The incidence of pulmonary thrombosis or thromboembolism was said to be lower in Japan than in western countries but it has been increasing recently in Japan. The reasons of this increase must be the true increase in this disease and the advance of diagnostic techniques. The incidence, and clinical and laboratory features of pulmonary thrombosis or thromboembolism were studied in 274 autopsied cases of cerebrovascular diseases (102 cerebral hemorrhage, 82 subarachnoid hemorrhage and 89 cerebral infarction cases). Pulmonary thrombosis or thromboembolism was confirmed in 20 cases (7.5%) in 274 cases of cerebrovascular disease by autopsy. Pulmonary infarct was observed in 13 cases from 20 cases of pulmonary thrombosis or thromboembolism. Therefore, the incidence of pulmonary thrombosis or thromboembolism was 8.8% in cerebral hemorrhage, 7.3% in subarachnoid hemorrhage and 4.5% in cerebral infarction, respectively. Pulmonary infarct was confirmed by autopsy in 6.5% of cerebral hemorrhage, 3.7% of subarachnoid hemorrhage and 3.4% of cerebral infarction. The thrombus in the vene cava inferior was found in a case of pulmonary infarct. Bronchopneumonia was complicated in 3 cases in pulmonary thrombosis or thromboembolism without pulmonary infarct.
The characteristic signs and symptoms of pulmonary thrombosis or thromboembolism were dyspnea, chest pain, cyanosis and tachycardia as well known. The abnormal laboratory findings were very often see in the increased blood WBC counts and the raised serum level of LDH. Serum GOT level was normal in about a half cases of pulmonary thrombosis or thromboembolism with the raised serum LDH level. Chest X-ray did not show any specific findings. The shadows of pneumonia, pleural effusion, and athelectasis were observed sometimes. Sinus tachycardia was most frequently observed in pulmonary thrombosis or thromboembolism. In addition, atrial fibrillation, ST segment depression in limb leads I and II or precordial leads V₁, V₂, V₅, and V₆, prominant Q wave in lead III, and T wave inversion in leads III, V₁, and V₂ were noticed in several cases. The elevation of ST segment was seen in 3 cases.
Pathological examination revealed that pulmonary occlusion was caused by the multiple systemic thrombosis in seven cases. In other 13 cases, pulmonary occlusion was due to the pure pulmonary throbosis or thromboembolism. Pulmonary occlusion was caused by the embolization by thrombus in 10 out of those 13 cases. Cardiac thrombus was found in a half of them. Pulmonary infarction was not found even when pulmonary occlusion existed in 7 from 20 autopsy cases. In those cases except one, fresh multiple thrombi or emboli were found in small peripheral pulmonary arteries.

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A case of cerebrovascular disorder (CVD) caused by toxemia of pregnancy was reported.
The patient was a 25-year-old primipara in the 9th month of the pregnancy. On March 24, 1983, she was brought to our hospital because of an attack of cerebral apoplexy. On admission, she was in a comatose state, and neurological examination revealed right hemiparesis and conjugate deviation of the eyes to the left side. The blood pressure was 160/100 mmHg, while the pulse rate 75 beats per minute and regular. Respiration was distressed.
Computerized tomography (CT) on admission showed high density areas in the basal ganglia regions on both sides (mainly on the left side) surrounded by low density areas, and high density areas in the third, fourth and bilateral ventricles. The patient was saved with critical care and emergency treatment such as bilateral ventricular drainages. The baby was delivered by cesarean section and showed normal development later on.
Cerebral angiograms obtained three days after the attack showed diffuse cerebral vasospasm in the anterior and middle cerebral arteries of both sides and basilar artery. The venticular drainages were effective and contunued for 12 days. The neurological condition gradually improved. Repeated CT three weeks after the onset showed a decrease in size of the high density area and its surrounding low density area in the left basal ganglia region, disappearance of the other high and low density areas, and near normalization of the ventricles.
Forty-two days after the attack, cerebral angiography was again perfomed, but the diffuse cerebral vasospasm had disappeared. No aneurysm, or arteriovenous malformation was seen. The clinical course was good and the patient was discharged on the 50th hospital day, by which time her consciousness had become clear, right hemiparesis had recovered well and the blood pressure had been normal. CVD caused by toxemia of pregnancy is rare, and the main lesions of the brain had edema, focal ischemia, thrombosis and hemorrhage. They may be related to cerebral vasospasm. This paper suggests that cerebral vasospasm and subsequent ischemic changes are observed at times with severe toxemia of pregnancy, and in addition to them our case might be associated with so called hemorrhagic infarction caused by severe pregnancy induced hypertension.

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A rare case of cerebral infarction due to traumatic occlusion of the right common carotid artery is reported with reference to its pathogenetic mechanisms associated with dog bite injury.
A 59-year-old man developed disturbance of consciousness, left hemiparesis and dysarthria immediately after he was bitten by a dog on the right side of his neck. On admission he was stuporous and there were several dog bite wounds in paralell with the right sternocleidomastoid muscle. He exhibited a conjugate ocular deviation to the right side, a right Homer's syndrome, severe dysarthria, right hemiparesis including his face, and a left hemisensory deficit. He also showed anosognosia of the left hemiparesis and unilateral spatial agnosia of the left. Upon admission, the cranial CT which demonstrated an extensive low density area in the territory of the right middle cerebral artery and a localized low density area in the right thalamic region. Digital subtraction angiography revealed a complete occlusion of the right common carotid artery at its origin. The cervical CT showed a lack of contrast in the right common carotid artery. Since the cerebral infarction had already occurred, surgical treatment was not carried out for this traumatic arterial lesion. The patient had been treated with hypertonic solution and anti-platelet aggregation agent. The followup angiography performed on 12th day of admission failed to show recanalization of the occluded right common carotid artery.
This occlusive lesion of the right common carotid artery was considered to be directly associated with the dog bite injury. The usual time lapse between the trauma to the carotid artery and onset of neurological symptoms is reportedly about 8-10 hours. This interval is believed to correspond to the time necessary for the evolution of the thrombus and subsequent occlusion of the lumen of the vessel. Our patient was different from those with thrombotic occlusion due to the traumatic intimal laceration in having developed neurological symptoms immediately after the trauma. Two other possible pathogenetic mechanisms were considered for the traumatic occlusion of the right common carotid artery in this case. One is a traumatic dissection of the intima that occluded the true lumen of the artery. Another possibility is a hemorrhage in the media or subintimal planes.

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We studied the changes of cerebral blood flow (CBF) before and after intravenous administration of dopamine and at the same time measured dopamine, adrenaline, and noradrenaline in serum. The CBF was measured by the Xe-133 inhalation method and calculated by initial slope index (ISI) modified by Risberg. The subjects comprised of 18 patients with acute cerebral thrombosis within one week after the ictus (5 cases : stenosis of internal carotid artery, 2 : occlusion of middle cerebral artery, 3 : stenosis of middle cerebral artery, and 8 : normal findings on angiographic examinations). Both cerebral embolism from cardiac origin and transient cerebral ischemic attacks were excepted.
The CBF was significantly increased from 34.3 ± 2.6 to 37.9 ± 2.7 (11% increase) in the affected hemisphere and from 36.7 ± 2.0 to 41.5 ± 36.1 (13% increase) in the non-affected side in 6 cases with more than 100 ng/ml of serum dopamine concentration after intravenous infusion of dopamine at a rate of 10 μg/kg/min. Four cases of these patients had also a raise of systemic arterial pressure, but the others had no blood pressure changes.
On the other hand, 12 patients below 100 ng/ml of dopamine concentration in serum there was no constant tendency in CBF change. In these groups any chnages of systemic blood pressure was also not observed.
Dopamine (above 100 ng/ml in serum) might be an effective drug for acute cerebral thrombosis because this agent can significantly increase CBF without any overt changes in the systemic blood pressure and can be clinically used safely by intravenous infusion at a rate of 10 μg/kg/min. Relevant literatures were reviewed, and discussion was focused on the effect of domamine to cerebral blood flow.

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The giant posterior cerebral artery aneurysm is very rare.
The authors have encounted only 25 cases through published literatures up to this date.
We experienced a case of unruptured giant aneurysm of posterior cerebral artery.
A 31-year-old woman was brought to our attention with a chief complaint of progressive headache in the right occipital lesion aboout a year ago. No abnormalities were noted by a series of neurological examinations, however, CT scan revealed a high density area of round shape at the right cerebral peduncle to have been remarkably enhanced by 60% Conley drip infusion.
V.A.G. revealed a giant aneurysm on P₂-P₃ junction of the right posterior cerebral artery.
Sugita's clip was put on the P₂ segment just proximal to the neck of aneurysm, because the dome was tightly adhered to the brain stem and the distal side of the neck could not be identified.
The postoperative angiography revealed to be free of the aneurysm, but a CT scanning did reveal it a month later. Ever since, the patient has not complained of any headache or neurologiacal deficits.
The diagnosis of giant cerebral aneurysm should only be justified with angiographic findings, since they do not always reveal the acutual size due to the thickened wall and thrombus formation. In such cases, an enhanced CT scanning enables us to diagnose the actual size of aneurysmal dome.
Consequently, we recommend that the diagnosis of giant aneurysm be justified by an enhanced CT scan presenting the aneurysmal dome of its maximum diameter less than 25 mm, although a conventional definition of the diagnosis as exceeding 25 mm by the angiography.

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The authors experienced 8 cases of the cerebral arteriovenous malformation associated with aneurysm during a period of 6 years. CT scan and cerebral angiography were performed in all of them. During the same period, they had 143 cases of the intracranial saccular aneurysm. The etiology and surgical treatment of the aneurysm in association with AVM were discussed. Followings are conclusions.
1) The etiology of these aneurysms could be explained by hemodynamic stress theory, because all aneyrysms were on the feeding vessels of the AVMs and in a patient with an unresectable AVM, a newly formed aneurysm was found in a follow-up angiogram.
2) Both AVM and aneurysm should be treated in one stage operation.
3) The aneurysms with unresectable AVMs and unruptured AVMs of the aged should be clipped.

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Three cases of fulminant hypertensive intracerebral hematoma with volumes of 100 ml or more are reported.
Superacute evacuation was accomplished under local anesthesia within three hours of ictus. In all cases, the results proved very favorable.
On admission to our service, all three cases showed mydriasis, decerebrate limb posture and respiratory distress, suggesting tentorial herniation. Immediate hematoma cavity drainage was performed under local anesthesia and approximately 30 to 40% of the hematoma was manually evacuated. Evacuation of the residual hematoma was completed by infusing 6, 000 i.u. of urokinase solution into the hematoma cavity every 6 hours. Immediately after the initial aspiration, all of the cases showed improvement in respiration while level of consciousness also increased from somnolence to stupor. There was no incidence of rebleeding.
One patient, a 70-year-old female with a left-sided intracerebral hemorrhage, died from aggravated pulmonary cancer two months after the surgery. Yet, she was alert until just before her death, although she suffered from motor aphasia.
Another case, a 46-year-old male with a right-sided intracerebral hemorrhage, recovered to the point he could stand and walk with assistance within one month after the surgery. Now, five months postoperatively, he is leading a significant home life despite persistant paralysis in his left upper limb.
The third case, a 72-year-old male with a right-sided hemorrhage, who had already suffered from a previous left putaminal hemorrhage 5 years before the present hematoma, remains. Slightly apathetic with left hemiparesis 4 months postoperatively.
Experiences with these cases suggests that, even in fulminant intracerebral hemorrhage, evacuation of the hematoma in the superacute state may save life or even assure the patient a significant survival. In addition, this surgery can be carried out under local anesthesia without complicated stereotactic equipment. Thus, we can say that superacute evacuation is a simple and valuable technique for hypertensive intracerebral hemorrhage.

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A study was made on the clinical implication of the electrocardiographic (ECG) abnormalities observed during the acute stage of subarachnoid hemorrhage (SAH) secondary to rupture of intracranial aneurysm. The patients selected for the present study were 121 cases who were hospitalized to day 3 (the onset day as day 0) and who underwent ECG, CT and bilateral carotid angiography (CAG) at the time of admission with no past history of cardiac disease. Nine findings were examined on the ECG such as sinus bradycardia, sinus tachycardia, arrhythmia including extrasystole, AV block, atrial fibrillation and flutter, QTc prolongation, ST abnormality, giant T wave, inverted T wave, U wave abnormality and left ventricular hypertrophy (LVH). Each of these findings was examined in relation to neurological grading, site and intensity of subarachnoid clot on CT, rupture site of aneurysm and vasospasm on CAG.
Among the 121 cases, abnormality of some nature was observed on the ECG in 116 cases. The incidence of such findings was 19% for sinus bradycardia, 13% for sinus tachycardia, 57% for QTc prolongation, 23% for giant T wave, and 13% for inverted T wave. Evaluation of neurological grading at the time of admission showed 17 cases in grade 1, 41 cases in grade 2, 37 cases in grade 3, 20 cases in grade 4, and 6 cases in grade 5. With elevation in severity, an increase in the frequency of arrhythmias excluding bradycardia and of S-T abnormality was observed, but no difference in the frequency of sinus bradycardia and QTc prolongation could be observed by the neurological grading. The more the subarachnoid clot on CT, the higher was an incidence of abnormal ECG findings. But no difference in incidence of abnormal ECG findings could be observed by difference in laterality of the clot on CT. The rupture site of the aneurysm was anterior communicating artery (AcoA) in 49 cases, internal carotid artery (ICA) in 34 cases, middle cerebral artery (MCA) in 32 cases, and other sites in 6 cases. There was no difference in the incidence of arrhythmias excluding sinus bradycardia and of QTc prolongation by rupture site, but the incidence of sinus bradycardia was high in the cases with rupture of AcoA aneurysms. In examining the relationship of vasospasm observed on repeated CAG conducted on day 7-10 to ECG findings at the time of admission, no difference in the incidence of each findings excluding LVH could be observed.
It is considered that study of each ECG findings may provide valuable suggestions in not only developing clinical measures but also in elucidating the etiology of ECG abnormalities. The etiology of ECG abnormalities in the patients with SAH is discussed.

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Experimental cerebral infarction was produced in dogs by injecting one or two silicone rubber cylinders through the cervical internal carotid artery (permanent group). In some dogs the rubber cylinder was removed by pulling out the monofilament suture thread after 6 hours of temporary embolization (temporary group). Twenty-four hours after embolization, the animals were killed.
In ultrathin sections of capillary endothelium in the ischemic cerebral cortex of both groups, surface infolding and pericapillary fluid collection were recognized, but no findings of opening of tight junctions were ascertained.
In replica preparations of both groups, no definite findings of opening junctions were certificated. The average number per square μm of pinocytotic vesicles was increased. On the luminal front of protoplasmic face, it reached to 28 ± 6 equally in both groups as compared to 7 ± 1 in the normal cortex. The size of vesicle was also enlarged, 4, 713 ± 868 nm² in permanent group and 3, 684 ± 570 nm² in temporary group as compared to 3, 491 ± 507 nm² in normal group. The arteriole-venule in the ischemic cortex of temporary group also showed increased and enlarged pinocytoticvesicles, but no opening of tight junctions.
The results indicated that transcellular transport by pinocytotic vesicles plays an important role in the increase of capillary permeability observed in ischemic model of both groups. The vascular ultrastructural differences between permanent and temporary groups were not statistically significant in either cortex.

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A series of 49 patients with cerebral hemispheric arterior-venous malformations (AVM) operated on is presented.And the operability for cerebral hemispheric AVM, especially for unruptured cases, are discussed.
The success rate of surgical excision were 78.5% in patients with ruptured AVM and 81% with unruptured AVM. In cases with ruptured AVM, the surgical outcome were favorably affected by preoperative conditions of the patients due to intracerebral hematoma rather than by the operation. Postoperative intracerebral hematoma caused by residual AVM had a strong effect on the surgical results in cases with unruptured AVM. Therefore, the relationship between the surgical results and age of patients, size and location of AVM, demarcation of AVM, and feeding arteries supplying AVM was studied in cases with unruptured AVM. Patients with AVM smaller than 5 cm in diameter, even if they situated in the speech-motor-angular regions, had a better surgical results than did those with large AVM (5 cm or more in diameter). In addition to the size of AVM, two other factors had an effect on the surgical results. The first of them was the number and sort of arteries supplying the AVM. By using anatomical grading according to Luessenhop which corresponds to the number of participating arteries, surgical results were studied. Grade I, II or III patients of anatomical grading had no mortality or morbidity. However, patients with grade IV AVM, especially supplied by lenticulo-striate and/or anterior chorodial arteries, had a higher rate of mortality and morbidity than did those with grade I, II or III AVM. The second factor was the demarcation of AVM. The incidence of mortality and morbidity caused by postoperative intracerebral hematoma due to residual AVM was significantly higher in cases with poorly demarcated AVM compared with patients who had well demarcated AVM. Age of patients had no effects on the surgical results.
Conclusions : In most patients with AVM smaller than 5 cm in diameter a total extirpation of the AVM is possible without creating neurological deficits, even if they situate in speech-motor-angular regions. There is the possibility to excise totally the unruptured large AVM without operative risk which is well demarcated, and is not supplied by lenticulo-striate and/or anterior choroidal arteries. However, surgical excision is not indicated for patients with unruptured large AVM classified as anatomical grade IV, especially supplied by lenticulo-striate and/or anterior choroidal arteries, and with poorly demarcated AVM.

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To elucidate effects of various food-intakes, cigarette smoking and alcohol drinking on development of cerebrovascular diseases (CVD) among a general population, a 15 year follow-up study was carried out in Hisayama, Kyushu Island, Japan. With the food frequency interview method, data concerning frequencies of taking rice, meat, fish, milk, green vegitable, “tukemono” (pickled vegetables), “miso-shiru” (miso soup), cigarette smoking and alcohol drinking were obtained from 94 per cent of the residents, aged 40 to 69 years, in 1965. Blood pressure, body height, weight, serum protein and serum total cholesterol were determined at the time of the adults health examination in the summer of 1965, prior to the food frequency interview. Detailed information about development of CVD was available for the subjects who had been followed-up since 1961 as a cohort of the Hisayama Study, an ongoing longitudinal epidemiological study. As a result, it was confirmed that 111 out of 1, 110 subjects who belonged to the Hisayama cohort had newly developed the first attack of CVD during the follow-up period. Out of 111 subjects, 77 died and 73 of them underwent post mortem examination (the autopsy rate was 95 per cent). The types of CVD were as follows; cerebral thrombosis 72, cerebral embolism 1, cerebral hemorrhage 23, subarachnoid hemorrhage 12 and ill-defined type of CVD 3.
Using Cox's proportional hazard model and its computer software PHGLM in SAS, multivariate analysis showed that elevated level in systolic blood pressure, male sex, and advancing age were selected, in stepwise, as significant risk factors (p<0.05) for developing CVD as a whole. For development of cerebral thrombosis, advancing age and alcohol drinking were selected as significant, based on the frequency of food intakes and when the items of the above mentioned measurements were added to the model, elevated systolic blood pressure, male sex, advancing age and elevated diastolic blood pressure were selected. When the data were analysed after dividing by sex and age, elevated systolic blood pressure was selected as the most significant risk factor for CVD as a whole, in both sexes and agegroups. As the second one, however, low intake of meat was selected for the middle-aged (40 to 54 years) male subjects and low intake of fish for the old-aged (55 to 69 years) male subjects, respectively. For development of cerebral thrombosis, among the old-aged male subjects, low intake of fish remained as the second significant risk factor next to high systolic blood pressure.
Although the food intake frequency method is not quantitative, it represents some dietary pattern for a long time period. The results of the present study suggest that the consumption of fish may be of preventive value for arterial thrombosis as reported in the recent papers from the longitudinal prospective epidemiological studies for coronary heart disease in Europe.

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Two cases of mycotic aneurysms in the intracavernous portion of the internal carotid artery were reported.
Case 1 : A 48 years old woman was admitted to the hospital because of a severe headache and a spike fever of three days' duration. She had a clinical feature of bacterial meningitis and had been treated with antibiotics. Over the next six days she presented with diplopia and drooping of the left eyelid, followed by total ophthalmoplegia. Cerebral angiography performed two weeks after admission revealed a giant aneurysm in the left intracavernous portion of the internal carotid artery. Cerebral angiography repeated a month later showed a reduction in the size of the aneurysm with a slight improvement of ophthalmoplegia. Since follow-up angiography which was performed after an intreval of one year demonstrated a significant enlargement of the aneurysm, ligation of the internal carotid artery was carried out.
Case 2 : A 33 years old man was admitted to a local hospital with a diagnosis of bacteremia. A month later he was referred to the hospital because of progressive deterioration of left ophthalmoplegia. Crebral angiography carried out on admission revealed a giant aneurysm in the left intracavernous portion of the internal carotid artery. Repeated angiography performed on the 15th day following admission showed a further enlargement of the aneurysm. Ligation of the internal carotid artery obviously improved ophthalmoplegia.
To our knowledge 24 cases with mycotic aneurysms in the intracavernous portion have been previously reported in the literature. Frequently encountered causes were bacterial meningitis and cavernous sinus thrombophlebitis secondary to infection in the adjacent area. Rupture of an aneurysm occurred in only one case. it is suggested that patients with mycotic aneurysms in this portion had a relatively good prognosis and follow-up angiography was useful for the management of aneurysms.

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