梭曼作为一种有机磷神经毒剂，通过不可逆地抑制乙酰胆碱酯酶活性，使乙酰胆碱在神经突触和肌肉接头处蓄积，从而引发持续性癫痫状态、呼吸衰竭等致命症状。尽管目前已有标准治疗方案，但其疗效高度依赖早期干预，延迟治疗往往无法阻止神经损伤和死亡。即使患者在中毒后20 min内及时用药，若未能有效控制癫痫活动，仍可造成多脑区广泛神经病理损害，显著增加死亡率。因此，进一步探索新的联合用药策略，拓宽治疗时间窗，改善延迟救治的预后，对于梭曼中毒的紧急救治具有重要意义。本文主要对梭曼发挥神经毒性作用的机制及最新的治疗药物进展进行综述，旨在为进一步开发梭曼中毒的治疗新策略提供参考。

As an organophosphorus nerve agent， soman exerts its neurotoxic effects by irreversibly inhibiting acetylcholinesterase activity. This inhibition leads to the accumulation of acetylcholine at neural synapses and neuromuscular junctions， triggering persistent epileptic states and potentially fatal symptoms such as respiratory failure. Despite the existence of standard treatment protocols， their efficacy heavily relies on early intervention， as delayed treatment often fails to prevent neurological damage and death. Even with timely administration of medication， uncontrolled epileptic activity within 20 min can cause widespread neuropathological damage across multiple brain regions， significantly increasing the mortality rate. Further exploration of novel combination therapy strategies， expansion of the therapeutic time window， and improvement of outcomes for delayed treatment are crucial for emergency response to soman poisoning. This article provides a comprehensive review of the neurotoxic mechanisms of soman and recent advancements in therapeutic drugs， aiming to offer a reference for the further development of new treatment strategies for soman poisoning.