Burst Suppression Pattern on Electroencephalogram Secondary to Valproic Acid-Induced Hyperammonemic Encephalopathy.

BACKGROUND: Valproic acid may induce hyperammonemic encephalopathy. Various electroencephalogram (EEG) abnormalities have been documented in association with this condition, but not burst suppression, an abnormal EEG pattern that is associated with severe encephalopathy. METHODS: Serial EEGs, clinical observations, and laboratory findings were analyzed. PATIENT DESCRIPTION: This 13-year-old girl with autism and intractable epilepsy experienced increased seizures; her valproic acid dose was increased and other antiepileptic drugs were administered. She became lethargic, and her EEG showed a burst suppression pattern. Her ammonia concentration was increased to 101 µmol/L and her valproic acid level was increased to 269.9 mg/L. Valproic acid was discontinued and carnitine was administered. Subsequently she became more alert, her ammonia concentration decreased, and her EEG changed from a burst suppression pattern to a continuous pattern. Within three days, she was back to her baseline level of functioning. CONCLUSIONS: Valproic acid-induced hyperammonemic encephalopathy can produce a burst suppression EEG patternin the patient's.

Extensive apoptosis in a case of intractable infantile status epilepticus.

A previously healthy 8 1/2-month-old girl underwent epilepsy surgery for intractable focal seizures with secondary generalization that progressed to status epilepticus. The major neuropathologic finding was extensive apoptosis. Investigations did not reveal any etiology for the apoptosis or the seizures. This is the first report of apoptosis, without necrosis, in association with intractable status epilepticus in the developing human brain. The findings suggest that new treatment strategies targeted to prevent apoptosis may be useful in children with prolonged status epilepticus.