Abstract
One third of all stroke survivors develop post-stroke depression (PSD). Depressive
symptoms adversely affect rehabilitation and significantly increase risk of death
in the post-stroke period. One of the theoretical views on the determinants of PSD
focuses on psychosocial factors like disability and social support. Others emphasize
biologic mechanisms such as disruption of biogenic amine neurotransmission and release
of proinflammatory cytokines. The “lesion location” perspective attempts to establish
a relationship between localization of stroke and occurrence of depression, but empirical
results remain contradictory. These divergences are partly related to the fact that
neuroimaging methods, unlike neuropathology, are not able to assess precisely the
full extent of stroke-affected areas and do not specify the different types of vascular
lesions. We provide here an overview of the known phenomenological profile and current
pathogenic hypotheses of PSD and present neuropathological data challenging the classic
“single-stroke”-based neuroanatomical model of PSD. We suggest that vascular burden
due to the chronic accumulation of small macrovascular and microvascular lesions may
be a crucial determinant of the development and evolution of PSD.
Keywords
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Publication history
Published online: March 05, 2009
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© 2009 Elsevier B.V. Published by Elsevier Inc. All rights reserved.
