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Roger Kurlan, MD; Eric Caine, MD; Allen Rubin, MD; Charles B. Nemeroff, MD, PhD; Garth Bissette, PhD; Robert Zaczek, PhD; Joseph Coyle, MD; Fred J. Spielman, MD; Carrie Irvine; Ira Shoulson, MD

Arch Neurol. 1988;45(8):881-883.

Abstract
• Patients with Huntington's disease (HD) commonly have concomitant depressive disorders. Prompted by reports of elevated corticotropin releasing factor (CRF) and reduced 5-hydroxyindoleacetic acid (5-HIAA) concentrations in lumbar cerebrospinal fluid (CSF) of patients with major depression, these CSF constituents were examined in 56 nonmedicated patients who were in the early stages of HD. Elevated CRF concentrations were found in patients with HD in comparison with a control group of 21 subjects without neurologic illness. The CSF 5-HIAA concentrations in patients with HD did not differ from that in four normal volunteers. Patients with HD who had depressive disorders (major depression or dysthymia) did not differ from those without depression with respect to CSF 5-HIAA or CRF concentration. However, a positive correlation was observed between severity of major depression and CRF concentration. These findings suggest that the depression associated with HD may differ neurochemically from that seen in other major depressive disorders, and support the notion that clinically significant depressive symptoms reflect heterogeneous pathophysiologic conditions with different neurochemical correlates.

Author Affiliations
From the Departments of Neurology (Drs Kurlan, Caine, Rubin, and Shoulson and Ms Irvine) and Psychiatry (Drs Caine and Rubin), University of Rochester (NY) School of Medicine and Dentistry; the Departments of Psychiatry and Pharmacology and Center for Aging and Human Development, Duke University Medical Center, Durham, NC (Drs Nemeroff and Bissette); the Department of Child Psychiatry, The Johns Hopkins University School of Medicine, Baltimore (Drs Zaczek and Coyle); and the Department of Anesthesiology, University of North Carolina, Chapel Hill (Dr Spielman).

Footnotes
Accepted for publication April 4, 1988.

Reprint requests to Department of Neurology, Box 673, University of Rochester School of Medicine, 601 Elmwood Ave, Rochester, NY 14642 (Dr Kurlan).

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