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Longitudinal increase in the volume of white matter hyperintensities in late‐onset depression
Author(s) -
Nebes Robert D.,
Reynolds Charles F.,
Boada Fernando,
Meltzer Carolyn C.,
Fukui Melanie B.,
Saxton Judith,
Halligan Edythe M.,
DeKosky Steven T.
Publication year - 2002
Publication title -
international journal of geriatric psychiatry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.28
H-Index - 129
eISSN - 1099-1166
pISSN - 0885-6230
DOI - 10.1002/gps.635
Subject(s) - hyperintensity , depression (economics) , stroop effect , psychology , trail making test , cardiology , late life depression , executive dysfunction , leukoaraiosis , neuropathology , longitudinal study , cognitive decline , medicine , cognition , psychiatry , dementia , magnetic resonance imaging , disease , neuropsychology , pathology , radiology , economics , macroeconomics
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.