Chebaro, K.

Introduction Although Valsalva maneuvers and strenuous exercise are commonly discouraged in patients with intracranial aneurysms (IAs), the cerebrovascular stress they induce remains poorly characterized. To our knowledge, no prior review has systematically quantified their effects on hemodynamic surrogates of rupture risk. Objective To characterize the acute intracranial hemodynamic effects of strenuous physical activity and Valsalva maneuvers in individuals with and without IAs. Methods We searched PubMed, Embase, Scopus, Web of Science, and Cochrane (February 2025; PROSPERO ID: CRD42025637608) following PRISMA. Eligible studies reported acute changes in SBP, ICP, central venous pressure (CVP), cerebrovascular transmural pressure (CVTMP), middle cerebral artery (MCA) velocity, or CFD‐derived parameters (wall shear stress [WSS], oscillatory shear index [OSI], relative residence time [RRT]) in response to physical exertion or Valsalva. Populations included individuals with or without IAs. Acute neurological symptoms were also reviewed. Results From 2,859 records, 14 studies met inclusion criteria. Eight studies assessed real‐time hemodynamic responses during exercise (91 participants without IAs). Three studies (n=39) showed that resistance exercise increased SBP (mean Δ+21.8 mmHg). Two studies (n=22) showed significant MAP elevation (mean Δ+24.7 mmHg). When combined with a Valsalva maneuver, SBP increased further (mean Δ+26 mmHg; range 20–30). Three studies (n=38) evaluating isolated Valsalva identified significant ICP elevation (mean Δ+15 mmHg; range 5.7–24.3), primarily driven by CVP increases (mean Δ+52.0 mmHg; range 39–56). Breath‐holding during exertion reduced MCA velocity (mean Δ–11.6 cm/s), while continuous ventilation preserved more stable flow. In seven patients, resistance exercise without Valsalva increased CVTMP by 24.5%. In contrast, Valsalva alone raised ICP and CVP without increasing SBP, yielding a CVTMP 11% lower than during exercise alone. These paired observations suggest that Valsalva may transiently offset exercise‐induced transmural stress by raising ICP alongside SBP. However, this effect may be time‐limited and reverse during early recovery—when SBP remains elevated as ICP quickly normalizes—potentially producing a CVTMP rebound above exercise‐only levels. Six CFD studies (11 aneurysms; diameter 6.3–23 mm; 2 ruptured) reported exercise‐related increases in time‐averaged WSS (mean +21.7%, range –4.4% to +50%) and peak WSS (mean +382.3%, range +100% to +628%). Exercise‐induced changes in heart rate and flow pulsatility led to complex redistributions of intra‐aneurysmal WSS, potentially exposing the aneurysmal wall to focal mechanical stress. Conclusion Resistance exercise, especially with breath‐holding, provokes dynamic, time‐sensitive cerebrovascular stress. Valsalva maneuver may transiently lower CVTMP during effort, yet its release with lingering SBP elevation can precipitate delayed transmural pressure surges. The proposed biphasic effect of Valsalva offers a novel conceptual framework for prospective. Our findings underscore the need to define safe, individualized activity thresholds for patients with IAs with patient‐specific validation integrating concurrent physiology and CFD to reduce the risk of IA growth and rupture.

Introduction The risk of aneurysmal subarachnoid hemorrhage (aSAH) during exercise is not well quantified. We assessed temporal clustering of aSAH around physical exertion and around Valsalva‐like activities (defecation or urination). Objectives To estimate the proportion of aSAH cases temporally linked to strenuous activities using reported exposure‐to‐onset window uwing within‐person odds of rupture from case‐crossover studies. Methods We searched PubMed/MEDLINE, Embase, Scopus, Web of Science, and the Cochrane Library from inception through January 2025, and hand‐searched reference lists (PRISMA‐aligned; PROSPERO CRD42025637608). Eligible studies reported the activity at aSAH onset or within a defined pre‐onset window. Exposures were analyzed separately (exertion; defecation/urination). Primary proportional estimates used each study's own exposure‐to‐onset window as reported. To improve comparability, subgroup analysis was performed with only a prespecified subset pooled consecutive case series that explicitly used a ≤2‐hour window between the index activity and aSAH. Within‐person odds ratios (ORs) were abstracted from case‐crossover studies. Risk of bias for observational exposure studies was assessed with ROBINS‐E by two independent reviewers. Results Sixteen studies (published 1980–2022) from 10 countries were included with 5,815 cases of aSAH (mean age 55 years; 60.6% female). Designs comprised 10 case series, 3 case reports, 2 case‐crossover studies, and 1 case‐control study. Activity‐at‐onset was recorded for 4,219/5,815 (72.6%); among these 4,219 patients, mean age was 52.7 years. Using each study's reported window, 308/4,219 (7.3%) aSAH occurred during or within the study‐defined window after physical exertion, and 387/4,219 (9.2%) during/within the window after defecation or urination 695/4,219 (16.5%) were temporally linked to either exposure. In the subset of 10 consecutive case series restricted to ≤2 hours, 275 (5.4%) were linked to exertion and 385 (7.6%) to defecation/urination (combined 660; 13.0%). Study‐specific proportions ranged from 0.8–21.3% for exertion and 2.0–15.4% for defecation/urination. Two case‐crossover studies reported higher within‐person odds of rupture after moderate‐to‐vigorous exertion (OR 2.4–2.7). Temporal clustering of aSAH around exertion or straining was observed in 13–17% of cases, depending on dataset and inclusion criteria. Conclusions Although this relatively high rate of temporal association between aSAH and exercise might suggest an increased risk of aneurysm rupture during strenuous activity, variable definitions and unstated exposure‐to‐onset windows do not permit causal inference. Prospective or registry‐embedded case‐crossover studies using standardized exposure definitions (intensity, duration) and objective exposure capture are needed to refine immediate‐risk estimates and identify patient‐level susceptibility modifiers.