Aneurysms located on the posterior inferior cerebellar artery are rare, and treatment guidelines for them have not yet been established. In this paper, we present the results of a retrospective study which analyzes the management and treatment of 15 patients with posterior inferior cerebellar artery aneurysms from 2004 to 2013. The aneurysms were ruptured and presented with a subarachnoid hemorrhage. Of the 15 aneurysms, ten were of saccular, three fusiform, and two were dissecting. Computed tomography angiography or digital subtraction angiography revealed other aneurysms or intracerebral artery hypoplasia in seven patients. Either surgical or endovascular treatment was performed depending on the localization and morphology of the aneurysm. Six aneurysms were coiled, and surgery was performed in nine cases. Of the nine surgically treated patients, six (75%) had good outcomes. Of the six patients treated using endovascular procedures, three patients (50%) recovered. Patient outcomes were classified using the Hunt&Hess scale. Patients with Hunt&Hess 1-3 recovered without a neurological deficit. On the other hand, patients with Hunt&Hess 4-5 had a risk of up to 93% of death or a poor outcome. In two cases of endovascular and in two cases before any therapy, aneurysmal rebleeding occurred and resulted in deterioration of clinical state of the patient and a poor prognosis with high risk of death. This study shows the necessity of acute treatment of posterior inferior cerebellar artery aneurysm, of thorough diagnostic, and of interdisciplinary cooperation.
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.
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.
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