Brain–heart coupling at the P300 latency is linked to anterior cingulate cortex and insula—A cardio-electroencephalographic covariance tracing study

Panitz, Christian; Wacker, Jan; Stemmler, Gerhard; Mueller, Erik M.

doi:10.1016/j.biopsycho.2013.05.017

Cited by 17 publications

(22 citation statements)

References 53 publications

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“…CECTs were computed as in prior studies (Mueller et al, 2012;Mueller et al, 2013;Mueller et al, 2010;Panitz et al, 2013). To allow CECT computation across the 350-420 trials available for analysis per individual after artifact screening, EEG segments were divided into 50 bins of 15.625 ms each, ranging from 0 ms (stimulus onset) to 781.25 ms. HP segments were divided into 10 bins of 500 ms, ranging from 0-5 s. Next, CECTs were computed by correlating (Pearson's r) each EEG bin with each HP bin across trials within subjects, resulting in a 10 Â 50 cross-correlation CECT matrix.…”

Section: Discussionmentioning

confidence: 99%

“…This phenomenon has been labeled 'N300H' to indicate a negative (N) association between EEG amplitude at 300 ms and HP. The putative N300H brain source is the anterior cingulate cortex (Panitz et al, 2013), a key region for central control of the viscera (Critchley et al, 2003). Consequently, we focus on N300H for this initial test for disturbed brain-heart coupling in PD.…”

Section: Introductionmentioning

confidence: 99%

“…Because the N300H has been best validated for gambling tasks in which trial-by-trial feedback is given (Mueller et al, 2010;Panitz et al, 2013), we also used a gambling task in the present paradigm to evoke N300H.…”

Section: Introductionmentioning

confidence: 99%

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Panic Disorder and Serotonin Reuptake Inhibitors Predict Coupling of Cortical and Cardiac Activity

Mueller

Panitz

Nestoriuc

et al. 2013

Neuropsychopharmacol

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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 corticocardiac interactions in the absence of acute panic. Human participants with PD (n ¼ 22), major depression (MD, clinical control group, n ¼ 21) or no psychiatric diagnosis (healthy control group, n ¼ 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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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Panic Disorder and Serotonin Reuptake Inhibitors Predict Coupling of Cortical and Cardiac Activity

Mueller

Panitz

Nestoriuc

et al. 2013

Neuropsychopharmacol

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“…Using the effects of feedback on task performance during a gambling paradigm (which is associated with a negative potential within the EEG at 300 ms poststimulus), there is a strong association between heart rate interval during this test, and two dipole localizations one within the ACC, and the other within the left insula (247). Since the ACC is considered to be involved in the cardiac response to motivationally relevant stimuli and this is moderated by the left insula, this association has been suggested to relate to activation of cardiac parasympathetic pathways.…”

Section: Human Functional Studiesmentioning

confidence: 95%

The Insular Cortex and the Regulation of Cardiac Function

Oppenheimer

Cechetto

2016

Comprehensive Physiology

175

128

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Cortical representation of the heart challenges the orthodox view that cardiac regulation is confined to stereotyped, preprogrammed and rigid responses to exteroceptive or interoceptive environmental stimuli. The insula has been the region most studied in this regard; the results of clinical, experimental, and functional radiological studies show a complex interweave of activity with patterns dynamically varying regarding lateralization and antero-posterior distribution of responsive insular regions. Either acting alone or together with other cortical areas including the anterior cingulate, medial prefrontal, and orbito-frontal cortices as part of a concerted network, the insula can imbue perceptions with autonomic color providing emotional salience, and aiding in learning and behavioral decision choice. In these functions, cardiovascular input and the right anterior insula appear to play an important, if not pivotal role. At a more basic level, the insula gauges cardiovascular responses to exteroceptive and interoceptive stimuli, taking into account memory, cognitive, and reflexive constructs thereby ensuring appropriate survival responses and maintaining emotional and physiological homeostasis. When acquired derangements to the insula occur after stroke, during a seizure or from abnormal central processing of interoceptive or exteroceptive environmental cues as in psychiatric disorders, serious consequences can arise including cardiac electrophysiological, structural and contractile dysfunction and sudden cardiac death.

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“…Such corticocardiac coupling has been shown to be evoked and modulated by motivationally significant stimuli. More precisely, centromedial activity in the single‐trial EEG around 250–500 ms has repeatedly been found to predict cardiac modulation 2–5 s later (Mueller, Evers, Wacker, & van der Veen, ; Mueller, Panitz, Nestoriuc, Stemmler, & Wacker, ; Mueller, Stemmler, Hennig, & Wacker, ; Panitz, Wacker, Stemmler, & Mueller, ). Accordingly, heart beat modulation in the time window of the cardiac fear response is functionally coupled with preceding brain activity.…”

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confidence: 99%

Conditioned and extinguished fear modulate functional corticocardiac coupling in humans

2015

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Although the conditioned cardiac fear response is an important index of psychophysiological fear processing, underlying neural mechanisms remain unclear. N = 22 participants underwent differential fear conditioning and extinction with face pictures as conditioned stimuli (CS) and loud noise bursts as aversive unconditioned stimulus (US) on Day 1 and a recall test 1 day later. We assessed ERPs, evoked heart period (HP), and time-lagged within-subject correlations of single-trial EEG amplitude and HP as index for corticocardiac coupling in response to the CS. Fear-conditioned stimuli (CS+) triggered cardiac deceleration during fear acquisition and recall. Meanwhile, only during Day 1 acquisition, CS+ evoked larger late positivities in the ERP than CS-. Most importantly, during Day 2 recall, stimulus-evoked single-trial EEG responses in the time window between 250 and 500 ms predicted the magnitude of cardiac fear responses 2 to 5 s later. This marker of corticocardiac coupling selectively emerged in response to not previously extinguished CS+ but was absent in response to CS- or previously extinguished CS+. The present results provide first evidence that fear conditioning and extinction modulate functional corticocardiac coupling in humans. Underlying mechanisms may involve subcortical structures enhancing corticocardiac transmission to facilitate processing of consolidated conditioned fear.

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Brain–heart coupling at the P300 latency is linked to anterior cingulate cortex and insula—A cardio-electroencephalographic covariance tracing study

Cited by 17 publications

References 53 publications

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

The Insular Cortex and the Regulation of Cardiac Function

Conditioned and extinguished fear modulate functional corticocardiac coupling in humans

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