ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2014
Panic disorder and serotonin reuptake inhibitors predict coupling of cortical and cardiac activity.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Neurochemical and genetic factors in panic disorder: a systematic review.Translational psychiatry · 2024Pooled it
- Lifestyle Behaviours Add to the Armoury of Treatment Options for Panic Disorder: An Evidence-Based Reasoning.International journal of environmental research and public health · 2015Article
- Interoception and stress.Frontiers in psychology · 2015Review
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
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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