Acute subdural hematoma (aSDH) is a common pathology encountered after head trauma. Only a minority of aSDHs have an arterial source. In this article, we report a case of aSDH originating from a traumatic pseudoaneurysm of the distal segment of posterior cerebral artery (PCA), diagnosed several days after the initial minor trauma and successfully treated with endovascular coiling. This case emphasizes the importance of searching for vascular pathology when the localization, severity or relapsing course of the intracranial hemorrhage does not fully correspond to the severity of initial trauma and when the bleeding has a delayed onset. Characteristics, diagnostics and treatment possibilities of traumatic cerebral aneurysms, an important cause of arterial aSDH, are described in the article.

Background/Objectives: Antiplatelet therapy after emergent carotid stenting (eCAS) represents a challenge in balancing the risk of intracerebral hemorrhages (ICHs) and in-stent thrombosis (IST). Post-procedural platelet function monitoring may guide antiplatelet therapy and could potentially improve outcomes due to fewer post-procedural complications. Methods: Consecutive eCAS patients (2019–2021) were included in a single-center retrospective observational study. Patients treated with eCAS received peri-procedural eptifibatide followed by dual antiplatelet treatment with aspirin and clopidogrel. The effect of platelet ADP inhibition by clopidogrel was monitored using the Multiplate^® Analyzer (Roche). Clopidogrel non-responders were changed to ticagrelor treatment. The primary outcome was defined as a favorable outcome at 90 days using the modified Rankin Scale (mRS) of 0–2 versus 3–6. Safety outcomes included ICH, IST, and mortality. Data were analyzed and compared in clopidogrel- and ticagrelor-treated patients using Fischer’s exact test and multivariate logistic regression. Results: A total of 105 patients had eCAS, and 28 patients (27%) were clopidogrel non-responders and were changed to treatment with ticagrelor. The favorable outcome was more frequent in ticagrelor-treated patients, 23 (82%), than in clopidogrel-treated patients, 44 (57%), p = 0.036. Numerically, ICH, IST, and mortality were more frequent in clopidogrel-treated patients, but none of the differences were statistically significant. In multivariate analyses, ticagrelor treatment was significantly associated with the favorable outcome, OR = 3.89 (95% CI: 1.09–13.86), p = 0.036. Conclusions: One in four eCAS patients were clopidogrel non-responders. This study suggests that personalized antiplatelet treatment therapy was safe, and that changing treatment to ticagrelor in clopidogrel non-responders was associated with better outcomes in eCAS patients.