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From Wikipedia, the free encyclopedia

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 typpi Middle pharyngeal constrictor, Inferior pharyngeal constrictor, visceratyppi Middle pharyngeal constrictor, Inferior pharyngeal constrictor, viscera rass
MeSH    Vagus+Nerve

Vagus nerve - dissection

Cranial nerves
CN I – Olfactory
CN II – Optic
CN III – Oculomotor
CN IV – Trochlear
CN V – Trigeminal
CN VI – Abducens
CN VII – Facial
CN VIII – Vestibulocochlear
CN IX – Glossopharyngeal
CN X – Vagus
CN XI – Spinal accessory
CN XII – Hypoglossal

The vagus nerve (pron.: /ˈveɪɡəs/ VAY-gəs), also called pneumogastric nerve or cranial nerve X, is the tenth of twelve (excluding CN0) paired cranial nerves. Upon leaving the medulla between the medullary pyramid and the inferior cerebellar peduncle, it extends through the jugular foramen, then passes into the carotid sheath between the internal carotid artery and the internal jugular vein down below the head, to the neck, chest and abdomen, where it contributes to the innervation of the viscera. Besides output to the various organs in the body, the vagus nerve conveys sensory information about the state of the body's organs to the central nervous system. 80-90% of the nerve fibers in the vagus nerve are afferent (sensory) nerves communicating the state of the viscera to the brain.[1]

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.

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.

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

The Dorsal nucleus of vagus nerve - which sends parasympathetic output to the viscera, especially the intestines
The Nucleus ambiguus - which gives rise to the branchial efferent motor fibers of the vagus nerve and preganglionic parasympathetic neurons that innervate the heart
The Solitary nucleus - which receives afferent taste information and primary afferents from visceral organs
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


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


    Auricular 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

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


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).

Vagus nerve - dissection

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 anteriorly to the right subclavian artery and runs posterior to the superior vena cava and 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 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 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, notable ones being:

    Cricothyroid muscle
    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 (via action of the posterior cricoarytenoid muscle, the only abductor of the vocal folds). 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).

Functional components

The vagus nerve carries axons of type GVE, general visceral efferent, which provides parasympathetic innervation to glands of mucous membranes of the pharynx, larynx, organs in the neck, thorax, and abdomen.

The vagus nerve also carries axons of type GVA, general visceral afferent, which carries information from the thoracic and abdominal viscera; aortic body and arch.

The vagus nerve also carries axons of type SVA, special visceral afferent, which carry taste of the epiglottis region of the tongue.

The vagus nerve also carries axons of type GSA, general somatic afferent, which carry sensation from the external auditory meatus and tympanic membrane.

The vagus nerve also carries axons of type SVE, special visceral efferent, which innervate skeletal muscle of the pharynx and larynx.

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

The vagus nerve and the heart

Parasympathetic innervation of the heart is controlled by the vagus nerve. To be specific, the vagus nerve acts to lower the heart rate. 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, 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 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). Atropine is no longer indicated for the treatment of pulseless electrical activity (PEA) or asystole per the 2010 ACLS guidelines, as it has not been shown to improve outcomes in these clinical scenarios.

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.[2] A non-invasive VNS device that stimulates an afferent branch of the vagus nerve is also being developed and will soon undergo trials.[citation needed]

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. [2]

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.[3] Patients with supraventricular tachycardia,[3] 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.[4]

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.[5] 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.[6]

One serious side-effect of a Vagotomy is a vitamin B12 deficiency later in life - i.e., 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.[7]
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 because of a sudden drop in blood pressure and heart rate. 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.[8][9]

Liver - 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[10][11]

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.

Additional images

Interior view of the human brain, with the cranial nerves labeled.

Vagus nerve

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 tracheobronchial lymph glands

Section of the medulla oblongata at about the middle of the olive

Hind- and mid-brains; postero-lateral view

Upper part of medulla spinalis and hind- and mid-brains; posterior aspect, exposed in situ

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 position and relation of the esophagus in the cervical region and in the posterior mediastinum, seen from behind

The thyroid gland and its relations

The thymus of a full-term fetus, exposed in situ

Vagus nerve

Vagus nerve

Vagus nerve

Vagus nerve

Vagus nerve

Muscles, arteries and nerves of neck. Newborn dissection.

Muscles, arteries and nerves of neck. Newborn dissection.

Muscles, nerves and arteries of neck.Deep dissection. Anterior view.

« Last Edit: November 04, 2013, 10:43:17 AM by dennis100 » Logged
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« Reply #1 on: November 04, 2013, 05:26:15 AM »

J Physiol. 1934 September 19; 82(2): 211–241.
PMCID: PMC1394249
The action of a single vagal volley on the rhythm of the heart beat
G. L. Brown and J. C. Eccles
Copyright and License information ►
This article has been cited by other articles in PMC.
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« Last Edit: November 04, 2013, 05:33:39 AM by dennis100 » Logged
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« Reply #2 on: November 04, 2013, 06:01:38 AM »

Henry Gray (1821–1865).  Anatomy of the Human Body.  1918.
5j. The Vagus Nerve

(N. Vagus; Tenth Nerve; Pneumogastric Nerve)

The vagus nerve (Figs. 791, 792, 793) is composed of both motor and sensory fibers, and has a more extensive course and distribution than any of the other cranial nerves, since it passes through the neck and thorax to the abdomen.   

  The vagus is attached by eight or ten filaments to the medulla oblongata in the groove between the olive and the inferior peduncle, below the glossopharyngeal. The sensory fibers arise from the cells of the jugular ganglion and ganglion nodosum of the nerve, and, when traced into the medulla oblongata mostly end by arborizing around the cells of the inferior part of a nucleus which lies beneath the ala cinerea in the lower part of the rhomboid fossa. These are the sympathetic afferent fibers. Some of the sensory fibers of the glossopharyngeal nerve have been seen to end in the upper part of this nucleus. A few of the sensory fibers of the vagus, probably taste fibers, descend in the fasciculus solitarius and end around its cells. The somatic sensory fibers, few in number, from the posterior part of the external auditory meatus and the back of the ear, probably join the spinal tract of the trigeminal as it descends in the medulla. The somatic motor fibers arise from the cells of the nucleus ambiguus, already referred to in connection with the motor root of the glossopharyngeal nerve.
 The sympathetic efferent fibers, distributed probably as preganglionic fibers to the thoracic and abdominal viscera, i. e., as motor fibers to the bronchial tree, inhibitory fibers to the heart, motor fibers to the esophagus, stomach, small intestine and gall passages, and as secretory fibers to the stomach and pancreas, arise from the dorsal nucleus of the vagus.
 The filaments of the nerve unite, and form a flat cord, which passes beneath the flocculus to the jugular foramen, through which it leaves the cranium. In emerging through this opening, the vagus is accompanied by and contained in the same sheath of dura mater with the accessory nerve, a septum separating them from the glossopharyngeal which lies in front (Fig. 792). In this situation the vagus presents a well-marked ganglionic enlargement, which is called the jugular ganglion (ganglion of the root); to it the accessory nerve is connected by one or two filaments. After its exit from the jugular foramen the vagus is joined by the cranial portion of the accessory nerve, and enlarges into a second gangliform swelling, called the ganglion nodosum (ganglion of the trunk); through this the fibers of the cranial portion of the accessory pass without interruption, being principally distributed to the pharyngeal and superior laryngeal branches of the vagus, but some of its fibers descend in the trunk of the vagus, to be distributed with the recurrent nerve and probably also with the cardiac nerves.
 The vagus nerve passes vertically down the neck within the carotid sheath, lying between the internal jugular vein and internal carotid artery as far as the upper border of the thyroid cartilage, and then between the same vein and the common carotid artery to the root of the neck. The further course of the nerve differs on the two sides of the body.
 On the right side, the nerve passes across the subclavian artery between it and the right innominate vein, and descends by the side of the trachea to the back of the root of the lung, where it spreads out in the posterior pulmonary plexus. From the lower part of this plexus two cords descend on the esophagus, and divide to form, with branches from the opposite nerve, the esophageal plexus. Below, these branches are collected into a single cord, which runs along the back of the esophagus enters the abdomen, and is distributed to the postero-inferior surface of the stomach, joining the left side of the celiac plexus, and sending filaments to the lienal plexus.
 On the left side, the vagus enters the thorax between the left carotid and subclavian arteries, behind the left innominate vein. It crosses the left side of the arch of the aorta, and descends behind the root of the left lung, forming there the posterior pulmonary plexus. From this it runs along the anterior surface of the esophagus, where it unites with the nerve of the right side in the esophageal plexus, and is continued to the stomach, distributing branches over its anterosuperior surface; some of these extend over the fundus, and others along the lesser curvature. Filaments from these branches enter the lesser omentum, and join the hepatic plexus.
 The Jugular Ganglion (ganglion jugulare; ganglion of the root) is of a grayish color, spherical in form, about 4 mm. in diameter.
  Branches of Communication.—This ganglion is connected by several delicate filaments to the cranial portion of the accessory nerve; it also communicates by a twig with the petrous ganglion of the glossopharyngeal, with the facial nerve by means of its auricular branch, and with the sympathetic by means of an ascending filament from the superior cervical ganglion.   

  The Ganglion Nodosum (ganglion of the trunk; inferior ganglion) is cylindrical in form, of a reddish color, and 2.5 cm. in length. Passing through it is the cranial portion of the accessory nerve, which blends with the vagus below the ganglion.

 Branches of Communication.—This ganglion is connected with the hypoglossal, the superior cervical ganglion of the sympathetic, and the loop between the first and second cervical nerves.   
 Branches of Distribution.—The branches of distribution of the vagus are:     

In the Jugular Fossa… Meningeal.

In the Neck………… Pharyngeal.
Superior laryngeal.
Superior cardiac.

In the Thorax………. Inferior cardiac.
Anterior bronchial.
Posterior bronchial.

In the Abdomen……. Gastric.
 The Meningeal Branch (ramus meningeus; dural branch) is a recurrent filament given off from the jugular ganglion; it is distributed to the dura mater in the posterior fossa of the base of the skull.
 The Auricular Branch (ramus auricularis; nerve of Arnold) arises from the jugular ganglion, and is joined soon after its origin by a filament from the petrous ganglion of the glossopharyngeal; it passes behind the internal jugular vein, and enters the mastoid canaliculus on the lateral wall of the jugular fossa. Traversing the substance of the temporal bone, it crosses the facial canal about 4 mm. above the stylomastoid foramen, and here it gives off an ascending branch which joins the facial nerve. The nerve reaches the surface by passing through the tympanomastoid fissure between the mastoid process and the tympanic part of the temporal bone, and divides into two branches: one joins the posterior auricular nerve, the other is distributed to the skin of the back of the auricula and to the posterior part of the external acoustic meatus.
 The Pharyngeal Branch (ramus pharyngeus), the principal motor nerve of the pharynx, arises from the upper part of the ganglion nodosum, and consists principally of filaments from the cranial portion of the accessory nerve. It passes across the internal carotid artery to the upper border of the Constrictor pharyngis medius, where it divides into numerous filaments, which join with branches from the glossopharyngeal, sympathetic, and external laryngeal to form the pharyngeal plexus. From the plexus, branches are distributed to the muscles and mucous membrane of the pharynx and the muscles of the soft palate, except the Tensor veli palatini. A minute filament descends and joins the hypoglossal nerve as it winds around the occipital artery.
  The Superior Laryngeal Nerve (n. laryngeus superior) larger than the preceding, arises from the middle of the ganglion nodosum and in its course receives a branch from the superior cervical ganglion of the sympathetic. It descends, by the side of the pharynx, behind the internal carotid artery, and divides into two branches, external and internal.
 The external branch (ramus externus), the smaller, descends on the larynx, beneath the Sternothyreoideus, to supply the Cricothyreoideus. It gives branches to the pharyngeal plexus and the Constrictor pharyngis inferior, and communicates with the superior cardiac nerve, behind the common carotid artery.
 The internal branch (ramus internus) descends to the hyothyroid membrane, pierces it in company with the superior laryngeal artery, and is distributed to the mucous membrane of the larynx. Of these branches some are distributed to the epiglottis, the base of the tongue, and the epiglottic glands; others pass backward, in the aryepiglottic fold, to supply the mucous membrane surrounding the entrance of the larynx, and that lining the cavity of the larynx as low down as the vocal folds. A filament descends beneath the mucous membrane on the inner surface of the thyroid cartilage and joins the recurrent nerve.
 The Recurrent Nerve (n. recurrens; inferior or recurrent laryngeal nerve) arises, on the right side, in front of the subclavian artery; winds from before backward around that vessel, and ascends obliquely to the side of the trachea behind the common carotid artery, and either in front of or behind the inferior thyroid artery. On the left side, it arises on the left of the arch of the aorta, and winds below the aorta at the point where the ligamentum arteriosum is attached, and then ascends to the side of the trachea. The nerve on either side ascends in the groove between the trachea and esophagus, passes under the lower border of the Constrictor pharyngis inferior, and enters the larynx behind the articulation of the inferior cornu of the thyroid cartilage with the cricoid; it is distributed to all the muscles of the larynx, excepting the Cricothyreoideus. It communicates with the internal branch of the superior laryngeal nerve, and gives off a few filaments to the mucous membrane of the lower part of the larynx.
 As the recurrent nerve hooks around the subclavian artery or aorta, it gives off several cardiac filaments to the deep part of the cardiac plexus. As it ascends in the neck it gives off branches, more numerous on the left than on the right side, to the mucous membrane and muscular coat of the esophagus; branches to the mucous membrane and muscular fibers of the trachea; and some pharyngeal filaments to the Constrictor pharyngis inferior.
 The Superior Cardiac Branches (rami cardiaci superiores; cervical cardiac branches), two or three in number, arise from the vagus, at the upper and lower parts of the neck.
 The upper branches are small, and communicate with the cardiac branches of the sympathetic. They can be traced to the deep part of the cardiac plexus.
 The lower branch arises at the root of the neck, just above the first rib. That from the right vagus passes in front or by the side of the innominate artery, and proceeds to the deep part of the cardiac plexus; that from the left runs down across the left side of the arch of the aorta, and joins the superficial part of the cardiac plexus.
  The Inferior Cardiac Branches (rami cardiaci inferiores; thoracic cardiac branches), on the right side, arise from the trunk of the vagus as it lies by the side of the trachea, and from its recurrent nerve; on the left side from the recurrent nerve only; passing inward, they end in the deep part of the cardiac plexus.
  The Anterior Bronchial Branches (rami bronchiales anteriores; anterior or ventral pulmonary branches), two or three in number, and of small size, are distributed on the anterior surface of the root of the lung. They join with filaments from the sympathetic, and form the anterior pulmonary plexus.
 The Posterior Bronchial Branches (rami bronchiales posteriores; posterior or dorsal pulmonary branches), more numerous and larger than the anterior, are distributed on the posterior surface of the root of the lung; they are joined by filaments from the third and fourth (sometimes also from the first and second) thoracic ganglia of the sympathetic trunk, and form the posterior pulmonary plexus. Branches from this plexus accompany the ramifications of the bronchi through the substance of the lung.
 The Esophageal Branches (rami æsophagei) are given off both above and below the bronchial branches; the lower are numerous and larger than the upper. They form, together with the branches from the opposite nerve, the esophageal plexus. From this plexus filaments are distributed to the back of the pericardium.
 The Gastric Branches (rami gastrici) are distributed to the stomach. The right vagus forms the posterior gastric plexus on the postero-inferior surface of the stomach and the left the anterior gastric plexus on the antero-superior surface.
 The Celiac Branches (rami cæliaci) are mainly derived from the right vagus: they join the celiac plexus and through it supply branches to the pancreas, spleen, kidneys, suprarenal bodies, and intestine.
 The Hepatic Branches (rami hepatici) arise from the left vagus: they join the hepatic plexus and through it are conveyed to the liver.

« Last Edit: November 21, 2013, 09:04:00 AM by dennis100 » Logged
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« Reply #3 on: November 04, 2013, 06:44:09 AM »

A Complete Health E-Guide

Vagal inhibition
May 31, 2012 | Filed under: Forensic Medicine,General Health | Posted by: admin

Vagal inhibition is condition that causes sudden death to occur within seconds or a minute or two due to minor trauma or relatively simple and harmless peripheral stimulation.
Pressure on the baroreceptors situated in the carotid sinuses, carotid sheaths, and the carotid body (located in the internal carotid artery just above the bifurcation of common carotid artery, and situated about the level of angle of mandible) causes an increase in blood pressure in these sinuses with resultant slowing of the heart rate, dilatation of blood vessels and a fall in blood pressure. The vagal inhibition leaves the person dead instantly.
In normal persons, pressure on the carotid sinus causes minimal effects with a decrease in heart rate of less than six beats per minute, and only a slight reduction (less than 10 mm. Hg) in blood pressure. Some individuals show marked hypersensitivity to stimulation of the carotid sinuses, characterized by bradycardia and cardiac arrhythmia ranging from ventricular arrhythmias to cardiac arrest.
vagal inhibition

Stimulation of the corotid sinus baroreceptors causes impulses to pass via Herring nerve to the afferent fibers of the glossopharyngeal nerve (9th cranial nerve) ; these in turn link in the brain stem to the nucleus of the vagus nerve (10th cranial nerve) causing the vagal inhibition.
Parasympathetic efferent impulses then pass to the heart via the cardiac branches of the vagus nerve. Stimulation of these fibers causes a profound bradycardia. This reflex arc is independent of the main motor and sensory nerve pathways. There is wide network of sensory nerves in the skin, pharynx, glottis, pleura, pentoneum covering viscerr or extending into the spermatic cord, cervix, urethra, perineum and coeliac plexus.
Afferent fibers from these tissues pass into the lateral tracts of the spinal cord, effect local reflex connections over several segments and also pass to the brain. The vagal nucleus is controlled by the synaptic connections in the spinal cord, which may be facilitated from both the sensory central cortex and from the thalamic centres. The latter may be responsible for emotional tone noted in the vagal reflex.
Parasympathetic stimulation of the heart can be initiated by high neck compression, pressure on carotid sinus or sometimes by direct pressure over the trunk of the vagus nerve.
Causes of vagal inhibition

(1) The commonest cause of such vagal inhibition is pressure on the neck particularly on the carotid sinuses as in hanging or strangulation.
(2) Unexpected blows to the larynx, chest, abdomen and genital organs.
(3) Extensive injuries to the spine or other parts of the body.
(4) Impaction of food in larynx or unexpected inhalation of fluid into the upper respiratory tract.
(5) Sudden immersion of body in cold water.
(6) The insertion of an instrument into the bronchus, uterus, bladder or rectum.
(7) Puncture of a pleural cavity usually for producing a pneumothorax.
(8 ) Sudden evacuation of pathological fluids, e.g., ascitic or pleural.
(9) Sudden distension of hollow muscular organs, e.g., during attempts at criminal abortion, when instruments are passed through the cervix or fluids are injected into the uterus.
(10) In degenerative diseases of the heart, e.g., sinus bradycardia and partial or complete A-V block; parasympathetic stimulation further depress the heart rate and may induce a Stokes-Adams attack which may be fatal. There is great variation in individual susceptibility.
Death from vagal inhibition is accidental and caused by microtrauma. The stimulus should be sudden and abnormal for the reflex to occur. The reflex is exaggerated by a high state of emotional tension, and also any condition which lowers voluntary cerebral control of reflex responses, such as a mild alcoholic intoxication, a degree of hypoxia or partial narcosis due to incomplete anesthesia.
When death results from vagal inhibition, there are no characteristic postmortem appearances. The cause of death can be inferred only by exclusion of other pathological conditions, and from the accurate observations by reliable witnesses, concerning the circumstance of death.
A soldier was dancing with his girl friend in the presence of many others in a hall. While dancing, he playfully ‘tweaked” (pinched) her neck. She dropped down dead on the spot. There were no injuries or signs of asphyxia. Death was as a result of vagal inhibition.

Related Posts:
•Sudden death
•Modes of death – Asphyxia, Coma and Syncope
•Syncope (fainting) – causes, symptoms and treatment
•Anticholinergic syndrome
•Brain stem death
« Last Edit: November 14, 2013, 10:43:32 PM by dennis100 » Logged
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« Reply #4 on: November 04, 2013, 08:42:12 AM »

How can damage to the vagus nerve cause immediate death?
Cardiovascular Health Questions>Wiki Answers>Categories>Health>Cardiovascular Health

Best Answer

Nervus vagus belongs to parasympathetic nervous system which inhibits the contraction of heart, decreases its excitability and frequency of generated nerve impulses in heart. By overstimulating n.vagus these effects on heart are more intense - it could lead to total inhibiton of heart contractions, which would eventually lead to death within a little while.
Very intense slap behind ear or intensive pressure on neck area could lead to death as n.vagus is overstimulated. It is very rare though.
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« Reply #5 on: November 04, 2013, 09:36:04 AM »

Model Number 101
Event Date 05/02/2005
Event Type  Injury  
Patient Outcome  Life Threatening;
Event Description
Reporter indicated that after increasing programmed parameters, the pt experienced a choking sensation. During the episode, the pt's eyes became dilated and pt passed out. Treating neurologist was unable to get a pulse for a short period of time, but reported that the pt regained consciousness after prgrammed settings were reduced to original parameters. The pt was sent home in good condition after resting in the doctor's office. It was reported that programmed parameters were increased due to an increase in seizures activity; however, investigation to date has been unable to determine whether the increase was above pre-vns baseline frequency. At follow-up office visit two days later, device diagnostic testing with within normal limits, indicating proper device function. Normal mode output current was reduced from 1. 25ma to 1. 0ma.

Event Date 01/07/2011
Event Type Injury
Patient Outcome Life Threatening; Required Intervention
Event Description
It was reported that the pt went to the clinic to have the vns turned on. The pt was programmed to 0. 25 ma and could feel stimulation. When the nurse left the room for a few minutes, the pt's parent alerted that the pt had collapsed on the floor, was non-responsive and chalky white. The nurse thought this may have been due to the vns and turned the device off. The pt was resuscitated and transferred to intensive care unit and now reported to be recovering. The pt's heart rate after device switched off and during resuscitation was 60 bpm. There are no further plans to date.

Model Number 17876
Event Date 02/17/2010
Event Type Death
Event Description
My daughter, (b)(6) , had a vns implanted on (b)(6) 2010. She went to her neurologist on (b)(6) 2010 and had the device turned on. She died suddenly on (b)(6) 2010. It is my belief that this device was responsible for her death. The medical examiner removed the vns during the autopsy and sent it back to the mfr for diagnostics. I asked the medical examiner if i could have the device and i was told no. I asked that the device be sent to a third party that was not involved since i was not allowed to take the unit myself. The mfr is cyberonics. The serial number is: (b)(4), generator number: 17876 and lead number 302. I do not know what cyberonics did with my daughter's device nor have i ever received any info with any findings. It is my belief that the vns caused her heart to stop. She meant everything to me and she died leaving 2 children who were only 5 months and 15 months old. It is my hope that this device be removed from the market. I do not care how many have benefited from use of it, because no amount of good results are ever worth someone's life. We were not even told that there was a risk of death.

Event Date 03/25/2004
Event Type Death
Patient Outcome Death;
Event Description
Reporter indicated that vns patient had passed away. It was reported that the patient was walking into a room and simply dropped dead. Treating neurologist indicted that the death may be cardiac-related, but is not sure as autopsy results are pending. Cause of death is not known at this time. There is no evidence at this time that the ncp system caused or contributed to the reported event.

Event Date 05/29/2001
Event Type Injury
Patient Outcome Other; Required Intervention
Event Description
An article about the histological appearance of a chronically stimulated vagus nerve in a pediatric reporter indicated vns therapy moderated a patient's atonic episodes, but the patient experienced "occasional hospitalizations for status epilepticus. " the patient passed away due to asphyxiation (reported on medwatch 1644487-2008-02703). The vns therapy system was explanted with "1. 5 cm of unstimulated nerve superiorly and inferiorly. " the electrodes were dissected from the nerve "revealing grossly normal nerve above and below the stimulator. " "abundant inflammatory cells were present around the stimulated nerve section. " "severe myelin loss and occasional myelin digestion chambers were seen in the nerve fibers. With modified trichrome and luxo fast blue stains, this loss was estimated to be nearly 90%. " good faith attempts to obtain additional information have been unsuccessful to date.


« Last Edit: October 29, 2015, 04:22:27 AM by dennis100 » Logged
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« Reply #6 on: November 04, 2013, 09:37:16 AM »

DR. COSTELLO: Good afternoon, Dr. Wilkinson and members of the panel. This afternoon, I will be discussing issues regarding the safety and effectiveness of the vagus nerve stimulation device......................One-third of the patients had some type of an increase in seizures, with 17 percent having greater than a 25 percent increase.................This slide shows each of the studies and the percent seizure increase. As you can see, in each of the studies, there were patients who had greater than a 100 percent increase. In the E05 study, the range went up to a 234 percent increase, while in the E04 study, it went even higher, to a 680 percent maximum range.

pg. 125

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« Reply #7 on: November 04, 2013, 09:38:30 AM »

1997 FDA CDRH Neurological Devices Panel

DR. PIANTADOSI: Yes; well, one of the things that's concerning me is that the endpoint being measured in all of these studies is, in some sense, a surrogate, counting the number of seizures. I realize that to the patient and to others, it is a very important endpoint, but it may not be as definitive as some other things that we could measure. And there are numerous examples in the methodologic literature about the weaknesses of accepting clinical trial data based on surrogate outcomes, and I would point to, as a recent and a very dramatic example, the cardiac arrhythmia suppression trial, in which the study was designed and the endpoint was selected on the basis of looking at arrhythmias and suppressing them with a drug. And the studies originally seemed to show that the drug was effective in suppressing arrhythmias. The problem was that it was so good in suppressing arrhythmias that it was killing people, and the mechanism was not understood until much later and wasn't even believed until the results of the randomized trial. So, I am very nervous when I see high mortality rates associated with a supposed benefit, even though we don't have a way biologically right now to connect the two. So, that is why I have harped on this this morning and why I am still very nervous with this high death rate. What's your sense of that? I mean, I'm struggling to get some reassurance that my concerns are not well-founded.

Pg. 135

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« Reply #8 on: November 04, 2013, 09:38:45 AM »

1997 FDA CDRH Neurological Devices  Panel

DR. PIANTADOSI: Could I just ask the FDA very directly--I'm not confused about what the company thinks, and I really am not interested in the nuances of how SUDEP is defined. Is the FDA satisfied that this device is not associated with an elevated risk of death, all-cause mortality, whatever you want?
DR. COSTELLO:............So, to answer your question, I don't believe it has been shown that the high death rate is directly related to the device. However, we only have 2,000 patient years of  experience and a limited number of patients...............I cannot say that I believe that there is an  increased risk right now, but I would not want to rule it out either. I think that would require a longer-term study.
Pg. 142

The VNS was approved 19 days later
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« Reply #9 on: March 12, 2014, 01:26:13 PM »

VNS in Reader's Digest,4490.0.html

Nothing good happens when the vagus nerve is zapped 30 seconds every 3 or 5 minutes, 24 hours a day, 7 days a week, 365 days a year. Doing something that stupid will only result in permanent nerve damage. The reason for all the late onset adverse events is the vagus nerve slowly is becoming destroyed. You eventually will die via vagal inhibition unless it's shut off.

Why hasn't the FDA made any attempt to remove this device from the market? Because the VNS was designed to produce vagal inhibition. The placebo effect is what sells the device. Doctors are aware of that fact. They know what's going on! The VNS is a placebo, a very deadly one!
« Last Edit: October 24, 2015, 01:57:54 PM by dennis100 » Logged
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