Clancy Kevin, Ding Mingzhou, Bernat Edward, Schmidt Norman B, Li Wen
Department of Psychology, Florida State University, Tallahassee, FL, USA.
J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, FL, USA.
Brain. 2017 Jul 1;140(7):2041-2050. doi: 10.1093/brain/awx116.
Post-traumatic stress disorder is characterized by exaggerated threat response, and theoretical accounts to date have focused on impaired threat processing and dysregulated prefrontal-cortex-amygdala circuitry. Nevertheless, evidence is accruing for broad, threat-neutral sensory hyperactivity in post-traumatic stress disorder. As low-level, sensory processing impacts higher-order operations, such sensory anomalies can contribute to widespread dysfunctions, presenting an additional aetiological mechanism for post-traumatic stress disorder. To elucidate a sensory pathology of post-traumatic stress disorder, we examined intrinsic visual cortical activity (based on posterior alpha oscillations) and bottom-up sensory-driven causal connectivity (Granger causality in the alpha band) during a resting state (eyes open) and a passive, serial picture viewing state. Compared to patients with generalized anxiety disorder (n = 24) and healthy control subjects (n = 20), patients with post-traumatic stress disorder (n = 25) demonstrated intrinsic sensory hyperactivity (suppressed posterior alpha power, source-localized to the visual cortex-cuneus and precuneus) and bottom-up inhibition deficits (reduced posterior→frontal Granger causality). As sensory input increased from resting to passive picture viewing, patients with post-traumatic stress disorder failed to demonstrate alpha adaptation, highlighting a rigid, set mode of sensory hyperactivity. Interestingly, patients with post-traumatic stress disorder also showed heightened frontal processing (augmented frontal gamma power, source-localized to the superior frontal gyrus and dorsal cingulate cortex), accompanied by attenuated top-down inhibition (reduced frontal→posterior causality). Importantly, not only did suppressed alpha power and bottom-up causality correlate with heightened frontal gamma power, they also correlated with increased severity of sensory and executive dysfunctions (i.e. hypervigilance and impulse control deficits, respectively). Therefore, sensory aberrations help construct a vicious cycle in post-traumatic stress disorder that is in action even at rest, implicating dysregulated triangular sensory-prefrontal-cortex-amygdala circuitry: intrinsic sensory hyperactivity and disinhibition give rise to frontal overload and disrupt executive control, fuelling and perpetuating post-traumatic stress disorder symptoms. Absent in generalized anxiety disorder, these aberrations highlight a unique sensory pathology of post-traumatic stress disorder (ruling out effects merely reflecting anxious hyperarousal), motivating new interventions targeting sensory processing and the sensory brain in these patients.
创伤后应激障碍的特征是威胁反应过度，迄今为止的理论解释主要集中在威胁处理受损和前额叶皮质 - 杏仁核神经回路失调。然而，越来越多的证据表明创伤后应激障碍存在广泛的、与威胁无关的感觉亢进。由于低级别的感觉处理会影响高级操作，这种感觉异常可能导致广泛的功能障碍，为创伤后应激障碍提供了另一种病因机制。为了阐明创伤后应激障碍的感觉病理学，我们在静息状态（睁眼）和被动连续图片观看状态下，检查了内在视觉皮层活动（基于后阿尔法振荡）和自下而上的感觉驱动因果连接（阿尔法波段的格兰杰因果关系）。与广泛性焦虑症患者（n = 24）和健康对照受试者（n = 20）相比，创伤后应激障碍患者（n = 25）表现出内在感觉亢进（后阿尔法功率降低，源定位到视觉皮层 - 楔叶和楔前叶）和自下而上的抑制缺陷（后→前格兰杰因果关系减少）。随着感觉输入从静息状态增加到被动图片观看，创伤后应激障碍患者未能表现出阿尔法适应，突出了一种僵化的、固定模式的感觉亢进。有趣的是，创伤后应激障碍患者还表现出额叶处理增强（额叶伽马功率增强，源定位到额上回和背侧扣带回皮质），同时自上而下的抑制减弱（额叶→后因果关系减少）。重要的是，不仅阿尔法功率抑制和自下而上的因果关系与额叶伽马功率增强相关，它们还与感觉和执行功能障碍的严重程度增加相关（分别为过度警觉和冲动控制缺陷）。因此，感觉异常在创伤后应激障碍中形成了一个恶性循环，即使在休息时也在起作用，这涉及到三角感觉 - 前额叶皮质 - 杏仁核神经回路失调：内在感觉亢进和去抑制导致额叶过载并破坏执行控制，加剧并延续创伤后应激障碍症状。这些异常在广泛性焦虑症中不存在，突出了创伤后应激障碍独特的感觉病理学（排除了仅仅反映焦虑性过度觉醒的影响），促使针对这些患者的感觉处理和感觉脑的新干预措施的出现。
