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Intoxication with various psychotropic agents, including lithium, tricyclics, and neuroleptics, may occasionally mimic aspects of Creutzfeldt–Jakob disease (CJD). Here we describe a case of chronic carbamazepine toxicity exhibiting virtually all clinical, EEG, and biologic features of typical sporadic CJD.
Case report.
A 71-year-old patient, treated for high blood pressure, myocardial infarct, and chronic atrial fibrillation, developed a left trigeminal neuralgia which, after being initially responsive to low doses of carbamazepine, became rapidly refractory despite dosage of 1,200 mg daily. Alcohol infiltration of Gasser’s ganglion produced only marginal and transient benefit. Four months after carbamazepine initiation, he developed a progressive cognitive decline characterized by memory deficits, confusion, psychomotor slowness, hypersomnia, dysphasia, and postural instability with falls. All symptoms evolved at a rapid pace into severe abulia and dependency in most activities of daily living. On neurologic examination, he was disoriented and exhibited marked generalized bradykinesia, hypomimia, rigidity with cogwheeling, and bilateral and synchronous myoclonus on a background of a low amplitude postural …
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