A 36-year-old housewife who had bilateral pulmonary arteriovenous fistulae had a sudden attack of basilar artery occlusion. At onset loss of consciousness accompanied by double hemiplegia with left-side predominance, myosis, paralytic pontine exotropia was observed. The lesion might be lower pons level. In the recovery period transient asymmetrical ocular bobbing appeared under the condition of r-MLF, PPRF and abducens palsy. She gradually recovered, and on the course such a rare symptom as right gaze palsy with nocturnal right conjugate deviation was noticed. Strong impulses from vestibulo-ocular reflex arc during sleep may explain this phenomenon. She returned home one year later at the level of independence on eating and excretion, living using wheelchair. Since the previous attack at the age of thirty, she had not been able to understand any spoken language (word deafness) due to bilateral temporal infarctions. This time she lost her speech ability because of pseudo-bulbar palsy, although she was able to make a voice. On angiography basilar artery was occluded just proximal to the branch of superior cerebellar artery. In the following six months both vertebral and basilar arteries became gradually narrow and the territory of internal carotid artery extended. As to the etiology of this infarction paradoxical embolism brought to the basilar artery through the pulmonary shunt was considered.

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A case of aortitis syndrome with recurrent intracranial hemorrhages is reported. A 63-year-old female was admitted to the Department of Neurosurgery, Washokai Sadamoto Hospital with headache, aphasia and vomiting on December 7, 1983. Seven years prior to admission, she had a left hemiparesis due to cerebral infarction. At that time, weakness of the left radial artery pulse was noticed and systolic bruits were heard on the left supraclavicular fossa and the abdomen. The patient was suspected as having an aortitis syndrome. Seven months prior to admission, she was diagnosed as having cerebellar hemorrhage by CT. On admission, blood pressure was 150/80 mmHg, at the right arm, but it was difficult to palpate the pulsation of the left radial artery. Systoric bruits were audible of supraclavicular fossa and the abdomen. Neurological examination revealed only sensory dominant aphasia. A plain CT scan on admission demonstrated a 5 cm × 3 cm × 3 cm sized high density area in the left temporal lobe. Aortography revealed the stenosis of the thoratic and abdominal aorta and subclavian artery, and the obstruction of the celiac trunk, left subclavian and vertebral arteries. Cerebral angiography revealed no abnormal findings.
In cases of aortitis syndrome, intracranial hemorrhagic disease is rarer than ischemic diseases. But the cerebral hemorrhage due to hypertension is one of the most frequent causes of the death in the cases of the aortitis syndrome. Here we discuss the possible mechanism of hypertension in the case of the aortitis syndrome, and suggest that it is important to controal the blood pressure to prevent intracranial hemorrhage in the cases of aortitis syndrome.

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As an index implying the severity of damages in cerebral circulations in patients with cerebrovascular diseases (CVD), CO₂-reactivity (CO₂-R) is important. However, in the past, measuring the CO₂-R has sometimes needed invasive procedures and real-time recording of the cerebral circulation fluctuating with CO₂ has been difficult. We employed the transcranial Doppler flowmetry as a casual tool to measure the CO₂-R and investigated the reliability of this method in comparison with cerebral blood flow studies by the Argon inhalation method.
Fifteen patients thirteen with cerebral infarctions, one with aortitis syndrome, one with orthostatic hypotension were monitored middle cerebral artery blood velocity (MCAV), cerebral blood flow (CBF), and arterial gases in the condition of hyperventilation, normoventilation, and 3%, 5%, 7% CO₂ load. MCAV was measured by the use of a transcranial pulsed Doppler blood velocimeter (Aaslid et al., 1982). Basal CBF was directly measured by the Argon inhalation method based on the Fick's principle using the mass spectrometry of Argon at an artery and an internal jugular vein and CBF changes were calculated from the changes in arterio-venous oxygen differences. CO₂-R was calculated as k value in the formula of LnCBF=kpCO₂ + A presented by Olesen et al.
The mean value of MCAV was 34.5, 54.4, 62.4, 80.1, 96.8 cm/sec and the mean value of CBF was 27.3, 44.1, 49.8, 65.8, 86.2 ml/100 g/min in the condition of hyperventilation, normoventilation, and 3%, 5%, 7% CO₂ load, respectively. The CO₂-R in MCAV was 0.0391 ± 0.0062 (mean ± S.D.) and the CO₂-R in CBF was 0.0406 ± 0.0060 (mean ± S.D.). The association of the CO₂-R in MCAV with that in CBF was significant with a coefficient of correlation r=0.89 (p<0.001).
These data suggested that the transcranial Doppler flowmetry on the middle cerebral artery provided reliable information about the vasomotor reactivity of the cerebrovascular system and could be utilized in monitoring patients with CVD or metabolic crises and in the evaluation of the efficacy of the therapeutic regimens.

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A case of persistent primitive trigeminal artery (PTA) associated with Walenberg's syndrome is reported. Cerebral angiogram revealed hypoplastic vertebral arteries, occlusion of left posterior inferior cerebellar artery (PICA) and PTA on the right side.
Vertebrobasilar insufficiency with PTA has been supposed to be due to microembolization from an atherosclerotic carotid artery to basilar artery (BA) via PTA. However, in our case, this mechanism is not proper, both because occluded vessel is PICA arising from vertebral artery proximal to the junction of PTA and BA and angiogram showed neither atherosclerotic plaque at the carotid artery nor stenosis.
It is considered likely that the patient's illness was due to a thrombotic occlusion of PICA, probably atherosclerosis and abnormal vertebrobasilar circulation caused by hypoplasia of vertebral arteries.

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Disorders of the central nervous system (CNS) had been reported to occur frequently following cardiovascular surgery. Many reports tended to focus on the cerebral infarction based on hypotension and microembolism.
The cases with subdural hematoma (SDH), which had direct relation to cardiovascular surgery, had scarcely been reported.
Eight cases of SDH were found among 39 cases of major cerebral dysfunction following cardiovascular surgery in the National Cardiovascular Center for the past three years. Seven cases of them were under anticoagulation therapy. The mean duration of the occurrence of the symptoms after cardiovascular surgery was 8.3 days, and clinical course in the cases had aggravated in several days. In the previous reports SDH cases after cardiovascular surgery were only regarded as a complication of long term anticoagulation therapy. From the evidence that all of our cases occurred during the term of postoperative management, SDH as well as cerebral infarction should be regarded as the CNS complication directly related to the cardiovascular surgery.

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In spontaneously hypertensive rats (SHR), hemorrhagic hypotension (from 140-200 to 20-50 mmHg, 15-60 min) reduced cerebral blood flow to around 4 ml/100 g/min although no ischemic brain damage was observed. In contrast, SHR with unilateral carotid ligation showed a greater decrease in ipsilateral blood flow to 2 ml/100 g/min at the blood pressure level of about 60 mmHg or 30% of control, and developed ischemic lesions after 60 min hypotension.
These findings indicate that reduction of blood pressre below 30% of control for over 60 min causes cerebral damages due to ischemia ipsilateral to the occluded large artey supplying the brain.

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Dissecting aneurysm in the cervical portion of the internal carotid artery (ICA) is known to occur in patients with fibromuscular dysplasia (FMD). However, only a few cases have been recorded in the literature. We report a case of cerebral infarction due to spontaneous dissection of the ICA associated with FMD.
A 45-year-old healthy woman had transient blindness in the left eye and sudden onset of weakness of the right extremities. On the following day she was admitted to the hospital because of progressive weakness. On neurological examination, she was noted to have right homonymous hemianopsia, moderately affected right-side hemiparesis and expressive aphasia. A CT scan examined on admission revealed a small low density area in the left basal ganglia. Carotid angiography demonstrated a severe stenosis in the cervical portion of the left ICA which was suggestive of dissecting aneurysm. In addition, so called “string of beads” appearance which was characteristic findings in FMD was shown in the bilateral ICA. The patient received conservative treatment with a continous infusion of antithrombotic agent (MD-805). All these symptoms gradually imporved after admission and almost completely disappeared within 14 days of onset. The repeated angiography performed on the 13th day of onest revealed marked improvement in the narrowed lumen of the left ICA. Althought surgical treatment has been recommended for dissecting aneurysm in the ICA, conservative therapy also appears to be effective since spontaneous restoration of the narrowed lesion may occur as shown in the present case.

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A 39-year-old woman suddenly developed generalized convulsion after periodic administration of oral contraceptives (norgestrel 0.5 mg, ethinylestradiol 0.05 mg) for 5 months. CT scan showed small scattered intracerebral hemorrhage in the left frontal lobe and intravenous digital subtraction angiogram (IV-DSA) repeatedly demonstrated occlusion of the superior sagittal sinus at the anterior two third. Platelet aggregabilities were decreased on 9th day after onset. Intracranial pressure was well controlled by administration of mannitol and the patient was recovered without neurological deficits. Three months later, superior sagittal sinus was well recanalized at the anterior two third in the follow-up IV-DSA. Superior sagittal sinus thrombosis related to the oral contraceptives was still rare in Japan, and clinical features and hematological mechanism in relation to the thrombosis were discussed from the literature.

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As means for detecting platelet activation, an estimation of platelet aggregability in vitro and measurement of plasma levels of in vivo secreted platelet specific proteins are two major methodological approaches in clinical study. Although several studies have been reported on the platelet activity in cerebrovascular diseases using these methods, the significance of platelet activity in acute phase of cerebral infarction is yet to be determined. This is why differences in pathogenetic mechanisms of cerebral infarction (thrombotic or embolic occlusion) and in the significance between in vitro platelet aggregability and plasma levels of in vivo secretecd platelet specific proteins, were not taken into accounted in these studies.
In the present study, plasma β-thromboglobulin (β-TG) levels were determined in patients with cerebral infarction within 3rd days after onset who had no artificial vascular damages such as intraarterial cathetarization, blood withdrawal etc. The patients were devided according to pathogenetic mechanisms into five groups as follows : 1) infarction due to atherothrombotic lesion of cortical branches including main trunk (Th-c), 2) infarction due to thrombotic lesion of perforating branches (Th-p), 3) hemodynamically induced infarction (I-h), 4) embolic infarction of cardiac origin (E-c), and 5) embolism, (E-a).
1) Th-c group showed the highest value of β-TG, 208 ng/ml, which was significantly higher than those of other groups except for E-a group. This may reflect the fact that thrombus formation in this group was most active, which might have promoted the onset of cerebral infarction.
2) Th-p group showed diverse pattern of β-TG values. Of 22 patients, 13 cases (60%) showed the values less than 60 ng/ml, and 8 cases (36%) more than 90 ng/ml. Other factors such as blood viscosity may partly have a share in the promotion of cerebral infarction of this type.
3) I-h group had the lowest activity of platelet, whose plasma level of β-TG was 28 ng/ml, among these 5 groups. This indicates that new thrombus formation did not play a role in the pathogenesis of this type of infarction.
4) In E-c group the plasma level of β-TG was the second lowest, 51 ng/ml, indicating that the detachment of intracardiac thrombus did not follow the activation of platelet function, but that it may have been resulted from increased fibrinolytic activity.
5) Values of β-TG in E-a group were variable ranging from 25 ng/ml to 277 ng/ml, which may probably be due to differences of the composition of the thrombus on the atheromatous arterial wall.
Using the above results that there were significant differences in β-TG levels between patients with atherothrombotic arterial occlusion and cardiogenic embolism, it appears to be possible to differentiate these major two types of cerebral infarction which are pathogenetically different.

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Four cases of bilateral internal carotid occlusion are reported with respect to clinical features, hemodynamics and various image diagnosis. MRI is applied to three cases.
The patients comprised 2.08% of all cerebral occlusive diseases treated during the past five years at our clinic. One case is of abrupt onset and three cases are progressing profiles. In one of these cases, collateral circulation is supplied mainy by leptomeningeal anastomosis of the posterior cerebral artery and posterior pericallosal artery branching from the basilar artery. In two of them, they are supplied through the circle of Willis.
Middle cerebral artery occlusion, occlusio supra occlusionem, however, causes decisive ischemic lesion in its teritory. Applying MRI, complicated ischemic lesions, such as lacunar infarction, paraventricular lesion, deep white matter lesion and border zone infarction can clearly be identified. In the case of total aphasia, the lesions responsible are demonstrated clearly by MRI, but only vaguely by X-ray CT.

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We studied the angiograhpic finding on subarachnoid hemorrhage of unknon etiology (Unknown group).
The subjects consisted of 19 cases of Unknown group, 181 cases of cerebral aneurysm (An group) and 110 cases of control group (C group).
The incidence of vascular variation or anomaly such as A1 hypoplasia, fetal type posterior cerebral artery, azygos anterior cerebral artery or A2 fenestration was 63.2% in Unknown group, 65.8% in An group and 52.7% in C group. No remarkable difference in the frequency could be observed between Unknown and An group.
But the incidences of these two groups were significantly higher than that of C group. Hemodynamic stress on the weakened arterial wall due to vascular anomalies or variation should participate in the subarachnoid hemorrhage.
Nine cases (47.3%) out of 19 patients in Unknown group were accompanied by hypertension and angiographic arteriosclerosis was observed in 6 cases (31.6%).
The authors have discussed about the source of hemorrhage in Unknown group with case presentation.

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The present study was designed to investigate whether the sympathetic nervous system modulates the cerebellar dysautoregulation during supratentorial ischemia. We used SHRs in which blood flows to the parietal coretex (CBF) and to the cerebellar cortex (CeBF) were measured by H2 clearance method. The rats were divided into alpha-blockade group (Phenoxybenzamine 1.5 mg/kg i.v.) and beta-blockade group (Propranolol 3.0 mg/kg i.v.). Autoregulations of CBF and CeBF were tested during hemorrhagic hypotension (-15% and -30% of the baseline mean arterial pressure) before and during acute cerebral ischemia induced by bilateral carotid ligation.
Phenoxybenzamine did not affect the resting CBF and CeBF, nor did autoregulations of both CBF and CeBF at the preischemic state. At 30 min ischemia, however, CBF was reduced to 5 ml/100 g/min and autoregulation in the cerebrum was severely damaged. On the other hand, CeBF was preserved better than CBF, i.e., CeBF was 93% and 87% of the resting flow by 15% and 30% reduction of blood pressure, respectively. At the preischemic state, autoregulations of CBF and CeBF were not affected by administration of propranolol. At 30 min ischemia, however, autoregulations in both cerebrum and cerebellum were markedly impaired. CeBF decreased to 77% (p<0.01) and 62% of the resting flow (p<0.01) by 15% and 30% reduction of blood pressure, respectively.
Present results indicate that cerebellar dusautoregulation to hemorrhagic hypotension during supratentorial ischemia is at least in part affected by activation of alpha-adrenoceptor of sympathetic nervous system.

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Transient ischemic attacks (TIA) following hypotension are thought to be very rarer than TIA of microembolic cause. Six cases of hemodynamic TIA which occurred following hypotension were reported and its causal relations among various cerebral hemodynamic parameters were analyzed.
Mean age of four male and two female cases was 73 years old. Mean value of habitual mean arterial blood pressure was 113 mmHg and mean value of arterial blood pressure at the time of the attacks was 83 mmHg. 23% fall of mean arterial blood pressure occurred at the time of the attacks.
The causes of hypotension were vasovagal reflex in one case, complete atrioventricular conduction block in two, orthostatic hypotension in one, and antihypertensive medication in the other two.
Cerebral angiography revealed large vessel occulsion or severe stenosis of the brain in five cases. Mean hematocrit value at the time of the attack was 44% and was significantly elevated as compared to the value of interictal state (38%).
From these evidences it was suggested that the occurrence of hemodynamic TIA was closely connected to the hemorheological factors as well as systemic hypotension and large cerebral vessel occlusions.

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