Dropcho E J
Department of Neurology, Indiana University Medical Center, Indianapolis 46202, USA.
J Neurol Sci. 1998 Jan 8;153(2):264-78. doi: 10.1016/s0022-510x(97)00296-7.
Several neurologic paraneoplastic disorders are believed to be caused by an autoimmune reaction against antigen(s) co-expressed by tumour cells and neurons. Of the paraneoplastic syndromes, the evidence for an autoimmune etiology is strongest for the Lambert-Eaton myasthenic syndrome, in which autoantibodies downregulate voltage-gated calcium channels at the presynaptic nerve terminal. For other syndromes, including cerebellar degeneration, multifocal encephalomyelitis, sensory neuronopathy, limbic encephalitis, opsoclonus-myoclonus, stiff person syndrome, and retinal degeneration, the autoimmune theory is supported by the presence of specific antineuronal antibodies. These antibodies serve as a useful diagnostic tool, but their actual role in causing neuronal injury and clinical disease remains unclear. Further understanding of immunopathogenesis awaits successful experimental models. Among different syndromes, a varied proportion of patients shows neurologic improvement with immunosuppressive treatments; it is likely that many patients have already suffered irreversible neuronal injury at the time of diagnosis.
几种神经系统副肿瘤性疾病被认为是由针对肿瘤细胞和神经元共同表达的抗原的自身免疫反应引起的。在副肿瘤综合征中,自身免疫病因的证据在兰伯特-伊顿肌无力综合征中最为确凿,在该综合征中,自身抗体下调突触前神经末梢的电压门控钙通道。对于其他综合征,包括小脑变性、多灶性脑脊髓炎、感觉神经元病、边缘性脑炎、眼阵挛-肌阵挛、僵人综合征和视网膜变性,自身免疫理论得到了特定抗神经元抗体存在的支持。这些抗体是一种有用的诊断工具,但其在导致神经元损伤和临床疾病中的实际作用仍不清楚。对免疫发病机制的进一步了解有待成功的实验模型。在不同的综合征中,不同比例的患者在接受免疫抑制治疗后神经功能有所改善;很可能许多患者在诊断时已经遭受了不可逆的神经元损伤。