[en] Internal carotid artery (ICA) occlusion presents a broad spectrum of clinical manifestations ranging from death due to extensive infarction to absence of neurological deficit and infarction. In order to evaluate the relationship between the obstructive mechanism of ICA occlusion and the effect of this phenomenon on cerebral parenchyma, both CT scans and angiograms of forty-eight cases of ICA occlusion (eighteen cases of embolism and thirty of thrombosis) were reviewed. The size and location of low density areas (LDA), the presence of mass effect and the responce to contrast enhancement demonstrated on CT scans were analysed in relation to angiographic findings. About 90% of these cases demonstrated various sizes of LDA on CT. In this study, a large infarction was defined as LDA larger than 2/3 of the hemispheric area and a small infarction as LDA smaller than 1/3 of the hemispheric area. 61% of patients with embolism presented with large infarctions, with many being total infarctions of the cerebral hemisphere or middle cerebral artery (MCA) territory. On the contrary, small infarctions accounted for 67% of thrombotic cases. Most of them were partial infarctions of MCA territory; other small infarctions were distributed in various regions including watershed infarctions (27% of thrombotic cases). The frequency of mass signs was higher in embolism (78%) than in thrombosis (17%). Contrast enhancement was seen in 97% of embolic cases and 44% of thrombosis. (J.P.N.)

[en] In order to evaluate the relationship between CT and angiographic findings, especially the degree of collateral circulation estimated by 4-vessel study, 47 cases with internal carotid artery occlusion were studied. The CT findings showed large infarction in 16 cases and small infarction in 24, but 7 cases had no infarction. The angiography demonstrated contralateral internal carotid stenosis in 5 cases, contralateral A₁-hypoplasia in 3 cases, and occlusio-supra-occlusionem in 6 cases, in addition to internal carotid artery occlusion (5 cases with pilateral internal carotid artery occlusion). Markedly apparent collaterals were seen; ophthalmic anastomoses (Oph.) in 30 %, via the circle of Willis (CW) in 53 %, and leptomeningeal anastomoses (LM) in 30 %. In CW, cross-filling was seen, mainly through the anterior communicating artery in the anterior cerebral artery (ACA) and middle cerebral artery (MCA) region. LM was seen mainly as back-flow from posterior cerebral artery to ACA/MCA region. Among the various combinations of collaterals, 46 % were Oph (-) + CW (++), + LM (- ∼ +). The size of the infarcted area generally depended on CW. But since 28 % of CW (++) presented large infarctions of the MCA region it is likely that either an occlusio-supra-occlusionem or a propagation of secondary thrombosis from occluded site temporarily blocked the cross-filling through CW. On the other hand, in CW (- ∼ +) the combination of Oph and LM determined the size of the infarcted area. But large infarctions were seen in 36 % of the Oph(+)/LM(++) combination, suggesting that the speed of occlusion of the internal carotid artery influenced the formation of an infarction. That is, the rapid occlusion made the infarcted area larger due to arteriolo-arteriolo anastomoses of Oph and LM. (J.P.N.)

[en] Twenty-one cases of acute cerebral infarction with a midline shift on the CT scan were studied with respect to the development of the midline shift, the angiographic findings, the clinical pictures and the outcome of these patients. The CT findings of hemorrhagic infarction were also studied. No cases showed a midline shift on a CT scan taken within 6 hours after the onset. A midline shift was, however, noted as early as 9 hours after the onset, and it reached its peak between the 2nd and 7th day of the onset. It gradually disappeared by the end of the third week. Hemorrhagic infarction was diagnosed in 6 patients by either spinal tap or autopsy. The CT findings of these hemorrhagic infarction were divided into two types, solid hemorrhages with an unequivocal high density within the low-density area, and small, scattered hemorrhagic of almost the same density as normal brain tissue within the low-density area. In 19 of 21 patients, an round-edged occlusion and/or embolus were observed on the initial angiograms. The recanalization of the occluded vessels was proved in 10 of 14 patients by subsequent angiographic studies. Twenty of 21 patients showed a sudden development of neurological symptoms, and 15 patients had a history of various kinds of heart disease, such as atrial fibrillation, valvular heart disease and myocardial infarction. The patients had atrial fibrillation on EKG on admission. These angiographic findings and clinical pictures strongly suggest that the infarction with a midline shift on the CT scan may be caused by a cerebral embolism of cardiac origin. Eight patients died of cerebral herniation between the 2nd and 6th day of the onset. Taking these poor outcomes into consideration, surgical as well as medical decompression of the brain would seem to be most important when the CT scan shows a midline shift. (author)

[en] Thirty-eight patients with occlusive cerebrovascular disease were followed with regional cerebral blood flow (rCBF) measurement, angiography and computerized tomography (CT). The rCBF study was carried out by the ¹³³Xe intracarotid injection method. They were allocated to two groups according to the findings on angiogramsF; 15 patients having any change of occlusive lesion (the group of norecanalization) and 23 patients showing reopening of occluded vessels (the group of recanalization). In the group of no-recanalization, a mean value of rCBF (mean rCBF) in acute stage was well correlated to the severity of ischemic stroke. Sequential change of mean rCBF was not promineFnt in the group of no-recanalization. However, rCBF change was conspiculous in the group of recanalization. In acute stage of recanalization, rCBF were markedly affected by the presence of mass sign (cerebral edema) on CT. The inhomogeneity of rCBF was characteristic in cases with recanalization. The focal hyperemia usually disappeared within one week in cases of minor stroke and lasted until 2 or 3 weeks in cases of major stroke. In chronic stage, mean rCBF decreased, and there was no significant difference of averaged rCBF between two groups. Those findings suggests that the main factor influenced on the sequential change of rCBF is reopening of occluded vessels. Regional CBF may depends both on the degree of cerebral edema and the extent of vasoparesis after revascularization. In chronic stage CBF value is not always dependent to the presence of occlusive lesion but might be reflected in the total brain function. (J.P.N.)

[en] Fifty-two patients with carotid TIA'(s) (transient ischemic attack) were investigated by angiography, and computed tomography (CT) was also performed in 29 cases. Regional CBF (cerebral blood flow) was measured in 16 cases. About two third of the patients has the stenotic lesion(s) on angiograms. The incidence of the lesion is greater (double) in intracranial arteries than in extracranial artery. Of twenty-four intracranial stenotic lesions, thirteen (54%) were found in horizontal portion of the middle cerebral artery (M₁). Regional CBF was slightly reduced in five of seven patients with severe arterial stenosis, while rCBF was normal in most (eight of nine) patients with mild arterial stenosis or without stenosis. An abnormal CT finding was found in nine of 29 patients; namely, eight had a small low density area in the basal ganglia near the internal capsule, and one had a low density area in temporal lobe. In three of nine patients with small low density area in the basal ganglia, the lesion was enhanced after contrast infusion about two weeks after TIA. This indicates that the enhanced area seems to contribute to TIA. Of eight patients with small low density area in the basal ganglia on CT, five (63%) had a mild or severe stenosis of M₁, and the incidence of M₁ stenosis was significantly higher than that of the patients with normal CT (20%). None of them had a stenotic lesion in cervical internal carotid artery. These findings strongly suggest that the cause of TIA in patients with low density area in the basal ganglia is due to ischemia of the distribution of lenticulostriate artery. An atheromatous change of M₁ or lenticulostriate artery itself may cause blood flow disturbance near the internal capsule. (author)

[en] Twenty-five patients were diagnosed as having hemorrhagic infarction by autopsy (4 cases), by an operation (3 cases), or by the combination of CT and a spinal tap (18 cases). Angiography was repeated to identify the recanalization as far as possible. The progression or resolution of the mass sign (brain edema) and the contrast enhancement were observed by CT, which was performed at intervals of from one to seven days in almost all cases. The CT findings of hemorrhagic infarction were as follows: 1) Appearance of the foci of an increased density in the low-density area; Generally the foci were indicated as a high-density area, but sometimes they were presented as isodensity in the acute stage of a stroke. Adjacent severe brain edema in the acute stage was supposed to be the main cause of the reduction in the CT number. 2) Ring-formed contrast enhancement in the subacute stage; a ring-formed contrast enhancement was seen on post-contrast scans after the resorption of the hemorrhage. According to our data, hemorrhagic infarction was found not only in the acute stage (within 4 days of the stroke, 9 cases) but also in the subacute stage (over 7 days after the stroke, 19 cases). The acute type of hemorrhage was usually associated with marked cerebral edema. On the other hand, the subacute type of hemorrhage usually appeared when enhancement after contrast infusion was observed and the cerebral edema was being resolved. On angiograms, a recanalization of the occlusion was frequently observed (18 cases, 68%). A comparative study of angiography and CT revealed the difference in the timing of the hemorrhage between the acute and subacute types of hemorrhages. The acute type of hemorrhage usually appeared in response to the angiographical recanalization, but the subacute type of hemorrhage sometimes occurred unrelated to that of angiographical recanalization. (author)

[en] Computed tomography (CT) is a very useful method for the diagnosis of cerebrovascular diseases, especially in the acute stage. In the subacute stage, however, it is difficult to determine whether a lesion is a hematoma or an ischemia. It is necessary to use contrast agents to differentiate these two types of lesions. Therefore, it is very important to study the plain and the enhanced CT findings of these lesions in the acute and subacute stages. The author analysed the sequential CT findings of cerebral hemorrhage (60 cases), ischemic infarction (22 cases), and hemorrhagic infarction (22 cases) and reaches the following conclusions: 1) In cerebral hemorrhage, the high-density area disappears within weeks at a rate related with the length (cm) of the maximum diameter of the high-density area in the first week, contrast enhancement also disappears within months in parallel with the length of the maximum diameter of the high-density area in the first week. 2) In contrast-enhanced CT, cerebral hemorrhage showed a ring enhancement in all stages and sometimes showed a slit enhancement in the chronic stage. In general however, ischemic infarction did not show ring enhancement. 3) Mass effect and contrast enhancement disappear within the first month in ischemic infarction, but continue for two months in hemorrhagic infarction. (author)