Background/Objectives: Non-saccular aneurysms are a rare subtype of intracranial aneurysms with complex morphologies. Although treatment strategies for ruptured non-saccular and saccular aneurysms differ significantly, large-scale comparisons of the outcomes between the two types remain limited. We aimed to compare the clinical characteristics, procedure-related complications, and functional outcomes between patients with subarachnoid hemorrhage (SAH) caused by non-saccular or saccular aneurysms. Methods: We retrospectively analyzed 1176 consecutive patients with aneurysmal SAH from a population-based stroke registry in Kochi Prefecture, Japan. Aneurysms were classified as saccular or non-saccular based on the morphology, and clinical variables, radiological features, and treatment modalities were compared. Additionally, 840 patients who underwent intervention for their aneurysms within 3 days of onset were further investigated to evaluate the impact of the non-saccular aneurysm shape on poor functional outcomes, defined as a modified Rankin Scale score ≥ 3 at discharge. Results: Non-saccular aneurysms were more common in younger patients and located in the posterior circulation. Procedure-related ischemic complications were more likely to occur in non-saccular aneurysms than in saccular aneurysms (odds ratio [OR]: 2.57, 95% confidence interval [CI]: 1.56–4.97, p < 0.001). In a multivariable logistic regression analysis, a non-saccular morphology was an independent risk factor of poor outcomes (OR: 2.92, 95% CI: 1.34–6.32, p = 0.007) after adjustment for potential confounders. Interaction and subgroup analyses revealed that the negative effects of non-saccular aneurysms on functional outcomes were more prominent in younger patients aged ≤ 60 years. Conclusions: Non-saccular aneurysms are independently associated with ischemic complications and poor outcomes after SAH, particularly in younger patients.

Background/Objectives: Clazosentan reduces cerebral vasospasm and delayed cerebral ischemia following aneurysmal subarachnoid hemorrhage (aSAH). However, concerns that clazosentan may cause cerebral edema and increase intracranial pressure (ICP) have discouraged its use in patients with poor-grade aSAH. Methods: This single-center retrospective study included 59 patients with aSAH who underwent continuous direct ICP monitoring, of whom 23 received clazosentan and 24 received fasudil. Most clazosentan-treated patients had poor-grade aSAH (WFNS 4–5, 95.7%). The primary outcome was the change in mean daily ICP in the clazosentan group between the pre-treatment and full treatment periods, with a secondary analysis restricted to the first 7 days and stratified by the presence of intracerebral hematoma (ICH). Cerebral perfusion pressure (CPP) changes were assessed as secondary outcomes, and the fasudil group served as an exploratory comparator. Results: Among 21 clazosentan-treated patients available for primary analysis, median ICP did not change significantly between the pre-treatment and treatment periods (6.4 vs. 8.4 mmHg; median ΔICP +0.5 mmHg, 95% CI −1.74 to +2.64; p = 0.708), a finding consistent in the first 7 days and across subgroups by ICH status. In contrast, CPP increased significantly between the pre-treatment and treatment periods (69.1 vs. 84.5 mmHg; median ΔCPP +14.0 mmHg, 95% CI +8.93 to +17.44; p < 0.001). Conclusions: In this retrospective single-center cohort, no statistically significant ICP elevation was observed during clazosentan administration under standard neurosurgical management. Although the small sample size limits statistical power and a false-negative result cannot be excluded, these findings may help inform clinical decision-making regarding clazosentan use in patients with poor-grade aSAH.

Background/Objectives: Aneurysmal subarachnoid hemorrhage (SAH) requires prompt treatment, yet hospital admission is occasionally delayed, and the optimal treatment strategy for such patients remains to be established. We aimed to investigate treatment modality, treatment timing, and outcomes in patients with SAH with respect to early versus delayed admission. Methods: A total of 1080 patients with SAH and a defined onset date were included in this prefecture-wide, multicenter, registry-based study. Baseline characteristics, late SAH complications (including vasospasm), and functional outcomes were compared between early and delayed admission groups at Day 4 or later (Day 0 = SAH onset). Additionally, the association of treatment choice (endovascular therapy or direct surgery) with treatment timing was analyzed in the delayed admission group. Results: Delayed admission was observed in 69 (6.4%) patients. The neurological status upon admission was significantly better in the delayed admission group, with more World Federation of Neurological Societies grades I–II (89.8% vs. 56.2% in the early admission group). Delayed admission was significantly associated with an increased incidence of symptomatic vasospasm by multivariable logistic regression analysis (odds ratio 2.51: 95% confidence interval 1.26–5.00, p = 0.009), while a significant difference in poor functional outcomes (modified Rankin scale 3–6) was not revealed. Although endovascular therapy use did not increase in the delayed admission group, the interval from admission to endovascular therapy was significantly shorter than that in the direct surgery group (0 [0–1] days vs. 1 [1–8] days: median [interquartile range], p = 0.007, Mann–Whitney U test). Conclusions: Delayed admission was a risk factor for symptomatic vasospasm; however, functional outcomes were not exacerbated. These results were obtained under the treatment strategy of multiple institutions, where the timing of endovascular therapy was earlier than that of direct surgery in patients with delayed admission.