In view of the inconclusive and conflicting reports on the neuropathology of tardive dyskinesia, the authors performed a CT scan study of patients with severe, long lasting dyskinesia and of a matched control group. They sought answers to two questions: First, is there caudate atrophy in tardive dyskinesia, similar to that in Huntington's chorea? This seemed likely because of several phenomenologic and pharmacologic similarities between the two conditions. Second, does brain damage predispose to tardive dyskinesia? If it did, one might find more evidence of structural abnormalities in patients with dyskinesia compared with controls matched for age and especially for length of neuroleptic treatment. The bifrontal bicaudate ratio was significantly smaller in Huntington's chorea patients than in subjects with tardive dyskinesia. A small bifrontal bicaudate ratio indicates caudate atrophy. There were no significant differences between CT scans of dyskinesia patients and those of matched psychiatric controls on any of the variables studied. In each group, CT scans of patients receiving either no neuroleptics or less than 100 mg/day of chlorpromazine equivalents did not differ significantly from those of patients who were receiving more than 100 mg/day of chlorpromazine equivalents.
ASJC Scopus subject areas
- Psychiatry and Mental health