High resolution proton MR spectroscopy of cerebrospinal fluid in MS patients. Comparison with biochemical changes in demyelinating plaques
High resolution proton MR spectroscopy of cerebrospinal fluid in MS patients. Comparison with biochemical changes in demyelinating plaques
复制标题
DOI：
10.1016/s0022-510x(96)00224-9
复制
发表时间：
1996-12-01
影响因子：
4.4
通讯作者：
Livrea, P
中科院分区：
文献类型：
--
作者：
Simone, IL;Federico, F;Livrea, P
本文对53例多发性硬化（MS）、12例急性特发性多发性神经病、20例急性脑膜炎（病毒性和细菌性各10例）患者的脑脊液（CSF）进行了质子磁共振波谱（H-1-MRS）研究。光谱进行了比较，在18个神经控制。MS患者在复发-缓解期临床加重期间CSF乳酸水平较高（p = 0.036 vs.神经系统对照）。在具有Gd增强斑块的MRI证据的MS患者中，CSF乳酸高于具有MRI非活性斑块的患者（p = 0.017）。在具有临床活动性的MS患者（p = 0.05）以及具有MRI增强的MS患者（p = 0.003）中，CSF乳酸盐与CSF单核细胞数量呈正相关。一个比较H-1-MRS研究在体内局部脱髓鞘区证实了一个升高的乳酸信号在Gd增强（61%）比在未增强（22%）斑块更频繁（p = 0.03）。活动斑块中乳酸信号高的MS患者在CSF中显示高乳酸水平。急性脑膜炎和特发性多发性神经病患者脑脊液乳酸增加。这些数据表明，乳酸水平的变化可能取决于无氧糖酵解代谢灭活白细胞在炎症性疾病。在活动期和非活动期临床阶段，MS患者的CSF甲酸盐水平降低（分别与神经系统对照组相比，p = 0.037，p = 0.05）。甲酸盐的变化可能与MS的胆碱-甘氨酸循环紊乱有关。H-1-MRS在体内显示急性斑块中胆碱显著增加，而慢性斑块中N-乙酰天冬氨酸减少;这些代谢产物在CSF中检测不到。细菌性脑膜炎（p = 0.014）和神经系统对照（p = 0.05）的CSF葡萄糖水平低于病毒性脑膜炎（p = 0.014）。这些观察结果表明，H-1-MRS可能能够检测神经系统炎症性疾病的CSF代谢障碍。在MS中，一些CSF结果反映了脑脱髓鞘区发生的代谢变化，它们可能有助于评估疾病进展不同阶段的疾病活动。
Proton magnetic resonance spectroscopy (H-1-MRS) investigation was performed on CSF samples of patients with neurological inflammatory diseases including 53 cases of multiple sclerosis (MS), 12 acute idiopathic polyneuropathies, 20 acute meningitides (10 viral and 10 bacterial). Spectra were compared with those acquired in 18 neurological controls. High CSF lactate levels were found in MS patients during clinical exacerbation of relapsing-remitting course (p = 0.036 vs. neurological controls). In MS patients with MRI evidence of Gd-enhanced plaques CSF lactate was higher than in patients with MRI inactive plaques (p = 0.017). CSF lactate positively correlated with number of CSF mononuclear cells in MS patients with clinical activity (p = 0.05) as well as in MS patients with MRI enhancement (p = 0.003). A comparative H-1-MRS investigation in vivo on localized demyelinating areas confirmed an elevated lactate signal in Gd-enhanced (61%) more frequently than in unenhanced (22%) plaques (p = 0.03). MS patients with high lactate signal in active plaques showed high lactate levels in CSF. Increased CSF lactate was found also inpatients with acute meningitis and idiopathic polyneuropathy. These data suggest that changes in lactate levels may depend on anaerobic glycolytic metabolism inactivated leukocytes during inflammatory diseases. A decrease of CSF formate levels was found in MS patients during active and inactive clinical phase (p = 0.037, p = 0.05 vs. neurological controls respectively). Formate changes might be related to a disorder of choline-glycine cycle in MS. H-1-MRS in vivo showed significant increase of choline in acute plaques, whereas a decrease of N-acetyl aspartate was found in chronic plaques; these metabolites are undetectable in CSF. CSF glucose levels were lower in bacterial than in viral meningitis (p = 0.014) and in neurological controls (p = 0.05). These observations suggest that H-1-MRS may be able to detect CSF metabolic impairment in neurological inflammatory diseases. In MS some CSF findings reflect metabolic changes occurring in brain demyelinating areas, and they could be useful for evaluation of disease activity in different stages of disease evolution.