• D R Rutgers, M J P van Osch, L J Kappelle, W P T M Mali, and J van der Grond.
• Department of Radiology, E01.132, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands. d.rutgers@azu.nl
• Stroke. 2003 Mar 1; 34 (3): 648-52.

Background And PurposeThe goals of this study were to investigate (1) whether the concentrations of choline, creatine, and N-acetyl aspartate (NAA) in cerebral white matter are changed in patients with symptomatic occlusion of the internal carotid artery (ICA) and (2) whether possible changes in metabolite concentration are related to regional cerebral perfusion or cerebral vasoreactivity.MethodsIn 19 patients (mean+/-SD age, 60+/-9 years), white matter metabolite concentrations were measured with proton MR spectroscopic imaging on average 4+/-2 months after symptoms occurred. In selected voxels, corresponding cerebral blood flow and volume, mean transit time, and time-to-bolus peak were determined with dynamic susceptibility contrast MRI. Cerebral CO2 reactivity was determined with transcranial Doppler sonography.ResultsNo significant changes in choline and creatine concentrations were observed. NAA concentration was significantly reduced in the hemisphere on the side of the symptomatic ICA (9.1+/-1.7 mmol/L) compared with the contralateral hemisphere (10.5+/-1.7 mmol/L, P<0.005) and control subjects (10.5+/-0.9 mmol/L, P<0.01). Although no significant interhemispheric difference in NAA concentration was found in patients who presented with retinal ischemia, patients with cerebral ischemia had a significantly lower NAA concentration in the symptomatic hemisphere (9.0+/-1.7 mmol/L) compared with the asymptomatic hemisphere (10.4+/-1.6 mmol/L, P<0.05). In all patients, NAA concentration was not significantly correlated with quantitative cerebral perfusion parameters or CO2 reactivity.ConclusionsPatients with symptomatic ICA occlusion may show chronic neuronal damage in cerebral white matter as evidenced by reduced NAA concentration. This seems to be related to previous symptomatology rather than to the cerebral hemodynamic status in a chronic stage.

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