Ross Hauser, MD

In this article, I discuss:

• Why some people with hypermobile Ehlers-Danlos syndrome (hEDS) or a hypermobility spectrum disorder develop orthostatic intolerance, POTS, digestive problems, fatigue, headaches, and other symptoms of dysautonomia.
• How the sympathetic and parasympathetic nervous systems regulate heart rate, blood pressure, digestion, temperature, sweating, and other automatic functions.
• Why the vagus nerve is important to communication among the brain, heart, lungs, and gastrointestinal tract.
• What the medical literature shows about the overlap among hEDS, POTS, gastrointestinal disorders, and mast-cell symptoms.
• New 2026 research investigating transcutaneous auricular vagus nerve stimulation for dysautonomia in women with hEDS.
• Why that study is promising but does not prove that cervical instability caused the participants’ dysautonomia or that vagus nerve stimulation is an established treatment.
• When cervical instability may be considered as one possible contributor in a selected patient with significant neck symptoms, while recognizing that POTS and dysautonomia have many potential causes.

People who contact Caring Medical often describe a long and confusing list of symptoms: rapid heartbeat after standing, lightheadedness, near-fainting, fatigue, headaches, nausea, abnormal digestion, temperature intolerance, sweating changes, brain fog, poor concentration, sleep disruption, and anxiety-like sensations. Some already carry diagnoses of POTS, hEDS, a hypermobility spectrum disorder, migraine, gastroparesis, or mast cell activation syndrome. Others are still searching for an explanation.

These symptoms are real, but they do not point to one universal cause. Dysautonomia is an umbrella term, and POTS is a clinical syndrome with several recognized and proposed mechanisms. A careful evaluation should consider cardiovascular, neurological, endocrine, hematologic, gastrointestinal, medication-related, and musculoskeletal factors before symptoms are attributed to the cervical spine.

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.

What are dysautonomia and POTS?

The autonomic nervous system regulates body functions that normally occur without conscious effort, including heart rate, blood pressure, breathing, sweating, temperature control, pupil responses, bladder function, and digestion.

The sympathetic nervous system helps the body respond to exertion or stress. The parasympathetic nervous system supports recovery, digestion, energy conservation, and the slowing of heart rate after a demand has passed. Dysautonomia occurs when one or more aspects of this automatic regulation do not function normally.

Postural orthostatic tachycardia syndrome, or POTS, is one form of orthostatic intolerance. Current diagnostic criteria generally require chronic orthostatic symptoms together with a sustained heart-rate increase of at least 30 beats per minute in adults—or 40 beats per minute in adolescents—within 10 minutes of standing or head-up tilt, without the blood-pressure fall required to diagnose orthostatic hypotension. Other causes of tachycardia must also be excluded. (1)

POTS can involve different and overlapping mechanisms, including low circulating blood volume, excessive venous pooling, partial autonomic neuropathy, high sympathetic activation, deconditioning, immune-related factors, and secondary medical conditions. The diagnosis therefore describes a physiological pattern; it does not by itself identify the cause.

Common symptoms include:

• Lightheadedness, blurred vision, weakness, or near-fainting while upright
• Palpitations and a rapid heart rate after standing
• Exercise intolerance and prolonged fatigue
• Headache, brain fog, and impaired concentration
• Nausea, abdominal discomfort, bloating, constipation, or diarrhea
• Heat intolerance and abnormal sweating
• Tremulousness, sleep disturbance, and sensations that may resemble anxiety

Why do hEDS and POTS frequently overlap?

hEDS is a heritable connective-tissue disorder characterized by generalized joint hypermobility and other musculoskeletal and systemic features. A hypermobility spectrum disorder may produce similar problems in people who do not meet the complete diagnostic criteria for hEDS.

A major review of dysautonomia in Ehlers-Danlos syndromes and hypermobility spectrum disorders described POTS, orthostatic intolerance, gastrointestinal and bladder involvement, and thermoregulatory symptoms as important clinical issues in this population. (2) Earlier controlled research also found substantially more orthostatic hypotension, POTS, and uncategorized orthostatic intolerance among people with joint hypermobility than among controls. (3)

An orthopedic review of 61 patients with Ehlers-Danlos syndrome reported POTS in 38%, with greater representation among younger patients. The authors emphasized the effect on school, employment, and quality of life. (4) In a study of 102 adults with hEDS or a hypermobility spectrum disorder, POTS was identified in 48%, other orthostatic intolerance in 25.5%, and orthostatic hypotension in 3.9%. The investigators found heterogeneous autonomic profiles rather than one uniform pattern. (5)

Not every study has found that POTS with hEDS is physiologically distinct from POTS without hypermobility. In a comparison of 20 patients with POTS and hEDS and 20 POTS controls, autonomic test results were generally similar, although the hEDS group used more medications and healthcare resources and had a greater chronic-pain burden. (6) A pediatric series of 362 patients with POTS found EDS in 22.7% and a hypermobility spectrum disorder in 39%. (7)

These studies establish an association. They do not show that loose cervical ligaments are the cause of POTS in every hypermobile patient.

Exercise intolerance, deconditioning, and the problem of a self-reinforcing cycle

A retrospective cohort of 144 patients with hEDS or a hypermobility spectrum disorder found dysautonomia in 65% of women and 44% of men. Exercise intolerance was the most frequent complaint. After symptom flares, many patients became less active; the proportion described as sedentary increased from 44% to 85% among those with dysautonomia. Smaller cardiac chamber sizes were also reported, consistent with cardiovascular deconditioning in at least some patients. (8)

This creates a difficult cycle. Joint pain and instability may reduce activity. Reduced activity can worsen conditioning and orthostatic tolerance. More severe orthostatic symptoms can then make exercise even harder. Deconditioning does not mean that symptoms are imagined, nor does it explain every case. It may be one modifiable component of a multifactorial disorder.

The question of why hypermobility and dysautonomia overlap has remained open for years. Proposed explanations include abnormal vascular connective tissue, excessive venous pooling, altered sensory signaling, pain, deconditioning, small-fiber neuropathy, immune mechanisms, and structural contributors. (9)

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.

Gastrointestinal symptoms in hEDS and POTS

The autonomic nervous system is deeply involved in digestive function, but gastrointestinal symptoms in hEDS and POTS are not automatically caused by the vagus nerve or the cervical spine.

A review of joint-hypermobility syndromes described associations with functional gastrointestinal disorders, pelvic and bladder dysfunction, anxiety disorders, and orthostatic tachycardia. (10) In a tertiary-center study of patients with hEDS, gastrointestinal symptoms were common, and POTS was a significant predictor of diagnosed gastrointestinal dysmotility. Because the study was retrospective and referral-based, it cannot be used to estimate prevalence in all people with hEDS. (11)

Research in patients with functional dyspepsia found joint hypermobility syndrome in 55%, but objective measures such as delayed gastric emptying, impaired gastric accommodation, and sensitivity to distention did not differ significantly between hypermobile and non-hypermobile groups. (12) This is a useful reminder that similar symptoms may arise through different mechanisms.

A clinical review of gastrointestinal symptoms in POTS discusses altered motility, abnormal circulation, autonomic neuropathy, hEDS, and mast-cell disorders as possible contributors. It recommends evaluating the specific symptom and physiology rather than assuming that every gastrointestinal complaint shares one cause. (13)

POTS, hEDS, and mast-cell symptoms: overlap does not prove one disease causes another

POTS, hEDS, and mast cell activation syndrome can occur in the same person. A 2021 study of 195 patients found a higher proportion of diagnosed mast cell activation syndrome among patients who had both POTS and EDS than among those without that combination. (14)

Other authors have cautioned that evidence for a single causal “triad” remains limited, definitions vary, and many symptoms overlap across the conditions. (15) More recent research in 100 young patients with POTS again found that estimates of hEDS, hypermobility spectrum disorders, and mast-cell activation varied substantially according to the diagnostic definitions used. (16)

The practical message is that coexisting conditions should be evaluated on their own criteria. Flushing, hives, wheezing, food-related reactions, abdominal symptoms, and orthostatic complaints should not be assigned to mast-cell disease, POTS, hEDS, or cervical instability without appropriate assessment.

The vagus nerve and autonomic regulation

The vagus nerve is a major pathway of the parasympathetic nervous system. Most of its fibers carry sensory information from the body toward the brain. Other fibers send regulatory signals from the brain toward the heart, lungs, throat, and gastrointestinal tract.

The vagus nerve contributes to heart-rate regulation, swallowing, voice, breathing, nausea, gastric function, and gut-brain communication. Cardiovascular autonomic disorders can reflect abnormalities in the heart, blood vessels, baroreflexes, sympathetic activity, parasympathetic activity, or several systems at once. (17)

Because autonomic symptoms can include palpitations, tremor, shortness of breath, gastrointestinal distress, sleep disruption, and heightened bodily arousal, some patients are initially told that their condition is anxiety. Psychological stress can intensify autonomic symptoms, but that does not make the underlying physiology unreal. Research on neurovisceral function shows that brain-body signaling and autonomic reactivity can influence emotional and physical symptoms in both directions. (18)

Venous pooling is one proposed connection between connective tissue and orthostatic symptoms

One long-standing hypothesis is that abnormal connective tissue permits dependent veins to stretch more than usual when a person stands. Excessive pooling in the legs and abdomen could reduce the blood returning to the heart and increase the compensatory heart-rate response. A 1999 report described the overlap among Ehlers-Danlos syndrome, chronic fatigue, and orthostatic intolerance and proposed this vascular-connective-tissue mechanism. (19)

This hypothesis is biologically plausible, but it is not the only possible explanation. Blood volume, medications, neuropathy, cardiovascular conditioning, pain, endocrine factors, and other conditions can also influence orthostatic symptoms.

Can the cervical spine contribute to dysautonomia in selected patients?

The vagus nerves travel through the neck within the carotid sheaths, near the internal jugular veins and carotid arteries. The upper cervical region also contains the brainstem–spinal cord junction, sympathetic nerve pathways, baroreceptor-related neural connections, and important cerebrovascular structures. This anatomy provides a rationale for studying the cervical spine in selected patients whose autonomic symptoms occur alongside significant neck pain, abnormal motion, or reproducible positional symptoms.

It does not prove a cervical cause.

A small physiological study tested a neck-compression collar in 10 participants with POTS. During upright tilt, the collar reduced orthostatic symptom scores and altered several autonomic and respiratory measurements. The investigators proposed baroreceptor compression as one possible explanation. The study did not test cervical instability, and the benefit should not be interpreted simply as “stabilization of the neck.” (20)

A retrospective surgical series evaluated patients with hereditary connective-tissue disorders, atlantoaxial instability, and refractory syncope or presyncope. Autonomic symptoms reportedly improved after stabilization. The results are clinically interesting but remain preliminary because there was no nonsurgical control group and the patients had substantial structural pathology. (21) Earlier work also described occipitoatlantoaxial hypermobility, cranial settling, and Chiari I malformation in selected patients with hereditary connective-tissue disorders. These findings apply to a specialized population and should not be generalized to every patient with hEDS, headache, dizziness, or POTS. (22)

For a broader explanation, readers may review our articles on craniocervical and cervical instability and autonomic nervous system dysfunction and spinal instability.

Caring Medical’s proposed cervical mechanisms

In our published hypothesis paper, we proposed that progressive loss of normal cervical structure and ligamentous stability may, in some patients, affect the nerves and vascular structures traveling through the neck. Potential pathways include altered cervical sensory input, sympathetic activation, internal jugular vein narrowing, and effects on the vagus nerve. (23)

We later used the term cervicovagopathy to describe proposed vagus nerve dysfunction arising from cervical pathology. This is a mechanistic framework and hypothesis—not a universally accepted diagnosis or proof that cervical instability causes every symptom associated with dysautonomia. (24)

In a 2026 retrospective cross-sectional study, we reviewed 227 consecutive patients aged 20–50 who presented to our outpatient neck center with chronic “brain-based” symptoms. Forward-head posture, loss of cervical lordosis, C1–C2 instability, reduced internal jugular vein cross-sectional area, reduced vagus nerve cross-sectional area, and elevated optic nerve sheath diameter were common in this highly selected cohort. (25)

The study identified associations, not causation. It did not include a healthy control group, could not estimate how common these findings are in the general population, and did not establish that the imaging or ultrasound measurements caused any specific symptom. The observations require independent replication and prospective research.

New 2026 research: Auricular vagus nerve stimulation for dysautonomia in hEDS

A 2026 prospective pilot study examined transcutaneous auricular vagus nerve stimulation, or taVNS, in 14 women with hEDS and disabling dysautonomia. Auricular stimulation targets a sensory branch of the vagus nerve at the ear. It is not an injection, operation, or stimulation of the cervical vagus nerve. (26)

Participants received one supervised 60-minute session each week for eight weeks. Autonomic symptoms were assessed with the Composite Autonomic Symptom Score-31, or COMPASS-31, and quality of life was assessed with the SF-36 questionnaire.

What the researchers reported

• Mean COMPASS-31 scores decreased from 44.6 to 28.3, a reported reduction of 36.5%.
• Five of the 14 participants moved below the study’s score threshold for disabling dysautonomia.
• Gastrointestinal symptom scores remained statistically improved after correction for multiple comparisons.
• Orthostatic, vasomotor, and pupillomotor scores showed nominal improvement but did not remain statistically significant after that correction.
• The total SF-36 quality-of-life score increased from 30.3 to 38.7, but the overall change did not reach statistical significance.
• All participants completed the protocol. No serious cardiovascular or neurological adverse effects were attributed to stimulation; five participants reported mild temporary sensations such as tingling or warmth.

Why the findings are promising—but preliminary

This was a small, open-label, single-arm pilot study without sham stimulation, participant blinding, or a control group. Most outcomes were self-reported questionnaires. The investigators did not use objective autonomic testing, inflammatory biomarkers, cervical imaging, or cervical vagus nerve ultrasound to demonstrate a physiological change or identify the source of dysautonomia.

The study cannot separate a treatment effect from expectation, placebo effects, natural symptom fluctuation, regression toward the mean, or other influences. It supports larger randomized, sham-controlled trials; it does not establish taVNS as an effective treatment for hEDS dysautonomia.

Most importantly for this article, the study does not show that cervical instability injured the vagus nerve. Auricular stimulation may influence central autonomic pathways regardless of why a patient developed dysautonomia. The study did not test Prolotherapy, cervical curve correction, cervical vagus nerve hydrodissection, or any other neck-directed treatment.

Readers can learn more about the anatomy and tests discussed at our center on our page about vagus nerve function and dynamic assessment.

Evaluation should remain broader than the neck

Symptoms such as dizziness, palpitations, fatigue, fainting, headache, nausea, and brain fog have many possible causes. Depending on the presentation, conventional evaluation may include:

• Supine and standing heart rate and blood pressure measurements
• A 10-minute standing test or tilt-table testing
• Electrocardiography and, when appropriate, cardiac rhythm monitoring
• Review of medications, hydration, nutrition, and recent illness
• Blood testing for anemia, thyroid disease, electrolyte abnormalities, and other metabolic causes
• Assessment for migraine, vestibular disorders, neuropathy, autoimmune disease, endocrine disease, gastrointestinal disease, sleep disorders, and deconditioning
• Evaluation for hEDS or a hypermobility spectrum disorder when the history and examination support it

A cervical evaluation may be reasonable when a patient also has substantial neck pain, head or neck trauma, abnormal neck motion, neurological symptoms, or a consistent relationship between head position and autonomic complaints. It should complement—not replace—appropriate cardiovascular, neurological, and autonomic assessment.

Treatment is guided by the mechanism and the patient’s findings

Management of POTS commonly begins with education, avoidance of aggravating factors, appropriate hydration and sodium strategies when medically suitable, compression garments, and gradually progressed physical reconditioning. Medication may be considered according to blood pressure, heart rate, blood volume, sympathetic activation, and other individual factors. (1)

Intermittent intravenous saline has been associated with symptom and quality-of-life improvement in an observational study of 57 patients with medication-refractory POTS, but the absence of randomization and the risks of repeated venous access limit what can be concluded. (27)

A published case of a 16-year-old with joint hypermobility and orthostatic symptoms described improvement with increased fluids and sodium, postural measures, and a multidisciplinary rehabilitation program. One case cannot establish treatment effectiveness, but it illustrates the importance of nonoperative management and conditioning. (28)

At Caring Medical, our interest is in identifying patients whose cervical ligament injury or instability may be one contributor to their symptoms. That possibility is considered only in the context of the patient’s history, examination, imaging, and broader differential diagnosis. No injection, device, exercise program, or surgical procedure is appropriate for every patient with POTS, hEDS, or dysautonomia.

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.

Summary

Dysautonomia can produce a difficult combination of cardiovascular, gastrointestinal, neurological, and temperature-regulation symptoms. POTS is one form of dysautonomia, and it frequently overlaps with hEDS and hypermobility spectrum disorders. The overlap is well documented, but the underlying mechanisms differ among patients.

The vagus nerve is an important part of autonomic regulation. New 2026 research found improved autonomic symptom questionnaire scores after eight weekly auricular vagus nerve stimulation sessions in 14 women with hEDS. The study is encouraging but preliminary because it was small, uncontrolled, unblinded, and based mainly on self-reported outcomes.

The cervical spine may deserve evaluation in a selected patient who has significant neck symptoms or reproducible positional complaints. Current evidence does not support cervical instability as a universal explanation for hEDS dysautonomia or POTS. Our published cervical-instability research identifies associations and proposes mechanisms that require prospective and independent confirmation.

The most responsible approach is to identify the patient’s dominant physiological problems, consider reasonable alternative diagnoses, and distinguish established evidence from preliminary findings and clinical hypotheses.

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Medical disclaimer

This article is for educational purposes only and is not a substitute for individualized medical diagnosis or treatment. Dysautonomia, fainting, palpitations, chest pain, neurological symptoms, and symptoms attributed to cervical instability require evaluation by an appropriately qualified healthcare professional. Preliminary research should not be used to self-prescribe vagus nerve stimulation or to assume that one mechanism explains all symptoms.