0997 Ideal Sleep Midpoint and Inflammatory Activation in Wake-Up Stroke

Abstract Introduction Wake-up stroke (WUS) remains mechanistically unclear. Prior evidence suggests that circadian misalignment and intrinsic sleep timing may influence systemic inflammation, which could contribute to stroke onset during sleep. The ideal sleep midpoint—conceptually derived from the pristine time framework that reflects an individual’s preferred sleep timing under unconstrained conditions—may offer additional insight into sleep–inflammation interactions. This study compared pristine time–based sleep timing metrics, inflammatory markers, and clinical characteristics between WUS and non-WUS patients and explored whether these patterns support a preliminary conceptual model linking sleep timing, inflammation, and WUS. Methods We analyzed 250 acute ischemic stroke patients, categorizing them into WUS and non-WUS groups. Variables included demographics, risk factors of stroke, C-reactive protein (CRP), weighted total sleep time (wTST), pristine time-derived ideal sleep midpoint, ideal–actual sleep timing difference, and multiple sleep-related questionnaires. Group comparisons were performed to evaluate patterns potentially relevant to a sleep timing–inflammation pathway. Results Overall, 27.8% experienced WUS. Although differences were not statistically significant, the WUS group showed higher CRP levels, slightly shorter wTST, and a modestly later pristine time-derived ideal sleep midpoint compared with non-WUS group. Traditional risk factors of stroke and sleep questionnaire scores were similar between groups. While inconclusive, these directional trends are consistent with the hypothesized pathway linking intrinsic sleep timing and inflammation. Conclusion Although group differences did not reach statistical significance, the observed trends—higher CRP and a later pristine time–based ideal sleep midpoint in WUS—align with a potential sleep timing–inflammation mechanism. These findings should be interpreted as hypothesis-generating and support further investigation into a conceptual triangular model connecting intrinsic sleep timing (pristine time), systemic inflammation, and WUS. Support (if any)