Excerpt from EEG in Status Epilepticus

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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

For excellent patient education resources, visit eMedicine's Procedures Center and Brain and Nervous System Center. Also, see eMedicine's patient education articles Electroencephalography (EEG) and Epilepsy.

Please click here to view the full topic text: EEG in Status Epilepticus