Neural responses to emotional involuntary memories in posttraumatic stress disorder: Differences in timing and activity.
Neural responses to emotional involuntary memories in posttraumatic stress disorder: Differences in timing and activity.
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DOI：
10.1016/j.nicl.2018.05.009
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Rubin DC
中科院分区：
文献类型：
--
作者：
Hall SA;Brodar KE;LaBar KS;Berntsen D;Rubin DC
非自愿记忆是创伤后应激障碍（PTSD）的标志性症状，但对创伤后应激障碍（PTSD）非自愿记忆提取的神经基础的研究却很少。对创伤后应激障碍患者压力事件的非自愿记忆的神经相关性的研究集中在对记忆的自愿提取上，这些记忆有时被回忆为侵入性非自愿记忆，而不是在被扫描时的非自愿提取。在对照组中，无意识的记忆提取已被证明会引起海马旁回、楔前叶、顶叶下皮层和后中线区域的活动。然而，目前尚不清楚创伤后应激障碍中的非自愿记忆是否受到相同机制的支持。由于以前的工作表明，行为和神经反应在PTSD中减慢，我们研究了负性和中性非自愿记忆提取的神经活动的时空动态。21名PTSD患者和21名非PTSD患者在接受功能性磁共振成像扫描的同时，进行了非自愿记忆任务。环境的声音作为线索，良好的关联图片的负面和中性的场景。我们使用有限脉冲响应模型来分析神经反应中组之间的时间差异。与对照组相比，患有PTSD的参与者报告了更多的非自愿记忆，这些记忆更情绪化，更生动，但激活了类似的区域网络。然而，与对照组相比，PTSD患者在该网络中表现出延迟的神经反应，并增加了对负>中性刺激的vmPFC/ACC活性。创伤后应激障碍和非自愿记忆下的神经基质的控制之间的相似性表明，与自愿记忆不同，非自愿记忆在记忆检索的关键区域引起类似的活动。此外，PTSD中对非自愿记忆的延迟神经反应表明，影响PTSD中认知的因素，如增加的疲劳或回避行为，可以通过延迟认知处理所需区域的活动来实现。最后，与中性记忆相比，负性非自愿记忆引起vmPFC的过度活跃，而在PTSD中，在自愿记忆提取期间，vmPFC通常表现为低活性。这些模式表明，考虑认知过程的时间动态以及非自愿认知过程将改善现有的创伤后应激障碍的神经生物学模型。我们进行了第一个功能磁共振成像研究创伤后应激障碍的非自愿记忆（IM）检索。IM区域的活动在PTSD和对照组中相似，但在PTSD中延迟。在VMPFC的活性更高PTSD >阴性>中性IM的对照。PTSD患者比对照组有更多的IM。创伤后应激障碍的模型将受益于神经反应时间的研究。
Involuntary memories are a hallmark symptom of posttraumatic stress disorder (PTSD), but studies of the neural basis of involuntary memory retrieval in posttraumatic stress disorder (PTSD) are sparse. The study of the neural correlates of involuntary memories of stressful events in PTSD focuses on the voluntary retrieval of memories that are sometimes recalled as intrusive involuntary memories, not on involuntary retrieval while being scanned. Involuntary memory retrieval in controls has been shown to elicit activity in the parahippocampal gyrus, precuneus, inferior parietal cortex, and posterior midline regions. However, it is unknown whether involuntary memories are supported by the same mechanisms in PTSD. Because previous work has shown that both behavioral and neural responsivity is slowed in PTSD, we examined the spatiotemporal dynamics of the neural activity underlying negative and neutral involuntary memory retrieval. Twenty-one individuals with PTSD and 21 non-PTSD, trauma-exposed controls performed an involuntary memory task, while undergoing a functional magnetic resonance imaging scan. Environmental sounds served as cues for well-associated pictures of negative and neutral scenes. We used a finite impulse response model to analyze temporal differences between groups in neural responses. Compared with controls, participants with PTSD reported more involuntary memories, which were more emotional and more vivid, but which activated a similar network of regions. However, compared to controls, individuals with PTSD showed delayed neural responsivity in this network and increased vmPFC/ACC activity for negative > neutral stimuli. The similarity between PTSD and controls in neural substrates underlying involuntary memories suggests that, unlike voluntary memories, involuntary memories elicit similar activity in regions critical for memory retrieval. Further, the delayed neural responsivity for involuntary memories in PTSD suggests that factors affecting cognition in PTSD, like increased fatigue, or avoidance behaviors could do so by delaying activity in regions necessary for cognitive processing. Finally, compared to neutral memories, negative involuntary memories elicit hyperactivity in the vmPFC, whereas the vmPFC is typically shown to be hypoactive in PTSD during voluntary memory retrieval. These patterns suggest that considering both the temporal dynamics of cognitive processes as well as involuntary cognitive processes would improve existing neurobiological models of PTSD. We conducted the first fMRI study of involuntary memory (IM) retrieval in PTSD. Activity in IM regions was similar in PTSD and control groups but delayed in PTSD. Activity in the vmPFC was higher in PTSD > controls for negative > neutral IMs. People with PTSD had more IMs than controls. Models of PTSD would benefit from studies of the timing of neural responsivity.
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