另外研究表明[20]：早期严重的应激反应和治疗处理不当可以产生一连串的神经生物学改变潜在的影响持续的脑发育。这些改变表现在多重水平上，神经激素（下丘脑 —垂体—肾上腺（Hypothalamic_pituitary_adrental,HPA）轴系统）的结构和功能；白质并质体的中央部分和左侧新大脑皮层，海马及杏仁体发育变得稀疏，减低了额叶肢的电激惹能力和小脑蚓部的兴奋能力。由于眶额回的稀疏，以及前扣带回的稀疏，最后延及杏仁体的功能紊乱[21]，既在一定的刺激阈时，额叶不能执行较高级的对低层面调节功能，导致了右侧杏仁体的激活。缺乏对最先激活的神经系统层面的抑制，维持了高反应（负面的症状），也就减少了灵活的，更自动的调节功能（正面的症状）[22]。另外眶额回，前扣带回及杏仁体系统也与自主神经系统相联系[23]，上述系统的紊乱也导致自主神经系统的功能紊乱，它将在一段长时间内显示一对非相关联的事物的自动控制模式，既交感神经和副交感神经成分共同增加或减少，或不成对非相关事物的自动控制模式，既表现自主神经系统的反应部分分离：一部分改变缺失。也就是说，自主神经系统太容易被一种自动平衡壮态代替，一旦代替，就很难再建立平衡，既对从心理应激所表现的迷走神经的回缩和恢复的调节无能[24]。由于早期损害导致神经生物学改变，使这些个体更容易在成年易患PTSD。

目前的研究已经显示早期的精神创伤可以使个体发生神经生物学改变从而成为PTSD的易感者；也探讨了精神应激过于强烈或持久会导致有关记忆环路的损伤和调节中枢兴奋和抑制过程中的神经递质的表达改变，导致形成PTSD。但是其整个完整的病理机制的脑图谱尚未完全清楚，但是沿着精神应激记忆印痕的产生过程的探讨，特别是对其神经生物学和神经病理生理学的探讨，也许可以最终揭示其机制。

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