Cornell Study of Geriatric Depression Opens Door for Further Research on Treatment and Prevention

Feb 2, 1998

NEW YORK

A new hypothesis linking cerebrovascular disease to the onset of depression—referred to as "vascular depression"—in elderly patients provides impetus for the further study of the treatment and mechanisms of depression.

Dr. George Alexopoulos, the primary author in this work, is Director of the Cornell Institute of Geriatric Psychiatry at Cornell University Medical College. The article, which was published on October 15, 1997 in the Archives of General Psychiatry, cites studies that conclude that cerebrovascular disease is more likely to be present in patients with depression than non-depressive patients. According to papers published in the American Journal of Psychiatry (1983 and 1993) and the American Journal of Cardiology (1987), depression is highly prevalent in patients with hypertension, coronary artery disease and dementia brought on by vascular disease. At a National Institute of Mental Health (NIMH) conference in 1996, it was reported that 43% of patients undergoing coronary bypass surgery have significant depressive symptoms prior to surgery and 68% have these symptoms after surgery.

Lesions at the brain's deep white matter, the thalamus and basal ganglia, frequently occur in geriatric depression. Stroke often results in depression. Patients with late-onset depression (65 years and older) often have a "silent stroke," which shows no neurological signs.

Most depressed patients with "silent stroke" have lesions in one of two areas of the brain, either in the perforating arteries territory (49%) or both cortical and perforating artery areas (27%). Similarly, white matter lesions of elderly depression patients are most prominent in subcortical and frontal areas of the brain. Lesions that interfere with frontal lobe function may promote depression since the frontal lobe of the brain integrates sensory, emotional and neuroendocrine functions that are often impaired in depression.

According to Dr. Alexopoulos, all of these observations would suggest the need for further testing to ascertain whether (1) small strategically located lesions may precipitate vascular depression and (2) accumulation of lesions exceeding a threshold predispose to depression. The "vascular depression" hypothesis provides the theoretical background for treatment studies that may revolutionize the treatment and prevention of geriatric depression.

Guided by the "vascular depression" hypothesis, further studies are needed to investigate whether (1) drugs used in prevention and treatment of cerebrovascular disease reduce the risk for depression in patients with vascular risk factors or reduce impairment due to vascular depression, and (2) antidepressants known to promote neurological recovery after a vascular brain lesion are the most effective long-term treatment for vascular depression.

Drs. Barnett S. Meyers, Robert C. Young, Scott Campbell and David Silbersweig of the Department of Psychiatry; and Dr. Mary Charlson of the Department of Medicine contributed to this study.

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