No abstract

Abstract-Late-life depression is increasingly viewed as a vascular illness because of patients exhibiting characteristic white matter brain lesions and in vivo large artery endothelial dysfunction. However, the "vascular depression" hypothesis pertains to the microvasculature, and this circulation has not been studied in this context. Our objective was to examine structure and function of small subcutaneous arteries in patients with late-life depression. Thus, 16 patients aged 71.8Ϯ4.0 years with late-life depression were compared with 15 control participants aged 72.1Ϯ5.9 years. There were similar cardiovascular profiles between the 2 groups. All of the participants underwent MRI brain scans and subcutaneous gluteal fat biopsy from which small arteries were isolated and studied using pressure myography. Cerebral microvascular damage in depressed patients was confirmed by assessment of basal ganglia Virchow-Robin space scores (depressed patients 3.9Ϯ1.7 versus controls: 2.5Ϯ1.6; Pϭ0.01). Contractility to norepinephrine was equivalent in both groups, but relaxation of the small arteries to acetylcholine was significantly reduced in depressed patients (84.0Ϯ4.0%) compared with control participants (96.0Ϯ1.4%; Pϭ0.012). This difference in arterial relaxation was reduced but not entirely eliminated when NO synthase was inhibited. Depressed patients also exhibited hypertrophic wall growth with an increase in medial cross-sectional area (Pϭ0.035, multiple ANOVA and wall thickness; Pϭ0.04, multiple ANOVA).In conclusion, despite similar cardiovascular profiles, depressed patients with cerebral microvascular damage show abnormalities of subcutaneous small artery structure and function. (Hypertension. 2010;56:734-740.)

Neuropsychiatric syndromes are common in the setting of cerebrovascular disease. The most frequent psychiatric syndrome after stroke is depression. Emotionalism and apathy after stroke are also frequent and under-detected symptoms. Treatment principles are broadly similar to those currently used to treat non-organically ill patients. The evidence for pharmacological and psychological treatment for depression after stroke is scant, and of variable quality. Currently there is evidence of efficacy for both tricyclic antidepressants and SSRIs in the management of depression but the latter are better tolerated. Randomized controlled trials of antidepressants for post-stroke emotionalism are positive and this is encouraging. The current evidence base for psychological interventions either as first line or augmentative strategies is too limited and inconclusive to permit definite recommendations. Future studies might include multi-modal interventions using the principles of active case management and pharmacological studies which target both specific neuropsychiatric symptoms and underlying cerebrovascular disorder.