Prognostic Factors for Cognitive Decline After Intracerebral Hemorrhage

Abstract

Background and Purpose— Stroke and dementia are closely related, but no prospective study ever focused on poststroke cognitive decline in patients with intracerebral hemorrhage (ICH). We aimed to determine prognostic factors for cognitive decline in patients with ICH. Methods— We prospectively included 167 consecutive ICH survivors without preexisting dementia from the Prognosis of Intra-Cerebral Hemorrhage (PITCH) cohort. Median follow-up was 4 years (interquartile range, 2.3–5.4). We explored factors associated with cognitive decline using linear mixed models. Cognitive decline was determined based on repeated mini-mental state examination. We investigated each prognostic factor separately in univariate models. Next, we constructed clinical and radiological multivariable models. In a sensitivity analysis, we excluded patients with preexisting cognitive impairment. Results— Median age was 64 (interquartile range, 53–75) years, 69 (41%) patients were women, and median mini-mental state examination at 6 months was 27 (interquartile range, 23–29). Overall, 37% of the patients declined during follow-up. Factors associated with cognitive decline in univariate analyses were previous stroke or transient ischemic attack, preexisting cognitive impairment, microbleed presence, severity of white matter hyperintensities, and severity of cortical atrophy. In multivariable analyses, previous stroke or transient ischemic attack (β [SE], −0.55 [0.23]; P <0.05), preexisting cognitive impairment (β [SE], −0.56 [0.25]; P <0.01), and severity of cortical atrophy (β [SE], −0.50 [0.19]; P <0.01) remained independent prognostic factors. In patients without preexisting cognitive impairment (n=139), severity of cortical atrophy (β [SE], −0.38 [0.17]; P <0.05) was the only prognostic factor for future cognitive decline. Conclusions— Prognostic factors for cognitive decline after ICH are already present when ICH occurs, suggesting a process of ongoing cognitive impairment instead of new-onset decline induced by the ICH itself.