Seizure : the journal of the British Epilepsy Association
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The mechanisms underlying the hemiconvulsion-hemiplegia-epilepsy syndrome (HHE) remain unclear. The current proposed pathogenic mechanism is a neuronal injury induced by venous thrombosis and/or hypoxia. Previous abnormalities of the brain were suggested as underlying mechanism. ⋯ The pathological studies suggest that cytotoxic edema is responsible for neuronal damage. In HH syndrome, two mechanisms playing a role in the development of a later epilepsy could suggest delayed cell death induced by cytotoxic edema and/or thalamic dysfunction causing a disruption of thalamo-cortical circuit. In acute presentation, the use of anti-edema therapy should be discussed to prevent the cell injury.
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A retrospective case note study of the aetiology and course of children in convulsive status epilepticus (CSE) admitted to a large paediatric intensive care unit (PICU) was undertaken between January 1999 and April 2004. Status epilepticus was defined as a prolonged (>30 min) tonic-clonic seizure irrespective of whether the seizure had stopped prior to admission to PICU. During this period, 137 (74 male) children aged 1 month to 15 years were admitted to PICU with 147 episodes of status epilepticus. ⋯ No child died. Of the 70 children considered to be previously neurologically and developmentally normal prior to admission, only 1 child demonstrated a new gross neurological abnormality at the time of latest follow-up. Seven patients (5%) developed new or de novo epilepsy.