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ORIGINAL ARTICLES

The EEG of Status Epilepticus

Peter W. Kaplan

Summary: Gastaut noted that there are as many forms of statusepilepticus (SE) as there are seizure types. The pleomorphic EEGpatterns reflect this wide variety of clinical types. The differentelectroclinical types of status epilepticus share EEG characteristicsincluding rhythmic activity, epileptiform discharges, and often awaxing and waning evolution. Gray zones of interpretation exist inthe form of runs of epileptiform periodic discharges, typically oflower frequency, and lesser temporal variability. In diagnosing SE,clinical correlation and response to parenteral anti-epileptic drugs(AEDs) are of particular importance. Accurate diagnosis of electro-clinical SE type is essential, because it determines prognosis anddictates the intensity of therapeutic management. Some patients withbenign forms of SE may benefit from nonparenteral treatment, andbe followed up clinically and by spot EEGs. Conversely, intensivecare unit management with anesthesia and continuous monitoring,and parenteral AEDs may be required for refractory convulsive SE.

Key Words: Nonconvulsive status epilepticus, Encephalopathy,EEG, Triphasic waves, Periodic waves, PLEDs, BiPLED, GPEDs,Electrographic seizures, Periodic discharges.

(J Clin Neurophysiol 2006;23: 221–229)

As noted by Gastaut, “there can be as many forms of statusepilepticus as there are seizure types” (Gastaut, 1983).

The EEG of status epilepticus (SE), therefore, encompasses agreat variety of EEG seizure patterns. Nonetheless, particularsimilarities are present among the various types. In discussingthe EEG of SE, there is also the need to understand theusefulness and the uncertainties of interpreting the EEG. Toaddress some of these issues, this article will review thepatterns of epileptiform activity typical of SE, and those thatare controversial in the diagnosis or misdiagnosis of SE.Typical and atypical cases of SE will be used to illustratethese themes.

Status epilepticus remains an important subject, be-cause of the significant morbidity and mortality that attendssome types of SE. Such potential morbidity represents a

medical emergency, and engenders the need for rapid andaccurate diagnosis and for effective and safe treatments.

Obtaining good-quality EEGs or prolonged monitoringin either the emergency room or in intensive care units (ICUs)presents significant technical challenges. The recording envi-ronment may be plagued with artifact produced by movementaround the patient, nursing of the patient, intrusion of theeffects of machinery such as respirators, intravenous dripartifact and any machine that propagates 50 or 60 Hz elec-tromagnetic noise. The patient’s movement, vibrating beds,and muscle artifact can even produce tracings that may highlyresemble SE (Hirsch, 2005).

In a particular patient in an ICU, obtaining an EEG maybe difficult, because of the patient’s attendant needs forsterility; the presence of significant burns or open wounds (inthe burn unit); limited access created by bandages, or openwounds of the skull and scalp. There is also competition foraccess to the patient who needs to be nursed, changed,wounds dressed or may be sent off for other tests such as MRIor computed tomography.

DEFINITIONSStatus epilepticus was characterized by Gastaut in

1983 as being present “when an epileptic seizure is sofrequently repeated or so prolonged as to create a fixed andlasting condition” (Gastaut, 1983). Shorvon (2001, 2005)more recently enlarged on this definition, describing SE as“a term used to denote a range of conditions in whichelectrographic seizure activity is prolonged for 30 minutesor more and results in nonconvulsive clinical symptoms.”The determination of nonconvulsive status epilepticus(NCSE), however, presents other challenges. Because, bydefinition, convulsive movements must be absent for thisdiagnosis to be present, there is the need to identifywhether a state of ongoing seizure activity is present.Defining NCSE mandates the use of an EEG to establishthe presence of ongoing seizures. Much ambiguity re-mains, however, in what an electroencephalographerwould identify as seizures. Seizures are not merely thepresence of epileptiform activity lasting for 30 minutes,because there are a number of states with confusion andobtundation that may have an EEG correlate showingepileptiform morphologies. Some such states are triphasicwaves (TWs), the presence of profuse interictal activity, andsome patterns of epileptiform activity without ictal signifi-cance (rhythmic midtemporal theta of drowsiness or wicket-spikes). A convenient formulation of NCSE is the alterationof consciousness or behavior from baseline state for at least 30

Department of Neurology, Johns Hopkins University School of Medicine,Johns Hopkins Bayview Medical Center, Baltimore, Maryland, U.S.A.

Address correspondence and reprint requests to Professor Kaplan, Depart-ment of Neurology, Johns Hopkins University School of Medicine, JohnsHopkins Bayview Medical Center, B Bldg. 1 North, Rm. 125, 4940Eastern Avenue, Baltimore, MD 21224; U.S.A.; e-mail: [email protected].

Copyright © 2006 by the American Clinical Neurophysiology SocietyISSN: 0736-0258/06/2303-0221

Journal of Clinical Neurophysiology • Volume 23, Number 3, June 2006 221

minutes without convulsive movements, and the presence of oneor more of the following epileptiform patterns:

1. Repetitive focal or generalized epileptiform activity(spikes, sharp waves, spike-and-wave, sharp-and-slowwave complexes) or rhythmic theta or delta activity atmore than two per second.

2. The above EEG patterns at less than one per second, butwith improvement or resolution of epileptic activity andimprovement in the clinical state following intravenousinjection of a rapidly acting antiepileptic drug, such asa benzodiazepine.

3. A temporal evolution of epileptiform or rhythmic ac-tivity at more than one per second with change inlocation or frequency over time.

Some such patterns will be reviewed under a classifi-cation of NCSE into 1) complex partial status epilepticus(CPSE), and 2) generalized nonconvulsive status epilepticus(GNSE). A list of the different types of partial onset SE andprimary generalized SE is given in Tables 1 and 2.

Simple Partial Status EpilepticusSimple partial status epilepticus (SPSE) involves iden-

tifying a focal, subjectively perceived or visible, behavioralchange without mental status change. This may involvemotor activity, for example, nystagmus (Fig. 1), jerking ofhalf the face or the limbs on one side; sensory disturbance(e.g., with numbness, a burning sensation, or alteration insensory awareness of part of the body), “special sensory”alteration (e.g., visual, auditory, olfactory), autonomic (e.g.,sweating, salivation, pallor or pupillary dilatation); or psychic(anger, fear, happiness, illusions, hallucinations). The EEGcorrelates of such states vary from no perceptible change onthe EEG (largely because the seizure focus is too focal,circumscribed or too distant from the recording electrode) toictal patterns with combinations of spikes, spike and waves,polyspikes and rhythmic slow activity. Recordings with depthelectrodes have revealed that seizure activity is, indeed,present even while the scalp (surface) EEG remains normal(Wieser et al., 1985).

An example of motor partial status is epilepsia partialiscontinua (EPC), a focal process that may continue for days,months, or even years. Typical causes are encephalitis (orig-inally described as Russian Summer fever), nonketotic hy-perglycemia, occult or apparent malignancy, and neuromigra-tional disorders (Cockerell et al. 1996; Schomer, 1993). Atypical EEG, particularly with clinical facial or upper limbinvolvement, manifests epileptiform spikes over the rolandicregion. Some focal motor manifestations may, in fact, be“negative” i.e., asterixic in nature, in that with the epilepticspike there is a loss of tone in the outstretched arm. Theseconstitute one type of inhibitory motor seizures (Fig. 2)

(Kaplan, 1993). Many of these states clearly go unrecognizedboth because the clinical symptomatology is not thought to beepileptic and/or the EEG remains uninformative. In somecases, ictal single photon emission computed tomography(SPECT) scanning can reveal the focal, ictal nature of thedisorder (Fig. 3) (Kaplan, 1999).

The most common and arguably the most morbidtype of status is secondarily generalized convulsive statusepilepticus (SGCSE). It may be accompanied by coma andlead to death, often in a third of cases. There are manyetiologies, ranging from trauma, to infection, to malig-nancy, to underlying epilepsy, and it may occur at any age.As clearly demonstrated by Treiman et al. (1990), the EEGcorrelate of this dynamic condition often reflects a pro-gression from overt to subtle clinical and subtle EEGmanifestations (Treiman et al., 1990).

Primary Generalized Convulsive StatusEpilepticus

This rare entity is usually seen in patients with geneticepilepsies manifesting as convulsive seizures, who are non-compliant with their medication. In summary, the clinical andEEG progression are those of SGCSE with the exception thatthere is no progression to a state of “subtle status.”

Atonic Status EpilepticusAtonic SE predominantly affects infants. Clinical man-

ifestations can be relatively subtle with revulsion of the eyes,minor jerks, usually with coma. The EEG typically showsbilateral synchronous spike and slow-wave activity. Progno-sis is generally good.

Generalized Myoclonic Status EpilepticusGeneralized myoclonic SE as part of the myoclonic epi-

lepsies is extremely rare. It may affect children or adolescents,typically with idiopathic generalized epilepsies in which themyoclonus is irregular, bilateral, and with preserved conscious-ness. Alternately, it may be seen in secondary generalizedepilepsies in which there is asymmetric, asynchronous, mildermyoclonic movements, often with clouding of consciousness.The EEG may show bilateral, synchronous polyspikes (with aclinical myoclonus). Arrhythmic bursts of spiked waves, deltaactivity, or so-called recruiting rhythms have been described.

A continuous state of myoclonic movements in coma isfrequently seen after cardiac arrest. It is also referred to asstatus myoclonicus or status myoclonus. This common con-

TABLE 1. Types of Status Epilepticus (Partial Onset)

Simple partial status epilepticus (SPSE)

Complex partial status epilepticus (CPSE)

Secondarily generalized convulsive status epilepticus (SGCSE)

TABLE 2. Types of Status Epilepticus (Primary Generalized)

Generalized convulsive status epilepticus (GCSE)

Absence status epilepticus (ASE)

Atypical absence status epilepticus (AASE)

Generalized atonic status epilepticus (GASE)

Generalized myoclonic SE

Generalized clonic SE

Generalized tonic SE

Electrical status epilepticus of sleep (ESES)

P. W. Kaplan Journal of Clinical Neurophysiology • Volume 23, Number 3, June 2006

Copyright © 2006 by the American Clinical Neurophysiology Society222

dition almost invariably has a fatal outcome. The EEG mayshow spiked, polyspike, or spike slow-wave at various inter-vals from several per second to one every several seconds.

Generalized Clonic Status Epilepticus

Generalized clonic SE predominantly occurs in children(50% to 80%). When it is seen with normal children, there isusually an intercurrent fever. It may also be seen with mentalretardation usually in the setting of Lennox-Gastaut syndrome.The clinical correlate is of repeated, rhythmic, bilateral, smallclonic jerks, although these may often be asymmetric or arrhyth-mic. The EEG is variable typically showing bilateral synchro-

nous spikes, but may show spike bursts or recruiting rhythmsthat then progress to spike-waves.

Generalized Tonic Status EpilepticusGeneralized tonic SE is a rare condition that may occur in

either children or adults, usually those with Lennox-Gastautsyndrome. The seizures consist of brief, frequent clonic contrac-tions of the arms, often accompanied by eye revulsion; contrac-tion of the face, neck, and throat; and extension of the legs, oftenwithout return to baseline between contractions and seen everyfew minutes. There may be significant autonomic changes.Flexion of the spine may produce vertebral collapse and para-

FIGURE 1. This EEG shows motoractivity (nystagmus) with jerking ofhalf of the face or the limbs on oneside.

FIGURE 2. This EEG shows a typicalattack with right-arm weakness andjerking movements, and right-scalptwitching. Over the left parasagittalderivations (F3-C3, C3-P3, there arelow- voltage spikes with phase rever-sals (arrow A). Concurrently, there iscontralateral scalp electromyo-graphic artifact at F8-T4, T4-T6.T6-02 from ictal contraction of thecontralateral (right) scalp muscles(arrow B). Right-arm weakness wasalso present. From Kaplan PW. Focalseizures resembling transient isch-emic attacks due to subclinical isch-emia. Cerebrovasc Dis. 1993;3:241–243.

Journal of Clinical Neurophysiology • Volume 23, Number 3, June 2006 EEG of Status Epilepticus

Copyright © 2006 by the American Clinical Neurophysiology Society 223

plegia (personal observation). Seizures may be precipitated bybenzodiazepines. The EEG may show desynchronization, butmore typically shows low-voltage fast activity at 20 to 30 Hzthat gradually slows down to 10 to 20 Hz while increasing involtage (Fig. 4). Polyspikes and slow waves may be seen.Despite being refractory to a number of parenteral antiepilepticdrugs (personal observation), cognitive prognosis may be good.

Nonconvulsive Status Epilepticus

Complex Partial Status EpilepticusThe EEG patterns of complex partial status epilepticus

(CPSE) are highly variable. The morphology may includeisolated spikes, spike slow waves, and rhythmic theta or deltaactivity, with a frequency of 0.5 Hz to 1 Hz or upwards,largely lateralized to one side of the scalp. The patterns maybe continuous, waxing and waning, and may occur in burstswithout any typical diagnostic pattern, except that ictal later-alization predominates, or appears at onset. In some cases,lateralization is difficult to determine in that a mesiofrontalfocus can be responsible, producing secondary bilateral syn-chrony (Fig. 5).

Another form of CPSE from deep temporal structures islimbic SE (Fig. 6), which may have a highly variable clinicalstate with fluctuations in the level of consciousness fromwakefulness to catatonia, some with dream-like states. Apatient may be fearful, agitated, confused, or anxious.

Aside from the patterns previously described with CPSE,the scalp EEG may appear normal or be misdiagnosed as anencephalopathy because of the presence of rhythmic delta ac-tivity or of disorganized TWs (Fig. 7). In the case presented,theta-delta activity can be seen to alternate over the frontalregions as the frequencies slightly accelerate and decelerateindependently. Depth electrodes can sometimes reveal the ictalnature of the disorder (Wieser et al., 1985).

Generalized Nonconvulsive Status EpilepticusGeneralized nonconvulsive status epilepticus (GNSE)

is highly variable, with morphologies that include general-ized wave forms, spikes, spike-waves, polyspike-waves, andrhythmic theta or even delta activity. The frequency typicallymay vary from 0.5 to 1 Hz and upwards. The patterns areoften continuous, but may occur in bursts or in a waxing andwaning pattern. Again, no specific pattern is uniquely diag-nostic, but there is a generalized distribution with no domi-nating focal features (Fig. 8).

Atypical Absence Status EpilepticusAtypical absence status epilepticus (AASE) is rela-

tively rare, and is seen in infants or adolescents with mentalretardation, usually with Lennox-Gastaut syndrome. Clini-cally, the patients are confused with a change from identifi-able baseline despite their mental retardation. There may besubtle myoclonic movements, tonic and atonic seizures in thesame patient. The EEG can show generalized spike waveactivity typically varying from 1 to 2.5 Hz, often withgeneralized “recruiting rhythms” approaching 10 Hz. Anexample of AASE is given in Fig. 9.

FIGURE 3. This figure shows technetium Ceretec injectedintravenously at the start of one clinical seizure that yieldeda SPECT image showing increased perfusion of the righttemporal and temporoparietal regions. There was decreasedperfusion near previous left parietal and occipital infarcts.From Kaplan PW. Neurophysiological localization of epilepticnystagmus. Am J END Technol. 1999;39:77–83.

FIGURE 4. This EEG shows low-voltage fast spikes (20 Hz),which then slow to 10 Hz.



Electrical Status Epilepticus and Slow SleepThis nonconvulsive often generalized ictal state is rare and

merges, in part, with the Landau-Kleffner syndrome. Typicallyit affects children with mental retardation, though they areusually normal before the onset of electrical status epilepticusand slow sleep (ESES). The clinical state is that of multiple

seizure types (including partial seizures and atypical absenceseizures). The EEG when awake may show diffuse multifocal orgeneralized spikes or spike waves which then pervade therecording during non–rapid eye movement (non-REM) sleep tooccupy 85% of the record. There may be 1.5 to 2.0 Hz gener-alized spike waves. An example is given in Fig. 10.

FIGURE 5. This EEG (CPSE) showscontinuous, left-hemisphere rhyth-mic 2 to 3 Hz delta activity withsome waxing and waning evolution.

FIGURE 6. This EEG shows limbicstatus epilepticus with waxing andwaning independent bifrontal 3 to4 Hz activity (see text).



Periodic DischargesPeriodic discharges are stereotyped epileptiform dis-

charges which occur at regularly spaced intervals. Morphologiesmay include spikes, polyspikes, sharp waves, sharply contoured

slow-waves, or a mixture of spikes and slow-waves. The wavesmay be monophasic, biphasic, or triphasic, and are usually ofhigh amplitude (100 to 300 �V). They typically occur at regularor almost regular intervals of 0.3 to several seconds (Fig. 11).

FIGURE 7. This EEG shows CPSEwhere the scalp EEG could be misdi-agnosed as encephalopathy due tothe presence of theta-delta activityand triphasic morphologies. The EEGand patient improved within 3 min-utes of IV tornzepam.

FIGURE 8. This EEG shows general-ized, but predominantly synchronousfrontal epileptic discharges typical ofGNSE.



Several types of periodic EEG activity have beendescribed. Periodic lateralized epileptiform discharges(PLEDs) are unilateral, and were first described in theearly 1950s. Chatrian et al. (1963) introduced the termPLEDs and noted that they usually arose from structural or

focal lesions, co-occurred with seizures, and represented atransient phenomenon lasting usually less than 2.5 weeks.A rarer form, PLEDs-plus, was described in associationwith fast rhythmic discharges with an even greater asso-ciation with seizures. It was posited that these representedtransitional patterns where seizures appeared after a rhyth-mic buildup of PLEDs-plus morphologies (Reiher et al.,1991).

Bilateral Independent PseudoperiodicLateralized Epileptiform Discharges (BiPLEDs)

With BiPLEDs, the lateralized periodic or pseudoperiodicdischarges are seen independently over both hemispheres (Fig.12). Usually representing a more morbid underlying conditionthen PLEDs alone, the most common etiologies are anoxicencephalopathy, CNS infections, and chronic seizure disorders,each representing about a quarter of the causes. Almost threequarters of patients are comatose and mortality is high (about60%). Again, this pattern is highly associated with seizures (dela Paz and Brenner, 1981).

Generalized Periodic Epileptiform DischargesGeneralized periodic epileptiform discharges (GPEDs)

are generalized synchronous epileptiform discharges, usuallyappearing in a comatose patient (Fig. 13). Frequent causes areanoxic-ischemic coma after cardiorespiratory arrest, but theymay also be seen with metabolic encephalopathies or evenCreutzfeldt-Jakob disease. Typical CNS infections includeherpes simplex virus or following subacute sclerosing pan-encephalitis. Some forms of NCSE have largely a GPEDappearance. Finally, the pattern may be seen in the final

FIGURE 10. This EEG shows diffusemultifocal or generalized spikes orspike waves that then pervade thepervade the recording during non-REM sleep, and 1.5 to 2.0 Hz gener-alized spike waves.

FIGURE 9. This EEG shows diffuse generalized synchronouspolyspike discharges with eyelid fluttering. From PW Kaplan.Intravenous Valproate Treatment of Generalized Nonconvul-sive Status Epilepticus. Clin Electroenceph 1999;30:1–4.



stages of convulsive SE as it evolves toward subtle status(Husain et al., 1999).

One of the great challenges with periodic discharges isin deciding when they represent ictal (versus interictal) phe-nomena. Most electroencephalographers believe that PLEDsand BiPLEDs largely represent interictal discharges.

SUMMARYThe EEGs of SE typically show rhythmicity whether

represented by epileptiform morphologies or theta or deltaactivity; whether generalized or lateralized; and usually wax-ing and waning (at least to some degree). When clinical signsof convulsions or movement are absent, there is the challenge

FIGURE 12. This EEG shows bilat-eral, independent PLEDs occurringover the left and right frontal re-gions, without clinical correlate.

FIGURE 11. This EEG shows epilep-tiform discharges at regularly spacedintervals; monophasic, biphasic, ortriphasic; usually of high amplitude(100 to 300 �V); 1.5 to 2.0 Hz gen-eralized spike waves.



of differentiating impaired cognition or behavior with EEGchanges as an encephalopathy versus NCSE. The evolvingEEG picture, and clinical and EEG response to parenteralantiepileptic drugs may be pivotal. Finally, differentiatingepileptiform morphologies appearing periodically or pseudo-periodically, with or without a motor clinical correlate, froman active state of seizures, represents one of the importantgray zones of electroclinical diagnosis. Again, the pattern ofEEG evolution, and response to medication, along with theexpertise of the electroencephalographer and the “art” ofEEG interpretation, are central to this process.

REFERENCESChatrian G-E, White LE Jr. Electroencephalographic patterns resembling

those of sleep in certain comatose states after injuries to the head.Electroencephalogr Clin Neurophysiol. 1963;15:272–280.

Cockerell OC, Rothwell J, Thompson PD, et al. Clinical and physiologicalfeatures of epilepsia partialis continua: cases ascertained in the UK.Brain. 1996;119 (Pt 2):393–407.

de la Paz D, Brenner RP. Bilateral independent periodic lateralized epilep-tiform discharges: clinical significance. Arch Neurol. 1981;38:713–715.

Gastaut H. Classification of status epilepticus. In: Delgado-Escueta AV,Wasterlain CG, Treiman DM, Porter RJ, eds. Status epilepticus. NewYork: Raven Press, 1983:15–35.

Hirsch LJ, Brenner RP, Drislane FW, et al. The ACNS subcommittee onresearch terminology for continuous EEG monitoring: proposedstandardized terminology for rhythmic and periodic EEG pattersencountered in critically ill patients. J Clin Neurophysiol. 2005;22:128–135.

Hirsch LJ. Video EEG monitoring in the intensive care unit. Keynote address

at the annual meeting of the ACNS/AES, Washington, DC, December6, 2005.

Husain AM, Mebust KA, Radtke RA. Generalized periodic epileptiformdischarges: etiologies, relationship to status epilepticus, and prognosis.J Clin Neurophysiol. 1999;16:51–58.

Kaplan PW. Focal seizures resembling transient ischemic attacks due tosubclinical ischemia. Cerebrovasc Dis. 1993;3:241–243.

Kaplan PW. Neurophysiological localization of epileptic nystagmus. Am JEND Tech. 1999;39:77–83.

Kaplan PW. Intravenous Valproate Treatment of Generalized NonconvulsiveStatus Epilepticus. Clin Electroenceph 1999;30:1–4.

Kaplan PW, Tusa RJ. Neurophysiologic and clinical correlations of epilepticnystagmus. Neurology. 1993;43:2508–2514.

Reiher J, Rivest J, Grand’Maison F, Leduc CP. Periodic lateralizedepileptiform discharges with transitional rhythmic discharges: asso-ciation with seizures. Electroencephalogr Clin Neurophysiol. 1991;78:12–17.

Schomer DL. Focal status epilepticus and epilepsia partialis continua inadults and children. Epilepsia 1993;3 (Suppl 1):S29–36.

Shorvon S. The definition, classification and frequency of NCSE. In: Walker, M,Cross H, Smith S, Young C, Aicardi J, Appleton, Aylett S, Drislane D,Duncan J, Ferrie, C, Fujikawa D, Gray W, Kaplan P, Koutroumanidis M,O’Regan M, Plouin P, Sander J, Scott R, Shorvon S, Treiman D, Waster-lain C, Wieshmann U, eds. Nonconvulsive status epilepticus: EpilepsyResearch Foundation Workshop Reports. Epileptic Disord 2005;7:253–296.

Shorvon S. The management of status epilepticus. J Neurol NeurosurgPsychiatry 2001;70 (Suppl 2):ii22–27.

Treiman DM, Walton NY, Kendrick C. A progressive sequence of electro-encephalographic changes during generalized convulsive status epilep-ticus. Epilepsy Res 1990;5:49–60.

Wieser HG, Hailemariam S, Regard M, Landis T. Unilateral limbic epilep-ticus status activity: stereo EEG, behavioral and cognitive data. Epilep-sia 1985;26:19–29.

FIGURE 13. Generalized periodicepileptiform discharges. This EEGshows generalized pseudoperiodicdischarges every 0.5 to 1.5 secondsin a comatose patient with cardiore-spiratory arrest.



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