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Clinical Trials/NCT05639270
NCT05639270
Recruiting
Not Applicable

Pilot Study Before/After of Vagal Stimulation in Chronic Low Back Pain

University Hospital, Montpellier2 sites in 1 country30 target enrollmentFebruary 15, 2023
ConditionsLow Back Pain

Overview

Phase
Not Applicable
Intervention
Not specified
Conditions
Low Back Pain
Sponsor
University Hospital, Montpellier
Enrollment
30
Locations
2
Primary Endpoint
change from baseline pain at 1 month
Status
Recruiting
Last Updated
2 years ago

Overview

Brief Summary

Low back pain is a major public health problem. It is the leading cause of disability in the world. The factors that lead to chronicity of low back pain are multi-factorial and are essentially represented by psychosocial factors (catastrophism, kinesiophobia, algophobia job dissatisfaction, emotional problems such as depression, anxiety, stress, injustice, etc.).

Pain is a multimodal experience that involves different brain structures that are activated by the pain signal and involve the autonomic nervous system (ANS). The vagus nerve is the main actor of one of the two branches of the ANS, the parasympathetic system, which acts as a "slow-down".

The vagus nerve participates in the inter-neuronal transmission of key neurotransmitters for mood, alertness, attention and motivation.

Vagal stimulation has been used for many years as an analgesic device in chronic pain (vascular pain (facial vascular pain, fibromyalgia, visceral pain, gastrointestinal and pelvic pain...)

To date, no study has been conducted on the value of vagal stimulation in chronic low back pain.

Detailed Description

Low back pain is a major public health problem. It is the leading cause of disability in the world. The factors that lead to chronicity of low back pain are multifactorial, which explains the modest effectiveness of both drug treatments and multidisciplinary programs (analgesic drug interventions, non-pharmacological interventions with rehabilitation, physical exercise, psychotherapy, spinal ergonomics, meditation, yoga, etc.) in the treatment of low back pain. psychotherapy, spinal ergonomics, meditation, yoga...) in chronic forms. These factors of chronicization are essentially represented by psychosocial factors (catastrophism, kinesiophobia, algophobia, job dissatisfaction, emotional problems such as depression, anxiety stress, injustice...) In the chronic low back pain population, pain is a multimodal experience that involves different brain structures (insula, anterior cingulate cortex, amygdala and prefrontal cortex). These structures are activated by the pain signal and involve the autonomic nervous system (ANS). The vagus nerve is the main actor of one of the two branches of the ANS, the parasympathetic system, which acts as a "slow-down". The vagus nerve is involved in the inter-neuronal transmission of key neurotransmitters for mood, alertness, attention and motivation (serotonin, dopamine, oxytocin and noradrenaline). It is one of the longest nerves in the human body, originating from the base of the brain (nucleus tractus solitarius) and innervating most of the organs (heart, lung, stomach, liver, spleen, kidneys, gallbladder, pancreas, intestines). It allows the integration of information from the periphery (pain, stress, emotions), slows down the heart rate after a stress, reduces the caliber of the bronchial tubes to help breathing, reduces the inflammatory response, participates in digestion and in the communication with the digestive microbiota. Indeed, there seems to be an alteration of the vagal function in chronic pain patients patients: the vagus nerve is involved in the modulation of pain at different levels (medullary, cerebral) (medullary, cerebral) but also on the different components of pain (sensory, affective emotional, behavioral). The benefit of the stimulation of the vagus would be mediated by a modulation of afferent information (stress, pain, emotion) associated with a benefit of "relaxation" conveyed by the efferent fibers (cardiac, pulmonary effect...). This stimulation of the vagus nerve is done through an atrial electrode that stimulates the atrial branch of the vagus nerve. To date, no study has been conducted on the value of vagal stimulation in chronic low back pain. Because of the multifactorial mechanisms involved in this pathology, this type of therapy appears to be a useful complement to the management of our patients. This pilot study will allow us to evaluate the feasibility of a larger study with a placebo arm. The evaluation of tolerance and adherence to this therapy will be taken into account.

Registry
clinicaltrials.gov
Start Date
February 15, 2023
End Date
January 2024
Last Updated
2 years ago
Study Type
Interventional
Study Design
Single Group
Sex
All

Investigators

Responsible Party
Sponsor

Eligibility Criteria

Inclusion Criteria

  • Low back pain with a VAS greater than or equal to 40 that has been ongoing for more than 3 months
  • Failed or insufficiently relieved by private physiotherapy
  • Failed or insufficiently relieved or intolerant of level II analgesics
  • No change in therapy envisaged within one month.

Exclusion Criteria

  • Non-common low back pain will not be accepted (presence of red flags).
  • Auricular canal not adapted to the stimulation device.
  • Use of another type of electrical device (pacemaker or TENS).
  • History of vagotomy.
  • Heart rhythm disorder.
  • Presence of a cochlear implant on the stimulation side
  • Pregnancy in progress or planned during the study period
  • Adult protected by law or patient under guardianship or curator
  • Person unable to give consent.
  • Participation in other ongoing biomedical research

Outcomes

Primary Outcomes

change from baseline pain at 1 month

Time Frame: between baseline and 1 month

evaluated by a Visual Analog Scale (VAS, 0 the worst result and 100 the best result)

Secondary Outcomes

  • evaluation of device adherence at 1 month(between baseline and 1 month)
  • change from baseline anxiety and depression at 3 month(between baseline and 3 month)
  • change from baseline catastrophism at 1 month(between baseline and 1 month)
  • evolution of use of painkillers at 3 month(between baseline and 3 month)
  • change from baseline functional disability at 1 month(between baseline and 1 month)
  • change from baseline quality of life at 1 month(between baseline and 1 month)
  • change from baseline quality of life at 3 month(between baseline and 3 month)
  • change from baseline functional disability at 3 month(between baseline and 3 month)
  • change from baseline catastrophism at 3 month(between baseline and 3 month)
  • evaluation of device adherence at 3 month(between baseline and 3 month)
  • evaluation of device tolerance at 1 month(between baseline and 1 month)
  • evaluation of device tolerance at 3 month(between baseline and 3 month)
  • evaluation of device satisfaction at 3 month(between baseline and 3 month)
  • change from baseline anxiety and depression at 1 month(between baseline and 1 month)
  • evolution of use of painkillers at 1 month(between baseline and 1 month)
  • evaluation of device satisfaction at 1 month(between baseline and 1 month)
  • change from baseline vagal tone at 1 month(between baseline and 1 month)
  • change from baseline vagal tone at 3 month(between baseline and 3 month)

Study Sites (2)

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