Massachusetts General Hospital, Boston, MA, USA; Department of Psychiatry, Harvard Medical School, Boston, MA, USA.
Department of Psychiatry, Harvard Medical School, Boston, MA, USA; Division of Depression and Anxiety, McLean Hospital, Belmont, MA, USA.
J Psychiatr Res. 2024 Aug;176:173-181. doi: 10.1016/j.jpsychires.2024.06.009. Epub 2024 Jun 7.
The neurocardiac circuit is integral to physiological regulation of threat and trauma-related responses. However, few direct investigations of brain-behavior associations with replicable physiological markers of PTSD have been conducted. The current study probed the neurocardiac circuit by examining associations among its core regions in the brain (e.g., insula, hypothalamus) and the periphery (heart rate [HR], high frequency heart rate variability [HF-HRV], and blood pressure [BP]). We sought to characterize these associations and to determine whether there were differences by PTSD status. Participants were N = 315 (64.1 % female) trauma-exposed adults enrolled from emergency departments as part of the prospective AURORA study. Participants completed a deep phenotyping session (e.g., fear conditioning, magnetic resonance imaging) two weeks after emergency department admission. Voxelwise analyses revealed several significant interactions between PTSD severity 8-weeks posttrauma and psychophysiological recordings on hypothalamic connectivity to the prefrontal cortex (PFC), insula, superior temporal sulcus, and temporoparietaloccipital junction. Among those with PTSD, diastolic BP was directly correlated with right insula-hypothalamic connectivity, whereas the reverse was found for those without PTSD. PTSD status moderated the association between systolic BP, HR, and HF-HRV and hypothalamic connectivity in the same direction. While preliminary, our findings may suggest that individuals with higher PTSD severity exhibit compensatory neural mechanisms to down-regulate autonomic imbalance. Additional study is warranted to determine how underlying mechanisms (e.g., inflammation) may disrupt the neurocardiac circuit and increase cardiometabolic disease risk in PTSD.
神经心脏回路是对威胁和创伤相关反应进行生理调节的重要组成部分。然而,很少有直接研究大脑-行为与 PTSD 的可重复生理标志物之间的关联。目前的研究通过检查大脑核心区域(例如,岛叶、下丘脑)和外周(心率[HR]、高频心率变异性[HF-HRV]和血压[BP])之间的神经心脏回路来探究这些关联,并确定 PTSD 状态是否存在差异。参与者是从急诊部门作为前瞻性 AURORA 研究的一部分招募的 315 名(64.1%为女性)创伤后成年人。参与者在急诊部门入院两周后完成了一次深度表型分析(例如,恐惧条件反射,磁共振成像)。体素分析显示,创伤后 8 周 PTSD 严重程度与下丘脑与前额叶皮质(PFC)、岛叶、颞上回和颞顶枕叶交界处的连接的心理生理学记录之间存在几种显著的相互作用。在患有 PTSD 的人群中,舒张压与右侧岛叶-下丘脑连接直接相关,而在没有 PTSD 的人群中则相反。PTSD 状态以相同的方向调节收缩压、HR 和 HF-HRV 与下丘脑连接之间的关联。虽然这是初步的,但我们的发现可能表明,PTSD 严重程度较高的个体表现出代偿性神经机制来调节自主神经失衡。需要进一步研究来确定潜在机制(例如炎症)如何破坏神经心脏回路并增加 PTSD 中的心血管代谢疾病风险。