Cornwell Brian R, Garrido Marta I, Overstreet Cassie, Pine Daniel S, Grillon Christian
Brain and Psychological Sciences Research Centre, Faculty of Health, Arts and Design, Swinburne University of Technology, Hawthorn, Australia; National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland.
Queensland Brain Institute, Centre for Advanced Imaging and ARC Centre of Excellence for Integrative Brain Function, University of Queensland, Brisbane, Australia; School of Mathematics and Physics, University of Queensland, Brisbane, Australia.
Biol Psychiatry. 2017 Sep 15;82(6):447-454. doi: 10.1016/j.biopsych.2017.06.031. Epub 2017 Jul 6.
Anxious hypervigilance is marked by sensitized sensory-perceptual processes and attentional biases to potential danger cues in the environment. How this is realized at the neurocomputational level is unknown but could clarify the brain mechanisms disrupted in psychiatric conditions such as posttraumatic stress disorder. Predictive coding, instantiated by dynamic causal models, provides a promising framework to ground these state-related changes in the dynamic interactions of reciprocally connected brain areas.
Anxiety states were elicited in healthy participants (n = 19) by exposure to the threat of unpredictable, aversive shocks while undergoing magnetoencephalography. An auditory oddball sequence was presented to measure cortical responses related to deviance detection, and dynamic causal models quantified deviance-related changes in effective connectivity. Participants were also administered alprazolam (double-blinded, placebo-controlled crossover) to determine whether the cortical effects of threat-induced anxiety are reversed by acute anxiolytic treatment.
Deviant tones elicited increased auditory cortical responses under threat. Bayesian analyses revealed that hypervigilant responding was best explained by increased postsynaptic gain in primary auditory cortex activity as well as modulation of feedforward, but not feedback, coupling within a temporofrontal cortical network. Increasing inhibitory gamma-aminobutyric acidergic action with alprazolam reduced anxiety and restored feedback modulation within the network.
Threat-induced anxiety produced unbalanced feedforward signaling in response to deviations in predicable sensory input. Amplifying ascending sensory prediction error signals may optimize stimulus detection in the face of impending threats. At the same time, diminished descending sensory prediction signals impede perceptual learning and may, therefore, underpin some of the deleterious effects of anxiety on higher-order cognition.
焦虑性过度警觉的特征是感觉-知觉过程敏感化以及对环境中潜在危险线索存在注意偏向。这在神经计算层面是如何实现的尚不清楚，但可能会阐明诸如创伤后应激障碍等精神疾病中被破坏的脑机制。由动态因果模型实例化的预测编码为将这些与状态相关的变化建立在相互连接的脑区的动态相互作用基础上提供了一个有前景的框架。
在健康参与者（n = 19）接受脑磁图检查时，通过暴露于不可预测的厌恶性电击威胁来诱发焦虑状态。呈现听觉奇偶数序列以测量与偏差检测相关的皮层反应，并且动态因果模型量化与偏差相关的有效连接变化。参与者还接受了阿普唑仑治疗（双盲、安慰剂对照交叉设计），以确定急性抗焦虑治疗是否能逆转威胁诱发的焦虑对皮层的影响。
在威胁状态下，异常音调引发听觉皮层反应增强。贝叶斯分析表明，过度警觉反应最好由初级听觉皮层活动中突触后增益增加以及颞额叶皮层网络内前馈而非反馈耦合的调制来解释。使用阿普唑仑增加抑制性γ-氨基丁酸能作用可减轻焦虑并恢复网络内的反馈调制。
威胁诱发的焦虑在面对可预测感觉输入的偏差时产生了不平衡的前馈信号。放大上升的感觉预测误差信号可能会优化面对迫在眉睫的威胁时的刺激检测。同时，下降的感觉预测信号减弱会阻碍知觉学习，因此可能是焦虑对高阶认知产生一些有害影响的基础。
