Vagus nerve

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Nerve: Vagus nerve

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

Course and distribution of the glossopharyngeal, vagus, and accessory nerves.
Latin	nervus vagus
Gray's	subject #205 910
Innervates	Levator veli palatini, Salpingopharyngeus, Palatoglossus, Palatopharyngeus, Superior pharyngeal constrictor, Middle pharyngeal constrictor, Inferior pharyngeal constrictor
MeSH	A08.800.800.120.900

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.

1 Innervation
2 The vagus nerve and the heart
3 Medical treatment involving the vagus nerve
4 Physical and emotional effects
5 Effects of vagus nerve lesions
6 Additional images
7 References
8 External links

[edit] Innervation

The vagus nerve supplies motor parasympathetic fibers to all the organs except the suprarenal glands, from the neck down to the second segment of the transverse colon. The vagus also controls a few skeletal muscles, namely:

Levator veli palatini muscle
Salpingopharyngeus muscle
Palatoglossus muscle
Palatopharyngeus muscle
Superior, middle and inferior pharyngeal constrictors
Muscles of the larynx (speech).

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.

[edit] 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.

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

[edit] Medical treatment involving the vagus nerve

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. ^[1] A convenient, non-invasive VNS device that stimulates an afferant branch of the vagus nerve is also being developed and will soon undergo trials.

A degree of intermittent VNS can be achieved by daily breathing exercises (for example, Pranayama) over a period of several weeks. In some patients, such proactive relaxation exercises have been found to correlate with lower blood pressure and lower heart rate and more stable moods. The valsalva maneuver may activate the vagus nerve and is a 'natural' way to achieve the same effect in some patients. Patients with atrial fibrillation, supraventricular tachycardia and other illnesses may be trained to perform the valsalva maneuver (or find it for themselves).

Vagotomy (cutting of the vagus nerve) is a now-obsolete therapy that was performed for peptic ulcer disease.

[edit] 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.

[edit] Effects of vagus nerve lesions

The patient complains of hoarse voice, difficulty in swallowing and choking when drinking fluid.

[edit] Additional images

Section of the neck at about the level of the sixth cervical vertebra.	Transverse section of thorax, showing relations of pulmonary artery.	The arch of the aorta, and its branches.	Dura mater and its processes exposed by removing part of the right half of the skull, and the brain.
The right sympathetic chain and its connections with the thoracic, abdominal, and pelvic plexuses.	The celiac ganglia with the sympathetic plexuses of the abdominal viscera radiating from the ganglia.	The thymus of a full-time fetus, exposed in situ.

[edit] References

^ 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. link