Metabolic acidosis in cerebral ischemia is considered deleterious to cell function. Amelioration of systemic and focal cerebral acidosis by an alkalizing agent may reduce ischemic brain damage. We examined the effect of tris [hydroxymethyl] aminomethane (THAM) and NaHCO₃ on focal cerebral ischemia produced by occlusion of the middle cerebral artery (MCA) in cats. The animals were divided into three groups. In the control group, physiological saline was infused continuously. The THAM and NaHCO₃ group received continuous administration of 0.3 mol THAM and 7% NaHCO₃, respectively. PaO₂, PaCO₂ and the mean arterial blood pressure in each group were maintained within the normal range. The following experimental results were obtained. In the THAM and NaHCO₃ groups, the arterial pH was maintained within the normal range, whereas in the control group, it gradually fell from 7.39 at the start to 7.28 at 6 hours after the MCA occlusion. The local CBF measured by the hydrogen clearnace method in the marginal and suprasylvian gyri promptly decreased after the MCA occlusion and there were no significant differences among the three groups. The extracellular pH measured with a glass electrode on the marginal gyrus declined from 7.36 to 6.87 after 6 hours of ischemia in the control group. However, in the THAM and NaHCO₃groups, the extracellular pH failed to show significant changes during the 6 hours of occlusion. In the THAM group, the water content of the gray metter measured by the specific gravimetric method in the marginal gyrus was significantly decreased compared to that in the control and NaHCO₃ groups. The tissue lactate content measured by an enzymatic assay in the marginal gyrus fell singificantly following the administration of THAM, but was significantly increased in the NaHCO₃ group, as compared to the control group. These data suggest that alkalizing agents tend to improve the extracellular pH, but exert less effect on the cerebral circulation. We consider that the normalization of systemic and perifocal acidosis elicited by THAM is effective for reducing cortical edema at the early stage of focal cerebral ischemia. This effect of THAM is probably due to improvement of the cellular metabolism. NaHCO₃also normalized systemic and extracellular acidosis, but it exerted no effect on cerebral edema. The above results suggest therefore that NaHCO₃ infusion may lead to paradoxical intracellular acidosis, and that THAM is more effective than NaHCO₃ at the early stage of cerebral ischemia.

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The effect of Bifemerane hydrochloride, was evaluated by observing in vivo ³¹P-magnetic resonance spectra (MRS) in experimentally induced rat brain ischemia the rat brain ischemia was induced by a four-vessel occlusion model. After 30 min of ischemia, the circulation of the bilateral common corotid arteries was restored. During and after the ischemia, in vivo ³¹P-MRS were measured from the ischemic brain. The experimental, rats were divided into two groups : a non-treated control group and a Bifemerane hydrochloride-treated group. The survival time after ischemia, and changes in energy metabolism of the ischemic brain were estimated. The mean survival time of the control rats was 4. 8 days. On the other hadn, that of the treated group was 12.8 days. Immediately after the induction of ischemia, the energy metabolism of the brain changed. The creatine phosphate (PCr) and adenosine triphosphate (ATP) peaks decreased, and the inorganic phosphate (Pi) peak increased dramatically. The value of the pH, calculated from the value of the chemical shirt in the Pi peak, decreased showing an acidotic change in the ischemic brain tissue. After recirculation of the bilateral common carotid arteries, high energy phosphate metabolities such as PCr and ATPs recovered immediately, exhibiting rapid changes in the early stage of recovery. In the animals of the treated group, this rapid recovery of high energy phosphorus compounds was suppressed in a statistically significant manner. These findings indicate a supportive effect for Bifemerane hydrochloride on post-ischemic brain damage.

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The purpose of the present study was to ascertain whether or not basic fibroblast growth factor (bFGF) caused contraction of cerebral infarcts in rats with experimental ischemia. We permanently occluded the left middle cerebral artery (MCAO) of 21 Sprague-Dawley rats, and immediately infused bFGF (100 ng in physiological saline (PS)) and PS intraarterially in the bFGF and control groups, respectively. The cerebral infarct size determined at 24 hours after MCAO in the bFGF-treated group was significantly decreased (p<0.05 vs. control, unpaired Student's t test). Physiological parameters showed no significant inter-group differences. Thus, in a rat model of MCAO, bFGF elicited a contraction of infarcts.

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Hypertensive thalamic hemorrhage is often associated with intraventricular hemorrhage. The purpose of the present study was to evaluate the role played by intraventricular hemorrhage, especially cast formation, in the neurologic outcome. We reviewed 105 patients with intraventricular hemorrhage following hypertensive thalamic hemorrhage which we had experienced in our service over a period of 5 years and diagnosed by CT scan. Forty-five cases had cast formation and 60 cases did not. There were no significant differences between the group of 45 patients with cast formation and the group of 60 patients without cast formation as regards age, CT classification or volume of intraparenchymal hematoma. We found that, of the 45 patients in the cast formation group, 23 demonstrated a poor outcome such as a vegetative state or death, and the mortality rate was 35.6%. Of the 60 patients in the group without cast formation, 7 demonstrated a poor outcome and the mortality rate was 8.3%. It is considered therefore that cast formation is an important risk factor in the neurologic outcome for patients with hypertensive thalamic hemorrhage. The 45 patients in the cast formation group were assigned to one of two sub-groups according to the location of the cast formation. Type 1 included patients who had cast formation mainly in the third and/or fourth ventricles, whereas type 2 included those with cast formation in the lateral ventricles. The patients of type 1 had a worse outcome and a higher mortality rate than those of type 2. Patients with an intraparenchymal hematoma volume of less than 10 ml were investigated, and it was concluded that cast formation in the third and fourth ventricles represented the most important factor in the neurologic coutocme. There is no established evaluation procedure for intraventricular hemorrhage in patients with hypertensive hemorrhage. We developed a scoring system for intraventricular hemorrhage, and attempted to evaluate patients using a combination of lateral ventricle scores and third-fourth ventricle scores in each. We suggest that this provides a useful diagnostic method for identifying the severity of intraventricular hemorrhage.

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The level of basic fibroblast growth factor (bFGF) in the cerebrospinal fluid was measured by a two-sites sandwich enzyme immunoassay in 18 patients with moyamoya disease, 12 patients with atheros-clerotic occlusive cerebovascular disease involving the internal carotid or the middle cerebral arteries, and 15 patients with spinal dise disease. In the moyamoya patients, bFGF was found in 16 out of the 18 cerebrospinal fluid samples with a mean value of 85.5 pg/ml. In 4 patients with moyamoya disease, cerebrospinal fluid samples obtained during contralateral surgery performed 3 or 4 weeks after the first procedure also contained high levels of bFGF. bFGF was detected in only 5 out of the 12 patients with atherosclerotic occlusive cerebrovascular disease; however, the mean value was below the detection limit. In all the patients with disc disease, bFHG was not detected. Postoperative angiograms demonstrated the effectiveness of indirect bypass procedures in moyamoya patients whose cerebrospinal fluid contained a high level of bFGF, but any patient below the detection limit of bFGF was refractory to the indirect bypass procedures. An elevated level of bFGF may play an important role in the pathogenesis of moyamoya disease.

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We report three cases of new growth and rupture of cerebral aneurysm after successful surgical treatment of previous aneurysms at other sites. Two patients had ruptured newly-developed aneurysms at the junction of the internal carotid and posterior communicating arteries, one after dipping of anterior communicating artery aneurysm, and the other after distal anterior cerebral artery aneurysm. These two patients had suffered from hypertension before their second operation. In the third case, anterior communicating artery aneurysm developed and ruptured after treatment involving combined internal carotid artery occlusion and extracranial-intracranial anastomosis for a giant aneurysm of the internal carotid artery. In this case, the new aneurysm appears to have developed due to long-term hemodynamic stress. In all three cases, newly-developed aneurysms were successfully clipped, and rupture of them was confirmed.

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We report a case of lacunar infarction of the lateral lower medulla, showing rt. Horner's syndrome, hypalgesia under Th11 and thermohypoesthesia under Th10 on the right and truncal ataxia. CT scan revealed no obvious findngs in the brain stem, but MRI demonstrated a lacunar infarction in the lateral lower medulla. It was shown that segmental dissociated sensory disturbance without sensory deficit in the face could be caused by partial impairment of the lateral spinothalamic tract, which is arranged with the fibers from the sacral segments most lateral. Although segmental sensory disturbance is usually thought to be a sign of spinal cord disease, it is important that such sensory disturbance can also appear in patients with disease of the brain stem.

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A 29-year-old woman suffering from aplastic anemia was treated with low-dose anabolic steroid (oxymetholone, 5 mg/day) for 8 years. Four months after intrauterine fetal death associated with toxemic pregnancy, she experienced headache, followed by generalized seizures and right hemiparesis. Based on her angiographic findings, we diagnosed occlusion of the cerebral sinuses and veins. In the literature, we found 3 other patients with aplastic anemia complicated by cerebral sinus thrombosis. All previously reported patients had been taking either high-dose anabolic steroid or high-dose androgen for at least a few months, while out patient had, as mentioned, been taking low-dose analbolic steroid for about 8 years. Physicians should consider the possible complication of cerebral sinus thrombosis, when a patient with aplastic anemia on anabolic steroid or androgen therapy manifests both headache and a relatively rapid increase of platelet counts in the blood. In this situation, drug therapy should be discontinued immediately, or the dose decreased.

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The cerebral arteries are resistant to the usual procedures employed for atherosclerotic lesion induction in animal models. However, in a previous study, we performed localization and characterization of initial atherosclerotic lesions in the posterior cerebral artery, basilar artery and vertebral artery using hypertensive rabbits fed on a cholesterol diet. In the present study, we examined the ultrastructural changes of the intracortical fine vessels. Five hypertensive rabbits were fed on the cholesterol diet for 16 weeks, and perfusion fixation was carried out with 3% glutaraldehyde solution. Tissue blocks were taken from the cerebral cortex of the frontal lobe, and examined by transmission electron microscopy. Granule-laden perivascular cells were distributed around the fine vessels. The perivenular granule-laden cells contained secondary lysosomes, residual bodies, Golgi vesicles, fusion vesicles and vacuoles. However, in the periarterioar ones, secondary lysosomes and vacuoles were not prominent. These findings indicate that the granule-laden cells may be histiocytes which appear as a vascular reaction to hypertension and hypercholesterolemia, and the vascular reaction may occur more strongly in the veins in comparison with the arteries.

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A rare case of spontaneous cerebellar hemorrhage from hemangioblastoma is reported. A 47-year-old man with untreated hypertension complained of sudden onset of vertigo and vomiting. An initial CT scan showed no abnormal findings, and the patient was treated conservatively. A repeat CT scan taken 11 days after onset revealed a hemorrhage in the left cerebellar hemisphere. On the 15th day, the hematoma was enlarged and the patient became stuporous due to an upward transtentorial herniation. A suboccipital craniectomy was immediately performed. At operation, a dark reddish mass measuring 5 mm × 5 mm × 10 mm was noted in the wall of the hematoma cavity and was resected. Histological examinations demonstrated a hemangioblastoma with endothelial proliferation, foamy cells and various sizes of capillaries. We stress the importance of histological examinations in cases of atypical hemorrhagic intracerebellar lesions even in patients with hypertension.

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