Only 20 patients with RIND, who had been performed four vessel study, were analyzed to reveal the relationship between angiographic findings and clinical signs. The average of patients was 48.8 years lod.
The results are as follows;
1) The clinical signs were almost motor disturbance and speech disturbance. The time untill recovery is within 2 weeks, but patients with sensory disturbance had generally more time for the recovery.
2) The angiographic findings revealed almost atherosclerotic lesions at the region of interal carotid artery (ICA) as described previously. There were 3 cases (15%) without any cerebrovascular change.
3) The main factor, we thought to become RIND, was responsible for the cerebrovascular lesion. Also we found the otherwise lesion, cardiac (10%) and unclear (20%). Regard with the cerebrovascular lesion, we revealed ex-tracranial lesion in 6 cases, specially ulceration and stenosis of the carotid bifurcation. In 5 cases (25%), there were sclerotic change at the carotid siphon, and the remaining 3 cases (15%) were seen multiple cerebrovascular lesions.
4) We found RIND to tend to occur in the patient with history of TIA. These patient have atherosclerotic lesions at the carotid bifurcation and carotid siphon. Therefore atherosclerotic lesions at these region seen on angiography was though important pathologic factor for RIND.
It might be suggested that we were to deal with surgically when patients with RIND have any atherosclerotic lesions at the carotid bifurcation and carotid siphon.

View full abstract

The timing of the intracranial surgery of ruptured cerebral aneurysm is the most important for their treatments. The results of the acute stage operation were bad and delayed operation was recommended. While, authors have reported good results on acute stage operation.
Recently international cooperative study about the treatment of ruptured cerebral aneurysms in acute stage is proceeding, and in this paper, authors opinion and operative procedure of ruptured aneurysm in acute stage are reported comparing the results between arely and delayed operation.
Ninety-three cases with single episode of aneurysm rupture admitted within four days after the onset between February in 1981 and February in 1982. Patients condition on admission were relatively good-Fifty-five (59.2%) cases of grade one or two and only four (4.3%) cases of grade five in Hunt and Kosnik's classification. Forty-nine cases were operated upon intracranially soon after their admission and forty-four cases were not operated upon within four days after the onset. In thirty-two of such forty-four cases intracranial operations were carried out after then, but other twelve cases were out of our surgical indication and conservative treatments were performed.
The overall morbidity and mortality rate were followed up after two months from the onset comparing between these two groups-early operation group and others.
As the results of the morbidity rate there was no difference between them, but there was some difference in the mortality rate, there were three dead cases (6.1%) in early operation group and ten dead cases (22.7%) in the later group.
And in the later group there were four died cases due to rebleeding in spite of good condition on their admission.
From these results it was concluded that the cases with ruptured aneurysm must be admitted to neurosurgery soon after initial bleeding and be recommended to perform intracranial operation as early as possible after the admission under the correct surgical indication. But the management of early surgery of ruptured aneurysm is so difficult that authors have developed new device and techniques, for example, the method of evacuation of subarachnoid clots which will cause symptomatic vasospasm, the prolongation method of safety temporary occlusion time of the cerebral arteries preventing premature aneurysm rupture using 20% mannitol solution, the application of the continuous ventricle drainage during and after the surgery controlling the intracranial pressure, the method of prevention of the development of the post-operative vasospasms, converting oxy-hemoglobin which will be one of the strongest vasospasmogenic substance, into metho-hemoglobin using 10 mMol Nallo2 and so on. In this paper such methods were reported precisely.

View full abstract

In order to determine the distribution of adrenergic and non-adrenergic innervation of the cerebral arteries, quantitative analysis was performed on electron microscopic pictures of feline perivascular nerve terminals pretreated with 5-hydroxydopamine (5-OHDA).
In 5 cats, 15 minutes after intravenous injection of 5-OHDA (5 mg/kg body weight), the animals were fixed by perfusion of 2.5% glutaraldehyde through the left ventricle of the heart. Sections were taken from the proximal segment of the middle cerebral artery (MCA), the basilar artery (BA) and intracrainal portion of the vertebral artery (VA), post-fixed with osmium and processed for electron microscopic examination.
The diameter and number of adrenergic and non-adrenergic vesicles in the perivascular nerve terminals, and the distance between the nerve terminal and the muscle layer were measured by means of an image analyzed, Luzex 500 (Nihon Regulator Co.).
The diameter of the adrenergic vesicles of the MCA, BA and VA measured, 82.77 ± 0.66 nm (m±SEM), 81.30 ±0.79 nm, 79.94 ± 0.83 nm, respectively. Each of these values was significantly larger than that of the non-adrenergic vesicles of the corresponding arteries (57.22 ± 0.38 nm, 58.23 ± 0.35 nm, 54.44 ± 0.42 nm, respectively) (p<0.01).
The ratio of the number of the adrenergic nerve terminals to that of the non-adrenergic nerve terminals was approximately 2 : 1 in each vessel.
The average number of the adrenergic nerve terminals in the area of 1000 nm in length x full width of the muscle layer of the media in the MCA, BA and VA was 7.60, 4.30 and 4.70, respectively, while the number of the non-adrenergic nerve terminals in the MCA, BA and VA was 15.58, 11.20 and 10.30, respectively.
It is concluded that the MCA is more densely innervated than the BA and VA.

View full abstract

In order to determine the effect of unilateral superior cervical ganglionectomy on adrenergic and non-adrenergic nerve terminals of the middle cerebral artery (MCA) and vertebral artery (VA), quantitative analysis was performed on electron microscopic pictures of feline perivascular nerve terminals pretreated with 5-hydroxydopamine (5-OHDA).
In 5 cats, three weeks after the right superior cervical ganglionectomy, 5-OHDA (5 mg/kg body weight) was in-jected intravenously and 15 minutes later the animals were fixed by perfusion of 2.5% glutaraldehyde through the aortic arch. Sections were taken from the proximal segment of the MCA and intracranial portion of the VA of both sides and post-fixed with osmium and processed for electron microscopic examination.
The diameter and number of adrenergic and non-adrenergic vesicles in the perivascular nerve terminals were measured by means of an image analyzer, Luzex 500 (Nihon Regulator Co.). Four cats with a sham operation served as control.
In both MCA and VA, adrenergic and non-adrenergic vesicles were significantly larger on the ganglionectomized side than those of either the contralateral side or the control. In the MCA adrenergic and non-adrenergic vesicles were significantly smaller in the side opposite to the ganglionectomy than in the control, while no such difference was noted in the VA. The average number of adrenergic vesicles in a nerve terminal was significantly less on the ganglionec-tomized side than that on the contralateral side in the MCA and also than that in the control group.
It is concluded that the effect of unilateral superior cervical ganglionectomy is not confined to the ipsilateral adrenergic nerve terminals of the MCA and VA, but extends to the contralateral adrenergic nerve terminals of the MCA.

View full abstract

Antithrombin III has been known a potent antithrombotic factor in a venous thrombosis. However, the role of AT III in the ischemic cerebrovascular disease has not been fully elucidated.
In this study, we have investigated the time-course of AT III in 76 ischemic stroke patients with or without ad-ministration of aspirin and/or urokinase.
Materials and Methods : Materials were 53 thrombotic patients (38 males and 15 females), 16 embolic patients (13 and 3), and 7 TIA patients (5 and 2). The cerebral lesion were confirmed by CT scan and cerebral angiography. AT III was measured by single immunidiffusion method (Partigen, Hoechist). The normal level of AT III was 31.3 ± 4.3 mg/dl (mean±2SD) in age-matched healthy controles (68 males and 114 females).
Results : 1. The male patients under the age of 69 y.o. showed lower AT III level than that of sex-and age-matched controles (0.05<p<0.1). 2. AT III level was lower in the embolic group than the thrombotic group (0.05<p<0.1). 3. There was no significant difference of At III level among the groups which were divided by the stage of the stroke. 4. AT III level was significantly decreased in the thrombotic group either in the acute or subacute stage by the ad-ministration of urokinase (96000-46000IU/day). 5. Aspirin has significantly increased AT III level in the whole groups. This increses were marked in the lower AT III patients (AT III<27 mg/dl) and the earlier treated patients.
Conclusion : These results suggested that AT III is supposed to be useful practical indicator of the blood coagulability even in the antiplatelet therapy of the ischemic stroke.

View full abstract

We had a case of syndrome of inappropriate secretion of antidiuretic hormone induced by hemorrhage in the right caudate nucleus.
The patient was a 67 year old man. His chief complaints were left hemiplegia and gait disturbance. His present illness and its course prior to admission to our hospital were as follows : Left hemiparesis and gait disturbance were first noticed on the morning of Oct. 14, 1978. Therapy after admission was done at another hospital, and he was able to walk very well by himself in about one month. He was followed up as an outpatient after discharge, but gait distur-bance gradually became exaggerated again from January, 1980, so he visited our hospital on April 1, 1980.
After his admission to our hospital, rehabilitation through training and drug therapy improved his condition, but he suffered two attacks of cerebral thrombosis on Oct. 25, 1980 and on Dec. 23, 1980, respectively. For the purpose of protecting him from a reccurrence, anticoagulants had been administered to him since January 20, 1981. The gait disturbance and dysarthria caused by transient cerebral ischemic attacks, however, frequently occurred. Rigidity of the whole body and an excess of sweat were noticed by his wife at noon on March 31, 1981. A CT scan of the brain showed the high density area of the right caudate nucleus, the lateral ventricle and the third ventricle. These findings meant the hemorrhage in the right caudate nucleus had perforated the cerebral ventricular system.
As hyponatremia and hypokalemia were observed after the cerebral hemorrhage, hyperosmotic saline infusion was performed. Hyponatremia, however, continued for about three weeks. On the other hand, a potassium drug soon normalized hypokalemia. The chief laboratory data obtained during hyponatremia were composed of serum osmorality 262 mOsm/L, urinary osmorality 440 mOsm/L, urinary sodium excretion 5.2 g/day (the same as before cerebral hemorrhage) and blood pH 7.48. The concentration of ADH in perpheral venous blood was 1.5 pg/ml. The normal value of ADH would be caused by the blood sampling at the beinning of serum sodium normalization.
As no pretibial edema was pinpointed in this case and hypoosmotic fluid transfusion was not given to correct dehydration, the hyponatremia induced by cerebral hemorrhage belonged to neither hypervolemic nor hypovolemic hyponatremia. Therefore, in this case, hyponatremia was categorized as normovolemic. Generally there are many causes of pathogenesis of hyponatremia, and SIADH is one cause. This case fits Schwartz's criteria of SIADH except for renal dysfunction. As the attack of cerebral hemorrhage didn't influence the renal function, it seemed that renal dysfunction had not been a cause of hyponatremia in this case. After all, there was no discrepancy with Schwartz 's criteria of SIADH in this case, but whether secretion of ADH was appropriate or inappropriate could not be confirmed.
Conclusively this case was diagnosed as SIADH induced by hemorrhage in the right caudate nucleus.

View full abstract

One hundred and seventy-one initial episodes of cerebral infarction (CI) occured among 1, 621 males and females of Hisayama residents aged 40 and over during the period from 1961 to 1979. Long-term prognosis of CI and recurrence after the initial episode were assessed in relation to various factors estimated at entry.
Subjects suffered from CI less frequently survived than those of general population in Hisayama twon, and ageadjusted survival rate for CI was 51% and 36% at 5 and 10 yr follow-up which was accounted approximately as two-third and a half as that for general population, respectively. Incidentally, the survival curve for CI under 70 years of age was almost equal to that for non-suffered people aged 70 and over. Among the cases with CI, a poor prognosis was associated with old age (70 y.o. and over), poor ADL at one month after initial stroke and hypertention before stroke.
Out of 154 cases with CI who survived more than one month after the intial stroke, 31 (20%) had recurrent episodes, 48% of which ocurred within two years, and 84% within five years. Anuual rate for recurrence was calculated as 5.4% on average for 5-yr follow-up period. Recurrent attacks occured somewhat frequently among those with hypertention, with atrial fibrillation on ECG in both sexes and with diabetes mellitus in males.

View full abstract

α₂-adrenoceptor has been shown to exist in the noradrenergic nerve terminals and smooth muscles of the cerebral arteries, and also in the brainstem. In order to investigate the role of α₂-adrenoceptor in cerebral hemodynamics, the effects of clonidine, a potent α₂-agonist, on the diameter and autoregulatory response of feline pial arteries were observed.
Thirteen adult cats were anesthetized with intraperitoneal injection of α-chloralose (50 mg/kg) plus urethane (500 mg/kg), and ventilated with a respirator. The diameter of the pial arteries was measured continuously through a cranial window by means of a video camera system developed in our laboratory.
Intravenous injection of clonidine (100 μg/kg) produced an initial transient increase in arterial blood pressure followed by a gradual decrease. However, intracarotid administration of clonidine (10 μg/kg) reduced the blood pressure from the beginning but less markedly.
Clonidine injected either intravenously or intracarotidly produced a transient constriction of the pial arteries followed by a gradual dilatation, which was more marked in the latter group.
The effects of clonidine on the autoregulatory response of the pial arteries were observed during hemorrhage and reinfusion of the blood. After intravenous administration of clonidine, the vasoconstrictive response of the pial arteries during reinfusion of the blood was significantly disturbed compared with the vasodilatory response during hemorrhage of the blood. After intracarotid injection of clonidine, where the amount of the agent reached the brainstem was assumed to be relatively small, there was no marked change either in the vasodilatory or in the vasoconstrictive response of the pial arteries.
The above data suggest the importance of α₂-adrenoceptor both in regulation of pial arterial diameter and in autoregulation of cerebral blood flow.

View full abstract

The distribution of the lesions responsible for aphasia unassociated with right-sided hemiparesis was evaluated by cranial computed tomography (CT) among stroke patients. There were 18 patients with this syndrome, in which aphasia was Broca type in 2 patients, Wernicke in 7, transcortical motor in 2, transcortical sensory in 2, amnestic in 2 and global in 3.
The responsible lesions revealed by CT were as follows :
1) Broca aphasia; Aphasic symptoms were atypical of Broca aphasia in these 2 patients because writing or silent reading was preserved, and the lesions were far more localized than in ordinary Broca one.
2) Wernicke aphasia; In this group most patients showed relatively large lesions in the left superior temporal gyms, sometimes extending to supramarginal and angular gyri, which caused such additional symptoms as apraxia without motor paresis in some cases.
3) Transcortical motor aphasia; One patient showed the occlusion of the left internal carotid artery, though without obvious abnormality at CT. In another patient a circumscribed low density lesion was disclosed in the area anterior and superior to so-called Broca 's area.
4) Transcortical sensory aphasia; In this group the lesion involved the borderzone supplied by the left middle and posterior cerebral arteries.
5) Amnestic aphasia; One patient showed a lesion in the left parietal lobe, while in another no remarkable change was demonstrated.
6) Global aphasia; One had multiple isolated lesions in both anterior and posterior speech areas. Another showed a large lesion involving the whole territory of the left middle cerebral artery. In the remaining one a high density area was observed in the left superior temporal, supramarginal and angular gyri, not extending to the fronal lobe beyond wht sylvian fissure.
In summary, in sensory type of aphasia the responsible lesions were distributed in the areas almost compatible with those stated in literature. On the contrary, in aphasias of other types there were some discrepancies between the actual sites of lesion at CT and those predicted on basis of clinical symptoms. For example, in a patient with global aphasia a widespread lesion in the whole territory of the left middle cerebral artery caused no hemiparesis, while in another with this type of aphasia the lesion did not extend to the anterior speech area. In addition, CT revealed no lesions in one patient with transcortical motor and amnestic aphasia, respectively. Therefore, in interpreting CTs of such aphasic patients we must take account of not only the extent of the lesion but also the severity of destruction, that is, whether softening in complete or incomplete, because the extent with reduced blood perfusion could not be identical with that of low density at CT. Furthermore, in face of reduction in cerebral blood flow there may be a difference in threshold of affection between limb motor function and speech one as a higher cortical function, implying the latter usually being more vulnerable.

View full abstract

The purpose of this presentation is to report an autopsy case with cerebral infarction caused by tumor emboli and to describe the CT scan findings.
A 64-year-old male was admitted to Tokai Univ. Hosp. on Sep. 22, 1979. He had been admitted to another hospital because of expectoration since the beginning of August. Chest X-ray showed infiltrative shadow on RML (S4). In early September, he had developed dysarthria and weakness of the left upper extremity, which brought him to our hospital. On admission he was dyspneic, and rales were audible over the bilateral lower lungs posteriorly. Neurological examination revealed meningeal irritation signs, dysphonia, dysarthria and left hemiparesis including the face. On cranial CT scan, small LDA was seen in right internal capsule. On the 3rd hospital day, he died of respiratory failure with evidence of D.I.C.
The autopsy revealed poorly differentiated adenocarcinoma of the lung. Softening of the brain was seen in the posterior limb of the right internal capsule and right ventral portion of the pons. The latter showed hemorrhagic infarction. Perfusing arteries of the softened area were occluded by tumor emboli. The emboli were histologically identical to lung cancer. No metastasis was noted extravascularly. Tumor emboli were also seen in lung, pituitary gland, adrenal gland, liver, bone marrow and lymph nodes.
Case reports of brain tumor emboli are very rare. Twenty-five previously reported cases are reviewed here. It is concluded that there is a tendency for small, multiple infarctions in cases with spontaneous (non-operative) tumor emboli.

View full abstract