Post-stroke insomnia and the risk of post-stroke cognitive impairment and dementia: A large retrospective cohort study.

To evaluate the association between post-stroke insomnia (PSI) and the incidence of post-stroke cognitive impairment (PSCI), dementia, and all-cause mortality compared to stroke survivors without insomnia. We analyzed electronic health record data from the TriNetX Global Collaborative Network (119 healthcare organizations). Adults diagnosed with stroke between January 1, 2004, and September 30, 2017, were included. Patients with pre-existing insomnia were excluded. Patients were categorized as having PSI if diagnosed with insomnia after the index stroke, or as a non-insomnia comparator if no sleep disorder was recorded. Propensity score matching was used to balance baseline characteristics. The primary outcome was PSCI. Secondary outcomes included all-cause dementia, Alzheimer's disease, and all-cause mortality. Cox proportional hazard models were used to estimate hazard ratios (HRs) with 95% CIs. After propensity score matching, 35,144 patients were included in each cohort (PSI and non-insomnia). During follow-up, patients with PSI had significantly higher risks of PSCI (HR, 1.29; 95% CI, 1.24-1.34), all-cause dementia (HR, 1.30; 95% CI, 1.23-1.37), and Alzheimer's disease (HR, 1.28; 95% CI, 1.13-1.45) compared to the non-insomnia group. The risk of all-cause mortality was not different between the groups. Multivariable Cox model analyses revealed stronger associations of PSI with PSCI, dementia, and Alzheimer's disease in older adults, females, and those with diabetes, musculoskeletal diseases, hypertensive diseases, digestive disorders, specific head injuries, antidepressant use, NSAID use, and non-opioid analgesics use. In this large cohort study, PSI was associated with a significantly increased risk of cognitive decline, including PSCI, dementia, and Alzheimer's disease. These findings suggest that systematic screening and management of insomnia should be integrated into post-stroke care pathways to potentially mitigate long-term cognitive deterioration.