Kondziella Daniel, Danielsen Else R, Hansen Klaus, Thomsen Carsten, Jansen Erik C, Arlien-Soeborg Peter
Department of Neurology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.
J Neurol. 2009 Jun;256(6):970-9. doi: 10.1007/s00415-009-5057-y. Epub 2009 Mar 1.
Carbon monoxide (CO) intoxication leads to acute and chronic neurological deficits, but little is known about the specific noxious mechanisms. (1)H magnetic resonance spectroscopy (MRS) may allow insight into the pathophysiology of CO poisoning by monitoring neurochemical disturbances, yet only limited information is available to date on the use of this protocol in determining the neurological effects of CO poisoning. To further examine the short-term and long-term effects of CO on the central nervous system, we have studied seven patients with CO poisoning assessed by gray and white matter MRS, magnetic resonance imaging (MRI) and neuropsychological testing. Five patients suffered from acute high-dose CO intoxication and were in coma for 1-6 days. In these patients, MRI revealed hyperintensities of the white matter and globus pallidus and also showed increased choline (Cho) and decreased N-acetyl aspartate (NAA) ratios to creatine (Cr), predominantly in the white matter. Lactate peaks were detected in two patients during the early phase of high-dose CO poisoning. Two patients with chronic low-dose CO exposure and without loss of consciousness had normal MRI and MRS scans. On follow-up. five of our seven patients had long-lasting intellectual impairment, including one individual with low-dose CO exposure. The MRS results showed persisting biochemical alterations despite the MRI scan showing normalization of morphological changes. In conclusion, the MRS was normal in patients suffering from chronic low-dose CO exposure; in contrast, patients with high-dose exposure showed abnormal gray and white matter levels of NAA/Cr, Cho/Cr and lactate, as detected by (1)H MRS, suggesting disturbances of neuronal function, membrane metabolism and anaerobic energy metabolism, respectively. Early increases in Cho/Cr and decreases of NAA/Cr may be related to a poor long-term outcome, but confirmation by future studies is needed.
一氧化碳（CO）中毒会导致急性和慢性神经功能缺损，但对于具体的有害机制却知之甚少。氢质子磁共振波谱（1H MRS）或许能够通过监测神经化学紊乱来深入了解CO中毒的病理生理学，但迄今为止，关于该方法在确定CO中毒神经影响方面的应用仅有有限的信息。为了进一步研究CO对中枢神经系统的短期和长期影响，我们对7例CO中毒患者进行了研究，采用了灰质和白质MRS、磁共振成像（MRI）以及神经心理学测试。5例患者因急性高剂量CO中毒而昏迷1 - 6天。在这些患者中，MRI显示白质和苍白球信号增强，且主要在白质中胆碱（Cho）升高、N - 乙酰天门冬氨酸（NAA）与肌酸（Cr）的比值降低。在高剂量CO中毒早期，2例患者检测到乳酸峰。2例慢性低剂量CO暴露且未丧失意识的患者MRI和MRS扫描结果正常。随访发现，我们的7例患者中有5例存在长期智力损害，其中包括1例低剂量CO暴露者。尽管MRI扫描显示形态学改变已恢复正常，但MRS结果显示生化改变依然存在。总之，慢性低剂量CO暴露患者的MRS结果正常；相反，高剂量暴露患者经氢质子MRS检测显示，其灰质和白质中的NAA/Cr、Cho/Cr及乳酸水平异常，分别提示神经元功能、膜代谢及无氧能量代谢紊乱。Cho/Cr早期升高和NAA/Cr降低可能与长期预后不良有关，但仍需未来研究加以证实。
