Nonconvulsive status epilepticus (NCSE) was initially described in patients with typical and atypical absence status epilepticus (ASE) characterized by states of confusion varying in severity and in focal epilepsies with or without alteration of consciousness. Continuous EEG monitoring of critically ill patients has further refined the classification of NCSE into two main categories: with coma and without coma. Hypnotic, soporific or somniferous epileptic seizures do not exist. On the contrary, patients usually awaken when seizures occur during sleep, and their eyes remain open during ASE. Excessive sleepiness and coma alone are not ictal signs but are observed in the postictal phase of convulsive seizures. On the other hand, excessive sleepiness evolving into coma is a cardinal sign of metabolic/toxic encephalopathies with triphasic waves evolving to burst suppression patterns and ultimately to cerebral inactivity and death. NCSE alone does not directly cause coma. Comas are related to the underlying etiology, patient age and comorbidities, as well as the administration of intravenous sedative drugs to control epileptic seizures. In cases of severe brain injury, NCSE can explain the failure to awaken after the withdrawal of anesthetics and is only an aggravating factor of the neurological condition. In typical ASE, which is characterized by sustained, rhythmic, bilateral, synchronous and unreactive discharges with evolving spatiotemporal patterns (the best example of NCSE), there is no vigilance impairment. This contrasts with metabolic/toxic encephalopathies, which exhibit monomorphic generalized periodic discharges in which patients may become comatose and die. The extended concept of NCSE in comatose patients may lead to an inflated assessment of NCSE, implying a potentially worse prognosis compared to convulsive status epilepticus.
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