Longitudinal increase in the volume of white matter hyperintensities in late-onset depression

Background Cerebrovascular disease is thought to play a role in the pathogenesis of geriatric major depression. One finding supporting such a ‘vascular depression’ is the increased neuropathology in the form of white matter hyperintensities (WMH) found in patients diagnosed with a late‐onset depress...

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Bibliographic Details
Published in:International journal of geriatric psychiatry 2002-06, Vol.17 (6), p.526-530
Main Authors: Nebes, Robert D., Reynolds III, Charles F., Boada, Fernando, Meltzer, Carolyn C., Fukui, Melanie B., Saxton, Judith, Halligan, Edythe M., DeKosky, Steven T.
Format: Article
Language:English
Subjects:
Adult and adolescent clinical studies
Age of Onset
Aged
Biological and medical sciences
Case-Control Studies
Cerebral Cortex - blood supply
Cerebral Cortex - pathology
Cerebrovascular Disorders - complications
Cognition Disorders - physiopathology
Depression
Depressive Disorder - etiology
Depressive Disorder - physiopathology
Geriatrics
Humans
late-onset depression
Longitudinal Studies
Magnetic Resonance Imaging
Male
Medical sciences
Mental Status Schedule
Mood disorders
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
vascular depression
white matter hyperintensities
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Summary:Background Cerebrovascular disease is thought to play a role in the pathogenesis of geriatric major depression. One finding supporting such a ‘vascular depression’ is the increased neuropathology in the form of white matter hyperintensities (WMH) found in patients diagnosed with a late‐onset depression. However, at present there is little evidence that a longitudinal increase in WMH burden within an individual is associated with the onset of a late‐life depression. Methods This study examined three‐year longitudinal change in WMH volume and in cognition in: (a) an older man who developed his first episode of major depression during the study period, and (b) a comparison group of twelve older individuals who remained depression free. All subjects received at baseline and three years later a structural magnetic resonance imaging (MRI) using fast‐FLAIR technology. The images were analyzed with semi‐automated computerized software to obtain WMH volumes. Subjects also received at both time points the Mini Mental State Exam (MMSE) as well a series of cognitive tasks assessing executive abilities (verbal fluency, Trail Making Test and Stroop test) since executive dysfunction is thought to be characteristic of a vascular depression. Results The individual who became depressed during the followup showed an increase in WMH volume that exceeded the 95% Confidence Intervals (CI) for change in the comparison group. This individual also showed a similar decline on the measures of executive function but not on the MMSE. Conclusions These results are consistent with cerebrovascular disease being a factor in the pathogenesis of late‐onset depression (i.e. ‘vascular depression’). Copyright © 2002 John Wiley & Sons, Ltd.
ISSN:0885-6230
1099-1166
DOI:10.1002/gps.635