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A Comparison With Rates in Unipolar Depression and in Normal Controls

Lewis R. Baxter, Jr, MD; Michael E. Phelps, PhD; John C. Mazziotta, MD, PhD; Barry H. Guze, MD; Jeffrey M. Schwartz, MD; Carl E. Selin, MS

Arch Gen Psychiatry. 1987;44(3):211-218.

Abstract
• We studied 14 patients with obsessive-compulsive disorder (OCD) by positron emission tomography and the fluorodeoxyglucose method, looking for abnormalities in local cerebral metabolic rates for glucose in brain structures that have been hypothesized to function abnormally in OCD.These patients were compared with 14 normal controls and 14 patients with unipolar depression. The patients with unipolar depression and OCD did not differ in levels of anxiety, tension, or depression. In OCD, metabolic rates were significantly increased in the left orbital gyrus and bilaterally in the caudate nuclei. This was apparent on all statistical comparisons with both controls and unipolar depression. The right orbital gyrus showed at least a trend to an increased metabolic rate in all comparisons. The metabolic rate in the left orbital gyrus, relative to that in the ipsilateral hemisphere (orbital gyrus/ hemisphere ratio), was significantly elevated compared to controls and subjects with unipolar depression, and stayed high even with successful drug treatment. Though it was in the normal range in the morbid state, with improvement in OCD symptoms after drug treatment, the caudate/hemisphere metabolic ratio increased uniformly and significantly bilaterally. This ratio did not increase in patients who did not respond to treatment. Thus, OCD showed cerebral glucose metabolic patterns that differed from controls in both the symptomatic and recovered states.

Author Affiliations
From the Division of Biophysics and Nuclear Medicine, Department of Radiological Sciences (Drs Baxter, Phelps, Mazziotta, and Guze and Mr Selin), Department of Psychiatry and Biobehavioral Sciences (Drs Baxter, Guze, and Schwartz), and Department of Neurology (Dr Mazziotta), UCLA School of Medicine.

Footnotes
Accepted for publication Oct 14, 1986.

Presented in part at the Annual Meeting of the American College of Neuropsychopharmacology, Kaanapali, Maui, Hawaii, Dec 12, 1985.

Reprint requests to UCLA Neuropsychiatric Institute, 760 Westwood Plaza, Los Angeles, CA 90024 (Dr Baxter).

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