Archives of neurology · 2002
Brain damage after coronary artery bypass grafting.
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Bendszus Martin, Reents Wilko, Franke Dorothea, Müllges Wolfgang, Babin-Ebell Jörg, Koltzenburg Martin, Warmuth-Metz Monika, Solymosi Laszlo
Аннотация
BACKGROUND: Coronary artery bypass grafting (CABG) is associated with a risk for focal neurological deficits and neuropsychological impairment postoperatively.
OBJECTIVES: To examine the brain damage after CABG using diffusion-weighted magnetic resonance imaging and (1)H-magnetic resonance spectroscopy (MRS) and to correlate the results with neurological and neuropsychological findings.
PATIENTS AND METHODS: Thirty-five consecutive patients undergoing elective CABG were included. Patients underwent a neurological and neuropsychological examination before and after CABG. The magnetic resonance protocol was applied before and after (mean, 3 days) surgery and included a diffusion-weighted sequence and single-voxel MRS measurements in the frontal lobes.
RESULTS: None of the patients revealed a new focal neurological deficit after surgery. Diffusion-weighted magnetic resonance imaging demonstrated new ischemic lesions in 9 (26%) of the patients. The presence of an ischemic lesion was not related to impaired postoperative test performance (P>.50). The apparent diffusion coefficient values in the cerebellum and the centrum semiovale exhibited an increase after surgery (P<.01), consistent with vasogenic edema. Following surgery, MRS revealed a significant decrease in the metabolite ratio of N-acetylaspartate-creatine (mean +/- SD, 1.69 +/- 0.20 vs 1.52 +/- 0.19; P<.001). The extent of deterioration in neuropsychological test performance after surgery was closely related to the degree of the N-acetylaspartate-creatine ratio decrease (P<.01). A follow-up MRS scan revealed a normalization of the N-acetylaspartate-creatine ratio, which accompanied the recovery in psychological test performance.
CONCLUSIONS: Postoperative impairment in neuropsychological test performance is associated with a transient metabolic neuronal disturbance. Focal ischemic lesions after CABG are more frequent than the apparent neurological complication rate; however, they are not related to the diffuse postoperative encephalopathy.
OBJECTIVES: To examine the brain damage after CABG using diffusion-weighted magnetic resonance imaging and (1)H-magnetic resonance spectroscopy (MRS) and to correlate the results with neurological and neuropsychological findings.
PATIENTS AND METHODS: Thirty-five consecutive patients undergoing elective CABG were included. Patients underwent a neurological and neuropsychological examination before and after CABG. The magnetic resonance protocol was applied before and after (mean, 3 days) surgery and included a diffusion-weighted sequence and single-voxel MRS measurements in the frontal lobes.
RESULTS: None of the patients revealed a new focal neurological deficit after surgery. Diffusion-weighted magnetic resonance imaging demonstrated new ischemic lesions in 9 (26%) of the patients. The presence of an ischemic lesion was not related to impaired postoperative test performance (P>.50). The apparent diffusion coefficient values in the cerebellum and the centrum semiovale exhibited an increase after surgery (P<.01), consistent with vasogenic edema. Following surgery, MRS revealed a significant decrease in the metabolite ratio of N-acetylaspartate-creatine (mean +/- SD, 1.69 +/- 0.20 vs 1.52 +/- 0.19; P<.001). The extent of deterioration in neuropsychological test performance after surgery was closely related to the degree of the N-acetylaspartate-creatine ratio decrease (P<.01). A follow-up MRS scan revealed a normalization of the N-acetylaspartate-creatine ratio, which accompanied the recovery in psychological test performance.
CONCLUSIONS: Postoperative impairment in neuropsychological test performance is associated with a transient metabolic neuronal disturbance. Focal ischemic lesions after CABG are more frequent than the apparent neurological complication rate; however, they are not related to the diffuse postoperative encephalopathy.