Vagus

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The vagus nerve (also called pneumogastric nerve or cranial nerve X) is the tenth of twelve paired cranial nerves, and is the only nerve that starts in the brainstem (within the medulla oblongata) and extends, through the jugular foramen, down below the head, to the abdomen.

The medieval Latin word vagus means literally "Wandering" (the words vagrant, vagabond, and vague come from the same root). It is also called the pneumogastric nerve since it innervates both the lungs and the stomach.

Innervation

The vagus descends from the spinal cord in the carotid sheath, lateral to the carotid artery. It carries on past the aortic arch to dip inferiorly behind the left bronchus. Here it forms the pulmonary plexus, after giving rise to the recurrent laryngeal nerve.

The vagus nerve supplies motor parasympathetic fibers 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, namely:

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) and keeping the larynx open for breathing. It also receives some sensation from the outer ear, via the Auricular branch (also known as Alderman's nerve) and part of the meninges.

The vagus nerve and the heart

Parasympathetic innervation of the heart is mediated by the vagus nerve. The right vagus innervates the Sinoatrial node. Parasympathetic hyperstimulation predisposes those affected to bradyarrhythmias. The left vagus when hyperstimulated predisposes the heart to Atrioventricular (AV) blocks.

At this location Otto Loewi first proved that nerves secrete substances called neurotransmitters which have effects on receptors in target tissues. Loewi described the substance released by the vagus nerve as vagusstoff, which was later found to be acetylcholine.

The vagus nerve has three associated nuclei, the dorsal motor nucleus, the nucleus ambiguus and the solitary nucleus.

Drugs that inhibit the muscarinic cholinergic receptor (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(slow heart rate) and asystole, which is when the heart has no electrical activity. Anticholinergic drugs relax the detrusor muscle and cause constipation which again involves the vagus nerve.

Bulimics and anorexics have high vagal activity which is associated with the arrhythmias seen in these patients.


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, particularly having blood drawn. When the circulatory changes are great enough, vasovagal syncope results. Relative dehydration tends to amplify these responses.

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 because of a sudden drop in blood pressure and heart rate. Vasovagal syncope affects young children and women more often. It can also lead to temporary loss of bladder control under moments of extreme fear.

Research has shown that women who have complete transection of the spinal cord can experience orgasms through the vagus nerve, which can go from the uterus, cervix and probably the vagina to the brain (3).

Effects of vagus nerve lesions

The patient complains of hoarse voice, difficulty in swallowing (dysphagia) and choking when drinking fluid. There is also loss of gag reflex. Uvula deviates away from the side of lesion and there is failure of palate elevation.


References

  1. Nemeroff C, Mayberg H, Krahl S, McNamara J, Frazer A, Henry T, George M, Charney D, Brannan S (2006). "VNS therapy in treatment-resistant depression: clinical evidence and putative neurobiological mechanisms.". Neuropsychopharmacology 31 (7): 1345-55. PMID 16641939
  2. http://www.msnbc.msn.com/id/19563617/
  3. Komisaruk, B.R, Whipple, B., Crawford, A., Grimes, S., Liu, W-C., Kalin, 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."
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