抗神经表面抗原（反N-甲基-D-天门冬氨酸、反富含亮氨酸的胶质瘤抑制蛋白1和其他抗体）、自身免疫性癫痫（拉斯穆森脑炎、肿瘤相关脑炎、针对谷氨酸脱羧酶的抗体的颞叶癫痫）和带有胶质抗体的脑脊髓炎（神经视神经脊髓炎光谱障碍、髓鞘细胞糖蛋白抗体病）的自身免疫性脑炎的界定是神经学的一项重大进展。但是，这些炎症疾病如何“工作”？免疫系统和脑细胞之间的哪种相互作用会导致这些情况？回答这些问题的唯一直接方法是通过神经病理技术调查受影响的脑组织。它们提供了关于疾病过程的元素和定位的形态学和部分时间信息。分子技术扩展并支持这些数据。通过死亡检查和脑活组织检查，脑组织变得可用于诊断或治疗干预。介绍了神经病理病原学研究的局限性。最后，总结了自身免疫性脑炎和相关疾病的代表性神经病理学发现。

Delineation of the autoimmune encephalitides with antibodies against neural surface antigens (anti-N-Methyl-D-aspartate, anti-leucine-rich glioma-inactivated protein 1, and others), autoimmune-associated epilepsies (Rasmussen encephalitis, paraneoplastic encephalitides, temporal lobe epilepsy with antibodies against glutamic acid decarboxylase), and encephalomyelitides with glial antibodies (neuromyelitis optica spectrum disorder, myelin oligodendrocyte glycoprotein antibody disease) has been a major advance in neurology. But how do these inflammatory diseases "work"? What kind of interaction between elements of the immune system and brain cells leads to these conditions? The only direct way of answering these questions is to investigate affected brain tissue by neuropathological techniques. They provide morphological and, in part, temporal information on the elements and localization of the disease process. Molecular techniques broaden and support these data. Brain tissue becomes available through autopsies and brain biopsies, obtained for diagnostic or therapeutic interventions. The limitations of neuropathological pathogenic research are discussed. Finally, representative neuropathological findings in autoimmune encephalitides and related conditions are summarized.