Posttraumatic stress symptomatology and abnormal neural responding during emotion regulation under cognitive demands: mediating effects of personality.
Posttraumatic stress symptomatology and abnormal neural responding during emotion regulation under cognitive demands: mediating effects of personality.
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认知需求下情绪调节过程中的创伤后应激症状和异常神经反应：人格的中介作用。
DOI：
10.1017/pen.2020.10
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发表时间：
2020
影响因子：
--
通讯作者：
Sponheim,ScottR
中科院分区：
文献类型：
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作者：
Sun,Michael;Marquardt,CraigA;Disner,SethG;Burton,PhilipC;Davenport,NicholasD;Lissek,Shmuel;Sponheim,ScottR
创伤后应激障碍(PTSD)常伴有轻度创伤性脑损伤(MTBI)的后遗症。大脑状况的混合会导致情感和认知功能的异常，以及适应不良的行为。为了更好地了解大脑活动如何解释这些条件下的认知和情绪过程，我们使用情绪N-back任务和功能磁共振成像(FMRI)来研究美国退伍军人在部署到伊拉克和阿富汗后的神经反应。此外，我们试图检验不适应人格的层次维度模型是否可以解释认知和情感挑战下战斗相关的大脑状况和fMRI反应之间的关系。收集了93名退伍军人的fMRI数据、创伤后应激障碍症状学(PTSS)、冲击性脑损伤(BmTBI)严重程度和适应不良个性(MMPI-2-RF)的测量。研究对象为双侧杏仁核、双侧背外侧前额叶(DlPFC)和腹内侧额前/膝下扣带回(vmPFC-sgACC)。认知负荷增加了dlPFC的活动，减少了情绪反应脑区的活动。然而，PTSS较大的个体在双侧杏仁核和vmPFC-sgACC显示钝性失活，而在右侧dlPFC反应较弱。此外，我们发现情绪/内化功能障碍(EID)升高，特别是低积极情绪性(RC2)，是认知负荷增加下双侧杏仁核PTSS相关变化的原因。研究结果表明，PTSS可能导致杏仁核和vmPFC-sgACC活动抵抗认知需求的缓和，反映出尽管需要整合认知资源，但情绪调节失调。快感缺乏可能是改善创伤后应激障碍患者情感和认知功能的干预措施的重要目标。
Posttraumatic stress disorder (PTSD) is often complicated by the after-effects of mild traumatic brain injury (mTBI). The mixture of brain conditions results in abnormal affective and cognitive functioning, as well as maladaptive behavior. To better understand how brain activity explains cognitive and emotional processes in these conditions, we used an emotional N-back task and functional magnetic resonance imaging (fMRI) to study neural responses in US military veterans after deployments to Iraq and Afghanistan. Additionally, we sought to examine whether hierarchical dimensional models of maladaptive personality could account for the relationship between combat-related brain conditions and fMRI responses under cognitive and affective challenge. FMRI data, measures of PTSD symptomatology (PTSS), blast-induced mTBI (bmTBI) severity, and maladaptive personality (MMPI-2-RF) were gathered from 93 veterans. Brain regions central to emotion regulation were selected for analysis, and consisted of bilateral amygdala, bilateral dorsolateral prefrontal (dlPFC), and ventromedial prefrontal/subgenual anterior cingulate (vmPFC-sgACC). Cognitive load increased activity in dlPFC and reduced activity in emotional responding brain regions. However, individuals with greater PTSS showed blunted deactivations in bilateral amygdala and vmPFC-sgACC, and weaker responses in right dlPFC. Additionally, we found that elevated emotional/internalizing dysfunction (EID), specifically low positive emotionality (RC2), accounted for PTSS-related changes in bilateral amygdala under increased cognitive load. Findings suggest that PTSS might result in amygdala and vmPFC-sgACC activity resistant to moderation by cognitive demands, reflecting emotion dysregulation despite a need to marshal cognitive resources. Anhedonia may be an important target for interventions that improve the affective and cognitive functioning of individuals with PTSD.