Reperfusion after brain ischemia causes thrombus formation and microcirculatory disturbances, which are dependent on the platelet glycoprotein Ib-von Willebrand factor (VWF) axis. Because ADAMTS13 cleaves VWF and limits platelet-dependent thrombus growth, ADAMTS13 may ameliorate ischemic brain damage in acute stroke. We investigated the effects of ADAMTS13 on ischemia-reperfusion injury using a 30-minute middle cerebral artery occlusion model in Adamts13 ؊/؊ and wild-type mice. After reperfusion for 0.5 hours, the regional cerebral blood flow in the ischemic cortex was decreased markedly in Adamts13 ؊/؊ mice compared with wild-type mice (P < .05), which also resulted in a larger infarct volume after 24 hours for Adamts13 ؊/؊ compared with wild-type mice (P < .01). Thus, Adamts13 gene deletion aggravated ischemic brain damage, suggesting that ADAMTS13 may protect the brain from ischemia by regulating VWF-platelet interactions after reperfusion. These results indicate that ADAMTS13 may be a useful therapeutic agent for stroke. (Blood. 2010; 115:1650-1653) Introductionvon Willebrand factor (VWF) is a large multimeric protein that plays a key role in thrombus formation by tethering platelets at sites of vascular injury. 1 Smaller VWF multimers are less active, and the potent thrombogenic activity of ultra-large VWF (ULVWF) secreted from endothelium is regulated in vivo through cleavage by ADAMTS13. 2,3 The importance of this mechanism for normal hemostasis is supported by evidence that patients with deficiency of ADAMTS13 function, diagnosed with thrombotic thrombocytopenic purpura, have ULVWF in circulating blood and VWFdependent microvascular thrombosis. 2 Recently, we demonstrated that ADAMTS13 cleaves VWF on the surface of platelet thrombi in a shear force-dependent manner, which limits thrombus growth in vitro. 4 These data suggest that ADAMTS13 is a key molecule that maintains a physiologic balance between hemostasis and thrombosis through regulation of VWF function in vivo.ADAMTS13 function is crucial for preventing thrombosis in the cerebral microvasculature, as indicated by the occurrence of neurologic deficits in thrombotic thrombocytopenic purpura, but the role of ADMTS13 in the pathogenesis of reperfusion injury after arterial thrombosis has not been established. To address this issue, we investigated the role of ADAMTS13 in a transient middle cerebral arterial occlusion (MCAO) model of ischemia-reperfusion injury in the mouse brain 5 using Adamts Ϫ/Ϫ mice. 6 Because brain ischemia-reperfusion injury is dependent on the platelet glycoprotein Ib-VWF axis 7 and platelet thrombosis adversely affects the postischemic cerebral microcirculation 8-11 leading to secondary brain damage, 10 ADAMTS13 may reduce platelet thrombus growth and thereby ameliorate ischemic brain injury by improving the postischemic no-reflow phenomenon. 12 Here we demonstrate that Adamts13 gene deletion aggravates postischemic cerebral blood reflow, resulting in larger infarct volume. This result suggests that ADAMTS13 may indeed supp...

Neurogenic pulmonary edema (NPE), leading to cardiopulmonary dysfunction, is a potentially life-threatening complication in patients with aneurysmal subarachnoid hemorrhage (SAH). We sought to assess the clinical presentation and risk factors for the development of NPE after SAH. The database contained prospectively collected information on 477 patients with SAH. Baseline characteristics, clinical and radiologic severity of the bleeding, localization of the ruptured aneurysm, and clinical outcome of patients with NPE were compared with those of patients without NPE. Further, in patients with NPE, intracranial pressure, serum cardiac biomarkers, and hemodynamic parameters during the acute phase were evaluated retrospectively. The incidence of NPE was 8% (39 of 477 patients). Most patients with NPE were severely impaired and all of them presented with radiologically severe hemorrhage. The incidence of NPE was significantly higher in patients with ruptured aneurysm in the posterior circulation. Elevated intracranial pressure was found in 67%, pathologically high cardiac biomarkers in up to 83% of patients with NPE. However, no patient suffered from persistent cardiac dysfunction. Compared with patients without NPE, patients with NPE showed poor neurologic outcome (Glasgow outcome scale 1 to 3 in 25% vs.77% of patients). In conclusion, patients with NPE have a high mortality rate more likely due to their severity grade of the bleeding. Morbidity and mortality due to cardiopulmonary failure might be reduced by appropriate recognition and treatment. The awareness of and knowledge about occurrence, clinical presentation, and treatment of NPE, are essential for all those potentially confronted with patients with SAH in the acute phase.

Higher IL-6 levels are associated with worse clinical outcome and the occurrence of DINDs. Because IL-6 levels were significantly elevated in the early phase, they might be a useful parameter to monitor.

5-ALA-induced fluorescence is a useful and promising intraoperative tool for the visualization of meningioma tissue. The novel findings demonstrated in this study in terms of high fluorescence and poor correlation with histological findings highlight the usefulness of this technique as a routine visual tool to achieve optimal resection of meningiomas.

Prolonged systemic hypothermia may be considered as a last-resort option for a carefully selected group of SAH patients with intracranial hypertension or CVS resistant to conventional treatment. However, complications associated with hypothermia require elaborate protocols in general intensive care unit management.

A retrospective analysis of 32 patients with tuberculum sellae meningiomas who underwent surgery via a unilateral pterional approach was performed. A selective extradural anterior clinoidectomy (SEAC) technique was added in 20 patients. All patients had visual dysfunction preoperatively. Macroscopically complete removal with Simpson grade II was performed in 28 patients (87.5%). The postoperative visual function improved in 25 (78.1%), did not change in 3 (9.4%), and worsened in 4 patients (12.5%). The SEAC technique was effective, especially for removal of the tumour extending into the sellae/pituitary stalk (9 patients), the optic canal (4 patients) and hypothalamus (4 patients) with preservation of the visual and endocrinological function. These results were superior to those of surgery without SEAC technique. This technique is therefore recommended for complete resection of the tuberculum sellae meningiomas extending to the surrounding anatomical structures as the SEAC procedure reduces the risk of intraoperative optic nerve injury considerably.

No abstract

Addi"ional informa"ion is available a" "he end of "he chap"er h""p://dx.doi.org/10.5772/57336 . IntroductionChronic subdural hematoma cSDH is one of the most frequent neurosurgical entities caused by head trauma. Since cSDH affects mainly elderly patients and the population continues to age, it has become a common neurosurgical disease seen by both general and specialized health-care practitioners. Despite the increasing prevalence of cSDH, class I studies, and evidence regarding the management of this disease is lacking. We provide an overview of the epidemiology, pathophysiology and etiology of cSDH and discuss several controversial aspects of its management including indication and timing of surgery, steroid treatment, the effectiveness of anti-epileptic prophylaxis, comparative effectiveness of various techniques for surgical evacuation, the timing of postoperative resumption of anticoagulant medication, and protocols for mobilization following evacuation of cSDH. Complications of surgical evacuation such as recurrent hematoma, postoperative epilepsy, brain injury and/or iatrogenic intracerebral bleeding due to hematoma evacuation, drainage insertion or irrigation, and ways to avoid them are also discussed. "s the incidence of cSDH is expected to increase and most treatment aspects lack clear consensus, further large prospective studies are needed. For this reason, a randomized, prospective study evaluating one aspect of the management of cSDH is currently in progress at our institution.. Definition " chronic subdural hematoma cSDH is defined as chronic ≥ weeks intracranial bleeding between the dura mater which adheres to the skull , and the arachnoid mater which envelops © 2014 Soleman e" al.; licensee InTech. This is a paper dis"rib""ed "nder "he "erms of "he Crea"ive Commons A""rib""ion License (h""p://crea"ivecommons.org/licenses/by/3.0), which permi"s "nres"ric"ed "se, dis"rib""ion, and reprod"c"ion in any medi"m, provided "he original work is properly ci"ed. the brain . The underlying cause of cSDH is usually traumatic tearing of the bridging veins which connect the brain surface with the dura mater.[ ]. . EpidemiologyThe incidence of cSDH is estimated at . -per ' people, rising up to per ' people in patients above the age of [ -]. The average age of patients with cSDH is approximately years old [ ]. "s the population continues to mature, incidence is expected to double by the year [ , ]. " large demographic study found the prevalence of cSDH in patients older than to be significantly higher % vs. % [ ]. In addition, men are more frequently affected than women % vs. % . In % of the cases, the patient has suffered a fall in the past and % of the patients were either treated with oral anticoagulants or platelet aggregation inhibitors. The reported recurrence rates range from . % to % [ -]. The most common risk factors are advanced age, alcohol abuse, seizures, cerebrospinal fluid CSF shunts, coagulopathies, blood thinners, and patients at risk for falling e.g. hemiplegia . In -% of the cases, cSDHs are b...