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Published on: May 19, 2015
A controlled study of MRI signal hyperintensities in older depressed patients with and without hypertension
B S Greenwald1, E Kramer-Ginsberg, K R Krishnan
1Department of Psychiatry, Long Island Jewish Medical Center, Glen Oaks, New York 11004, USA.
Objectives:
To compare the frequency/severity of signal hyperintensities--likely markers of cerebrovascular disease--in the subcortical gray and deep white matter on magnetic resonance imaging (MRI) scans of brains of hypertensive and normotensive older depressed and nondepressed comparison subjects.
Design:
Between-groups comparison of cross-sectional MRI data employing analyses of covariance controlling for the effects of age, gender, and height.
Setting:
A comprehensive inpatient-outpatient geriatric psychiatry service in a university hospital.
Participants:
Nondemented older depressed (n = 81) and nondepressed comparison (n = 70) subjects divided into four groups (hypertensive depressed (n = 40), hypertensive normals (n = 21), normotensive depressed (n = 41), normotensive normals (n = 49)).
Measurements:
Signal hyperintensities were rated on T-2 weighted MRI scans blind to patient diagnoses employing two standardized hyperintensity rating systems (Fazekas, Boyko).
Results:
Hypertensive depressives had significantly more- severe hyperintensity ratings in both subcortical gray and deep white matter than did normotensive depressives and controls (P < .05) and significantly more-severe hyperintensity ratings only in subcortical gray matter (P < .05) than did hypertensive controls. Hypertensive controls had significantly more-severe ratings in deep white matter than either normotensive group (P < .05).
Conclusions:
Findings suggest a relationship between deep white matter hyperintensities and hypertension (regardless of depressive state), and a particular role of subcortical gray matter hyperintensities (possibly interacting with more-severe deep white matter lesions) in older depressed hypertensives, as compared with older depressed normotensives of similar ages and severity of depression. These data support possible heterogeneous pathogenic contributions in late-life depression subgroups, one of which appears to be influenced by cerebrovascular disease.
