Nonconvulsive Status Epilepticus in Adults: Types, Pathophysiology, Epidemiology, Etiology, and Diagnosis

Nonconvulsive status epilepticus (NCSE) poses a significant multidimensional challenge for emergency and intensive care physicians as well as neurologists [1, 2]. This primarily starts with the diagnosis and related detection and confirmation of NCSE, and continues through optimal therapy and difficult prognosis [3]. Although a convulsive status epilepticus (CSE) needs only to be distinguished from a non-epileptic dissociative convulsive state, in the differential diagnostic spectrum and in appearance, NCSE can range from migraine, stroke, coma or delirium to psychiatric disease patterns such as stupor and psychosis [4, 5]. Nowadays all paroxysmal focal (and sometimes even global) deficits are basically considered events suspicious of stroke, and therefore initially evaluated as such. While this may still be correct with respect to focal impairments such as paralysis or aphasia, focal impairments with temporary changes in – or loss of – consciousness occur only with considerable vertebrobasilar insufficiency of an ischemic nature, more frequently they are indicative of an epileptic, metabolic-toxic or migrainous origin. It should also be noted that a “plus” symptomology (movements, paresthesia, olfactory, visual, emotional, acoustic impressions) is predominantly present in epileptic seizures and status epilepticus, whereas in cases of stroke there is a “minus” symptomology (paralysis, hypesthesia, aphasia, amaurosis, etc.). The picture is obscured by the fact that “minus” symptoms can occur during epileptic episodes (paresis, aphasia, apraxia), while during strokes “plus” symptoms (hyperkinesia – limb-shaking TIAs, paresthesia, visual phenomena, etc.) may be observed. The following presents the definition, various manifestations and types, classification, causes, epidemiology, brief pathophysiology as well as the diagnosis of NCSE.