Cerebral Metabolism of Patients With Stenosis or Occlusion of the Internal Carotid Artery

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Abstract
Background and Purpose Occlusion or severe stenosis of extracranial vessels may lead to hypoperfusion without overt infarction of brain tissue. The aim of this study was to investigate whether occlusion of the internal carotid artery or stenosis with reduction in diameter of more than 70% leads to altered cerebral metabolism in regions in which no infarcts are visible with magnetic resonance imaging. Methods We studied 10 control subjects and 55 patients with transient or nondisabling cerebral ischemia (25 patients with severe unilateral stenosis, 15 patients with unilateral occlusion, and 15 patients with bilateral severe stenosis or occlusion of the internal carotid artery). All subjects underwent magnetic resonance imaging and 1 H magnetic resonance spectroscopic imaging. Cerebral metabolism was studied by assessing ratios of N -acetyl aspartate (NAA) to choline and to creatine as well as lactate from noninfarcted frontal, mesial, and parietal regions in the centrum semiovale in both hemispheres. Results All patients with unilateral stenosis or occlusion of the internal carotid artery had decreased NAA/choline ratios in noninfarcted areas in the hemisphere on the side of the stenosis or occlusion and normal NAA/choline ratios in the contralateral hemisphere. Patients with bilateral stenosis or occlusion had decreased NAA/choline ratios in both hemispheres. In one third of all patients, cerebral lactate was found in regions without abnormalities on magnetic resonance imaging. Conclusions A severe reduction in the diameter of the internal carotid artery affects cerebral metabolism in regions that are not infarcted. These changes are reflected in a decreased NAA/choline ratio and a high incidence of cerebral lactate. These regions are probably at risk for infarction in the long term or if cerebral perfusion decreases further.

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