4.2 Article

Stroke lesion in cortical neural circuits and post-stroke incidence of major depressive episode: A 4-month prospective study

Journal

WORLD JOURNAL OF BIOLOGICAL PSYCHIATRY
Volume 12, Issue 7, Pages 539-548

Publisher

TAYLOR & FRANCIS LTD
DOI: 10.3109/15622975.2011.562242

Keywords

Cingulate gyrus; depression disorder; magnetic resonance imaging; prefrontal cortex; stroke

Categories

Funding

  1. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES) Foundation
  2. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
  3. Aspect Medical Systems
  4. Forest Laboratories
  5. Janssen Pharmaceutica

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Objective. Little is known about the relevance of lesion in neural circuits reported to be associated with major depressive disorder. We investigated the association between lesion stroke size in the limbic-cortical-striatal-pallidal-thalamic (LCSPT) circuit and incidence of major depressive episode (MDE). Methods. We enrolled 68 patients with first-ever ischemic stroke and no history of major depressive disorder. Neurological and psychiatric examinations were performed at three time-points. We diagnosed major depressive episode, following DSM-IV criteria. Lesion location and volume were determined with magnetic resonance imaging, using a semi-automated method based on the Brodmann Cytoarchitectonic Atlas. Results. Twenty-one patients (31%) experienced major depressive episode. Larger lesions in the left cortical regions of the LCSPT circuit (3,760 vs. 660 mm(3); P = 0.004) were associated with higher incidence of MDE. Secondary analyses revealed that major depressive episode was associated with larger lesions in areas of the medial prefrontal cortex including the ventral (BA24) and dorsal anterior cingulate cortex (BA32) and subgenual cortex (BA25); and also the subiculum (BA28/36) and amygdala (BA34). Conclusions Our findings indicate that depression due to stroke is aetiologically related to the disruption of the left LCSPT circuit and support the relevance of the medial prefrontal cortex dysfunction in the pathophysiology of depression.

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