Information

Unilateral damage to vagus nerve

Unilateral damage to vagus nerve


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

Context: The vagus nerves supply the neck viscera, heart, lungs and gastrointestinal tract. They join around the oesophagus to form the oesophageal plexus.


Question: Would damage to one vagus nerve in the neck have significant impact on heart rate and gastrointestinal tract function?


Thoughts: If the heart and GIT lie below the oesophageal plexus, which then continue in the inferior direction towards the cardiac and gastric plexuses, then surely a major functional failure in either the heart or GIT would require damage to both vagus nerves (?). I'm trying to make sense of the effect of their fusion, and whether or not this provides a compensating mechanism in the event that one of the two nerves is damaged.


Would damage to one vagus nerve in the neck have significant impact on heart rate and gastrointestinal tract function?

Not that much, because fibers from both sides are fused, so each nerve carries about a 50% of fibers originated from the one side and about 50% from the contro-lateral. Consider that fibers are rewired after each plexus.

References:

wikipedia page about vagus nerve

wikipedia category about vagus nerve


Vagus Nerve Symptoms: How to Detect Damage and Stimulate Your Vagus Nerve

There are 12 cranial nerves. The vagus nerve is the longest of them, and some might say the most important. No matter what the issues are, your vagus nerve is critical to optimal health. Being the longest cranial nerve, the vagus nerve extends from the brainstem to the abdomen, passing through important organs like the heart, lungs, and esophagus. The vagus nerve contains motor and sensory fibers, and has the widest distribution in the body. The nerve commands unconscious body procedures like maintaining your heart rate and controlling digestion.


The importance of understanding vagus nerve activity

Among its many roles in the body, the vagus nerve is involved in suppressing damaging inflammation. Following on from research in which they mapped this inflammatory reflex, a team of researchers have now developed a new recording method for the vagus nerve in mice to further our understanding. This method is detailed in an article published today in Bioelectronic Medicine, an open access journal published by BMC in partnership with the Feinstein Institute for Medical Research. Here we interviewed one the authors of paper, Dr. Harold Silverman, to find out more.

2

Could you tell us about the vagus nerve and its function in the body?

The vagus nerve is the tenth cranial nerve. It is a paired nerve on the right and left. In the human body, each vagus nerve contains 80,000 to 100,000 nerve fibers 80% are sensory, sending information to the brain. In Latin, Vagus means “wanderer,” an apropos name for this nerve, because it travels to the heart, lungs, spleen, liver, stomach, and intestines. The vagus network coordinates everyday bodily functions from digestion to breathing, and even immune function.

Vagus nerve activity varies from person to person, but it can be measured during an electrocardiogram to measure heart rate. The strength of the vagal response is known as vagal tone. Low vagal tone has been associated with many chronic inflammatory conditions, including rheumatoid arthritis.

Inflammation is a key component of the immune response, helping the body heal. However, in the case of excessive inflammation this response becomes harmful. In Dr. Kevin J. Tracey’s Laboratory of Biomedical Sciences at the Feinstein Institute for Medical Research we study the vagus nerve’s role in suppressing the inflammatory response. This work has led to the discovery of the “Inflammatory Reflex.” This reflex is mediated through the vagus nerve to stop damaging inflammation.

The inflammatory reflex is mediated through the vagus nerve to stop damaging inflammation.

Please could you describe what you did in your study?

In our study we looked at developing a standardized methodology for recording the electrical signals that are transmitted through the vagus nerve in mice. By recording this activity, we can begin to understand the language of the peripheral nervous system.

We investigated differences between electrodes used in recording vagus nerve activity, level of anesthesia, nutritional status, and strain effects on baseline vagus nerve activity. Several of these conditions have a significant effect on vagus nerve signals. However electrode configuration can make a significant difference in the quality of the recording.

Anesthetics affect neuronal function, and we demonstrated how isoflurane anesthesia can suppress vagus nerve signaling. Interestingly vagus nerve signals are also affected by feeding behavior. Administration of bacterial endotoxin caused a significant increase in vagus nerve activity. Our results outline a method that is both standardized and can be used to identify these short term electrical changes in vagus nerve activity.

How might these methods inform future research?

The method reported here have broad implications to inform future research on the vagus nerve. Mice are important in studying mechanisms, and our methodology can help us better understand the language of the nervous system in transgenic and knockout mice.

Signaling through the vagus nerve has links to cardiac function, pulmonary function, immune function, and metabolism. Understanding these signals can inform methods to use these signals to stimulate nerves to correct irregular signals.

What are the implications of this research in this field?

Previous work in our lab have mapped the inflammatory reflex. The new recording methods described here, in mice, give another layer to this understanding, as a wide variety of genetic mouse models are available. Taking this together this research with our prior work should accelerate the development of new detection methods, and treatments, for inflammatory disorders.

Dr. Silverman began his studies at Binghamton University, earning a Bachelor of Science degree in Anthropology in 2010 and a Master of Science degree in Biomedical Anthropology in 2012. He went on to earn his Doctor of Philosophy in the Molecular Basis of Medicine from the Donald and Barbra Zucker School of Medicine in 2018. His PhD work was done in Dr. Kevin J. Tracey’s Laboratory of Biomedical Sciences at the Feinstein Institute for Medical Research. There, Dr. Silverman studied the inflammatory reflex, focusing on understanding the role of sensory vagus nerve signaling in inflammation. He has over 10 publications in peer reviewed journals and has guest lectured at Binghamton University, as well as at the Elmezzi School for Molecular Medicine. His work has been presented at various international conferences, including the SHOCK Society meeting, the Society for Neuroscience, and the New York Academy of Sciences 13th Key Symposium on Bioelectronic Medicine- Technology Targeting Molecular Mechanisms.


Critical Care Neurology Part II

K.N. Sheth , E. Nourollahzadeh , in Handbook of Clinical Neurology , 2017

Cranial nerve deficits and peripheral neuropathy

Most periprocedural CN deficits and peripheral neuropathies are transient and management is conservative. Intraoperative measures, such as use of NCS to further delineate the pertinent CNs during CEA, or use of pericardial insulation pads to minimize hypothermic injury to the phrenic nerve, are some of the possible preventive approaches. Patients with failed conservative management of vagus nerve injury can be assessed for surgical options. For instance, patients with vocal cord paralysis can undergo Teflon injection to increase tension and further support the vocal fold. Dysphagia can sometimes be treated with cricopharyngeal myotomy, as it can relieve the persistent spasm from the cricopharyngeus muscle ( Buchholz and Neumann, 1997 ). The recovery of unilateral vocal cord dysfunction due to recurrent laryngeal neuropathy can take up to 1 year ( Shafei et al., 1997 ). Patients with severe phrenic nerve injury may be candidates for diaphragm plication. This procedure can be performed with an open or minimally invasive approach, in which the diaphragm dome is flattened to provide larger expansion volume for the lungs. If plication fails to improve conditions, the diaphragm can be repaired or reinforced with synthetic or bioprosthetic mesh ( Bowen et al., 1982 Tsakiridis et al., 2012 ).


Functions of Vagus Nerve

The vagus nerve is the 10th cranial nerve in the body and has different types of functions. They are as follows.

Sensory Functions:-

The sensory functions of the vagus are divided into two different components.

One is somatic components which refer to the sensations felt by the brain from the skin as well as muscles.

If the sensations felt by the brain due to the organs of the body, then those components are known as visceral components.

Besides these components, the sensory functions performed by the Vagus nerve are as follows-

They help to provide the information from the brain to the skin, middle parts of the throat, and external parts of the ear.

The larynx, heart, esophagus, trachea, lungs, and most of the digestive tract receive visceral information through the brain.

Also contributes to providing the information of taste at the bottom part of the tongue. This part is also known as the root part of the tongue. This function is nothing but a special sensory function of the Vagus nerve.

[Image will be Uploaded Soon]

Motor Functions

The motor functions of the Vagus nerves majorly include the transferring of information for the larynx and pharynx.

Provides information and stimulates a muscle of the fleshy part around the tongue and mouth. These parts include the larynx, firings, and a soft palate.

It also has a major part in reducing the resting heart rate.

A motor function that helps to contract the involuntary muscles of the stomach, intestine and helps to move the food through a tract.

These are the different functions performed by the vagus nerve present in the body. Also, some cardiac functions were known as parasympathetic functions of the Vagus nerve. The vagus nerves supply all types of information to various parts of the body. Every function of the vagus nerves has its cell bodies, unique name, etc.

Bottom Line

Hence, the vagus nerve helps to supply various information to various parts of the brain and vice versa. This is the 10th cranial nerve present in the body. The Roman number is used to represent its notation. One should keep all the cranial nerves properly and healthy. Especially the vagus should be healthy as it performs various functions.


Patients and methods

The medical records of 53 patients diagnosed and treated as unilateral vocal fold paralysis at Ear, Nose and Throat department in King Hussein medical center between January 2003 and October 2010 were studied retrospectively.

The diagnosis of unilateral vocal fold paralysis was based on a detailed history taking and thorough general physical and local examination. All patients were subjected to indirect laryngescopy and or fibreoptic examination or rigid laryngoscope with a stroboscope to confirm the diagnosis.

All patients were investigated to find out the cause of paralysis and theses included plain chest radiographs, thyroid sonography, and esophagoscopy and when central nervous system lesions were expected brain imaging such as computed tomography or magnetic resonance were carried out. Neck and/or chest computed tomography was performed when needed depending on the suspected pathology.

Unilateral vocal fold paralysis was labeled as idiopathic when the clinical and radiological examination failed to reveal the cause after 12 months of follow-up.

Exclusion criteria were cases of unilateral vocal fold paralysis due to

Malignancies of pharyngeal and laryngeal origin.

Patients with intubation injuries and cricoarytenoid joint ankylosis.

Patients with incomplete examinations and follow-ups.

Data regarding age, sex, duration of symptoms, etiology, and side of paralysis were recorded.


You might also Like

I have had Fibromyalgia for over 20 years, but that is a side affect I think, of damaged vagus nerves, this nerve is so important to the body as it regulates all parts of it and if it's not working correctly the damage is mega.

My symptoms are asthma, skin problems, diabetes, heart attacks, obviously the pain and tiredness that comes with FM but FM also mimics other illness that feel so real like kidney pain, liver problems, urinary problems, chest pains that feel like heart attacks, (but having had a few heart attacks there is a subtle difference. One trick is to gulp ice cold water and the pain will go away. If it doesn't then that's your heart attack. Also fizzy drinks do the trick too). There's a long list of things, but O don't want to bore you. I have recently discovered that I have had a hiatal hernia for many years without really noticing I had one (these are called silent hernias). This has caused barrats syndrome so if you have heartburn with no explanation to why you have it, get it checked out.

I have discovered that a hiatal hernia causes all of the above by damaging the vagus nerve that controls and regulates your body. That gets damaged and the rest follows, a hyper vagus nerve causes people to faint a lot. Do your own research on these subjects.

I have swapped over to herbication rather than medication, pharmaceutical treatment just made me worse, so much so that I couldn't get out of bed, now I have a part time job, walk daily and feel as if I can actually function in this world. There's promising new treatment coming up for FM so don't despair, but in the meantime check out your medical herbalist and see what they can do for you. Good luck. anon993839 December 20, 2015

If someone has one of these problems for vagal damage (e.g. swallowing difficulty, painful speaking, etc.), how can it be healed, especially if gabapentin and anti-depressants aren't helping? anon355355 November 15, 2013

Can a damaged vagus nerve cause seizures? anon342027 July 17, 2013

Do vagus nerve disorders also cause chronic nausea and dizziness? Also what doctor would diagnose this condition? anon295379 October 6, 2012

I want to know about vagus nerve damage and how we can avoid vagus nerve problems through yoga. BostonIrish March 5, 2011

This is true, but there are some key differences. You can chop the branches from a tree and the tree will do fine. If you lose particular nerve branches, or even damage them, however, the human system cannot function. It is important to recognize and address issues with nerve damage as soon as possible, especially if you lose feeling altogether in a particular branch. Leonidas226 March 3, 2011

This is an interesting point, because the human nervous system looks much like a tree, with the backbone being the main trunk and shaft of the system. Nerve signals are fed throughout the body after capturing light through the optic system, much like trees capture sunlight and transfer them throughout the tree. Renegade March 2, 2011

The pain which results from nerve damage can be particularly excruciating if it occurs near the back. This is because most nerves travel down a central spinal nerve "highway" to transmit signals between the brain and the rest of the body. FitzMaurice February 28, 2011

The vagus nerve is just one nerve in the huge human nervous system. These all work together like ligaments and branches of a tree to provide perfect functioning of the human body in terms of responses and involuntary processes like digestion. Damage to any one of these nerves can have painful and dangerous results.


Bulbar palsy

Question 27 from the first paper of 2019 asked for the lesions of bulbar palsy, and their coresponding cranial nerves. There was nowehere else to put it, and so it remains here, even though the glossopharyngeal and vagus nerves are not the only ones involved.

Basically, bulbar palsy involves nerves IX, X, XI and XII, which makes little sense because this palsy is bulbar, and therefore involves all things of the bulb, which is an archaic term for the medulla oblongata and occasionally for the brainstem as a whole. Why we persist with this rather than calling it medullary palsy is not entirely clear. In extension of this, it is unclear as to why we still use the archaic term "palsy", as it appears to take its origin from the Latin paralysis, mangled by centuries of illiterate Anglo-Normans.

Anyway. According to LITFL and the CICM examiners, the clinical features of bulbar palsy are pure lower motor nerve signs of the medullary cranial nerves. Kühnlein et al (2008) is probaby the best description of these features writing about ALS patients:

Absent gag reflex: due to bilateral lesions of CN IX and X

Soft palate paralysis which results in "im­precise consonants, hypernasality, and a decreased range of pitch and loudness" (because the weakness of the soft palate and pharyngeal muscules causes insufficient nasopharyngeal closure and reduced oral airflow). The resulting speech is breathy, quiet and the patient is generally unable to generate long phrases because they need to pause to take another breath. This is due to bilateral lesions of CN IX and X a unilateral lesion of the same mechanism would cause a deviation of the uvula.

Paralysis of the laryngeal muscles: this causes a "soft, weak, low-pitched and
mono­tonous voice"
which is the result of CN X paralysis. In bulbar palsy the volcal cords are hypoadducted, which promotes aspiration.

Tongue wasting and fasciculations due to CN XII paralysis which also contributes to the inarticulate speech.

Dysphagia occurs because the process of swallwoing normally requires all the bulbar nerves to work in concert, and their weakness therefore results in an incoordinated swallow. Realistically, this is due to the dysfunction of nerves IX, X and XII, but also V and VII.

Drooling, because there is a loss of tone and strength in the muscles that control lip closure (CN VII). At the same time, due to decreased laryngeal sensitivity and motor function, there is progressive pooling of food and saliva in the vallecula and piriform recesses.


Course of the Vagus Nerves and RLNs

The vagus nerves and RLNs are not directly visualized at CT. Therefore, knowing their expected courses is essential when searching for disease (Fig 1 ) (9).

Drawings illustrate the normal anatomy of the vagus nerves (VN) and RLNs. (a) Left anterior oblique dissected view shows the left vagus nerve exiting the skull base through the jugular foramen and descending through the neck posterolateral to the internal carotid arteries (ICA) and common carotid arteries (CCA). As the left vagus nerve passes anterolateral to the aortic arch, the left RLN branches off and passes below the arch posterior to the ligamentum arteriosum. It then ascends within the left tracheoesophageal groove to enter the larynx posteriorly at the level of the cricoarytenoid joint. The right vagus nerve descends posterolateral to the internal and common carotid arteries from the right jugular foramen, giving rise to the right RLN as it passes anterior to the right subclavian artery (SCA). The right RLN then passes posterior to the right brachiocephalic artery (BCA) before ascending to the larynx within the right tracheoesophageal groove. JV = jugular vein. (b) At the level of the skull base, each vagus nerve is found within the posterolateral aspect of its respective jugular foramen (the pars vascularis) and posterolateral to the internal carotid artery. CCA = common carotid artery, JV = jugular vein. (c) At the level of the origin of the right subclavian artery (SCA), the right vagus nerve passes anterior to the subclavian artery, with the RLN crossing the mediastinum immediately below this point to reach the right tracheoesophageal groove. BCA Bifurc. = brachiocephalic artery bifurcation, CCA = common carotid artery, Tr = trachea. (d) At the level of the aortic arch (AoA), the left vagus nerve gives rise to the RLN, which passes below the arch to reach the left tracheoesophageal groove. SVC = superior vena cava, Tr = trachea.

The RLN is grouped within the vagus nerve as it exits the nucleus ambiguus in the medulla of the brainstem. The vagus nerve (cranial nerve X) crosses the lateral cerebellomedullary cistern and exits the skull base via the pars vascularis of the jugular foramen, located within a dural sheath shared with the spinal accessory nerve (cranial nerve XI) (10). The “superior ganglion” of the vagus nerve is located within the jugular foramen, contains the vagal parasympathetic and sympathetic cell bodies, and is not directly involved in skeletal muscle control. Conversely, the “inferior ganglion,” located immediately below the jugular foramen, is the exit point of the pharyngeal branches and the superior laryngeal nerve, both of which provide muscular innervation. The pharyngeal branches provide motor fibers to the pharyngeal plexus, which supplies the pharyngeal muscles and palate, including the uvula (11). The pharyngeal plexus also contains sensory branches of the glossopharyngeal nerve (cranial nerve IX) and vasomotor sympathetic fibers from the superior cervical ganglion. The superior laryngeal nerve provides motor fibers to the cricothyroid and superior pharyngeal constrictor muscles (12). Extracranially, the vagus nerve (still containing the RLN tracks) descends through the neck posterolateral to the internal carotid arteries within the carotid sheath and is located posteromedial to the adjacent jugular vein.

The RLNs enter the larynx posterior to the cricoarytenoid joints and innervate the intrinsic laryngeal muscles. The cricothyroid muscle is the only intrinsic laryngeal muscle not supplied by the RLN, instead receiving its motor supply from the superior laryngeal nerve branch of the vagus nerve as mentioned earlier (14). The posterior cricoarytenoid muscle is the main vocal cord abductor, receiving its innervation from the ipsilateral RLN. Paralysis of the posterior cricoarytenoid muscle causes the arytenoid cartilage to subluxate anteromedially, resulting in medialization of the posterior aspect of the true cord, and is responsible for many of the CT signs of VCP. Moreover, the posterior cricoarytenoid muscle is the only intrinsic laryngeal muscle capable of separating the vocal cords during normal respiration. If this muscle is paralyzed on both sides, the inability to abduct the vocal folds leads to dyspnea.


Lab 10 - Cranial Nerve Nuclei and Brain Stem Circulation

The axons of the nucleus ambiguus innervate the muscles of the palate, larynx and pharynx via three cranial nerves:

  • The axons of the most rostral portion of the nucleus ambiguus contribute fibers to the glossopharyngeal (IX) nerve.
  • The axons of the mid-portion of the nucleus ambiguus join the vagus (X)nerve.
  • Axons from the caudal pole of the nucleus ambiguus emerge from the lateral surface of the medulla caudal to the lowest filaments of the vagus nerve to join the accessory (XI)nerve. These cranial accessory fibers later join the vagus nerve and innervate the intrinsic muscles of the larynx.

Unilateral damage to the lower motor (nucleus ambiguus) neurons produces an ipsilateral paralysis of the palate, pharynx and larynx. Speech disorders, hoarseness, dyspnea (shortness of breath) and dysphagia (difficulty in swallowing) occur. Bilateral lesions may result in death due to the complete paralysis of the larynx (i.e., inability to abduct the vocal cords during inspiration).

The nucleus ambiguus receives short connecting fibers from the neighboring cranial sensory nuclei, i.e., the spinal trigeminal nucleus and nucleus solitarius. These fibers complete reflex arcs controlling swallowing, coughing, vomiting and control laryngeal motor output.

The cortical input to the nucleus ambiguus is bilateral and indirect. Unilateral damage of the corticobulbar tract produces mild forms of weakness. Bilateral lesions produce a weakness or absence of the ability to speak, swallow and breathe.

Instructional design and illustrations created through the Academic Technology


Watch the video: Nervenentzündung: Schädigt eine Entzündung die Nerven u0026 das Gehirn? Neuritis Symptome u0026 Therapie (June 2022).


Comments:

  1. Maushakar

    This has stumbled upon it! This has come to you!

  2. Keanan

    This message is incomparable)))

  3. Selwin

    A very fun idea



Write a message