eMedicine Specialties > Neurology > Electroencephalography and Evoked Potentials
EEG in Status Epilepticus
Updated: Feb 27, 2007
Introduction
The first description of what might have been a case of status epilepticus (SE) can be found in the 25th and 26th tablets of the Sakikku cuneiform dating from 718-612 BC. The SE described in this classical period usually consisted of grand mal or generalized tonic-clonic convulsions (ie, generalized convulsive SE [GCSE]). Sporadic descriptions of other forms of SE appeared, but not until the advent of EEG were these other forms systematically described. GCSE was quickly recognized as a medical emergency, and the other forms usually grouped together as nonconvulsive SE (NCSE) were not considered emergencies. This gave rise to the first practical classification of SE into GCSE and NCSE.
This classification soon was considered inadequate. It grouped together SE consisting of absence or petit mal seizures (ie, absence SE, or ASE) and SE consisting of complex partial seizures (ie, complex partial SE, or CPSE), both of which could lead to clinically similar twilight states.
At the 10th Marseille Colloquium in 1962, the traditional definition of SE was extended to consist of epileptic seizures that were so prolonged or repeated as to constitute a fixed and durable epileptic state. This definition implied that as many types of SE existed as did seizures and that SE classifications should be similar to a seizure classification. The World Health Organization (WHO) dictionary defines SE as "a condition characterized by epileptic seizures that are sufficiently prolonged or repeated at sufficiently brief intervals so as to produce an unvarying and enduring epileptic condition." This was modified in the 1981 version of the international classification to describe SE as a condition in which "a seizure persists for a sufficient length of time or is repeated frequently enough that recovery between attacks does not occur."
Currently, some controversy exists with regard to the exact definition of SE. Gastaut (according to Shorvon) suggested that the episode should last at least 30-60 minutes to be considered SE. Most current studies accept a cutoff of 30 minutes. DeLorenzo and coworkers compared patients with seizures that lasted 10-29 minutes to patients whose seizures lasted 30 minutes or more. Shorter seizures were much more likely to stop without antiepileptic drugs (AEDs); they were also associated with a much lower mortality rate.
Shinnar and coworkers identified a subpopulation of children predisposed to prolonged (>30 min) seizures and concluded that their data supported starting treatment of any seizure that lasts for 5-10 minutes and retaining the 30 minute cutoff in the definition of SE. Lowenstein, Bleck, and MacDonald argued that basing a definition on the onset of neuronal injury is questionable. Because isolated seizures rarely last longer than a few minutes, they proposed a revised operational cutoff of 5 minutes for adults with GCSE.
However, many recognize that the best definition would be based on the physiology of SE and that such a definition should include failure of normal seizure-terminating mechanisms. Although some biochemical changes that take place during SE (eg, loss of GABA-A receptor sensitivity) are known, sufficient experimental data are lacking to formulate such a definition, which might need to encompass many different mechanisms. Fountain and Lothman suggested a pathophysiological classification based largely on presentations found on EEG. First, he differentiated between isolated seizures (transient neuronal dysfunction) and SE (enduring neuronal dysfunction). SE was then subdivided based on the presence or absence of typical spike-wave (SW) complexes on the EEG, into SW SE and non-SW SE.
Pathophysiology of non-SW SE is thought to be the impairment of GABAergic (primarily GABA-A) inhibition and accentuation of glutamatergic excitation. Adenosine is speculated to play a role in the termination of SE. In SW SE, GABAergic (primarily GABA-B) inhibition is enhanced first, hyperpolarizing thalamic neurons and causing the wave. This then "de-inactivates" excitatory (speculatively, T-type calcium) channels, depolarizing the neuron, causing the spike, and resulting in more GABAergic hyperpolarization. This process perpetuates the cycle.
Patient education
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Epidemiology
Extrapolating from their data from Richmond, VA, and empirically correcting for underreporting, DeLorenzo et al estimated that in 1 year, 152,000 patients in the United States experience SE (incidence 61 cases per 100,000 population) for a total of 195,000 episodes (incidence 78 cases per 100,000 population).
They found that SE most frequently occurred in infants in their first year of life and adults older than 60 years. In children, the etiology was a systemic, non-CNS infection in over half of cases. Low AED levels and remote causes (including congenital malformations) also explained a significant number of cases. In adults, the distribution of etiologies was more even: low AED levels, stroke, and remote causes being the 3 major etiologic classes. In adults aged 60 years or older, acute or remote strokes caused 61% of cases.
Shorvon estimated the incidence of SE as 44.1-64.6 cases per 100,000 per year. Of these, 18-28 are GCSE, 3.5 CPSE, and 0.1 typical ASE. He also estimated that 8 cases per 100,000 are newly diagnosed epilepsies presenting with SE. Wu and coworkers found that the incidence of SE in California was 6.2 cases per 100,000 and that the incidence had fallen 42% from 1991-1998.
Morbidity And Mortality
Determinants
Determinants of mortality and morbidity include type of SE, etiology, age of patient, and duration of SE. Mortality rates in children are lower than in adults. Low-mortality causes include low AED levels and systemic infections. High-mortality causes include hypoxia and anoxia, cerebrovascular disease, metabolic disturbances, and tumors.
Waterhouse et al recently showed that SE consisting of intermittent seizures has a lower mortality rate than SE consisting of a continuous seizure; this finding was statistically significant in adults but not children.
DeGiorgio et al showed that serum neuron-specific enolase (a marker of acute brain damage) is elevated in GCSE, CPSE, and subclinical or subtle GCSE. The levels were lowest in GCSE, higher after CPSE, and highest after subclinical or subtle GCSE. These findings suggest that all of those forms of SE can cause neuronal damage. The authors concluded that the high levels after subtle GCSE are related to the poor outcome generally associated with that presentation. The intermediate levels after CPSE reflect long duration and potential for brain damage.
Krumholz believes that GCSE and CPSE have been well documented to cause brain damage and that, although ASE has not been definitively documented to cause brain damage, it does pose a significant problem of recurrence. Drislane has countered that the various forms of human NCSE have not yet been shown to cause permanent brain damage, at least not unequivocally enough to justify urgent treatment.
Jordan believes that when NCSE occurs in the setting of brain injury, the 2 conditions act synergistically to increase brain damage.
Generalized convulsive status epilepticus
The most significant mortality and morbidity rates in SE occur in patients with GCSE. Recent estimates of mortality in patients with GCSE range from 8-32%. In the past, rates have been as high as 50%. Effects of GCSE can be subdivided into systemic effects and CNS effects, which can be further subdivided into those resulting from systemic physiologic changes and those resulting from neuronal activity (excitotoxicity).
Hauser and Hesdorffer believed that the deaths from SE in patients with acute CNS insult did not appear to be due to SE but to systemic complications such as aspiration, compression fracture, acute tubular necrosis, hypotension, and the effect of the underlying pathology, which is the progressive lesion in the CNS.
Early in GCSE, physiologic changes are characteristic of sympathetic overdrive, probably related to increased circulating catecholamines. In this early (or compensated) stage, the body changes to meet the demands of the neurons in the brain for increased oxygen and glucose and removal of metabolic waste products. Cerebral blood flow increases 200-600%.
The patient passes into stage II, or decompensated SE, 30-60 minutes later. Blood pressure falls, metabolic needs of the cerebral neurons are no longer met by homeostatic mechanisms, and cell death occurs. Fountain and Lothman stated that supply/demand mismatch does not occur until SE has continued for hours. High-energy phosphates continue to be available into late stages of SE. They conclude that the causes of histopathologic changes can be independent of cerebral physiology.
One of the cellular events that may lead to GCSE is the release of glutamate, an excitatory neurotransmitter. Glutamate is toxic to neurons (ie, an excitotoxin). Elaboration of glutamate triggers a sequence of intracellular events that begins with increased intracellular calcium, which then proceeds to dysfunction of multiple intracellular systems, finally resulting in cell death.
Complex partial status epilepticus
Morbidity rates in CPSE are much lower than in GCSE. CPSE is not a medical emergency. Krumholz described several patients with persistent neurological deficits thought to be secondary to CPSE. The patient does not experience the violent motor manifestations seen in GCSE. Therefore, systemic physiologic changes do not occur in CPSE.
The mechanism of CNS damage is thought to be similar to the excitotoxic neuronal death seen in GCSE. The long-term prognosis of CPSE is dependent on the underlying disease process.
Absence status epilepticus
No definite examples of long-term sequelae of ASE have been reported. This is consistent with the fact that different cellular mechanisms underlie the different types of SE. Snead et al separated typical and atypical ASE. Typical ASE occurs in the context of primary generalized epilepsy, and, clinically, typical ASE may greatly differ in children compared with adults. The prognosis of patients with typical ASE is usually good. The distinction between typical and atypical ASE is made more on etiologic than on clinical grounds. Typical ASE is most commonly observed in patients with the Lennox-Gastaut syndrome. EEG may sometimes be useful in distinguishing typical from atypical ASE.
During prolonged seizures, the 3-Hz SW pattern characteristic of typical absence seizures often slows to 1.5-2.5 Hz, resembling the slow SW pattern characteristic of epileptic encephalopathies. Prognosis of atypical ASE is poor, which probably reflects the severity of the underlying disease.
Electroencephalography (EEG)
Muscle and movement artifact frequently obscure EEG during an episode of GCSE; thus, the usefulness of EEG during this situation may be limited. In diagnosis, EEG can be used to distinguish SE from other causes of altered mental status. Praline and coworkers found that the 3 most frequent indications for emergent EEG were brain death (13%), convulsive status epilepticus (CSE) after treatment (12.1%), and NCSE (10.6%).
Varelas and coworkers found that emergent EEGs were ordered in their institution 60.2% of the time for a question of SE and an additional 7.3% of the time for NCSE. When they divided the requests into those coming from an intensive care unit (ICU) or non-ICU source, significantly more requests citing SE (but not NCSE) came from the ICU setting. A diagnosis of CSE was made in only 6.1% of cases and a diagnosis of NCSE in 4.6%. Cardiopulmonary arrest and suspicious clinical activity predicted the diagnosis of CSE. Cardiopulmonary arrest also predicted the occurrence of either CSE or NCSE. None of the clinical or historical variables tested predicted NCSE alone; however, a prolonged emergent EEG made a demonstration of NCSE 5 times more likely. EEG is also useful in classifying SE into SW and non-SW forms, in choosing and monitoring therapy, and in formulating prognosis.
Darbin and coworkers found that aging alters the appearance of EEG readings rats with experimental SE. Fernandez-Torre and coworkers studied NCSE in elderly persons and emphasized that the diagnosis can be very difficult to make on clinical grounds alone and that an EEG is important in the evaluation for possible NCSE in elderly persons.
Animals with experimentally induced GCSE progress through a sequence of EEG stages according to Treiman's classification. These include discrete generalized seizures with interictal slowing, merged discrete seizures with waxing and waning of frequency and amplitude, continuous seizure discharge, almost continuous seizure discharge interrupted by flat periods, and periodic epileptiform discharges (PEDs) on a flat background (ie, periodic lateralized epileptiform discharges [PLEDs]).
Disagreement exists regarding the number of stages and the descriptions of individual stages, but enough independent descriptions indicate some sort of progression, at least in experimental animals, to support this proposal. However, Mikati and coworkers found that younger rats are less likely to progress through the 5 orderly stages than older rats. Treiman believes that most cases of human GCSE are in fact secondarily GCSE. Whether a similar sequence of changes occurs in primarily GCSE is uncertain. The full sequence has not been reported in humans. Although all stages have been reported in various individuals (sometimes several in a single individual), some investigators believe that humans, unlike experimental animals, do not always progress through a predictable sequence of EEG changes during SE. Whether PEDs comprise an ictal pattern or a marker of severe cortical dysfunction is still a subject of disagreement.
Nowack and Shaikh have reported fragments of Treiman's sequence in human patients with CPSE. Such a sequence may occur in cases of partial-onset (probably non-SW) human SE. In partial SE, Grand'Maison et al have described a somewhat different set of stages than Treiman has.
Granner and Lee studied EEGs from 85 episodes of NCSE. They speculate that many cases with generalized-appearing ictal discharge (especially those with focal predominance) may actually have focal onset of the SE and that diazepam can be a useful tool for distinguishing between generalized and focal onset in this heterogenous group.
A patient who displays the violent motor manifestations of GCSE usually presents no diagnostic difficulty. However, Walker et al reported that almost half of patients referred to a specialized center for "refractory SE" had nonepileptic conditions that mimic SE. Howell et al discussed the difficulties of differentiating SE from pseudostatus epilepticus. Kaplan described 25 patients with NCSE in whom diagnosis was delayed up to 5 days because of presentations that suggested other entities. EEG can be helpful in making the correct diagnosis. Privitera et al reported that 74 of 198 patients with altered levels of consciousness but no clinical convulsions had EEG evidence of definite or probable non–tonic-clonic SE. They believed that clinical signs alone could not be used to determine the correct diagnosis. Their conclusion was that an emergency EEG should be obtained in all patients with altered levels of consciousness.
Experimental evidence suggests that patients with EEG patterns in late stages of SE respond better to phenobarbital than to more standard AEDs. However, Treiman found that the later the EEG stage of the SE, the harder it is to control. Whether to treat PEDs and, by extrapolation, any NCSE in critically ill patients is disputed. Husain et al used a combination of EEG and clinical findings to identify patients in whom PEDs should be treated. Patients whose EEGs showed higher voltage between PEDs responded more frequently to treatment.
Treiman described subtle GCSE, in which SE persists after partial treatment has eliminated convulsive movements of overt GCSE. EEG may be necessary to differentiate between partial and adequate treatment of GCSE. DeLorenzo found that NCSE can follow partial treatment of CSE and felt that EEG can be useful is detecting such incomplete treatment. He also found that most NCSE following partial treatment of CSE was CPSE. EEG monitoring following treatment of CSE can guide treatment plans.
Jaitly et al evaluated EEGs performed after the treatment of SE. They found that the presence of burst suppression or posttreatment ictal discharges was strongly (statistically) associated with mortality. The presence of PLEDs was also highly correlated (but not as strongly) with mortality and poor outcome. Drislane did a retrospective study of patients with focal SE and found no difference with regard to outcome or response to medications between the groups with continuous focal epileptiform discharge and the group with discrete electrographic seizures. He excluded patients with PLEDs with longer intervals (ie, those that recurred with a frequency of <1.5 Hz). Normalization of EEG correlated with a good outcome. Using a somewhat different set of EEG features, Nei et al found that any detected presence of PEDs in the EEG predicted poorer outcome.
Reviewing 100 consecutive patients with NCSE from a SE database, Shneker and Fountain found that the presence of generalized SW discharges on the EEG of patients with NCSE did not affect mortality.
Differential Diagnosis
Usually, the initial diagnosis of GCSE is not difficult. GCSE is a medical emergency. Treatment should not be delayed while waiting for results of laboratory tests. Myoclonus that accompanies hypoxic or toxic insults may be confused with GCSE. Keep in mind that Treiman considers some cases of toxic or hypoxic myoclonus to be a subtle form of GCSE. Psychogenic SE is uncommon but may be a source of confusion. If differentiating the type of seizure is not possible on clinical grounds, EEG usually makes the distinction. Well-modulated alpha rhythm during or immediately after a spell suggests a psychogenic etiology. Presence of postictal slowing, especially focal, suggests an epileptic etiology.
Differential diagnosis of other forms of SE is more complicated because of polymorphic presentations. Nonconvulsive forms of SE (eg, CPSE, ASE) can be confused with psychiatric syndromes or toxic, metabolic, or other encephalopathies. Differential diagnosis of one form of NCSE should always include the other; CPSE and ASE cannot be distinguished on clinical grounds. Finally, always consider CPSE and ASE in differential diagnoses of patients with altered mental status.
In general, the diagnosis of generalized nonconvulsive status epilepticus (GNCSE) is based on the EEG presence of ictal patterns for some period (usually 30 min) and the presence of altered mental status. The case of triphasic waves (TWs) illustrates the difficulties. TWs (see EEG Triphasic Waves) can be seen in metabolic encephalopathies and degenerative conditions; similar-appearing rhythmic waveforms can be seen in GNCSE (Young, 2006). Boulanger and coworkers have described some EEG differences between TW and similar-appearing GNCSE, such as the following:
- Higher frequency of epileptic discharges
- Presence of spikes with epileptic discharges
- Amplitude predominance of phase II in TW
- Increase of TWs in response to noxious or auditory stimulation
- Phase lag absent in cases of GNCSE but present in some cases of TWs
Even with those differentiating features, the differential diagnosis remains difficult. Some authorities have proposed abolition of the controversial patterns with intravenous benzodiazepines as a diagnostic test. Fountain and Waldman have shown that TWs are also abolished by benzodiazepines. To overcome that difficulty, the test has been expanded to require both (1) abolition of the questionable patterns and (2) improvement in level of consciousness.
Thomas and coworkers believe that confirmation with such a response is mandatory to make the diagnosis. Fountain and Shneker believe that such confirmation is not necessary. Criteria for making the diagnosis remain controversial.
Towne and coworkers have found that of comatose patients without clinical convulsive activity who have EEG evidence of SE, 8% have NCSE.
Treatment Of Status Epilepticus
Generalized convulsive status epilepticus
GCSE is a medical emergency; provide therapy immediately without waiting for EEG results or other laboratory tests. Several protocols exist, none of which has been proven significantly superior. Given the current knowledge, having a clear plan of approach is more important than recommending one of the protocols over another.
Stabilize coexisting medical problems, treat metabolic abnormalities, and ensure airway and oxygenation. Many medications used to treat SE depress respiration, so intubation and ventilation may be necessary. Adequate facilities for this procedure must be available. Obtain venous access; treatment should be intravenously administered. Test for hypoglycemia and treat if present. In adults, provide supplementary thiamine with glucose. Lumbar puncture is indicated if CNS infection is suspected.
Walker and Shorvon recommend dividing SE into premonitory, early, established, and refractory stages. The premonitory stage often occurs before the patient arrives at the hospital. At this point, rectal diazepam may abort SE. The early stage can be treated with intravenous benzodiazepines. Lorazepam (0.1 mg/kg) is the benzodiazepine of choice because of its long duration of action. Treiman et al have evaluated the initial treatment of SE, comparing outcomes of patients given phenobarbital, phenytoin, diazepam plus phenytoin, or lorazepam. In patients with verified diagnosis of overt GCSE, response rates were as follows: lorazepam, 64.9%; phenobarbital, 58.2%; diazepam and phenytoin, 55.8%; and phenytoin alone, 43.6%. In statistical comparison of the pairs, only the difference between lorazepam and phenytoin alone was significant.
The suggested treatment in the established phase of SE is a combination of intravenous phenytoin (20 mg/kg) and lorazepam (if not already given) or intravenous phenobarbital alone (15-20 mg/kg). Fosphenytoin, a water-soluble phenytoin precursor, is an alternative when stability of intravenous access is questionable since it does not have the tissue toxicity of extravasated phenytoin. It also can be intramuscularly administered, but absorption by this route is not fast enough to treat SE adequately.
Other medical treatments are available, but in refractory SE (ie, that which does not respond to either regimen above), use of general anesthesia is reasonable. A commonly used protocol for treatment of refractory SE is intravenous pentobarbital. A loading dose of 5 mg/kg is followed by 0.5-3 mg/kg/h titrated to cessation of seizures or a burst-suppression pattern on EEG. In a recent study of patients with refractory SE, Krishnamurthy and Drislane concluded that the survival rate was better in patients whose EEG was more suppressed. Hypotension is a risk of pentobarbital infusion. In patients who cannot tolerate pentobarbital, alternatives include continuous infusion of benzodiazepines (eg, midazolam or propofol).
Wasterlain and Chen have postulated a division of SE. The first minutes (15-30 min in the case of focal seizures) are impending SE, which evolves into SE (epidemiologically defined as at least 30 min of continuous seizure activity or 30 min of intermittent seizures without full recovery of consciousness between seizures). Perhaps these 2 stages are similar to the induction phase of self-sustaining SE and the maintenance phase that follows. Treatment of the induction phase is effective with many agents, possibly in small doses, which enhance inhibitory transmission or reduce excitatory transmission. Once seizures become self-sustained SE, the maintenance phase is entered, and treatment tends to be effective only with a few agents, and then only in high doses. Experimentally, those that block NMDA synapses or are presynaptic glutamate releasers tend to be most effective (Mazarati, 2006). This emphasizes the importance of making the diagnosis and instituting treatment quickly.
Complex partial status epilepticus
Favorable neurologic outcomes of CPSE have been reported regardless of whether medical treatment was successful. Few reports indicate serious sequelae complicating CPSE. Thus, the question of how aggressively to treat CPSE remains controversial. In general, pending a good, randomized trial, CPSE should be treated similarly to GCSE, except that treatment should stop before the use of general anesthesia (eg, pentobarbital coma).
In acute stages and for diagnosis, treatment with an intravenous benzodiazepine may be helpful. Often, out-of-hospital treatment with rectal or oral benzodiazepines aborts an episode. Williamson believes that, since most patients with CPSE have a history of epilepsy, concomitant AED therapy should be optimized.
Walker and Shorvon reported that, although most episodes of CPSE are self-terminating, recurrent episodes are encountered, and medical treatment is often disappointing. Patients who have medically refractory localization-related epilepsy should be evaluated for surgical therapy.
Absence status epilepticus
Walker and Shorvon reported that ASE responds rapidly to intravenous benzodiazepines. D'Agostino and coworkers believe that valproate is the medication of choice for ASE. Although effective, this treatment may result in complications such as sedation and respiratory depression. Kaplan summarized a case of a female with known absence epilepsy in which hospitalization was avoided by treating ASE with intravenous valproate. Snead et al stated that the more atypical the SE, the more difficult it is to control with benzodiazepines and other forms of therapy. Patients with primary generalized epilepsy should have optimized valproate or ethosuximide therapy to prevent recurrent episodes of ASE. Thomas et al reported that long-term anticonvulsant therapy might not be necessary in adults who are middle-aged or older at the onset of de novo ASE.
Keywords
SE, electroencephalogram, EEG, generalized convulsive SE, generalized convulsive status epilepticus, GCSE, subclinical GCSE, subtle GCSE, nonconvulsive SE, nonconvulsive status epilepticus, NCSE, absence status epilepticus, absence SE, ASE, typical absence status epilepticus, atypical absence status epilepticus, typical ASE, atypical ASE, complex partial status epilepticus, complex partial SE, CPSE, epileptic seizure, epileptic state, epilepsy, antiepileptic drugs, anti-epileptic drugs, AED, AEDs, neuronal dysfunction, spike-wave complex, SW SE, non-SW SE, decompensated SE, periodic epileptiform discharge, PED, periodic lateralized epileptiform discharge, PLED
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Further Reading
Keywords
SE, electroencephalogram, EEG, generalized convulsive SE, generalized convulsive status epilepticus, GCSE, subclinical GCSE, subtle GCSE, nonconvulsive SE, nonconvulsive status epilepticus, NCSE, absence status epilepticus, absence SE, ASE, typical absence status epilepticus, atypical absence status epilepticus, typical ASE, atypical ASE, complex partial status epilepticus, complex partial SE, CPSE, epileptic seizure, epileptic state, epilepsy, antiepileptic drugs, anti-epileptic drugs, AED, AEDs, neuronal dysfunction, spike-wave complex, SW SE, non-SW SE, decompensated SE, periodic epileptiform discharge, PED, periodic lateralized epileptiform discharge, PLED
