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Background: Microthrombosis and reactive inflammation contribute to neuronal injury after sub- arachnoid hemorrhage (SAH). ADAMTS-13 cleaves von Willebrand factor multimers, and inhibits thrombus formation and, seemingly, inflammatory reactions. Objective: To investigate the effect of ADAMTS-13 in experi- mental SAH. Methods: A total of 100 male C57/BL6 mice were randomly assigned to four groups: sham (n = 15), SAH (n = 27), vehicle (n = 25), and ADAMTS-13 (n = 23; 100 lL per 10 g of body weight of 100 lg of ADAMTS-13 per 1 mL of 0.9% NaCl; 20 min after SAH). Neurologic performance was assessed on days 1 and 2 after SAH. Animals were killed on day 2. The amounts of subarachnoid blood, microthrombi, apoptosis and degenerative neurons were compared. The degree of neuronal inflammation and vasospasm was also com- pared. In five mice each (SAH and ADAMTS-13 groups), bleeding time was assessed 2 h after SAH. Results: Systemic administration of ADAMTS-13 achieved significant amelioration of microthrombosis and improvement in neurologic performance. ADAMTS-13 reduced the amount of apoptotic and degenerative neurons. A ten- dency for decreased neuronal inflammation was observed. ADAMTS-13 did not show any significant effect on vaso- spasm. The degree of systemic inflammation was not changed by ADAMTS-13 administration. ADAMTS-13 neither increased the amount of subarachnoid blood nor prolonged the bleeding time. Conclusions: ADAMTS-13 may reduce neuronal injury after SAH by reducing micro- thrombosis formation and neuronal inflammation, thereby providing a new option for mitigating the severity of neuronal injury after SAH.

Despite the failure of the international extracranial-intracranial (EC-IC) bypass study in showing the benefit of bypass procedure for prevention of stroke recurrence, it has been regarded to be beneficial in a subgroup of well-selected patients with haemodynamic impairment. This report includes the EC-IC bypass experience of a single centre over a period of 14 years. All consecutive 72 patients with atherosclerotic occlusive cerebrovascular lesions associated with haemodynamic compromise treated by EC-IC bypass surgery were retrospectively reviewed. Pre-operatively, 61% of patients presented with minor stroke and the remaining 39% with recurrent transient ischemic attacks (TIAs) despite maximal medical therapy. Angiography revealed a unilateral internal carotid artery (ICA) stenosis/occlusion in 79%, bilateral ICA stenosis/occlusion in 15%, MCA stenosis/occlusion in 3% and other multiple vessel stenosis/occlusion in 3% of the cases. H(2)(15)O positron emission tomography (PET) or 99mTc-HMPAO SPECT with acetazolamide challenge was performed for haemodynamic evaluation of the cerebral blood flow (CBF). All the patients had impaired haemodynamics pre-operatively in terms of reduced regional cerebrovascular reserve capacity and rCBF. Standard STA-MCA bypass procedure was performed in all patients. A total of 68 patients with 82 bypasses were reviewed with a mean follow-up period of 34 months. Stroke recurrence took place in 10 patients (15%) resulting in an annual stroke risk of 5%. Improved cerebral haemodynamics was documented in 81% of revascularised hemispheres. Patients with unchanged or worse haemodynamic parameters had significantly more post-operative TIAs or strokes when compared to those with improved perfusion reserves (30% vs.5% of patients, p<0.05). In conclusion, EC-IC bypass procedure in selected patients with occlusive cerebrovascular lesions associated with haemodynamic impairment has revealed to be effective for prevention of further cerebral ischemia