Longitudinal increase in the volume of white matter hyperintensities in late-onset depression
Article first published online: 28 MAY 2002
Copyright © 2002 John Wiley & Sons, Ltd.
International Journal of Geriatric Psychiatry
Volume 17, Issue 6, pages 526–530, June 2002
How to Cite
Nebes, R. D., Reynolds, C. F., Boada, F., Meltzer, C. C., Fukui, M. B., Saxton, J., Halligan, E. M. and DeKosky, S. T. (2002), Longitudinal increase in the volume of white matter hyperintensities in late-onset depression. Int. J. Geriat. Psychiatry, 17: 526–530. doi: 10.1002/gps.635
- Issue published online: 28 MAY 2002
- Article first published online: 28 MAY 2002
- Manuscript Accepted: 4 DEC 2001
- Manuscript Received: 3 DEC 2001
- National Institute on Aging. Grant Numbers: AG 14051, AG 05133
- National Institute of Mental Health. Grant Numbers: MH 52247, MH 43832, MH 37869
- late-onset depression;
- vascular depression;
- white matter hyperintensities
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.
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.
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.
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.