Is Hypermobile Ehlers-Danlos Syndrome a Neuroplastic Condition?

I recently found myself reflecting on a chapter in Dr. Howard Schubiner’s book Unlearn Your Pain (see previous article here), in which he places hypermobile Ehlers-Danlos syndrome (hEDS) within a neuroplastic category of conditions. This raised some important questions and concerns for me, both as a psychologist who works with chronic illness and chronic pain, and as someone with lived experience of hEDS. Before going any further, I want to acknowledge that I have great respect for Dr. Schubiner’s contributions to the field of neuroplasticity and illness. His work has helped many people understand that chronic symptoms are not always a direct reflection of tissue damage and that the brain and nervous system can play a powerful role in generating and amplifying symptoms. However, I am concerned that placing all people with hEDS into a neuroplastic category is an oversimplification that does not adequately reflect the clinical and biological heterogeneity of the condition, including the clear presence of structural complications and mixed presentations in many individuals. This framing may be more appropriately placed within a mixed category, where both structural/connective tissue factors and neuroplastic (nervous system–mediated) processes contribute to the overall symptom presentation.

The Challenge of Categorizing hEDS

One of the difficulties with hEDS is that it presents very differently from person to person. Some individuals experience primarily joint hypermobility, chronic pain, fatigue, dysautonomia, gastrointestinal symptoms, headaches, and anxiety. Others develop more significant connective tissue complications, including pelvic organ prolapse, recurrent joint dislocations, cerebrospinal fluid (CSF) leaks, mitral valve prolapse, spinal curvature such as scoliosis or kyphosis, and various forms of cervical and cranial instability. In addition, many individuals show connective tissue features sometimes described as Marfanoid characteristics, such as unusually long limbs, long fingers, increased arm span relative to height, a narrow or high palate, or a generally elongated body habitus. These are not symptoms in the same way pain is a symptom; they are physical expressions of connective tissue differences. This raises an important question: When we talk about hEDS, are we talking about a single condition with a single mechanism, or are we talking about a broad diagnosis encompassing people with very different underlying experiences? In my view, there are at least three groups that deserve consideration.

Group One: Predominantly Neuroplastic Symptoms

There are undoubtedly people diagnosed with hEDS whose symptoms are heavily influenced by nervous system sensitization. Chronic pain, fatigue, headaches, gastrointestinal symptoms, dizziness, and other bodily sensations can become amplified through processes such as central sensitization, conditioning, hypervigilance, and fear of symptoms. Importantly, many people in this group still meet diagnostic criteria for hEDS and therefore still have hypermobile joints and perhaps other connective tissue features. However, their day-to-day symptom burden is more strongly driven by nervous system amplification of sensation rather than by major structural complications. For these individuals, approaches such as Pain Reprocessing Therapy (PRT), Emotional Awareness and Expression Therapy (EAET), somatic therapies, mindfulness-based approaches, and nervous system regulation may be extremely helpful. This may be the group that neuroplastic practitioners have primarily in mind when discussing hEDS.

Group Two: A Combination of Structural and Neuroplastic Factors

I suspect that many people with hEDS fall into this middle category. In these cases, there may be genuine connective tissue abnormalities alongside nervous system sensitization. The person may have joint instability, recurrent injuries, pelvic floor dysfunction, scoliosis or other spinal curvature (such as kyphosis), migraines, or other physical challenges. At the same time, years of pain, uncertainty, medical trauma, and repeated symptom monitoring can lead to central sensitization and increased nervous system reactivity. For example, a pelvic organ prolapse is a structural issue. However, the pain and distress associated with it may become amplified through sensitization. A person may have spinal curvature that creates real biomechanical strain, while central sensitization contributes to ongoing pain that extends beyond what would be expected from structural findings alone. A person may have mitral valve prolapse that is structurally present and clinically relevant, while also experiencing heightened bodily vigilance, anxiety, and symptom amplification. Joint instability may be real, while the nervous system contributes to ongoing pain long after tissues have partially adapted or healed. In these situations, structural and neuroplastic factors are not competing explanations. They coexist.

Group Three: Predominantly Structural Complications

There is also a subgroup of people with hEDS who experience significant structural complications that cannot reasonably be explained as neuroplastic phenomena. Examples might include confirmed CSF leaks, pelvic organ prolapse, recurrent joint dislocations, significant ligamentous injuries, marked scoliosis or kyphosis, mitral valve prolapse with functional significance, or forms of craniocervical instability. While neuroplastic processes may influence symptom severity, distress, coping, and secondary pain responses, they do not repair connective tissue, close a dural tear, correct spinal curvature such as scoliosis or kyphosis, reverse mitral valve prolapse, stabilize an unstable joint, restore pelvic support structures, or eliminate structural connective tissue fragility. This distinction matters because people with these complications may feel dismissed if structural pathology is interpreted primarily through a neuroplastic lens.

The Difference Between a Condition and Its Symptoms

Part of the confusion may stem from failing to distinguish between a diagnosis and the mechanisms contributing to symptoms. Saying that many symptoms experienced by people with hEDS involve neuroplastic processes is very different from saying that hEDS itself is a neuroplastic condition. The first statement is well supported by the scientific literature. Chronic pain, migraines, fatigue, gastrointestinal symptoms, dizziness, and other persistent symptoms can all be influenced by nervous system sensitization. The second statement is much harder to justify. hEDS is currently understood as a hereditary connective tissue disorder, even though the precise genetic mechanisms remain unclear for many patients. Connective tissue abnormalities are not neuroplastic phenomena; they reflect differences in structural proteins and tissue integrity. Recognizing the role of neuroplasticity does not require us to deny the existence of structural pathology. Both can be true at the same time.

A Broader Perspective on Chronic Illness

In many ways, this debate extends beyond hEDS. Most chronic illnesses involve some interaction between biological processes and nervous system functioning. Rheumatoid arthritis, inflammatory bowel disease, endometriosis, migraine, and many other conditions can involve central sensitization alongside underlying disease processes. The presence of neuroplastic mechanisms does not mean the illness itself is neuroplastic. A useful analogy is that a house can have both a faulty foundation and an oversensitive alarm system. Repairing the alarm system may reduce distress and unnecessary alerts, but it does not fix the foundation. Equally, repairing the foundation may not immediately calm an alarm system that has been activated for years. Both problems can exist simultaneously.

Moving Beyond Either/Or Thinking

Perhaps the most helpful way of understanding hEDS is not to place it entirely in a structural category or entirely in a neuroplastic category. Instead, we might recognize that people with hEDS exist along a spectrum. For some, symptoms may be predominantly neuroplastic. For others, symptoms may arise from a combination of structural and neuroplastic factors. For still others, significant structural complications may play a central role. A nuanced approach allows us to acknowledge both the realities of connective tissue disorders and the powerful influence of the nervous system on symptom experience. In my view, this is where the biopsychosocial perspective remains valuable, not because it reduces symptoms to psychology, but because it reminds us that biological, psychological, and social factors interact in complex ways. We do not have to choose between structure and neuroplasticity. In many cases, both are contributing to the person’s experience. The challenge is not deciding whether hEDS is “real” or “neuroplastic.” The challenge is understanding which mechanisms are operating for a particular person at a particular time, and tailoring treatment accordingly. That requires curiosity, humility, and a willingness to move beyond simplistic explanations in either direction.

If you liked this post or know someone who might find it useful, please share. You can also join my mailing list at www.ingelathuneboyle.com for regular blog notifications straight to your inbox! Please check out my other blog posts here.

------------------------------------------------

Dr. Ingela Thuné-Boyle is a licensed Practitioner Health Psychologist and a Doctor in Behavioural Medicine who specializes in improving the quality of life of people struggling with long-term health problems, chronic pain and trauma. She runs a private online (telehealth) practice at www.ingelathuneboyle.com. You can find out more about her background [here], and more about her approach to therapy [here].

📩 Contact: For therapy or other enquiries, you can contact her at info@ingelathuneboyle.com.

Please note: Advice given in this blog is not meant to take the place of therapy or any other professional advice. The opinions and views offered by the author is not intended to treat or diagnose, nor is it intended to replace the treatment and care that you may be receiving from a licensed physician or mental health provider. The author is not responsible for the outcome or results following their information and advice on this blog.