We report data from 346 admissions for generalized tonic-clonic convulsive status epilepticus (GC-SE); 68% had had epilepsy previously. Outcome was determined by underlying cause, SE duration of > 4 h, the presence of more than one medical complication, and the quality of therapy and management. Clonazepam (CZP), diazepam (DZP), and phenytoin (PHT) were most frequently used for treatment.

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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.

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Vigabatrin (gamma-vinyl-GABA or GVG) is an irreversible inhibitor of gamma-aminobutyric acid transaminase (GABA-T), which is an enzyme responsible for gamma-aminobutyric acid (GABA) catabolism. Inhibition of GABA catabolism increases brain concentration of GABA, a neural inhibitor. GVG has been found to be a potent new anti-epileptic drug, especially in the treatment of refractory epilepsy, in particular of complex partial seizures. Three patients who developed a severe status epilepitus while on GVG treatment are reported. A possible proconvulsive effect of GVG is hypothesized, which might result from disinhibition in the nigro-collicular pathway due to increased GABA-levels.