Summary:There is some evidence that long-term phenytoin (PHT) use may occasionaly give rise to irreversible cerebellar atrophy, but it is unclear whether such changes can occur after acute PHT intoxication. We describe a 38-year-old patient with accidental acute PHT overdose who developed severe cerebellar atrophy. This case provides evidence that acute PHT intoxication can, on rare occasions, result in irreversible cerebellar degeneration. Key Words: Cerebellar atrophy-Acute PHT intoxication.Acute phenytoin (PHT) intoxication gives rise to a cerebellar syndrome that is most often reversible; residual cerebellar atrophy is unusual, but a few case reports have suggested the possibility of such sequelae (1-3). We describe a patient with epilepsy in whom encephalopathy and cerebellar ataxia with severe cerebellar atrophy developed after accidental acute PHT overdose.
CASE REPORTA 38-year-old man was admitted to our hospital with delirium and ataxia. He had tonic-clonic seizures for 10 years, well controlled with PHT (300 mg/day). One month before admission, he had two generalized convulsions for which he was advised to double the dose of PHT for 1 day. After this, he had diplopia and mild ataxia. Investigations including CSF and computed tomographic (CT) scan of the brain were normal, and as the ataxia persisted, a diagnosis of viral cerebellitis was considered. He was admitted to a local hospital where he was given injectable methylprednisolone, and PHT was continued at 300 mg/day. Inadvertently, the patient's relatives continued to give him the dose of medication previously prescribed. As a result, he received 600 mg/ day of PHT for 2-3 weeks. The ataxia worsened, and he became confused and agitated. On admisssion to our hospital, he was frankly encephalopathic and incontinent of urine. He had severe ataxia with brisk reflexes and extensor plantars; vital parameters were well maintained. Serum PHT level on admission was 83.5 pg/ml (therapeutic range, 10-20 pg/ml). Blood investigations including serum electrolytes and renal-and liver-function tests were normal. Human immunodeficiency virus (HIV) antibodies were absent. Chest radiograph, ECG, and CSF examinations also were normal. A magnetic resonance (MR) scan of the brain showed mild generalized atrophic changes in the cerebrum and cerebellum (Fig. 1 A, B). EEG on admission showed marked bilateral slow waves with loss of normal alpha activity.With supportive treatment, the patient gradually improved. On discharge, after a month's stay in the hospital, cognition had markedly improved, but there continued to be slight impairment in memory and calculation. Speech was dysarthric, and severe ataxia persisted. Motor and sensory examinations were normal, but plantars were bilaterally extensor.A repeated EEG 6 months after discharge was normal. A repeated MR scan showed unchanged mild cerebral atrophy, but the degree of cerebellar atrophy was now severe (Fig. 2A, B). Clinical assessment 3 months later showed near-normal cognitive functions, but dysarthria and gross ataxi...
