Panic Disorder and Serotonin Reuptake Inhibitors Predict Coupling of Cortical and Cardiac Activity
Panic Disorder and Serotonin Reuptake Inhibitors Predict Coupling of Cortical and Cardiac Activity
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恐慌症和血清素再摄取抑制剂预测皮质和心脏活动的耦合
DOI：
10.1038/npp.2013.224
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发表时间：
2014
影响因子：
7.6
通讯作者：
Wacker
中科院分区：
文献类型：
--
作者：
Mueller;Panitz;Nestoriuc;Stemmler;Wacker
惊恐发作是惊恐障碍（PD）的主要症状，其特征是强烈的生理反应，包括心脏活动加速。虽然皮质过程被认为是触发和加强惊恐发作，但尚不清楚PD患者是否普遍倾向于表现出升高的皮质-心脏相互作用，这可能使他们在惊恐期间易受大脑驱动的心脏活动调节。与这一假设相一致，血清素，一种与恐慌和PD高度相关的神经递质，可能会影响心脏的皮质控制。因此，目前的研究旨在测试是否PD和5-羟色胺再摄取抑制剂（SRI）的摄入量与皮质-心脏的相互作用，在没有急性恐慌。患有PD（N= 22）、重度抑郁症（MD，临床对照组，N= 21）或无精神病诊断（健康对照组，N= 23）的人类参与者执行赌博任务。为了测量皮质-心脏耦合，确定反馈呈现后单次试验EEG的受试者内协变和随后的心动周期变化。与先前的研究一样，EEG和心脏活动存在显著的时滞协变，表明反馈诱发EEG振幅的逐个试验波动决定了几秒钟后心脏活动加速的程度。重要的是，这种协变模式在PD与对照参与者中显著增强。此外，同时摄入SRI进一步增强了PD和MD患者的脑-心协变。目前的研究结果表明，PD和5-羟色胺与非恐慌情况下改变的脑-心相互作用有关。未来的工作应该澄清脑-心耦合是否在PD中起因果作用，例如通过促进恐慌发作。
Panic attacks, the cardinal symptom of panic disorder (PD), are characterized by intense physiological reactions including accelerated heart activity. Although cortical processes are thought to trigger and potentiate panic attacks, it is unknown whether individuals with PD have a general tendency to show elevated cortico–cardiac interactions, which could predispose them for brain-driven modulations of heart activity during panic. Consistent with this hypothesis, serotonin, a highly relevant neurotransmitter for panic and PD presumably affects the cortical control of the heart. The current study thus aimed to test whether PD and serotonin reuptake inhibitor (SRI) intake are related to cortico–cardiac interactions in the absence of acute panic. Human participants with PD (N= 22), major depression (MD, clinical control group, N= 21) or no psychiatric diagnosis (healthy control group, N= 23) performed a gambling task. To measure cortico–cardiac coupling, the within-subject covariation of single-trial EEG after feedback presentation and subsequent changes in heart period was determined. As in prior studies, there was a significant time-lagged covariation of EEG and heart activity indicating that trial-by-trial fluctuations of feedback-evoked EEG amplitude determined how much heart activity accelerated seconds later. Importantly, this covariation pattern was significantly potentiated in PD vs control participants. Moreover, concurrent SRI intake further augmented brain–heart covariation in individuals with PD and MD. The present findings demonstrate that PD and serotonin are associated with altered brain–heart interactions in a non-panic situation. Future work should clarify whether brain–heart coupling has a causal role in PD, for example by facilitating panic attacks.
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