Electroencephalography (EEG) in the diagnosis of seizures and epilepsy

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.

●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 are advised to periodically switch montages during interpretation of every recording and to review any potential abnormality with more than one montage.

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 at nearly regular intervals (varying by <50 percent from one cycle to the next in most cycle pairs), for at least six cycles, typically greater than 0.5 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 has also been called frontal intermittent rhythmic delta activity (FIRDA). Once thought to be associated primarily with deep midline cerebral lesions and raised intracranial pressure, frontally predominant GRDA 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 photoparoxysmal response can also be a familial trait [82] 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 [83].

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 [84-86]. 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 [85]. Another study found that a sleep-deprived EEG had significantly higher yield compared with drug-induced sleep [87]. 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 hydrate sedation is significantly longer, and in one study was not associated with a higher yield of IED detection [88]. Melatonin may be superior to chloral hydrate at increasing the rate of detection of IEDs in routine EEGs in children [89].

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 [90]. 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 [91]. 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 [92-95].

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 [96]. 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 [97]. 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 [12,22,84,85,98].

●Normal EEG – It is important to remember that a normal EEG never rules out epilepsy [3,99]. 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) [86,99]. 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 [36,86].

●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 [84,85,98,100]. These include (table 1) [85,101,102]:

•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 [103]. However, even among experienced, board-certified neurophysiologists, interobserver agreement is only moderate [2,9,104].

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 5^th to 6^th 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 10^th to 12^th 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.)