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

被引:47
作者
Nebes, RD
Reynolds, CF
Boada, F
Meltzer, CC
Fukui, MB
Saxton, J
Halligan, EM
DeKosky, ST
机构
[1] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA
[2] Univ Pittsburgh, Sch Med, Dept Radiol, Pittsburgh, PA USA
[3] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA USA
关键词
late-onset depression; vascular depression; white matter hyperintensities;
D O I
10.1002/gps.635
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
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 (C) 2002 John Wiley Sons, Ltd.
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页码:526 / 530
页数:5
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