vagus physiology: answers to critical questions you didn’t know you had – part II

Can different pathophysiological mechanisms and risk factors leading to various diseases be linked with altered nerve transmission via one common pathway? The authors of a 2012 scientific article published in the journal, Clinical Science, (3) hypothesized that adequate vagal nerve activity reduces the risk of major diseases through common basic mechanisms..

• There are 3 basic mechanisms that contribute to many chronic diseases. These are: 1) local oxidative stress and DNA damage; 2) inflammatory reactions; and 3) excessive sympathetic responses, all of which are inhibited by vagal nerve activity.
• Efferent vagal activity can be easily monitored noninvasively by measuring Heart Rate Variability (“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, gastrointestinal, neurological, endocrine and urinary-like disorders that we 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 (4) found:

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 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.

how the vagus nerve impacts so many body functions

The caption of the image below 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.

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 side 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 is 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 below, 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.

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.

vagus nerve as the “sixth sense” or “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.

vagus nerve and 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 via the glossopharyngeal nerve. The spinal accessory nerve is responsible for muscle movement of the neck and shoulders.

Cervical instability can also be responsible for almost all painful neuralgias of the head and face including occipital and trigeminal nerve neuralgia, as well as structural headaches including tension, migraines, and cluster. A 2019 German study (5) 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 but 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 (6) 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 damaged 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 a 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 wears away bone

I would like to offer a side note about vascular compression and how it can cause a great amount 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 (7) 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.

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 the 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: the carotid sheath at the cranio-cervical 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.

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, 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 to 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 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 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.

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” that old proteins and lipids are pulled away from the nucleus and new proteins and lipids are sent to the nucleus.

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. (8)

“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, 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, the more the brain stem and the vagus nerves get 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.

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.

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.

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. (9)

• 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 haemorrhage (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. (10)

The researchers wrote: “Neurogenic pulmonary oedema is the most serious complication of subarachnoid haemorrhage. As vagal nerves have vital roles in lung functions, vagal ischemia may have a causative role in the pathogenesis of Neurogenic pulmonary oedema.” 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 haemorrhage.”

The animals used in this study presented meningeal (the layers of the membrane covering the brain) irritation signs. 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 neurogenic lung edema vagus nerve.

Above we discussed axon damage. That is what happened in this study, the researchers (11) 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. (12)

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. (13)

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

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.

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.

** See previous blog https://neurosoma.net/2022/01/01/how-to-map-your-nervous-system-polyvagal-theory-part-2/

This blog is Part 2 of an edited article originally published by Caring Medical Regenerative Medicine Center. Parts II and III will look at understanding treatment for Cervicovagopathy and treatment modalities.

About the author: Ross Hauser MD. Medical Director, Caring Medical Regenerative Medicine Center, Fort Myers, Florida, USA

Board Certified Physiatrist (or Physical Medicine and Rehabilitation Specialist): completed residency training in Physical Medicine and Rehabilitation at Loyola Medical Center in Chicago; MD University of Illinois, Chicago; and Bachelor of Science undergraduate degree from the University of Illinois, Urbana-Champaign.

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