In a new paper published in Alimentary Pharmacology and Therapeutics, researchers from the Wingate Institute of Neurogastroenterology at the Blizard Institute have demonstrated that transcutaneous vagal nerve stimulation (t‐VNS) prevents the development of and/or reverses established visceral hypersensitivity in a previously validated model of acid‐induced oesophageal pain.
Visceral pain hypersensitivity is a condition when the gut becomes more sensitive so that even normal events such as passage of food or mild acid reflux can trigger pain. This is an important factor in chronic abdominal pain felt in functional gastrointestinal disorders such as functional chest pain and irritable bowel syndrome. In a previous study, the researchers demonstrated that physiologically increasing parasympathetic vagal tone, using deep slow-paced breathing, prevents the development of acid‐induced oesophageal pain hypersensitivity. The acid‐induced oesophageal pain procedure was used as a validated model on which the current study was based.
In this study, the researchers used a transcutaneous vagal nerve stimulation (t-VNS) device to administer electrical stimulation to healthy participants aged 18‐60 years, who had no past medical history. The device consisted of an earplug‐like electrode which sits on the cymba conchae of the outer ear, and a handheld battery‐powered electrical stimulator which produces electrical pulses to stimulate the auricular branch of the vagus nerve located directly under the skin of the cymba concha. The participants received either administration of electric shocks to the cymba concha (t‐VNS group), or through administration of shocks to the external earlobe (sham t-VNS).
In the first study, the researchers infused hydrochloric acid into the distal oesophagus while administering t‐VNS/sham to evaluate whether the intervention would prevent the development of acid‐induced oesophageal pain hypersensitivity. The results showed participants who received t-VNS tolerated more pain compared to those who received the sham stimulation, providing evidence that vagus nerve stimulation prevents the development of oesophageal hypersensitivity.
In the second study, t‐VNS/sham was applied after the development of acid‐induced oesophageal pain hypersensitivity to evaluate whether it could be reversed. The results showed participants who received t-VNS tolerated more pain compared to those who received the sham stimulation, providing evidence that vagus nerve stimulation reverses established oesophageal hypersensitivity.
The findings could lead to nonpharmacological treatments of chronic pain, particularly in functional gastrointestinal disorders. A substantial proportion of patients being treated for acid reflux fail to respond to existing drug treatments such as protein-pump inhibitors used to treat heartburn and chest pain. These symptoms are mediated, in part, by oesophageal hypersensitivity. Therefore, the results from this study highlight a potential area of nonpharmacological intervention which could be beneficial to patients exhibiting these symptoms.
Professor of Neurogastroenterology and Director of the Wingate Institute of Neurogastroenterology, Professor Qasim Aziz, said: "These results are exciting because they demonstrate that non-invasive methods like application of an electrical stimulus to the vagus nerve via the skin can not only prevent development of pain after an injury but can reverse established pain. This method therefore has the potential to prevent and treat pain arising from the gut and therefore further research is now required to assess its effectiveness in disease states."