MRI abnormalities in tardive dyskinesia

• Published in: Psychiatry research 1991-11, Vol.40 (3), p.157-166
• Main Authors: Mion, Carmen C., Andreasen, Nancy C., Arndt, Stephan, Swayze, Victor W., Cohen, Gregg A.
• Format: Article
• Language: English
• Subjects: Adult; Antipsychotic Agents - adverse effects; Antipsychotic Agents - therapeutic use; Basal Ganglia - drug effects; Basal Ganglia - pathology; Biological and medical sciences; Caudate Nucleus - drug effects; Caudate Nucleus - pathology; Chronic Disease; Drug toxicity and drugs side effects treatment; Dyskinesia, Drug-Induced - pathology; Female; Globus Pallidus - drug effects; Globus Pallidus - pathology; Humans; Magnetic Resonance Imaging; Male; Medical sciences; Middle Aged; Neurologic Examination; Pharmacology. Drug treatments; Putamen - drug effects; Putamen - pathology; Schizophrenia - drug therapy; Schizophrenia - pathology; Schizophrenic Psychology; striatum; Tardive dyskinesia; Toxicity: nervous system and muscle
• ISSN: 0925-4927; 0165-1781; 1872-7506; 1872-7123
• DOI: 10.1016/0925-4927(91)90007-D

Most investigators studying tardive dyskinesia (TD) hypothesize that 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 designed to detect possible neuropathological abnormalities in 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 used to measure the volumes of the caudate, putamen, globus pallidus, lateral ventricle, and intracranium. The volumes of the caudate nuclei of the patients with TD were significantly smaller than the volumes of the caudate nuclei of the patients 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 neuroleptic use. Further studies are necessary to confirm our findings and to determine the pathophysiologic nature of these structural alterations and the role played by neuroleptics, whether primary or secondary.