Why It Matters How We Conceptualize hEDS

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.

In a previous article, I reflected on a chapter in Dr. Howard Schubiner's book Unlearn Your Pain, in which he appears to classify hypermobile Ehlers-Danlos syndrome (hEDS) as a neuroplastic condition (you can find it here). Before I begin, I want to emphasize that I have a great deal of respect for Dr. Schubiner and his contributions to the field. His work has helped many people understand something profoundly important: symptoms are not always a direct reflection of tissue damage, and the brain and nervous system can play a significant role in generating, amplifying, and maintaining symptoms. I agree with that. However, the classification of hEDS as a neuroplastic condition does not align with how hEDS is defined within current diagnostic frameworks. hEDS is a heritable connective tissue disorder with specific clinical diagnostic criteria. These criteria describe a systemic disorder of connective tissue integrity, not a condition whose primary mechanism is joint hypermobility and neuroplastic symptom generation.

While neuroplastic processes may influence symptom expression, severity, and persistence in individuals with hEDS (as they may in any chronic condition), this does not change the underlying classification of hEDS itself. This is not simply a matter of academic disagreement or terminology. It reflects a fundamental distinction between a diagnosed connective tissue disorder and explanatory models of symptom persistence. Ideas about classification matter because they shape clinical practice, research priorities, education, and healthcare decision-making, and ultimately influence patient outcomes. When conditions are misclassified, even with good intentions, the implications can extend far beyond theoretical discussion.

Why hEDS Is Not a Neuroplastic Condition

To understand why this matters, we first need to be clear about what hEDS actually is. hEDS is a hereditary connective tissue disorder. It is diagnosed on the basis of generalized joint hypermobility together with a range of systemic connective tissue features and other clinical criteria. Importantly, hypermobility alone is not sufficient for diagnosis. (For readers unfamiliar with the current diagnostic criteria, they can be found here.) Many people are hypermobile but do not have hEDS. The diagnosis requires evidence that something broader is occurring within the connective tissue system. This may include manifestations such as mitral valve prolapse, hernias, pelvic organ prolapse, rectal prolapse, bladder prolapse, skin abnormalities, atrophic scarring, dental crowding, arachnodactyly, and other recognized connective tissue features. These are not neuroplastic phenomena. A prolapse is not neuroplastic. A hernia is not neuroplastic. Abnormal connective tissue integrity is not neuroplastic. The fact that an individual with hEDS may also experience neuroplastic pain, central sensitization, or other neuroplastic symptoms does not transform the underlying connective tissue disorder into a neuroplastic condition. To suggest otherwise confuses a mechanism that may contribute to some symptoms with the nature of the disorder itself.

Why This Distinction Matters

At first glance, some readers may wonder whether this distinction is important. After all, if neuroplastic processes are contributing to symptoms, does it really matter how we categorize the condition? I believe it does, because diagnostic labels influence thinking. They influence how symptoms are interpreted. They influence what clinicians look for. They influence what patients pay attention to. They influence what gets investigated and what does not, and they influence what may be missed.

The Risk of Missing Serious Medical Complications

One concern I have is that framing hEDS as a neuroplastic condition may unintentionally increase the risk that some symptoms are prematurely interpreted through a neuroplastic lens. Take headaches as an example. Migraine-like headaches are common in hEDS. Many headaches may indeed involve sensitization, nervous system dysregulation, or other neuroplastic processes. However, hEDS is also associated with an increased risk of cerebrospinal fluid (CSF) leaks (I know, I have had them). CSF leaks can present with severe headaches that are easily mistaken for migraine or other primary headache disorders. The management is entirely different. A patient with a CSF leak requires appropriate medical evaluation and treatment. If patients, therapists, or healthcare professionals become accustomed to viewing hEDS primarily as a neuroplastic condition, there is a risk that some symptoms may be interpreted too quickly as manifestations of nervous system sensitization rather than possible signs of a medical complication. The problem is not that neuroplastic explanations are wrong. The problem is that they may become the default explanation, and default explanations sometimes cause us to stop looking. The same principle applies to other recognized complications associated with connective tissue disorders. Symptoms may sometimes signal instability, structural changes, prolapse, hernias, or other biological processes that warrant assessment. A conceptual framework that focuses primarily on neuroplasticity risks making these possibilities less visible.

Consequences for Patients

Many people with hEDS spend years fighting to have the biological reality of their condition recognized. They are often told that nothing is wrong, that they are anxious, that they are catastrophizing, that their symptoms are stress-related, and that they simply need reassurance. Receiving an hEDS diagnosis (assuming the diagnosis is correct) can be validating because it acknowledges that there is an identifiable connective tissue disorder underlying many of their experiences. To then describe hEDS itself as neuroplastic risks creating confusion about the nature of the condition. Patients may begin questioning whether their diagnosis represents a genuine connective tissue disorder or merely a nervous system phenomenon. Some may become uncertain about when symptoms should be medically evaluated and when they should be approached through neuroplastic strategies. Others may feel that the biological aspects of the condition are once again being minimised. Given the history of dismissal experienced by many individuals with hEDS, these concerns should not be taken lightly.

Consequences for Therapists

Therapists are increasingly encountering neuroplastic models of pain and persistent symptoms. In many ways, this is positive. These models offer powerful tools for understanding fear, conditioning, symptom monitoring, avoidance, and nervous system sensitization. However, therapists are not typically trained to diagnose connective tissue disorders or recognize their complications. If hEDS is conceptualized primarily as a neuroplastic condition, there is a risk that therapists may become overly confident in neuroplastic explanations while underestimating the relevance of medical assessment. This could lead to situations where symptoms requiring medical attention are inadvertently conceptualized as manifestations of fear, sensitization, conditioning, or symptom focus. The issue is not bad practice. The issue is that clinicians inevitably interpret symptoms through the frameworks they have been taught.

Consequences for Physicians

The same concern applies within medicine. Doctors are not immune to cognitive biases; none of us are. When a particular explanatory model becomes influential, clinicians may become more likely to interpret symptoms through that model. Psychologists refer to this as confirmation bias. Once a clinician begins expecting neuroplastic explanations, symptoms that fit that expectation tend to stand out, while contradictory information becomes easier to overlook. This does not mean that physicians would stop recognizing prolapse, hernias, CSF leaks, or other complications, but it does mean that the threshold for considering alternative explanations may gradually shift. History shows that medicine is particularly vulnerable to this phenomenon. When one explanatory framework dominates, competing explanations often receive less attention.

Consequences for Research and Education

The implications extend beyond individual patient encounters. Conceptual frameworks shape research priorities. They influence funding decisions. They influence educational materials. They influence how future healthcare professionals are trained. If hEDS becomes increasingly conceptualized as a neuroplastic condition, there is a risk that research attention shifts disproportionately toward nervous system mechanisms while fundamental questions about connective tissue pathology remain underexplored. This is particularly concerning given how much remains unknown about hEDS. The biological basis of the condition is still incompletely understood. Many important questions remain unanswered. This is not the time to narrow our focus.

Replacing One Reductionism with Another

One of the great contributions of the neuroplastic movement has been challenging the idea that all symptoms must be explained by structural pathology. That contribution has been enormously valuable. However, there is a danger that the pendulum swings too far. Historically, patients were sometimes reduced to tissue pathology. Now there is a risk that some conditions become reduced to neuroplasticity. Neither approach adequately reflects the complexity of human illness. hEDS is not simply a collection of symptoms generated by the brain, nor is it simply a connective tissue disorder devoid of psychological and social influences. It is a complex condition in which biological, psychological, and social factors interact, but the existence of those interactions does not change the fundamental nature of the disorder.

Final Thoughts

Neuroplastic symptoms can occur in people with hEDS. Neuroplastic pain can occur in people with hEDS. Central sensitization can occur in people with hEDS. All of that is true, but hEDS itself is not a neuroplastic condition. It is a hereditary connective tissue disorder. That distinction matters because once we misclassify a condition, we risk changing how patients understand their symptoms, how clinicians interpret clinical presentations, how researchers prioritize questions, and how future professionals are trained. The concern is not theoretical; it is practical. When influential voices shape the way a condition is understood, those ideas inevitably influence healthcare decisions. And when a connective tissue disorder is reframed as a neuroplastic condition, there is a real risk that important biological manifestations become less visible, not because clinicians stop caring, but because the conceptual lens through which they are viewed has changed. That is why this distinction matters. Not because neuroplasticity is unimportant, but because accurate classification is.

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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.