183.Prediction and Pathophysiology of Poststroke Depression

Article type: Letter to the Editor
Article title: Prediction and Pathophysiology of Poststroke Depression

Journal: Journal of Marine Medical Society
Year: 2025
Authors: Jamir Pitton Rissardo, Ana Letícia Fornari Caprara
E-mail: jamirrissardo@gmail.com

ABSTRACT
Poststroke depression is the most common noncognitive neuropsychiatric complication after stroke, affecting approximately 33% (95% confidence interval [CI]: 29%–36%) of stroke survivors. The Diagnostic Statistical Manual of Mental Disorders-5 lists poststroke depression as a depressive disorder due to an underlying medical condition, explaining that the pathophysiology of poststroke depression is a consequence of another disease. Interestingly, the pathophysiology of poststroke depression involves five main hypotheses: lesion location, decreased neurogenesis, immune dysfunction, neurotransmitter dysfunction, and increased cortisol levels. It is worth mentioning that a previous history or a family history of any neuropsychiatric disorder could influence the etiology of depression after a stroke. Herein, we would like to discuss the current literature on poststroke depression.
Keywords: post-stroke depression, homocysteine, c-reactive protein, inflammation, neurogenesis.

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DOI
10.4103/jmms.jmms_8_24

Citation
Rissardo JP, Caprara AL. Prediction and pathophysiology of poststroke depression. J Mar Med Soc 2025;27:111-2.
Figure 1. Pathophysiology of poststroke depression. ACTH: Adrenocor ticotropic hormone, BDNF: Brain-derived neurotrophic factor, HPA: Hypothalamic-pituitary-adrenocortical, IFN: Interferon, IL: Interleukin, NT: Neurotransmitter, TNF: Tumor necrosis factor, VEGF: Vascular endothelial growth factor.