Neuroplastic Pain and the Biopsychosocial Model: Contradiction or Complement?

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

I have recently been reading Dr. Howard Schubiner's new book, "Unlearn You Pain," and found myself reflecting on his discussion of the biopsychosocial model. As I understand his argument, he is concerned that the model may inadvertently encourage some people with neuroplastic pain to continue searching for a structural explanation for their symptoms. This raises an interesting question: is neuroplastic pain theory fundamentally different from the biopsychosocial model, or is it better understood as a more specific explanation operating within it? While I understand the concern, I believe the disagreement may be less about the biopsychosocial model itself and more about how it is interpreted and applied in clinical practice.

What Counts as "Biology"?

One of the central issues in this debate is that the word biological is often interpreted in different ways. When patients hear that their pain has biological, psychological, and social influences, the biological component is frequently understood as referring to structural damage or an ongoing physical abnormality that has not yet been identified. For someone experiencing neuroplastic pain, this interpretation can understandably lead to repeated investigations, ongoing symptom monitoring, heightened health anxiety, and a continued search for a missing diagnosis. In turn, these patterns can reinforce fear, uncertainty, and the neural pathways associated with persistent symptoms. From this perspective, it is understandable why some clinicians working in the neuroplastic pain field worry that the biopsychosocial model may inadvertently keep people anchored to a tissue-damage explanation for their symptoms. However, this concern is quite different from the idea that the biopsychosocial model itself defines biology solely in terms of structural pathology.

In contemporary pain science, neuroplastic pain mechanisms are widely understood as biological processes in their own right. Central sensitization, predictive processing, conditioned responses, learned neural pathways, autonomic nervous system dysregulation, and neuroplasticity all involve the functioning of the brain and nervous system. The nervous system is biology. For this reason, many clinicians working in pain psychology, health psychology, rehabilitation, and modern pain science continue to use the biopsychosocial framework while also integrating neuroplastic pain concepts. These approaches are not seen as contradictory. Rather, neuroplastic pain is understood as one example of how biological, psychological, and social factors interact to shape symptom experience. In this sense, Schubiner's work can be viewed not as rejecting the biological domain, but as expanding what counts as biological. Instead of focusing solely on tissues, joints, muscles, discs, or structural abnormalities, attention is directed toward the brain, nervous system, learning processes, and neural networks. Neuroplastic pain theory is, in fact, deeply biological; it simply locates the biological mechanisms in different systems.

Recovery Versus Coping

Another important aspect of this discussion concerns the goals of treatment. Historically, many chronic pain programs have emphasized coping, adaptation, and acceptance. Patients were encouraged to improve quality of life, maintain meaningful activity, and build fulfilling lives despite ongoing symptoms. This approach developed partly because many people do not experience complete symptom resolution, and supporting wellbeing in the presence of pain is an essential clinical goal. At the same time, some advocates of neuroplastic pain treatment have argued that this framing can become limiting if it is interpreted as meaning that pain is necessarily permanent and that acceptance is the best possible outcome. Schubiner, Alan Gordon, and others have challenged this assumption by emphasizing that substantial improvement and complete recovery is possible when symptoms are primarily driven by learned neural pathways rather than ongoing tissue pathology. For many people, this has offered an important and hopeful reorientation. However, recovery and coping do not need to be positioned as opposites. People can work toward symptom reduction and recovery while also developing skills that allow them to live meaningful, engaged lives in the present. These are not mutually exclusive pathways but complementary ones.

The Perspective of Chronic Illness

This discussion becomes especially important when considering chronic medical conditions. For individuals living with rheumatoid arthritis, multiple sclerosis, Ehlers-Danlos syndrome, or other chronic illnesses, it would be inaccurate to suggest that no biological disease process is present. These conditions involve genuine physiological changes that require appropriate medical assessment and management. At the same time, symptom severity, including pain, fatigue, disability, and distress, is often influenced by far more than disease activity alone. Nervous system sensitization, stress physiology, emotional states, cognitive expectations, sleep disturbance, trauma history, social context, and environmental demands all contribute to how symptoms are experienced and interpreted. For this reason, many clinicians adopt a both-and approach rather than an either-or framework. Structural pathology and nervous system processes can coexist.

Neuroplastic mechanisms may be present alongside identifiable disease processes, and they may also occur independently of structural pathology. Recognizing one does not require denying the other. From this perspective, recovery can take different forms. For some individuals, it may involve full resolution of symptoms. For others, it may involve meaningful reduction in symptom intensity, improved function, increased participation in life, and greater emotional wellbeing. The presence of biological disease does not eliminate the possibility of improvement, nor does it negate the role of the nervous system in shaping symptom experience.

Symptom Perception and the Biopsychosocial Model

More recent theories, such as the symptom perception model and neuroplastic pain theory, can be viewed as refinements of the biopsychosocial model rather than alternatives to it. The biopsychosocial model tells us that biological, psychological, and social factors all contribute to symptoms; symptom perception models help explain how this occurs. According to these theories, symptoms emerge through the interaction of bodily processes, learned neural pathways, previous experiences, emotions, attention, expectations, beliefs, and environmental context. This helps explain why pain may persist even when there is no longer sufficient tissue damage to account for its intensity. Importantly, this does not mean the pain is imagined or "all in the mind." The pain is real, but the processes generating and amplifying it may involve the brain and nervous system rather than ongoing tissue injury. From this perspective, the symptom perception model does not replace the biopsychosocial model; it provides a more detailed account of one of the mechanisms through which biopsychosocial factors influence symptom experience.

Is the Biopsychosocial Model Incompatible with Recovery?

For these reasons, I would be cautious about framing the biopsychosocial model as inherently incompatible with recovery. The model itself does not make predictions about prognosis. Rather, it offers a framework for understanding the multiple interacting influences that shape health, illness, symptoms, and functioning. Whether recovery is considered possible depends largely on how the biological component is conceptualized. If biology is defined only in terms of fixed structural damage, then recovery may appear unlikely. However, if biology also includes neuroplasticity, nervous system learning, sensitization, predictive processing, and conditioned neural pathways, then recovery becomes entirely compatible with biological processes. The nervous system is capable of change. Learning can be revised. Neural pathways can be reshaped. Sensitization can reduce. These are all biological realities.

A Framework and a Mechanism

A useful way to understand this debate is to distinguish between levels of explanation. The biopsychosocial model operates as a broad framework, identifying the domains that contribute to health and symptoms. Neuroplastic pain theory and symptom perception models operate at a more specific level, describing mechanisms through which these domains interact within the nervous system.

Rather than replacing the biopsychosocial model, these newer theories can be understood as operating within it. The biopsychosocial model tells us which factors matter; neuroplastic pain and symptom perception models help explain how those factors can produce and maintain symptoms.

Seen in this way, the two perspectives are not competitors but complements. One provides the overarching structure, while the other offers a more detailed account of specific processes within that structure. Far from undermining the biopsychosocial model, neuroplastic pain science arguably deepens it, expanding our understanding of biology to include the adaptability of the nervous system and the complex processes through which symptoms are generated and sustained. In fact, when communicated well, it can be a highly validating framework for patients.

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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.