Two cases of carotid steno-occlusive disease with pulsatile tinnitus are reported.
Case 1. A 57-year-old hypertensive woman complained of pulsatile tinnitus on the right side. Bilateral cervical and right orbital bruits were heard with the stethoscope. Compression of the right carotid artery decreased both the tinnitus and the bruits. Angiography revealed stenoses of the right internal carotid artery at its bifurcation and the siphon. Stenosis of the eustachian tube was found, the inflation of which resulted in attenuation of her tinnitus.
Case 2. A man of 54 years complained of pulsatile tinnitus on the left side five months before he had left hemiparesis and anosognosia. Angiography showed occlusion of both the right internal carotid artery and the right middle cerebral artery. Collateral circulation from the left internal carotid artery was found. A CT scan revealed a right parietal infarction. Two months later, the patient began to walk and his tinnitus reappeared. Through auscultation of the neck we found a systolic carotid bruit on the left side. Both the bruit and the tinnitus disappeared after compression of the left carotid artery.
An absolute stenosis of the carotid artery, possibly of atheromatous origin, might have resulted in the pulsatile vascular tinnitus in case 1.
A relative stenosis, contralateral occlusion of the carotid artery, might have caused tinnitus in case 2.
Pathophysiological mechanisms of pulsatile vascular tinnitus were discussed.

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A case of neurofibromatosis and cerebral arteriovenous malformation is reported. A 50-year-old man was admitted to St. Mary's Hospital because of generalized convulsive seizures. Examination showed light brown colored spots of different size and small subcutaneous tumors disseminated on the trunk and extremities. Neurological examination revealed no abnormal findings after cessation of the convulsive seizures. A skull X-ray film showed a dysplasia of the right superior orbital fissure. The left common carotid angiogram revealed a vascular stain in the region of the lower portion of the supramarginal gyrus. Venous drainage occurred during the early arterial phase via the superficial cortical vein. Histological examination of the resected vascular lesion showed a combination of arterial and venous components. The biopsied subcutaneous tumor was histologically a typical neurofibroma.
A review of the literature disclosed only one related case report. The etiology of neurofibromatosis associated with cerebral arteriovenous malformation is discussed from an embryological point of veiw.

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Effect of thromboxane A₂ synthetase inhibitor (OKY-046) on occurrence of cerebral vasospasm and infarction was analyzed in 24 consecutive patients of ruptured aneurysm (OKY-046 group), in comparison with another 15 consecutive patients (control group) which were admitted within same period. All these patients belonged to Hunt and Hess grade I to III and were surgically treated within 72 hours after SAH. Both groups of patients had similar age distribution and preoperative neurological condition. The agent was begun postoperatively to drip intravenously and continuously at 5 μg/kg/min for 4 to 21 days (mean; 10.1 days). Efficacy of the agent was evaluated from vasospasm grade on angiography, postoperative resting clot score on repeated CT scans and activity of daily living (ADL) one month after SAH. Further, regional cerebral blood flow at the 2nd week after SAH was measured. And also, level of thromboxane B₂, 6-keto PGF_1α and 12-HETE like substance in plasma obtained from internal jugular vein and, level of 5-HETE like substance in cerebrospinal fluid were analyzed in relation to vasospasm grade. This study was concluded as follows, 1) OKY group had clinically higher incidence of asymptomatic vasospasm than control group, whereas OKY-046 treatment could not prevent occurrence of symptomatic vasospasm, especially in most cases with severe resting subarachnoid clot postoperatively. 2) From result of r-CBF analysis possibility of protective effect of OKY-046 against cerebral ischemia was suggested, 3) There were no significant differences in plasma level of TXB₂, 6-keto PGF 1α and, 12- and 5-HETE like substance in SAH patients between control and OKY groups, and also between asymptomatic and symptomatic vasospasm.

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During the past 4 years we experienced 68 cases of subcortical hematoma, excluding one secondary to trauma or ruptured aneurysm. Among these we had 17 cases of hypertensive subcortical hematoma (hypertensive group) and 28 cases of so-called spontaneous subcotical hematoma. The so-called spontaneus hematoma was further subdivided into two groups; one (13 cases) is cryptic AVM group in which small angiomatous malformations were confirmed histologically (cryptic AVM group), the other (15 cases) is unknown group in which any clear etiology could not be found (unknown group). Three groups were clinically analyzed. Especially in cryptic AVM group, the age ranged from 3 months to 73 years with the mean age of 40 years and there were 2 males and 11 females. Initial symptoms of cryptic AVM group were mild onset with headache, nausea, vomiting, and delayed loss of consciousness and/or hemiparesis. On the other hand, initial symptoms of hypertensive group were sudden onset with hemiparesis and/or speech disturbance. The hematoma site was predominant in the parietal lobe in hypertensive and cryptic AVM group, and in the occipital lobe in unknown group.
CT scan was useful for diagnosis of subcortical hematoma, but there were no characteristic differences in shape and size of hematoma among 3 groups. Cryptic AVM showed no contrast enhancement in our cases. Angiographically, most cases with subcortical hematoma were demonstrated avascular mass with displacement of vessels. Only 5 cases of cryptic AVM showed abnormal findings such as early venous filling or extravasation. Since cryptic AVM is rarely found by angiography, it must be emphasized to search fully during surgery, even if considered to hypertensive hematoma preopeartively. And it is necessary to remove the cryptic AVM completely to prevent rebleeding. Microscopically, all cases of cryptic AVM showed arterio-venous malformations.
The outcome of subcortical hematoma was good even though the state of the consciousness were poor on admission. Out of the total 45 patients, 5 died of systemic complications postoperatively. Four of 5 dead cases were aged more than 70 years. Therefore, the outcome seemed to depend on the age of patient.

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Up to December, 1983, 1935 cases of cerebral aneurysms were operated in our clinic. Among them, 35 cases were the patients over 70 years of age. Their preoperative neurological grade, according to the classification of Hunt & Kosnik, were 0 in 3 cases, I in 7 cases, II in 9 cases, III in 10 cases, Ia in 4 cases and IV in 2 cases. Four cases were operated within 48 hours after the onset of subarachnoid hemorrhage. Two cases were operated on the day 3 and one case was operated on the day 6. Remaining 25 cases were operated after ninth day from the onset.
One of the most difficult problem for operation of cerebral aneurysms over 8th decade is cerebral arteriosclerosis. Usually, we use temporary clips on the parent arteries of the aneurysm for treatment of the aneurysm neck. However, in this series, severe arteriosclerosis of the parent arteries was seen in 31 cases (89%). We had to give up to use temporary clips in 8 cases bacause all of the arteries in the operative field were hard and yellow. Treatment of the aneurysm neck was abanodoned in 11 cases, because a severe arteriosclerosis existed around it or aneurysm had broad neck. Body clipping and/or ligation of the aneurysm were performed for these cases and aneurysm neck was wrapped by muscle with aron α adhesive.
Combined diseases have been emphasized as risk factor in aneurysm surgery of aged patient. Care of these diseases was one of the most important problem, however, most of combined diseases could be controlled by careful management. Operative results at discharge were as follows : excellent in 18 cases, good in 4 cases, fair in 4 cases, poor in 7 cases and dead in 2 cases. Operative results were bad in the patients of Grade IV and Ia. Results of peracute surgery in Grade III was poor. Patients with postoperative vascular occlusion or vasospasm had bad outcome. When the patients had pathological condition with or without symptoms in their brain or cerebral arteries, operative result was sometimes disappointing.
Follow-up study was performed 6 months to 10 years after the operation. Twenty-four cases (68.6%) were excellent or good at follow-up or until the death of other causes. One case was fair and one case was poor at follow-up. Other 7 cases were died of complications after dischange.
Conclusion : Good operative results could be get even the cases of aneurysm over 70 years of age, by precise preoperative evaluation and careful operation.

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A few reports of posterior inferior cerebellar artery (P.I.C.A.) located more proximal to the superior retrotonsillar segment are recognized. However, non traumatic or non mycotic aneurysms located on the peripheral branch more distal to this segment of P.I.C.A. are very rare.
Clinical and anatomical features of the aneurysms located on the peripheral branch of P.I.C.A. are analized based on four previously reported cases together with four present series.
The average age at the onset was 48 years. All the patients presented classical symptoms of SAH : severe headache followed by nausea and vomiting. All the aneurysms in this category were very small. They were less than 5 mm in diagmeter except for one case which was preveously reported (8 × 4 mm). One of the present series the size was extremely small. It was 2 × 2 mm in size and was only demonstrated by magnified angiogram. Multiple aneurysms were found in 3 cases out of the 8 cases and all of them were arising from the same P.I.C.A. In two of the cases, the multiple aneurysms were complicated with AVM's. In these cases, the aneurysms were located on the proximal portion of the same branch of which AVM's located. In these cases, increased of blood flow caused by the existense of AVM was though to be a main cause which facilitates aneurysm formation. CT finding in the present series was very characteristic. In all the cases, hemorrhage was noted in the fourth ventricle and the subarachnoid space over the cerebellum but no hemorrhage was recognized in the basal cisterns.
In the unknown origin of SAH when CT showed the characteristic appearance one should strongly suspect the presence of ruptured aneurysm of the P.I.C.A. peripheral branch, and all efforts should be made to demonstrate by angiography.

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The following conclusions were obtained from the analysis of CT findings of 26 cases with ruptured anterior communicating aneurysm showed postoperative mental symptoms.
1) Many cases with diffuse and symmetrical high density in subarachnoid spaces on CT in the acute stage, showed severe mental symptoms in the chronic stage. In particular, serious mental symptoms of the chronic stage were recognized in cases with high density in not only subarachnoid space but also in brain tissues and ventricles.
2) Mental symptoms of the chronic stage were severe in cases showed relatively large low density area and with low density in frontal lobe.

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Twenty-three patients who developed an acute stroke during hospitalization in our clinic from 1971 to 1983 were retrospectively studied. Of those, 16 cases were of cerebral infarction and 7 of hemorrhagic stroke. Complete clinical data before and after stroke, including daily or frequent blood pressure measurements, hematology and blood chemistry were available in 12 cases of cerebral thrombosis (6 hypertensives and 6 normotensives). Our own criteria, described elsewhere, were used for diagnosis of hypertension. In 4 of the 6 hypertensives, a marked reduction of the blood pressure, ranged from 33 to 69 mmHg in mean arterial blood pressure, following antihypertensive treatment was observed before the occurrence of cerebral thrombosis. On the other hand, the blood pressure changed little in all normotensive patients except one who had congestive heart failure.
It had been known that cerebral autoregulation in hypertensive patients is adapted to a high blood pressure and its lower limit is shifted upwards. Therefore longstanding or severe hypertensive patients may be at risk to develop cerebral ischemia even at the blood pressure that is well tolerated by normotensive subjects. Our present results suggest that a considerably rapid and marked lowering of the blood pressure by antihypertensive treatment in hypertensives is one of the important factors for developing cerebral thrombosis.

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The cerebrovascular diseases have been generally believed to be under the influence of seasonal factors.
We investigated the occurrence and rupture of intracranial aneurysms in subtropical area, Okinawa prefecture. Our cases of aneurysm were surgically operated and proved by cerebral angiograms in several main neurosurgical clinics during the period of 1974 to 1983.
They are consisted of 412 cases including 364 cases of single and 48 cases of multiple aneurysm.
Seasonal changes, especially in temperature and humidity, were not major factors for the rupturing of intracranial aneurysm. The annual incidence of aneurysm in the present series is 4.8-6.2 per 100, 000 people. The incidence was predominant in women to men in a ratio about 1.8 : 1. Age distribution of aneurysm shares at the 5th to 7th decade (324 in 412 total cases : 79%). Aneurysm is located mainly at internal carotid A. (37%) anterior communicating A. (24%) and middle cerebral A. (19%) amongst of 364 cases of single aneurysm. Multiple aneurysm is found in 48 cases (12%) of our series.

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A case of MLF syndrome developed immediately after a basilar aneurysm surgery was reported. This 48-year-old lady with proven subarachnoid hemorrhage was admitted on day 9 in grade II (Hunt & Kosnik) and a neck clipping of the basilar bifurcation aneurysm was performed via a pterional approach on day 14. The operation was smooth and uneventful, and neither a temporary occlusion of the parent artery nor an induced hypotension was necessary during the operation. Immediately after the operation, however, the patient presented the MLF syndrome with disturbance of convergence (anterior type of MLF syndrome by Cogan). No other brain stem signs were present.
Solitary MLF syndrome unassociated with other brain stem signs is very rare, and the aneurysm surgery as a cause of the MLF syndrome has not been reported. The etiology of the syndrome in this patient was briefly discussed.

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Diagnosis of Wallenberg's syndrome has been made by typical neurological symptoms and signs which are compatible with those of lesion in the lateral aspect of medulla oblongata. Although X-ray CT is an extraordinary useful measure for detecting lesions in the central nervous system, brainstem lesion is difficult to be evaluated by it because of varieties of artifact. A recent advance in techniques of magnetic resonance imaging (MRI) made it possible to produce fairly good images of infratentorial structure without artifact. But, there are no reports on patients with Wallenberg's syndrome whose lesion was clearly delineated by MRI.
A 44 year-old man with a history of hypertension was referred to our hospital because of vertigo, pain on the right side of the face, disturbance of swallowing and hiccup 22 days after onset. On admission, neurological examination revealed right Horner's sign, decreased gag reflex and cerebellar ataxia on the right side, and dissociated sensory impairment on the right side of the face and left extremities. Clinical diagnosis of Wallenberg's syndrome was made, but X-ray CT showed no definite lesion in the infratentorial structure.
Cerebral angiography revealed occlusion of the right vertebral artery without reflux of contrast media from the left vertebral artery. Then, there was no visualization of the right posterior inferior cerebellar artery.
MRI using Magnetom (0.35 Tesla of static magnetic field produced by superconducting magnet) clearly delineated low intensity area in the right lateral aspect of the medulla oblongata.
This is the first case of Wallenberg's syndrome whose anatomical lesion was demonstrated by MRI.

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We observed two patients with acute onset hypersomnia and memory disturbance who had unilateral infarction in the anteromedial thalamus.
The first case is a 62-year-old, right-handed woman, who showed hypersomnia and memory disturbance. CT scan revealed a small low density area in the right anteromedial thalamus, which involved the anterior, intralaminar, centromedian, ventral anterior, ventral lateral, and dorsomedial nuclei and mamillothalamic tract. Angiography showed no occlusion in the major cerebral arteries, except for stenosis and wall irregularity in the circummesencephalic portion of the right posterior cerebral artery.
The second case is a 68-year-old, right-handed man, who had been suffering from hypertension and diabetes mellitus for ten years. He showed hypersomnia, memory disturbance and dyscalculation. Other symptoms included Homer's syndrome and a mild weakness and dysesthesia in the right arm. CT scan revealed a small low density area in the left anteromedial thalamus. Angiography showed no stenosis or occlusion in the major cerebral arteries. In both cases hypersomnia disappeared two weeks after onset.
It can be postulated that the intralaminar, centromedian and dorsomedial nuclei which are related to the ascending reticular activating system could play a chief role of the occurence of hypersomnia. It is suggested that the thalamic lesion on either dominant or nondominant hemisphere could cause memory disturbance.

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In an attempt to clarify the abnormality of lipid metabolism in ischemic cerebrovascular diseases (ICVD), serum lipid components, including apoliprotein A-I, A-II (apo A-I, apo A-II) HDL-Cholesterol (HDL-C) were simultaneously investigated in 81 patients with ICVD.
Apo A-I was significantly decreased in the acute stage of ICVD, keeping a good correlation with HDL-C. While apo A-I returned to almost normal level in 3 months period, HDL-C remained low for much longer period. Namely, it was strongly suggested that a direct trigger for the development of cerebral infarction could be decrement of apo A-I, and that apo A-I could also be related to repairing process of the infarction.
Though, apo A-II also decreased slightly in the acute stage of cereberal infarction, the change was not statistically significant. In cases with TIA or RIND, no changes were seen in apo A proteins indicating that the developing mechanism of those minor attacks should be attributed to some factors other than lipid metabolism.
In conclusion, it was proved that serum apo A-I level should be an useful predictive factor for the development of cerebral infarction, and also be a good prognostic indicator.

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Thirty-seven patients with cerebrovascular disease were studied with N-isopropyl-p- (I-123) iodoamphetamine (IMP) and single-photon emission computed tomography (SPECT) comparing with X-ray CT findings. SPECT was performed using a rotating gamma camera or a whole body multislice SPECT scanner. Focal decrease of IMP was observed in 37/43 (86%) studies of these patients. Twenty eight of them (76%) showed larger perfusion defects than those observed in X-ray CT scans. In 4/6 patients without abnormal findings in SPECT with IMP, X-ray CT scans revealed small localized abnormalities in basal ganglia or cerebellum. Crossed cerebellar diaschisis was observed in 15/39 (38%) studies of 34 patients, in which SPECT with IMP demonstrated extensive abnormalities in unilateral cerebral hemisphere, while there was no correlation between X-ray CT abnormalities and crossed cerebellar diaschisis.
SEPCT with IMP would be of great value in evaluating abnormal cerebral perfusion, although X-ray CT scan was more sensitive to detect small abnormalities.

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It has been known that exfoliation of endothelial cells is a factor of atherogenesis. We observed the circulating exfoliated endothelial cells in man with Giemsa staining in accordance with the method of Hladovec, further with Ruthenium Red staining and direct immunofluorescent staining using anti-human factor VIII serum and using antihuman α₂-macroglobulin serum.
For the purpose of examining our studies that circulating endothelial cells can cause cerebral infarction, endothelial cells were injected into common carotid artery in rabbits. As control examination, blood clots or arachidonic acid was injected into common carotid artery in rabbits.
The subjects were 72 healthy persons, 23 hemodialysis patients and the male rabbits which were 3-4 kg of body weight.
Results obtained were as follows;
1) With Giemsa staining, cells to be thought as endothelial cells were shown, as a rule, polygonal shape, often with folded or rolled suggesting a marked flatness. The membrane of the cell was stained with Ruthenium Red and by the fluorescent staining, and we could observe the intence fluorescence in the cell with using anti-human factor VIII and anti-human α₂-macroglobulin serum.
2) When blood is taken with a syringe, endothelial cells may be detached and taken together. To prevent it, blood was taken from arterial side tube of extracorporeal circulation in hemodialysis patients. These samples, also showed the presence of cells suggesting the endothelial cells. The average of the circulating cell numbers in healthy subjects was 1.59 cells/9 μlPRP, and that of hemodialysis patients was 1.29 cells/9 μlPRP, showing no significant difference between healthy subjects and hemodialysis patients.
3) By injections of endothelial cells into common carotid artery in rabbits, cerebral embolisms could not be observed. But, by injections of blood clots or arachidonic acid into common carotid artery, cerebral embolisms could be observed. It was suggested from above results that the increasing of circulating endothelial cells cannot cause embolism by itself.

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