The usefulness of helical CT for detecting intracranial aneurysms was evaluated. The diagnostic accuracy of helical CT was compared with that of conventional cerebral angiography in 83 aneurysms of 64 patients. The scanning parameters were 135 KV, 250 mA and a 1-mm slice thickness. The couch top was moved at 1-2 m/s during the scanning of 30s. For postprocessing, 3-D CT images by a volume-rendering technique and MPR images were provided using a work station. The detection rates by helical CT and angiography were 96.4% and 97.6%, respectively. Helical CT was superior to conventional angiograms in its multi-directional display of the circle of Willis, including base view projections for visualizing small aneurysms such as blister-like aneurysms or aneurysms surrounded by complicated arteries and thrombosed aneurysms. All aneurysms located above the anterior clinoid process could be observed retrospectively. The smallest aneurysms with a diameter of 1-2 mm were demonstrated by this technique. Multiple reconstruction images provided information on the intra-aneurysmal thrombous or calcified parts and associated vascular anomlies. Conventional angiograms were superior to helical CT in revealing intraclinoid small aneurysms with a diameter of less than 6 mm and perforating branches of less than 1 mm in diameter. With respect to larger aneurysms with diameters of over 12 mm, helical CT tended to be more useful than conventional angiography for delineating the aneurysmal blebs, neck and orifice of the aneurysms, as well as the relation to the surrounding vessels. From the standpoint of preoperative simulation, helical CT provided useful information on the anatomical relationship with the parent artery, inner view of the aneurysm and bony structures around the aneurysm. From the neurosurgical viewpoint, helical CT is considered more useful than conventional angiography for delineating intracranial aneurysms.

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We studied the risk factors for small-vessel disease revealed by magnetic resonance imaging (MRI) of the brain. In total, 133 patients with asymptomatic or symptomatic cerebral infarction were randomly selected for the study, including 64 males and 69 females with an average age of 66.7 ± 10.1, and age range of 40 to 85 years old. Among them, 91 patients had a history of symptomatic cerebral infarction, 46 patients of hypertension, and 28 patients of diabetes mellitus. Patients with large cortical infarctions, cerebral hemorrhage, demyelinating disease or mass lesions were excluded. The MRI scans were reviewed for areas with increased signal intensity on T2-weighted images. The grade of periventricular lesions, and the number of small infarctions in the subcortical white matter, basal ganglia and brainstem increased significantly with advancing age. It was thus reconfirmed that age is an important risk for demonstrating small-vessel disease on brain MRI. In addition, the degree of small-vessel disease on brain MRI was more extensive in patients with symptomatic cerebral infarction than with asymptomatic cerebral infarction. The detailed results suggest that small-vessel disease on brain MRI in patients with asymptomatic cerebral infarction might represent preclinical lesions for symptomatic cerebral infarction. The numbers of small infarctions in both the subcortical white matter and basal ganglia associated with advancing age, and histories of cerebrovascular accident and hypertension, suggest that common underlying mechanisms may exist in small-vessel disease in both the medullary arteries, which arise from cortical arteries, and perforating arteries. In the subcortical white matter, the number of patchy lesions was more strongly correlated with histories of hypertension and diabetes mellitus than was the number of spotty lesions, suggesting that the risk factors differed depending on the size of the lesions. The present study revealed that the degree of small-vessel disease on brain MRI was not correlated with the serum concentration of total cholesterol, triglyceride or HDL-cholesterol. The data thus indicate that the risk factors for small-vessel disease are distinct from those for large-vessel disease.

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The circles of Willis in 2011 patients were examined by 3-dimensional time-of-flight MR angiography in order to evaluate the variations. The Al segment of the anterior cerebral artery was not found in 4.8% on the right side and in 3.4% on the left side. In the older patients, MRA failed to demonstrate either the right or left Al segment. A fetal configuration, whereby P1 segments had a smaller diameter than the posterior communicating artery and the posterior cerebral artery derived predominantly from the carotid artery, occurred in 19.8% on the right side and in 16.7% on the left side. MRA did not reveal the posterior communicating artery to be more common in the elderly. The circulatory states in the circle of Willis may alter with aging.

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Endothelin-1 (ET-1) is a recently identified 21-amino acid peptide produced by the vascular endothelium and is the most potent known vasoconstrictor. The present study attempted to evaluate the interaction between the level of ET-1 and the concentration of noradrenalin in the plasma over a period of 2 weeks following an episode of cerebral hemorrhage. Thirty-seven patients with cerebral hemorrhage were examined. We estimated the immunoreactive ET-1 by radioimmunoassay. The level of ET-1 during the acute stage (day 7) was 4.03 ± 1.32 pg/ml, which was significantly higher than that (2.03± 1.38 pg/ml) during the subacute stage (day 8 to day 14). During the acute stage, a close relationship existed between the ET-1 (X) and noradrenalin (Y). Linear regression analysis yielded the following equation : Y= 148.62X -18.38 (r = 0.555, p <0.01). Also, during the subacute stage, the increase in level of ET-1 (X) with noradrenalin (Y) revealed an excellent linear relationship (Y=251.1X + 196.08; r = 0.867, p<0.01). These linear regressions obtained during the acute stage and during the subacute stage displayed a significant difference (p < 0.01). In conclusion, the time course of interaction between ET-1 and noradrenalin may be closely related to the functional sequence of derangement of both the endothelium and noradrenalin nervous system.

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The purpose of the present study was to evaluate the clinical profile of silent cerebral infarction patients, based on consecutive patients with lacunar lesions detected by cranial CT. From among a series of patients who had undergone CT at Fukuoka University Hospital between January 1983 and April 1989, 3006 patients without apparent lesions on CT were extracted. Of these 294 patients (193 men and 101 women; age, 64.5 ± 12.5 yr. mean ± SD) with lacunar lesions were examined in this study. The subjects were divided into two groups : 164 who had no clinical stroe episodes (silent infarction group) and 130 who had stroke episodes (infarction group). The CT findings and vascular risk factors were compared between the two groups. The number and size of lacunar lesions were smaller in the silent infarction group than in the infarction group. In the silent infarction group, the number of lacunar lesions increased as the age of the patients increased. Among the risk factors, hypertension, values for the hemoglobin, hematocrit, uric acid and total cholesterol levels were found to difer between the two groups. The complication of hypertension and actually measured blood pressure were significantly lower in the silent infarction group than in the infarction group. The values for the hemoglobin, hematocrit, uric acid and total cholesterol in the silent infarction group were lower although within the normal ranges than those in the infarction group. Multivariate analysis suggested that the values of the nematocrit. In the asymtptomatic group, 35.3% of the subjects had no vascular risk factors and involved patients who were diagnosed as having malignant tumors. Our study demonstrated that silent cerebral infarction patients had fewer vascular ris factors as compared to cerebral infarction patients.

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The brain perfusion index (BPI) and cerebral blood flow in the territory of the middle cerebral artery (mca CBF) using 99m-TcHPMAO-SPECT were evaluated in comparison with the severity of large vessel stenosis in the carotid system in 17 patients (mean age, 64 ± 6 years old) with lacunar stroke. We defined mean mcaCBF of 4 regions of interest in the territory of the middle cerebral artery in the lesion site hemisphere in relation to those of the contralateral hemisphere as the % decrease in mcaCBF. The severity of stenosis of the internal carotid or middle cerebral artery was evaluated from the grading score of the narrowing of the artery on angiograms, as follows : score 0, narrowing of less than 50%; score 1, narrowing of 50-75%; score 2, narrowing of 75-90%; score 3, narrowing of 90-99%; and score 4, complete occlusion. The patients with scores of more than 3 showed a significantly lower % decrease in mcaCBF than did those with scores of less than 2. Although the BPI and mcaCBF were influenced by collateral blood flow and diaschisis in lacunar stroke, stenotic lesions of the carotid system of more than 90% significantly lowered the cerebral circulation in the lesion site hemisphere. In conclusion, quantitative assessments of the cerebral circulation may be needed for secondary or tertiary preventive strategies in patients with lacunar stroke.

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Activated protein C resistance (APC-R) has recently been reported to be the most common hereditary blood coagulation disorder associated with familial thrombosis. APC-R is characterized by a poor anticoagulant response to APC in the plasma of patients the and is due to a defect of factor V. However, all the data relating to APC-R have been derived from Westerners, and little information is yet available on APC-R in Japan. We therefore studied 82 patients suffering from stroke and 33 patients with neurological disease who remained free of vascular disease, by measuring the activated partial thromboplastin time (aPTT) with and without addition of APC. We also determined whether a mutation (Arg506→ Gln) of the factor V gene was present or absent. All patients revealed an APC ratio within the normal range, and the mutation was absent in all of them. We conclude that the incidence of APC-R is very low in Japan.

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In the present study, the inhibitory effect of trapidil, a receptor antagonist of platelet-derived growth factor (PDGF), on the proliferative organic changes occurring in cerebral arteries after subarachnoid hemorhage (SAH) was examined experimentally. In an in vivo study, we evaluated the preventive effect of trapidil on the development of organic changes in experimental SAH. Twenty-eight cats were divided into 4 groups : the SAH (n=8), trapidil-treated (n=8), non-surgical control (n=7), and trapidil-control (n= 5) groups. SAH was produced by transorbital rupture of the right middle cerebral artery (MCA). In the trapidil-treated group, trapidil (20 mg/kg/day, i.m.) was administered daily, from 2 days before through 14 days after SAH. At 2 weeks after SAH, the animals were sacrificed by infusion of periodic, lysine-paraformaldehyde solution into the right common caroid artery. The right MCA was dissected out, and prepared for light and electron microscopic examination. Organic changes demonstrating narrowing and wall thickening on light microscopy and subintimal proliferation of smooth muscle-like cells and increased extraccellular matrix in the media on electron microscopy, were present in the SAH group. Such changes were not observed in the trapidil-treated animals. In an in vitro study, we evaluated the effect of trapidil on the contraction of collagen type I gels populated by rat vascular smooth muscle cells, a model of vascular remodeling. Contraction was quantified as the decrease in gel diameter. Trapidil suppressed the gel contraction in a concentration-dependent manner (10 and 100 μg/ml). Trapidil may inhibit the proliferative organic changes that occur after SAH. Furthermore, trapidil may be clinically useful for preventing delayed ischemic deficits caused by cerebrovascular organic changes and may enhance the vasodilatory effect of calcium antagonists following SAH.

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A 41-year-old man noticed nausea, left occipital pain, numbness of the left face and right hemiparesis. He had left Horner's sign, rightward nystagmus, left soft palate paralysis, dysphagia, hoarseness, dysarthria, diminished sensation of temperature and pain on the left side of the face and right side of the body, and ataxic gait at the 3rd day when he was admitted to our hospital. He was diagnosed as having lateral medullary syndrome. Left vertebral artery dissection was suspected. On admission, duplex ultrasound sonography demonstrated occlusion of the left vertebral artery after the branching of the posterior inferior cerebellar artery. Vertebral artery dissection was further suspected because of tapering occlusion on cerebral angiography. On the 17th day, MRI disclosed a septum (intimal flap) in the left vertebral artery. Dissection in the intracranial vertebral artery was confirmed by the intimal flap and sequential changes in findings for the intensity in the vertebral artery by MRI.

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A 36-year-old woman was hospitalized because of left hemiplegia with sudden early morning onset. She had untreated hypertension, and had taken tranquilizers for the past 7 months because of emotional instability accompanied by mild mental retardation which had developed after severe head trauma at 5 years of age. However, she had never demonstrated a bleeding tendency. On admission, her skin and mucosa showed no signs of hemorrhage or vascular anomaly. A CT scan revealed a massive hematoma in the right putmen. On the 12th hospital day, hemorrhage recurred in the left putamen. The bleeding time (BT) increased from that on admission, although the platelet count, prothrombin time, activated partial thromboplastin time, thrombo test, plasma fibrinogen level, and activity of coagulation factors were normal. After increasing for 4 weeks, the BT then normalized. Platelet functions examined during the 6th hospital week were normal. Brain MRI demonstrated no vascular anomaly. This patient represented a rare case of recurrent intracerebral hemorrhage probably due to hypertension. The transient prolongation of the BT appeared to aggravate the hemorrhage, but the factors causing the prolongation remain uncertain. Among 37 patients with acute intracerebral hemorrhage without a bleeding tendency hospitalized between 1992 and 1994, two showed a transiently prolonged BT. There is a possibility therefore that intracerebral hemorrhage itself may prolong BT.

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The patient was a 59-year-old man with progressing ischemic stroke associated with polycythemia vera despite phlebotomy a period of 3 months. He had a history of polycythemia 3 years previously. The symptoms began with numbness and weakness in the left hand, and were slowly progressing to include consciousness disturbance, tetraparesis and global aphasia despite phlebotomy and antiplatelet therapy. Brain CT images showed extension of low density areas in the bilateral supratentorial regions. When treatment with alkylating agent was strated, the polycythemia and thrombocytosis gradually subsided, and the patient's symptoms became stable. Cerebral angiography revealed M2 occlusion of the left middle cerebral artery. Polycythemia vera, age, phlebotomy, hypertension, diabetes, and delay in chemotherapy may be factors of progressing ischemic stroke. If a patient with polycythemia vera displays of progressing ischemic stroke despite phlebotomy, early chemotherapy is needed.

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We report a 38-year-old man who developed lateral medullary syndrome and vertebral artery dissection, probably as a complication of neck rotation during golf exercise. He noticed pain in the neck, after golf exercise for 4 hours. Two hours later, he had numbness in the left hand and ataxic gait, followed by hiccups. On the 4th day when he was admitted to our hospital, he showed right lateral medullary syndrome. On the 5th day, right vertebral angiography disclosed an irregular wall (string signs) from the V3 portion of the vertebral artery to the junction of both vertebral arteries, which disappeared on the 56 th day. We therefore diagnosed the patient as traumatic vertebral dissection due to quick rotation and/ or extension of the neck and head during golf exercise.

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