Vagus nerve compression in the neck: Symptoms and treatments

Ross Hauser, MD

The vagus nerve plays a key role in regulating many of our body’s functions. Its name best describes its physical characteristics, Vagus is Latin for “fugitive,” or “wanderer.” It is the longest and most widely extended of the nerves of the body. The vagus nerves keep us alive by their innervation (nervous system function) of the internal organs of the body and their interactions with the brain, spinal cord, cranial nerves, upper cervical spinal nerves, and sympathetic nervous system.

Sensory functions of the vagus nerve are critical for conscious perception and for monitoring visceral functions in the cardiopulmonary and gastrointestinal systems. As such the vagus nerve has a critical role in the maintenance of bodily homeostasis (balance) in diverse functions relating to digestion, satiety, respiration, blood pressure, and heart rate control. Its profound role is illustrated by abnormalities in it that can lead to far-reaching consequences including gastroesophageal reflux disease, heart failure, failure of respiratory control, gastroparesis, vasovagal syncope, and chronic pain.

The interconnectedness of the vagus nerve and other nerves helps patients and doctors understand mysterious and bizarre symptoms.  For instance, a woman says that when she puts her contact lenses in, will often have horrible stomach pain. Some doctors may attribute this to psychiatric factors. Is it? Does she need a psychiatrist? For doctors, understanding the neurology of the vagus nerve may discover that this is an exaggerated oculo-emetic (eye reflex) and oculocardiac (the reduction in heart rate when pressure is exerted on the eye) reflex. Because there is a connection between the trigeminal nerve and the vagus nerve, any stimulation of the trigeminal nerve (pressure on the eyeball) can stimulate the vagus nerve.

Likewise, the patient that said every time she “poops I get a headache.” The act of defecation stimulates the vagus nerve and this in turn can cause the firing of the trigeminal nerve and give facial pain or headache. The trigeminal-vagus nerve connection explains a lot of episymptoms.

Vagus nerve compression in the neck

The vagus nerve seems to extend everywhere; consider: the supradiaphragmatic vagus nerve innervates the skin of the external acoustic meatus (auricular branch) and the dura of the posterior cranial fossa (meningeal branch), larynx, pharynx, and upper esophagus (pharyngeal branches), aortic arch (cervical cardiac branches), trachea and esophagus (recurrent laryngeal), lungs and heart. The right vagus nerve (more so than the left) innervates the SA node and the AV node of the heart. (This is why vagus nerve stimulators are placed on the left side). The subdiaphragmatic vagus nerve innervates the liver, pylorus, antrum, pancreas, intestine, and stomach. Efferent vagus branches reach the uterus, adrenal gland, and gallbladder. Vagus nerve fibers innervate the thymus and travel to abdominal adipose tissue. The vagus nerve has many branches that interact with the enteric nervous system and provide central coordination of everything related to the digestive tract, including sensation, absorption, motility, and even sphincter control.

The vagus nerve is a 2-way messenger network, passing messages and signals between the organs and brain to maintain heart rate, blood pressure, circulation, breathing, internal organ distension (for example the moving of food through the digestive system), secretions, and inflammation. As we will see below the vagus nerve helps us talk, swallow, focus vision, hear, and understand. The vagus nerve also sends out messages as part of the parasympathetic nervous system that “calms down” the body after physical exertion or in response to stress in a “fight or flight” situation.

The caption reads: Upper cervical instability is the structural cause of vagus nerve destruction at the nodose ganglion (nerve center).

Article summary

In this article, I will briefly discuss an incredible number of symptoms and conditions in the human body that can be caused by disruption of and interference of the vagus nerve signals. I will also provide more detailed information on each disorder and symptom through links to companion articles on this website.

I will also focus on one mechanism by which vagus nerve dysfunction can be altered. That is through the mechanism of cervicovagopathy. Cervico – a structural problem in the neck that is causing “vago” vagus nerve “pathy” or disease or illness. See my article Cervical Myelopathy – Cervical Degenerative Disc Disease – Cervicovagopathy. Cervicovagopathy is then the neck’s altered or broken structure causing compression or disease on the vagus nerve and then on to produce a myriad of:

In many patients, we can help identify this myriad of symptoms as either structural and/or systemic disease causes.

A very complex medical history

As described above, have seen many patients who have a very complex medical history. In some cases, they would describe a dozen or more disorders. The patient will tell us that if they had gastrointestinal distress, the gastrointestinal specialist treated them. If they had cardiovascular-type symptoms, a slow or racing heartbeat for example, or spells of passing out, they were referred to the heart specialist. For problems with hearing or tinnitus they were sent to the otologist, problems with vision would send them to the ophthalmologist, skin problems were seen by the dermatologist, urinary problems by the urologists, etc. Sometimes a psychiatrist would often be referred.

Sometimes the psychiatrist would be the last referral because the patient has started a process of denial. Not because they denied they had all these things wrong with them, but because they started to deny that the treatments they were getting were in fact getting anywhere.  These people would summarize the above experiences as years of each disorder being treated as its own cause and effect, in isolation, with symptomatic treatment. Rarely were all these problems that these people addressed through a singular cause.

Intuitively patients knew that “something had to be at the bottom of all this.” Somehow dizziness, digestive problems, ringing in the ears, blurry vision, itching, poor body temperature control, brain fog, choking sensations, depression, anxiety, inability to focus and other symptoms had to somehow all be related.

As mentioned above and to reiterate: The vagus nerve supplies every organ from the neck down to the transverse colon (except adrenal glands), including the heart, lungs, stomach, small intestine, gallbladder, liver, spleen, one kidney, and some of the colon. It is involved with speech, swallowing, some taste perception, and some tissues in the throat, neck, and even part of the ear.  Stress raises the body’s level of epinephrine and norepinephrine, which stimulates the sympathetic nervous system to override the parasympathetic nervous system, of which the vagus nerve is the main component. So most people’s normal lives are characterized by an under-active vagus nerve, which becomes worse when rotatory atlantoaxial instability or other forms of cervical instability, disrupt vagus nerve impulses. Since the vagus nerve runs very close to the C1-C3 vertebrae, can easily be affected by upper cervical malrotations from instability.

The vagus nerve could be called the nervous systems commander-in-chief in the field, monitoring all the important systems of the body including inflammation, heart rate variability, digestion, bowel movements (flow of food through the digestive tract), breathing, thinking, feeling, hunger, satiety, and hormone secretion. There is a drastic difference in how the body functions between someone with increased vagal tone (health) and decreased vagal tone (disease). Let’s get to the clinical and research aspects of this article.

Sensory functions of the vagus nerve

The vagus network

In the neck, the vagus nerve connects to the inferior, middle, and superior cervical sympathetic ganglion (SCSG), as well as the upper cervical nerves and many of the cranial nerves, and descends all the way down to the celiac plexus, the nerves that innervate the abdomen.

Vagus nerve compression from disease

Vagus nerve compression can occur in the carotid spaces not just from dysstructure of the cervical spine but also from space-occupying lesions. For instance, paragangliomas, schwannoma, or neurofibromas at the jugular foramen or at the ganglion nodosum (at the level of the C1 lateral mass) can compress the vagus nerve giving symptoms of dysphagia, hoarseness, vocal cord paralysis, pulsatile tinnitus, hearing loss or vertigo. (1) For this reason it is important for a person with vagopathy (vagus nerve dysfunction) to get high-resolution magnetic resonance imaging of the neural and ligament anatomy of the neck, especially in the craniocervical junction.  MRI is the gold standard technique in the study of the cranial nerves.  Most MRIs that are done on people’s necks, do not have the resolution that is needed to see adequately the small structures (in the order of 1-3mm) such as the transverse and alar ligaments, sympathetic ganglion and cranial nerves such as the vagus and glossopharyngeal.

The vagus nerve, the inferior cervical sympathetic ganglion, and cardiovascular-like problems, breathing, and thyroid dysfunction.

The inferior cervical sympathetic ganglion is a nerve complex located between the C7 and the top rib. Messages between the vagus nerve and inferior cervical sympathetic ganglion influence blood flow between the heart, brain, and neck.

Altered messages between the vagus nerve and the inferior cervical sympathetic ganglion can impact the function of the following:

  • Subclavian arteries supply blood to the thorax, head, neck, shoulder, and arms.

Fainting, loss of blood flow to the brain:

  • Subclavian arteries branch off into the vertebral artery which supplies blood to the back of the brain through the basilar, posterior cerebral, and cerebellar arteries. Dysfunction can cause blackouts, fainting, and vascular problems.

Thyroid 

  • The vagus nerve connects to the external laryngeal nerves which act upon the inferior thyroid artery.

Symptom: Cardiovascular risks and Cardiovascular risks linked to hypothyroidism.

The thyroid receives its nerve supply mainly from the middle cervical ganglion but also is innervated by the superior and inferior cervical ganglions.

A study published in the North American Journal of Medical Sciences (2) investigated the link between sympathovagal imbalance (Sympathovagal imbalance is the disruption and dysfunction in which the sympathetic and vagal components of the autonomic nervous system run either too high or too low. In other words, too much “flight-fight” or too little problems with energy, fatigue, and digestion among many symptoms) to cardiovascular risks and the plausible mechanisms of cardiovascular risks in hypothyroidism. What the researchers suggested was Sympathovagal imbalance could be implicated in:

  • Increased diastolic pressure (the bottom number of a blood pressure reading).
  • Decreased HRV (Heart rate variable) and increased low-frequency to high-frequency ratio (LF-HF) of HRV.
  • Dyslipidemia (Cholesterol problems).
  • Increased high-sensitive C-reactive protein (inflammation)

All these symptoms were observed in hypothyroid patients and all these parameters had a significant correlation with the heart rate variability. Sympathovagal imbalance due to sympathetic activation and vagal withdrawal occurs in hypothyroidism.

A February 2018 study in the journal Biomed Central Research (3) notes examined the effect of propranolol (blood pressure medication) on heart rate variability (HRV) in hyperthyroidism before antithyroid treatment. This was a before-and-after study, on ten patients presenting overt hyperthyroidism who had no previous treatment.

HRV parameters including sympathovagal balance estimate by low-frequency to high-frequency ratio (LF-HF) ratio remained unchanged. Although a significant reduction in heart excitability, propanolol failed to restore a good sympathovagal balance in hyperthyroidism.

Various surgeries and the vagus nerve

Neurosurgeons, orthopedic Surgeons, and Ear Nose, and Throat surgeons who operate on the anterior neck and base of the skull are keenly aware of the vagus nerve. These surgeries including thyroid surgery, carotid endarterectomy, anterior cervical fusion and base of skull operations stretch the vagus nerve. Recurrent laryngeal nerve stretch injury is an ever-present problem for them because of the operations they do. Mechanisms of injury include traction injuries from retractors, clamping injuries, interruption of neurovascular supply, compression injury, sharp dissection, electrosurgery and even stretch from intubation.  Pathophysiology of injury is thermal damage, stretch, cutting, compression, and vascular compromise.

In my practice, we have seen patients where overextension of the neck occurred not only in surgery, or a simple diagnostic procedure such as endoscopy or laryngoscopy but also with a simple dental examination or procedure, going to a beauty salon and the washing of your hair.

The experience and research on nerve physiology give insight into how fragility of the vagus nerve.  Studies thus have been done to try to elicit why there are so many nerve (including vagal) injuries during anterior neck surgeries and show (4)

  1. For surgical exposures (retraction) the recurrent laryngeal nerve is at 13% to 44% stretch
  2. 6% for one hour shows a 70% action potential amplitude decrease
  3. 12% stretch for one hour blocks action potential completely
  4. 15% stretch causes complete intraneural ischemia
  5. 50 grams of tension for 5 minutes causes a significant loss of function

A March 2024 study (5) in the journal Annals of Surgical Oncology describes a group of 85 patients who had developed left recurrent laryngeal nerve palsy after minimally invasive McKeown esophagectomy.

  • Twenty-two (25.8%) patients successfully recovered from left recurrent laryngeal nerve palsy.
    • Patients who did not fully recover were seen to be smokers
    • or it was the surgical approach identified as a key cause of complication.

A March 2022 study in the Plastic and Reconstructive Surgery Global Open (6) discusses surgical injury. “Iatrogenic glossopharyngeal nerve injuries are commonly associated with procedures such as a tonsillectomy, carotid endarterectomy, and endotracheal intubation.” In this case report, doctors present a previously unreported complication of a thread lift procedure (cosmetic procedure) in the jowl region, causing damage to the glossopharyngeal nerve through compression. The glossopharyngeal nerve because of its connection to the vagus nerve, may cause cardiovascular complications associated with the vagus nerve.”

The connection to neck pain and a history of cervical spine surgery and injury.

Many of the people that we see in our practice have been on a long medical journey as described above. They are at our center because a connection between neck pain and neck injury has been made. There is a suspicion that a structural cause, that is cervical instability, or floating vertebrae or neck bones, is the cause of the compression on the vagus nerve and a condition of Cervicovagopathy. This would be seen in patients with a medical history of post-concussion syndrome, Whiplash Associated Disorder, cervical spine fusion or cervical spine laminectomy, and hypermobility Ehlers-Danlos Syndrome.

How does one come to a condition of Cervicovagopathy or wandering floating neck bones?  This condition is caused by weakened, loose, and damaged cervical spine ligaments. Ligaments are the soft-tissue structure that holds the vertebrae in place. When these ligaments no longer hold the vertebrae in place the structure of the neck falters and the natural curve of the cervical spine is lost. This condition is described in the image below.

The caption reads Cervical degenerative dysstructure: The progressive nature of cervical instability that leads to a breakdown of the cervical curve resulting in destructive forces (compression, grinding, and impingement of blood vessels and nerves) being placed on vital neurovascular structures including the cervical spinal cord and vagus nerves.

To the left, we see:

  • NORMAL posture.
  • MILD cervical spine instability, the head is moving forward causing a mild stretch of the nerves and blood vessels. When blood vessels are stretched, the vessels narrow.
  • MILITARY Neck: This condition is called a military neck because the neck is standing up straight. This is not a good thing. The spine acts as a shock absorber and is built like a spring with a curve to it.
  • KYPHOTIC. The cervical spine instability has become so severe, that the curve of the neck has reversed itself and is now backward.

This all occurs because of damage to the cervical spine ligaments that hold the bones in proper alignment.


Treatment for loss of natural neck curve structure is directed to improve the structural integrity of the cervical spine and the symptoms and conditions it causes, including cervicovagopathy and increased intracranial pressure. Treatment modalities can include dynamic (chiropractic) ortho-neurological adjustments for the vertebral subluxations (malrotations), curve correction to restore lordosis, and Prolotherapy to repair injured ligaments. The diagnostic tests used to discover cervical instability and resultant pathophysiology can also be used to monitor progress during treatment. These treatment options are discussed below.

Please see our article on treatments for Atlas displacement c1 forward misalignment.

The etiology of the cause of vagal or parasympathetic dysfunction has many chemical and emotional etiologies

The etiology of the cause of vagal or parasympathetic dysfunction has many chemical and emotional etiologies, including diabetes, heavy metals, medications, and emotional or financial stress, but a cause that is overlooked is structural injury. As the list of symptoms and diseases, including chronic pain, depression, tinnitus, migraine headache, seizures, heart failure, Alzheimer’s dementia, and systemic inflammation continues to grow, it is prudent that clinicians and the patients they treat understand the vagus nerve anatomy, injury, and the pathophysiology it causes.

External laryngeal nerves – voice, breathing, swallowing problems

  • The plexus (bundle of nerves and blood vessels) on the inferior thyroid artery talks with the recurrent and external laryngeal nerves, with the superior cardiac nerve, and with the plexus on the common carotid artery.
  • Laryngeal nerve dysfunction can cause loss of voice, hoarseness, swallowing difficulties,
  • a sense of breathing obstruction.

The phrenic nerve – breathing, swallowing, and problems with hiccups

  • The phrenic nerve sends messages through the thorax to assist in regulating breathing, and controlling the cough reflex, and the hiccup reflex. For a detailed discussion on the interaction between the phrenic nerve and the vagus nerve, please see my article Hiccups, Cough, Neck Pain, and Vagus and Phrenic Nerve Injury.

What are we seeing in this image?

This is the superior cervical sympathetic ganglion in its native habitat. Surrounded by blood vessels (internal carotid artery and internal jugular vein) and nerve networks and near the C2 vertebrae. When the vertebrae wander out of position, it takes these veins, arteries, nerves, and nerve bundles with it, causing compression and stretching of these vital structures. In the context of this article, this compression and stretching can not only cause pain but disrupt nerve signals causing cardiovascular-like symptoms and conditions already outlined in this article.

The vagus nerve has five main components contained within the nerve, which make up the five fascicles or nerve bundles seen in the vagus nerve cross-sections. (See figure). These are branchial motor, visceral sensory, visceral motor, and special and general sensory fibers. (See Figure). These five vagus nerve components can be summarized:

  1. Special visceral afferent (SVA, motor) – these motors are special because they supply motor innervation to skeletal muscles of branchial arch origin which include all the muscles of the pharynx, larynx, and soft palate.
  2. General visceral efferent (GVE, motor) – contains the parasympathetic motor part of the nerve that innervates the smooth muscles of the trachea, bronchi, and gastrointestinal tract and regulates heart rhythm. When we talk about the vagal tone we are talking about this part of the vagus nerve primarily. It is the part that slows the heart rate and is responsible for sinus arrhythmia with breathing. 
  3. General visceral afferent (GVA, sensory) – general sensory to the abdominal viscera including the trachea, larynx, and esophagus digestive tract.
  4. Special visceral afferent (SVA, sensory) – taste sensation to the epiglottis and root of the tongue.
  5. General sensory afferent (GSA)– these fibers carry general sensation ( touch, pressure, pain, and temperature) from cutaneous structures and mucous membranes of the head, and general proprioception from somatic structures such as muscles, tendons, and joints of the head and neck. The trigeminal, facial, glossopharyngeal, and vagus nerves transmit GSA input to the spinal nucleus of the trigeminal nerve. One important innervation is to the skin of the external acoustic meatus, which is used for transcutaneous auricular vagus nerve stimulation.

Cervicovagopathy is defined as degeneration of the vagus nerve and/or interruption of vagal nerve impulses

The role of vagus nerve function in health and disease cannot be overemphasized. The hallmarks of dysautonomia (conditions and symptoms caused by problems with the autonomic nervous system (ANS))—parasympathetic dysfunction causing sympathetic dominance, or what is termed “sympathovagal imbalance”—are paramount to understanding the pathophysiology of most medical conditions. The role of sympathovagal imbalance, discussed briefly above will continue to be a dominating theme within this article.

Cervicovagopathy is defined as degeneration of the vagus nerve and/or interruption of vagal nerve impulses from the effects of damaged ligaments causing cervical instability, with or without significant cervical dysstructure or advanced cervical structural problems, leading to harmful effects on the body. Cervicovagopathy is one of the most devastating effects of cervical instability, upper cervical instability, and cervical dysstructure.

In the image below we see x-ray evidence of cervical spine misalignment, cervical dysstructure, and cervical spine instability.

  • In the top panel, we see a misalignment of the C2.
  • In the center panel, we see cervical dysstructure and a comparison of where a normal cervical curve should be and a significant curve structural problem causing the vertebrae to be displaced by 2 – 3 inches. The vagus nerve is associated with C1.
  • In the lower panel, we see how far off-set the vertebrae are from each other and from C2-C6.

Now let’s re-examine the discussion we had above about Heart Rate Variable

Homeostasis of the human body is under the control of the autonomic nervous system (ANS); while the sympathetic nerve system (SNS) allows us to handle stress, the parasympathetic nervous system (PNS) allows us to live. As the vagus nerve is the primary sensory input and effector for the parasympathetic nervous system, its compromise has many long-ranging detrimental effects on human homeostasis and health.

When the autonomic nervous system (ANS) balance becomes sympathetic dominant, a rise in the LF/HF ratio is seen on Heart Rate Variable parameters. This rise in LF/HF ratio is frequently found in many chronic diseases, which brings up the hypothesis that the chronic symptoms these conditions produce may have as their etiology the breakdown of the cervical curve, affecting the precise balance between sympathetic and parasympathetic function—a condition known as dysautonomia. If this is true, then treatment should be directed at improving the cervical structure and stability to restore the body’s vagal tone.

“You may need the vagus nerve to understand the pathophysiology and to treat diseases.”

“You may need the vagus nerve to understand the pathophysiology and to treat diseases.” This is the title of a 2012 scientific article published in the journal Clinical Science (7) whose premise is, “Can different pathophysiological mechanisms and risk factors leading to various diseases be linked with altered nerve transmission of signals by one common pathway?”

The authors hypothesized that adequate vagal nerve activity reduces the risk of major diseases via common basic mechanisms and interim risk factors.

  • There are 3 basic mechanisms that contribute to many chronic diseases, that is local oxidative stress and DNA damage, inflammatory reactions, and excessive sympathetic responses, all of which are inhibited by vagal nerve activity.
  • Efferent vagal activity can be easily monitored noninvasively by measuring HRV.
  • It is this interconnection between the vagus nerve and the whole body that allows vagus nerve stimulation to relieve chronic pain and reduce the number of cardiovascular-like, gastrointestinal-like, neurological-like, endocrine-like, and urinary-like disorders that we will discuss throughout this article.

As a side-note to this research, an October 2021 paper in the journal Public Library of Science One PLoS 1 (8) found that “Patients with COVID-19 present with a variety of clinical manifestations, ranging from mild or asymptomatic disease to severe illness and death. Whilst previous studies have clarified these and several other aspects of COVID-19, one of the ongoing challenges regarding COVID-19 is to determine which patients are at risk of adverse outcomes of COVID-19 infection. It is hypothesized that this is the result of insufficient inhibition of the immune response, with the vagus nerve being an important neuro-immuno-modulator of inflammation. Vagus nerve activity can be non-invasively indexed by heart-rate-variability (HRV).”

The researchers of this study found higher HRV predicts greater chances of survival, especially in patients aged 70 years and older with COVID-19, independent of major prognostic factors. Low HRV predicts ICU indication and admission in the first week after hospitalization.

This study above is an example of how vagus nerve disruption can cause a myriad of symptoms not only related to inflammation but the general well-being.

The image below offers an explanation as to how the vagus nerve impacts so many body functions.

The caption of the image reads: The vagus nerve origin in the brainstem: The vagus nerve exits and enters the medulla part of the brain stem and from there goes into the neck and into the body and up from there it goes into other parts of the brainstem and brain. The vagus nerves’ unique location at the main relay station of the body the craniocervical brainstem junction is why it has such a wide-ranging influence over how the body feels reacts and functions in both stressful situations and peaceful situations.

The vagus nerve origin in the brainstem

Of note in the above illustration to the right is the nodose ganglion. The vagus nerve facilitates messages back and forth from the brain to the heart. Afferents (messages in) go through the nodose ganglion (nerve bundle) which sits in front of the atlas (C1 vertebra). If the C1 vertebra is unstable and causes problems of “nerve pinching” this is how upper cervical instability can affect the heart rate variability. The C1 vertebrae would sit between the left and right sides Nodose Ganglion.

Location, location, location. Compression, compression, compression.

What are we seeing in this image? The superior cervical sympathetic ganglion is isolated so we can observe its proximity to the C2 vertebrae.  Cervical instability that can lead to a “wandering” C1, C2, and C3 vertebrae will impact the proper nervous system function of the vagus nerve and the superior cervical sympathetic ganglion.

Compression and stretching of the vagus nerve in the neck

The vagus nerves are most vulnerable to stretch, traction or pull, and compression in the cervical region, as they lie in a specific space called the carotid space. The carotid space is a paired space defined by the carotid sheath, a connective tissue boundary in the neck that is made up of superficial, middle, and deep layers of the cervical fascia.

Carotid sheath compression

What are we seeing in this image? An ultrasound of the neck shows the three main structures in the carotid sheath. The internal jugular vein, the Vagus Nerve, and the carotid artery.

The carotid sheath encases the carotid artery, jugular vein, vagus nerve, and the sympathetic plexus of nerves. Instability of the cervical spine can cause compression on the carotid sheath due to its location. The cervical compression can cause arterial ischemia (inadequate blood flow to the brain) leading to drop attacks, brain fog, and other symptoms.

The vagus nerve and many other structures are vulnerable to injury here, especially at the craniocervical junction around the atlantoaxial joint, the most mobile and vulnerable of the spinal joints to injury.

What are we seeing in this image?

Cervical instability-induced vagus nerve compression:

The most common structural condition that leads to poor vagus nerve function is upper cervical instability. (As we will discuss later in this article, we believe an effective treatment for cervical spine instability is Prolotherapy. An injection treatment to strengthen weak and cervical spine ligaments.)

In the four-panel illustration, panel A shows a far view of the nerves of the anatomy. In the B panel,  a close-up lateral side view of the cervical spine and the interwoven nerve network. In C: Rotation and smashing or compression of the vagus nerve. In panel D the view from the bottom up.

Cervical instability induced vagus nerve compression:

The upper cervical segments are the most mobile, thus the “loosest” sections of the spinal column, and the most vulnerable to instability. When the atlantoaxial joint becomes unstable, muscles in both the anterior and posterior neck, including the longus colli, are recruited to help stabilize the joint. Please see my article and video on Upper cervical instability and Atlantoaxial instability symptoms including compression of the brainstem.

  • Prolonged forward head posture causes flexion (forward bending) in the mid-lower cervical spine and extension (backward tilt of head)  of the upper cervical (sub-occipital) spine, as well as shortened cervical flexors (muscle bundles)—which is another point of stretch for structures in the carotid sheath, including the vagus nerves.
  • As the vagus nerves are interconnected to some of the most important nerve structures of the face, head, and brain, interruption of vagus inputs can result in wide-ranging detrimental consequences.

The Vagus nerve is the “sixth sense” the “gut feeling.”

The vagus nerve is our sixth sense and our “gut feeling.” Since the vagus nerve meanders and extends its branches to multiple tissues and organs, its role in health must be immense. It regulates homeostasis by connecting three interwoven systems: the nervous, endocrine, and immune systems. Brief demonstrations of this impact were given in some of the research citations above and will be demonstrated again below.

The exchange of information between the nervous, endocrine, and immune systems plays an important role in various physiological, as well as pathological, processes.

The Vagus nerve and its branches to other nerves

In the cervical region, the vagus nerve supplies branches to the:

  • Facial nerve. The interaction of the two nerves controls facial expression and the taste sensation on the tongue
  • Glossopharyngeal nerve.
    • The vagus nerve and glossopharyngeal nerve control the muscles of the throat. Dysfunction can cause swallowing difficulties.
    • The nerves serve to help drain blood from the brain into the carotid sinus into the carotid artery in your neck. Dysfunction would cause brain drainage problems and high blood pressure problems.
    • The nerves serve to sense fullness in the ear. Tinnitus and Meniere’s Disease may be a by-product of nerve dysfunction.
    • The nerves serve to regulate the parotid (saliva) gland. Dysfunction can cause too much or too little or no saliva production.
    • The Facial nerve was described above as providing a taste sensation in the tongue. It does this by regulating two-thirds of the tongue’s surface. The glossopharyngeal nerve helps you taste food in the back third of your tongue.
    • Voice and swallowing dysfunction can occur if the vagus and glossopharyngeal nerve send distorted messages to the stylopharyngeus muscle which lifts the larynx out of the way when you are eating.
  • The spinal accessory nerve. The nerve is responsible for muscle movement of the neck and shoulders.
  • Trigeminal nerve. Cervical instability can also be responsible for almost all painful neuralgias of the head and face including occipital and trigeminal neuralgia, as well as structural headaches including tension, migraines, and clusters. A 2019 German study (9) wrote: “In patients with episodic cluster headache, successful transient therapy with transcutaneous stimulation of the vagus nerve may be required.”
  • Hypoglossal nerves are the nerves that move your tongue.

The vagus nerve is mostly tied to the glossopharyngeal nerve, as they travel together down the carotid sheath and innervate the pharynx and esophagus. Irritation of these nerves can therefore lead to such horrific stabbing or lightning-like pharyngeal pain that it can make it hard to swallow and is associated with nausea and vomiting. The condition is called is vago-glossopharyngeal neuralgia. The attacks of pain are brought on by swallowing, talking, coughing, sneezing, touching the tragus of the ear, and turning the head or rolling toward the side of the pain.

Vascular compression is indicated in cervical spine instability.

A 2011 French study by Neurologists affiliated with the University of Lyon (10) evaluated the anatomy of the central myelin (the insulation that protects the nerves) portion and the central myelin-peripheral myelin transitional zone (the sensory and parasympathetic division of a nerve) of the trigeminal, facial, glossopharyngeal and vagus nerves.

The aim was also to investigate the relationship between the length and volume of the central myelin portion of these nerves with the incidences of the corresponding cranial dysfunctional syndromes caused by their compression to provide some more insights for a better understanding of mechanisms.

The researchers were looking at the damage caused by compression on these structures to help explain how such problems as Trigeminal Neuralgia, Peripheral and Central Facial Nerve Palsy (Side of and lower half muscle paralysis or weakness in the face), eye muscle problems such as headaches, eye strain, blurred vision, and double vision, floating eye or problems with eye movement.

The findings: “At present, it is rather well-established that primary trigeminal neuralgia, hemifacial spasm, and vago-glossopharyngeal neuralgia have as one of the main causes of vascular compression.”

Vascular compression would be the entanglement of these nerves and the blood vessels leading out of the brain and into the neck. Vascular compression is indicated in cervical spine instability.

Vascular compression not only compresses nerves it also wears away bone

I would like to offer a side note about vascular compression and how it can cause a great number of symptoms it does and to demonstrate that this is something seen by many doctors. In May 2014, doctors at the Hospital for Special Surgery published a case history (11) of a patient with a stretched-out vertebral artery that rubbed away and destroyed a portion of her C1-C2 facet complex and caused cervical instability resulting in a clinical presentation of severe occipital headache.

Such is the power of vascular compression.

The superior cervical sympathetic ganglion

In the neck specifically, there are direct communications between vagus nerves and the superior cervical sympathetic ganglion, glossopharyngeal nerves, spinal accessory nerves, and cervical spinal nerves #1, 2, 3, and 4. The most important of these communications is with the superior cervical sympathetic ganglion.

Above I touched on the role of these nerves and superior cervical sympathetic ganglion in symptoms and disease when they are in a state of dysfunction. Here I will go further in helping the understanding of the relationship between the vagus nerve and the superior cervical sympathetic ganglion.

The superior cervical sympathetic ganglion innervates the eye and lacrimal (tear) gland and causes vasoconstriction of the iris and sclera, pupillary dilation, widening of the palpebral fissure (the “whites of your eyes” the open area between the lower and upper eyelid), and reduces tear production. It has been implicated in many conditions and symptoms, including elevations of intraocular pressure (pressure within the eye), glaucoma, photophobia, and macular degeneration.

Eye problems: Kinking of the carotid sheath at the craniocervical junction.

Let’s take a moment to discuss these eye and vision problems before we move on. The caption of this image reads: The carotid sheath contents include the internal carotid artery, internal jugular vein, vagus nerve, glossopharyngeal nerve, and spinal accessory nerves. They can be functionally compromised as they make a sharp turn up to a 90-degree angle in the C1 atlas transverse process area into the brain through the jugular and carotid foramen pathways. This kinking or compression of these nerves, including the vagus nerve, and the blood vessels can lead to increased intracranial pressure, localized Cerebrospinal fluid and resultant cerebral atrophy, and increased eye pressure.

The vulnerability of the vagus nerve and the sympathetic ganglia

The superior cervical sympathetic ganglion is not a structure that one would like to leave vulnerable to compression. The superior cervical sympathetic ganglion connects with numerous organs, vessels, muscles, bones, joints, the last 4 cranial nerves, the vertebral plexus, the vagus nerve, the facial ganglion, and the phrenic nerve. It supplies the upper cervical spinal nerves (C1-C3) with gray rami communications (“uninsulated” nerve fibers to the spinal nerves) and sends off vascular fibers to the internal and external carotid arteries. Autonomic branches pass the ganglion to the larynx, pharynx, and heart, and together with vascular plexuses to the salivary and lacrimal glands, pituitary, thyroid, and parathyroid gland, as well as to primary and secondary lymph organs in the cervical region, including the thymus and submaxillary/submandibular lymph nodes. There are also connections with the middle cervical ganglion and the tympanic plexus. It can give fibers to a branch of the vagus nerve from the external branch of the superior laryngeal nerve. Lastly, but very importantly, the SCSG sends projections to the pineal gland and the suprachiasmatic nucleus that are key to normal (ideal) circadian rhythms. A person’s biological clock can be negatively affected, causing circadian rhythm sleep disorders and circadian dysrhythmias, from cervical instability impacting the superior cervical sympathetic ganglion.

As you can see, many body functions can be altered and functionally compromised by compression or damage to the superior cervical sympathetic ganglion.

The vagus nerves and sympathetic ganglia in the neck and upper thoracic area sit on either side of the longus muscles, capitis, or colli, which flex the neck. The longus capitis and longus colli muscles attach to the occiput (back of the skull) and atlas, respectively, and originate in the transverse process of the lower cervical and upper thoracic vertebrae. These muscles are extremely tight in forward head posture.

In the image below we see muscle tightness from chronic forward head posture – the posture of looking down at cell phones. 

As it is the longest nerve in the body, the vagus nerve is especially prone to being “stuck”

As it is the longest nerve in the body, the vagus nerve is especially prone to being “stuck,” or not able to translate normally because of musculoskeletal changes that occur in the neck with the forward head-face down lifestyle, and is prone to injury by all these mechanisms. The net effect is that if the forces on the vagus nerve do not stop, there is a risk of vagal (and other) neurons dying.

The forward head posture can be a cause of cervical dysstructure or a broken neck structure. It can lead to progressively worse nerve damage in the cervical nerves, vagus nerve, and superior cervical sympathetic ganglion.

In the image below we can follow a path:

We start with Normal Healthy Nerves and normal nerve function > as the cervical spine structure starts to fail or becomes broken the patient can move onto Neuralgia. Here the nerve is now stretched and has the start of compression but the nerve is not yet damaged > Next is Neuritis, inflammatory damage around the nerve is present, and the nerve sheath becomes damaged. > At the end state we have Neuropathy, the death of neurons. When neurons die there are fewer communications and neurologic-like disorders become dominant.

When a nerve is subjected to long-term compression or stretch forces

When a nerve is subjected to long-term compression or stretch forces, whether from changes in bony or muscular anatomy or within the nerve sheath (cerebrospinal fluid [CSF]) or nerve (arterial/venous compromise, swelling) itself, neuron cell death can occur.

The pressure on the vagus nerve.

First an explanation: Axonal transport is a body system that is the main component of essential neuronal function (the ability of your nerve cells to communicate with your brain and your brain to be able to respond back). The Axon is a “cable” within the neuron. The Axonal transport, among its functions, removes old proteins and lipids from the neuron and replaces them with fresh proteins and lipids

The anatomy of a neuron, the anatomy of a nerve. In this illustration, we see the anatomy of a nerve. Attached to the nucleus in the Axon and as you can see the “long” cable or “chute” old proteins and lipids are pulled away from the nucleus and new proteins and lipids are sent to the nucleus.

The anatomy of a neuron, the anatomy of a nerve

When a nerve is subjected to long-term compression or stretch forces, whether from changes in bony or muscular anatomy or within the nerve sheath (cerebrospinal fluid [CSF]) or nerve (arterial/venous compromise, swelling) itself, neuron cell death can occur. It has been shown that both slow and fast axonal transport is impaired in the cervical vagus nerves by low pressures of compression, such as those levels of compression comparable with those found in human compression neuropathies such as carpal tunnel syndrome.

Compression of the vagus nerve can stop or impede the Axonal transport system. 

In animal studies in the 1980s and 1990s researchers found that when rabbit vagus nerves were compressed and then the compression was removed, lingering effects occurred.  Nerve transmission could be blocked or altered for one or more days depending on the level of compression and how long that compression lasted. Compression can occur as a result of pinching or stretching.  Stretch or other deformation injuries to the axons can cause loss of axon transport and the accumulation of toxic substances that can destroy either transport or the axon itself. Also note that cervical kyphosis and compensatory hyperextension of the cervical spine can cause bending and strain of the lower brainstem and upper spinal cord, in addition to other damaging effects on localized nerves and nerve ganglia. 

In medical research, Axonal transport is often described as motor proteins “trucking” their cargo of proteins and lipids back and forth along the axon. For good reason, that is what is occurring. A disruption in this trucking is seen in a 2019 paper in the journal Nature Reviews. Neurology. (12)

“motor proteins actively navigate microtubules (in simplest terms storage structures) to deliver diverse cargoes, such as organelles (the stuff that makes cell function happen), from one end of the axon to the other and is widely regarded as essential for nerve development, function, and survival. Mutations in genes encoding key components of the transport machinery, including motor proteins, motor adaptors, and microtubules, have been discovered to cause neurological disease. Moreover, disruptions in axonal cargo trafficking have been extensively reported across a wide range of nervous system disorders. However, whether these impairments have a major causative role in, are contributing to, or are simply a consequence of neuronal degeneration remains unclear. Therefore, the fundamental relevance of defective trafficking along axons to nerve dysfunction and pathology is often debated.”

What is being suggested is, is the disruption of the axonal transport system within the nerves, the vagus nerve specifically, is the cause of neurological disease and neurological-like symptoms or is it a result of neurological disease. Both scenarios may be correct. Equally, can disruption of the axonal transport system be caused by cervical neck instability?

Compression and stretch. 

In the illustration below, the more the head moves forward, the result of degenerative cervical ligament damage, and the more the brain stem and the vagus nerves get stretched.

the more the head moves forward, the result of degenerative cervical ligament damage, the more the brain stem and the vagus nerves gets stretched.

Above we discuss disruption, compression, and stretch of the signals of the vagus nerve and its branches to and from other nerves and the nerve center ganglia. Now, what about the vagus nerve and blood flow?

If the vagus nerve is the most important nerve in the body, then surely the ascending pharyngeal artery, the vagus’s primary blood supply, is one of the most important blood vessels in the body. The ascending pharyngeal artery is a branch of the external carotid artery, the main collateral blood supply to the brain when the internal carotid artery is compressed. It is difficult to comprehend the enormity of the function of the vagus nerve (at only 2 mm in diameter) and the ascending pharyngeal artery (only 1 mm in diameter) that supplies these two structures are responsible for.

This little ascending pharyngeal artery provides vascularization of:

  • the oropharynx, which needs blood from the pharyngeal artery for the back third of the tongue, the soft palate, the side and back walls of the throat, and the tonsils.
  • the nasopharynx which is the airway behind the nasal passages. Also contained within the nasopharynx are the adenoids chronically implicated in breathing problems, especially through the mouth),
  • the eustachian tube, and the middle ear, (problems of ear fullness and hearing – please see my article Neck pain Chronic Sinusitis and Eustachian Tube Dysfunction),
  • the skull base, the occipital bone and the foramen magnum,
  • the dura,  the outermost layer of the three meninges (the outer layer of membrane) that surrounds and protects the brain and spinal cord. Blood supply helps dura matter leaks and punctures heal.
  • the hypoglossal canal, where the hypoglossal nerve transmits signals to the tongue,
  • the vasa nervorum of the lower cranial nerves, (this is a group of small arteries that bring nutrients to the nerves).
  • and the superior cervical sympathetic ganglion.

As the space narrows in the front of the neck between bones and muscle compartments, the small blood vessels are at risk for occlusion, as is the health of the tissues they supply.

It is therefore very possible that some of the symptoms implicated in cervical spine instability and its impact on vagal tone or vagus nerve function are actually from vascular injury as well. In an interesting twist, if the blood supply through the external carotid artery gets compromised, the vagus nerve sends inhibitory (relax, calm down) signals to the superior cervical sympathetic ganglion to dilate the blood vessel and improve blood flow. Not panic signals to try to push more blood through by increasing circulation.

Vessel stretch can result in intimal (the membrane or “skin” inside the vessels) injury, creating the potential for vessel dissection (separation of vessel wall tissue layers) or intramural thrombus (blood clot) formation, leading to vessel stenosis or complete blockage. It should be noted that the symptoms of an exogenous (from the outside as in herniation or compression) artery occlusion causing vagus nerve injury can be similar to a compressive vagus nerve injury alone.

These symptoms include:

  • ipsilateral (same side) headache,
  • carotidynia (throbbing facial pain),
  • ocular (eye) pain,
  • tinnitus,
  • neck pain, and
  • amaurosis fugax (temporary loss of vision or darkness in the eye). It is important to remember the carotid sheath contains the internal carotid artery, whose last branch before entering the brain is the ophthalmic artery, which branches off right at the craniocervical junction. The ophthalmic artery and its branches supply the eyeball and areas around the eyeball, including the lacrimal glands, eyelids, conjunctiva (the connective tissue covering the eyeball), posterior uveal tract (the tissue between the cornea and the retina), extraocular muscles, and others.

Treatment vagus nerve stimulation

Vagus nerve stimulation is an umbrella term to describe any medical technique, electrical stimulation, manual manipulation, self-help technique, or health regimen that stimulates the vagus nerve.

In June 2022 a paper in the journal Biological Psychology (13) discusses the “recently proposed role of the vagus nerve in limiting inflammation. This has led to the adoption of an earlier developed technique for epilepsy treatment, i.e., electrical stimulation of one vagus nerve bundle in the neck, but now for immune diseases like rheumatoid arthritis, the scope is even widening to depression and cluster headaches. However, the problem in the application of whole vagus nerve stimulation is the lack of specificity: there is no way to titrate the stimulation to an observable effect variable. All nerves in the bundle, incoming and outgoing, can be ‘hit’, leading to side-effects which limit the intended application.”

In July 2022, researchers in Italy wrote in the Journal of Electroconvulsive Therapy (14) that vagus nerve stimulation can be effective for treatment-resistant depression. In this study, five patients treated with implanted with electronic vagus nerve stimulation were followed for 6 to 12 years after implantation.

  • The VNS implant was associated with a sustained response (more than 10 years) in terms of clinical response and social, occupational, and psychological functioning in 3 patients.
  • Two patients dropped out after 6 and 7 years of treatment, respectively.
  • Vagus nerve stimulation was well tolerated by all patients, who reported only mild adverse effects.

Symptoms of Cervicovagopathy Dysautonomia

Above we have laid a basic groundwork describing structural problems, or cervical dysstructure, in the neck.  Now we will discuss the vagus nerve and dysautonomia.

Let’s first touch on some new research developments that will help explain the impact of vagus nerve dysfunction on health and the role of cervical instability.

First dysautonomia

Dysautonomia is a dysfunction of the nerves that regulate the involuntary functions of the body. Vagus nerve degeneration can be so serious that widespread arterial vasospasm (blocking off blood flow to the body including the brain) can occur. Everything that happens in the body involuntarily, including cardiovascular, gastrointestinal, genitourinary, ocular, respiratory, thermoregulatory, vasomotor homeostatic functions, and a host of other involuntary reflexes can be affected by vagus nerve degeneration. The PNS, led by the vagus nerve, helps the body rest, digest, and ultimately repair, without which the body goes into disrepair. The sympathetic and parasympathetic systems are in a finely tuned interplay. When sympathetic dominance occurs over a long period of time, characteristic signs and symptoms occur.

Let’s examine the illustration below. Below the illustration are explanatory notes.

Vagus and nodose ganglion degeneration findings

Animal studies are done in preliminary research, sometimes animal studies are done when the risk of producing the same study in human beings would be considered unsafe.

The amount of neuron (nerve) degeneration correlates with the level of coronary artery vasospasm and animal (rabbit) death. (15)

  • The researchers summarized their findings this way: “We found that there is a causal relationship between nodose ganglion degeneration and coronary vasospasm. Our finding could be the reason that many cardiac events occur in patients with subarachnoid hemorrhage (bleeding around the brain). Vagal pathway paralysis (among other conditions, impacting the heart function) induced by indirect sympathetic overactivity (increased heart rate, increased respiration, increased blood pressure) may trigger coronary vasospasm and heart rhythm disturbances.”

Vagal ischemia (loss of blood supply) induces lung (cell and area death) in respiratory arrest from pulmonary artery vasospasms. (16)

  • The researchers wrote: “Neurogenic pulmonary edema is the most serious complication of subarachnoid hemorrhage. As vagal nerves have vital roles in lung functions, vagal ischemia may have a causative role in the pathogenesis of Neurogenic pulmonary edema.” The researchers examined whether there was a relationship between vagal complex ischemia and lung immune complexes occupying the lymph node infarct (cell death) in subarachnoid hemorrhage.”
    • The animals used in this study had meningeal (the layers of the membrane covering the brain) irritation signs:
      • convulsive attacks
      • fever
      • apnea
      • cardiac arrhythmia
      • and breathing difficulties.

Degeneration of the vagal renal (kidney) branches caused extreme parenchyma (functional tissue) spastic renal arteries leading to Glomerulonephritis (inflammation of the small filters in your kidneys) and kidney cell death at a 17 times greater rate than normal. This problem also results in sodium retention leading to severe hypertension in the neurogenic lung edema vagus nerve.

  • Above we discussed Axon damage. That is what happened in this study, the researchers (17) noted significant degenerated axon density of vagal nerves.

Vagus nerve degeneration causes Auerbach network (responsible for intestinal peristaltic movement) degeneration. The Auerbach plexus or myenteric plexus is a group of ganglia that run throughout the entire gastrointestinal tract and innervate its multiple layers of smooth muscle. (18)

  • The research noted that: Ultimately intestinal gland atrophy resulted in 200 times more cell deaths and ulcers. One of the main findings again was Axon damage along the gastric branches of the vagus nerve. (19)

The illustration above helps explain the wide-ranging symptoms and conditions of vagus nerve dysfunction along with the nerve network.

The hallmark feature of dysautonomia is dysfunction of the vagus nerve.

The most common symptoms of vagus nerve dysfunction include chronic pain, fatigue, dizziness, lightheadedness, spinning or pulling sensation (in a particular direction), weight loss, poor focusing, exercise intolerance, emotional lability, inflammation, heartburn, bloating, diarrhea, tinnitus, headache, anxiety, depression, brain fog, swallowing difficulty, vision changes, and inability to handle stress well.

One clue that there is a neck cause to a person’s dysautonomia is when turning of the head or facial movements such as laughing, chewing, or speaking cause what we term “episymptoms,” which are symptoms that are manifested by activities that don’t normally cause those symptoms, such as flushing, sweating, temperature dysregulation, headaches, vision changes, electric shocks, palpitations, tachycardia, or other autonomic symptoms.

Signs include changes in blood pressure, impaired thermoregulation, fatigue, changes in mental state (such as an increase in stress or lightheadedness), dilated pupils, uvula deviation to one side, and an inability of the palate to rise normally, decreased gag reflex, and dilated pupils. Many of these symptoms are signs of vagopathy.

The nitty-gritty of how you know you have a vagus nerve problem

  • One pupil is significantly larger than the other along with light sensitivity)
  • Resting heart rate over 100 beats per minute
  • Uvula deviates
  • Uvula does not rise
  • Uvula rises more on one side versus the other side.
  • You slow your breathing down but your heart rate does not.

In the image below, right vagopathy is evidenced by the lack of palatal elevation on the right side when saying “Ahhh.” This is caused by weakness in this patient’s right levantor veli palatini muscle which is innervated by the right vagus nerve.

Dysautonomia and cervical instability caused by ligament damage or weakness are progressive disorders. As vagal nerve function struggles, the autonomic nervous system’s (ANS) ability to regulate the body gets more compromised. Eventually, when it can no longer maintain blood pressure, orthostasis occurs (loss in blood pressure when standing), and ultimately multisystem atrophy that can include all the internal organs, in what is termed “pure autonomic failure.” When a person with cervical instability caused by ligament damage experiences symptoms that occur suddenly or increase in severity, it is often because they are starting to have autonomic collapse.

Summary and contact us. Can we help you? How do I know if I’m a good candidate?

We hope you found this article informative and that it helped answer many of the questions you may have.  Just like you, we want to make sure you are a good fit for our clinic prior to accepting your case. While our mission is to help as many people with chronic pain as we can, sadly, we cannot accept all cases. We have a multi-step process so our team can really get to know you and your case to ensure that it sounds like you are a good fit for the unique testing and treatments that we offer here.

References:

1 Lee KY, Oh YW. Extradrenal pargangliomas of the body: imaging features. Am J Roentgenol. 2006;187:492-504. [Google Scholar]
2 Syamsunder AN, Pal GK, Pal P, Kamalanathan CS, Parija SC, Nanda N. Association of sympathovagal imbalance with cardiovascular risks in overt hypothyroidism. North American Journal of Medical Sciences. 2013 Sep;5(9):554. [Google Scholar]
3 Tankeu AT, Azabji-Kenfack M, Nganou CN, Ngassam E, Kuate-Mfeukeu L, Mba C, Dehayem MY, Mbanya JC, Sobngwi E. Effect of propranolol on heart rate variability in hyperthyroidism. BMC Research Notes. 2018 Dec;11(1):1-4. [Google Scholar]
4 Myssiorek D. Recurrent laryngeal nerve paralysis: anatomy and etiology. Otolarynngol Clin North Am. 2004;37(1):25-44. [Google Scholar]
5 Kuo CT, Chiu CH, Fang TJ, Chao YK. Prognostic factors for recovery from left recurrent laryngeal nerve palsy after minimally invasive Mckeown esophagectomy: a retrospective study. Annals of Surgical Oncology. 2024 Mar;31(3):1546-52. [Google Scholar]
6 Mingazova LR, Karpova EI, Murakov SV, Danishuk OI, Bychenko VG, Orlova OR, Soykher MI, Nikolenko VN, Sinelnikov MY. Iatrogenic glossopharyngeal neuropathy in aesthetic practice: a case report. Plastic and Reconstructive Surgery–Global Open. 2022 Mar 1;10(3):e4166. [Google Scholar]
7 De Couck M, Mravec B, Gidron Y. You may need the vagus nerve to understand pathophysiology and to treat diseases. Clinical science. 2012 Apr 1;122(7):323-8. [Google Scholar]
8 Mol MB, Strous MT, van Osch FH, Vogelaar FJ, Barten DG, Farchi M, Foudraine NA, Gidron Y. Heart-rate-variability (HRV), predicts outcomes in COVID-19. PLoS One. 2021 Oct 28;16(10):e0258841. [Google Scholar].
9 Diener HC, Gaul C, Holle-Lee D, Jürgens TP, Kraya T, Kurth T, Nägel S, Neeb L, Straube A. Headache-an Update 2018. Laryngo-Rhino-Otologie. 2019 Mar 7;98(3):192-217. [Google Scholar]
10 Guclu B, Sindou M, Meyronet D, Streichenberger N, Simon E, Mertens P. Cranial nerve vascular compression syndromes of the trigeminal, facial and vago-glossopharyngeal nerves: comparative anatomical study of the central myelin portion and transitional zone; correlations with incidences of corresponding hyperactive dysfunctional syndromes. Acta neurochirurgica. 2011 Dec;153(12):2365-75. [Google Scholar]
11 Taher F, Bokums K, Aichmair A, Hughes AP. C1–C2 instability with severe occipital headache in the setting of vertebral artery facet complex erosion. European Spine Journal. 2014 May;23(2):145-9. [Google Scholar]
12 Sleigh JN, Rossor AM, Fellows AD, Tosolini AP, Schiavo G. Axonal transport and neurological disease. Nature Reviews Neurology. 2019 Dec;15(12):691-703. [Google Scholar]
13 Karemaker JM. The multibranched nerve: vagal function beyond heart rate variability. Biological Psychology. 2022 Jun 7:108378. [Google Scholar]
14 Pigato G, Rosson S, Bresolin N, Toffanin T, Sambataro F, Olivo D, Perini G, Causin F, Denaro L, Landi A, D’Avella D. Vagus Nerve Stimulation in Treatment-Resistant Depression: A Case Series of Long-Term Follow-up. The Journal of ECT.:10-97. [Google Scholar]
15 Yolas C, Kanat A, Aydin MD. Unraveling of the effect of nodose ganglion degeneration on the coronary artery vasospasm after subarachnoid hemorrhage: an experimental study. World Neurosurg. 2016 Feb;86:79-87 [Google Scholar]
16 Atalay C, Gundogdu B, Aydin MD. Vagal ischemia induced lung immune component infarct following subarachnoid hemorrhage: an experimental study. Turk Neurosurg. 2017 Jan 1;27(4):509-15. [Google Scholar]
17 Soyalp C, Kocak MN, Ahiskalioglu A, Aksoy M, Atalay C, Aydin MD, Cakir M, Calikoglu C, Ozmen S. New determinants for casual peripheral mechanism of neurogenic lung edema in subarachnoid hemorrhage due to ischemic degeneration of vagal nerve, kidney and lung circuitry. Experimental study. Acta Cirúrgica Brasileira. 2019 Mar 18;34. [Google Scholar]
18 Shahrestani J, Das JM. Neuroanatomy, auerbach plexus. StatPearls [Internet]. 2021 Jun 4. [Google Scholar]
19 Cakir M, Ahiskalioglu A, Karadeniz E, Aydin MD, Malcok UA, Soyalp C, Calikoglu C, Sengul G, Sipal S, Yayik AM. A new described mechanisms of intestinal glandular atrophy induced by vagal nerve/Auerbach network degeneration following subarachnoid hemorrhage: The first experimental study. Journal of Clinical Neuroscience. 2019 Jan 1;59:305-9. [Google Scholar]

Get Help Now!

You deserve the best possible results from your treatment. Let’s make this happen! Talk to our team about your case to find out if you are a good candidate.