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Departments of Radiology (Drs. Mayberg and Dannals), Psychiatry (Drs. Mayberg, Starkstein, Peyser, Brandt, and Folstein), Neurology (Dr. Mayberg), and Environmental Health Sciences (Dr. Dannals), The Johns Hopkins Medical Institutions, Baltimore, MD.
We measured regional cerebral glucose metabolism using 2-[18F]-fluoro-2-deoxy-D-glucose and positron emission tomography in depressed and nondepressed patients with early Huntington's disease (HD), compared with appropriately matched controls. Caudate, putamen, and cingulate metabolism was significantly lower in patients with HD than in control subjects, independent of mood state. Orbital frontal-inferior prefrontal cortex hypometabolism, however, differentiated depressed patients from both nondepressed patients and normal controls. These findings implicate selective dysfunction of the paralimbic regions of the frontal lobes in the mood disorder of HD. The metabolic pattern is similar to that in depression associated with Parkinson's disease, suggesting that the integrity of pathways linking paralimbic frontal cortex and the basal ganglia may be integral to the normal regulation of mood.
Supported in part by National Institutes of Health grants NS15080 and NS16375.
Address correspondence and reprint requests to Dr. Helen Mayberg, Research Imaging Center, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78284-6240.
Received October 9, 1991. Accepted for publication in final form February 17, 1992.
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