Vol 1 n° 2 - Depression in the Elderly
Past issues Contributors How to publish Contributions and comments Home
 
he National Institutes of Health (NIH) Con- sensus Development Conference noted that depression is one of the most frequent psychiatric disorders of old age, with a prevalence of 1% for major depression, 2% for dysthymia, and 8% to 15% for clinically significant depressive  symptoms.1   Over  50%  of  hospitalized depressed elderly patients are in their first episode.2 Epidemiological studies have shown that the majority of individuals suffering from major depression or dys- thymia have no history of previous psychiatric treat- ment.3 Earlier we suggested that late-onset depression is a het- erogeneous syndrome, which, among others, encom- passes patients with brain disorders that may or may not be clinically evident when the depression first appears.4 Vascular depression: a new view of late-onset depression George S. Alexopoulos, MD; Martha L. Bruce, PhD; David Silbersweig, MD; Balu Kalayam, MD; Emily Stern, MD B a s i c   r e s e a r c h T Address for correspondence and reprints: Prof George S. Alexopoulos, Director Cornell Institute of Geriatric Psychiatry, Weill Medical College of Cornell University, 21 Bloomingdale Road, White Plains, NY 10605, USA
(e-mail: gsalexop@mail.med.cornell.edu) Author affiliations: Weill Medical College of Cornell University, White Plains, NY, USA. Professor of Psychiatry, Director Cornell Institute of Geriatric Psychiatry (George S. Alexopoulos); Associate Professor of Sociology in Psychiatry (Martha L. Bruce); Associate Professor of Psychiatry and Neurology (David Silbersweig); Associate Professor of Clinical Psychiatry (Balu Kalayam) Keywords: vascular depression; treatment resistance; recovery from ischemia; disability 6 8 We have suggested that cerebrovascular disease may predispose, precipitate, or perpetuate some late-life depressive syndromes. The mechanisms of “vascular depression” include disruption of cortico-striato-pal- lido-thalamo-cortical (CSPTC) pathways or their modulating systems. This view is supported by the pre- sentation of vascular depression, which consists of depressive symptoms, cognitive abnormalities, as well as neuroimaging findings that may result from CSPTC impairment. Moreover, clinical and electrophysio- logical evidence of CSPTC impairment, an abnormality frequently found in patients with vascular depres- sion, appears to be associated with poor response to antidepressant treatment and early relapse and recur- rence. The vascular depression hypothesis provides the conceptual background for studies that may have clinical and theoretical impact. Agents influencing dopamine, acetylcholine, and opioid neurotransmit- ters may be studied in vascular depression, since these are essential neurotransmitters of the frontostri- atal circuitry. Drugs used for prevention and treatment of cerebrovascular disease may be shown to reduce the risk for vascular depression or improve its outcomes. The choice of antidepressants in vascular depres- sion may depend on their effect on neurological recovery from ischemic lesions. Finally, identification of specific relationships between specific symptoms, cognitive deficits, and disability may lead to interven- tions that target the patients’ deficits as well as their interactions with psychosocial factors known to con- tribute to depression. Research can clarify the pathways to vascular depression by focusing on the site of lesion, the resultant brain dysfunction, the presentation of depression and time of onset, and the contri- bution of nonbiological factors. George S. ALEXOPOULOS