Non-convulsive status epilepticus: causes, treatment, and outcome in 65 patients.

Abstract

The incidence of non-convulsive status epilepticus (NCSE) The first description of complex partial status epilepticus (CPSE) was in 1956 by Gastaut.4 The clinical presentation has been described extensively by others.510 NCSE in The Netherlands Our study concerns patients admitted to hospital. We tried to find out how the diagnosis of a particular type of NCSE had been made and we were especially interested in clinical presentation, management, and outcome. Some patients with NCSE will not be diagnosed, or will not be sent to a hospital if the NCSE subsided spontaneously. Others are known to have had previous epilepsy or previous episodes of NCSE and immediate admission to hospital is not always required. MethodsThe population of The Netherlands is about 15 million. The incidence of patients with NCSE in The Netherlands is not known. We asked for the cooperation of neurologists in 50 medical centres in The Netherlands. Fourteen, from all parts of the country, agreed to cooperate, information from two was inadequate. Also two of the three epilepsy centres were included.The study was limited to NCSE in patients over 15 years of age admitted to hospital during 1980-7. Only patients with a minimum seizure duration of 30 minutes were included. Outcome is the condition at discharge from the hospital. Morbidity is all new neurological signs occurring because of the status epilepticus. Therapy was considered insufficient when an insufficient dose had been administered, when the route of administration was wrong (for example, diazepam given intramuscularly), when unnecessary delay was present (for instance waiting for more than one hour after diazepam injection, while seizures continued, before giving a second agent), when mechanical ventilation was not started despite signs of respiratory insufficiency or the presence of various medical complications, or when EEG monitoring was not done in patients treated with antiepileptic drugs together with curarisation.

A Descriptive Analysis of Prognostic Indicators in Patients with Non-Convulsive Status Epilepticus in a Tertiary Hospital Population

“…We've again shown that a history of epilepsy is a favourable prognostic indicator [11,34], as our low mortality rate of 8% in this population compares well with that of 2% -3% found by others [14,35]. In fact, our single death in a patient with a known seizure disorder was clearly not epilepsy-related as it occurred in the context of a cardiac arrest with postanoxic NCSE.…”

“…Yet there have been no large controlled studies of NCSE, with most of the literature centering on small case series [10,11,21,24,28,31,32,35,48,49] and a case control study of 19 elderly [20]. Aside from a single paper assessing morbidity and mortality in 100 patients with NCSE [14], our series is the largest descriptive study of NCSE to date and the only one to systematically correlate NCSE clinical and electrographic variables with functional disability at discharge.…”

Nonconvulsive status epilepticus: a diagnostic and therapeutic challenge in the intensive care setting

“…Owing to the favourable clinical outcome of CPSE itself and the lack of neurological or neuropsychological sequelae [Scholtes et al 1996a;Cockerell et al 1994;Williamson et al 1985], further treatment escalation including iv anaesthetics should be performed reluctantly [Drislane, 2000;Kaplan, 2000]. Aggressive pharmacological treatment seems to have a greater risk concerning morbidity and mortality [Ropper, 2003] than continuing nonconvulsive seizure activity [Kaplan, 1999].…”

Neuronal Sodium Channels in Neurodegeneration and Neuroprotection

“…Na + / Ca 2 + exchanger, leads to a cascade of cellular death The pharmacological basis for achieving neuroprotection mechanisms involving delayed Ca 2 +-mediated apoptotic against ischemic injury with sodium channel blockers is processes of cellular degradation [21]. unresolved but changes in ionic sodium dynamics influencIn this study we have used a model of temporary MCAo ing ischemic injury have been clearly established [36]. and reperfusion to produce brain injury in the rat closely Although the brain only comprises 2% of the total human resembling clinical stroke pathology [28].…”

“…Following MCAo to relieve the excitotoxic effects of cerebral ischemia due surgery, animals were placed in recovery cages with to the membrane stabilizing properties of these compounds ambient temperature maintained at 22 'C. Sham-treated [36]. Most therapeutic sodium channel blocking comanimals received all surgical procedures but the filament pounds are use-dependent and only significantly block was not inserted into the MCA.…”