Abstract
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.
Angiograms, mostly performed within one week after the onset of attack, revealed that collateral circulation (CC), which was derived from three major routes, was present in various combinations, i.e.
1) CC via the circle of Willis (CW) was present in 66.7% of the thrombotic cases. Good filling of both the anterior and middle cerebral arteries from the contralateral ICA was seen in 16 cases. Embolism had the same percentage, although good filling was seen in only half of the cases.
2) CC via the ophthalmic anastomoses was present in 36.7% of the thrombotic cases and 11.1% of the embolic cases.
3) CC via the leptomeningeal anastomoses was present in 53.4% of the thrombotic cases and 44.4% of the embolic cases.
The analysis of the CT scans correlated with the angiograms, leading to the conclusion that the size of the infarcted area depended on the degree of collateral flow and that the CC of embolism mainly relied on CW. Therefore, cases with sufficient collateral flow developed either no or minimal infarction. In contrast, absent or insuffcient collateral flow through the CW resulted in a large infarction in spite of the presence of collateral flow from the other routes.
In thrombosis, the role of collateral flow from the CW seemed not to be as important as in embolism. Six cases failing to show collateral flow through the CW developed small infarctions with the presence of collateral flow from other routes.
A higher frequency of intracranial occlusio-supra-occlusioneum and propagation of secondary thrombosis distal to the occlusion in embolism may be attributed to the extension of infarction due to reduced collateral flow.
