Ross Hauser, MD.

At Caring Medical, many patients are evaluated with hypermobile Ehlers-Danlos syndrome (hEDS) and chronic neck symptoms. One of the challenges in these patients is determining whether symptoms attributed to degenerative disc disease, cervical arthritis, or other structural abnormalities may also involve ligamentous cervical instability and abnormal cervical motion.

In our 2026 study, we published “Characterizing Initial Cervical Spine and Neurovascular Findings in 84 Consecutive Patients with Hypermobile Ehlers-Danlos Syndrome: A Retrospective Study” in the Journal of Clinical Medicine. (1)

We examined 84 consecutive patients with hEDS, ages 20–50. Patients with previous neck surgery or significant traumatic neck injury were excluded, allowing us to examine cervical findings in an hEDS population without these major confounding factors. We assessed cervical structure and instability as well as neurovascular findings involving structures traveling through the neck.

Our study reported a high prevalence of abnormalities involving cervical alignment, upper cervical instability, internal jugular vein dimensions, and vagus nerve measurements. These findings are important because hEDS is fundamentally a connective-tissue disorder associated with joint hypermobility and ligamentous laxity. When this laxity involves the cervical spine, the vertebrae may potentially move beyond their normal physiological limits.

From our clinical perspective, this raises an important question:

• In some patients with hEDS and chronic neurological, autonomic, or head and neck symptoms, could cervical ligament instability be an overlooked component of the problem?

We feel the importance of our study is that it examines cervical instability beyond the traditional discussion of neck pain and degenerative discs. The cervical spine is surrounded by important neurological and vascular structures. These include the spinal cord, vertebral arteries, internal jugular veins, vagus nerves, sympathetic nerves, and cerebrospinal fluid pathways. Our findings suggest that abnormal cervical structure in hEDS may coexist with measurable changes involving some of these structures.

This does not establish that cervical instability causes every neurological or autonomic symptom experienced by patients with hEDS. The study was retrospective and observational and did not include an asymptomatic hEDS control group. Therefore, the findings demonstrate associations rather than proving causation.  Nevertheless, the study provides a framework for further investigation into the relationship between connective-tissue laxity, cervical biomechanics, and neurovascular function.

The concept that spinal instability can occur in EDS is not new.

In a widely cited 2017 review in the American Journal of Medical Genetics, (2) researchers discussed neurological and spinal manifestations of Ehlers-Danlos syndromes.

The authors described segmental instability, scoliosis, kyphosis, early degenerative disc disease, and spondylosis among the spinal problems encountered in EDS. They further discussed how cervical and thoracic instability and disc disease may contribute to loss of normal cervical lordosis and increasing kyphosis, potentially producing mechanical neck pain and, in severe circumstances, progressive neurological compromise. We built upon this earlier understanding by providing clinical imaging and neurovascular observations from a specific group of patients with hEDS.

From ligament laxity to cervical dysstructure

We have also proposed a broader model explaining how ligamentous instability may progressively alter cervical structure. In our 2024 Frontiers in Neurology paper (3), we described how chronic cervical ligament injury and instability may contribute to deterioration of the normal cervical curve, forward head posture, and what the authors term cervical dysstructure.

As the cervical curve deteriorates, mechanical loading on the supporting ligaments may increase. In susceptible patients, this could potentially create a cycle:

• Ligament laxity → excessive cervical motion → altered cervical alignment → abnormal mechanical loading → further instability.

For patients with hEDS, this proposed mechanism is particularly relevant because ligamentous laxity is already part of the underlying connective-tissue disorder.

Cervical instability, the vagus nerve, and internal jugular veins

Another important  concerns structures located immediately adjacent to the cervical spine. The vagus nerves and internal jugular veins travel through the carotid sheath anterior to the cervical vertebrae. Changes in cervical alignment and excessive vertebral motion could therefore theoretically influence the space available to these structures.

In our 2025 Frontiers in Neurology paper, (4) we proposed the concept of “cervicovagopathy,” in which cervical ligament instability and cervical dysstructure could potentially contribute to stretching or compression of the vagus nerve.

Our 2026 hEDS study provides additional clinical observations relevant to this hypothesis because the investigators evaluated both vagus nerve and internal jugular vein measurements in their hEDS cohort. These proposed relationships remain an evolving area of research. They should not be interpreted to mean that cervical instability is the cause of dysautonomia, gastrointestinal problems, dizziness, brain fog, or other systemic symptoms in every patient with hEDS.

Rather, the research suggests another possible mechanism that may warrant investigation in carefully selected patients.

Why this may matter when surgery is considered

Patients with hEDS can present difficult treatment decisions because the visible abnormality on an MRI may not necessarily represent the entire mechanical problem. A patient may have disc degeneration, cervical stenosis, loss of lordosis, or other degenerative changes. However, if significant ligamentous laxity and abnormal vertebral motion are also present, treating a single degenerative segment may not address the broader biomechanical problem.

This does not mean that patients with hEDS should avoid surgery.

For patients with severe craniocervical instability, neurological compromise, and appropriate radiographic findings, stabilization surgery can be beneficial. A 2024 outcomes study of patients with EDS undergoing occipito-cervical fusion reported significant improvements in several clinical outcomes following carefully selected surgical treatment. (5)

The important issue is therefore patient selection and identification of the underlying pain and instability generators.

Looking beyond the conventional cervical MRI

A conventional cervical MRI provides valuable information about discs, spinal stenosis, spinal cord compression, arthritis, and other structural abnormalities.

However, an MRI obtained while the patient remains relatively motionless may not answer every question about ligamentous instability or abnormal motion.

For this reason, the Caring Medical approach to an hEDS patient with chronic cervical symptoms may include asking questions beyond: How much degeneration is visible on the MRI? The evaluation may also ask: Is ligamentous cervical instability contributing to abnormal motion, altered cervical alignment, or the patient’s symptoms?

Our research strengthens the rationale for investigating this question. It documents a pattern of cervical structural and neurovascular abnormalities in a consecutive cohort of patients with hEDS and provides a foundation for future controlled studies examining how these findings relate to symptoms and treatment outcomes.

For patients with hEDS, understanding the role of ligament integrity and cervical stability may therefore become an increasingly important part of determining whether conservative care, regenerative injection treatment such as Prolotherapy, or surgical stabilization represents the most appropriate treatment strategy.

References

1 Hauser RA, Griffiths M, Watterson A, Matias D, Rawlings BR. Characterizing Initial Cervical Spine and Neurovascular Findings in 84 Consecutive Patients with Hypermobile Ehlers–Danlos Syndrome: A Retrospective Study. Journal of Clinical Medicine. 2026 Mar 14;15(6):2212. [Google Scholar]
2. Henderson Sr FC, Austin C, Benzel E, Bolognese P, Ellenbogen R, Francomano CA, Ireton C, Klinge P, Koby M, Long D, Patel S. Neurological and spinal manifestations of the Ehlers–Danlos syndromes. InAmerican Journal of Medical Genetics Part C: Seminars in Medical Genetics 2017 Mar (Vol. 175, No. 1, pp. 195-211). [Google Scholar]
3. Hauser RA, Matias D, Rawlings B. The ligamentous cervical instability etiology of human disease from the forward head-facedown lifestyle: emphasis on obstruction of fluid flow into and out of the brain. Frontiers in Neurology. 2024 Nov 27;15:1430390. [Google Scholar]
4. Hauser RA, Matias D, Rawlings BR. Cervicovagopathy: ligamentous cervical instability and dysstructure as a potential etiology for vagus nerve dysfunction in the cause of human symptoms and diseases. Front Neurol. 2025;16:1572863. [Google Scholar]
5. Henderson Sr FC, Schubart JR, Narayanan MV, Tuchman K, Mills SE, Poppe DJ, Koby MB, Rowe PC, Francomano CA. Craniocervical instability in patients with Ehlers-Danlos syndromes: outcomes analysis following occipito-cervical fusion. Neurosurgical review. 2024 Jan 2;47(1):27. [Google Scholar]