Shigeharu Suzuki

Incidence and Significance of Early Aneurysmal Rebleeding Before Neurosurgical or Neurological Management

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 (P <0.01). 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 >160 mmHg 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.

Impact of Cerebral Microcirculatory Changes on Cerebral Blood Flow During Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

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 (r=0.429, P=0.0006). Peripheral CCT showed strong inverse correlation with rCBF (r=-0.767, P<0.0001). 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.

Cerebrovascular disorders associated with von Recklinghausen's neurofibromatosis: a case report.

A 28-year-old woman with von Recklinghausens 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.

Morphological changes of intraparenchymal arterioles after experimental subarachnoid hemorrhage in dogs.

OBJECTIVE Morphological and microcirculatory changes in intraparenchymal vessels after subarachnoid hemorrhage (SAH) have not yet been fully clarified. We conducted this experimental study to investigate the serial morphological changes of intraparenchymal arterioles after SAH. METHODS SAH was produced by injecting autologous arterial blood into the cisterna magna twice at 48-hour intervals in 30 dogs. The dogs were killed 3, 7, or 14 days after SAH, and then perfusion-fixed specimens of both anterior sylvian giri were obtained by using two methods. Microvascular corrosion casts produced by arterial injection of polyester resin were examined using scanning electron microscopy, and the widths of 40 arterioles of each animal were measured. Sectioned slices from the brain surface to 500 microns deep were examined by light microscopy, and external diameter, internal diameters, and wall thickness of the arterioles at depths of 50, 200, and 500 microns from the brain surface were morphometrically evaluated in 40 arterioles of each animal. In control animals receiving cisternal injections of mock cerebrospinal fluid (n = 10) and in healthy control animals (n = 10), the same examination and evaluation were performed. RESULTS Corrosion casts of arterioles showed tapered narrowing with folding after SAH, and the width of the arterioles significantly decreased 3 and 7 days after SAH (P < 0.01). Morphometric examination by light microscopy showed a significant decrease of internal diameter of arterioles associated with a significant increase of wall thickness at any depth from the brain surface 3 and 7 days after SAH (P < 0.05 or P < 0.01). These findings improved 14 days after SAH. Control animals receiving cisternal injections of mock cerebrospinal fluid showed no significant differences compared with healthy control animals. CONCLUSION These results suggest that constriction of intraparenchymal arterioles occurs after SAH and may contribute to delayed cerebral ischemia.

Dissecting Aneurysms of Intracranial Carotid Circulation

Background and Purpose— Clinical features of nontraumatic dissecting aneurysms of intracranial carotid circulation remain unclear because investigation of this disease has been limited to case reports. The aim of this study was to investigate the clinical features of this disease through the use of cooperatively collected cases. Methods— The cases diagnosed as dissecting aneurysms of intracranial carotid circulation on the basis of clinical signs and neuroradiological findings in 46 stroke centers from 1995 through 1999 were collected, and their clinical features were analyzed. Results— Forty-nine cases of dissecting aneurysms of intracranial carotid circulation were collected. Thirty-two patients presented with subarachnoid hemorrhage (SAH), and 17 presented with cerebral ischemia. The ratio of this disease to all intracranial dissecting aneurysms treated in the same institutes for the same period was 19.1%, and the ratio of SAH resulting from this disease to SAH of unverified origin treated in the same institutes for the same period was 6.2%. The predominant site of lesion was the internal carotid artery in 18 of 32 patients (56%) with SAH and the anterior cerebral artery in 13 of 17 patients (76%) with cerebral ischemia. The predominant angiographic findings were that stenosis with dilatation occurred in 20 of 32 patients (63%) with SAH and stenosis without dilatation was seen in 11 of 17 patients (65%) with cerebral ischemia. Poor prognosis was seen in 21 of 32 patients (66%) with SAH, which was due largely to rebleeding seen preoperatively, during operation, and even postoperatively when clipping or wrapping of the aneurysmal bulge was performed. Conclusions— Nontraumatic dissecting aneurysm of intracranial carotid circulation is not as rare as expected. It seems to be one of the important causes of SAH of unverified origin.

Meningiomas with brain edema: Radiological characteristics on MRI and review of the literature

OBJECT Despite their benign characteristics, meningiomas are often accompanied by perifocal brain edema. The aims of this study are to determine what kind of characteristics on magnetic resonance (MR) image are indicative of a meningioma that produces brain edema and to investigate the mechanism responsible for brain edema accompanying meningiomas. METHODS Fifty-one patients with meningioma were examined by magnetic resonance imaging (MRI), and tumor size, tumor location, shape of tumor margin, peritumoral rim, and signal intensity of tumor on T2-weighted image (T2WI) were compared and correlated with the presence versus absence of brain edema. Surgical histopathology was also examined and correlated with the MRI findings and brain edema. RESULTS Shape of tumor margin, peritumoral rim, and signal intensity of tumor on T2WI correlated with brain edema on multivariate analyses. CONCLUSION Invasive pattern of brain-tumor interface and hyperintensity on T2WI were indicative factors of meningiomas producing brain edema.

Role of platelet function in symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

To evaluate the role of platelet function in the pathogenesis of cerebral vasospasm, we compared sequential changes of platelet aggregability and beta-thromboglobulin and thromboxane B2 concentrations in blood samples from the internal jugular and peripheral vein of 13 patients with aneurysmal subarachnoid hemorrhage. Platelet function in blood from the internal jugular vein tended to be enhanced during days 0-1 but recovered to the normal range during days 2-4. After day 5, platelet function showed various patterns depending on the presence of symptomatic vasospasm. In patients without symptomatic vasospasm, sequential changes were relatively minor, with normal or slightly high values. Patients with symptomatic vasospasm already showed high platelet aggregability during the early stage of vasospasm. The concentration of beta-thromboglobulin increased several days after the onset of vasospasm, reaching 80 ng/ml or more in patients with a poor prognosis. Two of the five patients with symptomatic vasospasm showed markedly high concentrations of thromboxane B2 after day 8. These results suggest that vasospasm activates platelets and promotes aggregability and that the resulting increased tendency for thrombus formation may affect the patients prognosis during the advanced stage.

Importance of monitoring the circulating blood volume in patients with cerebral vasospasm after subarachnoid hemorrhage.

We used the isotope dilution technique to monitor circulating blood volume (CBV) in three patients with ruptured cerebral aneurysms who developed pre- or postoperative ischemic symptoms that responded well to intravascular volume expansion therapy with blood transfusion and plasma expanders. In the first and second cases, predeterioration CBVs were obtained. Both of these patients showed hypovolemia and a decreased red blood cell volume at the time of neurological deterioration. A predeterioration CBV was not available for the third patient for comparison, but his red cell volume was also markedly decreased. Postrecovery CBVs were obtained in the second and third cases. Our data suggested that a depleted red blood cell volume was more responsible for neurological deterioration than was a lowered plasma volume. To prevent the occurrence of hypovolemia and anemia in aneurysm patients, we should monitor CBV not only at the time of neurological deterioration, but also at the time of admission and during the immediate postoperative period.

Role of Multiple Cerebral Microthrombosis in Symptomatic Cerebral Vasospasm: With a Case Report

In our studies of the pathogenesis of cerebral vasospasm, we have been emphasizing that microthrombosis may play an important role in the induction of cerebral ischemic symptoms or cerebral infarction. In this report, multiple microthrombi are demonstrated histologically to be a major cause of cerebral infarction in the autopsied brain of a 63-year-old woman who died from typical cerebral vasospasm that occurred after the rupture of an anterior communicating artery aneurysm. We discuss the significance of thrombus formation and subarachnoid perivascular acidosis in vasospasm.

Risk Factors for Aneurysmal Subarachnoid Hemorrhage in Aomori, Japan

Background and Purpose— Japan is known to have an incidence of aneurysmal subarachnoid hemorrhage (SAH) as high as that in Finland, where SAH is especially common. However, the risk factors for SAH in Japan are unknown. The purpose of this study was to identify the risk factors and then examine their possible roles in cases of SAH in Japan. Methods— Case-control data were collected in the Aomori prefecture between June 2000 and May 2001 and in the Shimokita area between 1989 and 1998. A history of hypertension, cigarette smoking, alcohol consumption, hypercholesterolemia, and diabetes mellitus were examined as possible risk factors for SAH by using stepwise logistic regression analysis. Results— Stepwise logistic regression analysis showed that a history of hypertension and current smoking increased the risk of SAH and that a history of hypercholesterolemia decreased the risk of SAH. Alcohol consumption and a history of diabetes mellitus were excluded from the model, because their log-likelihood ratios were not significant. The adjusted odds ratios, obtained by forcing matching factors, were 2.29 for a history of hypertension (95% CI, 1.66 to 3.16), 3.12 for current smoking (95% CI, 2.05 to 4.77), and 0.41 for a history of hypercholesterolemia (95% CI, 0.24 to 0.71). The prevalence of hypertension in control subjects was 27% in men and 31% in women, whereas the prevalence of cigarette smoking in control subjects was 46% in men and 9% in women. Conclusions— Hypertension and cigarette smoking seem to be independent risk factors for SAH in Japan. The high prevalence of hypertension in both sexes and the high prevalence of cigarette smoking in men in the general population might contribute to the high incidence of SAH in Japan.