Halperin J J, Heyes M P
Department of Neurology, SUNY, Stony Brook.
Neurology. 1992 Jan;42(1):43-50. doi: 10.1212/wnl.42.1.43.
Although neurologic dysfunction occurs frequently in patients with Lyme borreliosis, it is rarely possible to demonstrate the causative organism within the neuraxis. This discordance could arise if neurologic symptoms were actually due to soluble neuromodulators produced in response to infection. Since immune stimulation is associated with the production of quinolinic acid (QUIN), an excitotoxin and N-methyl-D-aspartate (NMDA) agonist, we measured levels of CSF and serum QUIN, and lymphokines. Samples were obtained from 16 patients with CNS Borrelia burgdorferi infection, eight patients with Lyme encephalopathy (confusion without intra-CNS inflammation), and 45 controls. CSF QUIN was substantially elevated in patients with CNS Lyme and correlated strongly with CSF leukocytosis. In patients with encephalopathy, serum QUIN was elevated with corresponding increments in CSF QUIN. Lymphokine concentrations were not consistently elevated. We conclude that CSF QUIN is significantly elevated in B burgdorferi infection--dramatically in patients with CNS inflammation, less in encephalopathy. The presence of this known agonist of NMDA synaptic function--a receptor involved in learning, memory, and synaptic plasticity--may contribute to the neurologic and cognitive deficits seen in many Lyme disease patients.
尽管莱姆病患者经常出现神经功能障碍，但在神经轴内很少能证实致病生物体的存在。如果神经症状实际上是由于感染引发的可溶性神经调节剂所致，那么就可能出现这种不一致的情况。由于免疫刺激与喹啉酸（QUIN，一种兴奋性毒素和N - 甲基 - D - 天冬氨酸（NMDA）激动剂）的产生有关，我们检测了脑脊液和血清中QUIN以及淋巴因子的水平。样本取自16例中枢神经系统伯氏疏螺旋体感染患者、8例莱姆脑病患者（意识模糊但无中枢神经系统内炎症）以及45名对照者。中枢神经系统莱姆病患者的脑脊液QUIN显著升高，且与脑脊液白细胞增多密切相关。在脑病患者中，血清QUIN升高，脑脊液QUIN也相应增加。淋巴因子浓度并非持续升高。我们得出结论，在伯氏疏螺旋体感染中脑脊液QUIN显著升高——在有中枢神经系统炎症的患者中升高显著，在脑病患者中升高程度较小。这种已知的NMDA突触功能激动剂（一种参与学习、记忆和突触可塑性的受体）的存在，可能导致许多莱姆病患者出现神经和认知缺陷。
