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Monte S. Buchsbaum, MD; Lynn E. DeLisi, MD; Henry H. Holcomb, MD; John Cappelletti; Anna Catherine King; Jeannette Johnson, PhD; Erin Hazlett; Susan Dowling-Zimmerman; Robert M. Post, MD; John Morihisa, MD; William Carpenter, MD; Robert Cohen, MD, PhD; David Pickar, MD; Daniel R. Weinberger, MD; Richard Margolin, MD; Robert M. Kessler, MD

Arch Gen Psychiatry. 1984;41(12):1159-1166.

Abstract
• Local cerebral uptake of deoxyglucose labeled with fluorine 18 was measured by positron emission tomography in 16 patients with schizophrenia and 11 patients with affective disorder. Patients received no medication a minimum of 14 days and an average of 39.8 days. The subjects were administered the deoxyglucose 18F just before receiving a 34-minute 1/s series of unpleasant electrical stimuli to the right forearm while resting with eyes closed in a darkened, acoustically attenuated psychophysiologic testing chamber. Following monitored stimulation in the controlled environment, subjects were scanned and images converted to values of glucose use in micromoles per 100 g per minute according to Sokoloff's model. Data were analyzed with a four-way analysis of variance (ANOVA) with independent groups (normals, schizophrenics, and affectives) and repeated measures for slice level (supraventricular, midventricular, and infraventricular), hemisphere (right, left), and anteroposterior position (four sectors). Both normal subjects and patients showed a significant anteroposterior gradient in glucose use with highest values in the frontmost sector. Patients both with schizophrenia and with affective illness showed less of an anteroposterior gradient especially at superior levels, which was statistically confirmed by ANOVA. Absolute glucose levels in patients, which were actually higher in posterior regions rather than lower in frontal regions, were the largest contributors to the effect. Neither group differences in whole brain glucose use nor left-right asymmetries reached statistical significance. These results are consistent with our earlier reports of a relative hypofrontal function in schizophrenia compared with controls. This report extends this finding to affective illness, sharing a lack of diagnostic specificity with many biologic measures.

Author Affiliations
From the Department of Psychiatry (Dr Buchsbaum and Ms Hazlett), University of California, Irvine; the Laboratory of Psychology and Psychopathology (Drs DeLisi, Holcomb, Johnson, and Cohen, Mr Cappelletti, and Mss King and Dowling-Zimmerman), the Biological Psychiatry Branch (Dr Post), the Section on Clinical Neuropsychiatry and Neurobehavior (Drs Morihisa and Weinberger), and the Division of Clinical and Behavioral Research (Dr Pickar), National Institute of Mental Health, and the Nuclear Medicine Department, Clinical Center (Drs Margolin and Kessler), National Institutes of Health, Bethesda, Md; and Maryland Psychiatric Research Center (Dr Carpenter), University of Maryland, Baltimore.

Footnotes
Accepted for publication Jan 30, 1984.

Reprint requests to Department of Psychiatry, University of California, Irvine, CA 92717 (Dr Buchsbaum).

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