Department of Radiology, Weill Medical College of Cornell University, New York, NY 10021, USA.
NMR Biomed. 2012 Sep;25(9):1073-87. doi: 10.1002/nbm.2772. Epub 2012 Jan 27.
Chronic fatigue syndrome (CFS) is a complex illness, which is often misdiagnosed as a psychiatric illness. In two previous reports, using (1)H MRSI, we found significantly higher levels of ventricular cerebrospinal fluid (CSF) lactate in patients with CFS relative to those with generalized anxiety disorder and healthy volunteers (HV), but not relative to those with major depressive disorder (MDD). In this third independent cross-sectional neuroimaging study, we investigated a pathophysiological model which postulated that elevations of CSF lactate in patients with CFS might be caused by increased oxidative stress, cerebral hypoperfusion and/or secondary mitochondrial dysfunction. Fifteen patients with CFS, 15 with MDD and 13 HVs were studied using the following modalities: (i) (1)H MRSI to measure CSF lactate; (ii) single-voxel (1)H MRS to measure levels of cortical glutathione (GSH) as a marker of antioxidant capacity; (iii) arterial spin labeling (ASL) MRI to measure regional cerebral blood flow (rCBF); and (iv) (31)P MRSI to measure brain high-energy phosphates as objective indices of mitochondrial dysfunction. We found elevated ventricular lactate and decreased GSH in patients with CFS and MDD relative to HVs. GSH did not differ significantly between the two patient groups. In addition, we found lower rCBF in the left anterior cingulate cortex and the right lingual gyrus in patients with CFS relative to HVs, but rCBF did not differ between those with CFS and MDD. We found no differences between the three groups in terms of any high-energy phosphate metabolites. In exploratory correlation analyses, we found that levels of ventricular lactate and cortical GSH were inversely correlated, and significantly associated with several key indices of physical health and disability. Collectively, the results of this third independent study support a pathophysiological model of CFS in which increased oxidative stress may play a key role in CFS etiopathophysiology.
慢性疲劳综合征（CFS）是一种复杂的疾病，常被误诊为精神疾病。在之前的两项研究报告中，我们使用（1）H MRSI 发现，与广泛性焦虑症和健康对照组（HV）相比，CFS 患者的脑室脑脊髓液（CSF）乳酸水平显著升高，但与重度抑郁症（MDD）患者相比则没有升高。在这项第三次独立的横断面神经影像学研究中，我们研究了一个假设，即 CFS 患者 CSF 中乳酸的升高可能是由氧化应激增加、脑灌注不足和/或继发性线粒体功能障碍引起的病理生理模型。我们对 15 名 CFS 患者、15 名 MDD 患者和 13 名 HV 进行了以下研究：（i）（1）H MRSI 测量 CSF 中的乳酸；（ii）单体素（1）H MRS 测量皮质谷胱甘肽（GSH）作为抗氧化能力的标志物；（iii）动脉自旋标记（ASL）MRI 测量局部脑血流（rCBF）；（iv）（31）P MRSI 测量脑高能磷酸化合物作为线粒体功能障碍的客观指标。我们发现 CFS 和 MDD 患者的脑室乳酸升高，GSH 降低，与 HV 相比。两组患者之间的 GSH 没有显著差异。此外，我们发现 CFS 患者的左前扣带回皮质和右侧舌回的 rCBF 低于 HV，但 CFS 患者与 MDD 患者之间的 rCBF 无差异。三组在任何高能磷酸代谢物方面均无差异。在探索性相关性分析中，我们发现脑室乳酸和皮质 GSH 水平呈负相关，与身体健康和残疾的几个关键指标显著相关。总的来说，这项第三次独立研究的结果支持了 CFS 的病理生理模型，其中氧化应激的增加可能在 CFS 的发病机制中发挥关键作用。
