Uncertainty in anticipation of uncomfortable rectal distension is modulated by the autonomic nervous system — A fMRI study in healthy volunteers

Rubio, Amandine; Oudenhove, Lukas Van; Pellissier, Sonia; Ly, Huynh Giao; Dupont, Patrick; Micheaux, Hugo Lafaye de; Tack, Jan; Dantzer, Cécile; Delon‐Martin, Chantal; Bonaz, Bruno

doi:10.1016/j.neuroimage.2014.11.043

Cited by 49 publications

(42 citation statements)

References 93 publications

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“…However, pharmacological brain imaging studies have implicated alterations in the corticotropin-releasing factor (also known as corticoliberin)–corticotropin-releasing receptor 1 64,83 and norepinephrine–α adrenergic receptor signalling system in this network. 84 …”

Section: The Nervous System Componentmentioning

confidence: 99%

Towards a systems view of IBS

Mayer

Labus

Tillisch

et al. 2015

Nat Rev Gastroenterol Hepatol

224

220

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Despite an extensive body of reported information about peripheral and central mechanisms involved in the pathophysiology of IBS symptoms, no comprehensive disease model has emerged that would guide the development of novel, effective therapies. In this Review, we will first describe novel insights into some key components of brain–gut interactions, starting with the emerging findings of distinct functional and structural brain signatures of IBS. We will then point out emerging correlations between these brain networks and genomic, gastrointestinal, immune and gut-microbiome-related parameters. We will incorporate this new information, as well as the reported extensive literature on various peripheral mechanisms, into a systems-based disease model of IBS, and discuss the implications of such a model for improved understanding of the disorder, and for the development of more-effective treatment approaches in the future.

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Section: The Nervous System Componentmentioning

confidence: 99%

Towards a systems view of IBS

Mayer

Labus

Tillisch

et al. 2015

Nat Rev Gastroenterol Hepatol

224

220

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“…Anxiety has been demonstrated to modulate gastrointestinal symptoms in healthy 21 and symptomatic individuals 22 . Sharma et al showed that anxiety increases acid-induced esophageal hyperalgesia 23 .…”

Section: Introductionmentioning

confidence: 99%

Anxiety can significantly explain bolus perception in the context of hypotensive esophageal motility: Results of a large multicenter study in asymptomatic individuals

Cisternas

Scheerens

Omari

et al. 2017

Neurogastroenterology Motil

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“…5,17,27,37,63 For example, neuroimaging evidence indicates that threat evoked by anticipation of a painful event modulates pain processing by activating cortical and subcortical nociceptive circuits, including the primary somatosensory cortex, anterior cingulate cortex, insula, thalamus, prefrontal cortex, periaqueductal grey, and hippocampal network. 5,17,26,[37][38][39]52,54,55 Threat also seems to engage descending brain-to-spinal cord mechanisms to modulate nociceptive input at the spinal level. For example, Willer et al 63 demonstrated that anticipation of a painful ankle shock could augment the nociceptive flexion reflex (NFR, a spinally mediated withdrawal reflex used as an indicator of spinal nociception).…”

Section: Introductionmentioning

confidence: 99%

Does pain catastrophizing contribute to threat-evoked amplification of pain and spinal nociception?

Terry

Thompson²,

Rhudy³

2016

Pain

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Unpredictable threat amplifies pain and spinal nociception (as measured by the nociceptive flexion reflex, NFR), but it is unknown whether pain catastrophizing mediates this threat-related amplification. To examine this, the present study experimentally reduced catastrophizing and examined the effect on threat-evoked pain/NFR facilitation. Healthy pain-free participants (N 5 113) were randomly assigned to a brief 30-minute intervention designed to reduce catastrophic thoughts or a control intervention that involved education about pain neurobiology. Before the interventions, participants underwent a block of 8 pseudorandomly ordered periods of safe (no abdominal shock) and threat (abdominal shock possible) during which pain and NFR were evoked by electric stimulations to the ankle. After the safe/threat periods, participants rated pain intensity, pain unpleasantness, and situation-specific pain catastrophizing. The same test block was delivered after the intervention to examine changes in catastrophizing and threat-evoked pain/NFR facilitation. As expected, pain catastrophizing was reduced by the catastrophizing reduction intervention, relative to the control group. Furthermore, pain intensity, unpleasantness, and NFR magnitudes were higher during threat periods than safe. However, this threat-related pain/NFR amplification was not attenuated by the catastrophizing reduction intervention at the group level, although the intervention generally led to lower pain ratings (but not reduced NFR), regardless of the context. Nonetheless, bootstrapped mediation analyses found that reductions in catastrophizing mediated reductions in threat-related amplification of pain, but not NFR. This suggests that catastrophizing is partly responsible for threat-evoked pain amplification and provides further evidence that catastrophizing does not amplify pain at the spinal level.

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Uncertainty in anticipation of uncomfortable rectal distension is modulated by the autonomic nervous system — A fMRI study in healthy volunteers

Cited by 49 publications

References 93 publications

Towards a systems view of IBS

Towards a systems view of IBS

Anxiety can significantly explain bolus perception in the context of hypotensive esophageal motility: Results of a large multicenter study in asymptomatic individuals

Does pain catastrophizing contribute to threat-evoked amplification of pain and spinal nociception?

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