Imaging Research Laboratories, Robarts Research Institute, Schulich School of Medicine and Dentistry, The University of Western Ontario, 100 Perth Drive, London, ON, Canada, N6A 5K8.
Brain. 2012 Feb;135(Pt 2):461-8. doi: 10.1093/brain/awr328. Epub 2011 Dec 15.
Alterations in motor function in cervical myelopathy secondary to degenerative disease may be due to local effects of spinal compression or distal effects related to cortical reorganization. This prospective study characterizes differences in metabolite levels in the motor cortex, specifically N-acetylaspartate, creatine, choline, myo-inositol and glutamate plus glutamine, due to alterations in cortical function in patients with reversible spinal cord compression compared with healthy controls. We hypothesized that N-acetylaspartate/creatine levels would be decreased in the motor cortex of patients with cervical myelopathy due to reduced neuronal integrity/function and myo-inositol/creatine levels would be increased due to reactive gliosis. Twenty-four patients with cervical myelopathy and 11 healthy controls underwent proton-magnetic resonance spectroscopy on a 3.0 Tesla Siemens Magnetom Tim Trio MRI. Areas of activation from functional magnetic resonance imaging scans of a finger-tapping paradigm were used to localize a voxel on the side of greater motor deficit in the myelopathy group (n = 10 on right side and n = 14 on left side of the brain) and on each side of the motor cortex in controls. Neurological function was measured with the Neck Disability Index, modified Japanese Orthopaedic Association and American Spinal Injury Association questionnaires. Metabolite levels were measured relative to total creatine within the voxel of interest. No metabolite differences were detected between the right side and left side of the motor cortex in controls. The myelopathy group had significantly decreased neurological function compared with the control group (Neck Disability Index: P < 0.001 and modified Japanese Orthopaedic Association: P < 0.001). There was a significant decrease in the N-acetylaspartate/creatine metabolite ratio in the motor cortex of the myelopathy group (1.21 ± 0.07) compared with the right (1.37 ± 0.03; P = 0.01) and left (1.38 ± 0.03; P = 0.007) motor cortex in controls suggesting neuronal damage or dysfunction distal to the lesion in the spine. No difference was observed in levels of myo-inositol/creatine. Thus, cortical levels of N-acetylaspartate/creatine may be a meaningful biomarker in cervical myelopathy, indicative of neuronal damage or dysfunction.
由于脊髓压迫的局部影响或与皮质重组相关的远端影响,退行性疾病引起的颈髓病变中的运动功能改变可能归因于局部效应。本前瞻性研究的特点是,与健康对照组相比,由于可逆性脊髓压迫患者皮质功能改变,运动皮质中的代谢物水平(特别是 N-乙酰天冬氨酸、肌酸、胆碱、肌醇和谷氨酸加谷氨酰胺)存在差异。我们假设,由于神经元完整性/功能降低,颈髓病变患者的运动皮质中的 N-乙酰天冬氨酸/肌酸水平降低,而由于反应性神经胶质增生,肌醇/肌酸水平升高。24 例颈髓病变患者和 11 例健康对照者在 3.0 特斯拉西门子 Magnetom Tim Trio MRI 上进行质子磁共振波谱检查。从手指敲击范式的功能磁共振成像扫描中获得的激活区域用于在颈髓病变组(病变侧大脑的 10 个右侧和 14 个左侧)和对照组的每个运动皮质侧定位一个体素。神经功能通过颈痛指数、改良日本矫形协会和美国脊髓损伤协会问卷进行测量。代谢物水平相对于感兴趣体素内的总肌酸进行测量。在对照组中,在运动皮质的右侧和左侧之间未检测到代谢物差异。与对照组相比,颈髓病变组的神经功能明显下降(颈痛指数:P<0.001;改良日本矫形协会:P<0.001)。颈髓病变组运动皮质中的 N-乙酰天冬氨酸/肌酸代谢物比值(1.21±0.07)明显低于对照组的右侧(1.37±0.03;P=0.01)和左侧(1.38±0.03;P=0.007),提示脊柱病变的远端存在神经元损伤或功能障碍。肌醇/肌酸水平无差异。因此,皮质 N-乙酰天冬氨酸/肌酸水平可能是颈髓病变的有意义的生物标志物,表明神经元损伤或功能障碍。