Cerebral vasospasm and subsequent delayed ischemic neurological deficit is a typical sequela of acute subarachnoid hemorrhage after aneurysm rupture. The occurrence of vasospasms after uncomplicated surgery of an unruptured aneurysm without history of suspected rupture is extremely rare. The pathogenesis and severity of cerebral vasospasms is typically correlated with the amount of blood breakdown products extravasated during subarachnoid hemorrhage. In rare cases, where vasospasms occur after unruptured aneurysm surgery, the pathogenesis is most likely multifactorial and unclear. We present two cases of vasospasms following uncomplicated clipping of middle cerebral artery (MCA) aneurysms and a review of literature. Early diagnosis and therapy of this rare complication are necessary to achieve optimal clinical outcomes.

Brain ischemia after central nervous system (CNS) bleeding significantly influences the final outcome of patients. Catalytic activities of aspartate aminotransferase (AST) in the cerebrospinal fluid (CSF) to detect brain ischemia were determined in this study. The principal aim of our study was to compare the dynamics of AST in 1956 CSF samples collected from 215 patients within a 3-week period after CNS hemorrhage. We compared concentrations of the AST catalytic activities in the CSF of two patient groups: survivors (Glasgow Outcome Score (GOS) 5–3) and patients in a vegetative state or dead (GOS 2–1). All statistical evaluations were performed using mixed models and the F-test adjusted by Kenward and Roger and the Bonferroni adjustment for multiple tests. The significantly higher catalytic activities of AST in the CSF from patients with the GOS of 2–1 when compared to those who survived (GOS 5–3, p = 0.001) were found immediately after CNS haemorrhage. In the further course of time, the difference even increased (p < 0.001). This study confirmed the key association between early signs of brain damage evidenced as an elevated AST activity and the prediction of the final patient’s clinical outcome. The study showed that the level of AST in the CSF could be the relevant diagnostic biomarker of the presence and intensity of brain tissue damage.

Extravasation of blood in the central nervous system (CNS) represents a very strong damaged associated molecular patterns (DAMP) which is followed by rapid inflammation and can participate in worse outcome of patients. We analyzed cerebrospinal fluid (CSF) from 139 patients after the CNS hemorrhage. We compared 109 survivors (Glasgow Outcome Score (GOS) 5-3) and 30 patients with poor outcomes (GOS 2-1). Statistical evaluations were performed using the Wilcoxon signed-rank test and the Mann–Whitney U test. Almost the same numbers of erythrocytes in both subgroups appeared in days 0–3 (p = 0.927) and a significant increase in patients with GOS 2-1 in days 7–10 after the hemorrhage (p = 0.004) revealed persistence of extravascular blood in the CNS as an adverse factor. We assess 43.3% of patients with GOS 2-1 and only 27.5% of patients with GOS 5-3 with low values of the coefficient of energy balance (KEB < 15.0) in days 0–3 after the hemorrhage as a trend to immediate intensive inflammation in the CNS of patients with poor outcomes. We consider significantly higher concentration of total protein of patients with GOS 2-1 in days 0–3 after hemorrhage (p = 0.008) as the evidence of immediate simultaneously manifested intensive inflammation, swelling of the brain and elevation of intracranial pressure.

Objectives: The goal of this study is to establish the incidence of high on-treatment platelet reactivity (HTPR) to aspirin and clopidogrel in patients undergoing carotid stenting and to evaluate the efficacy of ticagrelor and ticlopidine in patients with HTPR to clopidogrel. Methods: In a single institutional setting spanning eight years, every consecutive patient who underwent carotid artery stenting was incorporated into a study. Subsequently, a retrospective analysis of their platelet function was executed. Prevalence of high on-treatment reactivity to aspirin, clopidogrel, ticlopidine and ticagrelor was assessed. Platelet function testing was conducted by light transmission aggregometry and Multiplate^®. Results: A total of 216 patients were tested for antiplatelet therapy efficacy. The high on-treatment reactivity to clopidogrel was observed in 68 patients (31.4%). No patients with high on-treatment reactivity to ticagrelor or ticlopidine were observed. There was a significant reduction in platelet reactivity with ticagrelor (p < 0.000) and ticlopidine (p < 0.000) in patients with HTPR to clopidogrel. Conclusions: High on-treatment platelet reactivity to clopidogrel is common in patients undergoing carotid artery stenting. Ticagrelor is a viable alternative to overcome HTPR to clopidogrel. These findings suggest that platelet function testing can identify patients who may benefit from tailored antiplatelet therapy in reducing thromboembolic complications after carotid stenting.