Preliminary report: modulation of parasympathetic nervous system tone influences oesophageal pain hypersensitivity

Botha, Claude; Farmer, Adam D.; Nilsson, Matias; Brock, Christina; Gavrila, Ana D; Drewes, Asbjørn Mohr; Knowles, Charles H.; Aziz, Qasim

doi:10.1136/gutjnl-2013-306698

Cited by 65 publications

(90 citation statements)

References 43 publications

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“…Traditionally, it is thought that visceral pain afferent information is primarily conducted via spinal afferents although there is an increasing appreciation that the ANS is involved in pain genesis in maintenance across a number of chronic pain syndromes including CP 16,18,34. Of note, Botha et al20 demonstrated that physiological accentuation of vagal tone, using DSB, could prevent the development of acid-induced esophageal hypersensitivity in a validated model in healthy volunteers. Moreover, it was shown that the analgesic effect of DSB could be abolished with coadministration of the vagolytic agent atropine.…”

Section: Discussionmentioning

confidence: 99%

“…Physiological vagal stimulation was undertaken with a validated deep breathing protocol, consisting of breathing at full inspiratory capacity for 4 seconds, followed by exhaling to forced expiratory vital capacity for 6 seconds, repeated at a frequency of 0.1 Hz (i.e., six breaths per minute) 20. For the sham breathing procedure, patients were asked to breathe normally and count their breaths.…”

Section: Methodsmentioning

confidence: 99%

“…Vagal activity can be therapeutically accentuated either physiologically, with deep slow breathing (DSB), or electrically, using vagus nerve stimulation (VNS), which can be applied invasively or noninvasively through the skin. In healthy volunteers, DSB and noninvasive transcutaneous electrical vagal nerve stimulation (t-VNS) of the auricular branch of the vagus nerve have been shown to decrease experimental pain and increase GI motility 19,20. Hence, combined physiological and electrical modulation of vagal tone, using DSB and t-VNS, respectively, may represent an alternative non-pharmacological treatment modality for pain and GI dysmotility in CP.…”

Section: Introductionmentioning

confidence: 99%

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Acute physiological and electrical accentuation of vagal tone has no effect on pain or gastrointestinal motility in chronic pancreatitis

Juel¹,

Brock²,

Olesen³

et al. 2017

JPR

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BackgroundThe effective management of pain in chronic pancreatitis (CP) remains a therapeutic challenge. Analgesic drugs, such as opioids, and the underlying pathology can impair gut function. The autonomic nervous system influences hormone secretion and gut motility. In healthy volunteers, electrical (using noninvasive transcutaneous vagal nerve stimulation [t-VNS]) and physiological (using deep slow breathing [DSB]) modulation of parasympathetic tone results in pain attenuation and enhanced gut motility. Thus, the aims were to investigate whether t-VNS and DSB could enhance the parasympathetic tone, decrease pain sensitivity and improve gut motility in CP.Patients and methodsA total of 20 patients (12 males, mean age=61 years, range: 50–78 years) with CP were randomized to short-term (60 minutes) t-VNS and DSB, or their placebo equivalent, in a crossover design. Cardiometrically derived parameters of autonomic tone, quantitative sensory testing of bone and muscle pain pressure, conditioned pain modulation (CPM) and assessments of gastroduodenal motility with ultrasound were performed.ResultsIn comparison to sham, t-VNS and DSB increased cardiac vagal tone (CVT) (P<0.001). However, no changes in pain pressure thresholds for bone (P=0.95) or muscle (P=0.45) were seen. There was diminished CPM (P=0.04), and no changes in gastroduodenal motility were observed (P=0.3).ConclusionThis explorative study demonstrated that t-VNS and DSB increased CVT in patients with CP. However, this short-lasting increase did not affect pain sensitivity to musculoskeletal pain or gastroduodenal motility. The chronic pain in CP patients is complex, and future trials optimizing neuromodulation for pain relief and improved motility are needed.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Acute physiological and electrical accentuation of vagal tone has no effect on pain or gastrointestinal motility in chronic pancreatitis

Juel¹,

Brock²,

Olesen³

et al. 2017

JPR

Self Cite

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“…The technique of deep breathing allowed an increase in cardiac vagal tone and increased pain threshold in healthy individuals subjected to an acid challenge to the esophagus [Botha et al 2015]. Atropine prevented both effects, again reinforcing the relevance of the vagal cholinergic anti-inflammatory pathway in visceral pain perception.…”

Section: The Vagus Nervementioning

confidence: 77%

What goes around comes around: novel pharmacological targets in the gut–brain axis

González-Arancibia

Escobar-Luna

Barrera-Bugueño

et al. 2016

Therap Adv Gastroenterol

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Abstract:The gut and the brain communicate bidirectionally through anatomic and humoral pathways, establishing what is known as the gut-brain axis. Therefore, interventions affecting one system will impact on the other, giving the opportunity to investigate and develop future therapeutic strategies that target both systems. Alterations in the gut-brain axis may arise as a consequence of changes in microbiota composition (dysbiosis), modifications in intestinal barrier function, impairment of enteric nervous system, unbalanced local immune response and exaggerated responses to stress, to mention a few. In this review we analyze and discuss several novel pharmacological targets within the gut-brain axis, with potential applications to improve intestinal and mental health.

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“…Second, the deep breathing could have induced a hypoalgesic effect of itself, which makes the interpretation of the study effects complicated. It has been shown that slow, deep breathing results in lower heat pain intensity ratings36 and increased thermal pain thresholds,37 induces hypoalgesia for suprathreshold electrical stimulations38 and prevents the development of acid-induced esophageal hypersensitivity 35. It is thought that HR variability and thus parasympathetic activity during deep breathing might contribute to the hypoalgesic effect by shared cardiorespiratory and nociceptive neurophysiological pathways,35,37 although this is not consistently found 38…”

Section: Discussionmentioning

confidence: 99%

Influence of exercise on visceral pain: an explorative study in healthy volunteers

Weerdenburg

Brock

Drewes

et al. 2016

JPR

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Background and objectivesContradictory results have been found about the effect of different exercise modalities on pain. The aim of this study was to investigate the early effects of aerobic and isometric exercise on different types of experimental pain, including visceral pain, compared to an active control condition.MethodsFifteen healthy subjects (6 women, mean [standard deviation] age 25 [6.5] years) completed 3 interventions consisting of 20 minutes of aerobic cycling, 12 minutes of isometric knee extension and a deep breathing procedure as active control. At baseline and after each intervention, psychophysical tests were performed, including electrical stimulation of the esophagus, pressure pain thresholds and the cold pressor test as a measure for conditioned pain modulation. Participants completed the Medical Outcome Study Short-Form 36 and State-Trait Anxiety Inventory prior to the experiments. Data were analyzed using two-way repeated measures analysis of variance.ResultsNo significant differences were found for the psychophysical tests after the interventions, compared to baseline pain tests and the control condition.ConclusionNo hypoalgesic effect of aerobic and isometric exercise was found. The evidence for exercise-induced hypoalgesia appears to be not as consistent as initially thought, and caution is recommended when interpreting the effects of exercise on pain.

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Preliminary report: modulation of parasympathetic nervous system tone influences oesophageal pain hypersensitivity

Abstract: The development of oesophageal hyperalgesia is prevented by physiologically increasing parasympathetic tone. This effect is pharmacologically blocked with atropine, providing evidence that the PNS influences the development of oesophageal pain hypersensitivity.

Cited by 65 publications

References 43 publications

Acute physiological and electrical accentuation of vagal tone has no effect on pain or gastrointestinal motility in chronic pancreatitis

Acute physiological and electrical accentuation of vagal tone has no effect on pain or gastrointestinal motility in chronic pancreatitis

What goes around comes around: novel pharmacological targets in the gut–brain axis

Influence of exercise on visceral pain: an explorative study in healthy volunteers

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