Dysautonomia, POTS, and the hEDS patient with a long list of symptoms and conditions

Ross Hauser, MD

In this article Dr. Hauser discusses:

We get many emails from people suffering themselves or with children suffering from Ehlers-Danlos Syndrome and Postural Orthostatic Tachycardia Syndrome. They are being treated for tachycardia (rapid heartbeat), dizziness, fainting, headaches, vertigo, excessive fatigue, digestive problems including nausea, weight loss. Because of the fainting symptoms, especially the “blackouts” these people would find themselves in the emergency room, hooked up to various cardiovascular assessment machines and devices looking for the initial and subsequent causes of these events. This is typically the beginning of their POTS treatment journey. Sometimes it is at an emergency room visit where it was also initially speculated that the person has a joint hypermobility problem or hEDS, hypermobile Ehlers-Danlos Syndrome. This may have happened to you.

Confusion of which path to take in treatment. “Everything is newly discovered”

Some of these people will relate that they had many trips to the emergency room and that in some of the earlier trips to the emergency room, without a “solid” diagnosis of what was happening to them, their visit would often conclude with a confusing or misdiagnosis of their condition. They would be told that they have a  virus, the flu, a mysterious infection, or it was something they ate. After a few visits to the ER, these explanations would lose credibility as they continued to fall under the “mysterious” umbrella. However, reassured by the doctors and now armed with a handful of prescriptions, these people hoped and thought they would soon return to school or work and this event would pass. Yet their symptoms progressed.

As time went on, some people reported that the frequency of their events increase to the point that every time they got to their feet or stood up, their heart would race. Sometimes their heart would race wildly after eating which lead to the belief it was “something they ate” or more medically “something that was causing a reaction of some type.” Eventually, some would be diagnosed with panic disorders and be sent on a different path of treatment, one towards physiatrists and mental health professionals and months, possibly years of testing various anxiety and panic disorder medications that seemingly did not help, and worse accelerated “bad thoughts.” Please see our companion article: Dissociation, Anxiety, and Depression – Uncontrolled emotion in cervical spine instability patients. Some, as we will see later in this article were accused of simply being “attention seekers.”

Yet all these doctors and all these treatments did not lessen or slow down the development of symptoms.

Many of these people will then relate their stories of the amount of or better yet “over amount” of medical care they required from “countless” specialists. Because of their myriad of symptoms and no “easy answers” they were recommendations to gastroenterology specialists, numerous second opinion visits to cardiologists for chest pain and shortness of breath, and the aforementioned mental health specialists. Yet all these doctors and all these treatments did not lessen or slow down the development of symptoms.

Some will tell us that their doctors were left without any idea how to proceed forward. In some patients, failure of treatment can be as equally a mystery as the cause of the symptoms and diagnosis of Dysautonomia, POTS, and the hEDS. In some, and the reason that many of these people contact us is that they suspect that their issues are in whole or in part being caused by craniocervical instability. In their quest for answers, some people have now come down this path of cervical myelopathy or instability. These are the people we see. People with many problems in the neck possibly cause compression on the nerves, veins, and arteries that pass through the cervical spine. Some of the things we hear from people are:

“I have over 50 symptoms every day”

People who reach out to us can present with very difficult and challenging symptoms and cases.  For most people, there is no easy fix and a path to treatment may require months to achieve some or all of their treatment goals. The treatment itself can be exhausting. Even with a clear-cut plan to alleviate symptoms, treatment programs must be realistically assessed and the candidacy of the patient to achieve their treatment goals must be thoroughly examined.

If you are reading this article because you yourself have been facing years of symptomology or you are researching for a loved one, you, or they are probably thinking now, “I probably have dozen of symptoms. I have lost track.”

People, maybe like yourself, send us emails like this where they describe symptoms that also include problems in the cervical spine. Treating problems of the cervical spine as causation of the myriad of symptoms described in this article is our primary plan to restore the patient to a better quality of life.

hEDS and cervical stenosis

I have connective tissue disorder – Hypermobile Spectrum Disorder, Dysautonomia, and Mast Cell Activation Syndrome. I have also been diagnosed with cervical stenosis and bulging discs. I also have Kyphosis. I have over 50 symptoms every day, and these issues have been going on for years, however, the neck symptoms got worse about a year ago, causing severe vertigo whenever I move my head.

Dozens of diagnoses: Craniocervical instability secondary to hEDS

Here is another of the many types of emails we receive where a person reported many symptoms of cardiological, neurological, immunological, and gastrological-like problems.

Dozens of symptoms, 50 symptoms a day, how can these people possibly be treated? Again, I want to stress for most people, there is no easy fix and a path to treatment may require months to achieve some or all of their treatment goals. Even with a clear-cut plan to alleviate symptoms, treatment programs must be realistically assessed and the candidacy of the patient to achieve their treatment goals must be thoroughly examined.

Dysautonomia-Autonomic nervous system malfunction: Digestive, immune, and cardiac-like disorders: Some of the symptoms of Autonomic nervous system dysfunction.

As we progress our way through this article we will examine together the role of cervical spine instability and neurologic-like, cardio-vascular-like, and gastrointestinal-like problems that may be the secondary result of cervical spine compression on vital nerves, arteries, and nerves.

In this examination I will refer to my previous article Neurologic, digestive, cardiac, and bladder disorders: Some of the symptoms of Autonomic nervous system dysfunction and treatment options and summarize some of those findings here.

Some people will have a diagnosis of dysautonomia. In most general terms, their nervous system is not communicating messages correctly.

Some people will have a diagnosis of dysautonomia. In most general terms, their nerves are not communicating correctly. These symptoms can manifest themselves as problems with blood pressure and heart rate. Some will have a concurrent diagnosis of Ehlers-Danlos Syndrome and Hypermobility Spectrum Disorders. The list of symptoms some people display seemingly goes on and on as we discussed above. Where are all these problems coming from? For some people, the problem may arise from an underlying cervical or lumbar spinal instability leading to autonomic nervous system dysfunction.

Let’s review the basic concepts of autonomic dysfunction and malfunction. 

The autonomic nervous system (ANS) is made up of nerves that control the automatic functions throughout the body. It is the master regulator, controlling heart rate, blood pressure, temperature, respiration, sweating, digestion, and other vital functions. These systems operate without you consciously thinking about them because the autonomic nervous system provides the nerve messaging connection between these system organs and the brain. Let’s start thinking about the path these nerves have to take from the heart or digestive system to the brain, where does everything have to pass to get to and from the brain? The neck. Everything goes through the neck.

The autonomic nervous system is made up of two subsystems: the sympathetic autonomic nervous system (SANS) and the parasympathetic autonomic nervous system (PANS). Most organs are directed by both the sympathetic and parasympathetic systems. The sympathetic autonomic nervous system is usually more of a stimulatory system, increasing heart rate and blood pressure when necessary.

Where the parasympathetic autonomic nervous system, generally slows bodily processes, such as reducing heart rate and blood pressure. There are certainly exceptions. Digestion and urination, for instance, are stimulated by the parasympathetic autonomic nervous system and slowed by the sympathetic autonomic nervous system. The sympathetic autonomic nervous system triggers emergency responses or the “fight or flight” responses to prepare for stressful situations and controls the body’s response to stress. The parasympathetic autonomic nervous system conserves energy and restores tissues for ordinary functions, helping to return the body’s equilibrium to the resting state.

Where do many symptoms come from? Dysautonomia

Dysautonomia refers to problems of or dysfunction of the autonomic nervous system. Since the autonomic nervous system regulates automatic or involuntary bodily functions, such as controlling the activities of organs, glands, smooth muscles, and cardiac muscles, when the autonomic nervous system malfunctions, the organs it regulates malfunction. For this reason, when individuals suffer from dysautonomia, they often exhibit numerous maladies and symptoms.

What are we seeing in this image?

This is a graphic that displays the sympathetic autonomic nervous system and parasympathetic autonomic nervous system. Many organ systems are maintained and controlled by the autonomic nervous system. When the autonomic nervous system is compromised, many systems can teeter on the brink of collapse and cause dozens of symptoms.

Autonomic Nervous System

Orthostatic intolerance

When the autonomic nervous system is compromised, orthostatic intolerance can develop. Orthostatic intolerance is a common problem in autonomic dysfunction and presents with lightheadedness, palpitations, and tremulousness during standing. When in the upright posture other symptoms include visual changes, discomfort in the head or neck, the throbbing of the head, poor concentration, tiredness, weakness, and occasionally fainting. Many of the symptoms are relieved by lying down.

Other symptoms of dysautonomia include exercise intolerance, due to an inability to alter heart rate and regulate the cardiovascular system. Excessive or insufficient sweating is a problem due to problems regulating temperature. Slow digestion causes nausea, loss of appetite, bloating, diarrhea or constipation, and difficulty swallowing. Urinary problems can include difficulty starting urination, incontinence, and incomplete emptying of the bladder. Problems with vision include blurry vision or the failure of the pupils to react quickly enough to changes in light. And the list goes on…Fatigue, abnormal breathing patterns, dyspnea, vertigo, syncope, gait problems, hypoglycemia, “anxiety,” insomnia/non-restorative sleep, and peripheral paresthesias. Any or all of these symptoms may be present in varying degrees of severity.

How does this happen? One path of diagnosis and treatment follows the vagus nerve. What are we seeing in this image?

Here we see the “normal sequence of events” of how messages go from your brain through the vagus nerve to the heart. The messages between brain and heart are simple adjustments to maintain heart rate. Once the message is received the heart sends a message back to the brain via the glossopharyngeal nerve and the vagus nerve on heart rate and blood pressure.

What if the message from the brain to the heart is distorted? What if the message from the heart to the brain is distorted or garbled?

In the video below, Dr. Hauser will discuss the role of the vagus nerve. Here are summary learning points, they will be discussed in further detail below.

The main highway of heart to brain communication via the autonomic nervous system is the vagus nerve

As discussed above, the sympathetic nervous system helps make adaptations to your current situation by adjusting your heart rate, blood pressure, and breathing rate to dramatically increase when exercising or physical demand. The parasympathetic nervous system is an energy management center. When you are done being in “fight or flight mode,” or are using techniques to end a panic attack or to catch your breath, or calm yourself down. The parasympathetic nervous system helps automatically reduce heart rate and blood pressure.

The main highway of communication is the vagus nerve 

So here we have the autonomic nervous system and its components, the sympathetic nervous system and parasympathetic nervous system, that among its duties regulate your heart rate. Its main highway of communication is the vagus nerve of which there are two running down each side of the neck. The vagus nerve has a great impact on heart function, as the cardiovascular afferents (afferents – simply the nerve fibers that send messages to the brain as opposed to efferents, nerve fibers which send the response back) make up the greatest extent (compared to other organs) of the 85-90% of sensory fibers which make up the vagus nerve.

In other words, the majority of work the vagus nerve does is getting messages back and forth from brain to heart. These 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.


In this video Ross Hauser, MD highlights some of the most common reasons why cervical instability or cervical dysstructure (broken neck syndrome) can be the underlying structural cause of low vagal tone and associated poor heart function, leading to POTS, or dysautonomia.

Postural Orthostatic Tachycardia Syndrome (POTS)

Often more simply referred to as Postural Orthostatic Tachycardia Syndrome, POTS, is the most common form of dysautonomia and is characterized by orthostatic intolerance, with or without associated orthostatic hypotension, and excessive autonomic excitation. Symptoms manifest with the body’s inability to make the necessary adjustments to counteract gravity when standing up.

What are we seeing in this image? How blood pressure can be affected by c1-c2 nerve compression of the Vagus and glossopharyngeal nerves – the impact on blood flow

“Dysautonomias, the result of an autonomic nervous system malfunction, is often found in patients with cardiovascular symptoms”

A June 2020 paper in the Journal of Atrial Fibrillation (1), describes a racing heart and the problem of heart rate messaging miscommunication in the autonomic nervous system.

“The cardiovascular branch of the autonomic nervous system (ANS) is responsible for the regulation of heart rate, blood pressure, and maintaining homeostasis during physiological stress such as exercise and standing upright. The autonomic nervous system constantly controls the rate and force of heart contractions and the vascular tone with the aim to maintain the sufficient tissue perfusion with oxygenated blood and secure venous return to the heart.” (In other words, the normal function of the heart, blood rich in oxygen travels the body and it returns to the heart the oxygen-poor blood to send to the lungs to be re-oxygenated).

“Dysautonomias, the result of an autonomic nervous system malfunction, is often found in patients with cardiovascular symptoms. Apart from the most prevalent one, arterial hypertension (high blood pressure), the cardiovascular dysautonomic continuum (simply the function of the heart to bring blood to the body and return it to the lungs for oxygen) encompasses other important although less known conditions: Postural Orthostatic Tachycardia Syndrome, inappropriate sinus tachycardia, orthostatic hypotension and reflex syncope (fainting from loss of blood pressure). Moreover, heart diseases may evoke autonomic imbalance by themselves; cardiac pump failure is usually associated with sympathetic hyperactivity (rapid heart rate, rapid breathing, increased blood pressure), neuroendocrine vasopressor activation (the release of hormones that constrict the blood vessels), higher heart rate, reduced heart rate variability, and baroreflex hyposensitivity), all of which are predictors of adverse outcomes.”

The last sentence describes baroreflex hyposensitivity. What is that? The Baroreceptors (blood pressure sensors) will notice the drop in blood pressure by sensing that the arterial walls are relaxed, or, too relaxed. The concerned Baroreceptors will start then sending urgent messages to the vagus nerve to decrease its vagal tone. Simply, the vagus nerve is responsible for slowing the heart rate or bringing the heart rate down after an event that causes it to raise, exercise, do something strenuous, fear, anxiety, panic, fright.

Sometimes the vagus nerve does not get this message. Why? Because something is blocking or interfering with the message. The basis of this article will present one possibility, a problem of cervical instability and vagus nerve compression.

“What they suggest is that the inability to maintain constant blood pressure through an autonomic dysfunction may lie at the cause of POTS in hypermobile Ehlers-Danlos Syndrome and baroreflex sensitivity”

In May 2020, University researchers in Italy published an observational study in the journal Monaldi Archives for Chest Disease. (2) In this study they explored a further association between joint hypermobility, hypermobile Ehlers-Danlos Syndrome (hEDS), and different forms of orthostatic intolerance.

What they observed was “abnormal results in (heart rate, blood pressure and baroreflex sensitivity (the baroreflex or baroreceptor reflex is the mechanism that tries to hold a steady blood pressure) were estimated in 102 hEDS/HSD subjects during deep breathing, Valsalva maneuver, standing up: 30-15 ratio, Head-Up Tilt and sustained handgrip.)

Among the patients, it was found that:

The researchers observed that a “high rate and heterogeneity (many reasons why) of abnormal autonomic regulation in hEDS/HSD, and suggests the baroreflex sensitivity might distinguish comorbid POTS from other profiles in this subgroup of patients. Abnormal autonomic regulation is common in adults with hEDS/HSD and should be regularly assessed for tailoring the management approach.”

What they suggest is that the inability to maintain constant blood pressure through an autonomic dysfunction may lie at the cause of POTS in hypermobile Ehlers-Danlos Syndrome.

The many symptoms of Dysautonomia, POTS, and the hEDS patient. Observations noted in the medical research

The type of symptomology we see in patients at our center is not unique to our center. Hospitals, leading research centers, emergency rooms, and private practice physicians see them too. It is not a debate as to if these people have these symptoms, the debate in the medical community is over whether many of the symptoms are actually real or imagined and where are the real ones coming from. In this section, we will explore recent medical research.

Recently, there has been more attention given to the idea that some type of musculoskeletal issue may be the cause of this myriad of neurologic-like, digestive-like, cardiac-like, and bladder-like disorders that these patients suffer from. Not in every patient, but in some. There is an idea of these symptom problems are not primary, meaning that your digestive problems are not being caused by the digestive system itself, but are secondary in nature. This means the digestive symptoms are being caused by something influencing the function of the digestive system, possibly nerve dysfunction. It is possibly cervical instability and compression of the spinal cord, arteries, veins, and nerves in the cervical spine.

A 2018 study from the Department of Internal Medicine, Texas Tech University Health Sciences Center Paul L. Foster School of Medicine offered these observations in The American Journal of the Medical Sciences. (3)

“Joint hypermobility is a common, primarily benign finding in the general population. However, in a subset of individuals, joint hypermobility causes a range of clinical problems mainly affecting the musculoskeletal system and, to a lesser extent, extra-articular disorders. Joint hypermobility often appears as a familial (Family) trait and is shared by several inherited connective tissue disorders, including the hypermobility subtype of Ehlers-Danlos Syndrome (hEDS) and Benign Joint Hypermobility Syndrome (BJHS/JHS).

Although joint hypermobility has primarily been thought of as a rheumatological disorder, increasing evidence shows significant associations between both hEDS and BJHS with specific extra-articular (inflammatory) disorders. To date, the strongest associations of these two conditions are with anxiety disorders, orthostatic tachycardia, various functional gastrointestinal (GI) disorders, and pelvic and bladder dysfunction.”

Mast Cell Activation System is an immune, inflammatory disorder. A suggestion is that something is causing a misfiring of the autoimmune system. Could it be cervical spine instability?

Postural Tachycardia Syndrome (POTS), hypermobile Ehlers-Danlos syndrome (EDS), and Mast Cell Activation Syndrome (MCAS)

Doctors at Tufts University School of Medicine, Boston wrote in the journal Allergy and Asthma Proceedings (4) May 2021: Postural Tachycardia Syndrome, hypermobile Ehlers-Danlos Syndrome, and Mast Cell Activation Syndrome (MCAS) can occur in the same patient.

In this study, the researchers investigated the relationship among these three syndromes to establish the relationship of MCAS in patients diagnosed with POTS and hypermobile EDS as well as to characterize the demographics of the patients affected by these syndromes. In other words, can people suffer from all three of these syndromes simultaneously, and what is the patient profile, or, who is the type of patient at risk for this.

Mast Cell Activation Syndrome

I am going to take some time to comment on Mast Cell Activation Syndrome. We see many patients who have suffered from prolonged illness including POTS and Mast Cell Activation Syndrome. What we observe in our own patients and what we see in people that we talk to who are interested in becoming patients is that among their many symptoms is neck pain. However for some, their neck pain was seen as a manifestation of their illnesses, rarely was it seen as the cause of their illnesses.

So many of these people have taken it upon themselves to explore upper cervical instability and cervical spine instability as not a symptom, but rather a cause. These people then make appointments with cervicocranial specialists who examine them and take imagining studies. In some of these images, the patients learn that they degenerative disc disease in their cervical spine and a loss of the cervical curve contributing to kyphosis.

The confusion is some of these people’s diagnosis stems from not what is the answer to help them, but rather what is the question that is not being asked of them. Namely, which came first the autonomic nervous dysfunction (the source of symptoms in the cervical spine) or the immune-mediated allergy?  At a minimum, we know they are interconnected. A lot of antigen-antibody immune complexes and a host of histamine release are going to excite the autonomic nervous system throughout and likewise, autonomic nervous system dysfunction makes antigen-antibody reactions more likely. The patient has the symptoms, is it the neck? Is it the allergies? For more discussion on this subject please see my article: Neurologic-like symptoms and conditions of Cervical Spine Instability.

Let’s return to the study from Tufts University School of Medicine. Discussing POTS, hypermobile Ehlers-Danlos Syndrome, and Mast Cell Activation Syndrome (MCAS). There was a marked percentage of MCAS among the patients with diagnoses of POTS and EDS.

In this study, the doctors looked at the case histories of 195 patients. What they found was “statistically significant.” The percentage of MCAS within the group of POTS and EDS was 31% in comparison with 2% within the non-POTS and EDS group. Conclusion: There was a marked percentage of Mast Cell Activation Syndrome among the patients with diagnoses of POTS and EDS.

In summary: Mast Cell Activation Syndrome is primarily found in young hypermobile females, including those with EDS and POTS. Dysautonomia being 3-10 times more common in EDS, POTS, and allergic-type disorders than in the general population. Mast Cells are in the connective tissues, near blood vessels, and in enteric mucosa, where they store and release histamine and other immune-modulating substances in response to antigen and other pathological stimuli associated with tissue injury, inflammation, and autoimmunity. Mast Cells are critical for proper microbial defense, epithelial integrity, immune regulation, and proper neurological activity of vagal innervated organs and tissues. 

hEDS and EDS patients are at risk for Mast Cell Activation Syndrome through many mechanisms including loose connective tissue in the GI tract and blood, being on medications that raise histamine levels as well as ligamentous upper cervical instability-induced Cervicovagopathy (dysfunction of the vagus nerve). While treatments directed at the structural neck issues are helpful for histamine-induced symptoms they have to be combined with dietary changes to reduce synthetic and histamine-containing foods, as well as eliminate drugs that raise histamine levels. These include antibiotics, diuretics, H2 receptor antagonists, antidepressants, analgesics, muscle relaxants, and antihypertensive medications.

GI manifestations, mast cell activation syndrome, POTS, and hEDS

Doctors at the Divisions of Gastroenterology, Department of Medicine and St. Louis University, the University of Louisville, Department of Cardiac Sciences, Cumming School of Medicine, Libin Cardiovascular Institute, at the University of Calgary and the Division of Cardiology, Department of Medicine, St. Louis University teamed up to examine gastrointestinal manifestations in Postural Orthostatic Tachycardia Syndrome patients. Here is what they wrote in the journal Neurogastroenterology and Motility in December 2020. (5)

“Postural Orthostatic Tachycardia Syndrome (POTS) is a disorder of orthostatic intolerance associated with many GI manifestations that can be broadly classified into two different categories: those present all the time (non-positional ) and those that occur with orthostatic position change.

There are also many conditions that can co-exist with POTS such as Mast Cell Activation Syndrome and the hypermobile form of Ehlers-Danlos Syndrome (hEDS) that are also oftentimes associated with GI symptoms.”

In their paper, the doctors noted previous research to help conclude that hEDS-POTS patients were more likely to have more than one GI organ involved compared to patients with hEDS alone, and certain GI symptoms were also more common in the hEDS-POTS cohort.”

POTS was found to be an independent predictive factor for GI dysmotility.

An April 2020 study (6) from the Cleveland Clinic examined the prevalence and predictor factors of gastrointestinal dysmotility in Hypermobile Ehlers-Danlos Syndrome patients. Here are the highlights of this study:

“Ehlers-Danlos syndrome (EDS), specifically the hypermobility type (hEDS), is associated with a variety of gastrointestinal conditions. In this study, the researchers evaluated the prevalence of and factors associated with gut dysmotility in patients with hEDS.”

The researchers found a total of 218 patients with hEDS previously treated at the Cleveland Clinic who met the criteria for inclusion in this study.

In my article Cervical spine instability and digestive disorders: Indigestion and irritable bowel syndrome caused by cervical spondylosis, I offer a connection between cervical spine instability and digestive disorders and describe the challenges faced by the hEDS patient. Digestive problems are part of the symptomology of hypermobile type Ehlers-Danlos Syndromes. We often find that the joint instability that they suffer in their neck can lead to compression of the spinal cord, vital arteries and veins, and their nervous system with a focus on the Vagus Nerve.

Gastrointestinal symptoms and vagus nerve compression

In this video Ross Hauser, MD. discusses a myriad of gastrointestinal symptoms that may be caused by vagus nerve compression typically found in cervical spine instability.

The argument that none of this is real: “my neurologist and neurosurgeon are claiming not to understand my symptoms”

An email we received: “I have severe symptoms that seem to match Dysautonomia and Postural Orthostatic Tachycardia Syndrome (POTS), but my neurologist and neurosurgeon are claiming not to understand my symptoms, they say they are unrelated to my spine injury.”

A June 2020 paper in the journal Clinical Reviews in Allergy & Immunology (7) published these findings:

“In recent years, an association between hypermobile Ehlers-Danlos Syndrome (hEDS), Mast Cell Activation Syndrome (MCAS), and Postural Orthostatic Tachycardia Syndrome (POTS) has garnered attention and patients are increasingly presenting with this triad. However, a real relationship between these entities is unclear due to a lack of scientific validity.”

What these researchers did was conduct an extensive review of the medical research. They could not find conclusive evidence that there is an association between hypermobile Ehlers-Danlos Syndrome, Mast Cell Activation Syndrome, and Postural Orthostatic Tachycardia Syndrome. They wrote:

“All three clinical entities are controversial in either existence or pathogenesis. Mast cell Activation Syndrome is a poorly defined clinical entity, and many studies do not adhere to the proposed criteria when establishing the diagnosis. Patients previously diagnosed with EDS hypermobility type may not meet the new, stricter criteria for hEDS but may for a less severe hypermobility spectrum disorder (HSD). The pathophysiology of POTS is still unclear. An evidence-based, common pathophysiologic mechanism between any of the two, much less all three conditions, has yet to be described.”

“(This study) Our review of the literature shows that current evidence is lacking on the existence of Mast cell activation syndrome or hEDS as separate or significant clinical entities. Studies proposing a relationship between the three clinical entities are either biased or based on outdated criteria. The reason behind the purported association of these entities stems from an overlapping pool of vague, subjective symptoms, which is inadequate evidence to conclude that any such relationship exists.”

A different opinion: “it is important to identify these patients in routine clinical practice to ensure that the comorbidities are suitably recognized and well managed”

A November 2020 paper in the journal Clinical and Translational Gastroenterology (8) came from the Department of Gastroenterology, Neurogastroenterology & Motility, Translational Research in Gastrointestinal Disorders at the University of Leuven in Belgium and the Barts and The London School of Medicine and Dentistry, Wingate Institute of Neurogastroneterology, Centre for Neuroscience and Trauma, Blizard Institute Queen Mary University of London.

Here the research team suggested: “an association among POTS, increased Mast Cell Activation, and gastrointestinal symptoms have been observed, again suggesting an additional link to immunological factors. Given that these are treatable conditions, which can also lead to improvement in gastrointestinal symptoms, it is important to identify these patients in routine clinical practice to ensure that the comorbidities are suitably recognized and well managed.”

When Mast Cell Activation Syndrome and Immune Response is not seen as a primary mover for symptoms related to POTS and hEDS

In the above section, I focused on Mast Cell Activation Syndrome and the inflammatory response as culprits in the symptomology some people suffer from. As with many medical disorders, trying to find the source of the patient’s health challenges can daunting, specifically in cases of a long list of symptoms and conditions related to Dysautonomia, POTS, and hypermobile Ehlers-Danlos Syndrome. Mast Cell Activation Syndrome response caused by cervical instability may be one possible explanation. The idea that cervical instability can also cause deepening and accelerated symptoms and conditions related to Dysautonomia, POTS, and hypermobile Ehlers-Danlos Syndrome without the presence of Mast Cell Activation Syndrome can lead to the suggestion that in some people, the core problem is cervical neck instability causing nerve, vein and arterial compression and a compromising of the autonomic nervous system.

Researchers and their quest for answers admit a lack of knowledge asking: “How exactly are joint hypermobility syndrome (JHS) and POTS associated?”

Many doctors understand that many of the mysterious ailments that they see in their patients with problems of Dysautonomia, POTS, hEDS, and joint hypermobility are exactly that “mysterious ailments ” without a known or consistent path of treatment.

In 2010 Shomu Bohora, MD, DM, of the Baroda Heart Institute and Research Centre, Vadodara, India published an editorial in the leading medical publication Indian Pacing and Electrophysiology Journal. (9) This is what Dr. Bohora suggested:

“There still remain some unanswered, but important, questions. How exactly are joint hypermobility syndrome (JHS) and POTS associated? Why do both POTS and JHS have female preponderance? Is it related to genetic, hormonal, or environmental modification of the nervous system along with differences in musculoskeletal structure in patients that predispose to the above, or is there a single cause of all these contiguous syndromes which we are yet to discover?”

Is there a single cause of all these common syndromes which we are yet to discover?

The same questions in 2010 are still being asked in 2021. There have been updated classifications, there have been updated observational studies, yet the questions still remain. What is causing hEDS and joint hypermobility syndromes patients their problems with POTS and dysautonomia?

Postural tachycardia in hypermobile Ehlers-Danlos syndrome dysautonomia – is it still not clear?

In 2017, doctors at the Department of Neurology and the Department of Psychiatry at Stanford University Medical Center wrote in the journal Autonomic Neuroscience: Basic & Clinical (10): “It is not clear if patients with postural tachycardia syndrome (POTS) and Ehlers-Danlos syndrome (hEDS) differ from patients with POTS due to other etiologies.”

The point of this statement was to assess if a subgroup of patients, those with clinically diagnosed POTS and hEDS should be separated out and treated differently than patients with a primary POTS diagnosis.

What the researchers then did was to take patients with POTS + hEDS (a total of 20 patients) and POTS controls without hypermobility (a total of 20 patients) and tested them for autonomic dysfunction in addition to reviewing their medical records to determine the number and types of medications patients were taking, as well as the number of outpatients, emergency department, and inpatient visits over the prior year. The point of all this was to best determine if a separate treatment strategy was needed for the POTS + hEDS patients or if the current POTS treatment guidelines would be sufficient.


Conclusions: “While autonomic testing results were not significantly different between groups, patients with POTS+hEDS took more medications and had greater markers of healthcare utilization, with chronic pain likely playing a prominent role.” In other words, POTS + hEDS patients took more medications because of more pain.

One-fifth of pediatric patients with POTS had EDS and over one-third of patients had hypermobility spectrum disorder

A March 2021 study published in the journal Autonomic Neuroscience: Basic & Clinical (11) examined the prevalence of joint hypermobility syndromes in pediatric Postural Orthostatic Tachycardia Syndrome.

Here are some of the observations of this paper:

In this study:


The researchers concluded: “Our evaluation of a large series of pediatric patients with POTS revealed that over one-fifth of patients had EDS and over one-third of patients had HSD. The awareness of the prevalence of comorbidities such as hypermobility disorders may help inform providers diagnosing and caring for these patients.”

There is a strong connection between Dysautonomia, Joint Hypermobility Syndrome and Ehlers-Danlos Syndrome 

There is a strong connection between Joint Hypermobility Syndrome (JHS) and autonomic nervous system dysfunction. In fact, significant dysautonomia is observed in JHS patients with symptoms such as syncope and pre-syncope, orthostatic intolerance, palpitations, chest discomfort, fatigue, and heat intolerance. These symptoms are significantly more common among hypermobile patients. Another study making this connection was published in the journal Frontiers in Neuroscience. (12) Here orthostatic hypotension, Postural Orthostatic Tachycardia Syndrome, and uncategorized orthostatic intolerance were found in over three-quarters of the hypermobile patients in comparison to one-tenth in the controls.

Ehlers-Danlos Syndrome (EDS) involves the presence of joint hypermobility as well as other musculoskeletal and extra-articular connective tissue difficulties.

The term “Ehlers-Danlos Syndrome” (EDS) groups together an increasing number of heritable connective tissue disorders mainly featuring joint hypermobility and related complications, with skin, joints, blood vessels, and internal organs variably affected. EDS-hypermobility type (EDS-HT), which is one of the most common variants, is still a clinical diagnosis based on subtle and likely unspecific features and shows a nearly complete phenotypic overlap with Joint Hypermobility Syndrome (JHS), a heritable rheumatologic condition defined by the Brighton criteria. Some classify both Joint Hypermobility Syndrome and Hypermobile Ehlers-Danlos Syndrome as the same condition; however, the question of whether hEDS and JHS are also identical at the molecular level is still a matter of debate.

Poor aerobic fitness and cardiac atrophy

A July 2021 study (13) comes from the Icahn School of Medicine at Mount Sinai and was published in the American Journal of Medical Genetics. Part A. In this study, the problem of physical deconditioning and poor aerobic fitness was examined in hEDS patients. Here are the summary highlights:

“In this study, the prevalence of dysautonomia, range of associated symptoms, patient-reported physical activity levels, and echocardiographic features were assessed retrospectively in a cohort of 144 patients (94% female) with hypermobile Ehlers-Danlos syndrome (hEDS) or hypermobility spectrum disorder (HSD).

“Dysautonomia was identified in 65% of female and 44% of male subjects and was associated with a high burden of symptomatology, most commonly exercise intolerance (78%).

Exercise capacity was limited by dysautonomia, often postural symptoms, in half of all patients.”

What the researchers observed was something that is commonly reported in patients: A reduction in physical activity following the onset of a significant flare of hEDS/HSD symptoms. The researchers noted: “most strikingly noting the proportion of dysautonomic patients with a sedentary lifestyle, which increased from 44% to 85%. (Joint Hypermobility)-related dysautonomia was associated with smaller cardiac chamber sizes, consistent with the previous reports in positional orthostatic tachycardia syndrome.”

Cervical Instability in Ehlers-Danlos Syndrome and POTS

Ross Hauser, MD explains the approach used at Caring Medical Regenerative Medicine Clinics for treating cervical instability and its various debilitating manifestations. With patients suffering from conditions caused by disabling chronic neck instability due to Ehlers-Danlos Syndrome and/or suffering from POTS, Prolotherapy, simple dextrose injections that help rebuild collagen tissues in the cervical ligaments, may be an effective treatment. Since 1993, our clinic has been helping patients with EDS.

Summary transcript of this video with explanatory notes:

When a person comes to our center with Ehlers-Danlos Syndrome or other types of genetic hypermobility disorders causing joint instability and a history of dislocating joints or their joints are hyper-flexible, we assess whether or not they have neck instability. If a person with Ehlers-Danlos Syndrome has neck instability, we may be able to realistically assess that this neck instability can be the cause of Postural Orthostatic Tachycardia Syndrome, Mast Cell Activation Syndrome, Leaky gut syndrome, digestive problems in addition to the symptoms and conditions that we may see in people with cervical instability such as migraine headaches, dizziness, ringing in the ears, tinnitus, concentration difficulties, terrible fatigue among many other symptoms. Please see my article Symptoms and Conditions of Craniocervical Instability. In this article, I have put together a summary of some of the symptoms and conditions that we have seen in our patients.

We can assess cervical instability with digital motion scanning. In other words, we basically take a movie camera picture of the movement of the bones with various motions of the neck. What we are looking for in excessive movement or hypermobility of the neck of the vertebrae. Then we can target the treatment. The treatment we utilize is cervical Prolotherapy, the use of simple dextrose injections to rebuild and restore the collagen matter of the cervical spine ligaments. The hope is that the injections, given at points of ligament weakness, will restore these ligaments to a more natural function and alleviate or eliminate issues related to cervical instability.

Once we can restore stability in a patient, the symptoms start to go away and for the person who has an abnormal curvature of the cervical spine, what we do is do cervical realignment therapy (explained below) so for a person with Ehlers-Danlos Syndrome and cervical instability would start with Prolotherapy.

In May 2021 doctors at the Department of Neurosurgery, University of Maryland Capital Region Health Center, and the Department of Pediatrics, Johns Hopkins University School of Medicine discussed difficult to treat Syncope and Presyncope and its association with Atlantoaxial Instability. These are the summary points of their findings published in May 2021 in the journal World Neurosurgery. (14)

The 20 patients of this study

“Postoperatively, subjects reported a statistically significant improvement in lightheadedness, presyncope, and syncope, and in the frequency of other symptoms related to autonomic function, such as nausea, exercise intolerance, palpitations, tremors, heat intolerance, gastroesophageal reflux, and sleep apnea. This study draws attention to the potential for Atlantoaxial Instability to present with syncope or presyncope that is refractory to medical management, and for surgical stabilization of Atlantoaxial Instability to lead to improvement of these and other autonomic symptoms.”

In this study, the suggestion is made that cervical fusion can alleviate the symptoms these patients face. For many people, surgery can be very beneficial. Some patients may not be good surgical candidates, some may not want to have fusion surgery, some had the surgery with less than hoped-for results. It is this second group of patients that we typically see.

Unstable C1-C2 and Stable C1-C2 under Digital Motion X-ray

One of the most revealing tests we do in our office for upper cervical instability is a digital motion x-ray (DMX), which includes looking at how the C1 and C2 vertebrae align when tilting the head. In this video, Ross Hauser, MD shows an unstable and stable upper cervical digital motion x-ray from 2 different patients.

What are we seeing in this image?

This is a case study 35-year-old female patient seen at Caring Medical. The patient was diagnosed with Ehlers Danlos Syndrome and POTS. We first saw this patient in 2018 for neck pain and cervical instability symptoms. Symptoms at her initial visit were neck pain, vertigo, brain fog, trouble concentrating, a feeling of instability and “discs moving” in the neck, muscle tightness,  intermittent radiculopathy in both her hands, migraines, constant headaches, visual disturbances, nausea, facial pain, a feeling that something is stuck in her throat, increased heart rate with flexion, anxiety and slight movements would put her out of alignment. The patient was wearing an aspen collar planning to see us.

Currently patient has no need for the collar and his symptoms have resolved after treatments with Prolotherapy and NUCCA maintenance. NUCCA is the National Upper Cervical Chiropractic Association chiropractic treatment guidelines for upper cervical instability.

Recently we did two NRRIT procedures on the vagus nerves. NRRIT is a nerve hydrodissection technique that can be successful in releasing nerve entrapments and restoring homeostasis. The nerve’s ability to receive, pass on and transmit correct messages between the brain and the body organs including the heart. After NRRIT and continued Prolotherapy the patient was able to get off of two of her three blood pressure medications. Medication was used to raise her blood pressure due to POTS. The patient is also now able to get out of bed right away in the morning instead of slowly taking her time sitting up before getting up because POTS allowed her to discontinue two or three of her medications for POTS and all of her symptomology including the POTS is almost completely dissolved.

In the image below we see an illustration of an injection around a compressed vagus nerve.

The story of a 16-year-old girl in a cardiology journal

Doctors are assessing the many ways to treat Dysautonomia, POTS, and hEDS. At our center, we rely on non-surgical and if possible, non-pharmacological methods. These treatments were briefly outlined above and will be explained in better detail below. Some doctors do rely on pharmacological methods to achieve patient treatment goals. The people who have success with these treatments are not the people that we typically see. We see the people who still suffer from a constellation of symptoms and conditions that are progressing.

Doctors at the  National University of Colombia published an April 2021 patient case in the Case Reports in Cardiology (15). It is the story of a 16-year-old girl with a 4-year history of snapping sounds in the joints of hips, elbows, and knees, especially in extension, with non-inflammatory polyarthralgia (pain in multiple joints) and persistent headache. Her medical history included recurrent neurocardiogenic syncopal episodes. She had sudden drops in heart rate and blood pressure leading to fainting since the age of 12, along with spontaneous recovery as if nothing happened.

She had joint hyperlaxity in hands, elbows, wrists, knees, and hips, with a Beighton score of 7/9 (High risk or having achieved a high level of hypermobility on the Beighton hypermobility scoring test). Skin hyperlaxity was also observed.

Elbow radiography showed radial head dislocation, while 24-hour Holter and blood pressure monitoring were normal. The tilt table test was compatible with mixed neurocardiogenic syncope and orthostatic intolerance syndrome.

Due to her history of neurocardiogenic syncope and joint hypermobility syndrome, she was diagnosed with joint hypermobility syndrome associated with Orthostatic Postural Tachycardia Syndrome (POTS). Nonpharmacological treatment was initiated, as well as increased fluid intake, sodium, postural therapy, among others. Clinical improvement was achieved due to a decrease in the frequency of syncopal episodes.

How did this patient achieve good treatment results?

In this case, the doctor’s goal was to provide successful nonpharmacological measures such as increased fluid intake, sodium, postural therapy, and rest, along with a multidisciplinary rehabilitative approach, looking to increase muscle strength and prevent further muscle loss. Based on this outcome in the 16-year-old-patient, her doctors suggested that:

“Patients should perform physical activity 3 to 4 times per week for at least 45 minutes, achieving a frequency between 75 and 80% of the expected maximum heart rate with a progressive increase, mainly from aerobic exercise.

Using elastic compression stockings in the lower limbs is also recommended with a pressure of at least 20 mmHg (compression socks can often be found with labels  “20-30 mmHg”) to improve venous (blood) return. Pharmacological therapy, such as the administration of fludrocortisone (corticosteroid) at doses of 0.05 to 0.2 mg per day, seeks to increase sodium retention to achieve blood volume expansion.”

A note on compression socks: 

The common hypothesis about POTS and hEDS is that the abnormal connective tissue hEDS patients may have may compromise blood vessels permitting the veins to distend excessively in response to ordinary hydrostatic pressures. This would lead to peripheral vascular pooling (blood pooling in the veins) and its hemodynamic (blood flow disorders) and symptomatic consequences such as orthostatic intolerance. Simply put, this connective tissue abnormally allows excessive amounts of blood to pool in these patients’ lower limbs when they stand. This idea was developed in a 1999 study (16) from Johns Hopkins University School of Medicine in a paper describing Chronic Fatigue Syndrome and orthostatic intolerance in a group of younger patients with hEDS. Here the doctors wrote: “We propose that the occurrence of these syndromes together can be attributed to the abnormal connective tissue in dependent blood vessels of those with EDS, which permits veins to distend excessively in response to ordinary hydrostatic pressures. This in turn leads to increased venous pooling and its hemodynamic and symptomatic consequences. These observations suggest that a careful search for hypermobility and connective tissue abnormalities should be part of the evaluation of patients with CFS and orthostatic intolerance syndromes.”

Connective tissue abnormalities and the cervical spine ligaments – Instability and hypermobility in the neck

In this section, we will discuss further the role of connective tissue abnormalities in cervical instability. Above we saw research that recommended that upper cervical instability treated with upper cervical fusion could alleviate some problems related to Dysautonomia, POTS, and the hEDS patient. The idea of the fusion is to prevent the bones of the neck from wandering around and thereby prevent possible compression on arteries, veins, nerves, and spinal cord that travel through the neck. But how does the body do this naturally? The body holds the bones of the neck in place with ligaments.

The ligaments of the cervical spine are bands of dense connective tissue bundles made up of collagenous fibers. Individuals with hEDS have multiple joints that are unstable because of the laxity of ligaments and tendons due to collagen variants. Let’s take a look first at the instability and laxity of ligaments this collagen disorder causes in the neck.

When the capsular ligaments of the neck become elongated, exhibit laxity, and cause excessive movement of the cervical vertebrae, a few things occur:

1) At the upper cervical spine instability  (C0-C2), can cause a number of symptoms including, but not limited to, nerve irritation and vertebrobasilar insufficiency with associated vertigo, tinnitus, dizziness, facial pain, arm pain, and migraine headaches.

2) In the lower cervical spine (C3-C7), this can cause muscle spasms, crepitation, and/or paresthesia in addition to chronic neck pain.

In either case, the presence of excessive motion between two adjacent cervical vertebrae cause these associated symptoms similar to those described in dysautonomia.

The occipito-atlanto-axial complex also has a unique anatomical relationship with the vertebral arteries. In the lower cervical spine, the vertebral arteries lie in a relatively straightforward course as they travel through the transverse foramina from C3-C6.

C1 and C2 are held in proper position by the transverse and alar ligaments-helping to protect the spinal cord, brain stem, and nervous system from excess movement in the upper cervical spine. When the ligaments are lax and elongated from hypermobility, this protective barrier is inefficient. Cervical instability can provoke irritation of both the vertebral and sympathetic nerves. Damage to ligaments and ensuing irritation to the surrounding nerve endings may alter the firing patterns from these nerve endings, which may cause increased activation of the sympathetic nervous system.

A cervical neck collar alleviates symptoms of cardiorespiratory and cerebrovascular function in POTS

An April 2020 study (18) from the School of Kinesiology and Health Science, York University and the Division of Cardiology, Department of Medicine, McMaster University Canada examined the effect of a neck compression collar on cardiorespiratory and cerebrovascular function in Postural Orthostatic Tachycardia Syndrome (POTS).

The goal of the study was to see if Postural Orthostatic Tachycardia Syndrome symptoms of reduced brain blood flow, autonomic dysfunction, and orthostatic intolerance could be improved by wearing a neck compression collar that could increase brain blood flow and influence autonomic reflexes. (The proper function of the autonomic nervous system).

In participants with POTS, wearing the Q-collar reduced orthostatic symptoms.

What does all this mean? 

The collar provided stability to the neck and prevented the bones from wandering this as noted above: the researchers found that using a neck compression collar alleviated orthostatic symptoms in an upright posture in participants with postural orthostatic tachycardia syndrome (POTS).

Many of you reading this article may have already had a cervical collar prescribed or you bought one of your own because you needed help “holding your head up.” Cervical collars can help, they may also make a situation worse. Please see our article Cervical collars – why do they help some people and not others? In this article, we discuss cervical collars to help alleviate the patient’s symptoms by stretching the spinal vertebrae to relieve pressure and pain on the nerves that transverse the cervical vertebrae. For many patients, this will provide relief of symptoms. For some patients, the cervical collar may cause more problems than it was designed to help. The automatic prescription of a cervical collar in instances of neck pain should not be automatic, but, carefully considered in each patient’s situation to maximize benefit and minimalize complications.

A case history of one of our patients.

As with any medical treatment, no guarantees or claims of cures are made as to the extent of the response to treatment that every person experiences. The video represents only the featured person/people’s experience or opinion. Every therapy/treatment has patients who experience varying levels of success and failure. Results may not be the same from patient to patient, even with a similar diagnosis, as the body’s internal status is unique to each individual patient.

Every doctor I went to would just kind of blow me off saying there was nothing wrong with me I was only attention-seeking.

How do I explain it? There would be episodic periods of time ranging from three to four months where I  wasn’t able to really eat right and my right side was constantly in pain. Every doctor I went to would just kind of blow it off, saying I was attention-seeking, which honestly if anybody hears that is just going to break their heart because internally you know something’s wrong but for some reason, the doctors can’t show you the inside what’s actually going on.

The doctors just trust the results, trust the blood tests and send you on your way. I got my official diagnosis two, three years ago. I was diagnosed with Mast Cell Activation Disorder and then we have POTS and then we have gastroparesis and Ehlers-Danlos Syndrome type III.

Dr. Hauser asks: When you came here if we said to you what would be the top three things that you would want to be helped the most with, what would you say they were?

I would probably start with gastroparesis because this is the main reason why I get hospitalized

I would probably start with gastroparesis because this is the main reason why I get hospitalized, ninety-nine percent of the time I’m in the hospital for a week and the doctors have to pump medications in me in order to get my nutrients level back up.

What is in gastroparesis that causes you to get hospitalized?

I had two gastric emptying scans (as many of you are aware this is a test to determine how fast you digest a meal). My numbers were really high.

A brief explanation of what “the numbers were really high” means.

The gastric emptying scan has a set of percentages of how quickly a meal should be digested.

Here our patient is reporting that her numbers were really high, 35% when it should have been 10% meal retention at four hours. Further, it took her a full eight hours to digest a full meal. This would cause her pain, discomfort, nausea, rapid weight loss, she would drop ten pounds in a week. She was advised to gain weight so that she could handle the rapid weight loss problems.

Saline infusions treatment

At 2:35 of the video, Dr. Hauser asks Stefanie why does she have an IV port in her heart area?

The first diagnosis I got was for POTS and my doctors were considering different treatment methods. But, because I would be at normal blood pressure in a supine position but when I stood up I would have low blood pressure, my doctors had to readjust my treatment methods. Beta-Blockers because of the normal reading on the supine position was ruled out. So I was given saline infusions to help regulate my blood pressure.

Brief research explanation: In the Journal of Interventional Cardiac Electrophysiology (17) researchers from the University of Toledo explain:

At 4:30 an update after three treatments. This video clip inserted here begins at the 4:30 mark

Stefanie describes her condition now 5 weeks after treatment.

As with any medical treatment, no guarantees or claims of cures are made as to the extent of the response to treatment that every person experiences. The video represents only the featured person/people’s experience or opinion. Every therapy/treatment has patients who experience varying levels of success and failure. Results may not be the same from patient to patient, even with a similar diagnosis, as the body’s internal status is unique to each individual patient.

Ehlers-Danlos Syndrome, Atlanto-axial instability, and Craniocervical instability

In my article Ehlers-Danlos Syndrome, Atlanto-axial instability, and Craniocervical instability, I write that “treatment of Ehlers-Danlos Syndrome-related craniocervical instability is challenging enough. Not having an initial, accurate diagnosis can make it more challenging. A lack of a diagnosis can send patients on a many-year journey searching for help that they cannot get because they and their doctors are chasing the wrong problem.” At our center, we concentrate on the diagnosis aspect of craniocervical instability and then provide links to treatments.

I invite you to read that article for more information on our treatments. Included in that article are summaries of:

  • C1-C2 bone spurs in a patient with Ehlers-Danlos Syndrome and symptoms of upper cervical instability
  • Very little research in exploring a myriad of problems seen in patients with hEDS and Craniocervical instability.
  • “Refine diagnosis and treatment of the various neurological and spinal manifestations of Ehlers-Danlos Syndrome.” The challenges of diagnosis
  • Neurological manifestations in hEDS – “abnormal stretching of or pressure on peripheral nerves”
  • The Alar Ligaments and Neurological manifestations
  • Patients with Ehlers-Danlos and their high risk for ligament incompetence put them and their atlantoaxial joint at a higher risk for instability.
  • Repairing the ligaments and curve for a long-term fix

What are we seeing in this image?

Here we see the before and after of neck curve corrections. Ligament laxity or looseness or damage, whether the cause is from trauma, genetic as in cases of Ehlers-Danlos Syndrome, ultimately causes a kyphotic force on the cervical spine, stretching the posterior ligament complex of the neck. As can be seen in the x-rays of this image, patients with a whiplash injury, Joint Hypermobility Syndrome, and Ehlers-Danlos Syndrome can have their cervical curve restored with Prolotherapy injections and the use of head and chest weights.

In this illustration we see the before an after of neck curve corrections. Ligament laxity or looseness or damage, whether the cause is from trauma, genetic as in cases of Ehlers-Danlos syndrome, ultimately causes a kyphotic force on the cervical spine, stretching the posterior ligament complex of the neck. As can be seen in the x-rays of this image, patients with a whiplash injury, Joint Hypermobility Syndrome, and Ehlers-Danlos syndrome can have their cervical curve restored with Prolotherapy Injections and the use of head and chest weights, documented below.

How do I know if I’m a good candidate?

We hope you found this article informative and it helped answer many of the questions you may have surrounding the challenges that you may be facing. 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.

Please visit the Hauser Neck Center Patient Candidate Form

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This article was updated September 1, 2021

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