11 EEG in Adult Epilepsy

MOHAMAD Z. KOUBEISSI • ELSON L. SO

Introduction Ictal EEG in Focal Epilepsy

Interictal Epileptiform Discharges Ictal EEG in Generalized Epilepsy
Focal IED Limitation of Interictal and Ictal Scalp EEG
Generalized IED Summary
Photo-Epileptiform Discharges (Photoparoxysmal References
Response)
Ictal EEG
Features of Scalp-Recorded Ictal Discharges

Introduction abnormalities “applies to distinctive waveforms or complexes resembling

those recorded in a proportion of human subjects suffering from epi-
The use of EEG in the evaluation of seizure disorders typically begins in the leptic disorders and in animals rendered epileptic experimentally” (1).
outpatient setting as a procedure performed using scalp electrodes during the Another definition of epileptiform waveforms or patterns is that they are
interictal period. Ictal EEG is now commonly performed with simultaneous EEG abnormalities that are associated with a predisposition to experi-
video recording, in either outpatient or inpatient setting. The objective of this encing or developing epileptic seizures. The word predisposition is used
chapter is to discuss the types of interictal epileptiform discharges (IEDs) and to indicate that the association between epileptiform abnormalities and
ictal discharges recorded from the scalp in adults. The emphasis of this chapter seizure disorders is not absolute. Presence of epileptiform discharges
is on the features of IEDs and ictal discharges and their clinical correlation. does not necessarily indicate that the patient has a seizure disorder (2).
However, the detection of epileptiform abnormalities does increase the
Interictal Epileptiform Discharges likelihood of an epileptic seizure disorder being present. When the find-
ing is taken together with the clinical history and other diagnostic test
According to the International Federation of Societies for Elec- results, epileptiform abnormalities help in establishing the diagnosis of
troencephalography and Clinical Neurophysiology, “epileptiform” epileptic seizure disorders.
315
316 EEG in Adult Epilepsy

Focal IED Spikes/sharp waves are often followed by a slow wave that can be smaller
or larger than the spike/sharp wave discharges themselves. The spike/sharp
Spikes/Sharp Waves wave with its after-going slow wave may be referred to as a “spike-and-slow-
Spikes are transient waveforms with pointed peaks when displayed at a screen wave complex” (i.e., a complex is a series of two or more individual waves).
resolution of approximately 30 mm per second (Fig. 11.1). By definition, du- The accompaniment of spikes/sharp waves by an after-going slow wave may
ration of spikes varies from 20 to 70 milliseconds, whereas sharp waves are not be constant in the same patient and at the same location. When the
wider with duration between 70 and 200 milliseconds (1). The distinction in spike/sharp wave is of negative polarity, as is most often the case, the after-
this regard between spikes and sharp waves is somewhat arbitrary. The two coming wave will be negative as well. Separating these two will be a deflec-
types of waves often occur in the same clinical disorder or the same patient. tion of positive polarity.
Spikes/sharp waves should have sufficient amplitudes to distinguish them
from the background, such as by a factor of two. They are often polyphasic, Focal Spikes/Sharp Waves
but the main component is usually surface-negative. Surface-positive IEDs Common locations of focal spike/sharp-wave discharges, in the approximate
are rare, and can occur at the site of craniotomy (3), particularly if lateral order of frequency, are temporal, frontal, centrotemporal, parietal, occipi-
convexity cortex is removed, but not more mesial cortex. Central positive tal, and midline central and/or paracentral. The clinical correlation of focal
sharp waves can be observed in infants with intraventricular hemorrhage or spikes/sharp waves is with focal epilepsy; however, the likelihood that a given
periventricular white matter injury, but the discharges are a better indication focal spike/sharp wave is associated with epilepsy varies with its location (5).
of encephalopathy than of epileptogenicity (4). For instance, the association is higher for temporal spikes/sharp waves than

Figure 11.1: Left midtemporal spike in a 33-year-old woman who had

been experiencing spells of smelling burnt rubber, followed by lip smack-
ing and behavior of confusion. This spike discharge is not followed by
an after-going slow wave. MRI showed a cavernous angioma at the left
temporal lobe, despite lack of left temporal slowing during wake EEG.
 EEG in Adult Epilepsy 317

for rolandic or occipital spikes/sharp waves. Approximately 90% of children with periventricular hemorrhage or leukomalacia and in young children with
with anterior temporal spikes have seizures, whereas seizures are present in multifocal spikes/sharp waves, especially in the presence of global encepha-
only 38% of those with rolandic spikes. Temporal lobe tissues, especially the lopathy, such as with ischemic injury or lipid storage diseases (9,10).
hippocampus and the amygdala, are some of the most epileptogenic. The The identification of focal spikes/sharp waves is very important in the di-
temporal lobes are also frequently involved in pathologic conditions, such as agnosis of benign, age-related epilepsy syndromes (see Chapter 10). Spikes/
hypoxia, strokes, tumors, trauma, and vascular malformations. In contrast, sharp waves in these syndromes have distributions, morphology, and activa-
many children with occipital IED do not have epilepsy; in fact, about 60% of tion factors that are characteristic for each syndrome. The most common
children with occipital spikes do not have epileptic seizure disorders (6), and is benign epilepsy of childhood with centrotemporal spikes (also known as
occipital IEDs are even encountered in nonepileptic persons with migraine benign epilepsy with centrotemporal spikes, BECT, or benign rolandic epi-
disorders (7). Other occipital discharges, known as “needle spikes,” can be ob- lepsy). Other childhood syndromes of focal epilepsy are benign childhood
served in the EEG of children who have congenital blindness but not epilepsy epilepsy with occipital paroxysms and the syndrome of early-onset child-
(8). These occipital spikes are low in amplitude and sharp in configuration. hood seizures with occipital spikes (Panayiotopoulos syndrome) (11).
Most focal spikes/sharp waves are surface negative at the scalp. Positive
spikes/sharp waves are not common in the adult patient. They can be seen Multifocal Spikes
postoperatively when overlying convexity cortex is removed, but more mesial Multifocal spikes/sharp waves refer to the presence of multiple indepen-
cortex remains. Synchronous, but spatially separated, positive and negative dent foci of spikes or sharp waves that involve both hemispheres (Fig. 11.2).
spikes are evident when the spike voltage field is tangential rather than radial. Although this abnormality can be seen at any age, it is most frequently
Positive-polarity discharges are more frequently encountered in newborns observed in children aged 4 to 7 years (12). Background EEG slowing is

Figure 11.2: Multifocal spikes appearing at F4, F8, P8, O1, and bisyn-
chronously at the occipital regions. The patient had medically refractory
seizures since childhood. Note also the generalized slowing in the back-
ground. EEG is displayed in Laplacian montage. The patient had other
EEG abnormalities, which, together with the clinical history, suggest LGS
(see Figs. 11.7 and 11.9).
318 EEG in Adult Epilepsy

present in nearly all these patients, and 94% of them have seizures. General- distribution within a hemisphere, or more diffusely affecting a whole hemi-
ized motor seizures are the most common, occurring in 76% of patients (13). sphere. The temporo-parietal-occipital region is most frequently involved.
Seizures are typically frequent, with half of the patients experiencing daily PLEDs are highly associated with acute cerebral disorders, especially those
seizures. Concomitant neurological abnormalities are also common; 45% producing structural lesions such as stroke (infarct or hematoma), brain
of these patients have motor deficits and 82% have mental retardation and trauma, herpes encephalitis, tumor, and abscess. Rare causes include met-
developmental delay. The majority (71%) have underlying structural brain abolic encephalopathy, Creutzfeldt-Jakob disease, migraine, and toxic en-
abnormalities or a history of brain injury. cephalopathy (e.g., aminophylline or alcohol intoxication).
Fifty percent of patients with PLEDs will develop seizures, most often
Periodic Lateralized Epileptiform Discharges of a focal nature, with or without secondary generalization. Reiher and
Periodic lateralized epileptiform discharges (PLEDs) are epileptiform dis- colleagues (17) observed that PLEDs may be multiphasic and burst-like in
charges or complexes that recur with a regular periodicity in one hemi- appearance. PLEDs-plus is the term they coined for this type of periodic
sphere, usually every 0.3 to 4 seconds (14) (Fig. 11.3). This periodic activity activity, as opposed to the less complex morphology of PLEDs-proper.
may take the form of monophasic or polyphasic spikes or sharp waves, PLEDs-plus carries a much higher association with clinical seizures
which may or may not have accompanying slow waves (15,16). Although and status epilepticus. In fact, ictal activity is commonly recorded with
very focal PLEDs have been observed, usually the discharges are regional in PLEDs-plus.

Figure 11.3: Periodic lateralized epileptiform discharges (PLEDs) at

the right hemisphere in a 40-year-old man who had a small right ­frontal
­tumor. The patient experienced a generalized convulsive seizure 12 hours
­before the EEG recording was performed.
 EEG in Adult Epilepsy 319

PLEDs are transient and they may transform over days or weeks into in- Nearly 90% of patients with multifocal PLEDs have seizures. Prognosis is
termittent monomorphic slow waves with or without sporadic spikes/sharp dependent on the underlying cerebral disorder. For example, patients with
waves. The interval between discharges typically lengthens over time as well. acute cerebral lesions or infections have a higher mortality than those whose
These intermittent slow waves eventually disappear, possibly leaving resid- PLEDs follow a bout of multiple seizures.
ual focal slowing, which reflects the sequela of underlying brain damage.
When PLEDs are recorded bilaterally, the term BIPLEDs is commonly Temporal Intermittent Rhythmic Delta Activity
used. These discharges may be temporally dependent or independent (18). Temporal intermittent rhythmic delta activity (TIRDA) consists of inter-
They are encountered in patients with severe hypoxic encephalopathy or mittent sinusoidal trains of rhythmic delta waves from the temporal region
bilateral hemisphere destructive lesions. BIPLEDs, particularly when inde- that typically last several seconds (Fig. 11.4) (20,21). The most common
pendent, are associated with a poor prognosis for survival or recovery of frequency is 2 to 3 Hz. Although anterior temporal is the predominant loca-
normal neurological functions. tion, posterior TIRDA can also be observed. TIRDA may appear in wake-
In multifocal PLEDs, there are at least three foci of periodic activity in- fulness or sleep, but it is often most easily identified in drowsiness. Reiher
volving both hemispheres (19). Multifocal PLEDs are encountered in pa- and colleagues (20) have demonstrated that TIRDA is highly correlated with
tients with severe and diffuse brain dysfunction or with multifocal lesions a history of temporal lobe seizures. In a case-control study, all patients with
of both cerebral hemispheres. Etiologies include multifocal strokes, infec- TIRDA were shown to have complex partial epilepsy (21), and the major-
tion, a state of seizure exacerbation, and toxic/metabolic encephalopathy. ity also had temporal spikes/sharp waves on their EEGs. Temporal depth

Figure 11.4: Temporal intermittent rhythmic delta activity (TIRDA; indi-

cated by a circle) at the right temporal lobe in a 32-year-old patient with
medically refractory epilepsy. MRI showed evidence of right mesial tem-
poral sclerosis, in the form of hippocampal atrophy and fluid-attenuated
inversion recovery (FLAIR) signal abnormality.
320 EEG in Adult Epilepsy

electrode recording during TIRDA on the scalp showed active spiking from (HV) or drowsiness. These bilateral bursts are synchronous in timing and
the amygdalohippocampal structures. TIRDA is commonly associated with symmetric in amplitude between hemispheres, although shifting asymmetry
underlying structural lesions. In fact, two-thirds of the patients in the study is common from burst to burst. On close inspection, latency differences be-
had pathology of the temporal lobe. tween hemispheres can be detected, but usually by no more than 20 millisec-
onds. The amplitude of these discharges may be upward of several hundred
Generalized IED microvolts and typically most prominent in the midline frontal region.
3-Hz spike-and-wave discharges are the EEG signature of absence epilepsy.
Generalized IEDs have a variety of forms—3-Hz spike-and-waves, atypical It is now known that even a brief burst can interfere with mental functioning.
spike-and-slow-waves, slow spike-and-wave discharges, hypsarhythmia, and The effect is subtle and may not be apparent by visual observation; however,
generalized repetitive fast discharge (GRFD). neuropsychological testing has demonstrated that even a 1- or 2-second burst
will briefly interrupt continuous motor tasks (22). Bursts of 3 seconds or
3-Hz Spike-and-Wave longer duration are more consistently accompanied by the clinical signs of
As the name implies, 3-Hz spike-and-wave discharges are runs of bilateral an absence seizure, namely, behavioral arrest, staring, and/or eye fluttering.
spikes and after-coming slow waves that repeat rhythmically at a rate of three HV is a standard procedure for activating absence seizures and 3-Hz
cycles per second (Fig. 11.5). Each burst typically lasts between 1 and 3 sec- spike-and-wave bursts during EEG recording. However, clinicians must be
onds, but longer runs occur, especially when activated by hyperventilation aware of pseudo-absence events that can occur in some children without

Figure 11.5: Hyperventilation-induced paroxysm of 3-Hz spike-and-

waves in an 11-year-old girl who had behavioral arrest and eyelid flutter-
ing during the paroxysm. (Interval between gridlines is 200 milliseconds.)
 EEG in Adult Epilepsy 321

epilepsy (23). This nonepileptic phenomenon has EEG features of runs of bursts. The atypical spike-and-slow-wave pattern is more likely to occur as
high-voltage, semirhythmic to rhythmic, delta waves that may be slower than single bursts rather than in long repetitive runs. Drowsiness and non-REM
the usual HV buildup. This slowing is widely distributed, but often with a sleep activate generalized atypical spike-and-slow-wave discharges, and they
maximal amplitude at the anterior head regions. However, careful analysis may be entirely absent during wakefulness in some patients.
of the EEG in pseudo-absence spells shows that spikes are lacking, unlike The clinical correlation of the generalized atypical spike-and-slow-wave
real 3-Hz spike wave. Unfortunately, the clinical appearance of pseudo-­ abnormality is with primary generalized epilepsy, including benign myo-
absence spells can mimic that of genuine absence seizures (24). Accordingly, clonic epilepsy of early childhood, myoclonic-astatic epilepsy of early child-
an EEG recording is required to differentiate the two. hood, juvenile myoclonic epilepsy (JME) of Janz, juvenile absence epilepsy,
atypical absence epilepsy, epilepsy with grand mal on awakening, and pho-
Generalized Atypical Spike-and-Slow-Waves tosensitive epilepsy (26).
Generalized atypical spike-and-slow-wave discharges are bilaterally synchro- In patients with both 3-Hz and atypical spike-and-slow waves, it is not
nous complexes that resemble 3-Hz spike-and-wave discharges, but differ in uncommon for focal spikes of low amplitude to appear during drowsiness
that they have variable rates, although mostly close to 4 Hz. Also, the spike in the frontal or temporal regions. These do not indicate an accompanying
component of the complexes is often polyphasic (25) (Fig. 11.6). Moreover, focal seizure disorder, as long as they are not abundantly present at a single
the complexes vary greatly in amplitude and morphology within and between location during wakefulness or sleep.

Figure 11.6: Generalized atypical spike-and-slow-wave complexes in a

19-year-old woman who since age 13 years has had sporadic generalized
tonic-clonic seizures on awakening in the morning. The patient did not
have myoclonic jerks or absence spells, but the recorded paroxysms,
such as the one shown in this figure, were sometimes accompanied by
brief arrest of activity.
322 EEG in Adult Epilepsy

Slow Spike-and-Waves (Sharp-and-Slow-Wave Complexes) pattern is commonly seen as one of the EEG features of Lennox-Gastaut
As the name indicates, the slow spike-and-wave discharge pattern is charac- syndrome (LGS) in children and adults.
terized by complexes that occur slower than the “prototypical” 3-Hz spike-
and-wave discharge pattern of absence epilepsy (Fig. 11.7), namely, around Generalized Repetitive Fast Discharge
1.0 to 2.5 Hz. Moreover, the complexes are not as rhythmic, and the spike GRFD is also known as paroxysmal fast rhythm, generalized paroxysmal
component is replaced by longer-duration sharp waves (27). Compared to fast activity, or “runs of rapid spikes” (28,29). This pattern consists of bursts
3-Hz spike-and-wave pattern, persistent or fluctuating asymmetry of am- of repetitive spikes in the alpha or beta frequency range (Fig. 11.8). The
plitude between hemispheres occurs more commonly with the slow spike- bursts are generalized in distribution, typically last less than 10 seconds, and
and-wave pattern. This pattern is also more likely to occur during waking as are of low to medium amplitude.
a single discharge of one or a few complexes. However, drowsiness or non- Most GRFD occurs during sleep. It can be considered an ictal rhythm,
REM sleep may activate trains of repeating slow spike-and-wave complexes, because tonic seizure activity sometimes accompanies it. However, this tonic
sometimes similar to electrical status epilepticus during sleep (ESES). HV, seizure activity may be subtle and take the form of tonic slow eye opening.
but not photic stimulation, may enhance slow spike-and-waves, but not as GRFD may also be accompanied by transient apnea or bradycardia in some
reliably as it does the 3-Hz spike-and-wave pattern. The slow spike-and-wave children. A particular type of GRFD, referred to as an electrodecrement,

Figure 11.7: Slow spike-and-wave, also called sharp-and-slow wave (in-

dicated by arrow), in the patient in Figs. 11.2 and 11.9. (Interval between
gridlines is 200 milliseconds.)
 EEG in Adult Epilepsy 323

Figure 11.8: GRFD during sleep, in the patient in Figs. 11.2 and 11.7.
(Interval between gridlines is 200 milliseconds.)

is characterized by a sudden, brief, generalized attenuation of background discharges are generally believed to be more highly associated with sei-
EEG. High-frequency, but low-amplitude, spiking is thought to underlie zure disorders; however, two studies showed no difference in seizure pro-
electrodecremental events. Patients with GRFD usually also have general- pensity (32,33).
ized spike-and-wave complexes or especially slow spike-and-wave discharges. Photo-epileptiform discharges can also be divided into four categories ac-
Bursts of GRFD may be preceded or followed by these other discharges. cording to their scalp distribution: (a) generalized (Fig. 11.9); (b) bilateral
GRFD is often associated with catastrophic epilepsy syndromes, especially posterior dominant (Fig. 11.10); (c) bilateral occipital; and (d) focal unilat-
in children, such as the LGS (29,30). eral (34). Of the four categories, generalized photo-epileptiform discharges
are the most common, and focal unilateral discharges are the least com-
mon. When focal, photo-epileptiform discharges usually occur in the occipi-
Photo-Epileptiform Discharges tal region, and they have a high association with a structural abnormality
(Photoparoxysmal Response) ipsilateral to the discharges. Up to 77% of individuals with generalized
photo-epileptiform discharges have seizure disorders, whereas epilepsy is
Photo-epileptiform discharges are spikes/sharp waves or complexes of less common in those with bilateral occipital discharges. In general, primary
spike-and-waves that are elicited by repetitive photic stimulation. Photo- generalized epilepsy is most commonly associated with photo-epileptiform
epileptiform discharges have been divided into two types—“self-­limited,” discharges. Focal seizure disorders are rarely associated with this phenom-
if the discharges do not exceed the duration of the stimulation; and enon, but those rare instances when focal seizures are activated by photic
“self-sustaining,” if they outlast the stimulation (31). Self-sustaining stimulation, they usually begin in the occipital region.
324 EEG in Adult Epilepsy

Figure 11.9: Example of generalized photo-epileptiform discharge

(photoparoxysmal response).

Ictal EEG the EEG morphology of the metamorphic seizure pattern evolves through
different stages of the seizure. This pattern is most typical of focal seizures,
An EEG recording during a patient’s habitual episode and documenting an but it can be seen in both primary and secondary generalized tonic-clonic
ictal discharge are essential parts of the evaluation of patients with parox- seizures.
ysmal episodes, particularly for differentiating epileptic from nonepileptic Defining what constitutes an ictal pattern can be difficult. It is usually, but
spells. In patients with epilepsy, ictal EEG recording is often needed to help not always, associated with seizure symptoms or signs in the patient. Ictal
determine seizure type and epilepsy syndromes. Ictal recordings are also an onset is generally marked by a clear change in the background EEG rhythm,
indispensable part of the presurgical evaluation of patients with pharmaco- which may be manifested as an increase or decrease of the frequency, field,
resistant seizures (35). morphology or amplitude of activity as the seizure evolves. Seizures are
most recognizable when the EEG pattern consists of an organized rhythm
Features of Scalp-Recorded Ictal Discharges that is different from normal background activity and has apiculate or sharp
waveforms. Fortunately, ictal EEG patterns typically evolve through several
Seizure patterns can be isomorphic or metamorphic. Isomorphic patterns stages, which is an important distinguishing feature.
lack clear evolution between multiple phases of an ictal event. EEG mor- In certain situations, it may be difficult to distinguish EEG seizures from
phology changes little throughout the seizure. A typical example is the physiological or nonictal pathological findings. Specifically, EEG fea-
spike-and-slow wave discharge of an absence seizure. On the other hand, tures related to transition from sleep to wakefulness or transition between
 EEG in Adult Epilepsy 325

Figure 11.10: Example of bilateral posterior dominant photo-­

epileptiform discharge (photoparoxysmal response).

different depths of coma may resemble seizures. In addition, differentiating or signs, depending on the brain region affected. Seizure semiology is often an
frequent spiking from seizures may not be straightforward. The same pat- important indicator of the area of seizure onset. For example, elemental audi-
tern may represent ictal discharges in some patients (36,37). In comatose pa- tory seizures strongly suggest onset in Heschl gyrus, whereas elemental visual
tients, ictal-like activity may not have a clear clinical correlate, which further phenomena often originate from regions within or close to the primary visual
makes its designation as ictal more difficult. cortex. Other ictal symptoms, however, are less specific in indicating the loca-
tion of seizure onset, such as olfactory or psychic auras. While such auras are
Ictal EEG in Focal Epilepsy often seen in temporal lobe epilepsy, they may also be seen in orbitofrontal,
insular, or neocortical temporal epilepsy. When ictal activity is recorded by
Simple Focal Seizures scalp electrodes during simple focal seizures, it is often indistinguishable from
Simple focal seizures frequently occur without a detectable ictal correlate on that seen with complex focal seizures, namely, focal fast-frequency discharge
scalp EEG. The low electrographic yield is a consequence of the restricted in the alpha or beta frequency, focal rhythmic slowing in the delta or theta
nature of and limited propagation from the seizure focus. In one study, only frequency, or, less commonly, focal repetitive spike discharge. Focal, irregular,
21% of all simple partial seizures were associated with discernible ictal dis- nonrhythmic delta or theta activity is an unlikely ictal pattern.
charge on the EEG (38). The percentage was higher in those seizures that
involved motor manifestations (33%) and lower in seizures that had no motor Complex Focal Seizures
manifestations (15%). This may be explained by the fact that motor phenomena The EEG almost always shows changes in association with complex ­focal
frequently reflect a wider seizure propagation. Clinical manifestations of focal seizures, with the exception of some of frontal or parietal lobe origin (39).
seizures include motor, sensory, autonomic, cognitive, and psychic symptoms Inferring the location of the epileptogenic zone by using ictal scalp recordings
326 EEG in Adult Epilepsy

is not always straightforward. The morphologic appearance of the ictal and sphenoidal electrodes may not detect deviations from the baseline EEG.
pattern is not specific to the area of seizure onset. For example, the classic However, with the involvement of neocortical areas, the scalp EEG and the
theta frequency ictal discharge, often typical of mesial temporal genera- sphenoidal EEG are more likely to detect an ictal activity. The mesial tempo-
tors, can be seen in other focal seizures that later spread to the temporal ral structures are connected with numerous cortical regions. These include
lobe (40). One generally accepted rule is that the closer the recording elec- the orbitofrontal cortex, the insula, the frontal pole, the posterior cingulate
trode is to the ­ictal-onset zone, the higher the recorded frequencies. In con- area, as well as the temporal neocortex and temporo-occipital region (40).
trast, seizure generators that are deep in the brain or far from the recording Thus, in nonlesional cases that have seizures that are semiologically and clin-
electrodes tend to be associated with slower-frequency discharges on scalp ically consistent with temporal lobe epilepsy, intracranial electrode evalua-
EEG. Gloor (41) suggested that when faster frequencies are recorded early tion is often recommended to sample regions known to have connectivity
in the seizure, they reflect proximity of the recording electrodes to the site with the mesial temporal structures. For example, patients can have extra-
of origin, whereas slower frequencies often represent propagation from a temporal epilepsy, but with seizures that are clinically and electrographi-
distant site. Indeed, intracranial electrodes often record high-frequency cally typical of mesial temporal lobe epilepsy (40). The opposite scenario
activity when implanted at or close to the epileptogenic zone, whereas may sometimes occur when seizures of mesial temporal origin result in an
scalp-recorded ictal discharges start as slow waveforms before progressing initial scalp ictal discharge over a different brain region due to propagation
into higher frequencies. (Fig. 11.11). In some patients who have hippocampal sclerosis on one side,
In most complex focal seizures, evolution of the ictal EEG pattern is a but scalp-recorded seizure onset on the contralateral side, intracranial elec-
fundamental feature that helps differentiate a seizure from the stable mono- trode recording has revealed the seizure onset on the side of sclerosis (45).
morphic appearance of normal activity, such as benign variants. Typically, A 5- to 9-Hz ictal-onset rhythm recorded from the inferior temporal scalp
the evolution is from lower voltage and higher frequencies to higher-voltage electrodes has been reported to be highly associated with hippocampal
and lower-frequency waveforms as the seizure propagates to more brain onset seizures (46). Commonly, a synchronous positive polarity rhythm is
regions. However, some focal seizures, particularly those originating from observed at the vertex or parasagittal region, particularly in a common aver-
temporal neocortex, can begin as repetitive spikes or sharp waves. Progres- age reference montage. This represents the positive field maximum of the
sively slower spike and wave discharges commonly mark the ending of ictal inferior temporal dipolar source. On the other hand, seizures originating in
activity. A sudden termination is the hallmark of most such seizures. Post- temporal neocortex are often associated with irregular, polymorphic, 2- to
ictal EEG changes also help in distinguishing seizures from benign vari- 5-Hz lateralized activity. This pattern is sometimes preceded by repetitive or
ants. These changes may include generalized or focal slowing, amplitude periodic sharp-wave discharges at the temporal region.
attenuation, or an increase in the focal spike frequency (42,43). When pres- One of the early signs of ictal EEG changes in temporal lobe epilepsy is
ent, focal postictal slowing has lateralizing or sometimes localizing value diffuse attenuation of the EEG and cessation of IEDs (47). This pattern
for the ictal-onset zone (44). The latency between the first clinical sign of may have localizing value. Blume and colleagues (48) studied 66 seizures of
a seizure and the ictal EEG onset should always be assessed. If the onset temporal lobe origin and found that the initial EEG change consisted of
of ictal behavior precedes the EEG onset, it may signify that the ictal EEG attenuation in 10% of the seizures, rhythmic discharge without epileptiform
pattern is coming from a region to which the seizure has propagated, rather features in 43%, and repetitive epileptiform discharges in 41%. A typical ic-
than its origin. tal pattern that evolves shortly after onset in temporal lobe epilepsy is that
of a theta rhythm or organized spiking, often centered in the anterior-to-
Temporal Lobe Complex Focal Seizures mid temporal region or in sphenoidal electrodes (Fig. 11.12). This temporal
Temporal lobe seizures have been the most thoroughly studied because they rhythm is seen in 50% to 80% of the mesial temporal lobe seizures (49). Some
comprise the most common type focal epilepsy. These seizures often origi- seizures, however, may not be accompanied by clear EEG correlates at their
nate from the hippocampus or other mesial temporal structures and propa- onset. Neocortical-onset seizures are more likely to be of this category (46).
gate to involve the basal and lateral temporal lobe cortices, as well as frontal Intracranial EEG recordings typically provide better temporal resolu-
lobe regions. When the ictal discharge is limited to the hippocampus, scalp tion of seizure activity. Whereas scalp-recorded ictal discharges may lag
Figure 11.11: A 24-year-old man presented with a history of intrac-
table complex focal epilepsy since age 12. His risk factors include an
episode of meningitis at age 7 years. Video-EEG monitoring with scalp
electrodes suggest seizure onset in the left frontopolar region with later
propagation to the left temporal region. Because his brain MRI revealed
left hippocampal atrophy, invasive monitoring with depth electrodes
was conducted. This figure shows his seizure onset in two consecutive
EEG pages consisting of simultaneous scalp and depth electrode re-
cordings. His seizure onset zone proved to be in the left hippocampus,
with secondary spread to the left frontopolar region. The scalp record-
ings missed the initial high-frequency hippocampal discharge (inset), but
showed a frontopolar ictal discharge only after seizure propagation to
the frontal pole. M1–6 are medial frontopolar contacts, L1–6 are lateral
frontopolar contacts, HH1–3 are in the head of the hippocampus, and
HB1–2 are in the hippocampal body.

327
328 EEG in Adult Epilepsy

Figure 11.12: The patient is a 36-year-old, left-handed woman with a

history of epilepsy since 9 years of age. She has frequent generalized
tonic-clonic seizures preceded by cephalic auras lasting 10 to 20 sec-
onds. She had a normal brain MRI and routine EEGs in the past. Upper
panel of this figure shows EEG without, and lower panel with, sphenoi-
dal electrode recording. A: Interictal EEG showing low-voltage, poorly
defined spike at channel T7–P7, but simultaneous sphenoidal recording
shows high-amplitude spike activity. B: Ictal EEG showing rhythmic delta
discharge more obvious at the sphenoidal electrode recording than the
simultaneous scalp recording.

behind the clinical onset, intracranially recorded ictal discharges are often ictal-onset discharge of beta frequency is independently predictive of ex-
concomitant with, or appear before, behavioral signs. Indeed, interictal and cellent outcome following lesional or nonlesional frontal lobe surgery, with
ictal discharges that are limited to the hippocampus are often undetectable 90% of the patients becoming seizure-free (52). Unfortunately, only 25% of
by sphenoidal or scalp electrodes, and the ictal pattern becomes evident on frontal lobe surgery patients have this type of discharge that is visually de-
scalp recordings only after the seizure has involved significant portions of the tectable. Computer-aided power spectrum analysis of the EEG is sometimes
basal and lateral temporal neocortex (Fig. 11.13). The frequency of scalp- required (Fig. 11.15A and B).
recorded seizure discharges can be in the alpha, beta, or delta range (48). Parietal lobe seizures may be accompanied by sensory hallucinations, par-
Intracranial electrodes can record the higher-frequency and lower-­amplitude esthesias, and rarely ictal pain. Scalp EEG recordings of parietal lobe sei-
beta or gamma activity, which is typical of the seizure onset, whereas scalp zures often do not show localizing findings and sometimes not even a clear
electrodes can appreciate only the slower frequencies that evolve with seizure ictal correlate (53).
spread. Occipital lobe seizures are often associated with semiology, which helps
identify the site of origin. These include elemental or complex visual hal-
Extratemporal Complex Focal Seizures lucinations and other eye movement phenomena such as eye deviation and
In contrast to patients with temporal lobe seizures, who often have auras, forced blinking (54). It is common for occipital lobe seizures or parietal
slowly developing automatisms, and postictal states, patients with frontal lobe seizures to propagate to the ipsilateral temporal lobe, as well as to
lobe seizures tend to exhibit no auras, abrupt hypermotor activity, rapid the contralateral temporal lobe (Fig. 11.16). Following propagation, the
propagation, and little or no postictal confusion. These contribute to the seizure semiology would include alteration of awareness and automatic be-
decreased EEG yield in frontal lobe seizures (50). Frontal lobe seizures have haviors typical of temporal lobe seizures. Propagation to the frontal lobe
a myriad of clinical manifestations and are often poorly localized by scalp and insula from occipital lobe foci has also been described. This is more
EEG (39) (Fig. 11.14). Only about half of the complex focal seizures origi- likely associated with clonic or tonic seizure behavior. Scalp recordings of
nating from the frontal lobe appear to show a clearly localizing EEG pat- occipital seizures commonly show a clear focal ictal pattern over the oc-
tern, and many simply movement and muscle artifact (51). However, a focal cipital region.
 EEG in Adult Epilepsy 329

Scalp electrodes
Figure 11.13: The patient is a 44-year-old woman with history of intrac-
table epilepsy since age 19. Her seizures manifest as abdominal aura fol-
lowed by alteration of awareness and oral automatisms, and infrequent
secondary generalization. Her video-EEG monitoring with scalp elec-

Depth electrodes
trodes captured habitual seizures that electrographically appeared to be
of left temporal origin, but the ictal discharge occurred at least 20 ­seconds
after the clinical onset. Because she had a normal brain MRI, invasive
monitoring was performed with depth electrodes in the left temporal
lobe and other brain regions, including frontal, insular, and posterior cin-
gulate regions. Simultaneous depth and scalp recordings confirmed ictal
onset in the left hippocampus, which explained the delayed scalp EEG

Scalp electrodes
appearance. A: Seizure onset in the hippocampus (H1, 2) was associated
with normal tracings on simultaneous scalp EEG. B: Seizure propagation
to the amygdala (AM1, 2) also did not result in clear changes on scalp
EEG. C: Attenuation of the posterior basic rhythm and some evolving
rhythms started to manifest on the scalp EEG as the intracranial seizure

Depth electrodes
discharge involved temporal neocortical (TN1) regions. D:  Further syn-
chronization of the ictal discharge over the temporal neocortex (TN1–4)
30 seconds after seizure onset, resulting in a clear rhythmic ictal discharge
at the scalp recording of the left temporal region.

Figure 11.14: This EEG is of a 38-year-old right-handed man with epi-

sodes of alteration of awareness since 15 years before. They were occa-
sionally preceded by “smelling sweet smells.” His interictal EEGs in the
past were normal. This figure shows scalp EEG during a nocturnal seizure
that manifested as right hand and mouth automatisms, facial grimac-
ing, and smiling. Awareness and language appeared to be preserved in
the immediate postictal period, typical of frontal lobe seizures. The ictal
EEG shows diffuse, frontal-maximum, delta-range rhythmic discharge
with no clear lateralizing features.
330 EEG in Adult Epilepsy

Secondary generalized seizures may evolve from complex focal seizures, used when a nongenetic, intra- or postnatal cause of the epilepsy is known.
which in turn may evolve from simple focal seizures. Scalp EEG of secondary “Cryptogenic” is used when a nongenetic cause is suspected but not clearly
generalized seizures is best distinguished from that of primary generalized identified.
seizures by the focal or lateralized onset, a focal or regional predominance
of the seizure pattern, and focal or lateralized postictal slowing. Idiopathic Generalized Epilepsy
Idiopathic generalized epilepsy includes juvenile and childhood absence
Ictal EEG in Generalized Epilepsy epilepsies, JME, and generalized tonic-clonic epilepsy. These syndromes
are associated with several seizure patterns. However, common characteris-
Generalized epilepsies are defined by the International League Against tics are that the ictal and interictal discharges are bilateral, symmetric, and
Epilepsy as epileptic disorders with generalized seizures. Generalized
­ consist of synchronous spike-and-slow-wave activity of varying frequencies.
­seizures are defined as ones originating at some point within, and rapidly Because these are “primary” epilepsies without obvious brain damage, the
engaging, bilaterally distributed networks. These networks can include EEG background is typically within normal limits, and the bilateral ictal
cortical and subcortical structures, but do not necessarily involve the en- discharges typically appear and terminate abruptly. Although widespread
tire cortex (55). There are two major categories of generalized epilepsy: and termed “generalized,” the ictal discharge is often maximal over bilateral
idiopathic and symptomatic/cryptogenic. In the “idiopathic” category, in- superior frontal regions. As the run of spike-and-wave activity progresses,
terictal and ictal EEG findings are usually bilateral, synchronous, and sym- its frequency slows and the spike component may become less obvious. The
metrical. The etiology is presumably genetic. The term “symptomatic” is EEG returns to a normal baseline immediately after seizure termination,

Figure 11.15: A: Scalp EEG recording showing midline and left fron-
tal seizure discharge onset in the beta frequency (i.e., focal ictal beta
discharge), which soon develops into a higher-amplitude but lower-­
frequency activity that spreads. B: Power spectrum analysis of the fre-
quencies of the same scalp-recorded seizure activity, showing peaks of
17-Hz beta-frequency activity (arrow) occurring just after the fifth second
at the left (F3–C3), but not at the right (F4–C4) fronto-central region.
 EEG in Adult Epilepsy 331

Figure 11.15: (continued)

except in cases of generalized convulsive seizures, when there will be postic- of the paroxysm, and only 4% had normal reaction times during the first
tal slowing. This seizure type tends to be readily responsive to medications, second of the discharge. The term “complex absence” describes absence sei-
although some may be medically intractable. zures with prominent automatisms (57).
The ictal discharge of an absence seizure is typically abrupt in onset and
Absence Epilepsy offset. There is no postictal slowing. In childhood absence epilepsy, the ictal
Most patients with absence seizures are neurologically and cognitively in- pattern consists of repetitive, spike-and-slow wave complexes at the aver-
tact, and the EEG at baseline is within normal limits. Absence seizures are age frequency of 3 Hz. These discharges typically have a higher frequency
often subtle in their clinical manifestation, and the distinction between in- at seizure onset (approximately 3.5 Hz) and a slower frequency by seizure
terictal and ictal behavior may be difficult. Discharges that last longer than termination (approximately 2.5 Hz) (see Fig. 11.5). Absence seizures can be
3 seconds will often have clinical correlates. Testing patient responsiveness brief or last tens of seconds. At times, there are polyspike and wave com-
with motor or verbal tasks may help assess the alteration of awareness in ab- ponents to the ictal pattern. Occasionally, the spike and waves may be more
sence seizures. Browne et al. (56) studied auditory reaction times and found prominent posteriorly (57). Absence seizures in other epilepsy syndromes
them to be within normal limits immediately prior to the epileptic discharge. may show irregular spike-and-wave complexes, slow spike-and-wave activ-
However, fewer than half the subjects had normal reaction times at the start ity, or generalized paroxysmal fast activity (58).
332 EEG in Adult Epilepsy

Figure 11.16: This EEG is of a 58-year-old man with seizures following a re-
mote history of intracerebral hemorrhage that necessitated surgical evacu-
ation. After years of seizure control, the patient presented with recurrent
seizures manifesting as decreased responsiveness and left facial twitching.
A: FLAIR MRI shows right parieto-occipital encephalomalacia. B: EEG sei-
zure onset consists of low-voltage, alpha-range rhythmic discharge over P4.
C: Discharge evolves in amplitude, frequency, morphology, and distribu-
tion within 30 seconds after seizure onset. D: Emergence of rhythmic activ-
ity at Fz–Cz and F4–C4, denoting seizure propagation into frontal regions.
E: Ninety seconds after seizure onset, EEG shows further seizure propaga-
tion into the whole right hemisphere, including the temporal region, and
also into the left hemisphere to a lesser degree. F: Heralding seizure ter-
mination, slowing and disorganization of the ictal discharge occurred at
­approximately 120 seconds after seizure onset.

Juvenile Myoclonic Epilepsy will have a generalized photo-epileptiform discharge (photoparoxysmal

JME typically starts in the teenage years and is marked by myoclonic and response).
generalized tonic-clonic seizures. The EEG often shows bursts of bilateral, During myoclonic seizures, the EEG shows a high-voltage, 10- to 16-Hz
frontally dominant, irregular, spike-and-wave, and polyspike-and-slow-wave spike discharge. This may be preceded by irregular slow spike-wave com-
discharge with or without an associated myoclonic jerk (Fig. 11.17). Myo- plexes (at 2 to 5 Hz) (59). Absence seizures can be seen in JME, and its 3-Hz
clonic jerks tend to occur shortly after arousal, and some are induced by spike-and-wave discharge is indistinguishable from other absence epilepsies.
intermittent photic stimulation. Approximately one-third of the patients However, such discharges in JME may start as a rapid polyspike-and-wave
 EEG in Adult Epilepsy 333

Figure 11.17: This EEG is of a 21-year-old woman with a recent history

of an episode of loss of consciousness and fall. She also had arm jerks
for several years, which were worst after sleep deprivation and when
she played video games. EEG shows a burst of generalized, bifrontal-­
maximum, polyspike-and-slow wave discharges. Such discharges
­occurred at times in association with myoclonic jerks. Both clinical h
­ istory
and EEG abnormalities are typical of JME.

activity before slowing to 3 Hz. Panayiotopoulos and colleagues (57) stud- generalized rhythms that gradually increase in amplitude and decrease in
ied absence seizures in patients with JME by using continuous video-EEG frequency to approximately 10 Hz (i.e., the “epileptic recruiting rhythm”).
monitoring. They found that clinical seizures were often subtle and notice- Another early EEG change in generalized tonic-clonic seizures is that of
able only if the patient was engaged in certain activities. Polyspike and wave paroxysmal fast activity at about 10 Hz, which increases in voltage (57). This
complexes of irregular frequencies were often the EEG correlate. paroxysmal fast activity becomes intermixed with rhythmic slow activity af-
ter approximately 10 seconds, and the blend gives rise to polyspike-and-slow
Generalized Tonic-Clonic Seizures wave complexes. With the evolution of the seizure, the ictal rhythm slows
Polyspike-and-slow wave discharges may herald the tonic phase of a gener- to approximately 4 Hz and tonic muscle contraction gives way to the clonic
alized tonic-clonic seizure. This tonic phase is associated with low-voltage, activity. During the clonic phase of the seizure, each spike burst is associated
high-frequency activity of 20 to 40 Hz. This pattern is often followed by with a bilateral muscular jerk, whereas the slow wave that follows the spike is
334 EEG in Adult Epilepsy

associated with muscle relaxation. Both the EEG and motor manifestations Atypical Absence Seizures
gradually slow and finally stop abruptly. Postictal EEG voltage attenuation Atypical absence seizures are characterized by a more gradual onset and
ensues, the length of which is a function of the seizure duration. Gradually, offset than childhood absence seizures. Atypical absence seizures may be as-
cerebral rhythms return, starting with diffuse delta activity, which in turn is sociated with decreased muscle tone (62). These seizures typically occur in
followed by more normal rhythms of increased voltage and frequency. The patients with diffuse brain disease and cognitive impairment. They usually
duration of the postictal phase varies from a few minutes to tens of minutes, begin between 1 and 8 years of age, and are they frequently refractory. Atypi-
but it tends to be longer in younger children and after longer seizures. cal absence seizures are common in LGS, as are tonic seizures, atonic seizures,
Clonic-Tonic-Clonic Seizures and, to a lesser extent, myoclonic seizures. The EEG can help to diagnose
LGS if it shows generalized, bifrontal slow spike-and-slow wave complexes
Clonic-tonic-clonic seizures are often seen in individuals with genetic gen- (1.5 to 2.5 Hz) (see Fig. 11.7). These seizures may initially resemble severe
eralized epilepsy (60). The initial clonic jerks are associated with a diffuse myoclonic epilepsy of infancy (Dravet syndrome) and m ­ yoclonic-astatic
10- to 16-Hz spike discharge, which is followed by voltage attenuation with epilepsy (Doose syndrome). Other ictal patterns associated with atypical
superimposed low-amplitude, high-frequency activity of 20 Hz or more absence seizures include slow spike-and-wave activity, which may not be
during the tonic phase. During the second clonic phase, the EEG typically easily distinguished from the patient’s diffusely slow background EEG, and
shows diffuse high-voltage fast spikes interrupted by slow waves (59). ­hypersynchronous slow-and-spike-wave discharge (63). This generalized
Generalized Tonic-Clonic Seizures on Awakening slowing is indicative of diffuse encephalopathy associated with the second-
ary or ­symptomatic epilepsies in which there is obvious brain damage.
Generalized tonic-clonic seizures on awakening are rather uncommon type
of idiopathic generalized epilepsy. These patients semiologically have nei- Tonic Seizures
ther absence spells nor myoclonic jerks (58). Their EEG shows generalized In tonic seizures, there is a sudden and sustained contraction of muscle
bursts of 3 Hz or faster polyspike-and-slow wave discharges, which can be groups, which is commonly associated with falls and loss of consciousness.
irregular in morphology and frequency. They occur principally in individuals with global or multifocal brain impair-
ment. The most common ictal EEG correlate is diffuse low-voltage attenua-
Symptomatic Generalized Epilepsies tion with superimposed fast activity. This pattern may gradually increase in
These epilepsies generally start during infancy or early childhood, although amplitude as the frequency decreases, similar to the early phase of a gener-
they can present at any age. The clinical and EEG manifestations are vari- alized tonic-clonic event. Alternatively, the ictal discharge of tonic seizures
able and age-dependent. may consist of an initial high-voltage slow-wave discharge, followed by volt-
age attenuation (64).
Symptomatic Generalized Tonic-Clonic Seizures
Symptomatic generalized tonic-clonic seizures have EEG correlates that are Clonic Seizures
similar to those seen in idiopathic generalized tonic-clonic seizures. Clas- Patients seldom have clonic seizures alone. Clonic seizures result in less se-
sically, the tonic phase is associated with an electrodecremental pattern or vere metabolic dysfunction and postictal confusion than generalized tonic-
the paroxysmal fast-activity pattern (61). During sleep, these discharges are clonic seizures. The ictal pattern observed with clonic seizures resembles that
subclinical, whereas the pattern is more likely to be accompanied by clinical of the clonic phase of a generalized tonic-clonic seizure. These discharges
manifestations during wakefulness. The frequency of paroxysmal fast activ- are often generalized, repetitive, high-amplitude spike or sharp waves, usu-
ity ranges between 10 and 25 Hz, and its duration often averages 3 to 5 sec- ally with some degree of after-coming slow wave.
onds, before it gives rise to sharp-and-slow wave complexes. The amplitude
of spikes in the fast activity may decrease as the discharge progresses. These Atonic Seizures and Akinetic Seizures
patterns are bilaterally synchronous and frontally dominant, although they Atonic seizures present as brief loss of muscle tone in association with brief
may rarely be unilateral. loss of consciousness, thus often resulting in injurious falls. They last for a
 EEG in Adult Epilepsy 335

Figure 11.18: This case is of a 7-year-old with LGS. His seizures started
at 5 days of age and have been resistant to multiple antiepileptic medi-
cations and the vagus nerve stimulation. His seizure types include clonic,
generalized tonic-clonic, and atonic. EEG during an atonic seizure
is characterized by head drop. Such seizures occur at a frequency of
20 times per day on average. Note the sudden electrodecrement with
superimposed fast activity that evolves within 2 seconds into a gener-
alized, frontal-maximum, alpha-range activity. This is followed by the
reemergence of the interictal pattern consisting of high-voltage gener-
alized slowing and slow spike-and-wave activity.

few seconds, with little or no postictal confusion. Atonic seizures tend to Scalp electrodes often fail to record an ictal discharge in seizures that do
occur in individuals with multifocal or diffuse brain disease (49). The ictal not involve an alteration of consciousness (67). Thus, the absence of ictal
EEG in atonic seizures consists of diffuse voltage attenuation with superim- EEG changes with simple focal seizures does not exclude epilepsy. The di-
posed generalized fast activity, generalized spike-and-slow wave discharges, agnosis of simple focal seizures, rather than psychogenic nonepileptic spell,
or generalized fast activity (Fig. 11.18). Paroxysms of multiple spike-and- commonly depends on the entire clinical presentation, including their ste-
slow waves or slow spike-waves have been described as well (65). Clinically, reotypical nature, their duration, and findings on brain imaging. Conversely,
atonic and myoclonic seizures may be difficult to distinguish from one an- seizures that include alteration of awareness usually show EEG changes (68).
other, if they are brief, and drop attacks may be due to tonic seizures instead Scalp EEG recordings are limited primarily because they can detect only
of atonic seizures. Akinetic seizures are characterized by the sudden onset a small portion of the underlying brain activity. Cortical discharges need be
of behavioral arrest with no impairment in the muscle tone. Their EEG cor- synchronized over an area of 10 cm2 or more before they can be detected
relates are similar to those of atonic seizures. by scalp electrodes (69), and the amplitude of recorded brain signals is in-
versely proportional to the square of the distance between the recording
Limitation of Interictal and Ictal Scalp EEG electrode and the cortical generator (70). Moreover, the impedance of the
meninges, cerebrospinal fluid, skull, and scalp will attenuate all intracranial
Scalp ictal recordings have limitations. In patients with a known brain le- frequencies as they behave like a high linear frequency filter and, together
sion, especially in the temporal lobe, spatial concordance between the lesion with the electrodes, function as an EEG averager (71).
and the scalp-recorded ictal discharge will often support resective surgery An additional important factor is the location and number of the elec-
and provide a good outcome (66). However, in nonlesional epilepsy, scalp trodes attempting to characterize the EEG dipole generator. Without suf-
ictal recordings can be insufficient or misleading, and intracranial electrodes ficient recording locations in both the top and bottom half of the head, the
implantation and recording are often required before resective surgery is angle subtended by any of the standard 10 to 20 electrodes with the cortical
possible. generator may be insufficient to measure its signal. This principle is also true
336 EEG in Adult Epilepsy

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