Macmillan C S A, Wild J M, Wardlaw J M, Andrews P J D, Marshall I, Easton V J
Department of Clinical Neurosciences, University of Edinburgh, Western General Hospital, Edinburgh, UK.
Acta Neurochir (Wien). 2002 Sep;144(9):853-62; discussion 862. doi: 10.1007/s00701-002-0966-x.
To look for evidence of early ischaemic neurochemical changes in patients suffering severe traumatic brain injury (TBI) and severe subarachnoid haemorrhage (SAH). Proton metabolite concentrations were measured in normal and abnormal areas of brain on T2 MR imaging, in regions considered particularly vulnerable to ischaemic injury.
Intensive care patients underwent T2 weighted imaging in a 1.5 Tesla MR scanner and proton magnetic resonance spectroscopy (single voxel or chemical shift imaging). Metabolite values in areas that appeared 'normal' and 'abnormal' on T2 MR imaging were compared with those obtained from normal controls.
18 TBI and 6 SAH patients were imaged at 1 to 26 days. N-acetyl aspartate (NAA) was lower in TBI and SAH patients compared to controls in both T2 normal and T2 abnormal areas (p<0.0005). SAH, but not TBI patients also had increased choline and creatine compared to controls in the T2 normal (p<0.02, p<0.02 respectively) and T2 abnormal (p=0.0003, p=0.003) areas. No lactate was found in TBI or SAH patients.
Significant loss of normal functioning neurones was present in TBI and SAH, but no evidence of anaerobic metabolism using lactate as a surrogate marker, questioning the role of 'ischemia' as a major mechanism of damage. Increased choline and creatine were found in SAH patients suggestive of increased cell-wall turnover. Current theories of brain injury after TBI or SAH do not explain these observed neurochemical changes and further research is required.
寻找重度创伤性脑损伤（TBI）和重度蛛网膜下腔出血（SAH）患者早期缺血性神经化学变化的证据。在T2磁共振成像上，对被认为特别易受缺血性损伤的脑区正常和异常区域的质子代谢物浓度进行测量。
重症监护患者在1.5特斯拉磁共振扫描仪中接受T2加权成像和质子磁共振波谱分析（单体素或化学位移成像）。将T2磁共振成像上显示“正常”和“异常”区域的代谢物值与正常对照组获得的值进行比较。
18例TBI患者和6例SAH患者在1至26天进行了成像。在T2正常和T2异常区域，TBI和SAH患者的N-乙酰天门冬氨酸（NAA）均低于对照组（p<0.0005）。与对照组相比，SAH患者（而非TBI患者）在T2正常区域（分别为p<0.02，p<0.02）和T2异常区域（p=0.0003，p=0.003）的胆碱和肌酸也增加。在TBI或SAH患者中未发现乳酸。
TBI和SAH患者存在正常功能神经元的显著丧失，但没有以乳酸作为替代标志物的无氧代谢证据，这对“缺血”作为主要损伤机制的作用提出了质疑。SAH患者中发现胆碱和肌酸增加，提示细胞壁周转率增加。目前关于TBI或SAH后脑损伤的理论无法解释这些观察到的神经化学变化，需要进一步研究。
