Atlantic Health System, Morristown.
Biomedical Research Institute of New Jersey, Cedar Knolls.
Clin Infect Dis. 2018 Jun 18;67(1):80-88. doi: 10.1093/cid/ciy019.
Lyme encephalopathy, characterized by nonspecific neurobehavioral symptoms including mild cognitive difficulties, may occur in patients with systemic Lyme disease and is often mistakenly attributed to central nervous system (CNS) infection. Identical symptoms occur in many inflammatory states, possibly reflecting the effect of systemic immune mediators on the CNS.
Multiplex immunoassays were used to measure serum and cerebrospinal fluid (CSF) cytokines in patients with or without Lyme disease to determine if there are specific markers of active CNS infection (neuroborreliosis), or systemic inflammatory mediators associated with neurobehavioral syndromes.
CSF CXCL13 levels were elevated dramatically in confirmed neuroborreliosis (n = 8), less so in possible neuroborreliosis (n = 11) and other neuroinflammatory conditions (n = 44). Patients with Lyme (n = 63) or non-Lyme (n = 8) encephalopathy had normal CSF findings, but had elevated serum levels of interleukins 7, 17A, and 17F, thymic stromal lymphopoietin and macrophage inflammatory protein-α.
CSF CXCL13 is a sensitive and specific marker of neuroborreliosis in individuals with Borrelia-specific intrathecal antibody production. However, it does not distinguish individuals strongly suspected of having neuroborreliosis, but lacking confirmatory intrathecal antibodies, from those with other neuroinflammatory conditions. Patients with mild cognitive symptoms occurring during acute Lyme disease, and/or after appropriate treatment, have normal CSF but elevated serum levels of T-helper 17 markers and T-cell growth factors, which are also elevated in patients without Lyme disease but with similar symptoms. In the absence of CSF abnormalities, neurobehavioral symptoms appear to be associated with systemic inflammation, not CNS infection or inflammation, and are not specific to Lyme disease.
莱姆病性脑炎的特点是非特异性神经行为症状，包括轻度认知困难，可能发生在系统性莱姆病患者中，并且经常被错误地归因于中枢神经系统 (CNS) 感染。许多炎症状态下会出现相同的症状，这可能反映了系统性免疫介质对 CNS 的影响。
使用多重免疫分析检测有或没有莱姆病的患者的血清和脑脊液 (CSF) 细胞因子，以确定是否存在活跃的中枢神经系统感染 (神经莱姆病) 的特定标志物，或与神经行为综合征相关的系统性炎症介质。
在确诊的神经莱姆病 (n = 8) 中，CSF CXCL13 水平显著升高，在可能的神经莱姆病 (n = 11) 和其他神经炎症疾病 (n = 44) 中则升高较少。莱姆病 (n = 63) 或非莱姆病 (n = 8) 性脑炎患者的 CSF 发现正常，但白细胞介素 7、17A 和 17F、胸腺基质淋巴生成素和巨噬细胞炎症蛋白-α的血清水平升高。
在具有 Borrelia 特异性鞘内抗体产生的个体中，CSF CXCL13 是神经莱姆病的敏感和特异性标志物。然而，它不能区分强烈怀疑患有神经莱姆病但缺乏确认性鞘内抗体的个体与其他神经炎症疾病的个体。在急性莱姆病期间出现轻度认知症状的患者，和/或在适当治疗后，CSF 正常，但血清中 T 辅助 17 标志物和 T 细胞生长因子水平升高，这些标志物在没有莱姆病但有类似症状的患者中也升高。在没有 CSF 异常的情况下，神经行为症状似乎与系统性炎症有关，而与 CNS 感染或炎症无关，并且与莱姆病无关。
