Electroencephalography (EEG) in The Diagnosis of Seizures and Epilepsy - UpToDate

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Electroencephalography (EEG) in the diagnosis of

seizures and epilepsy
Authors: Jeremy Moeller, MD, Hiba Arif Haider, MD, Lawrence J Hirsch, MD
Section Editor: Paul Garcia, MD
Deputy Editor: John F Dashe, MD, PhD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2022. | This topic last updated: Feb 23, 2022.
INTRODUCTION
The diagnosis of epilepsy is often not straightforward, and misdiagnosis is not rare [1]. A
detailed and reliable account of the event by an eyewitness is the most important part of the
diagnostic evaluation, but may not be available [2].
This topic discusses the use of EEG in the diagnosis of seizures and epilepsy. The use of
other diagnostic tests in the evaluation of patients with seizures and epilepsy are presented
separately. (See "Video and ambulatory EEG monitoring in the diagnosis of seizures and
epilepsy" and "Evaluation and management of the first seizure in adults" and
"Nonconvulsive status epilepticus: Classification, clinical features, and diagnosis".)
CLINICAL UTILITY
Electroencephalography (EEG) is an important diagnostic test in evaluating a patient with

possible epilepsy. It can provide support for the diagnosis of epilepsy and also assists in
classifying the underlying epileptic syndrome [3].
However, there are several reasons why EEG alone cannot be used to make or refute a
specific diagnosis of epilepsy:
● Most EEG patterns can be caused by a wide variety of different neurologic diseases.
● Many diseases can cause more than one type of EEG pattern.
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● Intermittent EEG changes, including interictal epileptiform discharges (IEDs), can be

infrequent and may not appear during the relatively brief period of routine EEG
recording.
● The EEG can be abnormal in some persons with no other evidence of disease.
● Not all cases of brain disease are associated with an EEG abnormality, particularly if the
pathology is small, chronic, or located deep in the brain.
In order to make the best clinical use of EEG in the evaluation of patients with possible
epilepsy, the clinician must understand the strengths and weaknesses of EEG, specifically as
they relate to the diagnosis of seizures and epilepsy.
ROUTINE EEG TECHNIQUE
During a routine EEG, electrical activity is recorded from standard sites on the scalp
according to the international 10 to 20 system of electrode placement ( figure 1). The EEG
recording depends upon differential amplification: the output is always expressed as the
difference between two inputs, in a tracing that is called a channel. Typically, 21 or more
channels are displayed in a montage, which forms the basis of EEG interpretation. With
modern digital EEG technology, the electroencephalographer has virtually infinite ability to
adjust the montages and other technical parameters in a given recording in order to
optimize interpretation and analysis.
Types of montages — There are two main types of montages:
● Referential montage – In of the referential montage, each channel consists of the

difference between a specific electrode and a reference. There are several types of
references that can be used:
• Common reference: Each electrode is compared with a common electrode, such as

Cz, ipsilateral or contralateral ear, or a noncephalic reference (eg, the rarely used
"balanced neck-chest" reference).
• Common average reference: Each electrode is compared with a weighted average of

the signal from all other head electrodes. Generally, electrode positions most
susceptible to artifact (Fp1, Fp2, O1, O2) are excluded from the average.
• Laplacian and weighted average references: Each electrode is compared with a

reference, which may consist of an average of the closest electrodes (Laplacian) or
an average in which different electrodes are given different weights (weighted
average). These montages are nonintuitive and require more extensive knowledge
of EEG technology, and so they are not in common usage.
● Bipolar montage – In the bipolar montage, each channel consists of a comparison of

two adjacent electrodes. There are several types of bipolar montages, including:
• Anterior-posterior longitudinal bipolar: The electrode pairs are arranged in an

anterior-posterior pattern in temporal and parasagittal chains, as well as a midline
chain. This is the most versatile montage and is the most commonly used montage
for interpretation of routine EEG recordings.
• Transverse bipolar: Electrode pairs are arranged in a left-right pattern, starting in

the front of the head and moving posteriorly. This is also called a "coronal"
montage.
• Others, such as hatband, mandibular notch montage, and institution-specific

bipolar montages: These montages are in much less frequent use, but may be
chosen in order to display particular patterns.
A discussion of the strengths and weaknesses of particular montages is beyond the scope of
this topic. In general, it is important to recognize that no montage is perfect at detecting all
types of abnormalities, and every montage is susceptible to artifact. For this reason,
electroencephalographers must be cautious to change montages during interpretation.
Amplitude and frequency — The electrical activity in each EEG channel can be described in
terms of amplitude and frequency. The amplitude of typical EEG recordings ranges from 5 to
200 microvolts, but most awake background EEG recordings are in the range of 20 to 50
microvolts. Frequency of EEG activity is expressed according to the following terminology:
● Delta – 0 to 4 Hz
● Theta – 4 to 8 Hz
● Alpha – 8 to 13 Hz
● Beta – 13 to 30 Hz
● Gamma – Greater than 30 Hz
NORMAL EEG FINDINGS
In the normal awake adult with eyes closed, there is an 8.5 to 12 Hz alpha rhythm, maximal
in the posterior part of the head. This is also referred to as the posterior-dominant rhythm.
The amplitude of the alpha falls off anteriorly, where there is lower-voltage beta activity. The
alpha rhythm becomes lower voltage (attenuates) or disappears altogether when the eyes
open, and becomes higher voltage (augments) when the eyes close.
In some patients (eg, children, patients with mild cerebral dysfunction), the frequency of the
"alpha" rhythm may be in the theta range, which introduces semantic confusion. Some
electroencephalographers therefore prefer to use the term "posterior-dominant rhythm"
instead.
With drowsiness (ie, stage N1 sleep), the alpha rhythm gradually disappears, fronto-central
beta activity may become more prominent, and diffuse theta activity emerges. The stages
and architecture of normal sleep are discussed in more detail elsewhere. (See "Stages and
architecture of normal sleep", section on 'Sleep staging'.)
EEG FINDINGS IN PATIENTS WITH EPILEPSY
Different EEG findings are variably associated with epilepsy. In the setting of potential
epilepsy, it is useful to classify EEG abnormalities as epileptiform and nonepileptiform.
● Examples of epileptiform activity include interictal epileptiform discharges (IEDs),

lateralized periodic discharges (LPDs; previously known as periodic lateralized
epileptiform discharges [PLEDs]) ( waveform 1), and generalized periodic discharges
(GPDs) ( waveform 2).
● Nonepileptiform abnormalities include slowing, which may be diffuse, regional, or

localized; amplitude changes or asymmetries; and other deviations from normal
patterns. (See 'Slowing' below.)
Only epileptiform discharges are associated with epilepsy at rates sufficient to be clinically
useful, and only when benign variants have been excluded. Nonspecific (nonepileptiform)
EEG abnormalities are relatively common, especially in older individuals, patients with
migraine, and those on centrally acting medications. These should not be interpreted as
supporting a diagnosis of epilepsy.
Interictal epileptiform discharges — To qualify as an IED, discharges should meet the

following criteria [4]:
● They must be paroxysmal and distinct from the patient's normal background activity.
● They must include an abrupt change in polarity occurring over several milliseconds
(ms).
● The duration of each transient should be less than 200 ms. A spike has a duration of
less than 70 ms; sharp waves have a duration between 70 and 200 ms.
● The discharge must have a physiologic field, with the discharge recorded from more
than one electrode, and a voltage gradient should be present.
● They must not be one of the known benign variants or normal discharges such as
wicket spikes, small sharp spikes (SSS), or vertex waves ( table 1 and
waveform 3A-G).
Most IEDs are of negative polarity at the scalp, and are followed by a slow wave (ie, a spike-
wave complex). While these two features are not required criteria, they are helpful in
distinguishing IEDs from other types of paroxysmal activity, including electrode or other
artifacts. They also relate closely to the underlying physiologic phenomena occurring at the
cellular level [5].
Sensitivity — An IED is found in 20 to 55 percent of persons with epilepsy on a first

"routine" EEG [6-10]. A number of factors can influence the sensitivity of a finding of IED for
the diagnosis of epilepsy.
● The number of EEG studies – With repeated recordings, the likelihood of finding IEDs
increases from 20 to 50 percent to as high as 80 to 90 percent when four or more EEGs
are obtained [7,8,10-13].
● EEG duration – A routine EEG is 30 to 45 minutes in length. Longer EEG monitoring

increases the yield of the study [14-18]. (See "Video and ambulatory EEG monitoring in
the diagnosis of seizures and epilepsy".)
● Seizure frequency – More frequent seizures are associated with a higher frequency of
IEDs on an EEG tracing [8,19]. In this regard, a finding of IEDs may also be predictive of
seizure recurrence. In a meta-analysis of 11 studies of EEG after a first unprovoked
seizure in adults, the probability of seizure recurrence in patients with epileptiform EEG
abnormalities was 50 percent compared with 27 percent in those with normal EEGs
[20,21]. Patients with an estimated risk of recurrent seizure of ≥60 percent after a single
unprovoked seizure are considered to have epilepsy [21]. (See "Evaluation and
management of the first seizure in adults".)
● Timing of EEG in relation to recent seizure – Clinical seizures are temporally

associated with more frequent IEDs [7,8,22]. In a study of more than 600 outpatients
with epilepsy or first seizure, the chance of finding epileptiform discharges on EEG
decreased as time elapsed since the last seizure: 62 percent if ≤24 hours, 51 percent if
25 to 48 hours, 40 percent if 49 to 72 hours, and 31 percent if >72 hours [23]. In
another case series, early performance of an EEG (within 24 hours of a seizure)
appeared to have a similar yield of epileptiform abnormalities as did a later-performed
sleep-deprived study [24]. (See 'Sleep and sleep deprivation' below.)
● Antiseizure medication therapy – There is limited information regarding the

suppressant effect of antiseizure medications on IED detection [4,25-28]. Treatment
with valproate, levetiracetam, and probably ethosuximide reduces the rate of

generalized IEDs. Diazepam and phenobarbital can suppress IEDs acutely, but chronic
therapy may have little impact. Another study found that antiseizure medication
withdrawal was associated with fewer spikes on EEG [29].
● Epilepsy syndrome – The EEG is more likely to be abnormal in certain epilepsy

syndromes. As examples, IEDs are almost invariably present in children with untreated
infantile spasms, Landau-Kleffner syndrome, and benign rolandic epilepsy. While
medial temporal lobe epilepsy is usually associated with an abnormal interictal EEG,
patients with frontal lobe epilepsy may have a normal interictal EEG [4,30]. However,
the presence of IEDs often influences both the diagnosis of epilepsy itself, as well as
the specific epilepsy syndrome; as a result, this may be a source of substantial bias.
● Specialized techniques – The use of activation procedures (hyperventilation, photic

stimulation, sleep deprivation, induced sleep, and medication withdrawal) and special
electrode placement can increase the yield of IEDs on an interictal EEG. Their use is
recommended on most follow-up EEGs in order to improve the sensitivity of the test.
(See 'Specialized techniques' below.)
● Age – Factors that are variably reported to be associated with the prevalence of IEDs in
persons with epilepsy include a younger age at the time of EEG, a longer duration of
epilepsy, and an earlier age at epilepsy onset [8,19].
Specificity — IEDs are rare in patients without a history of seizures. Studies in healthy flight
personnel reveal IEDs in 0.5 percent [31,32]. The prevalence of IEDs has been recorded to be
somewhat higher in healthy children (3.5 to 6.5 percent) and in hospitalized adults with
neurologic or psychiatric illness (2.0 to 2.6 percent) [33-36].
A finding of IEDs is most helpful if the clinical history strongly suggests epileptic seizure
[2,3,23]. However, certain caveats apply:
● The pattern of IEDs, along with the patient's age, impacts the specificity of these
findings. Spikes and sharp waves are common in normal neonates during quiet (non-
REM) sleep but disappear over the first six to eight weeks of life. By contrast, focal or
multifocal IEDs in adults are almost always associated with epilepsy [8,37-40]. In
children, IEDs are less specific for epilepsy. In particular, central-midtemporal
discharges, generalized spike-wave discharges, and photoparoxysmal responses may
be asymptomatic manifestations of genetic traits [31,32,34,41]. In one series of EEG
studies, only 40 percent of children with central-midtemporal spikes had epileptic
seizures [40,42].
The table ( table 2) lists IEDs that may be seen on EEG, their associated clinical
significance, and their likelihood of association with epilepsy [4].
● Some conditions are associated with the presence of IEDs on EEG, but do not imply
epilepsy. These include occipital spikes seen in blind people (especially those who are
congenitally blind) [43].
● Withdrawal from short-acting barbiturates and benzodiazepines, certain metabolic

derangements (eg, hypocalcemia, uremia, dialysis disequilibrium), as well as high drug
levels of lithium, neuroleptics (especially clozapine), bupropion, and tricyclic
antidepressants have been associated with IEDs even in the absence of accompanying
seizures [27,44,45]. These conditions are also associated with a lower seizure threshold.
● Inexperienced interpreters of EEG, unaware of benign variants and normal fluctuations

that are commonly seen on EEG, can misread EEGs and limit the specificity of the
findings. (See 'Pitfalls in interpretation' below.)
Lateralized periodic discharges — Lateralized periodic discharges (LPDs; previously known

as PLEDs) are defined by lateralized, persistent spikes, sharp waves, or sharply contoured
slow waves that occur with an almost regular repetition rate, typically 0.5 to 2 Hz
( waveform 1) [46].
These are most often seen in the setting of acute, relatively large, destructive lesions, such
as cerebral infarction or hemorrhage, encephalitis, abscess, or rapidly growing cerebral
malignancy [47-52]. In children, LPDs are also associated with chronic diffuse
encephalopathies [53].
LPDs are highly associated with seizures, especially nonconvulsive seizures in critically ill
patients [54]. Clinical seizures have also been reported in the majority of patients with LPDs
(50 to 100 percent, depending on the population) [49,52,55-57]. Focal motor seizures are the
most common seizure type associated with LPDs [55,56].
LPDs usually resolve over several days to weeks with recovery from the acute illness, but
their presence increases the risk of developing remote symptomatic epilepsy [55,56,58,59].
In a study of 118 patients with LPDs and at least three months of follow-up, 47 percent had
late seizures (after hospital discharge) [58]. Excluding those with prior epilepsy, 48 percent of
those with LPDs and seizures on continuous EEG monitoring developed late seizures
(qualifying as new-onset epilepsy), as did 17 percent of those with LPDs and no
electrographic seizures, and 38 percent of those with electrographic seizures but no LPDs.
Bilateral independent periodic discharges — Bilateral independent periodic discharges

(BIPDs; previously known as BIPLEDs) are most often observed in association with acute
central nervous system (CNS) infections (especially herpes simplex encephalitis), anoxic
encephalopathy, and severe chronic epilepsy [49,60]. This pattern is also highly associated
with seizures. Compared with LPDs, BIPDs are associated with more severe cerebral injury,
worse neurologic status, and higher mortality, probably related to the severity of the
underlying illness.
Generalized periodic discharges — GPDs ( waveform 2) are less common than LPDs, but
are still often observed in critically ill patients [61,62]. They are associated with seizures,
especially when seen in combination with superimposed rhythmic delta or fast activity
(GPDs-plus) [54]. (See "Nonconvulsive status epilepticus: Classification, clinical features, and
diagnosis", section on 'Uncertain EEG patterns in critical illness'.)
Slowing — Focal slow-wave activity and generalized slowing of background rhythms are

common postictal and interictal findings in patients with partial seizures and symptomatic
epilepsies. However, they are also frequently seen in other neurologic disorders, especially
focal structural lesions, regardless of whether there are associated seizures [63-65]. As an
example, two-thirds of patients with continuous, focal, polymorphic delta activity have a
structural lesion, but seizures occur in only approximately 20 percent [63]. In patients with
no clinical history of neurologic injury and a normal neuroimaging study, focal slowing is
more likely to suggest epilepsy.
Bilateral, synchronous, and symmetric slow activity in the delta frequency range (<4 Hz), or
generalized rhythmic delta activity (GRDA), does not usually imply epilepsy. In adults, this
pattern is most commonly intermittent and usually has an anterior predominance and is
known as frontal intermittent rhythmic delta activity (FIRDA, or frontally predominant GRDA).
Once thought to be associated primarily with deep midline cerebral lesions and raised
intracranial pressure, FIRDA is now recognized to be a nonspecific marker of encephalopathy
regardless of etiology, as well as neurodegenerative disease and generalized epilepsy. It can
occasionally be seen in normal individuals as well [66]. A large, multicenter study of 1513
critically ill patients with periodic or rhythmic activity found that GRDA was not associated
with an increased risk of seizures, even at higher frequencies (>2 Hz) [54].
Occipital intermittent rhythmic delta activity (OIRDA) is more common in young children and
is rarely seen in patients older than 15 years [67]. It is a frequent interictal finding in
generalized epilepsy syndromes, occurring in 15 to 38 percent of all patients with childhood
absence epilepsy, and implies a good prognosis [67-70].
Temporal intermittent rhythmic delta activity (TIRDA) ( waveform 4) is a particular form of

focal slowing (and a subtype of lateralized rhythmic delta activity [LRDA]; see next
paragraph) that is specific for temporal lobe localization in patients with refractory epilepsy.
TIRDA is observed in as many as 25 to 40 percent of patients being evaluated for temporal
lobe resection [71,72]. TIRDA is often associated with temporal IEDs and has a high positive
predictive value for temporal lobe localization in patients with refractory epilepsy. (See "Focal
epilepsy: Causes and clinical features", section on 'Mesial temporal lobe epilepsy'.)
LRDA ( waveform 5) is a form of focal rhythmic slowing. The two most common causes of
LRDA are acute brain injury and chronic seizure disorder. In one study, approximately 5
percent of critically ill patients had LRDA [73]. In this study, two-thirds of patients with LRDA
had either clinical or electrographic seizures during their acute illness, an identical frequency
to patients with LPDs in the same study. This suggests that the clinical significance of LRDA is
similar to that of LPDs, and much different than focal nonrhythmic slowing, in which much
lower rates of seizures are observed. LRDA and LPDs commonly coexist, and patients with
both patterns are at increased risk of acute seizures [54,73]. (See 'Lateralized periodic
discharges' above.)
Epilepsy syndrome diagnosis — The classification of seizures and epilepsy can be

important for prognosis and treatment. In adult patients, the most important distinction is
between primary-generalized and partial epilepsy.
The clinical history can be unhelpful or misleading in this regard. As examples, a patient with
staring spells may have absence or complex partial seizures, and a patient with generalized
convulsions may have primary or secondarily generalized epilepsy. Although the presence of
an aura strongly suggests partial-onset seizures, one study reported that symptoms
interpreted by the patient as a seizure aura (often brief, nonspecific dizziness) occurred in up
to 70 percent of those with primary generalized epilepsy [74].
Specific interictal EEG findings that are associated with specific epilepsy syndromes are listed
in the table ( table 3). Clinical correlation between the clinical seizure type and EEG
findings is also important. When these agree, this is generally sufficient to distinguish
generalized from partial epilepsies [75]. In addition, when focal IEDs are strongly lateralized
(more than 90 to 95 percent), they predict the side of seizure onset [38]. However, focal IEDs
can manifest as secondary bilateral synchronous discharges, while generalized epilepsy can
have fragmentary expression and appear more focal [76,77]. As a result, it is important to
consider the clinical as well as the EEG manifestations.
SPECIALIZED TECHNIQUES
Specific methods can be employed to improve the detection of interictal epileptiform

discharges (IEDs) and the sensitivity of the test.
Routine activating techniques — A standard routine EEG usually includes hyperventilation

and photic stimulation.
Hyperventilation — Hyperventilation increases the rate of generalized discharges in

childhood absence epilepsy and other generalized epilepsies [77]. It is less productive in
partial epilepsies, increasing the yield of focal IEDs by less than 10 percent [4,78]. Two
studies have suggested that the yield of hyperventilation in generalized epilepsy may also be
low, approximately 12 percent [79,80]. However, this activation procedure is very effort
dependent, and yield may vary as a result. One study in 80 patients undergoing long-term
EEG monitoring found that hyperventilation had an activating effect on EEG recording, but
only in those patients whose antiseizure medications were being tapered [81].
Photic stimulation — Photic stimulation induces IEDs in some individuals with idiopathic

generalized epilepsy, and infrequently in patients with focal seizures arising from the
occipital lobe [4,77]. A trait of photoparoxysmal response can also run in families, and in this
setting in particular, is a less specific finding for epilepsy than spontaneous IEDs. A
photoparoxysmal response that is both generalized and sustained (outlasting the period of
photic stimulation) and occurs at a different frequency than the photic stimulation is more
likely to be associated with epilepsy than when these features are absent [78].
In order to maximize the yield of photic stimulation, each laboratory should have a protocol
that includes testing at a number of frequencies between 1 and 60 Hz, and patients should
be tested with eyes both opened and closed at each frequency, if possible. The technologist
should document the patient's clinical response to photic stimulation at each frequency. The
procedures for photic stimulation vary widely, although there have been attempts to
establish standardized methodology [82].
Sleep and sleep deprivation — Sleep is a neurophysiologic activator of epilepsy; 20 to 40

percent of epilepsy patients with an initial normal recording will have IEDs on a subsequent
recording that includes sleep [83-85]. Sleep is sometimes captured on a routine EEG, but
sleep deprivation increases this likelihood. Sleep is also usually captured on prolonged EEG
monitoring and, alternatively, can be induced by administration of a sedative, usually chloral
hydrate.
In a cohort of 92 children aged 2 to 16 years with new-onset seizures, the yield of delayed
sleep-deprived EEG was similar to that of an early EEG, done within 2 to 24 hours of the
seizure (61 percent had epileptiform abnormalities on sleep-deprived EEG, compared with 57
percent on early EEG) [24].
Sleep deprivation appears to increase IEDs to an extent not fully explained by the greater
chance of recording sleep [6,39]. One study found that the additional yield of a sleep-
deprived EEG was similar whether or not sleep was recorded [84]. Another study found that
a sleep-deprived EEG had significantly higher yield compared with drug-induced sleep [86].
In this study, the sleep-deprived patients were also more likely to have a seizure during the
EEG compared with the sedated patients. The time it takes to perform an EEG with chloral
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hydrate sedation is significantly longer, and in one study was not associated with a higher
yield of IED detection [87]. Melatonin may be superior to chloral hydrate at increasing the
rate of detection of IEDs in routine EEGs in children [88].
When sleep-deprived EEG was compared with 24-hour ambulatory EEG monitoring in 46
patients with "presumed epilepsy," IED detection was similar (24 versus 33 percent) [40].
However, clinical seizures were also captured in 15 percent of the ambulatory EEGs and in
none of the sleep-deprived EEG. (See "Video and ambulatory EEG monitoring in the
diagnosis of seizures and epilepsy".)
It is generally agreed that a follow-up EEG in a patient with possible epilepsy and a normal
routine EEG should include sleep. Clinicians can order full or partial sleep deprivation, but it
is not clear how much this affects the yield [6]. The choice of test (sleep-deprived, sleep with
oral sedation, or prolonged EEG monitoring) should be individualized to the patient's
circumstances. Because sleep deprivation can be quite disruptive and carries some risk of
seizure exacerbation, we generally prefer 24-hour ambulatory EEG studies rather than sleep-
deprived studies. (See "Video and ambulatory EEG monitoring in the diagnosis of seizures
and epilepsy".)
Special electrode placement — Some highly epileptogenic areas, such as the mesial

temporal lobes, are not well explored by the standard scalp electrodes. Scalp coverage with
the standard 10-20 system detects only approximately 65 percent of epileptiform discharges
from the temporal lobes [89]. The classic temporal chain electrodes (F7/F8 and T7/T8) lie
close to the sylvian fissure and can record activity from both infra- and suprasylvian regions
( image 1).
Specialized electrode placement can improve detection of IEDs ( image 1). However, these
electrodes can be uncomfortable for patients and are associated with increased artifact,
which increases the potential for misinterpretation. (See 'Pitfalls in interpretation' below.)
● Sphenoidal electrodes are wires inserted through a needle cannula inferior to the
zygomatic arch, perpendicular to the sagittal plane, and parallel to the coronal plane, in
an attempt to record activity from the anterior tip of the temporal lobe ( image 1).
● Nasopharyngeal electrodes (Np1 and Np2) are inserted through the nostrils into the
nasopharynx to record from the anterior mesial surface of the temporal lobe
( image 1).
● Ear electrodes (A1 and A2) are inserted into the ear canal to lie next to the tympanic
membrane ( image 1).
● Superficial anterior temporal or Silverman's electrodes (T1 and T2) are placed 1 cm
above and one-third the distance along the line from the external auditory meatus to
the external canthus of the eye, to record from the anterior-basal areas of the temporal
lobe.
● Mandibular notch electrodes (Mn1 and Mn2) are placed 2.5 cm anterior to the external
auditory meatus, inferior to the zygomatic arch, at the insertion site for sphenoidal
electrodes ( image 1).
● Inferior temporal chain electrodes (F9/T9/P9 and F10/T10/P10) are an extra chain of
three electrodes placed a standard electrode distance inferior to the standard temporal
chain and recorded from the temporal lobes ( image 1).
Of these, sphenoidal electrodes have the highest yield and are associated with considerably
less artifact then nasopharyngeal electrodes [90]. In one study, sphenoidal electrodes
detected 99 percent of discharges, compared with a 57 percent yield for nasopharyngeal
electrodes and 54 percent yield for ear electrodes. However, these electrodes are invasive
and uncomfortable for patients and are not used routinely for diagnostic purposes.
The superficial anterior temporal and mandibular notch electrodes are slightly less sensitive
than sphenoidal electrodes, but are noninvasive and are equivalent or superior in sensitivity
and patient comfort to the nasopharyngeal, mandibular notch subdermal (also known as
minisphenoidal), and ear electrodes [91-94].
Limited electrode montages — Full-montage EEG is considered the gold standard for the
identification of suspected subclinical electrographic seizures, but cost, time, and availability
of trained technologists are limits to widespread utilization. In one report of urgent EEGs in
an inpatient setting, a reduced-montage EEG, using a device that could be applied without
the need for a technologist, had a high sensitivity for detecting seizures, with rates of
detection very close to full-montage EEG [95]. Overall, for the task of identifying whether or
not a patient was having seizures, the concordance between reduced-montage and full-
montage EEG was 95 percent. In addition, limited montage EEG had a 96 percent positive
predictive value for identifying clinically important abnormalities such as seizures,
epileptiform discharges, or periodic discharges.
While a full-montage EEG is always preferred, reduced electrode array could be considered
when resources are limited or if there is going to be a delay in obtaining the full-montage
EEG. The full-montage EEG should be used whenever it becomes available. (See
"Nonconvulsive status epilepticus: Classification, clinical features, and diagnosis", section on
'EEG electrode array and placement'.)
Quantitative and automated analysis of EEG — Several available quantitative measures

can be used as adjunctive methods for identifying seizures and other epileptiform
abnormalities on EEG. These include seizure detection algorithms, automated detectors of
epileptiform discharges, and quantitative parameters that aid in the visual detection of
patterns or trends suggestive of seizures in long-term EEG recording.
While these methods, in their current form, should not replace interpretation of standard
EEG patterns by a qualified reader, they do have several roles. Automated seizure and
epileptiform discharge detectors can serve as a screening method, especially in longer
recordings, pointing the EEG reader to areas that deserve particular scrutiny and helping to
ensure that subtle abnormalities are not missed [96]. These methods can also aid in the
quantification of spikes or seizures during longer recording periods, providing a perspective
on longer-term trends. With further improvement and use of machine learning techniques,
automated analysis is likely to be of more clinical utility in the near future.
PITFALLS IN INTERPRETATION
Misinterpretation of EEG findings or over-reliance on the EEG frequently contribute to

misdiagnosis [12,22,83,84,97].
● Normal EEG – It is important to remember that a normal EEG never rules out epilepsy
[3,98]. Even with repeated EEGs, use of specialized techniques, or prolonged
monitoring, a significant number of patients with epilepsy (10 to 20 percent) will have
not have interictal epileptiform discharges (IEDs) [85,98]. Even ictal recordings may not
have an identifiable scalp correlate in many frontal lobe seizures, as well as in simple
partial seizures from any location [30].
● Abnormal EEG – It is also important to note that "abnormal" EEG does not define
epilepsy; most abnormal findings are nonspecific. IEDs are the most specific finding for
epilepsy, but these can occur in approximately 0.5 percent of healthy adults and in 1.9
to 6.5 percent of normal children [36,85].
● Variation in EEG interpretation – There is also wide variation in how EEGs are
interpreted. When EEGs are read by clinicians without special training, a number of
benign or normal patterns are often misinterpreted as epileptiform [83,84,97,99].
These include ( table 1) [84,100,101]:
• Benign epileptiform transients of sleep (BETS), also termed small sharp spikes (SSS)
( waveform 3A)
• Wicket spikes ( waveform 3B)
• Rhythmic midtemporal theta of drowsiness (psychomotor variant) ( waveform 3C)
• 6 Hz "phantom" spike-and-wave complex ( waveform 3D)
• Subclinical rhythmic EEG discharge in adults (SREDA) ( waveform 3E)
• Positive occipital sharp transients of sleep (POSTS) ( waveform 3F)
• Breach rhythm ( waveform 3G)

• 14 Hz and 6 Hz positive spikes ( waveform 6)
• Hyperventilation-induced high-voltage paroxysmal slow waves
• Artifacts (such as over-filtered muscle potentials)
• Repetitive vertex waves, especially in children
Repeating the EEG or having it reinterpreted at a tertiary epilepsy center by a board-

certified electroencephalographer can be helpful. One meta-analysis found that a more
restrictive interpretation style that limits false-positive results improves diagnostic
accuracy [102]. However, even among experienced, board-certified neurophysiologists,
interobserver agreement is only moderate [2,9,103].
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Seizures and epilepsy
in adults" and "Society guideline links: Seizures and epilepsy in children".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
● Basics topics (see "Patient education: EEG (The Basics)" and "Patient education: Epilepsy
in adults (The Basics)" and "Patient education: Epilepsy in children (The Basics)")
SUMMARY AND RECOMMENDATIONS
● Clinical utility – Electroencephalography (EEG) is an important diagnostic test in

evaluating a patient with possible epilepsy, providing evidence that helps confirm or
refute the diagnosis. EEG also assists in classifying the underlying epileptic syndrome
and thereby guides management. (See 'Clinical utility' above.)
● Routine EEG – During a routine EEG, electrical activity is recorded from many different
standard sites on the scalp according to the international (10 to 20) electrode
placement system ( figure 1). In the normal awake adult with eyes closed, there is a
prominent 8.5 to 12 Hz alpha rhythm observed in the posterior part of the head. This
rhythm gradually disappears with drowsiness. The amplitude of the alpha falls off
anteriorly, where there is lower-voltage beta activity. (See 'Routine EEG technique'
above and 'Normal EEG findings' above.)
● EEG findings in patients with epilepsy – A single routine EEG has low sensitivity for
detection of interictal epileptiform discharges (IEDs) (20 to 50 percent) for patients with
epilepsy. The sensitivity can be increased by repeating the study, recording for a longer
period of time (such as overnight), including a recording of sleep (spontaneous, after
sleep deprivation, or via administration of a sedative), performing the EEG within 24
hours of a seizure, and using special electrodes for temporal lobe epilepsy. (See
'Sensitivity' above and 'Specialized techniques' above.)
A normal EEG, however, can never rule out epilepsy; 10 to 20 percent of patients with
definite epilepsy never have IEDs.
● Interictal epileptiform discharges – Overall, the specificity of IEDs for epilepsy is high,
more than 90 percent in adults. However, inexperienced EEG interpreters can mistake
artifact or benign EEG patterns for IEDs, lowering the specificity of the study. The
specificity of this finding is also influenced by the pattern of IEDs, and by the patient's
age, family history, and comorbid conditions. (See 'Specificity' above and 'Pitfalls in
interpretation' above.)
● Lateralized periodic discharges – Lateralized periodic discharges (LPDs; previously

known as periodic lateralized epileptiform discharges [PLEDs]) are usually seen in the
setting of acute, relatively large cerebral injury, such as stroke, encephalitis, or rapidly
growing cerebral malignancies. Patients with LPDs have an increased risk of acute
symptomatic seizures as well as new-onset remote symptomatic epilepsy after
recovery. (See 'Lateralized periodic discharges' above.)
● Slowing – Generalized or focal slowing on EEG is nonspecific and does not suggest
epilepsy. One exception is lateralized rhythmic delta (LRDA), which is associated with
seizures, including the specific subtype of temporal intermittent rhythmic delta activity
(TIRDA), which is highly associated with temporal lobe epilepsy. (See 'Slowing' above.)
Use of UpToDate is subject to the Terms of Use.

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Topic 2233 Version 29.0
GRAPHICS
International electrode placement system
The location of electrodes for recording electroencephalograms from the scalp,

nasopharyngeal, and external ear sites are shown. The leads placed on the
zygomatic arch beneath the eye allow for monitoring of eye movements.
Adapted from: Jasper HH. Report of the committee on methods of clinical examination in
electroencephalography: 1957. Electroencephalogr Clin Neurophysiol 1958; 10:370.
Graphic 78990 Version 2.0
Right hemisphere lateralized periodic discharges (LPDs)
Reproduced with permission from: Chong DJ, Hirsch, LJ. Which EEG patterns warrant treatment in the
critically ill? Reviewing the evidence for treatment of periodic epileptiform discharges and related
patterns. J Clin Neurophysiol 2005; 22:79. Copyright © 2005 Lippincott Williams & Wilkins.
Generalized periodic discharges (GPDs)
Reproduced with permission from: Chong DJ, Hirsch LJ. Which EEG patterns warrant treatment in the
critically ill? Reviewing the evidence for treatment of periodic epileptiform discharges and related
patterns. J Clin Neurophysiol 2005; 22:79. Copyright © 2005 Lippincott Williams & Wilkins.
Benign EEG variants
Waveform:
Patient: age /
morphology / Duration Distribution
state
frequency
Benign spike-like patterns
Small sharp Adults / drowsiness Monophasic or Phase <50 Bi-hemispheric

spikes and light sleep diphasic spikes msecs maximal-
anterior / mid
temporal
Wicket Adults / drowsiness Sharply contoured Few Bilateral

spikes and light sleep arch shaped / 6 to 11 seconds anterior / mid
Hz temporal
14- and 6-Hz Children and Arch shaped positive Less than 1 Bilateral
positive adolescents / sharp component / 4- to 2 posterior
bursts drowsiness and light 7 Hz and 13-17 Hz seconds temporal /
sleep range parietal
6 Hz spike Adolescents and Low voltage spike- 1 to 2 Generalized /

and wave young adults / relaxed high amplitude slow seconds at times
wakefulness and wave / 5 to 7 Hz maximal
drowsiness anterior or
posterior
Rhythmic patterns with an epileptiform morphology
Rhythmic Adolescents and Notched flat topped / Seconds Bilateral

temporal young adults / relaxed 5 to 7 Hz temporal
theta bursts wakefulness and
of drowsiness
drowsiness
Subclinical Adults >50 / Rhythmic sharply 40 to 80 Bilateral

rhythmic hyperventilation, contoured / 5 to 6 Hz seconds parietal /
EEG drowsiness posterior
discharge in temporal
adults
Midline Children and adults / Sinusoidal, arciform / 4 to 20 Midline,

theta awake, drowsy 5 to 7 Hz seconds maximal
rhythm centrally
Reproduced with permission from: Mushtaq, R, Van Cott, AC, Benign EEG variants. Am J Electroneurodiagnostic Technol
2005; 45:88. Copyright ©2005 American Society of Electroneurodiagnostic Technologists.
Small sharp spikes also known as benign epileptiform

transients of sleep (BETS)
Small sharp spikes (also known as benign epileptiform transients of sleep, or

BETS; see boxed area). This is a normal variant.
Courtesy of Drs. Lawrence Hirsch and Hiba Arif.
Wicket spikes
These may appear in clusters or singly in the temporal regions.
Rhythmical midtemporal theta of drowsiness
Rhythmical midtemporal theta of drowsiness (RMTD; see arrows); also known as

psychomotor variant. This is a normal variant.
Six-Hz spike-and-wave bursts
Six-Hz spike-and-wave bursts ("Phantom spike and wave"; see arrows):

three 1 second bursts from one routine EEG recording. (A) This pattern is
accentuated in an average referential montage, sensitivity 5 uV/mm. Note
the low amplitude, occipitally predominant "phantom" spikes (arrows), and
the frequency of approximately 6 per second (B) in a longitudinal bipolar
montage (7 uv/mm), this pattern is not as well-appreciated. This is a normal
variant.
Subclinical rhythmic EEG discharge of adults (SREDA)
Subclinical rhythmic EEG discharge of adults (SREDA) in a 52 year old

woman with headaches, preceded by a widespread, moderate-to-high
amplitude, biphasic waveform. This is a rare but normal variant.
Reproduced with permission from: BF, Westmoreland, Klass, DW. A distinctive rhythmic EEG
discharge of adults. Electroencephalogr Clin Neurophysiol 1981; 51:186. Copyright ©1981
Elsevier.
Positive occipital sharp transients of sleep (POSTS)
A) POSTS (Positive occipital sharp transients of sleep), in runs, in a bipolar

montage (red arrows). B) A referential recording confirms the positivity in the
occipital regions (downgoing waves; green arrows). These are normal discharges.
Breach rhythm
Breach rhythm noted at the C3 electrode in a 61-year-old man with

history of head trauma and a left frontoemporal craniotomy.
Reproduced with permission from: Mushtaq, R, Van Cott, AC, Benign EEG variants. Am J
Electroneurodiagnostic Technol 2005; 45:88. Copyright ©2005 American Society of
Electroneurodiagnostic Technologists.
Spike location and probability of epilepsy
Probability: Most often associated with:
High probability of epilepsy (>85%):
Anterior-mid temporal spikes* Mesial temporal lobe epilepsy
Midline spikes¶ Tonic-clonic seizures
Hypsarhythmia Infantile spasms (West syndrome)
Slow spike-wave Lennox-Gastaut syndrome
Generalized paroxysmal fast activity Lennox-Gastaut syndrome
Moderate probability of epilepsy (<75%):
Frontal spikesΔ Frontal lobe epilepsy
Generalized spike-wave (≥3 Hz) Absence epilepsy (3 Hz; CAE, JAE), juvenile
myoclonic epilepsy (>3 Hz), and other primary
generalized epilepsies
Centro-temporal spikes◊ Benign rolandic epilepsy of childhoood (BREC)
Occipital spikes§ Benign focal epilepsy of childhood (Gastaut and

Panayiotopolous syndromes: the 2 variants of
CEOP)
Photoparoxysmal response Primary generalized epilepsy
CAE: childhood absence epilepsy; JAE: juvenile absence epilepsy; BECTS: benign focal epilepsy of
childhood with centrotemporal spikes; BREC: benign rolandic epilepsy of childhood; CEOP:
childhood epilepsy with occipital paroxysms.
* >90% probability of seizures/epilepsy (adults)[1] .
¶ 76-91% probability of seizures/epilepsy (children)[2] .
Δ ~75% probability of seizures/epilepsy (children)[3] .
◊ ~40% probability of seizures/epilepsy (children)[3] .
§ 50% probability of seizures/epilepsy (children)[3] .
References:
1. Pedley TA, Mendiratta A, Walczak TS. Seizures and Epilepsy. In: Current Practice of Clinical
Electroencephalography, Ebersole JS, Pedley TA (Eds), Lippincott Williams & Wilkins, Philadelphia 2003 p.506.
2. Ehle A, Co S, Jones MG. Clinical correlates of midline spikes. An analysis of 21 patients. Arch Neurol 1981; 38:355.
3. Kellaway P. The incidence, significance and natural history of spike foci in children. In: Current clinical
neurophysiology: update on EEG and evoked potentials, Henry C (Ed), Elsevier, Amsterdam 1981 p.151.
Table modified and expanded from: Pillai J, Sperling MR. Interictal EEG and the diagnosis of epilepsy. Epilepsia 2006; 47
Suppl 1:14.
Temporal intermittent rhythmic delta activity
Temporal intermittent rhythmic delta activity (TIRDA; see boxes) in the left temporal region in a patient w
sclerosis on MRI.
Lateralized rhythmic delta activity (LRDA)
Lateralized rhythmic delta activity (LRDA; see boxes) in the left hemisphere, most pronounced in the left
Electroencephalographic features of some epilepsy syndromes
Epilepsy
EEG findings Additional EEG features
syndromes
Generalized
Absence 3-Hz generalized spike-and-slow Normal background; activation of

epilepsy wave; often repetitive trains of IEDs and seizures with
discharges hyperventilation
Atypical 1.5 to 2.5-Hz generalized spike-and- IEDs may be asymmetric, with

absence slow wave discharges shifting focal features
epilepsy
Juvenile 4 to 6-Hz generalized spike and Normal background; activation of

myoclonic multiple spike-and-slow wave IEDs with photic stimulation is
epilepsy common; more typical 2.5 to 3-Hz
spike-and-slow wave may be seen;
IEDs may be asymmetric, with
shifting focal features
Infantile Hypsarrhythmia and multifocal No clearly normal background

spasms spikes and sharp waves activity since the EEG is dominated by
the hypsarrhythmia pattern
Lennox- <2.5-Hz generalized sharp-and-slow Generalized background slowing and

Gastaut wave discharges paroxysmal fast activity; often
syndrome multifocal spikes and sharp waves
Progressive Generalized and multifocal spikes, Progressive background slowing with

myoclonic multiple spikes, and sharp waves disease progression; photic
epilepsy activation of IEDs in some cases
Partial
Benign Large-amplitude spikes or sharp Normal background; often

rolandic waves, maximal over the prominent activation of IEDs with
epilepsy centrotemporal region sleep; the discharge can be bilateral
or unilateral and often has an
anterior-posterior field of a
tangential dipole
Benign Bilateral or unilateral occipital spike- Occipital IEDs often attenuate with
occipital and-slow wave discharges eye opening; photic stimulation may
epilepsy precipitate seizures
Temporal lobe Temporal lobe spikes, sharp waves, Often intermittent or persistent
epilepsy and temporal intermittent rhythmic temporal slowing; may see
delta activity; often activated with independent IEDs from contralateral
drowsiness and sleep temporal lobe
Frontal lobe IEDs in the frontal region Mesial frontal discharges often are
epilepsy not detected by scalp EEG; secondary
bilateral synchrony can occur
EEG: electroencephalographic; IED: interictal epileptiform discharge.
Reproduced with permission from: Worrell GA, Lagerlund TD, Buchhalter JR. Role and limitations of routine and
ambulatory scalp electroencephalography in diagnosing and managing seizures. Mayo Clin Proc 2002; 77:991.
Copyright © 2002 Dowden Health Media.
Position of special electrodes with respect to the underlying brain
Standard temporal electrodes (F7/F8 and T7/T8) lie over the Sylvian fissure, and record
infra- and suprasylvian regions. Special inferior temporal electrodes (F9/F10 and T9/T10)
record the lateral temporal region. Superficial anterior temporal electrodes (T1/T2;
usually positioned slightly anterior to what is shown here) record the anterior temporal
region, as do mandibular notch electrodes (Mn1/Mn2). The inferior temporal region can
be recorded by ear (A1/A2), sphenoidal (Sp1/Sp2) and nasopharyngeal electrodes
(Np1/Np2).
Courtesy of Lawrence J Hirsch, MD, Hiba Arif, MD, and Jeremy Moeller, MD.
14 and 6-Hertz positive bursts
14- and 6-Hertz positive bursts (arrows). This is a normal variant, generally seen during drowsiness or lig
temporal region. The bursts are usually 14 Hz, although can occur at a rate of 6 to 7 Hz, and have a posit
negative phase.
Contributor Disclosures
Jeremy Moeller, MD No relevant financial relationship(s) with ineligible companies to disclose. Hiba
Arif Haider, MD Grant/Research/Clinical Trial Support: Nichols Foundation [Research support].
Other
Financial Interest: Springer Publishing [Author royalties].
All of the relevant financial relationships listed
have been mitigated. Lawrence J Hirsch, MD Consultant/Advisory Boards: Eisai [Epilepsy]; Neurelis
[Epilepsy]; Ceribell [Epilepsy]; Accure [Epilepsy]; Neuropace [Epilepsy]; Aquestive [Epilepsy]; Medtronic
[Epilepsy]; Marinus [Epilepsy]; UCB [Epilepsy]. Other Financial Interest: Wiley [Atlas of EEG]. All of the
relevant financial relationships listed have been mitigated. Paul Garcia, MD Equity Ownership/Stock
Options: EnlitenAI Inc [Epilepsy].
Consultant/Advisory Boards: Biogen [Epilepsy];EnlitenAI Inc
[Epilepsy];Moon Creative Lab [Epilepsy];Otsuka [Epilepsy].
All of the relevant financial relationships
listed have been mitigated. John F Dashe, MD, PhD No relevant financial relationship(s) with ineligible
companies to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

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24/8/22, 17:02 Electroencephalography (EEG) in the diagnosis of seizures and epilepsy - UpToDate

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Electroencephalography (EEG) in the diagnosis of

Electroencephalography (EEG) is an important diagnostic test in evaluating a patient with

● Intermittent EEG changes, including interictal epileptiform discharges (IEDs), can be

ROUTINE EEG TECHNIQUE

Types of montages — There are two main types of montages:

● Referential montage – In of the referential montage, each channel consists of the

• Common reference: Each electrode is compared with a common electrode, such as

• Common average reference: Each electrode is compared with a weighted average of

• Laplacian and weighted average references: Each electrode is compared with a

● Bipolar montage – In the bipolar montage, each channel consists of a comparison of

• Anterior-posterior longitudinal bipolar: The electrode pairs are arranged in an

• Transverse bipolar: Electrode pairs are arranged in a left-right pattern, starting in

• Others, such as hatband, mandibular notch montage, and institution-specific

NORMAL EEG FINDINGS

EEG FINDINGS IN PATIENTS WITH EPILEPSY

● Examples of epileptiform activity include interictal epileptiform discharges (IEDs),

● Nonepileptiform abnormalities include slowing, which may be diffuse, regional, or

Interictal epileptiform discharges — To qualify as an IED, discharges should meet the

Sensitivity — An IED is found in 20 to 55 percent of persons with epilepsy on a first

● EEG duration – A routine EEG is 30 to 45 minutes in length. Longer EEG monitoring

● Timing of EEG in relation to recent seizure – Clinical seizures are temporally

● Antiseizure medication therapy – There is limited information regarding the

with valproate, levetiracetam, and probably ethosuximide reduces the rate of

● Epilepsy syndrome – The EEG is more likely to be abnormal in certain epilepsy

● Specialized techniques – The use of activation procedures (hyperventilation, photic

● Withdrawal from short-acting barbiturates and benzodiazepines, certain metabolic

● Inexperienced interpreters of EEG, unaware of benign variants and normal fluctuations

Lateralized periodic discharges — Lateralized periodic discharges (LPDs; previously known

Bilateral independent periodic discharges — Bilateral independent periodic discharges

Slowing — Focal slow-wave activity and generalized slowing of background rhythms are

Temporal intermittent rhythmic delta activity (TIRDA) ( waveform 4) is a particular form of

Epilepsy syndrome diagnosis — The classification of seizures and epilepsy can be

Specific methods can be employed to improve the detection of interictal epileptiform

Routine activating techniques — A standard routine EEG usually includes hyperventilation

Hyperventilation — Hyperventilation increases the rate of generalized discharges in

Photic stimulation — Photic stimulation induces IEDs in some individuals with idiopathic

Sleep and sleep deprivation — Sleep is a neurophysiologic activator of epilepsy; 20 to 40

Special electrode placement — Some highly epileptogenic areas, such as the mesial

Quantitative and automated analysis of EEG — Several available quantitative measures

Misinterpretation of EEG findings or over-reliance on the EEG frequently contribute to

• Breach rhythm ( waveform 3G)

Repeating the EEG or having it reinterpreted at a tertiary epilepsy center by a board-

SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

SUMMARY AND RECOMMENDATIONS

● Clinical utility – Electroencephalography (EEG) is an important diagnostic test in

● Lateralized periodic discharges – Lateralized periodic discharges (LPDs; previously

Use of UpToDate is subject to the Terms of Use.

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