Vagus nerve stimulation attenuates heat- and formalin-induced pain in rats

Bohotin, C.; Scholsem, Martin; Bohotin, Valentin; Franzen, Rachelle; Schoenen, Jean

doi:10.1016/s0304-3940(03)00908-x

Cited by 22 publications

(13 citation statements)

References 15 publications

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“…Since overactive sympathetic outflow has been associated with pain, pain may be reversed by reducing sympathetic outflow while increasing parasympathetic outflow. Together with the antiinflammatory effect, autonomic modulation by vagal nerve stimulation can help manage pain [128] via suppression of pain neurons, as observed in animal models [129][130][131]. All these studies suggest a plausible role of vagal nerve stimulation in controlling and managing pain through multiple mechanisms.…”

Section: Vagal Nerve Stimulationmentioning

confidence: 81%

Molecular Aspects of Regional Pain Syndrome

Baronio

Sadia

Paolacci

et al. 2020

Pain Research and Management

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The purpose of this review is to summarize the pathophysiology of complex regional pain syndrome (CRPS), the underlying molecular mechanisms, and potential treatment options for its management. CRPS is a multifactorial pain condition. CRPS is characterized by prolonged or excessive pain and changes in skin color and temperature, and/or swelling in the affected area, and is generally caused by stimuli that lead to tissue damage. An inflammatory response involving various cytokines and autoantibodies is generated in response to acute trauma/stress. Chronic phase pathophysiology is more complex, involving the central and peripheral nervous systems. Various genetic factors involved in the chronicity of pain have been identified in CRPS patients. As with other diseases of complex pathology, CRPS is difficult to treat and no single treatment regimen is the same for two patients. Stimulation of the vagus nerve is a promising technique being tested for different gastrointestinal and inflammatory diseases. CRPS is more frequent in individuals of 61–70 years of age with a female to male ratio of 3 : 1. Menopause, migraine, osteoporosis, and asthma all represent risk factors for CRPS and in smokers the prognosis appears to be more severe. The pathophysiological mechanisms underlying CRPS involve both inflammatory and neurological pathways. Understanding the molecular basis of CRPS is important for its diagnosis, management, and treatment. For instance, vagal nerve stimulation might have the potential for treating CRPS through the cholinergic anti-inflammatory pathway.

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Section: Vagal Nerve Stimulationmentioning

confidence: 81%

Molecular Aspects of Regional Pain Syndrome

Baronio

Sadia

Paolacci

et al. 2020

Pain Research and Management

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show abstract

“…VNS significantly attenuated the increase of Fos‐immunoreactive neurons observed in ipsilateral TNC laminae I‐II after experimental pain by formalin injection into the left mystacial vibrissae. VNS reduced nociceptive behavior, ie, rubbing the face, on average by 96.1% during the early phase (0‐6 min), and by 60.7% during the late phase (6‐45 minutes) after formal injection . Chen et al found that low intensity stimulation (40 µA) of the sub‐diaphragmatic VN in rats activated Aδ‐fibers and reduced visceral pain.…”

Section: Recent Trials and Research On Vnsmentioning

confidence: 99%

“…VNS reduced nociceptive behavior, ie, rubbing the face, on average by 96.1% during the early phase (0-6 min), and by 60.7% during the late phase (6-45 minutes) after formal injection. 88 Chen et al found that low intensity stimulation (40 mA) of the subdiaphragmatic VN in rats activated Ad-fibers and reduced visceral pain. High-intensity (400 mA) VNS activated C-fibers but had no effect on the visceromotor response to colorectal distension.…”

Section: Recent Trials and Research On Vnsmentioning

confidence: 99%

Vagus Nerve and Vagus Nerve Stimulation, a Comprehensive Review: Part III

2015

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Vagus nerve stimulation (VNS) is currently undergoing multiple trials to explore its potential for various clinical disorders. To date, VNS has been approved for the treatment of refractory epilepsy and depression. It exerts antiepileptic or antiepileptogenic effect possibly through neuromodulation of certain monoamine pathways. Beyond epilepsy, VNS is also under investigation for the treatment of inflammation, asthma, and pain. VNS influences the production of inflammatory cytokines to dampen the inflammatory response. It triggers the systemic release of catecholamines that alleviates the asthma attack. VNS induces antinociception by modulating multiple pain-associated structures in the brain and spinal cord affecting peripheral/central nociception, opioid response, inflammation process, autonomic activity, and pain-related behavior. Progression in VNS clinical efficacy over time suggests an underlying disease-modifying neuromodulation, which is an emerging field in neurology. With multiple potential clinical applications, further development of VNS is encouraging.

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“…The analgesic effect of the vagal afferent stimulation has been reported in numerous behavioral pain tests in laboratory animals. For instance, the VNS-induced inhibition of the nociceptive digastric reflex induced by intense tooth-pulp stimulation (Maixner et al, 1991;Bossut et al, 1992), reduction of the cumulative duration of rubbing and scratching the injection site in the orofacial formalin test (Bohotin et al, 2003b), and latency increase of the tail-flick or the hind paw withdrawal response to noxious heat (Ren et al, 1989;Aicher et al, 1991;Thurston and Randich, 1991;Bohotin et al, 2003a) were reported. In epileptic patients treated with VNS, an increase in mechanical pain threshold was noted (Kirchner et al, 2000(Kirchner et al, , 2006.…”

Section: Introductionmentioning

confidence: 99%