The role of the circle of Willis in carotid occlusion: assessment with phase contrast MR angiography and transcranial duplex.
OBJECTIVE
To study the collateral pathways recruited after occlusion of the internal carotid artery (ICA), and to evaluate its influence on the impairment of hemispheric blood flow supply and development of low flow infarcts.


METHODS
38 patients with ICA occlusion (18 asymptomatic; five transient ischaemic attacks; and 15 strokes) were included. Infarcts on cerebral MR scanning were categorised in order to differentiate patients with territorial infarcts or no lesion (group I; n = 22) from those with brain damage due to low flow (group II; n = 16). Patency and direction of flow in the communicating arteries were assessed by means of cine phase contrast MR angiography (PC-MRA). Flow velocity in the middle cerebral artery (MCA) was measured by means of transcranial Duplex (TCD).


RESULTS
Cine PC-MRA revealed a reversed ophthalmic artery blood flow ipsilateral to the ICA occlusion in all except two patients in group I and one patient in group II (NS). Posterior to anterior flow in the ipsilateral posterior communicating artery (PCoA) was detected in 16 (73%) patients in group I and in 13 (81%) in group II (NS). In contrast, reversed blood flow in the ipsilateral A1 segment of the anterior cerebral artery, through a patent anterior communicating artery (ACoA), was identified in 19 (86%) patients of group I, vs. 7 (44%) of group II (p = 0.005). The relative risk of low-flow infarcts 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 flow 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 suggest 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-functioning ACoA is associated with an increased risk of developing low-flow infarcts.
D000293:Adolescent; D000328:Adult; D000368:Aged; D001783:Blood Flow Velocity; D001925:Brain Damage, Chronic / Q000175:diagnosis / Q000000981:diagnostic imaging; D002545:Brain Ischemia / Q000175:diagnosis* / Q000000981:diagnostic imaging; D002343:Carotid Artery, Internal / Q000000981:diagnostic imaging / Q000473:pathology; D016893:Carotid Stenosis / Q000175:diagnosis* / Q000000981:diagnostic imaging; D002536:Cerebral Arteries / Q000000981:diagnostic imaging / Q000473:pathology; D002544:Cerebral Infarction / Q000175:diagnosis* / Q000000981:diagnostic imaging; D002560:Cerebrovascular Circulation; D002941:Circle of Willis / Q000000981:diagnostic imaging / Q000473:pathology*; D003097:Collateral Circulation; D005260:Female; D006801:Humans; D002546:Ischemic Attack, Transient / Q000175:diagnosis / Q000000981:diagnostic imaging; D018810:Magnetic Resonance Angiography; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D008875:Middle Aged; D009880:Ophthalmic Artery / Q000000981:diagnostic imaging / Q000473:pathology; D012039:Regional Blood Flow; D013599:Systole; D017585:Ultrasonography, Doppler, Transcranial; D014654:Vascular Patency