Twenty six cases of internal carotid artery (ICA) occlusion confirmed by angiogram were classified into five groups according to CT findings; I) total infarction, low density area (LDA) involving most of a cerebral hemisphere, II) superficial infarction, cortical and/or subcortical LDA, III) deep infarction, LDA largely confined to the deeper, capsular territory of the middle cerebral artery, IV) both superficial and deep infarction, V) watershed infarction, LDA just located in the so-called anterior and/or posterior watershed area. Each group was evaluated regarding clinical features, collateral circulation and cerebral blood flow (CBF).
Watershed infarction observed in 35% of our cases was associated with mild, slowly completed symptom and good collateral circulation, while the cases with total infarction had poor collateral circulation and grave prognosis.
Furthermore, mean CBF of the ipsilateral hemisphere measured by ¹³³Xe inhalation method tended to be higher in watershed infarction than in any other infarction. The most cases with good collateral circulation had crossed circulation via anterior communicating artery (Acorn). As to the site of occlusion, the prognosis of proximal occlusion was better than that of distal occlusion. Seven cases (27%) had also LDA of the contralateral hemisphere, all of which located in watershed area. It suggested that CBF of the contralateral hemisphere should be reduced in some stage in these cases. Interhemispheric steal may play an etiologic role in two cases with both contralateral ICA stenosis and crossed circulation via Acom.
As a conclusion, the cases with watershed infarction diagnosed by CT had some clinical characteristics.

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The pathogenesis of transient ischemic attack (TIA) is assumed to be closely related to that of cerebral infarction (CI) from the standpoint of clinical symptomatology, but not many studies have ever been done to evaluate the pathogenetic relationship between TIA and CI. The present study was performed to investigate the pathogenetic importance of blood viscosity and platelet function in both diseases.
Several blood viscosity and platelet function parameters were measured in 20 patients with TIA at chronic stage, 15 patients with CI at chronic stage and 15 control subjects matched for age and sex.
The results were as follows :
1) In blood viscosity parameters, whole blood viscosity and hematocrit levels in both diseases were significantly high compared with those in controls and a positive correlation was found between whole blood viscosity and hematocrit (r=0.77, p<0.005).
2) In platelet function parameters, platelet aggregability, studied with optical density methods, in both diseases was significantly great compared with that in controls, and also levels of circulating platelet aggregates and plasma factor VIII/von Willebrand factor activity in both diseases were significantly high compared with those in controls.
3) In these parameters, no significant differences were found between TIA and CI.
These results suggest that blood viscosity and platelet function may be some common mechanism to TIA and CI. Pathogenetic implications of these parameters were discussed in the aspect of hemorheology and blood coagulation.

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Several reports have shown that subjects with coronary, cerebral, and peripheral artery diseases have elevated insulin responses to oral glucose compared with control subjects with no evidence of vascular diseases. In this study, 129 survivors of cerebral infarction (CI) were subdivided into two groups (cortical artery group and perforating artery group), and glucose, insulin (IRI), free fatty acid (FFA) and glucagon (IRG) responses to 50 g oral glucose were studied to assess the role of abnormal glucose metabolism in the pathogenesis of CI.
Patients with CI showed a significant rise in blood glucose levels after oral administration of glucose. In many of the patients the blood glucose values after oral administration of glucose satisfied the criteria for the diagnosis of diabetes mellitus (DM) of the Japan Diabetic Society, and the new diagnostic criteria for DM or impaired glucose tolerance (IGT) of WHO.
The patients with CI had abnormally delayed insulin responses after glucose. The mean concentration of IRI at 30 minutes in the perforating artery group was significantly lower than in healthy subjects and the cortical artery group, and the total IRI (sum of plasma IRI levels at 0, 30, 60 and 120 minutes) in the perforating aterty group was low. The plasma IRI in the cortical artery group showed a delayed response and reached a peak at one hour, but the mean concentration at two hours was significantly higher in the cortical artery group than in the healthy group. As a result, the total IRI was higher in the cortical artery group than in the healthy subjects and the perforating artery group.
The fasting FFA levels were higher in both groups of CI than in the healthy subjects. The plasma FFA fell rapidly after ingestion of glucose and no significant difference was found in the declining response.
Plasma glucagon in healthy subjects fell significantly after the adminstration of glucose, whereas the levels of plasma glucagon did not decrease after glucose ingestion in many patients with CI.
The findings suggest that diabetes with decreased insulin secretion accelerates the development of CI in the distribution of the perforating artety area more than in the cortical artery area, and that hyperinsulinism may play a role in the genesis of atherosclerosis of CI in the cortical artery area.

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The experimental study presented was undertaken to evaluate the role of platelet function contributing the cerebral microcirculatory disturbance during the post-cerebral ischemia, and to examine effects of antiplatelet agent, ticlopidine, on this condition.
Following Pulsinelli's method, rats were subjected to global cerebral ischemia by means of temorary clips on both common carotid for fifteen or thirty minutes after previous ligation of both vertebral arteries. The animals were assigned to three groups by administration of the drug as follow; 1) intact control group, 2) ischemic group without drug, 3) ischemic group with 100 mg/kg of ticlopidine given orally three hours before insult. The morphological changes of platelet were observed by scanning electron microscope and the platelet aggregability to ADP were recorded on each group at five minutes and thirty minutes after recirculation. The degree and distribution of no-reflow phenomenon after reperfusion was assessed by means of carbon black perfusion method in serial coronal section.
Compared with the intact control group, ischemic animals without ticlopidine showed significantly increased aggregability of platelet and increased numbers of activated from of platelet during their post-ischemic period. This group also had impaired reperfusion after ischemia on carbon black perfusion method.
While, in ischemic group treated with ticlopidine, platelet aggregability and number of activated form of platelet were significantly decreased and impaired reperfusion seemed to be also improved. Ticlopidine improved survival rate after fifteen minutes of cerebral ischemia but did not in cases of thirty minutes of ischemia.

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One hundred and fifteen measurements of regional cerebral blood flow were performed on 52 patients with rup-tured intracranial aneurysms. The value of mean hemispheric blood flow (mCBF) reduced significantly 2 to 3 weeks following the onset of subarachnoid hemorrhage in the patients with angiographically proved angiospasm compared with the value of mCBF in the patients without angiospasm (p<0.01). The reduction of mCBF correlated well with the pre-operative clinical grades according to neurological deficits (p<0.05) and also with the presence of angiospasm (p<0.01). However, the correlation between the degree of reduction in mCBF and the severity of angiospasm was present only in the patients with severe reduction of mCBF to less than 30 ml/100 g/min.
Focal ischemia occurred frequently in the patients with severe neurological deficits. Impaired CO₂ response was found several days to more than one month after the onset of subarachnoid hemorrhage and occurred frequently in the patients with severe neurological deficits of angiospasm.
It was worthy to note that the patients with intact CO₂ reactivity showed good operative results in 14 of 16 cases, wheareas the patients with impaired reactivity showed poor operative results in 9 of 13 cases.

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Circadian changes in plasma levels of norepinephrine (NE) and epinephrine (EP) were studied in 16 patients with subacute or chronic stage of stroke. Subjects were kept at bed rest during the study and blood samples were obtained through an indwelling venous catheter at every three-hour interval.
Plasma catecholamines were determined by the application of high speed liquid chromatograph combined with trihydroxy indole method. In patients with clear consciousness, the mean values for both plasma NE and EP reached the highest level during the daytime and showed the lowest level during the nighttime, exhibiting the existence of circadian rhythms. On the other hand, in patients with vegetative state due to severe brain damage, these diurnal changes of plasma catecholamines were found to be altered and plasma levels of catecholamines during the daytime were similar to those during the nighttime.
Twenty-four hour patterns of plasma catecholamines in 3 patients having locked-in syndrome were also different from those observed in patients with clear consciousness, implying the unsteadiness of the activity of the sympathetic nervous system after stroke.
These results suggested that the severe impairment of the central nervous system had an influence on the cir-cadian rhythm of plasma catecholamines.

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This 52 years old male with a left middle cerebral giant aneurysm suffered from subarachnoid hemorrhage, in-farction attack and rebleeding serially within short term. However, this case was followed using CT scan. Generally aneurysms are diagnosed by angiogram. Recently CT scan is developed rapidly, giving us many new informations for cerebral giant aneurysm, such as, the true size of aneurysm, calcification of wall and thrombosis of cavity.
In this case the aneurysm was localized at bifurcation of middle cerebral artery. CT scan on asmission showed homogeneous round high density area and enhanced effect was clearly shown at both cavity and wall equally. In-farction attack occurred on the 16th day following the inital bleeding. At the time carotid angiogram showed M, stenosis due to angiospasm and complete occlusion at middle cerebral bifurcation. CT number of aneurysm was higher than that on admission. Therefore we supposed that circulation of middle cerebral artery was slow due to angiospasm, thrombosis was produced in the cavity of the aneurysm and the thrombosis occluded middle cerebral artery. Later the patient suffered from rebleeding caused severe intracerebral and ventricular hematoma, and died.

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A case of a basilar thrombosis, showing a “locked-in” syndrome, following posttraumatic occlusion of vertebral artery was reported.
A healthy 47-year-old man trumbled and flung his head on a concrete when playing golf, and six hours later he became unconscious suddenly. On admission, he was comatose and showed no voluntary movements. Ocular bobbing was present, and he did not respond to either oculocephalic reflex or caloric test. Left vertebral angiography on ad-mission revealed the complete occlusion of left vertebral artery at 3 cm above its origin. The right brachial angiography revealed a narrow and hypoplastic right vertebral artery and no filling in the basilar artery.
Three days after admission there was some recovery in the consciousness, but the patient remained completely tetraplegic and was not able to speak, so called locked-in syndrome. During the locked-in syndrome, the patient showed occasional decerebrate posture and transient painfull tonic spasm in his lower extremities. A CT scan obtained on two weeks after admission showed a large area of low density in the ventral portion of pons.
One year later, he was still in the state of locked-in syndrome. A CT scan showed atrophic changes in the pons and even in the cerebral cortex.
To the best of our knowledge, this is the first case of the locked-in syndrome following the traumatic occlusion of verterbral artery in Japan. It might be considered that the hyperextension and rotation of the vertebral artery due to trauma induced the injury of the vertebral arterial intima and caused the occlusion of the vessel.

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