OBJECTIVES: To study the effect of the severity of internal carotid artery (ICA) lesions on cerebral haemodynamics. DESIGN: Cross-sectional study. MATERIALS AND METHODS: Magnetic resonance (MR) imaging, angiography (MRA) and spectroscopy (MRS) were used to study the prevalence of (border-zone) infarctions, volume flow in the main cerebropetal and middle cerebral arteries (MCA) and metabolic changes in the MCA territories in 170 patients with symptomatic ICA stenoses or occlusions and 25 control subjects. RESULTS: No significant correlation was found between severity of the carotid lesion and the prevalence of border-zone infarctions. Also, no significant correlation was found with changes in the N -acetyl-aspartate/choline ratio nor with the prevalence of cerebral lactate. In patients with at least one severe ICA lesion, flow in the basilar artery was increased. Flow in the MCA on the symptomatic and asymptomatic side was decreased when at least one ICA was occluded. Total cerebropetal flow (flow through the ICAs plus basilar artery) was decreased when at least one ICA was occluded. No significant correlation was found between changes in cerebropetal flow and the N -acetyl-aspartate/choline ratio nor with the prevalence of border-zone infarctions. CONCLUSION: Border-zone infarctions and ischaemic metabolic changes are not directly the result of cerebral hypoperfusion caused by severe ICA lesions.
OBJECTIVES: To study the effect of the severity of internal carotid artery (ICA) lesions on cerebral haemodynamics. DESIGN: Cross-sectional study. MATERIALS AND METHODS: Magnetic resonance (MR) imaging, angiography (MRA) and spectroscopy (MRS) were used to study the prevalence of (border-zone) infarctions, volume flow in the main cerebropetal and middle cerebral arteries (MCA) and metabolic changes in the MCA territories in 170 patients with symptomatic ICA stenoses or occlusions and 25 control subjects. RESULTS: No significant correlation was found between severity of the carotid lesion and the prevalence of border-zone infarctions. Also, no significant correlation was found with changes in the N -acetyl-aspartate/choline ratio nor with the prevalence of cerebral lactate. In patients with at least one severe ICA lesion, flow in the basilar artery was increased. Flow in the MCA on the symptomatic and asymptomatic side was decreased when at least one ICA was occluded. Total cerebropetal flow (flow through the ICAs plus basilar artery) was decreased when at least one ICA was occluded. No significant correlation was found between changes in cerebropetal flow and the N -acetyl-aspartate/choline ratio nor with the prevalence of border-zone infarctions. CONCLUSION: Border-zone infarctions and ischaemic metabolic changes are not directly the result of cerebral hypoperfusion caused by severe ICA lesions.