A 43 year old male presented with a sudden onset of gait disturbance and urinary incontinence. An emergency CT scan revealed a subarachnoid hemorrhage and a spherical calcification on the right side of the foramen magnum. He was admitted to the hospital with generalized deterioration (bradycardia and irregular respiration).
The patient's general condition stabilized after 2 weeks and a contrast enhanced CT scan and a cerebral angiogram were carried out. Aneurysms were noted at the trifurcation of the right middle cerebral artery, A₂ portion of the anterior cerebral artery and the M₂-M₃ portion of the left middle cerebral artery supratentorially. Infratentorially, the right vertebral artery was hypoplastic and no contrast material entered the spherical calcified lesion observed by CT.
Based on these findings, the subarachnoid hemorrhage was thought to be due to a rupture of a supratentorial aneurysm. These supratentorial aneurysms were therefore surgically clipped. Unfortunately, after the 2 month uneventful postoperative course, death occurred secondary to hemorrhage from the posterior surface of the aneurysm at the M₂-M₃ portion of the left middle cerebral artery.
The 9 prior cases of aneurysms of the central side of the VA-PICA bifurcation have been identified in the literature. The present case describes hemorrhage from the trunk of the M₂ portion of the left middle cerebral artey in the posterior surfase of the aneurysm treated with clipping. Hemodynamic changes before and after the clipping were the most likely cause of the fatal hemorrhage.

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Using spontaneously hypertensive rats, we studied the effect of allopurinol, a xanthine oxidase inhibitor, on lipid peroxidation in the cerebral tissue after reperfusion for 30 minutes following the occlusion of the bilateral common carotid artery for 3 hours. In the present study, the malonyldialdehyde (MDA) values were measured as indicators for lipid peroxides in the cerebral tissue, and compared them between the group pretreated with oral administrations of allopurinol (400 mg/kg) and the non-treated control group.
As a result, the MDA value measured were found to be 68.9 ± 3.46 n mol/gm in the Sham-operated group and 83.27 ± 5.18 n mol/gm in the control group. However, the allopurinol-treated group showed a level as low as 67.62 ± 3.28 n mol/gm which was significant compared to that of the control group (p<0.05).
These results suggest the possibility that allopurinol inhibits the lipid peroxidation caused by the xanthine oxidase-linked free radical induced by cerebral ischemia and reperfusion.

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A pathological study was performed on cerebral arteries of 22 elderly patients with mean age of 81 years old, who showed the pathological changes of progressive subcortical vascular encephalopathy of Binswanger type (PSVE). Cerebral arteries were examined on the following 4 portions in all cases; main stem of cerebral arteries, leptomeningeal arteries, medullary arteries in the cortex, and small medullary branches in the white matter. Arterial lesionsin PSVE were compared with those in the age-matched cases of non-embolic brain infarction and of cerebral hemorrhage.
The results were as follows;
1) Severe atherosclerosis of middle cerebral artery (MCA) with stenosis over 50% of lumen was found in 68.2% of PSVE, in 63.6% of cerebral infarction, and in 30% of cerebral hemorrhage. The severity of atherosclerotic lesions in MCA was not different between in the cases of PSVE and cerebral infarction. However, the diffuse stenotic type of main cerebral arteries, which was characterized by the severe stenosis of bilateral anterior cerebral arteries (ACA), MCA and posterior cerebral arteries (PCA), was observed in 59.1% of PSVE, only in 27.3% of cerebral infarction, and in 20% of cerebral hemorrhage.
2) Severe stenosis over 50% of lumen in the leptomeningeal arteries was observed in 22.7% of PSVE, in 9.1% of cerebral infarction, but not observed in cases of cerebral hemorrhage. Severe stenosis over 50% of lumen at the cortical portion of medullary arteries was found in 31.8% of PSVE patients. None showed severe stenosis of these arteries in cases of cerebral infarction or cerebral hemorrhage.
3) Hyalinotic vascular stenosis over 50% of lumen in the arterioles of cerebral white matter was found in 59.1% of PSVE patients, in 18.2% of cerebral infarction, and in 40% of cerebral hemorrhage.
4) Angionecrosis (fibrinoid degeneration) in the small arteries or in the arterioles was observed in 72.7% of PSVE patients, in 18.2% of cerebral infarction, and in 70% of cerebral hemorrhage.
5) In PSVE, 9 cases (41%) showed the diffuse stenotic type of main stems in ACA, MCA and PCA associated with the diffuse severe stenosis of arterioles in the cerebral white matter. Some of PSVE patients showed the severe stenosis in the leptomeningeal arteries and/or in the cortical portion of medullary arteries, with or without stenosis in the arterioles of cerebral white matter. Three cases of PSVE showed no severe arterial changes. Amyloid angiopathy in the leptomeningeal and cortical arteries was combined in 5 cases of PSVE.
6) Many of PSVE cases had the history of hypertension. But, 17 cases (77%) of PSVE showed sometimes the systolic blood pressure level under 120 mmHg during their clinical courses.
These observations suggest that PSVE can be induced not only by the hyalinotic changes and stenosis of arterioles in the white matter, but also by the diffuse atherosclerotic lesions of main cerebral arteries, and by the stenotic lesions of leptomeningeal or of main medullary arteries. Under the condition of those vascular lesions, a fall of blood pressure in the hypertensives can play a role to develop the PSVE.

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Using both the conventional low-frequency stimulation method (10 times per second) and the high-frequency stimulation method (50 times per second), auditory brainstem responses were consecutively recorded in a case of basilar artery occlution. A 71-year-old female suddenly fell unconscious. Several hours after, she was admitted to our hospital. On admission, she was stupor. Her eye movement was limited in horizontal direction. She showed ocular bobbing, right Horner's sign and left peripheral facial palsy. She was tetraplegic. All the tendon reflexes was absent. The plantar reflex was extensor. Cerebral angiography revealed an occlusion of basilar artery at the initial segment and the left vertebral artery at the proximal portion. Auditory brainstem responses were carried out. The auditory brainstem responses performed on the first and the second hospitalized day failed to reveal any abnormality. On the third day, the interpeak latency I-V was prolonged in the high-frequency stimulation method. On the forth day, the interpeak latency I-V became significant prolonged by both high- and low-frequency methods. This result suggests that high-frequency stimulation method is more sensitive in detecting the brainstem dysfunction than low-frequency stimulation method. Based on the clinical features and auditory brainstem responses, it can be assumed that the ischemic lesion might be initially localized in the basal part of the pons and extended to the dorsal part of the pons along with progression of the brain edema. It is suggested that auditory brainstem response will be more sensitive tool in evaluating the evolution of the brainstem function utilizing high-frequency stimulation method in addition to the conventional low-frequency stimulation method.

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A case of Down's syndrome with Moyamoya disease is reported. A 15-year-old girl was admitted to our hospital because she had sudden left-sided hemiparesis and could not speak at all. A diagnosis of trisomy 21 was confirmed by cytogenetic karyotype analysis and Moyamoya disease was identified by angiograms. After her admission her hemiparesis deteriorated progressively.
So operation of EDAS (Encephalo-duro-arterio-synangiosis) was performed and her hemiparesis became gradually improved.
An association of Moyamoya disease with Down#CQs syndrome is very rare. Only 6 patients have been reported in the past.
Cytogenetics may be important to discuss the relationship between the two disease.

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The authors analyzed 46 patients of reruptured aneurysms with special reference to the incidence of the symptomatic vasospasm, timing of the surgery and the outcome. Rerupture most often occurred within 24 hours and between 8 to 14 days after initial subarachnoid hemorrhage in our series. Reruptured cases showed high Hunt and Hess grades (III-IV) after rerupture because of complication of intraventricular or intracerebral hematoma in addition to severe subarachnoid hemorrhage.
Surgery was divided into acute (within 3 days after rerupture) and delayed surgery groups (14 days after rerupture) from timing of the operation and the outcome was better in delayed surgery groups than acute surgery groups except in cases in which rerupture occurred within 24 hours after initial subarachnoid hemorrhage, and reruptured cases even with low Hunt and Hess grades had no better outcome than those reuptured cases with high Hunt and Hess grades (III) because of high incidence of symptomatic vasospasm after surgery. From the above results, dalayed surgery should be recommended in reruptured aneurysmal cases to reduce the occurrence of symptomatic vasospasm after surgery.

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Lipids and apolipoproteins were analysed in 228 subjects with thrombotic cerebral infarction and 47 age and sex matched controls (group C) without remarkable atherosclerotic changes in the cerebral arteries. The stroke subjects were divided into two groups upon the findings of carotid angiography as follws, group E : 81 subjects with stenotic lesions in the extracranial carotid arteries/group I : 147 subjects without carotid lesions.
Both serum cholesterol (CHO) and triglyceride (TG) were significantly higher in group E than in group C (p<0.01).HDL-C was significantly lower in group E than in group C (p<0.001). However, differences of CHO, TG and HDL-C between group I and group C were not statistically significant. Atherogenic index (CHO-HDL-C/HDL-C) was significantly higher in both group E and I than in group C (p<0.001), suggesting it was recommended to use atherogenic index as a marker of risk factor for thrombotic cerebral infarction with or without extracranial carotid lesions. On the other hand, apoprotein A1 was significantly lower in both group E and I than in group C (p<0.01). Apoprotein B was significantly higher in both group E and I than in group C (p<0.01). However, no significant difference in apoprotein A2 was observed among 3 groups.
In the present study, it is suggested that there are some differences in the lipid and apolipoprotein abnormalities between the subjects with intracranial atherosclerosis and the subjects with extracranial atherosclerosis. In the stroke subjects, high serum CHO levels and low serum HDL-C levels may be more frequently associated with the development of extracranial carotid lesions. On the other hand, apolipoprotein abnormalities which were characterized by the increase in apoprotein B and the decrease in apoprotein A1 may play important roles on the development of both intra- and extracranial atherosclerosis.

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Clinical figure of cerebral infarction involving anterior cerebral artery (ACA) territory was studied in 1586 consecutive cases of acute cerebral infarction admitted into our stroke care unit. ACA territory infarction was found in 74 patietns, which corresponded to 4.7% of entire cases. The lesion was localized within ACA territory in 8 cases, while the infarct involved also other regions in 66. Localized ACA infarction was always caused by thrombosis except for one patient who had embolic ACA occlusion. In this particular patient, hypoplasia of the contralateral A₁ portion was observed angiographically. On the other hand, non-localized ACA infarction was produced mainly by embolism. Angiographical examination of the cases of ACA territory embolism showed high incidence of hypoplasia of the contralateral A₁ portoion or occlusion of the contralateral internal carotid artery. These two occlusive changes were probably facilitating factors for occurence of ACA territory embolism. Prognosis of the cases with localized ACA infarction was generally exellent, while that of the cases with non-localized infarction was poor and often resulted in brain death. The results of the present study indicate that the pathogenesis of localized and non-localized ACA territory infarctions are quite different.

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Involvement of platelet-activating factor (PAF) in atherogenesis has been increasingly recogenized in the past few years. PAF is degraded by the action of a specific enzyme, PAF acetylhydrolase; and the estimation of this enzyme activity in plasma may provide an effective measure for clinical studies of atherosclerotic disorders. Our previous study demonstrated an increased PAF acetylhydrolase activity in plasma from patients with cerebral thrombosis. The higher enzyme activity was accounted for by the increased plasma level of LDL, which had been known to carry a major part of plasma PAF acetylhydrolase. However, it was also true that the higher enzyme activity could not be attributed solely to hyperlipoproteinemia; and we hypothesized that platelet hyperfunction would play a critical role. To test this hypothesis, we have studied the relationship between platelet aggregability and plasma PAF acetylhydrolase activity in patients with ischemic stroke.
Thirty-two consecutive patients with cerebral infarction ranging in age from 49 to 81 (66 ± 9.3) years old and 73 age-matched healthy controls (63 ± 7.3 years old) were studied. Plasma PAF acetylhydrolase activity was determined by the method described by Stafforini and coworkers using [2-acetyl-³H] PAF as the substrate. Platelet aggregation induced either by 40 ng/ml PAF or by 2 μM ADP was observed according to Born.
The incidence of irreversible aggregation in response to 40 ng/ml PAF was significantly higher in patients than in controls (62.5% versus 11.0%, p<0.05). The average maximal aggregation in patients was 53 ± 24.3%, which was significantly higher than that in controls : 30 ± 12.2% (p<0.01). The plasma PAF acetylhydrolase activity in patients and controls were 107 ± 47.9 nmol/ml/min and 78± 34.2 nmol/ml/min, respectively; and there was a statistically significant difference between these two values (p<0.01). Among patients, those whose platelets responded with irreversible aggregation to 40 ng/ml PAF displayed a significantly higher plasma PAF acetylhydrolase activity than those with only reversible aggregation. There was no significant difference in the enzyme activity by the irreversibility of ADP-induced aggregation.
These results suggest that PAF may be involved in platelet hyperfunction in patients with cerebral infarction. Increased plasma PAF acetylhydrolase activity in these patients may be an adaptation to platelet hyperfunction. Augmented platelet function may be associated with increased production of PAF, which may bring about the induction of the metabolizing enzyme, PAF acetylhydrolase.

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The registration of intracranial aneurysm started on January 1985 with co-operation of 13 hospitals in Yamaguchi prefecture, which had the population of 1, 601, 627. These 13 hospitals include all neurosurgical clinics which can performed the radical operation of intracranial aneurysm in the area. The diagnosis of intracranial aneurysm was confirmed by angiography, operation or autopsy. The conclusions of the study is as follows.
1) 228 cases of intracranial aneurysm were admitted in the co-operative hospitals from January 1 to December 31, 1985. The incidence rate for 100, 000 population per year was 14.3.
2) The age distribution of these patients was from 14 to 81 years old with the average of 54.8 y.o. This series included 82 males and 146 females. Female dominancy of the disease seems to be characteristically in the west part of Honshu island and in Kyushu area. This area specificity should be confirmed whether statistically significant or not in future.
3) Considerably low incidence rate of the disease was seen in far distant area from co-operative hospitals compare with that observing in neighboring area. Therefore it must be emphasized that more precise education of this disease to the population living in low incidence area.
4) It has been reported that the cases from 11 to 35 per cent of subarachnoid hemorrhage succumbed within one day after bleeding. More attention and effective treatment should be considered to this group for improving the recovery rate.

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A case of dural arteriovenous malformation in the anterior cranial fossa is reported.
A 71-year-old, right handed, male was admitted on March 4, 1987 for the evaluation of sudden onset of consciousnes disturbance and right hemiparesis. Computed tomography scans showed severe subarachnoid hemorrhage and a hematoma in the left frontal lobe. Angiograms showed a dural arteriovenous malformation in the left frontal lobe fed by the bilateral anterior ethmoidal arteries and the superficial temporal arteries and drained by the abnormally dilated vein, so-called vascular sac or aneurysmal dilatation, and then, drained to the superior sagittal sinus. The patient was initially treated with spinal drainage for a while because of his advanced age and almost recovered from his complaints 40 days after the onset. The second computed tomography scans taken 29 days after the onset disclosed a small fresh hematoma without worsening his neurlogical signs. Suggesting recurrent hemorrhage, surgical evacuation of the hematoma and removal of the vascular sac were performed 92 days after the onset. The nidus at the bilateral olfactory grooves was coagulated. Post operative angiograms revealed complete absence of any vascular anomaly. The patient was discharged without any neurological deficits 30 days after the operation.
The clinical features, neuroradiological findings, and surgical procedures were discussed in the cases with this malformation reported in the literature.

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