04/23/2026
Very interesting article explaining nociplastic pain.
"Your scans are clean, so there's nothing wrong."
If you've ever been told that whilst sat in a doctor's office in actual pain, this post is for you. Because there is something going on. It has a name. And the pain research world has been slowly catching up with it for years.
It's called nociplastic pain. And it's one of the most important concepts for those with fibromyalgia, hypermobility and EDS to understand.
Right, so let me back up a bit.
For most of modern medicine's history, pain research has officially recognised two mechanistic categories. Nociceptive pain, which is pain from actual or threatened tissue damage (you roll your ankle, your ankle hurts, makes sense). And neuropathic pain, which is pain from a lesion or disease of the nerves themselves (think sciatica with a compressed root, or diabetic neuropathy).
For years, clinicians and researchers knew there were people who didn't fit either box. Fibromyalgia being the most obvious example. The pain was real, it was widespread, it was debilitating, and yet the scans were clean and there was no clear nerve damage anywhere.
So, various labels were used over the years to try and capture it. "Central sensitisation pain." "Dysfunctional pain." "Functional pain." "Idiopathic pain." None of them really stuck, and none of them were formally endorsed.
Then in 2017, the International Association for the Study of Pain officially adopted a third mechanistic descriptor. Nociplastic pain. In 2021, Eva Kosek and colleagues published formal clinical criteria and a grading system for it in the journal PAIN (Kosek et al., 2021). And in the same year, Mary-Ann Fitzcharles and colleagues wrote a major review in The Lancet (Fitzcharles et al., 2021) explicitly framing fibromyalgia as the textbook example of this type of pain.
This isn't fringe stuff. This is the biggest pain research body in the world saying, yeah, this is a real, measurable, neurobiological thing with its own mechanism.
Now, before we go any further, I want to clear up something that drives me up the wall.
Your nerves don't "send pain." I know that's the phrase everyone uses. We've all said it. But it's not how pain actually works. Your nerves send information. Mechanical stress, temperature, pressure, chemical changes, stretch, the lot. That information gets to your spinal cord, up to your brain, and your brain takes all of it and mixes it with context, memory, mood, attention, threat, past experience. Then the brain and nervous system decide whether to produce pain.
Pain is made by the brain and nervous system. Not delivered to it.
That distinction matters, and it matters a lot. Because in nociplastic pain, what's changed isn't the tissue. It's the processing. The system that decides how much pain to produce has been running in a turned-up state for so long that ordinary input starts getting processed as threatening.
Light touch hurts. Clothing hurts. Normal movement hurts.
A stressful week and everything flares. None of it is imagined and none of it is exaggerated. The system is genuinely working differently. And we can measure it.
So, what does this actually look like?
For those with fibromyalgia, they sit right at the centre of the nociplastic pain picture. The widespread pain that doesn't map to any one structure. The sensitivity to sound, light, temperature, smell. The non-restorative sleep. The fatigue. The cognitive problems (what most of you call fibro fog). The allodynia, where things that shouldn't hurt do. All of it fits the pattern.
Why does it happen?
The evidence points to changes at multiple levels of the nervous system. Increased activity in brain regions involved in pain processing, like the insula and somatosensory cortex. Reduced activity in the regions that normally inhibit pain. Altered neurotransmitters, with elevated substance P and glutamate in the cerebrospinal fluid, and reduced pain-inhibiting chemicals. At the spinal cord level, the amplification system (called wind-up, or temporal summation) is enhanced. The whole pain system is running hot.
And this is why the standard approach to pain tends not to work well for fibromyalgia. Anti-inflammatories, opioids, injections, surgery. These target peripheral tissue. Fibromyalgia isn't really a peripheral tissue problem. It's a nervous system processing problem. The Lancet review (Fitzcharles et al., 2021) is explicit about this. Peripherally-directed therapies work less well. Centrally-directed approaches (graded exercise, cognitive approaches, sleep optimisation, certain centrally-acting medications, pain neuroscience education) tend to work better.
None of this means fibromyalgia is imagined. It means it has a mechanism, and that mechanism is different from the one most healthcare has been trying to treat.
For those with hypermobility, this is where it gets really interesting, and where the two conditions start bridging.
Multiple studies have now shown that fibromyalgia and hypermobility overlap at rates that can't be a coincidence. Ofluoglu and colleagues (2006) found joint hypermobility in 64.2% of women with fibromyalgia, compared with 22% of controls. Sendur and colleagues (2007) found hypermobility in 46.6% of women with fibromyalgia versus 28.8% of controls. Numbers vary between studies because of different diagnostic thresholds, but the direction is always the same: people with fibromyalgia are significantly more likely to be hypermobile than the general population.
And then there's the mechanism question. Di Stefano and colleagues (2016) tested 27 people with hypermobile EDS and found no nerve damage, but lowered cold and heat pain thresholds and an increased wind-up ratio. In plain English, their nervous systems were hypersensitive and the pain amplification system was running hot. Exactly like fibromyalgia. The authors concluded that hypermobility and fibromyalgia share similar pain mechanisms, and that persistent nociceptive input from unstable joints probably triggers central sensitisation over time.
Which, when you think about it mechanistically, kind of has to be true. If your joints are sending lower-quality proprioceptive information every minute of every day, for years, and your nervous system is constantly working overtime to figure out where your limbs actually are and active tone sits high, that's a sensitising stimulus. The system gets noisier. The volume creeps up. And eventually you end up with both mechanical instability
AND a turned-up pain system layered on top of it.
So ,a huge proportion of people end up with both labels. Fibromyalgia AND hypermobility. Two diagnoses. Often, one underlying driver.
Now, I want to be honest. The evidence here isn't all tied up in a neat bow. The Di Stefano study had 27 people. The Ofluoglu and Sendur studies were in women only. We still need bigger, better-designed trials before anyone can say with certainty "X percent of hypermobile people develop nociplastic pain by Y age." It's also a bit of a chicken and egg situation. Some of you will have developed fibromyalgia-type pain secondary to years of hypermobility. Others may have arrived at both from different directions. The research is getting clearer year on year, but we're not at the finish line.
What we do know is enough to change how we think about this.
So what do you actually do with this?
First, if you've ever been dismissed because your scans are clean, that's not on you. The imaging was never going to show it. It's not that kind of pain.
Second, nociplastic pain responds differently to tissue pain. Chasing structural causes with more and more tests often leads nowhere. What does help, based on the evidence we've got, is different. Graded movement. Sleep. Nervous system regulation. Pain neuroscience education (just understanding the mechanism genuinely reduces pain for a lot of people). Centrally-acting medications where appropriate. Cognitive and behavioural approaches that work with the nervous system rather than against it.
Third, for those with hypermobility specifically, if the noisy proprioceptive input from your joints is part of what's driving the sensitisation, then improving that input becomes part of the long-term answer. Not "just get stronger," which is what everyone says and which doesn't fix it. But actually training the brain to feel your joints properly again. Improving the quality of the signal. That's the foundation of everything we do with our clients.
The takeaway. Pain can be real, measurable, and not in your head, whilst also not coming from tissue damage. That's nociplastic pain. It has a mechanism. It has formal criteria. It has treatment strategies that are genuinely different from tissue-based pain. And understanding which type (or which combination) you're dealing with changes everything about how you approach it.
