Is Hypermobile Ehlers-Danlos Syndrome a Neuroplastic Condition?

Although this article is aimed primarily at clinicians, researchers, and other healthcare professionals, readers with a personal interest in hEDS may also find it valuable. While some sections are necessarily more technical, I hope the broader discussion remains accessible to a wider audience.

I recently found myself reflecting on a chapter in Dr. Howard Schubiner’s recent book Unlearn Your Pain, in which he places hypermobile Ehlers-Danlos syndrome (hEDS) within a neuroplastic category of conditions. I found this categorization fundamentally at odds with both the clinical reality and diagnostic understanding of hEDS. This reaction arose not only from my lived experience of the condition, but also from my professional work as a health psychologist specializing in chronic illness and chronic pain.

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, categorizing hEDS as a neuroplastic condition represents a fundamental category error. It confuses the processes by which symptoms are experienced with the essence of the underlying disorder itself. hEDS is a hereditary connective tissue disorder characterized by structural manifestations that extend far beyond hypermobility and pain. Neuroplastic processes may contribute significantly to symptom generation and amplification in some individuals, sometimes profoundly, but that is not the same thing as saying that the condition itself is neuroplastic.

Recognizing the role of neuroplasticity in symptom generation does not justify redefining a connective tissue disorder as a neuroplastic illness. In fact, doing so risks obscuring the biological realities of the condition and the significant structural complications that many people with hEDS experience.

The Challenge of Categorizing hEDS

One of the difficulties with hEDS is that it presents very differently from person to person. Although all individuals with hEDS must meet the diagnostic criteria for a connective tissue disorder, the features that dominate their day-to-day experience can vary considerably. For some, chronic pain, fatigue, dysautonomia, gastrointestinal symptoms, headaches, dizziness, and anxiety are the most prominent and disabling aspects of the condition. Others experience more overt 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. Some individuals also experience respiratory and pulmonary complications associated with connective tissue laxity, including asthma-like symptoms, dysfunctional breathing patterns, sleep-disordered breathing, reduced chest wall stability, spontaneous pneumothorax (collapsed lung), tracheobronchomalacia (weakness and excessive collapse of the airways), and, in some cases, other structural abnormalities affecting lung function.

While these complications are not present in everyone with hEDS, they illustrate the wide-ranging effects that connective tissue differences can have throughout the body. These are not symptoms in the same way pain is a symptom; they are physical manifestations of connective tissue abnormalities. These differences raise an important question: are discussions about hEDS always referring to the same patient population? Before considering how neuroplastic processes may contribute to symptoms, it is worth examining how hEDS is actually diagnosed.

The Importance of Accurate Diagnosis

In Unlearn Your Pain, Dr. Schubiner’s discussion of hEDS appears to focus primarily on joint hypermobility and pain, alongside the observation that hypermobility itself does not reliably predict chronic pain. This is an important point and one that is supported by the research literature. Indeed, many people are hypermobile and never develop significant pain, while others experience substantial pain that cannot be fully explained by the degree of joint laxity alone. This observation provides a compelling argument for the role of neuroplastic processes, central sensitization, and other nervous system mechanisms in symptom generation.

However, hypermobility is only one component of the hEDS diagnostic criteria. The diagnosis is not made simply because a person is flexible or has a positive Beighton score. The 2017 International Diagnostic Criteria for hEDS are intentionally stringent and require the presence of multiple features across several domains. Since no definitive genetic marker has yet been identified for hEDS, diagnosis relies on a comprehensive clinical assessment, and an individual must meet all three major diagnostic criteria simultaneously.

The first criterion requires evidence of generalized joint hypermobility, typically assessed using the Beighton score. However, this is only the starting point. The second criterion requires additional evidence that the hypermobility is part of a broader connective tissue disorder. This includes systemic manifestations affecting multiple body systems, a confirmed family history, and/or specific musculoskeletal complications.

Importantly, to satisfy one aspect of this criterion, an individual must demonstrate at least five of twelve specified systemic features. These include characteristics such as soft or velvety skin, mild skin hyperextensibility, unexplained stretch marks, recurrent hernias, atrophic scarring, dental crowding, a high or narrow palate, arm-span-to-height disproportion, mitral valve prolapse, aortic root dilatation, and unexplained pelvic, uterine, rectal, or other organ prolapse. These are not simply subjective symptoms. They are objective manifestations of a connective tissue disorder.

The third criterion requires the exclusion of alternative explanations. Other forms of Ehlers-Danlos syndrome, Marfan syndrome, Loeys-Dietz syndrome, neuromuscular disorders, and other connective tissue conditions must be carefully considered and ruled out before a diagnosis of hEDS can be made.

Importantly, if an individual has symptomatic hypermobility but does not meet the full diagnostic criteria for hEDS, they may instead receive a diagnosis of Hypermobility Spectrum Disorder (HSD). HSD is a legitimate and often disabling condition that can involve chronic pain, instability, fatigue, and significant functional impairment. However, it is not synonymous with hEDS.

This distinction matters because Dr. Schubiner’s discussion appears to reduce hEDS largely to hypermobility and pain, while giving no attention to many of the connective tissue manifestations that form part of the condition's diagnostic framework. As a result, the discussion risks equating hEDS with symptomatic hypermobility rather than engaging with the full clinical reality of the disorder. These manifestations can include skin abnormalities, recurrent hernias, prolapse, atrophic scarring, cranio-cervical and spinal complications, cardiovascular involvement, respiratory complications such as tracheobronchomalacia, and other structural findings that extend well beyond joint flexibility alone. Consequently, while the observation that hypermobility does not predict pain supports the importance of neuroplastic mechanisms, it does not justify classifying hEDS itself as a neuroplastic condition. That conclusion confuses the mechanisms causing the symptoms with the nature of the underlying disorder.

Indeed, one of the examples presented in Unlearn Your Pain involves an individual described as having hEDS whose symptoms completely resolved following a neuroplastic approach. The section is even titled Recovery from Hypermobile Ehlers-Danlos Syndrome. While this example is entirely consistent with what we know about nervous system sensitization and symptom amplification, it does not demonstrate that hEDS itself is neuroplastic. At most, it demonstrates that neuroplastic processes were contributing to that individual's symptoms. Rather, it demonstrates that symptoms experienced by a person with hEDS may have been significantly influenced by neuroplastic processes. Improvement in pain, fatigue, dizziness, gastrointestinal symptoms, or other bodily sensations is not the same thing as reversing a connective tissue disorder.

A person whose chronic pain improves through Pain Reprocessing Therapy has not altered their collagen, repaired connective tissue fragility, reversed a prolapse, corrected scoliosis, eliminated mitral valve prolapse, resolved tracheobronchomalacia, stabilized structurally compromised tissues, or reversed the underlying connective tissue disorder itself. What may have changed is the way the nervous system processes and responds to bodily signals. That is a meaningful and valuable outcome, but it is not evidence that the underlying condition was neuroplastic in origin.

More broadly, Dr. Schubiner's argument appears to rest largely on the observation that people with hEDS often experience symptoms such as chronic pain, fatigue, dizziness, gastrointestinal problems, and other symptoms that overlap with conditions he conceptualizes as neuroplastic. While this symptom overlap is undeniable, similarity of symptoms does not imply similarity of underlying pathology. Many very different illnesses can produce fatigue, pain, cognitive difficulties, dizziness, gastrointestinal symptoms, and autonomic dysfunction. Many chronic illnesses also develop central sensitization over time. Classification should be based on the nature of the underlying disorder, not simply on the symptoms it shares with other conditions. Classifying hEDS as neuroplastic on the basis of symptom overlap risks shifting attention away from the defining feature of the condition: that it is a hereditary connective tissue disorder with established structural manifestations affecting multiple body systems.

There is also a practical concern here. When a condition is framed primarily as neuroplastic, there is a risk that genuine structural complications receive insufficient attention. Most neuroplastic practitioners would not advocate ignoring medical pathology, but patients may nevertheless come away with the impression that structural findings are unimportant or secondary. For individuals living with prolapse, recurrent dislocations, CSF leaks, cervical instability, cardiovascular complications, or respiratory complications such as tracheobronchomalacia, such a message can feel invalidating and may inadvertently contribute to the very forms of dismissal and misunderstanding that many people with hEDS already encounter within healthcare systems.

Heterogeneity Within hEDS

Even when the diagnosis is made accurately, people with hEDS can present very differently from one another. Some individuals experience chronic pain, fatigue, headaches, gastrointestinal symptoms, dizziness, and other symptoms that may be heavily influenced by nervous system sensitization and neuroplastic processes. For these individuals, approaches such as Pain Reprocessing Therapy (PRT), Emotional Awareness and Expression Therapy (EAET), mindfulness-based approaches, somatic therapies, and nervous system regulation may be particularly helpful. Others experience these same symptoms alongside significant connective tissue manifestations, including prolapse, recurrent dislocations, scoliosis, craniocervical instability, cardiovascular involvement, respiratory complications, or other structural abnormalities. In these cases, structural and neuroplastic factors coexist and interact.

Still others experience substantial structural complications that cannot reasonably be explained as neuroplastic phenomena. While neuroplastic processes may influence symptom severity, distress, coping, and secondary pain responses, they do not close a CSF leak, stabilize an unstable joint, repair connective tissue fragility, prevent airway collapse in tracheobronchomalacia, reverse a prolapse, repair a collapsed lung or a hernia, or correct spinal deformities. The key point is that hEDS is a heterogeneous condition. The relative contribution of structural and neuroplastic factors may vary considerably between individuals. Recognizing this complexity is very different from classifying the condition itself as neuroplastic.

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 conceptually difficult to defend. 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 tissue structure and integrity.

Put differently, the fact that symptoms can be neuroplastic does not mean that the condition itself is neuroplastic. Confusing these two risks obscuring the distinction between a connective tissue disorder and the mechanisms through which its symptoms are experienced. 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

hEDS is NOT a neuroplastic condition. By definition, it is a hereditary connective tissue disorder. Neuroplastic processes may contribute substantially to symptom generation, symptom persistence, and recovery, but they do not redefine the nature of the underlying condition. The more relevant question is not whether the condition itself is neuroplastic, but to what extent neuroplastic processes contribute to an individual's symptoms at a given point in time. Framing the condition itself as neuroplastic risks confusing the underlying disorder with the mechanisms that may influence symptom severity, persistence, and recovery.

A nuanced approach enables us to recognize both the realities of connective tissue disorders and the significant impact of the nervous system on how symptoms are experienced. 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. Recognizing the role of neuroplasticity does not require us to abandon the biological reality of connective tissue disorders, just as recognizing structural pathology does not require us to ignore the powerful influence of the nervous system on symptom experience.

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, scientific accuracy, and a willingness to move beyond simplistic explanations in either direction.

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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.