[创伤后应激障碍与创伤记忆消退学习的治疗]。

Nozomu Asukai
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摘要

创伤后应激障碍(PTSD)是暴露于创伤性事件后发展的一种使人衰弱的心理状况。创伤后应激障碍的典型症状是重新体验、逃避、精神麻木和过度觉醒。在过去的三十年里,关于创伤后应激障碍的生物学文献急剧增长。与重新经历创伤性事件有关的PTSD症状可以在恐惧条件反射框架内概念化。最近的研究结果表明,创伤后应激障碍与后天恐惧反应的灭绝学习失败有关。创伤后应激障碍的恐惧回路模型假设vmPFC无法抑制杏仁核,而杏仁核在恐惧学习中起着至关重要的作用。暴露疗法目前有大量的随机临床试验证明其疗效,并且在PTSD治疗指南中被推荐为具有实质性临床信心的疗法。在一项随机对照试验中,延长暴露(PE)对日本PTSD患者也有疗效(Asukai et al., 2010)。解释PE治疗机制的情绪加工理论可能与PTSD的神经生物学机制假说相一致。d -环丝氨酸(DCS)是一种NMDA部分激动剂,已被证明可以促进动物和人类的灭绝学习。临床上,DCS已被证明是PE的一个有希望的增强,特别是对于那些需要更长时间治疗的患者。
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[Treatment of posttraumatic stress disorder and extinction learning of traumatic memory].

Posttraumatic stress disorder (PTSD) is a debilitating psychological condition that develops following exposure to a traumatic event. The characteristic symptoms of PTSD are re-experience, avoidance, psychic numbing and hyper-arousal. The biological PTSD literature has been dramatically growing over the past three decades. PTSD symptoms related to re-experiencing the traumatic event may be conceptualized within a fear conditioning framework. Recent findings suggest that PTSD is associated with a failure of extinction learning of an acquired fear response. A fear-circuit model of PTSD posits that vmPFC fails to inhibit the amygdala, which has a crucial role in fear learning. Exposure therapy currently has the largest number of randomized clinical trials demonstrating its efficacy, and is recommended with substantial clinical confidence in treatment guidelines for PTSD. The efficacy of Prolonged Exposure (PE) was also shown for Japanese PTSD patients in a randomized controlled trial (Asukai et al., 2010). The emotional processing theory that accounts for the treatment mechanism of PE may be consistent with the hypothesis of a neurobiological mechanism in PTSD. D-cycloserine (DCS), an NMDA partial agonist, has been shown to facilitate extinction learning in animals and humans. Clinically, DCS has been shown to be a promising augmentation to PE, particularly for those who need longer treatment.

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