Background and Purpose-Rebleeding is a major cause of death and disability in aneurysmal subarachnoid hemorrhage (SAH); however, there has been no report focusing on rebleeding before hospitalization in neurosurgical or neurological institutions. The aim of this study was to clarify the incidence of prehospitalization rebleeding, its impact on the clinical course and prognosis in patients with aneurysmal SAH, and the possible factors inducing it. Methods-In 273 patients who were admitted to our institution within 24 hours after the initial SAH bleeding and whose clinical course before admission could be fully evaluated, the patients' clinical conditions and CT findings on admission, operability, prognosis, and possible factors inducing rebleeding were comparatively evaluated between the patients with and without an episode of prehospitalization rebleeding. Results-Of the 273 patients, 37 (13.6%) patients suffered from 39 episodes of rebleeding in the ambulance or at the referring hospital before admission to our hospital. The peak time of rebleeding was within 2 hours (77%), in which the incidence was statistically significant compared with that occurring 2 to 8 hours after the initial SAH bleeding (PϽ0.01).The group experiencing rebleeding showed more severe Hunt and Hess grades on admission, higher rates of intracerebral hematoma, of intraventricular hematoma, and of subdural hematoma on CT scan on admission, less operability, and poorer prognoses with statistically significant differences compared with the group that did not experience rebleeding. Systolic arterial pressure Ͼ160 mm Hg was a possible risk factor of rebleeding (odds ratio 3.1, 95% CI 1.5 to 6.8). Conclusions-Rebleeding during transfer and at the referring hospital is not rare. To improve overall outcome of aneurysmal SAH, the results obtained in this study should be made available to general practitioners and the doctors devoted to emergency medicine.

Background and Purpose-Cerebral microcirculatory changes during cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) are still controversial and uncertain. The aim of this study was to investigate the changes of cerebral microcirculation during cerebral vasospasm and to clarify the roles of microcirculatory disturbances in cerebral ischemia by measuring cerebral circulation time (CCT) and regional cerebral blood flow (rCBF). Methods-In 24 cases with aneurysmal SAH, rCBF studies by single-photon emission CT and digital subtraction angiography (DSA) were performed on the same day between 5 and 7 days after SAH and/or within 4 hours after the onset of delayed ischemic neurological deficits. CCT was obtained by analyzing the time-density curve of the contrast media on DSA images and was divided into proximal CCT, which was the circulation time through the extraparenchymal large arteries, and peripheral CCT, which was the circulation time through the intraparenchymal small vessels. They were analyzed in association with rCBF and angiographic vasospasm. Results-Severe angiographic vasospasm statistically decreased rCBF, and correlation between the degree of angiographic vasospasm and rCBF was seen (rϭ0.429, Pϭ0.0006). Peripheral CCT showed strong inverse correlation with rCBF (rϭϪ0.767, PϽ0.0001). Even in none/mild or moderate angiographic vasospasm, prolonged peripheral CCT was clearly associated with decreased rCBF. Conclusions-In addition to the marked luminal narrowing of large arteries detected as severe angiographic vasospasm, microcirculatory changes detected as prolonged peripheral CCT affected cerebral ischemia during cerebral vasospasm. These results suggested that impaired autoregulatory vasodilation or decreased luminal caliber in intraparenchymal vessels may take part in cerebral ischemia during cerebral vasospasm.

These results suggest that constriction of intraparenchymal arterioles occurs after SAH and may contribute to delayed cerebral ischemia.

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A 28-year-old woman with von Recklinghausen's neurofibromatosis (NF-1) had a huge hematoma in the left posterior nuchal region. Carotid and vertebral angiograms revealed marked stenosis at the C3 portion of the left internal carotid artery, slight moyamoya staining, occlusion of the left vertebral artery at the atlas level, and a right internal carotid artery aneurysm. The radiographic, clinical, and histological features of this case are discussed together with a review of 42 similar cases found in the literature.