Abstract and Introduction
Status epilepticus (SE) is a neurologic emergency that require immediate vigorous treatment in order to prevent serious morbidity or even death. Several investigators have suggested that the underlying etiology is the primary determinant of outcome. We believe that this may be true in aggressively treated SE, but not when the treatment is less than optimal. In this article, we will discuss the factors that have been implicated in affecting SE outcomes, and argue, on the basis of both human and experimental animal data, that aggressive treatment is necessary and appropriate for all presentations of SE in order to maximize the probability of a successful outcome even when the etiology suggests a poor prognosis.
Status epilepticus (SE) is a neurologic emergency that, when it presents as repeated generalized convulsions without full recovery of consciousness between convulsions, has been generally thought to require immediate vigorous treatment in order to prevent serious morbidity or even death.[1–5]
Although several studies have investigated and established the first line of treatment, the subsequent treatment steps remain controversial as, to date, there have been no class I studies that have investigated such a treatment. This is in part owing to the difficulty of conducting such trials on human patients. Furthermore, the necessity for urgent treatment in the case of subtle or nonconvulsive SE has been less widely accepted, and some have suggested that the underlying etiology is the primary determinant of outcome. This may be true in aggressively treated SE, but is not necessarily true when treatment is less than optimal. In this article we discuss the role of etiology and other factors on the outcome of generalized convulsive SE, but we argue, on the basis of both human and experimental animal data, that aggressive appropriate treatment for all presentations of SE will maximize the probability of successful outcome even when the etiology suggests a poor prognosis.
SE is defined as a single seizure lasting longer than 30 min or a series of epileptic seizures during which full function is not regained between ictal events. More recently others have suggested that continuous ictal activity without evolution lasting more than 10 min or even 5 min should be considered SE. Thus, any seizure type of sufficient duration or frequency can be considered SE. This allows the use of the International Classification of Epileptic Seizures to classify SE. However, advances in understanding of generalized convulsive SE require that we expand the classification of at least secondarily generalized SE to include overt, subtle and electrical presentations of this type of SE (Box 1).
The occurrence of frequent seizures without fulfilling the criteria for SE in the International Classification of Epileptic Seizures has been described by several authors utilizing different terms, such as seizures cluster, serial seizures or acute repetitive seizures. However, this concept of frequent seizures and its relationship to SE remains controversial. Some authors have suggested that seizure clusters can evolve into SE, or at least create a higher risk for developing convulsive SE, while others observed a decrease in the risk of developing SE after seizure clusters.
Physiologically, SE is a condition where the effects of a single seizure still persist when the next seizure begins or where seizure terminating mechanisms have failed, so that epileptic activity continues longer than the usual seconds-to-minutes duration of single seizures. These two scenarios result in a cumulative effect of seizure-induced pathophysiological changes, with the result that untreated or undertreated SE is a dynamic state. The dynamic nature of generalized convulsive SE, first recognized by Clark and Prout,[15–17] has been again appreciated in the last several decades.[5,18,19] We now recognize that untreated generalized convulsive SE can evolve from repeated overt convulsion without complete recovery of consciousness between the seizures, to more subtle, more-or-less continuous motor twitches of the face, abdomen or extremities, to complete cessation of motor activity even though ictal discharges continue on the EEG. This evolution is hypothesized to be due to an increasingly encephalopathic state that results in attenuation of transmission of messages from the motor cortex down the neuroaxis to the extremities to produce convulsions of the extremities. However, when the brain insult that induces generalized convulsive SE is sufficiently severe to induce an encephalopathic state from the beginning, patients may present in subtle or electrical generalized convulsive SE, without ever exhibiting overt convulsions.
Sometimes the term 'nonconvulsive SE' is used to apply to cases of subtle or electrical generalized convulsive SE. However, the concept of nonconvulsive SE is not well defined. Several investigators agree that nonconvulsive SE can be defined as a prolonged state of impaired consciousness or altered sensorium associated with continuous paroxysmal activity or electrographic discharges on the EEG. However, the term 'nonconvulsive SE' is also used to refer to complex partial SE and also to absence SE, so the terminology in this field is confusing. Furthermore, refractory SE is a term used by several investigators to define SE that has failed to respond to initial treatment (benzodiazepines and phenytoin), but again there is no general agreement regarding a precise definition of this term.
Expert Rev Neurother. 2011;11(12):1747-1758. © 2011 Expert Reviews Ltd.