Vagus nerve

• Pharyngeal nerve
• Superior laryngeal nerve
• Superior cervical cardiac branches of vagus nerve
• Inferior cervical cardiac branch
• Recurrent laryngeal nerve
• Thoracic cardiac branches
• Branches to the pulmonary plexus
• Branches to the esophageal plexus
• Anterior vagal trunk
• Posterior vagal trunk
• Hering–Breuer reflex in alveoli[3]

The vagus runs parallel to the common carotid artery and internal jugular vein inside the carotid sheath.

The vagus nerve includes axons which emerge from or converge onto four nuclei of the medulla:

1. The dorsal nucleus of vagus nerve – which sends parasympathetic output to the viscera, especially the intestines
2. The nucleus ambiguus – which gives rise to the branchial efferent motor fibers of the vagus nerve and preganglionic parasympathetic neurons that innervate the heart
3. The solitary nucleus – which receives afferent taste information and primary afferents from visceral organs
4. The spinal trigeminal nucleus – which receives information about deep/crude touch, pain, and temperature of the outer ear, the dura of the posterior cranial fossa and the mucosa of the larynx

H&E stained fibers of the vagus nerve (bottom right) innervate the sinoatrial node tissue (middle left)

Parasympathetic innervation of the heart is partially controlled by the vagus nerve and is shared by the thoracic ganglia. Vagal and spinal ganglionic nerves mediate the lowering of the heart rate. The right vagus branch innervates the sinoatrial node. In healthy people, parasympathetic tone from these sources is well-matched to sympathetic tone. Hyperstimulation of parasympathetic influence promotes bradyarrhythmias. When hyperstimulated, the left vagal branch predisposes the heart to conduction block at the atrioventricular node.

At this location, neuroscientist Otto Loewi first demonstrated that nerves secrete substances called neurotransmitters, which have effects on receptors in target tissues. In his experiment, Loewi electrically stimulated the vagus nerve of a frog heart, which slowed the heart. Then he took the fluid from the heart and transferred it to a second frog heart without a vagus nerve. The second heart slowed without electrical stimulation. Loewi described the substance released by the vagus nerve as vagusstoff, which was later found to be acetylcholine. Drugs that inhibit the muscarinic receptors (anticholinergics) such as atropine and scopolamine, are called vagolytic because they inhibit the action of the vagus nerve on the heart, gastrointestinal tract, and other organs. Anticholinergic drugs increase heart rate and are used to treat bradycardia.

Excessive activation of the vagal nerve during emotional stress, which is a parasympathetic overcompensation for a strong sympathetic nervous system response associated with stress, can also cause vasovagal syncope due to a sudden drop in cardiac output, causing cerebral hypoperfusion. Vasovagal syncope affects young children and women more than other groups. It can also lead to temporary loss of bladder control under moments of extreme fear.

Research has shown that women having had complete spinal cord injury can experience orgasms through the vagus nerve, which can go from the uterus and cervix to the brain.[9][10]

Insulin signaling activates the adenosine triphosphate (ATP)-sensitive potassium (KATP) channels in the arcuate nucleus, decreases AgRP release, and through the vagus nerve, leads to decreased glucose production by the liver by decreasing gluconeogenic enzymes: Phosphoenolpyruvate carboxykinase, Glucose 6-phosphatase.[11][12]

Vagus nerve stimulation (VNS) therapy using a neurostimulator implanted in the chest is a treatment used since 1997 to control seizures in epilepsy patients and has been approved for treating drug-resistant cases of clinical depression.[13] A non-invasive VNS device that stimulates an afferent branch of the vagus nerve is also being developed and will soon undergo trials.[14]

Clinical trials have started in Antwerp, Belgium, using VNS for the treatment of tonal tinnitus[15] after a breakthrough study published in early 2011 by researchers at the University of Texas – Dallas showed successful tinnitus-suppression in rats when tones were paired with brief pulses of stimulation of the vagus nerve.[16][17]

VNS may also be achieved by one of the vagal maneuvers: holding the breath for 20–60 seconds, dipping the face in cold water, coughing, humming or singing, or tensing the stomach muscles as if to bear down to have a bowel movement.[18] Patients with supraventricular tachycardia,[18] atrial fibrillation, and other illnesses may be trained to perform vagal maneuvers (or find one or more on their own).

Vagus nerve blocking (VBLOC) therapy is similar to VNS but used only during the day. In a six-month open-label trial involving three medical centers in Australia, Mexico, and Norway, vagus nerve blocking helped 31 obese participants lose an average of nearly 15 percent of their excess weight. As of 2008, a year-long 300 participant double-blind, phase II trial had begun.[19]

Vagotomy (cutting of the vagus nerve) is a now obsolete therapy that was performed for peptic ulcer disease. Vagotomy is currently being researched as a less invasive alternative weight-loss procedure to gastric bypass surgery.[20] The procedure curbs the feeling of hunger and is sometimes performed in conjunction with putting bands on patients' stomachs, resulting in an average of 43% of excess weight loss at six months with diet and exercise.[21]

One serious side effect of vagotomy is a vitamin B₁₂ deficiency later in life – perhaps after about 10 years – that is similar to pernicious anemia. The vagus normally stimulates the stomach's parietal cells to secrete acid and intrinsic factor. Intrinsic factor is needed to absorb vitamin B₁₂ from food. The vagotomy reduces this secretion and ultimately leads to deficiency, which, if left untreated, causes nerve damage, tiredness, dementia, paranoia, and ultimately death.[22]

Researchers from Aarhus University and Aarhus University Hospital have demonstrated that vagotomy prevents (halves the risk of) the development of Parkinson's disease, suggesting that Parkinson's disease begins in the gastrointestinal tract and spreads via the vagus nerve to the brain.[23] Or giving further evidence to the theory that dysregulated environmental stimuli, such as that received by the vagus nerve from the gut, may have a negative effect on the dopamine reward system of the substantia nigra, thereby causing Parkinson's disease.[24]

The neuropathy in Chagas disease spreads in part via the major parasympathetic branches of the vagus nerve.[25]

The hypersensitivity of vagal afferent nerves causes refractory or idiopathic cough.

Arnold's nerve ear-cough reflex though uncommon is a manifestation of a vagal sensory neuropathy and this is the cause of a refractory chronic cough that can be treated with gabapentin. The cough is triggered by mechanical stimulation of the external auditory meatus and accompanied by other neuropathic features such as throat irritation (laryngeal paresthesia) and cough triggered by exposure to nontussive triggers such as cold air and eating (termed allotussia). These features suggest a neuropathic origin to the cough.[26]

The Latin word vagus means literally "wandering" (the words vagrant, vagabond, vague, and divagation come from the same root). Sometimes the right and left branches together are spoken of in the plural and are thus called vagi (/ˈveɪdʒaɪ/ VAY-jy). The vagus was also historically called the pneumogastric nerve since it innervates both the lungs and the stomach.