Psychiatry Research: Neuroimaging, 40: IV- 166 Elsevier 157 M R I Abnormalities in TardiveDyskinesia Carmen C. Mion, Nancy C. Andreasen, Stephan Arndt, Victor W. SwayzeII, and Gregg A. Cohen Received August10, 1990; revised version received June 10, 1991; accepted July 13. 1991. zyxwvutsrqpo Abstract. Most investigators studying tardive dyskinesia (TD) hypothesizethat the condition is due to a neurochemical abnormality of the striatum. Recently, numerous CT studies have been done to verify brain abnormalities in patients with TD; the findings have, however, been conflicting. The present study was designedto detect possible neuropathological abnormalitiesin the basal ganglia in a young sample of schizophrenic patients with TD as compared with schizophrenic patients without TD and normal controls. Magnetic resonance imaging (MRI) was usedto measure the volumes of the caudate,putamen,globus pallidus, lateralventricle, and intracranium. The volumes of the caudatenucleiof the patients with TD were significantly smaller than the volumes of the caudate nuclei of thepatients without TD and normal controls. This abnormality in the caudate may be related to some previous condition, which may prove a substrate that is necessary for TD to establish itself in association with neurolepticuse. Further studies are necessary to confirm our findings and to determine the pathophysiologic nature of these structural alterations and the role played by neuroleptics, whetherprimary or secondary. Key Words. Tardive dyskinesia,striatum, magneticresonance imaging. Tardive dyskinesia (TD) is a disordercharacterized predominantly by choreo- athetoid movementsof the bucco-oro-lingual musculature. Although TD is associated with long-term neuroleptic use, its overall prevalence in psychiatric patients on long-term neuroleptic therapy is 20% (Jeste and Wyatt, 1987). Risk factorsthat havebeenidentified for the conditioninclude advanced age, femalegender, and affective disorder.Other possiblerisk factors includebrain damage, length of neuroleptic exposure, use of anticholinergic drugs, drug holidays, and poor schizophrenia outcome (Chouinard et al., 1988; Lohr and Bracha, 1988). For many years investigators have proposed the dopamine supersensitivity hypothesisfor tardive dyskinesia.It is postulatedthat prolongedneuroleptic blockade of striatal dopamine receptors leads to a chemical denervation of neurons and subsequent supersensitivity of postsynaptic neuroreceptors. Supportfor this hypothesis comes from pharmacological lines of evidence (Crane and Naranjo, 1971; Carmen C. Mion, M.D., is Visiting ResearchScientist;Nancy C. Andreasen, M.D., Ph.D., is Professor of Psychiatry; Stephan Amdt, Ph.D., is Associate Research Scientist in Psychiatry; Victor W. Swayze II, M.D., is Associate Professor in Psychiatry; and Gregg A. Cohen, M.S., is Systems Analyst, Department of Psychiatry, University of Iowa College of Medicine, Iowa City, IA. (Reprint requests to Dr. N.C. Andreasen, Dept. of Psychiatry,University of Iowa College of Medicine, 500 Newton Rd., Iowa City, IA 52242, USA.) 01651781/91/%03.50@ 1991 Elsevier Scientific Publishers Ireland Ltd.