Cerebral metabolic changes in patients with a symptomatic occlusion of the internal carotid artery: a longitudinal 1H magnetic resonance spectroscopy study.
The objective of this 1H magnetic resonance spectroscopy study was to investigate the time course of the brain metabolites N-acetyl-aspartate (NAA), choline, and lactate in patients with transient or minor disabling neurological deficits associated with an occlusion of the internal carotid artery (ICA). Fifty patients had had symptoms of hemispheric ischemia, and 16 had suffered symptoms of retinal ischemia. Single-voxel proton spectra were obtained from uninfarcted cerebral regions on three occasions: 0-6, 6-12, and 12-18 months after symptoms. Reference values were obtained from 29 control subjects. In the 0-6 month period, patients with hemispheric ischemia showed a significantly lower NAA/creatine ratio in the hemisphere ipsilateral to the ICA occlusion, compared with control subjects and patients with retinal ischemia, and a significantly higher choline/creatine ratio, compared with control subjects. The prevalence of lactate did not differ significantly between patient groups. In the following time periods, the NAA/creatine ratio in patients with hemispheric ischemia tended to return to control values and no longer differed from that in patients with retinal ischemia; the choline/creatine ratio decreased significantly and returned to control values. These results demonstrate that cerebral metabolism is altered in patients with an ICA occlusion who have had a hemispheric ischemic event, but returns (choline) or tends to return (NAA) to control values over time. The metabolic changes occur primarily in the hemisphere ipsilateral to the symptomatic ICA occlusion and are related to the occurrence of the hemispheric ischemic event.
Rutgers
D R
DR
Department of Radiology, University Medical Center Utrecht, The Netherlands. D.Rutgers@azu.nl
Klijn
C J
CJ
Kappelle
L J
LJ
van der Grond
J
J
D000368:Aged; D020757:Amaurosis Fugax / Q000175:diagnosis / Q000503:physiopathology; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D001921:Brain / Q000503:physiopathology*; D002343:Carotid Artery, Internal; D016893:Carotid Stenosis / Q000175:diagnosis* / Q000503:physiopathology; D002794:Choline / Q000378:metabolism; D003401:Creatine / Q000378:metabolism; D004292:Dominance, Cerebral / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology*; D005260:Female; D006801:Humans; D002546:Ischemic Attack, Transient / Q000175:diagnosis* / Q000503:physiopathology; D019344:Lactic Acid / Q000378:metabolism; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D009460:Neurologic Examination; D012016:Reference Values
D001224:Aspartic Acid; D019344:Lactic Acid; C000179:N-acetylaspartate; D003401:Creatine; D002794:Choline