A cross-sectional study investigating the underlying inflammatory mechanisms of post-stroke insomnia

It is widely postulated that inflammation contributes to the pathogenesis of both stroke and insomnia; and vice versa. However, the mechanism underlying post-stroke insomnia (PSI) remains ambiguous. Therefore, this study aims to elucidate the potential inflammatory mechanisms associated with PSI and evaluate its predictive value.

A cross-sectional study was conducted among patients with acute stroke who were enrolled in this investigation. Sleep quality was evaluated using the Pittsburgh Sleep Quality Index (PSQI), alongside the assessment of 12 cytokines and complement component 1q (C1q) levels. The anxiety (HAD-A) and depression (HAD-D) states of patients were assessed utilizing the Hospital Anxiety and Depression Scale. Statistical analyses were conducted to compare differences in each indicator among patients with various types of stroke and varying sleep quality.

The prevalence of sleep disorders among patients with acute stroke is as high as 75.7 %. There were no significant differences observed in the PSQI scores and cytokines across different subtypes of strokes. However, significant differences were found in Interleukin (IL)-6, Interferon-α(IFN-α), and C1q levels, as well as in HAD-A and HAD-D scores among PSI patients. Binary logistic regression analysis revealed that C1q, IL-6, IL-10, IL-12, HAD-A, and HAD-D had a significant impact on sleep quality. The receiver operating characteristic (ROC) curve indicated that only IL-6 and HAD-A scores predicted PSI.

Insomnia is common after acute stroke, potentially due to inflammation. IL-6 levels and anxiety could serve as predictors for PSI development, thereby presenting potential targets for therapeutic intervention.