivity seen
activity (OIRDA). in progressive myoclonic epilepsies
Slow spike and wave. These patterns (Table 2-2).
are seen in more catastrophic epilepsies
with multiple seizure types and cog- Normal Variants or Benign
nitive dysfunction (eg, Lennox-Gastaut Patterns That May Confuse
syndrome). Slow spike-and-wave dis- the Diagnosis
charges typically occur at 1.5 to 2.5 Hz There are many normal variants that
and are distributed in a generalized can be confused with epileptiform ac-
fashion but can have focal features. tivity and lead to an erroneous diagno-
The background EEG activity is typi- sis (Table 2-3, Figure 2-9). Therefore,
cally slow in these patients, and slow being familiar with these patterns is
spike and wave is associated with atyp- important for a practicing neurologist
ical absence. who reads outpatient EEGs routinely.
Rhythmic temporal delta. Rhythmic Rhythmic midtemporal theta and wick-
temporal delta activity can be encoun- et spikes are the most frequent normal
tered in records of patients with tem- variants on the EEG that can lead to the
poral lobe epilepsy (Figure 2-8). It is erroneous diagnosis of epilepsy.25 In a
rarely encountered in normal popula- study of 35,249 EEGs, benign variants
tion and has a high specificity and were identified in 3.4% of the record-
positive predictive value for temporal ings, with the most common being
lobe epilepsy.24 small sharp spikes (1.85%); others were

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 EEG and Epilepsy Monitoring

FIGURE 2-8 EEG of rhythmic temporal delta activity seen best in the right temporal leads during an abdominal sensation in a
patient with right hippocampal sclerosis. This activity appeared as an ictal pattern but also occurred at other times
without any clinical symptoms. The patient is seizure free after a right anterior temporal lobectomy.

KEY POINT rhythmic midtemporal theta of drows- in the intensive care unit. A patient
h EEG in status epilepticus iness (0.12%), subclinical rhythmic elec- may begin with convulsive status epi-
can show progressive trographic discharges of adults (SREDA) lepticus, and if it is untreated or does
changes.
(0.07%), wicket spikes (0.03%), 6-Hz not respond to treatment, it may
spike and wave (1.02%), and 14 and 6 convert into a nonconvulsive status
positive spikes (0.52%).26 epilepticus.
In humans and animal models, there
EEG PATTERNS IN STATUS is a predictable sequence of EEG pat-
EPILEPTICUS terns in convulsive status epilepticus,
Status epilepticus is rarely encountered and EEG findings vary on an EEG de-
in routine EEGs or in patients with no pending on which stage is captured.27
preexisting epilepsy. The patterns They are the following:
seen on EEG during status epilepticus
depend on the type of status epilep- 1. Discrete seizures
ticus, convulsive versus nonconvulsive; 2. Merging of discrete seizures
the latter can be subdivided into par- 3. Continuous ictal discharges
tial complex status epilepticus, absence 4. Continuous ictal discharges with flat
status epilepticus, or nonconvulsive periods
status epilepticus in a comatose patient 5. Periodic epileptiform discharges

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TABLE 2-2 Epileptic Encephalopathies and EEG Features

Age
Syndrome Predisposition Clinical Phenotype EEG Pattern
Ohtahara syndrome First 3 mo of life Tonic spasms Burst suppression
West syndrome 4 to 8 mo Epileptic spasms Hypsarrhythmia or modified
hypsarrhythmia
Dravet syndrome 1 to 3 y of age Infantile febrile convulsions Progressive background slowing,
followed by myoclonic jerks, generalized spike-wave and
atypical absences, and focal multifocal spike-wave discharges,
seizures with impaired photosensitivity
awareness
Lennox-Gastaut Peaks at 3 to Tonic, atonic, and atypical Generalized slow spike-and-wave
syndrome 5 y of age absence seizures discharges and paroxysms of
fast activity
Landau-Kleffner Peaks at 5 to Acquired aphasia, cognitive Multifocal spikes or posterior
syndrome 7 y of age and behavioral abnormalities, temporal spikes facilitated
clinical seizures infrequent markedly by sleep, seen
continuously in slow-wave sleep
Progressive myoclonic Age of onset 5 to Progressive myoclonus, 3Y6 Hz polyspike-wave discharges
epilepsies 20 y of age cognitive impairment, ataxia and photosensitivity

The stages of status epilepticus are Periodic EEG Patterns

important in that there is a progres- The EEG patterns in obtunded or co-
sive decline in treatment response matose patients are more complex and
based on animal study.28 controversial (Table 2-4, Figure 2-10).

TABLE 2-3 Benign Variants Commonly Encountered on EEG but Confused With
Epileptiform Patterns

Benign Variants EEG Features

Rhythmic midtemporal Seen in temporal leads, occurring in trains that wax and
theta of drowsiness wane in amplitude
(psychomotor variant)
Small sharp spikes Small in amplitude (G50 2V), phase reversing in temporal leads,
seen unilaterally or bilaterally
Wicket spikes Typically distributed in temporal leads, occur in isolation or in runs
resembling a wicket fence, unilateral or bilateral, seen in older adults
Phantom spike and wave Brief bursts of 1Y2 s, can be anterior or posterior predominant,
(6-Hz spikes) FOLD (female, occipital predominant, low amplitude and drowsiness)
and WHAM (wake, high amplitude, anterior, and male)
14 and 6 positive spikes Seen during drowsiness or light sleep, occurring in bursts of 0.5Y1.0 s,
positive and negative components, temporal leads maximum,
seen in adolescents
Subclinical rhythmic Seen while awake and during drowsiness, bursts of theta and delta
electrographic discharges lasting 10Y40 s, abrupt onset and offset, can be diffuse or temporal
of adults (SREDA) maximum, seen in older adults

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 EEG and Epilepsy Monitoring

FIGURE 2-9 Normal variants or benign patterns. A, EEG of psychomotor variant or rhythmic
midtemporal theta of drowsiness (RMTD). Note the theta range activity seen
bilaterally but maximally in the temporal leads as the patient is becoming
drowsy. B, EEG of small sharp spikes. Note the low-amplitude spikes of 50 2V or less in the
temporal leads and note that the patient is also in light sleep.
Continued on next page

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FIGURE 2-9 (Continued from page 610) Normal variants or benign patterns. C, EEG of wicket spikes. Note the phase-reversing
sharp wave in left temporal leads that do not have an after-following slow wave and a rhythm that looks like
a wicket fence. Note the sleep spindle/vertex wave later in the page suggesting light sleep. D, EEG of phantom
spike and wave. Note the bisynchronous burst of 6-Hz activity with a spike component and with an amplitude of about 60 2V,
occurring as a burst lasting 1 second.
Continued on next page

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 EEG and Epilepsy Monitoring

FIGURE 2-9 (Continued from page 611) Normal variants or benign patterns. E, EEG of 14 and 6 positive bursts. Note the
1-second burst of right-sided activity with spike components but occurring at 14 Hz in trains during drowsiness.
F, EEG of subclinical rhythmic electrographic discharges of adults (SREDA). This EEG is from a 60-year-old patient
during awake state where bilateral, sharply contoured theta activity is seen but does not alter the baseline alpha range activity
posteriorly and almost looks like an ictal discharge, but patients generally do not have change in awareness. It has abrupt onset
and offset and can be seen in wakefulness or during sleep.

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TABLE 2-4 Periodic Patterns Seen on EEG in the Critically Ill and Comatose Patient

Periodic Patterns Etiologies EEG Description

Periodic lateralizing Seen with herpes simplex, lesions Sharp- and slow-wave complexes
discharges of gray matter or white matter, of 1Y2 Hz, unilateral, high association
nonketotic hyperglycemia, alcohol with seizures
withdrawal states, and the use of
theophylline
Bilaterally independent Seen with anoxic injury, CNS Asynchronous discharges seen
periodic lateralizing infections, and chronic epilepsy bilaterally, higher mortality rate
discharges
Generalized periodic Seen with anoxic brain injury, Bilaterally synchronous discharges,
discharges subacute sclerosing panencephalitis, may have interspersed seizures
Creutzfeldt-Jakob disease, in known
epilepsy, and in acute neurologic
events
Stimulus-induced, Seen in critically ill patients with Periodic or rhythmic discharges
rhythmic, periodic, or or without neurologic injury induced by alerting stimuli,
ictal discharges may have ictal pattern
Triphasic waves Often seen with metabolic Bilaterally synchronous, symmetric,
encephalopathies but can be medium- to high-voltage triphasic
indistinguishable from waves occurring in rhythmical trains
nonconvulsive status epilepticus at 1.5Y2.5 Hz
May be associated with focal seizures
if unilateral
Suppression burst Seen after anoxic injury, severe Alternate periods of high-amplitude
encephalopathy, and with use of drugs slow waves and flat EEG pattern
such as propofol or barbiturates

In comatose patients, rhythmic or GPDs have been divided into periodic KEY POINTS
periodic patterns often do not clearly short-interval diffuse discharges and pe- h Several periodic EEG
fall into ‘‘ictal’’ or ‘‘nonictal’’ cate- riodic long-interval diffuse discharges. patterns are seen in
comatose patients in the
gories, and there is some controversy With increased use of the EEG in criti-
intensive care unit,
in the literature regarding which pat- cally ill patients, it has become apparent
many of which are
terns represent or indicate status epi- that some ‘‘epileptiform’’ patterns may indicative of status
lepticus and which do not. Moreover, not be specific for seizures, and the epilepticus, although
different patterns may be seen within guidelines for prolonged intensive care some are controversial
the same patient at different time unit (ICU) monitoring now refrain from (such as triphasic
points during the continuous EEG rec- using the term epileptiform.29 waves).
ording. The commonly seen periodic h Continuous EEG
patterns include rhythmic delta activity; USE OF CONTINUOUS EEG monitoring should be
generalized triphasic waves; periodic MONITORING IN THE INTENSIVE considered in any
lateralizing discharges (PLDs); general- CARE UNIT critically ill patient with
ized periodic discharges (GPDs); bilat- Continuous EEG (cEEG) monitoring is unexplained mental
erally independent periodic lateralizing performed over hours or days to obtain status changes,
discharges (BIPLDs); and stimulus- information about cerebral function especially those with
induced, rhythmic, periodic, or ictal among patients who are critically ill acute neurologic injury,
discharges (SIRPIDs). PLDs have been and have limited neurologic examina- as nonconvulsive
seizures may be
further divided by some authors into tion; it is often indicated among pa-
underrecognized.
‘‘PLDs proper’’ and ‘‘PLDs-plus,’’ and tients in a medical or neurologic ICU
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 EEG and Epilepsy Monitoring

FIGURE 2-10 Periodic EEG patterns. A, EEG of periodic lateralized discharges. Note that the EEG shows
periodic sharp-wave discharges phase reversing in the right temporal leads. B, EEG of
bilateral periodic discharges. Note the periodic discharges phase reversing in the frontal
leads bilaterally and sometimes occurring asynchronously.
Continued on next page

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FIGURE 2-10 (Continued from page 614) Periodic EEG patterns. C, EEG of generalized periodic
discharges where there are periodic discharges that are seen bilaterally in a synchronous
manner, with maximal amplitude frontally in a patient with anoxic brain injury.

Case 2-2
A 23-year-old woman had a several-year history of spells characterized by sudden loss of consciousness
associated with a fall preceded by lightheadedness. Some of these spells had been triggered by blood
draw. She had eight of these episodes over the past 2 years and may have had some posturing and
shaking involved. She also described episodes characterized by an aura of déjà vu followed by staring
and oral automatisms and at times speech arrest, which occurred twice a week. Both types of spells
continued despite two anticonvulsant medication trials either independently or in combination. Her
MRI results were normal, as were Holter monitoring and ECG as an outpatient. Routine outpatient EEG
findings were normal as well. The patient was then admitted for video-EEG monitoring.
Comment. The case posed a diagnostic challenge in that the patient had a history of episodes twice
a week of what sound like focal seizures with loss of awareness and automatic behavior suggestive of a
temporal lobe semiology, whereas the episodes of loss of consciousness preceded by lightheadedness
sounded like syncope. However, it is possible that these may represent generalized tonic-clonic seizures
as well.
When admitted to the epilepsy monitoring unit, the patient had a blood draw for labs shortly after
which she reported feeling dizzy and then lost consciousness; this was followed by a brief tonic
posturing, followed by brief tonic-clonic activity. At the end of the event she had no postictal state and
reported to the nurses that she had ‘‘passed out.’’ ECG during the event showed severe bradycardia
when the patient reported dizziness, followed by asystole for 15 seconds with gradual return to normal
sinus rhythm. EEG during the bradycardia showed loss of amplitude diffusely followed by flattening,

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 EEG and Epilepsy Monitoring

Continued from page 615

and as sinus rhythm resumed, diffuse slowing followed by return of posterior
dominant rhythm was noted (Figure 2-11). These clinical, ECG, and EEG findings were
consistent with neurocardiogenic (vasovagal) syncope.

FIGURE 2-11 EEG from the patient described in Case 2-2. A, Note the normal awake
pattern while patient is undergoing phlebotomy. B, Note the bilateral
high amplitude slowing followed by flattening of EEG associated
with muscle artifact that coincided with patient losing consciousness and having some
tonic posturing.

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 Continued from page 616

FIGURE 2-11 (Continued from page 616) EEG from the patient described in Case 2-2. C, Note
that the EEG remains flat along with muscle artifact with poorly discernible electrocerebral
activity likely due to hypoperfusion during the period of asystole. D, Note resumption
of EEG activity that coincided with the patient having a few clonic jerks and that
followed resumption of ECG rhythm.
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 EEG and Epilepsy Monitoring

Continued from page 617

Interestingly, later in the recording she also had bitemporal interictal spikes and four partial
complex seizures, which were bilateral. This case is an example of how EEG monitoring led to
a dual diagnosis of epileptic seizures and an episode of neurocardiogenic syncope following
phlebotomy.

FIGURE 2-11 (Continued from page 617) EEG from the patient described in Case 2-2. E, Note the recovery of normal
alpha activity that coincided with patient recovery of normal consciousness where she started answering
questions.

who are comatose where subclinical Among comatose patients in the ICU,
seizures or nonconvulsive status epilep- rates of status epilepticus have been
ticus is suspected. It is also utilized reported to vary from 8% to 37%31,32 on
among patients with acute neurologic cEEG monitoring. Similarly, noncon-
injury to monitor function, during treat- vulsive status epilepticus was found in
ment of status epilepticus to monitor up to 20% of patients with traumatic
treatment response, among patients brain injury and 6% of patients with
with subarachnoid hemorrhage to stroke or intracranial hemorrhage.33 In
monitor for vasospasm, and among many institutions across the United
patients with raised intracranial pres- States, cEEG monitoring is now per-
sure after traumatic brain injury.29,30 formed routinely in patients with

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 KEY POINTS
unexplained mental status or in ob- facts occur. In patients with epilepsy, h Ambulatory EEG may be
tunded patients with acute neurologic medications are not lowered because useful in diagnosing
injury. of inherent risks associated of seizures, spells or in classifying
and therefore the study may not cap- seizures in some cases.
USE OF AMBULATORY EEG ture the target event or seizure. h Video telemetry in the
MONITORING (WITH OR
epilepsy monitoring unit
WITHOUT VIDEO) IN DIAGNOSIS UTILITY OF INPATIENT should be readily
OF EPILEPSY AND SPELLS VIDEO-EEG MONITORING considered in classifying
The International League Against Epi- Scalp EEG Monitoring spells as well as in
lepsy recommends long-term EEG Video-EEG monitoring as an inpatient localizing seizures
monitoring in cases with spells; where procedure has long been used for diag- among those with
diagnosis of epilepsy is uncertain; to nostic purposes for patients with spells intractable epilepsy.
classify the epilepsy syndrome in pa- of uncertain etiology, for localization of h Gelastic seizures and
tients with known epilepsy; and for seizure onset, or for classification pur- frontal lobe seizures
electroclinical localization among pa- poses in patients with known epilepsy may have a poor or no
tients who are candidates for surgery. (Case 2-1 and Case 2-2). Epilepsy scalp EEG correlate
With advancement in technology and monitoring unit (EMU) evaluation can that may lead to an
devices now available, outpatient am- be very helpful in distinguishing psy- erroneous diagnosis of
nonepileptic events.
bulatory EEG monitoring can now be chogenic nonepileptic seizures (PNES)
done with or without video capability and nonepileptic paroxysmal events
to diagnose spells. It is an attractive from epileptic seizures (Case 2-2). Stud-
option for patients whose diagnoses ies show that among EMU admissions,
are in question and who have frequent about 25% of patients have PNES,
spells, or for whom the only purpose whereas between 9% and 15% of pa-
is to classify their epilepsy. tients have both epileptic seizures and
Initial studies utilized four to eight PNES.37,38 A comparison of EMU studies
channels, but more recent studies at a US Department of Veterans Affairs
have been done using 32 channels.34 (VA) hospital and a university hospital
Several studies have examined the revealed that in both cohorts PNES
clinical utility of ambulatory EEG mon- occurred in 25% of the patients. VA-
itoring. In these studies, diagnosis was hospital patients had 41% nondiagnostic
refined in anywhere from 50% to 75% studies compared to 27% in university-
of cases.34,35 The majority of ambulatory hospital patients.39
cases were done for diagnostic pur- The key feature in distinguishing
poses, and a minority for epilepsy PNES is the fact that EEGs are normal
classification or seizure frequency de- during the spell, with movement arti-
termination. In pediatric cases, similar facts seen and often the underlying
results were obtained, suggesting that it posterior dominant rhythm preserved
can be successfully used in pediatric even during the event. Postictally, the
cases of all ages36Van ultimate diagno- normal background resumes immedi-
sis of the spells in question or diag- ately after termination of the event.
nosis of epilepsy syndrome was The major caveat in using EMU
confirmed in 61% of cases. The main studies is that patients with simple
caveats are that (1) in general these gelastic seizures or frontal lobe epi-
ambulatory studies are artifact laden lepsy often may not have a surface
and (2) electrodes cannot be reattached EEG correlate, which can lead to an
in a timely fashion. Lack of video avail- erroneous diagnosis of PNES. There-
ability makes ambulatory monitoring fore, in situations where a surface EEG
difficult in cases where rhythmic arti- correlate is not evident or the EEG is
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 EEG and Epilepsy Monitoring

obscured by muscle or movement deficits. While resective surgery is per-

artifact, careful review of the events formed if seizure-onset zone is separate
is required to examine stereotypy and from eloquent cortex, multiple subpial
EEG changes immediately before the transections can be offered to patients
onset of the event or postictally for whose seizure-onset zone is too close
focal features. PNES are often non- or overlying eloquent cortex.
stereotyped, whereas epileptic sei-
zures are fairly stereotyped. Other SUMMARY AND CONCLUSIONS
distinguishing features include the EEG is an important tool in diagnosis
duration of the event (PNES are likely of epilepsy, in classification of an
to be much longer [more than 5 epilepsy syndrome, and for localiza-
minutes]),38 gradual onset and offset, tion of seizures in cases where surgery
eye closure during the events,40 stop- is being considered. Inpatient video-
and-go features (where patients have EEG monitoring is warranted in cases
brief pauses in the convulsive type where an outpatient EEG alone does
activity), and pelvic thrusting. not offer the diagnostic information or
Another pitfall may be that some- if the patient has intractable epilepsy.
times patients may have no events It is also important for a practicing neu-
during an admission and interictal EEGs rologist to recognize all of the normal
may be normal, making the study variants that can look epileptiform,
nondiagnostic. In these cases repeat distinguish them from clearly epilepti-
EMU admissions may be necessary and form patterns, and avoid the erroneous
often increase the diagnostic yield.41 diagnosis of epilepsy in patients with
spells. EEG monitoring can help distin-
Invasive Monitoring guish psychogenic nonepileptic events
Patients being evaluated for surgery and should be readily considered when
sometimes require invasive monitoring the diagnosis is in question and when
to further localize seizures. The most the events do not respond to appropri-
commonly used methods include ate treatment.
depth wires or subdural grid elec-
trodes. Intracranial depth electrodes REFERENCES
are often utilized among patients with 1. Buzsáki G, Anastassiou CA, Koch C. The
origin of extracellular fields and
localization-related epilepsy, especially currentsVEEG, ECoG, LFP and spikes. Nat
if seizures appear to have temporal lobe Rev Neurosci 2012;13(6):407Y420.
onset but cannot be clearly lateralized 2. Tao JX, Ray A, Hawes-Ebersole S, Ebersole JS.
on scalp EEG, especially among those Intracranial substrates of scalp EEG spikes.
who are nonlesional. Depth electrodes Epilepsia 2005;46(5):669Y676.

are placed surgically through burr holes 3. Devinsky O, Sato S, Kufta CV, et al.
Electroencephalographic studies of simple
either in the temporal lobes alone partial seizures with subdural electrode
(tangentially or longitudinally) or as an recordings. Neurology 1989;39(4):527Y533.
array in the temporal and frontal lobes 4. McCormick DA, Contreras D. On the cellular
bilaterally. and network bases of epileptic seizures.
Subdural grid electrodes are placed Ann Rev Physiol 2001;63:815Y846.
surgically when seizure-onset zone is 5. Jacobs J, Staba R, Asano E, et al. High
felt to be close to an eloquent area. frequency oscillations (HFOs) in clinical
epilepsy. Prog Neurobiol 2012;98(3):
Subdural grids offer the advantage of 302Y315.
mapping of eloquent cortex, such that
6. King MA, Newton MR, Jackson GD, et al.
seizure-onset zone can be separated Epileptology of the first-seizure presentation:
clearly so as to prevent postoperative a clinical, electroencephalographic, and

620 www.ContinuumJournal.com June 2013

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 magnetic resonance imaging study of 300 and epilepsy: a proposed terminology
consecutive patients. Lancet 1998;352(9133): and classification for clinical and EEG
1007Y1011. phenomenology. Epilepsia 2001;42:
692Y701.
7. Flink R, Pedersen B, Guekht AB, et al.
Guidelines for the use of EEG methodology 18. Wirrell EC, Camfield PR, Gordon KE, et al.
in the diagnosis of epilepsy. International Will a critical level of hyperventilation-
League Against Epilepsy: commission report. induced hypocapnia always induce an
Commission on European Affairs of the absence seizure? Epilepsia 1996;37(5):
International League Against Epilepsy: 459Y462.
Subcommission on European Guidelines.
19. Ellingson RJ, Wilken K, Bennett DR. Efficacy
Acta Neurol Scand 2002;106(1):1Y7.
of sleep deprivation as an activation
8. Fountain NB, Van Ness PC, Swain-Eng R, procedure in epilepsy patients. J Clin
et al. Quality improvement in neurology: Neurophysiol 1984;1(1):83Y101.
AAN epilepsy quality measures: Report 20. Fountain NB, Kim JS, Lee SI. Sleep
of the Quality Measurement and deprivation activates epileptiform
Reporting Subcommittee of the American discharges independent of the activating
Academy of Neurology. Neurology 2011;
effects of sleep. J Clin Neurophysiol 1998;
76(1):94Y99. 15(1):69Y75.
9. van Donselaar CA, Schimsheimer RJ, Geerts AT, 21. Degen R, Degen HE. Sleep and sleep
et al. Value of the electroencephalogram deprivation in epileptology. Epilepsy Res
in adult patients with first idiopathic Suppl 1991;2:235Y260.
untreated seizures. Arch Neurol 1992;49(3):
231Y237. 22. Boulanger JM, Deacon C, Lecuyer D, et al.
Triphasic waves versus nonconvulsive status
10. Krumholz A, Wiebe S, Gronseth G, et al. epilepticus: EEG distinction. Can J Neurol Sci
Practice Parameter: evaluating an apparent 2006;33(2):175Y180.
unprovoked first seizure in adults (an
evidence-based review): report of the 23. Fountain NB, Waldman WA. Effect of
Quality Standards Subcommittee of the benzodiazepines on triphasic waves:
American Academy of Neurology and the implication of nonconvulsive status
American Epilepsy Society. Neurology epileptius. J Clin Neurophysiol 2001;18(4):
2007;69(21):1996Y2007. 345Y352.

11. Beghi E, Ciccone A. Recurrence after a first

unprovoked seizure. Is it still a controversial 24. Brigo F. Intermittent rhythmic delta
issue? First Seizure Trial Group (first). activity patters. Epilepsy Behav 2011;20(2):
Seizure 1993;2(1):5Y10. 254Y256.

12. Pillai J, Sperling MR. Interictal EEG and 25. Benbadis SR, Lin K. Errors in EEG
the diagnosis of epilepsy. Epilepsia 2006; interpretation and misdiagnosis of epilepsy.
47(suppl 1):14Y22. Which patterns are overread? Eur Neurol
2008;59(5):267Y271.
13. Bozorg AM, Lacayo JC, Benbadis SR.
The yield of routine outpatient 26. Santoshkumar B, Chong JJ, Blume WT, et al.
electroencephalogram in the veteran Prevalence of benign epileptiform variants.
population. J Clin Neurophysiol 2010;27(3): Clin Neurophysiol. 2009;120(5):856Y861.
191Y192. 27. Treiman DM, Walton NY, Kendrick C.
14. Salinsky M, Kanter R, Dasheiff RM. A progressive sequence of
electroencephalographic changes during
Effectiveness of multiple EEGs in supporting
the diagnosis of epilepsy: an operational generalized convulsive status epilepticus.
curve. Epilepsia 1987;28(4):331Y334. Epilepsy Res 1990;5(1):49Y60.
28. Wang NC, Good LB, Marsh ST, Treiman DM.
15. Cavazzuti GB, Cappella L, Nalin A.
EEG stages predict treatment response in
Longitudinal study of epileptiform EEG
experimental status epilepticus. Epilepsia
patterns in normal children. Epilepsia 1980;
2009;50(4):949Y952.
21(1):43Y55.
29. Hirsch LJ, Brenner RP, Drislane FW, et al.
16. Seneviratne U, Cook M, D’Souza W. The
The ACNS subcommittee on research
electroencephalogram of idiopathic
terminology for continuous EEG monitoring:
generalized epilepsy. Epilepsia 2012;53(2):
proposed standard terminology for
234Y248.
rhythmic periodic patterns encountered in
17. Kasteleijn-Nolst Trenite DG, Guerrini R, critically ill patients. J Clin Neurophysiol
Binnie CD, Genton P. Visual sensitivity 2005;22(2):128Y135.

Continuum (Minneap Minn) 2013;19(3):598–622 www.ContinuumJournal.com 621

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 EEG and Epilepsy Monitoring

30. Sutter R, Fuhr P, Grize L, et al. Continuous 36. Wirrell E, Kozlik S, Tellez J, et al. Ambulatory
video-EEG monitoring increases detection electroencephalography (EEG) in children:
rate of nonconvulsive status epilepticus in diagnostic yield and tolerability. J Child
the ICU. Epilepsia 2011;52(3):453Y457. Neurol 2008;23(6):655Y662.
31. Oddo M, Carrera E, Claassen J, et al. 37. Benbadis SR, Agrawal V, Tatum WO 4th.
Continuous electroencephalography in the How many patients with psychogenic
medical intensive care unit. Crit Care Med nonepileptic events also have epilepsy?
2009;37(6):2051Y2056. Neurology 2001;57(5):915Y917.
32. Towne AR, Waterhouse EJ, Boggs JG, 38. Lobello K, Morgenlander JC, Radtke RA,
et al. Prevalence of nonconvulsive status et al. Video EEG monitoring in the
epilepticus in comatose patients. Neurology evaluation of paroxysmal behavioral events.
2000;54(2):340Y345 Epilepsy Behav 2006;8(1):261Y266.
33. Vespa PM, O’Phelan K, Shah M, et al. Acute 39. Salinsky M, Spencer D, Boudreau E, et al.
seizures after intracerebral hemorrhage: Psychogenic nonepileptic seizures in
a factor in progressive midline shift and US veterans. Neurology 2011;77(10):
outcome. Neurology 2003;60(9):1441Y1446. 945Y950.
34. Faulkner HJ, Arima H, Mohamed A. The 40. Chung SS, Gerber P, Kirlin KA. Ictal eye
utility of prolonged outpatient ambulatory closure is a reliable indicator of psychogenic
EEG. Seizure 2012;21(7):491Y495. nonepileptic seizures. Neurology 2006;
66(11):1730Y1731.
35. Tatum WO 4th, Winters L, Gieron M, et al.
Outpatient seizure identification: results 41. Elgavish RA, Cabaniss WW. What is the
of 502 patients using computer-assisted diagnostic value of repeating a
ambulatory EEG. J Clin Neurophysiol non-diagnostic video-EEG study. J Clin
2001;18(1):14Y19. Neurophysiol 2011;28(3):311Y313.

622 www.ContinuumJournal.com June 2013

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