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

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Title: Longitudinal increase in the volume of white matter hyperintensities in late-onset depression.
Authors: Nebes, Robert D., Reynolds III, Charles F., Boada, Fernando, Meltzer, Carolyn C., Fukui, Melanie B., Saxton, Judith, Halligan, Edythe M., DeKosky, Steven T.
Source: International Journal of Geriatric Psychiatry. Jun2002, Vol. 17 Issue 6, p526-530. 5p. 1 Chart.
Subjects: Mental depression, Etiology of diseases, Cerebrovascular disease, Neurological disorders, Magnetic resonance imaging
Abstract: 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. [ABSTRACT FROM AUTHOR]
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Database: Psychology and Behavioral Sciences Collection
Description
Abstract: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. [ABSTRACT FROM AUTHOR]
ISSN:08856230
DOI:10.1002/gps.635