Why the study?
Post-stroke depression worsens rehabilitation effectiveness, reduces treatment efficacy for concomitant diseases, and increases mortality, yet comprehensive understanding of its etiology, genetics, pathogenesis, and overlap with post-stroke anxiety remains critical.
Key points are not available for this paper at this time.
Design
Literature review
May inform biomarker-guided risk stratification in post-stroke depression; leaves open causal validation and therapeutic targeting.
Disability after store is caused not only by motor, speech, and other focal neurological symptoms but also by neuropsychiatric disorders. Post-stroke depression (PSD) complicates the effectiveness of rehabilitation measures, reduces the efficacy of treatment for concomitant diseases, exacerbates and increases mortality. This article reviews contemporary perspectives on the prevalence, etiology, pathogenesis, and genetics of post-stroke depression based on scientific literature. The pathogenesis of depression is significantly influenced by the metabolism of biogenic amines, thus particular attention is paid to genetic factors of serotonin metabolism disorders and its role in the development of ADD. Pro-inflammatory cytokines are considered as potential markers of high risk for depression development. Literature on post-stroke anxiety (PSA) is scarce, especially regarding the combination of PSA and PSD. However, the presence of anxiety in patients with PSD prolongs its duration, increases its severity, and significantly reduces the effectiveness of rehabilitation measures.
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Shishigin et al. (2025) studied this question.
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