Evidence against permanent neurologic damage from nonconvulsive status epilepticus

Nonconvulsive status epilepticus (NCSE) is much more common than is general ly appreciated and is certainly underdiagnosed, but its long-term effects a re largely undetermined and remain controversial. There is increasing exper imental evidence that generalized convulsive status epilepticus produces la sting neuropathologic damage in the hippocampus, but experimental models of ten include provocation of status epilepticus (SE) by physical (e.g., elect rical stimulation) and chemical (including excitotoxic) agents that may ind uce damage independent of the epileptiform discharges. Also, damage appears to be related to the intensity and duration of electrical stimulation. Suc h models usually include high-frequency discharges sustained over long peri ods, somewhat different from the electrical activity of typical human NCSE. Pathologic studies in humans pertain primarily to patients who have had ge neralized convulsive status epilepticus. Clinical studies of the effects of NCSE are mandatory, but conclusions are difficult to come by, in part beca use of diverse definitions of NCSE. An altered mental status is obligatory, but the pertinent EEG and medication response criteria are controversial. Response to medication can be delayed by many hours or even days. Absence S E appears to cause no lasting effects. Complex partial SE is less uniform. Most reported cases have returned to baseline neurologic function, but seve ral well-described patients have had prolonged memory deficits. The signifi cance of other deficits is difficult to interpret in light of concomitant v ascular and other diseases causing neurologic dysfunction. Clinical series usually lack premorbid neurologic and neuropsychologic assessment. The few exceptions are complicated by preexisting mental retardation and other defi cits, by the coexistence of progressive illness, by the later effects of re current seizures, and almost always by the confounding influence of anticon vulsant medications. Most morbidity appears attributable to the underlying illnesses rather than to the NCSE itself. It is possible that relatively in frequent cases of prolonged NCSE or those with the synergistic effect of co ncomitant systemic illness, focal lesions, or very rapid excitatory epilept iform discharges may suffer more long-lasting damage, but these observation s are still preliminary. NCSE should be treated expeditiously because of th e acute neurologic impairment of the patients, because of the attendant mor bidity including physical injury, and because it may go on to generalized c onvulsions. There is reasonable concern about possible long-term effects, b ut permanent neurologic damage from NCSE has not yet been established as a mandate for urgent treatment.