Epileptic disorders : international epilepsy journal with videotape
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Rare cases of levetiracetam-induced thrombocytopenia have been reported in the literature. We report a case of glioblastoma multiforme and partial epilepsy treated with levetiracetam with subsequent development of thrombocytopenia. After ruling out all other possible causes of a decreased platelet count, we conclude that levetiracetam was the cause of this adverse event.
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Benign convulsions associated with gastroenteritis are now recognized as a clinical entity, characterized by an acute cluster of afebrile seizures during an episode of mild diarrhoea with excellent prognosis. We observed 30 children who each experienced at least two seizures associated with mild gastroenteritis. The inclusion criteria were: afebrile seizures during gastroenteritis, dehydration at ≤ 5%, normal neurological findings, normal psychomotor development and no underlying pathology according to laboratory and neuroimaging studies. ⋯ At the end of follow-up, antiepileptic treatment was withdrawn for all but two patients. None developed epilepsy. Although the pathogenesis of this clinical entity is unknown, we hypothesize that mild gastroenteritis may provoke a transient brain dysfunction which in turn provokes seizures in children with genetically determined susceptibility.
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SCN1A mutations account for a large proportion of Dravet syndrome patients, and are reported in other cases of epilepsy, such as some families with genetic epilepsy with febrile seizures plus (GEFS+). While most Dravet syndrome cases are caused by de novo mutations, 5% inherit a mutation from a mildly affected or symptom-free parent. ⋯ D194N, is transmitted from a mosaic GEFS+ father to a child with Dravet syndrome. Mosaicism may be more common than assumed and should be considered regardless of the nature of the mutation.
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We present a patient with cryptogenic focal epilepsy and another with Dravet syndrome, who experienced seizure aggravation and negative myoclonus, associated with continuous spikes and waves during slow sleep, induced by levetiracetam. For both patients levetiracetam was discontinued, and there was significant improvement of this particular electroclinical picture.
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We describe the case of a 62-year-old man who developed stimulus-induced focal motor seizures after prolonged cardiac arrest. During a video-EEG study, these focal motor seizures progressed into a generalised myoclonic status epilepticus. Both the severely decremented background activity on the EEG, and the absence of median and trigeminal somatosensory evoked potentials were in keeping with a devastating post-hypoxic encephalopathy and the patient died. Our clinical and electrophysiology data suggest that generalised myoclonic status epilepticus may occur in patients in whom the existence of severe cerebral damage prevents a complete development of all phases of classic generalised tonic-clonic seizures.