The CT findings of 19 hemodialyzed patients with brain hemorrhage (BH) were evaluated. The 30-day mortality rate was 78.9%. The lesion locations in the 19 cases with BH were putaminal hemorrhage in 8 patients, putaminothalamic (mixed) hemorrhage in 7, thalamic hemorrhage in one, subcortical hemorrhage in one, and cerebellar hemorrhage in one. In the remaining patient, the bleeding was confined to the ventricular system. One remarkable CT finding was the formation of a massive hematoma in most cases. In some cases, the hematoma occupied the greater part of one cerebral hemisphere. Oral anticoagulants and/or antiplatelet drugs, and intravenous heparinization could produce massive accumulations of blood in the brain parenchyma. The second major finding was the low CT absorption values of the hematoma at the acute stage, as compared to that of hypertensive BH. This decreased absorption density resulted from a low hemoglobin concentration in the hematoma itself due to the severe anemia occurring in patients on long-term maintenance hemodialysis.

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As a focal ischemic model, occlusion of the middle cerebral artery (MCA) of rats is frequently employed, and many methods have been reported such as direct MCA occulusion or intravascular occlusion. One major problem in creating the infarction is the variability in size of the resultant ischemic lesion due to collateral circulation. To examine this variability, we observed the MCA in rats under an operative microscope and established a method for creating a reproducible infarcted region. Among 100 rats in which the MCA was investigated in this study, 35 were sacrificed between 24 and 48 hours after surgery and the sectioned brains were stained with TTC (2, 3, 5-triphenyltetrazolium chloride) and subjected to evaluation of the infarcted area. The MCA observed through the microscope within the operative field was divided into three sections by the olfactory tract and the inferior cerebral vein which runs just above the rhinal fissure. In a large number of cases (87 cases, 87%), a couple of branching arteries ran anterioly and posteriorly, and the MCA bifurcated into frontal and parietal branches. In addition to this standard type of branching pattern, 8 cases (8%) revealed an early bifurcation of the MCA, 4 cases (4%) showed a fenestrated MCA, and one case (1%) had no bifurcation within the operative fleld. To eliminate collateral blood circulation from the frontal branch through the anterior cerebral artery, we cauterized the MCA from its origin to the bifurcated region. Among the 35 cases evaluated by TTC staining, 33 (94%) demonstrated high-grade cortical infarction. We conclude that in order to create a reproducible cortical infarction in the rat by direct MCA occlusion, it is necessary to obliterate the MCA from its origin to just distal to the emerging frontal branch.

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The occurrence of complications after cerebral angiography is still too frequent to be ignored in spite of the numerous technical and methodological advances. A strict indication for this procedure is thus extremely important, especially in cases of chronic occlusive disease. We investigated the CBF perfusion reserve by acetazolamide activation using the Xe/CT method in 20 cases of chronic occlusive disease who were divided into an occlusive group with a major cerebral artery affected (13 cases) and a non-occlusive group (7 cases). In the non-occlusive group, the increases in CBF after administration of Diamox were 37.7 ± 11.2% in the affected hemisphere and 34 ± 23.1% in the area affected by the middle cerebral artery, and these observed increases were statistically significant. In the occlusive group, the increases in the affected hemisphere and the area of the middle cerebral artery were 16.0 ± 18.8% and 10.0 ± 21.7%, respectively, and in the area affected by the middle cerebral artery the increases in CBF were below 30% except in one case. CBF perfusion reserve studies by acetazolamide administration are thus useful for identifying any suspected severe stenosis or occlusion of a major cerebral artery. Further when the CBF increase in the affected middle cerebral artery region is below 30%, we strongly recommend that cerebral angiography be performed in order to secure an accurate diagnosis.

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The purpose of the present study was to clarify the effect of nitric oxide on glutamate release in the rat striatum during and after transient forebrain ischemia and to elucidate the role of nitric oxide in cerebral ischemia. Two microdialysis probes were inserted into the bilateral striata of Wistar rats. One hundred μM N-ω-nitro-L-arginine (L-NNA), a nitric oxide synthase inhibitor, was topically administered to the unilateral striatum through one of the microdialysis probes, while Ringer's solution was perfused in the contralateral striatum as the control. Eleven rats were subjected to transient forebrain ischemia for 14 min, and the extracellular glutamate concentrations on the two sides were compared. The extracellular glutamate concentration in the striatum during ischemia was statistically significantly higher on the L-NNA-perfused side than on the control side (11.27 ±4.07 μM vs. 8.31 ± 2.77 μM, respectively; p< 0.01). Moreover, the extracellular glutamate concentration in the striatum during the reperfusion phase was also significantly higher on the L-NNA-perfused side than on the control side (6.63 ± 2.58 μM vs. 4.17 ± 1.88 μM, respectively; p <0.01). When 100 μM L-NNA was perfused together with 500 μM L-arginine, the extracellular glutamate concentration did not differ from that on the control side. It appears that nitric oxide inhibits excessive release of glutamate during ischemia and reperfusion, and thus affords protection against ischemic neuronal damage.

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It has frequently been reported that patients with ischemic heart disease (IHD) develop ischemic cerebrovascular disease as a complication, while patients with ischemic stroke suffer fatal IHD. This demonstrates the clinical importance of investigating the relationship between atherosclerosis in the cerebral and coronary arteries. We studied 17 patients with suspected atherosclerotic ischemic strokes who underwent both cerebral and coronary angiography in our hospital between January 1989 and September 1993. Patients with embolic stroke were excluded. The severity of cerebral arterial atherosclerosis was evaluated by grading scores of the narrowing of the artery on the cerebral angiograms. Grade 0 represented an artery with narrowing of less than 25% of the diameter, grade 1 narrowing of 25-49%, grade 2 narrowing of 50-74%, grade 3 narrowing of 75-99%, and grade 4 occlusion of 100%, respectively. The severity of coronary arterial atherosclerosis was evaluated by Gensini's score (Gensini, 1983) and a coronary angiography score (Tanaka et al., 1992) / Gensini's score represented the total of the scores in 15 segmental coronary arteries, in which each score was calculated according to the narrowing of the arterial diameter and functional significance of the area supplied by the segmental artery. The coronary angiography score was defined as the number of affected coronary branches (right and left anterior descending branches and left circumflexus branch) with more than 75% narrowing of the diameter. Risk factors such as sex, hypertension, diabetes mellitus, hyperlipidemia, and smoking, were also examined. The results obtained may be summarized as follows. (1) All patients were males. (2) Ischemic heart diseases had preceded in 14 (82%) of the patients. (3) Smoking, hyperlipidemia and hypertension were evident as risk factors. (4) The severity of atherosclerosis of the extracranial cerebral arteries (bifurcation of the internal caroid artery and vertebral artery) was significantly correlated with that of the coronary artery (Spearman rank correlation, p < 0.05). (5) The severity of atherosclerosis of the intracranial arteries (intracranial portion of the internal caroid artery, M1 portion of the middle cerebral artery, posterior cerebral artery, and basilar artery) was not correlated with that of the coronary artery. The present data suggest that the atherosclerotic mechanism of the extracranial cerebral artery was similar to that of the coronary artery. Factors such as sex, smoking, lipid metabolism, and blood pressure, may be strongly related to the mechanism.

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MRI studies were carried out on 69 patients with multiple lacunar infarcts : 32 had hyperactive-type delirium and the other 37 were non-delirious controls. Between the two groups, there were no statistically significant differences in mean age and sex distribution. In the corona radiata and basal ganglia, the number of infarcts did not differ between the two groups. However, the extent of thalamic infarcts and periventricular hyperintensity (PVH), the maximal width of the third ventricle and Evans' ratio among the delirious patients were significantly larger than those in the controls. In conclusion, thalamic lesions and diffuse advanced PVH may have an intimate correlation in the development of hyperactive-type delirium in patients with multiple lacunar infarcts.

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We report a case of spontancous dissection of the intracranial internal carotid artery with plasminogen abnormality. A 41-year-old woman suffered from weakness of her right upper extremity and narrowing of the visual field in her left eye. Branch occlusion of left retinal artery was disclosed, and brain MRI revealed multiple brain infarction in the territory of the left middle cerebral artery. Left carotid angiography demonstrated a string sign in the cavernous portion, suggesting dissection of the intracranial internal carotid artery. Following anticoagulation therapy, cerebral angiography showed recanalization, although reocclusion occurred 27 days later, and MRI delineated a double lumen in the petrosal-cavernous portion. Since the patient suffered from another brain infarction 10 months later, we performed position emission tomography which demonstrated matched hypoperfusion of cerebral blood flow and oxygne metabolsim. Biopsy of the frontal branch of the superficial temporal artery revealed a multi-laminated basal lamina, mild intimal thickening amorphous materials, and decreased collagen, which suggested systemic vascular disease. We therefore, treated the patient conservatively without bypass surgery. She was also a case of familial plasminogen abnormality, which might be associated with progressive thrombus formation after dissection of the intermal carotid artery.

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We describe a 57-year-old man with positivity for anticardiolopin antibody complicated by two episodes of subcortical hemorrhage. Although a CT scan, MRI and cerebral angiography were repeatd, they did not reveal any abnormality suggestive of an etiology. Data for coagulation tests such as the bleeding time, prothrombin time and analysis of coagulation factors were also negative. Biopsy was not carried out, but the concentration of cystatin C in the cerebrospinal fluid was normal, indicating that hemorrhagic lesions were not induced by amyloid angiopathy. The only persistently abnormal finding in the laboratory studies was positivity for anticardiolipin antibody, i.e. antiphospholipid antibody. There was no serological evidence of SLE or other autoimmune diseases. We concluded therefore that anticardiolipin antibody may have played an important role in the repeated subcortical hemorrhage. Antiphospholipid antibody should be considered in cases of unexplained repeated intracerebral hemorrhage.

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We report 3 cases of bilateral medial thalamic infarction, 2 of which were associated with midbrain infarctions. All of the cases abruptly presented with transient deterieration of consciousness as an onset symptom. Hypersomnia, a hypoactive tendency and recent memory disturbance followed as common symptoms at the chronic stage, and the cases with midbrain infarctions revealed vertical gaze palsy. The etiologies of the infarction in our cases were assessed from the results of CT scans, MR imaging, and angiography to be as follows : 1) temporary occlusion of the vertebral artery at the time of head rotation, 2) emboli possibly originating from dissection of the basilar artery, and 3) thrombo-embolism of the perforating arteries due to diabetes mellitus. Although conservative therapy resulted in no mortality, both memory and intellectual impairments handicapped the patients' normal daily living. The correlation between the clinical featurs of cerebrovascular disease and vascular anatomy of the medial thalamus is discussed with a review of the literature.

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We report a female case of pontine lacunar infarction showing hemiataxia and homolateral sensory disturbance. The ataxia consisted of limb ataxia and truncal ataxia on the left side. The sensory disturbance appeared as paresthesia on the left half of the body and hypesthesia on the left half of the face. MRI revealed a small lacunar infarction at an opposite site in the upper pons. The lesion was situated in the border zone between the base and tegmentum, and almost on the midline. It was thought to be an infarction in the territory of the paramedian artery. Contralateral cerebellar signs were thought to have been caused by interruption of the precrossed pontocerebellar fibers or destruction of the reticular tegmental pontine nucleus. Further, destruction of the medial lemniscus and ventral trigeminothalamic tract was thought to have elicited sensory disturbance.

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We report 2 cases of systemic lupus erythematosus (SLE) with anti-phospholipid antibodies (aPLAb) presenting with cerebral hemorrhage after ischemic stroke. Case 1 was a 42-year-old man who had suffered from SLE 3 years previously, and was admitted to our hospital because of cerebral infarction. Thalamic hemorrhage occurred while he was hospitalized. Case 2 was a 37-year-old woman who had suffered from SLE 9 years previously, had 2 ischemic strokes prior to admission, and was admitted because of ischemic stroke. Thalamic hemorrhage with ventricular rupture occurred 1 year after the last ischemic stroke and she died. Both cases exhibited severe hypertension during their course. In case 2, a postmortem examination of the central nervous system was performed. Multiple large infarcts and massive cerebral hemorrhage were observed. Microscopic examinations revealed arteriolar thickening, small infarcts and hemorrhages, but angitits and angionecrosis were not detected. These findings differed from those in hypertensive cerebral hemorrhage. Although aPLAb may play an important role in the development of ischemic stroke in SLE, cerebral hemorrhage is a rare complication. We speculate that severe and uncontrolled hypertension is an important risk factor of cerebral hemorrhage in SLE patients with aPLAb.

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