Metronidazole-Induced Encephalopathy with Thiamine Deficiency

Metronidazole-induced encephalopathy (MIE) can be caused by excessive dose or prolonged metronidazole administration. The signal abnormalities in the cerebellar dentate nuclei, midbrain, dorsal pons and corpus callosum on magnetic resonance imaging are considered as the characteristic feature of MIE. Although the mechanism of MIE remains to be elucidated, various hypothesis have been proposed including the role of metronidazole as a thiamine antagonist. Here we report a 58-year-old woman with MIE who coincidentally presented with thiamine deficiency.

A Case of Juvenile Onset Lennox-Gastaut Syndrome Presenting as Atypical Absence / 대한간질학회지

Atypical absence is less understood than typical absence. Several conditions that produce atypical absence are known including Lennox-Gastaut syndrome, myoclonic astatic epilpsy and epileptic encephalopathy with continuous spike and waves in slow wave sleep. A 17-year-old girl with mental retardation had developed frequent loss of consciousness and occasional falling attack with traumatic facial injury for 2 years. The interictal EEG showed 2 Hz slow spike-and-wave complex with maximum over right frontotemporal area and the brain MRI was normal. Carbamazepin was prescribed initially but the drug seemed to worsen the seizures. Long term video-EEG monitoring showed very frequent atypical absence seizures consisting of sudden hypotonia of head and oral automatism with or without secondary generalization. Generalized 2 to 2.5 Hz slow spike-and-wave complexes with duration of 10 to 40 seconds were seen during ictal period. About 10% to 20% of the non REM sleep was occupied with generalized slow spike-and-wave complex and/or polyspikes or polyspikes-and-wave complex with duration of within 1 second. Valprorate monotherapy had failed, then lamotrigin was added. In spite of polytherapy, the seizure was intractable. We think this intractable atypical absence might be associated with juvenile onset Lennox-Gastaut syndrome.