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The EEG in Status Epilepticus

Status epilepticus (SE) is a prolonged seizure or a series of seizures without recovery between them. There are many forms of SE, with different clinical and EEG manifestations. Deciding which type of SE a patient has is important in directing proper management and in predicting the outcome. EEG is often a crucial part of that evaluation.

There are both convulsive and nonconvulsive forms of SE. Generalized convulsive SE (GCSE) is the best described type of SE and has the greatest morbidity, mortality, and clinical urgency for treatment. GCSE must be diagnosed and treated promptly, in part for concern that it may become refractory to treatment and have grave consequences. For most forms of nonconvulsive SE (NCSE), however, there is less evidence that it causes lasting (or in some cases, any) neurologic harm. Thus, the treatment imperative is less, but not negligible. NCSE has been referred to as “underdiagnosed and over-treated.” Continuous EEG recording can help elucidate the temporal pattern of recurrent seizures when subtle or no clinical signs are evident.

GENERALIZED CONVULSIVE STATUS EPILEPTICUS

Clinical and EEG manifestations of generalized convulsions and GCSE are usually symmetric from the onset (Figure 10.1), although some may exhibit focal or lateralizing features, particularly at the onset or end of the seizure. On the EEG, true generalized seizures associated with genetic generalized epilepsies (GGEs) typically begin with bilaterally symmetric epileptiform discharges. The initial sudden interruption in behavior is often accompanied by widespread voltage attenuation and faster frequency rhythms between 20 and 40 Hz, producing an “electrodecremental” appearance of the ictal EEG (more often encountered in children). This is often the time when muscle artifact obscures the EEG recording of the tonic and clonic phases of the convulsion, although sometimes, epileptiform discharges may be evident at the vertex. The superimposed electromyography (EMG) activity itself may exhibit a characteristic rhythmic appearance in synchrony with the clinical features of repetitive clonic jerks.

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Following an individual seizure, repetitive epileptiform discharges may decrease from several per second to a frequency less than 1 Hz. The discharges might not disappear entirely, often giving way to generalized periodic discharges (GPDs) or lateralized periodic discharges (LPDs), usually on a suppressed, lower voltage background, and usually for several minutes before the gradual return of a normal background—or prior to another convulsion if GCSE has not been terminated.

When GCSE is prolonged, the EEG becomes more discontinuous, and clinical manifestations may become minimal. When the visible motor manifestations of SE cease, this may be termed “subtle” GCSE. At this point, clinical signs are minimal and may include low amplitude eyelid or facial twitching, intermittent myoclonic jerks, repetitive or sustained nystagmus, or even the absence of all clinical movement. Persistence of regular and rhythmic GPDs at 2.5 Hz or greater suggests that nonconvulsive seizures are still ongoing and that the SE has become refractory despite the lack of clinical signs. At this stage, patients are typically comatose.

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Some authors have proposed that there is a characteristic sequence (Figure 10.2 A–E) of EEG changes during GCSE—based on EEG recordings on animals and humans at various stages of (usually generalized convulsive) SE, although all such stages are seldom observed in an individual patient. This sequence of EEG changes includes: (A) Discrete seizures that are repetitive and separated electrographically by background slowing and attenuation between recurrent seizures. (B) Seizures that merge gradually, with some fluctuation in voltage and frequency. (C) Continuous seizure activity, but sometimes with asymmetric epileptiform discharges, reflecting the focal or lateralized onset of many seizures. (D) Ongoing seizure activity interrupted by brief periods of a suppressed background, often for just a second or so. (E) In late SE, the background becomes suppressed, with GPDs or infrequent bursts of polyspikes (Figures 10.2 D–E and 10.3). “Subtle” SE often corresponds to EEG stages D and E.

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While the later phases of this EEG sequence are thought to reflect the uncoupling of the electrical and mechanical activity after prolonged SE, not all clinical neurophysiologists have found such a predictable sequence of EEG patterns in many patients. Still, these patterns may be useful in determining the approximate phase of SE a patient is in, and whether the SE is prolonged enough (electrographically, when not evident clinically) that treatment for refractory SE should be considered.

215FOCAL MOTOR STATUS EPILEPTICUS

There are many causes of focal motor SE (FMSE). Stroke (ischemic or hemorrhagic), trauma, and infection are the most common. SE occurs in about 1% of all acute strokes, although isolated seizures are much more common. Central nervous system (CNS) infection (e.g., meningoencephalitis, often with herpes simplex encephalitis) may be manifested clinically as FMSE. Other etiologies of FMSE include mass lesions, autoimmune disorders, vasculitis, multiple sclerosis, and, rarely, mitochondrial or degenerative disorders. Rarely, benign idiopathic focal epilepsies, such as self-limited epilepsy with centrotemporal spikes (SLECTS) can lead to FMSE, but seizures in these syndromes are often treated easily and seldom lead to SE.

In focal motor SE, ictal EEG features are quite variable. Epileptiform activity may consist of discrete, frequently recurrent, focal motor seizures that are localized or lateralized to one hemisphere or have an asymmetric bihemispheric involvement when consciousness is impaired (Figure 10.4). There may be clinical recovery between seizures, or there may be continuous electrographic seizure activity. Following individual focal seizures, or between electrographic focal seizures on EEG, there may be continued slowing or LPDs. In terms of diagnosis and clinical outcome, there does not appear to be a large difference between the discrete and continuous forms of FMSE.

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Clinically, FMSE may be manifested as prolonged regular jerking of an isolated area of the body such as the face, hand, or foot. This is referred to as epilepsia partialis continua (EPC) (Figure 10.5). EPC can last days or weeks. Almost always, there is a responsible focal lesion, but there are not always identifiable focal rhythmic epileptiform discharges on the surface EEG. Although repetitive discharges or rhythmic theta or delta slowing are also common patterns with EPC, some epileptic foci are generated in deeper cortex, have limited surface area involved (i.e., less than 10 cm²), or have a dipolar source that is not oriented “favorably” for detection by surface electrodes, so there is often minimal or no change detected on surface EEG despite ongoing focal seizures.

LPDs are repetitive spike or sharp and slow wave complexes (see also Chapter 11). They usually last 100 to 400 msec and typically recur at 0.5 to 2 Hz but sometimes have longer intervals. They are usually distributed broadly over most of one hemisphere, with an attenuated EEG background between discharges. Most epileptologists do not consider LPDs to be definite clinical seizures or SE per se, but rather on an ictal–interictal continuum, and often associated with clinical seizures and with acute, serious focal neurologic illness. LPDs have a greater correlation with the likelihood of clinical seizures occurring than do GPDs. In about 90% of cases there is a structural lesion. Stroke is the most common cause, although tumor, and occasionally, CNS infections, and severe metabolic disturbances, such as nonketotic hyperglycemia, may result in LPDs. Some types of epilepsy may also exhibit LPDs as an interictal or ictal phenomenon. In many cases, LPDs may be considered “the terminal phase of status epilepticus,” although they may also occur between seizures.

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While most LPDs are manifested on the EEGs as discharges recurring every 1 to 2 seconds, some intervals may be 10 seconds or longer. The more rapid discharges of ≥ 2.5 Hz are a definite EEG correlate of seizures, but most electroencephalographers consider that there is a significant risk of ongoing seizures when the frequency of LPDs exceeds 1.5 or 2.0 Hz. “LPDs+” is a term describing LPDs associated with low-voltage rhythmic epileptiform discharges or other rapid rhythms occurring between the high-voltage discharges. LPDs+ are more likely to be associated with epileptic seizures than are “LPDs proper” (Figure 10.6 A–C).

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