The Unpredictive Brain Under Threat: A Neurocomputational Account of Anxious Hypervigilance.

The Unpredictive Brain Under Threat: A Neurocomputational Account of Anxious Hypervigilance.
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DOI:
10.1016/j.biopsych.2017.06.031
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发表时间:
2017-09-15
影响因子:
10.6
通讯作者:
Grillon C
Grillon C
中科院分区:
医学1区
文献类型:
--
作者:
Cornwell BR;Garrido MI;Overstreet C;Pine DS;Grillon C

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焦虑性过度警觉的特征是敏感的感觉-知觉过程和对环境中潜在危险线索的注意偏向。这是如何在神经计算水平上实现的尚不清楚,但可以澄清在精神疾病如创伤后应激障碍中被破坏的大脑机制。预测编码,实例化的动态因果模型(DCM),提供了一个有前途的框架,接地这些状态相关的变化,在相互连接的大脑区域的动态相互作用。焦虑状态引起的健康参与者(N = 19)暴露于不可预测的,令人厌恶的冲击的威胁,同时进行脑磁图。听觉oddball序列被提出来测量与偏差检测相关的皮层反应,DCM量化了有效连接中与偏差相关的变化。参与者还接受阿普唑仑(双盲,安慰剂对照交叉),以确定是否通过急性抗焦虑治疗逆转威胁诱导的焦虑的皮质效应。异常音调引起的威胁下增加听觉皮层的反应。贝叶斯分析表明,高度警惕的反应是最好的解释增加突触后增益A1活动以及调制前馈,但不反馈,耦合内的颞-额叶皮层网络。阿普唑仑增加抑制性GABA(γ-氨基丁酸)能作用可减少焦虑并恢复网络内的反馈调节。威胁引起的焦虑产生不平衡的前馈信号在可预测的感官输入的偏差。放大上升的感觉预测误差信号可以在面临即将到来的威胁时优化刺激检测。与此同时,下降的感觉预测信号会阻碍感知学习,因此可能会加强焦虑对高阶认知的一些有害影响。
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 neuro-computational level is unknown, but could clarify the brain mechanisms disrupted in psychiatric conditions such as PTSD. Predictive coding, instantiated by dynamic causal models (DCM), 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 DCM 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 post-synaptic gain in A1 activity as well as modulation of feedforward, but not feedback, coupling within a temporo-frontal cortical network. Increasing inhibitory GABA (γ-aminobutyric acid)-ergic action with alprazolam reduced anxiety and restored feedback modulation within the network. Threat-induced anxiety produced unbalanced feedforward signalling 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.
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