Vagus Nerve and Neurogenic Inflammation: Their Role in GERD
Posted Feb 19 2012 12:36am
The autonomic nervous system (ANS or visceral nervous system) is part of the peripheral nervous system that acts as a control system functioning largely below the level of consciousness while it controls visceral (the “inner parts” of the body) functions. The ANS affects heart rate, digestion, respiration rate, salivation, perspiration, diameter of the pupils, urination and sexual arousal. Whereas most of its actions are involuntary, some, such as breathing, work in tandem with the conscious mind.
It is classically divided into two subsystems: the parasympathetic nervous system (PSNS) and the sympathetic nervous system (SNS). Relatively recently, a third subset of neurons have been named ‘non-adrenergic and non-cholinergic’ neurons (because they use nitric oxide as a neurotransmitter) have been described and found to be integral in autonomic function, particularly in the gut and the lungs. The enteric nervous system is sometimes considered part of the autonomic nervous system, and sometimes considered an independent system. Besides output to the various organs of the body, the vagus nerve conveys sensory information about the state of the body's organs to the central nervous system. Up to 80-90% of the nerve fibers in the vagus nerve are sensory nerves communicating the state of the viscera to the brain. The vagus nerve is also called the pneumogastric nerve because it innervates both the lungs and the stomach.
The lower esophagus is richly invested with vagal nerve endings and failure/relaxation of the lower esophageal sphincter allows digestive contents to leak in a retrograde fashion from the intestine and stomach. This allows corrosive digestive juices including acid and proteolytic enzymes to encounter, irritate and stimulate vagal nerve endings which over time become eroded and sensitized.Our brain receives the information via this communication network and, rightly so, becomes alarmed thus triggering involuntary protective reflex responses. Reilly's syndrome confirms that changes in vascular tone, and reticuloendothelial system via neurogenic inflammatory response produces protection in vulnerable tissues. This is where it gets really interesting. Either the severity of the reflux or the intensity of the body’s response to this dangerous insult can result in a clinical syndrome that has manifestations far-reaching beyond the origin of the endangered tissues. Thus regurgitation of digestive/intestinal contents into the lower esophagus can trigger vagal nerve response that results in tissues swelling, injury, scarring and mucus production in the paranasal sinuses as well as the larynx and pharynx without the affected tissues ever having come in direct contact with regurgitated digestive secretions. Artificial placement of acid into the lower esophagus is proven to result in inflammatory reaction of the paranasal sinuses. This is but one example of a myriad of potential effects that can occur anywhere in the distribution of the vagus nerve, or even the entire craniosacral nervous system. This phenomenon of vagal activation in the presence of regurgitated digestive contents explains the resolution of cardiac palpitations with successful therapy for gastroesophageal reflux disorder (GERD).