Introduction

Generalized convulsive status epilepticus (GCSE) is a medical emergency that causes brain injury in hippocampus, cerebellum, and cortex, even in paralyzed and mechanically ventilated animals (8, 10, 12, 21, 23). However, human studies of SE are limited and select for the most severe cases, which are frequently plagued by confounding variables, especially previous epilepsy, acute neurologic insults, hypoxia, and hypotension (8). The true degree of brain injury in human survivors of SE is poorly understood. With the decline in mortality from SE to 3%, there is increased emphasis on the neurologic sequelae of brain injury in survivors of status (18). Our concern has evolved from how best to stop status to how to minimize the degree of brain injury in survivors. Further, there is a growing consensus that subtypes of status, specifically subclinical and complex partial status, cause brain injury and should be treated earlier and more aggressively (7, 10, 16, 40).

In order to assess brain injury in human survivors of SE, markers of brain injury are needed. Without specific markers of brain injury, the degree of brain injury can only be inferred or estimated. Markers of brain injury could provide an estimate of the degree of brain injury in SE. Markers could define subtypes of SE requiring aggressive intervention, and could serve as an outcome measure for new treatments and interventions. For a marker to be valuable for clinical and experimental use in SE, it should be sensitive and specific for neuronal injury, sensitive to the duration and outcome of status, reliable, and easily measured. Such an in vivo marker could accelerate our understanding of the optimal treatment of SE and its subtypes. Neuron-specific enolase may be one such marker.