Vagus nerve

Vagus nerve

Plan of the upper portions of the glossopharyngeal, vagus, and accessory nerves.

Course and distribution of the glossopharyngeal, vagus, and accessory nerves.
Details
Innervates Levator veli palatini, Salpingopharyngeus, Palatoglossus, Palatopharyngeus, Superior pharyngeal constrictor, Middle pharyngeal constrictor, Inferior pharyngeal constrictor, visceratyppi Middle pharyngeal constrictor, Inferior pharyngeal constrictor, viscera rass
Identifiers
Latin nervus vagus
MeSH A08.800.800.122.901
TA A14.2.01.153
FMA 5731

Anatomical terms of neuroanatomy

The vagus nerve (/ˈveɪɡəs/ VAY-gəs), historically cited as the pneumogastric nerve, is the tenth cranial nerve or CN X, and interfaces with parasympathetic control of the heart, lungs and digestive tract. The vagus nerves are paired; however, they are normally referred to in the singular. It is the longest nerve of the autonomic nervous system in the human body.

Structure

Upon leaving the medulla oblongata between the pyramid and the inferior cerebellar peduncle, the vagus nerve extends through the jugular foramen, then passes into the carotid sheath between the internal carotid artery and the internal jugular vein down to the neck, chest and abdomen, where it contributes to the innervation of the viscera. Besides giving some output to various organs, the vagus nerve comprises between 80% and 90% of afferent nerves mostly conveying sensory information about the state of the body's organs to the central nervous system.[1]

Right and left vagus nerves descend from the cranial vault through the jugular foramina, penetrating the carotid sheath between the internal and external carotid arteries, then passing posterolateral to the common carotid artery. The cell bodies of visceral afferent fibers of the vagus nerve are located bilaterally in the inferior ganglion of the vagus nerve (nodose ganglia).

The right vagus nerve gives rise to the right recurrent laryngeal nerve, which hooks around the right subclavian artery and ascends into the neck between the trachea and esophagus. The right vagus then crosses anterior to the right subclavian artery, runs posterior to the superior vena cava, descends posterior to the right main bronchus, and contributes to cardiac, pulmonary, and esophageal plexuses. It forms the posterior vagal trunk at the lower part of the esophagus and enters the diaphragm through the esophageal hiatus.

The left vagus nerve enters the thorax between left common carotid artery and left subclavian artery and descends on the aortic arch. It gives rise to the left recurrent laryngeal nerve, which hooks around the aortic arch to the left of the ligamentum arteriosum and ascends between the trachea and esophagus. The left vagus further gives off thoracic cardiac branches, breaks up into the pulmonary plexus, continues into the esophageal plexus, and enters the abdomen as the anterior vagal trunk in the esophageal hiatus of the diaphragm.

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

Nuclei

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

Development

The motor division of the vagus nerve is derived from the basal plate of the embryonic medulla oblongata, while the sensory division originates from the cranial neural crest.

Function

The vagus nerve supplies motor parasympathetic fibres to all the organs except the suprarenal (adrenal) glands, from the neck down to the second segment of the transverse colon. The vagus also controls a few skeletal muscles, notable ones being:

This means that the vagus nerve is responsible for such varied tasks as heart rate, gastrointestinal peristalsis, sweating, and quite a few muscle movements in the mouth, including speech (via the recurrent laryngeal nerve). It also has some afferent fibers that innervate the inner (canal) portion of the outer ear (via the auricular branch, also known as Alderman's nerve) and part of the meninges. This explains why a person may cough when tickled on the ear, such as when trying to remove ear wax with a cotton swab.

Efferent vagus nerve fibres innervating the pharynx and back of the throat are responsible for the gag reflex. In addition, 5-HT3 receptor-mediated afferent vagus stimulation in the gut due to gastroenteritis and other insults is a cause of vomiting.[3]

The vagus nerve carries various types of axons. These include:

The vagus nerve and the heart

Fibers of the vagus nerve (right/bottom of image) innervate the sinoatrial node tissue (central and left of image). H&E stain.

Parasympathetic innervation of the heart is partially controlled by the vagus nerve and is shared by the thoracic ganglia. To be specific, vagal and spinal ganglionic nerves mediate the lowering of the heart rate. The right vagus branch innervates the sinoatrial node. Parasympathetic tone from these sources are obviously well matched to sympathetic tone in healthy people. 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 down without an 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.

Physical and emotional effects

Activation of the vagus nerve typically leads to a reduction in heart rate, blood pressure, or both. This occurs commonly in the setting of gastrointestinal illness such as viral gastroenteritis or acute cholecystitis, or in response to other stimuli, including carotid sinus massage, Valsalva maneuver or pain from any cause, in particular, having blood drawn. When the circulatory changes are great enough, vasovagal syncope results. Relative dehydration tends to amplify these responses. Symptoms of irritable Bowel Syndrome are thought to cause activation of the vagus nerve with many people reporting fainting, vision disturbances and dizziness, but there has been little research into this area as it is not deemed necessary and/or life-threatening.

Excessive activation of the vagal nerve during emotional stress, which is a parasympathetic overcompensation of 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, cervix, and, it is presumed, the vagina to the brain.[4][5]

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.[6][7]

Clinical significance

Vagus nerve stimulation

Vagus nerve stimulation (VNS) therapy using a pacemaker-like device implanted in the chest is a treatment used since 1997 to control seizures in epilepsy patients and has recently been approved for treating drug-resistant cases of clinical depression.[8] A non-invasive VNS device that stimulates an afferent branch of the vagus nerve is also being developed and will soon undergo trials.[9]

Clinical trials are currently underway in Antwerp, Belgium using VNS for the treatment of tonal tinnitus 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.[10]

VNS may also be achieved by one of the vagal maneuvers: holding the breath for a few seconds, dipping the face in cold water, coughing, or tensing the stomach muscles as if to bear down to have a bowel movement.[11] Patients with supraventricular tachycardia,[11] 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 has helped 31 obese participants lose an average of nearly 15 percent of their excess weight. A year-long 300-participant double-blind, phase II trial has begun.[12]

Vagotomy

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.[13] The procedure curbs the feeling of hunger and is sometimes performed in conjunction with putting bands on patients' stomachs, resulting in average weight loss of 43% at six months with diet and exercise.[14]

One serious side effect of a 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 the deficiency, which, if left untreated, causes nerve damage, tiredness, dementia, paranoia, and ultimately death.[15]

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.[16]

Chagasic disease

The majority of gradual devastation by neuropathy in Chagas disease is channeled to the major parasympathetic branches of the vagus nerve. Depending upon load, Chagasic vagal disease can cause megaesophagus, megacolon and cardiomyopathy.[17]

History

Etymology

The medieval Latin word vagus means literally "wandering" (the words vagrant, vagabond, and vague come from the same root). Sometimes the branches are spoken of in the plural and are thus called vagi (/ˈveɪdʒaɪ/, US dict: vā′·jī). The vagus is also called the pneumogastric nerve since it innervates both the lungs and the stomach.

Additional images

See also

This article uses anatomical terminology; for an overview, see Anatomical terminology.

References

  1. ↑ Berthoud, H. R.; Neuhuber, W. L. (2000). "Functional and chemical anatomy of the afferent vagal system". Autonomic Neuroscience. 85 (1–3): 1–17. doi:10.1016/S1566-0702(00)00215-0. PMID 11189015.
  2. ↑ Dutschmann, Mathias; Bautista, Tara G.; Mörschel, Michael; Dick, Thomas E. (2014). "Learning to breathe: Habituation of Hering–Breuer inflation reflex emerges with postnatal brainstem maturation". Respiratory Physiology & Neurobiology. 195: 44–49. doi:10.1016/j.resp.2014.02.009. ISSN 1569-9048.
  3. ↑ Mandal, Ananya (25 September 2013). "Vomiting Mechanism". News Medical. Archived from the original on 4 January 2015. Retrieved 27 June 2015.
  4. ↑ "Exploring the Mind-Body Orgasm". Wired. 2007-01-10.
  5. ↑ Komisaruk BR, Whipple B, Crawford A, Liu WC, Kalnin A, Mosier K (2004). "Brain activation during vaginocervical self-stimulation and orgasm in women with complete spinal cord injury: fMRI evidence of mediation by the vagus nerves". Brain Res. 1024 (1-2): 77–88. doi:10.1016/j.brainres.2004.07.029. PMID 15451368.
  6. ↑ Pocai, A; TK Lam; Gutierrez-Juarez R (2005). "Hypothalamic K(ATP) channels control hepatic glucose production". Nature. 434 (7036): 1026–1031. doi:10.1038/nature03439. PMID 15846348.
  7. ↑ Pagotto, U. (2009). "Where does insulin resistance start? The brain". Diabetes Care. 32 (2): S174–S177. doi:10.2337/dc09-S305.
  8. ↑ Nemeroff, Charles B.; et al. (2006). "VNS therapy in treatment-resistant depression: clinical evidence and putative neurobiological mechanisms.". Neuropsychopharmacology. 31 (7): 1345–55. doi:10.1038/sj.npp.1301082. PMID 16641939. link
  9. ↑ Eisenstein, Michael (2013). "Neurodevice startups target peripheral nervous system.". Nature Biotechnology. 31: 865–866. doi:10.1038/nbt1013-865.
  10. ↑ http://www.utdallas.edu/news/2011/1/13-8021_Findings-Show-Promise-in-Battle-Against-Tinnitus_article.html
  11. 1 2 Vibhuti N, Singh; Monika Gugneja (2005-08-22). "Supraventricular Tachycardia". eMedicineHealth.com. Retrieved 2008-11-28.
  12. ↑ Mayo Clinic. Device Blocking Stomach Nerve Signals Shows Promise in Obesity
  13. ↑ Ulcer surgery may help treat obesity - Diet and nutrition - MSNBC.com
  14. ↑ "Could nerve-snip spur weight loss?". CNN.com. Turner Broadcasting System. Archived from the original on 2007-07-13.
  15. ↑ The Pernicious Anemia Society
  16. ↑ Parkinson's disease may begin in the gut.
  17. ↑ Córdova, E; et al. (April 2010). "Neurological manifestations of Chagas' disease.". Neurological research. 32 (3): 238–44. doi:10.1179/016164110X12644252260637. PMID 20406601.

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