Phenytoin

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Cerebellar ataxia, hypometabolism, atrophy and cognitive affective syndrome following intoxication: case report A 20-year-old woman developed persistent cerebellar ataxia, bilateral cerebellar hypometabolism and atrophy and cerebellar cognitive affective syndrome following acute intoxication with phenytoin. The woman, presented with slurring of speech, blurred vision, excessive sleep, tremulousness of her upper limbs and imbalance of 6 weeks’ duration. Eight weeks before presentation, she developed right hemiplegia due to a left basal ganglia bleed and started phenytoin 300 mg/day [route not stated] for seizure prophylaxis. On presentation, examination revealed right hemiparesis with right facial palsy, scanning speech, titubation, nystagmus, extrapyramidal features including orofacial dyskinesias and chorea, and severe generalised hypotonia with truncal, gait and limb ataxia. Phenytoin toxicity was suspected, and tests revealed a phenytoin concentration of 55 µg/mL (therapeutic range 10–20 µg/mL). EEG revealed diffuse background slowing. Phenytoin was tapered to withdrawal, and the woman was subsequently more awake and alert. One week after tapering phenytoin, repeat EEG revealed normal background activity. Mental function evaluation revealed cognitive and affective changes, executive dysfunction and deficient abstract thinking and working memory. She was diagnosed with acute cerebellar dysfunction with orofacial dyskinesia and chorea with cerebellar cognitive affective syndrome due to acute phenytoin intoxication. Over 4 weeks of hospitalisation, she had near complete improvement of her right-sided weakness and dyskinesia. Positron emission tomography revealed bilateral cerebellar hypometabolism. Her ataxia and cognitive and affective dysfunction persisted at 6 months’ follow-up, while repeat MRI revealed resolving bleed in left gangliocapsular area with diffuse cerebellar atrophy. Author comment: "We finally hypothesize that acute [phenytoin] intoxication is responsible for persistent severe generalized cerebellar ataxia, cognitive and affective dysfunction along with bilateral cerebellar hypometabolism and atrophy; while diaschisis phenomenon is responsible for additional asymptomatic hypometabolism in right cerebellar hemisphere and left fronto-parietal cortex." Gupta M, et al. Persistent cerebellar ataxia with cerebellar cognitive affective syndrome due to acute phenytoin intoxication: A case report. Neurology Asia 18: 107-111, No. 1, Mar 2013. Available from: URL: http://www.neurology-asia.org/ 803086479 India

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Reactions 11 May 2013 No. 1451