Your Pain Is Real. Your Scans Are Clear. Here’s What’s Actually Going On.
Most people who arrive into this work with chronic pain have been carrying it for years, have done the rounds of GPs and specialists, have the scans and the bloods and a folder of letters that all use some version of the phrase no significant findings.
The pain hasn't gone anywhere. It moves around the back, or sits in the jaw, or wakes them in the small hours with their shoulders locked into the pillow. Somewhere along the way someone said the word stress, in the tone that means we don't know what to do with you, and the conversation about the pain quietly stopped.
The pain is real. The scans are accurate. Both of those things can be true at the same time, because the place the pain is being generated is not the place that the scans were looking.
Pain that persists past the point where a tissue injury would have healed is usually being driven by the central nervous system rather than by the tissue. The system that processes pain can stay sensitised long after the original cause has resolved, sometimes for years, and once it does, the relationship between what's happening in the body and what's showing up on imaging starts to come apart. There's a substantial clinical literature on this now, and it has a specific name.
A 2024 review in Current Medicinal Chemistry described central sensitisation as increased responsiveness of pain-processing neurons in the spinal cord and brain to normal or below-threshold input. The careful clinical language is doing a lot of work in that sentence. What it means in practice is that the alarm system has been turned up, signals that wouldn't normally register as pain start to, and signals that should be mildly uncomfortable get amplified into something much louder. Research in The Lancet Rheumatology documented features of central sensitisation across fibromyalgia, osteoarthritis, rheumatoid arthritis, chronic low back pain, headaches, tendinopathies, spinal pain, IBS, chronic pelvic pain. The list is long because the mechanism isn't condition-specific. It's a pattern in how the central nervous system holds and amplifies pain signalling once it's been doing so for long enough.
In 2017 the International Association for the Study of Pain added a third category to sit alongside nociceptive pain, caused by tissue damage, and neuropathic pain, caused by nerve damage. They called it nociplastic pain, and it describes pain that arises from altered processing in the central nervous system rather than from ongoing injury at the site. The cluster of symptoms that travels with nociplastic pain is the cluster most people in this position already recognise, pain plus fatigue plus disrupted sleep plus brain fog plus mood that won't sit still, because nociplastic pain and nervous system dysregulation share a physiology.
The consequence of this for someone reading their own MRI report is the part that usually gets lost in the conversation. The amount of pain you feel does not have to correlate with the amount of tissue damage on the scan. Two people with the same disc bulge can have completely different pain experiences, one functionally fine, the other unable to drive, and the difference is often not in the disc. It's in the central nervous system interpreting the signals coming from it. Central sensitisation is one of the better-evidenced explanations for why two MRIs that look almost identical can produce two completely different lives.
How chronic stress sits inside the pain
The relationship between chronic stress and chronic pain isn't psychological in the way it's sometimes implied to be. It's neuroinflammatory, and once the loop is running, it tends to keep running on its own. When the HPA axis stays activated for long enough, cortisol stops being a useful short-term signal and starts driving low-grade neuroinflammation through activation of the glial cells in the central nervous system. Activated microglia release inflammatory cytokines that sensitise pain pathways, lower thresholds, and keep the central nervous system in the kind of hyper-excitability that maintains pain after the original trigger has long since resolved. A review in Frontiers in Psychiatry described chronic stress as disrupting the blood-brain barrier and allowing inflammatory mediators to cross into the central nervous system, where they activate the microglia that perpetuate the cycle.
A Neurology: Neuroimmunology and Neuroinflammation review called microglia central protagonists in the chronic stress response, and noted that repeated stress exposure changes their phenotype and function in ways that sustain neuroinflammation. Those changes are not transient. They persist after the original stressor has resolved, which is one of the reasons people sometimes feel worse, not better, six months after the difficult thing has ended. The body is still running the inflammation that the difficulty produced, even though the difficulty is over.
For someone who has been running on cortisol for years, holding a demanding job through poor sleep, managing a family that needs them, caring for ageing parents, the central nervous system has been sitting in the exact neurochemical conditions that keep pain pathways sensitised. The pain and the depletion aren't separate problems with a coincidental relationship. They're the same physiology, in the same system, expressing itself in different parts of someone's life.
The autonomic state the scan didn't measure
The other piece that usually doesn't make it into the workup is the state of your autonomic nervous system. Research on fibromyalgia, one of the most studied nociplastic pain conditions, has consistently found reduced vagal tone in people with the condition, measured through heart rate variability. A review in Neuroscience and Biobehavioral Reviews read fibromyalgia through the polyvagal theory lens and described how autonomic dysregulation, specifically reduced ventral vagal activity alongside sympathetic dominance, is implicated not just in the pain but in the full cluster of symptoms, the fatigue, the sleep disturbance, the cognitive problems, the emotional reactivity.
The same autonomic pattern shows up in irritable bowel syndrome, chronic headache, interstitial cystitis, endometriosis. Research has proposed that these conditions share a common physiology rooted in chronic autonomic threat responses, a nervous system stuck in protective mode with dampened ventral vagal function and elevated sympathetic or dorsal vagal activity. The same dysregulation that makes someone feel wired in the evening and flat by Friday, that breaks the sleep, that makes them reactive in meetings they could once handle in their sleep, is the dysregulation amplifying the pain signals at the same time. The pain and the burnout aren't running on parallel tracks. They're running on the same one.
What this means for what's actually been tried
If a significant component of someone's pain is being maintained by central sensitisation, then interventions focused only on the peripheral site, more injections, more imaging, more procedures targeting a structural pain generator, won't always address what's actually driving the pain. The 2024 Current Medicinal Chemistry review made this point explicitly, noting that understanding central sensitisation can help avoid persisting with procedures or surgeries when no reliable pain generator can be identified. That isn't an argument for never having surgery. It's an argument for understanding which kind of pain you're working with before deciding what to do about it, because the answer to that question changes what counts as treatment.
What the research supports for reducing central sensitisation looks different from what most people in chronic pain have been offered. Pain neuroscience education, where understanding what's actually driving the pain changes the brain's response to it. Graded movement that works with the nervous system's current capacity rather than pushing through the pain. Stress reduction that addresses the physiological stress response, not stress reduction that consists of being told to relax. Approaches that target autonomic regulation directly. A 2024 randomised trial published in JAMA compared a modern pain neuroscience approach combining education, stress management, and cognition-targeted exercise against usual-care physiotherapy for chronic whiplash-associated disorders, a condition strongly associated with central sensitisation. The approach that addressed the nervous system, not just the structural injury, produced better outcomes.
This is where nervous system regulation work becomes relevant. Not as a replacement for medical care, and not as the missing magic bullet that solves the problem in six weeks. As an additional layer that addresses one of the actual mechanisms keeping the pain going. If the system is stuck in chronic defence, helping it find its way back into safer states is part of the clinical picture, not separate from it.
Where this leaves you
If you've been told the scans are clear and the pain is still there, you're not making it up. You're not exaggerating. The pain is real. The source isn't where the imaging was looking, which is a different problem to having no source at all. Pain that fluctuates with stress and sleep and emotional load is pain with a significant central component, and that's useful information, because it points at where the work needs to happen.
The pattern, when it's described carefully, is one system showing up in several places at once. Pain, fatigue, sleep that doesn't restore, a body that won't switch off, a mind that won't either. Treating each of those as a separate problem hasn't worked because they were never separate problems. Looking at the system underneath them is a different way in.
Genevieve Gray BHSc, C.Hyp, RTTP
Nervous System Educator & RTT® Practitioner