Autonomic dysfunction is implicated from clinical, neuroimaging and experimental studies in sudden and unexpected death in epilepsy (SUDEP). Neuropathological analysis in SUDEP series enable exploration of acquired, seizure-related cellular adaptations in autonomic and brainstem autonomic centres of relevance to dysfunction in the peri-ictal period. Alterations in SUDEP compared to control groups have been identified in the ventrolateral medulla, amygdala, hippocampus and central autonomic regions. These involve neuropeptidergic, serotonergic and adenosine systems, as well as specific regional astroglial and microglial populations, as potential neuronal modulators, orchestrating autonomic dysfunction. Future research studies need to extend to clinically and genetically characterized epilepsies, to explore if common or distinct pathways of autonomic dysfunction mediate SUDEP. The ultimate objective of SUDEP research is the identification of disease biomarkers for at risk patients, to improve post-mortem recognition and disease categorisation, but ultimately, for exposing potential treatment targets of pharmacologically modifiable and reversible cellular alterations.

自主神经功能障碍与癫痫猝死 (SUDEP) 的临床、神经影像学和实验研究有关。SUDEP 系列中的神经病理学分析能够探索与围发作期功能障碍相关的自主神经和脑干自主神经中心的获得性癫痫相关细胞适应。与对照组相比，SUDEP 的改变在延髓腹外侧、杏仁核、海马和中枢自主神经区域中被发现。这些涉及神经肽能、5-羟色胺能和腺苷系统，以及特定的区域星形胶质细胞和小胶质细胞群，作为潜在的神经元调节剂，协调自主神经功能障碍。未来的研究需要扩展到临床和基因特征的癫痫，探索自主神经功能障碍的共同或不同途径是否介导 SUDEP。SUDEP 研究的最终目标是识别高危患者的疾病生物标志物，以改善死后识别和疾病分类，但最终是为了揭示可药理学和可逆细胞改变的潜在治疗目标。