Posttraumatic Stress Disorder Subsequent to Apparent Mild Traumatic Brain Injury.

Posttraumatic Stress Disorder Subsequent to Apparent Mild Traumatic Brain Injury.
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明显轻度创伤性脑损伤后的创伤后应激障碍。

DOI:
10.1097/wnn.0000000000000264
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发表时间:
2021
期刊:
Cognitive and behavioral neurology : official journal of the Society for Behavioral and Cognitive Neurology
影响因子:
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通讯作者:
Williamson,JohnB
Williamson,JohnB
中科院分区:
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文献类型:
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作者:
Rieke,JakeD;Lamb,DamonG;Lewis,GregoryF;Davila,MariaI;Schmalfuss,IlonaM;Murphy,AidanJ;Tran,AmyB;Bottari,SarahA;Williamson,JohnB

文献摘要

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创伤后应激障碍 (PTSD) 在有创伤性脑损伤 (TBI) 病史的退伍军人中普遍存在;然而,TBI 和 PTSD 之间的关系尚不清楚。我们介绍了一位患有创伤后应激障碍 (PTSD) 的 31 岁男性退伍军人的案例,他在入伍前报告了创伤性脑损伤。据报道,伤势似乎很轻:他的头部被棒球击中,失去知觉约 10 秒钟。几年后,他在经历过战斗后患上了严重的创伤后应激障碍。他没有接受针对这些问题的临床服务,而是在一项研究中遇到的。我们进行了认知、自主神经和 MRI 评估,以评估大脑功能、结构和神经生理学。接下来,我们将杏仁核体积、钩束扩散、功能连接、面部情感识别和压力感受器一致性与对照组退伍军人 (n = 23) 进行比较。我们的退伍军人的核磁共振显示,右侧眶内前额叶有一个大的病变,周围有萎缩,神经放射学家将其解释为可能是由外伤引起的。与对照组的比较表明,前额叶边缘结构的结构和功能连接被破坏,情绪、认知和自主反应受损。在临床背景下,在战斗前检测到这种伤害是不可能的,因为我们的退伍军人报告了一种现象学上的轻微伤害,而创伤后应激障碍是对药物滥用、睡眠障碍和心理社会困扰的简单解释。然而,右前额叶边缘系统的破坏可能会导致 PTSD 的发展变得脆弱,并加剧了我们的退伍军人对 PTSD 的情绪反应和恢复。
Posttraumatic stress disorder (PTSD) is prevalent among veterans with a history of traumatic brain injury (TBI); however, the relationship between TBI and PTSD is not well understood. We present the case of a 31-year-old male veteran with PTSD who reported TBI before entering the military. The reported injury appeared to be mild: He was struck on the head by a baseball, losing consciousness for∼ 10 seconds. Years later, he developed severe PTSD after combat exposure. He was not receiving clinical services for these issues but was encountered in the context of a research study. We conducted cognitive, autonomic, and MRI assessments to assess brain function, structure, and neurophysiology. Next, we compared amygdala volume, uncinate fasciculus diffusion, functional connectivity, facial affect recognition, and baroreceptor coherence with those of a control group of combat veterans (n= 23). Our veteran’s MRI revealed a large right medial–orbital prefrontal lesion with surrounding atrophy, which the study neuroradiologist interpreted as likely caused by traumatic injury. Comparison with controls indicated disrupted structural and functional connectivity of prefrontal–limbic structures and impaired emotional, cognitive, and autonomic responses. Detection of this injury before combat would have been unlikely in a clinical context because our veteran had reported a phenomenologically mild injury, and PTSD is a simple explanation for substance abuse, sleep impairment, and psychosocial distress. However, it may be that right prefrontal–limbic disruption imparted vulnerability for the development of PTSD and exacerbated our veteran’s emotional response to, and recovery from, PTSD.