ArticleWorld journal of psychiatry2025
Correlation between anxiety-depression disorders and brain structural connectivity abnormalities after subarachnoid hemorrhage.
Article in World journal of psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Risk Factors for Anxiety or Depression in Patients With Stroke During the Acute and Recovery Phases: An Independent Cohort Study.Actas espanolas de psiquiatria · 2026Article
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5 authors.
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Abstract
backgroundSubarachnoid hemorrhage (SAH) is associated with high incidence of anxiety and depression disorders (27%-54% and 20%-42%, respectively), significantly affecting patient quality of life. However, the pathophysiological mechanisms underlying post-SAH emotional disorders remain poorly understood, limiting targeted therapeutic interventions.
aimTo identify potential biomarkers and therapeutic targets through comprehensive analysis of behavioral, neuroimaging, and inflammatory parameters in a rat SAH model.
methodsWe established a rat SAH model using cisternal injection of autologous blood and conducted comprehensive assessments including behavioral tests (elevated plus maze, forced swimming test, sucrose preference test), diffusion tensor imaging (DTI), and inflammatory factor detection. Seventy-two male SD rats were randomly divided into sham and SAH groups, with evaluations performed at multiple time points (1 hour to 72 hours post-hemorrhage). DTI parameters including fractional anisotropy (FA) and apparent diffusion coefficient were measured in limbic-prefrontal circuits. Serum and cerebrospinal fluid inflammatory markers [interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α] were quantified using enzyme-linked immunosorbent assay.
resultsSAH rats exhibited significant anxiety-like and depression-like behaviors at 12 hours, which further deteriorated at 24 hours (open arm time: 30.3 ± 4.7 seconds
conclusionThis study demonstrates that post-SAH emotional disorders result from a temporal cascade involving early neuroinflammation and progressive limbic-prefrontal circuit microstructural damage.
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