THE ROLE OF THE CIRCLE OF WILLIS IN CAROTID OCCLUSION - ASSESSMENT WITH PHASE-CONTRAST MR-ANGIOGRAPHY AND TRANSCRANIAL DUPLEX

Purpose: To study the collateral pathways recruited after occlusion of the internal carotid artery (ICA), and to evaluate its influence an t he impairment of hemispheric blood flow supply and development of low flow infarcts. Methods: 38 patients with ICA occlusion (18 asymptomati c; five transient ischaemic attacks; and 15 strokes) were included. In farcts on cerebral MR scanning were categorised in order to differenti ate patients with territorial infarcts or no lesion (group I; n = 22) from those with brain damage due to low flow (group II; n = 16). Paten cy and direction of flow in the communicating arteries were assessed b y means of cine phase contrast MR angiography (PC-MRA). Flow velocity in the middle cerebral artery (MCA) was measured by means of transcran ial Duplex (TCD). Results: Cine PC-MRA revealed a reversed ophthalmic artery bloodflow ipsilateral nl to the ICA occlusion in all except two patients in group I and one patient in group II (NS). Posterior to an terior flow in the ipsilateral posterior communicating artery (PCoA) w as detected in 16 (73%) patients in group I and in 13 (81%) in group I I (NS). In contrast, reversed blood flow in the ipsilateral A1 segment of the anterior cerebral artery, through a patent anterior communicat ing artery (ACoA), was identified in 19 (86%) patients of group I, vs. 7 (44%) of group II (p = 0.0051. The relative risk of low-flow infarc ts was significantly higher in those cases with non-functioning ACoA ( odds ratio = 8.1; p < 0.05). TCD showed a lower peak systolic velocity (PSV) in the ipsilateral MCA than in the contralateral one (60 +/- 9 cm/s vs. 90 +/- 11 cm/s; p < 0.005). Those patients without crossed fl ow through the ACoA, showed an even lower PSV in the ipsilateral MCA ( 55 +/- 7 cm/s vs. 64 +/- 9 cm/s; p = 0.03). Conclusions: These data su ggest that even though ICA occlusion may occur without cerebral damage , collateral blood supply is not enough to maintain normal hemispheric perfusion. The ACoA may be a key collateral pathway as a non-function ing ACoA is associated with an increased risk of developing low-flow i nfarcts.