Understanding Nociplastic Pain: Insights from Dr. John Quintner That Can Change How We See Chronic Pain

If you live with persistent pain that continues long after an injury or surgery seems resolved, or pain that appears without clear structural explanation despite normal imaging and laboratory results, you understand the frustration of seeking clarity. Many patients I see here in Toronto describe this situation: their clinicians report that tests look unremarkable, yet the pain remains tangible and life-altering. The concept of nociplastic pain has gained traction as a helpful way to frame these experiences, and Dr. John Quintner offers one of the most lucid and thoughtful explorations of it.

Dr. Quintner, a retired Australian rheumatologist and pain medicine specialist, volunteers with Arthritis and Osteoporosis Western Australia and maintains an active role in research and education. He has earned respect for his willingness to examine established ideas in pain science with rigor, especially when the evidence warrants reconsideration. In collaboration with colleagues such as Dr. Milton Cohen, his writings encourage a shift away from hunting for obscure muscle lesions or hidden damage and toward a clearer recognition of how the nervous system can produce and perpetuate pain.

A key publication that reshaped perspectives for many practitioners is the 2015 critical review by Dr. Quintner, Dr. Geoffrey Bove, and Dr. Milton Cohen in the journal Rheumatology. For years the dominant model attributed myofascial pain to discrete trigger points, supposed painful knots within muscle that formed taut bands and referred discomfort elsewhere. Standard approaches involved pressing, stretching, or needling these points to release them. Quintner, Bove, and Cohen scrutinized the available evidence and concluded that the case for primary muscle pathology as the central driver does not hold. They offered a more consistent account: the local tenderness and referred pain commonly labeled as trigger points often arise from irritation or sensitization of peripheral nerves, including the fine nervi nervorum that innervate the connective tissue sheaths of larger nerves. When these nerves experience mechanical or inflammatory irritation, the central nervous system interprets the input as originating in the nearby muscle. This perspective redirected attention toward peripheral nerve sensitization, aligning better with both clinical patterns and experimental data.

I had the privilege of contributing to that work indirectly. While Dr. Bove was collaborating with Dr. Quintner on the paper, I was deeply involved in his neurobiology laboratory at the University of New England. I assisted with editing and refining aspects of the manuscript during that time, and making it more relevant to manual therapists. Those years of close collaboration gave me firsthand insight into the careful reasoning behind their critique.

Our interest in the mechanisms of pain provided fertile ground for later discussions of nociplastic pain. In their 2025 article “Nociplastic pain: exploring the concept and ongoing discussions,” published in the Korean Journal of Pain, Dr. Quintner joined Dr. Asaf Weisman of Tel Aviv University’s Spinal Research Laboratory and Dr. Milton Cohen to examine the topic more fully. Conventional medical education has typically sorted pain into nociceptive pain, which signals actual or potential tissue damage (for example, a sprained ankle or arthritic flare), and neuropathic pain, which stems from identifiable damage or disease within the nervous system (such as diabetic neuropathy). However, many individuals, particularly those dealing with fibromyalgia, diffuse chronic pain, or symptoms that outlast apparent injury or postoperative recovery, fall outside these neat divisions. Diagnostic investigations frequently reveal little, yet the pain endures and may broaden in scope.

Nociplastic pain serves as a third descriptive category. At its core, it denotes pain that originates from altered nociceptive function within the nervous system, without requiring evidence of ongoing tissue injury or discrete nerve pathology. Sensitization occurs: the threshold for activation drops, signals amplify more readily, and activity can arise independently of external provocation. Quintner and his co-authors underscore that nociplastic pain functions as a mechanistic descriptor rather than a standalone diagnosis. It lends biological credibility to the patient’s report without necessitating perpetual searches for undetected lesions. Equally important, it questions the entrenched clinical assumption that ongoing pain invariably points to unresolved structural harm or inflammation. That traditional stance often left thoughtful patients feeling unheard or reduced to psychological explanations. Dr. Quintner and Dr. Weisman call for a more contemporary view: pain constitutes a perceptual experience generated by the brain and nervous system, one that can persist as a valid biological process even absent continuous tissue damage.

My laboratory research with Dr. Bove complements these ideas, particularly concerning the contribution of adhesions. Over more than ten years in his neurobiology lab, we explored the biological pathways through which soft-tissue alterations are formed and then sustain pain, concentrating on postoperative and post-injury adhesions and fibrosis. Our NIH-supported studies produced several peer-reviewed publications, most notably our 2017 paper in PLOS ONE, “Attenuation of Postoperative Adhesions using a Modeled Manual Therapy”. Our work seemed like an important analysis of what many manual therapists describe as “reducing scars”.

The results carry direct clinical implications. After surgery or trauma, scar tissue forms as part of ordinary repair. Yet when tissues lack sufficient early, gentle motion. Commonly due to pain, restricted activity, or medications that impair motility, adhesions may develop. These tether organs, muscles, or fascial planes that should slide freely relative to one another. The resulting mechanical strain on nerve endings fosters localized inflammation and peripheral nerve sensitization. Repeated nociceptor activation can then feed into wider nociplastic processes, enabling pain to become chronic or more diffuse.

Encouragingly, manual therapy can help break this sequence. In our controlled experiments, we applied a modeled visceral manipulation technique to rats shortly after surgery. When introduced early and repeated appropriately, the intervention reduced the frequency and extent of certain cohesive adhesions, diminished inflammatory and fibrotic markers, and decreased abnormal attachments between visceral structures and the abdominal wall. It also appeared to assist in disrupting immature adhesions before they consolidated. On a mechanistic level, the therapy interrupted sustained nociceptive firing from irritated nerves and supported restoration of normal neural responsiveness.

These outcomes reflect established physiology. Skillfully applied manual therapy delivers the mechanical stimulus tissues need for proper remodeling, eases aberrant tension on nerves, influences local inflammatory signaling, and reestablishes healthy gliding between layers. In my Toronto practice I draw on these principles when treating patients with post-surgical scarring, abdominal or pelvic adhesions, adhesive capsulitis, repetitive strain injuries, or longstanding spinal pain. Many have invested considerable time in trigger-point centered therapies that provided only short-term benefit. Addressing the nerve irritation and adhesion-related sensitization frequently leads to decreased pain, enhanced mobility, and greater confidence in the recovery process.

Dr. Quintner’s account of nociplastic pain integrates naturally with this body of work. Adhesions and fibrosis, though frequently undetectable on standard imaging, can act as ongoing peripheral contributors that maintain nervous system sensitization. The decade I spent working alongside Dr. Bove demonstrated that precise manual therapy exerts tangible effects on the mechanisms underlying many forms of chronic pain. It connects earlier muscle-focused models with the richer contemporary understanding of peripheral and central sensitization. It makes fascia less relevant, and interfaces of tissue where adhesions and nociception can occur more of a relevant model.

For readers who value a thoughtful, informed approach to their pain and healing, this synthesis offers real agency. It confirms that the pain has a sound biological grounding without implying fault or weakness. It also points toward practical strategies: education about nervous system sensitization paired with targeted manual techniques to manage adhesions and nerve irritation, supported by attention to movement, sleep quality, and broader nervous system regulation.

Pain science has progressed meaningfully, and the scholarship of Dr. Quintner, Dr. Bove, Dr. Weisman, and Dr. Cohen is fostering more precise, less stigmatizing care. If elements of nociplastic pain or adhesion-mediated sensitization seem relevant to your circumstances, our clinical practice can help you assess your pain, and perhaps bring about some clarity of thought surrounding the ‘why’.

Those interested in the source material may find value in the 2015 trigger-point review by Quintner, Bove, and Cohen; the 2025 nociplastic pain article by Quintner, Weisman, and Cohen; and our 2017 PLOS ONE study on modeled manual therapy and adhesions. Each rewards attentive reading for anyone seeking a deeper grasp of their own situation.

We are also witnessing a welcome evolution in the language used to describe pain. Older frameworks, such as the gate control theory from the 1960s, introduced important ideas about modulation in the spinal cord but still tended to portray pain primarily as a signal that could be gated or blocked. In clinical practice this sometimes slipped into unhelpful shorthand that left patients hearing their pain was “all in their head” when no clear tissue damage appeared. The shift toward terms like nociplastic pain moves us beyond that binary thinking. It acknowledges the nervous system’s capacity to generate genuine, biologically rooted pain experiences through sensitization processes, without requiring ongoing injury or invoking psychological dismissal. This more precise and respectful vocabulary helps patients and clinicians engage with chronic pain as a legitimate, multifaceted phenomenon worthy of serious attention and targeted care.

I will finish with my gratitude to Dr. Geoffrey Bove for the opportunity to learn and grow my knowledge through his love of the scientific method, and is innovations and contributions to the world of pain science.

Know that your pain is intelligible, and considered evidence-guided steps can lead to meaningful improvement in your wellbeing.

Susan Chapelle, RMT MBA and Katherine Ditterman, Physiotherapist

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