Non-invasive vagus nerve stimulation shows promise for treatment of rheumatoid arthritis

Summary: Non-invasive vagus nerve stimulation reduces inflammation and improves symptoms for those suffering from rheumatoid arthritis. The simulation technique helps inhibit the production of cytokines and reduces inflammatory response.

Source: Northwell Health

Bioelectronic medicine scientists at The Feinstein Institute for Medical Research collaborated with counterparts from Academic Medical Center at University of Amsterdam in the Netherlands to carry out a series of pilot clinical studies to assess the effect of a novel bioelectronic stimulation. These studies show that non-invasive stimulation at the external ear improves disease symptoms in patients with rheumatoid arthritis (RA). These findings were first published today in Bioelectronic Medicine. An emerging field of science, bioelectronic medicine draws on neuroscience, focuses on molecular targets, and deploys bioengineering to tap into the nervous system to treat disease and injury without the use of pharmaceuticals.

RA is a chronic inflammatory disease, which is characterized by pain, swelling and stiffness of joints. It affects around 1.3 million people in the United States and costs tens of billions of dollars annually to treat. Commonly, signs and symptoms of this condition are treated using synthetic and biological antirheumatic drugs. However, these medications can result in side effects and may not be effective in all RA patients.

In this pilot study, Sangeeta S. Chavan, PhD, Feinstein Institute professor, along with Meghan E. Addorisio, BS, tested the efficacy of non-invasive vagus nerve stimulation to reduce inflammation and improve disease severity in RA patients. They found that bioelectronic medicine treatment was effective in inhibiting the production of cytokines, proteins that mediate inflammation and reduce the inflammatory responses in patients with rheumatoid arthritis.

“Our primary objective was to observe if a non-invasive treatment using an external device will be effective in improving disease severity of rheumatoid arthritis that continues to plague more than one million across the country each year,” Dr. Chavan said. “We are pleased to observe that this novel bioelectronic treatment significantly reduces swelling and inflammation associated with RA.”

This shows a picture of neurons

They found that bioelectronic medicine treatment was effective in inhibiting the production of cytokines, proteins that mediate inflammation and reduce the inflammatory responses in patients with rheumatoid arthritis. The image is adapted from the Northwell Health news release.

“This clinical research suggests that non-invasive stimulation could suppress inflammation in rheumatoid arthritis patients,” said Kevin J. Tracey, MD, president and CEO of the Feinstein Institute, and co-author on the paper.

About this neuroscience research article

Source:
Northwell Health
Media Contacts:
David Robbins – Northwell Health
Image Source:
The image is adapted from the Northwell Health news release.

Original Research: Open access.
“Investigational treatment of rheumatoid arthritis with a vibrotactile device applied to the external ear”
Meghan E. Addorisio, Gavin H. Imperato, Alex F. de Vos, Steve Forti, Richard S. Goldstein, Valentin A. Pavlov, Tom van der Poll, Huan Yang, Betty Diamond, Kevin J. Tracey and Sangeeta S. Chavan. Bioelectronic Medicine 2019 5:4 doi:10.1186/s42234-019-0020-4

Abstract

Investigational treatment of rheumatoid arthritis with a vibrotactile device applied to the external ear

Background
Rheumatoid arthritis (RA) is a chronic and debilitating inflammatory disease characterized by extensive joint tissue inflammation. Implantable bioelectronic devices targeting the inflammatory reflex reduce TNF production and inflammation in preclinical models of inflammatory disease, and in patients with RA and Crohn’s disease. Here, we assessed the effect of applying a vibrotactile device to the cymba concha of the external ear on inflammatory responses in healthy subjects, as well as its effect on disease activity in RA patients.

Methods
Six healthy subjects received vibrotactile treatment at the cymba concha, and TNF production was analyzed at different time points post-stimulation. In a separate study, nineteen healthy subjects were enrolled in a randomized cross-over study, and effects of vibrotactile treatment at either the cymba concha or gastrocnemius on cytokine levels were assessed. In addition, the clinical efficacy of vibrotactile treatment on disease activity in RA was assessed in nine patients with RA in a prospective interventional study.

Results
Vibrotactile treatment at the cymba concha reduced TNF levels, and the suppressive effect persisted up to 24 h. In the cross-over study with 19 healthy subjects, vibrotactile treatment at the cymba concha but not at the gastrocnemius significantly reduced TNF, IL-1β, and IL-6 levels compared to pre-treatment baseline (TNF p < 0.05, IL-6 p < 0.01, IL-1β p < 0.001). In healthy subjects, vibrotactile treatment at the cymba concha inhibited TNF by 80%, IL-6 by 73%, and IL-1β by 50% as compared to pre-treatment baseline levels. In RA patients, a significant decrease in DAS28-CRP scores was observed two days post-vibrotactile stimulation at the cymba concha (DAS28-CRP score pre-treatment = 4.19 ± 0.33 vs post-treatment = 3.12 ± 0.25, p < 0.05). Disease activity remained significantly reduced 7 days following vibrotactile treatment (DAS28-CRP score 7 days post-treatment = 2.79 ± 0.21, p < 0.01). In addition, a persistent improvement in visual analogue scale scores, a patient derived measure of global health assessment, was observed in RA patients following vibrotactile treatment.

Conclusion
Application of a vibrotactile device to the cymba concha inhibits peripheral blood production of TNF, IL-1β, and IL-6 in healthy subjects, and attenuates systemic inflammatory responses in RA patients.

Trial registrations
ClinicalTrials.gov Identifier: NCT01569789 and NCT00859859. The AMC trial conducted in The Netherlands does not have a ClinicalTrials.gov Identifier.

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