Project Spectrum

Why Flexible seating should be in every classroom ⬇️

* Honouring different sensory needs: Some students focus better when they can move, bounce, or shift position.
* Supporting self-regulation: Options like wobble stools, cushions, or floor seating allow students to find what helps them feel calm and alert.
* Promoting body awareness and core engagement: Active sitting can improve postural control and endurance for learning tasks.
* Reducing cognitive load: When the body is supported, the brain is freer to engage in learning.
* Encouraging autonomy and inclusion: Students choose what works for them.

"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.

Can you relate to this?

Survival mode is how our nervous system protects us and most people on survival mode don’t even realise they are in it, until they come out and reflect back.

When we’ve faced stress or unpredictability (often from a young age), our bodies adapt by staying on high alert. The nervous system remembers those early experiences, so even in adulthood it can default to survival mode which is a way we show up as high functioning anxiety.

That’s why survival mode feels exhausting and we can feel stuck. It’s not laziness or lack of willpower, which is often what a high functioning person may believe about themselves.

Your body is simply trying to keep you safe.

But I want you to know that with awareness, compassion, and support, we can show our nervous system that it’s safe to step out of survival mode and shifting from just getting through to truly living.

The reason why our early experiences matter is because it helps us to understand why we show up the way we are and to release certain patterns that are no longer serving us.

Comment “Journal” and I’ll share some inner child journal prompts that can help you reflect on certain patterns that aren’t serving you.

You’re here to shine and learn to feel worthy with who you are Becasue you are enough.

Dr. L

fightorflight

Your heart is racing. Your breathing is shallow. Your hands are shaking.

And your immediate thought is: "Something is wrong with me."

But nothing is wrong with you. Your nervous system is doing exactly what it's supposed to do. It's trying to save your life.

Anxiety is a range of normal emotions. Worried. Nervous. Uneasy. Fear. Panic. Terror. And all of them are designed to do ONE thing: Alert you to a situation you need
to respond to.

Think of anxiety like an alarm system.

When your nervous system senses danger (real or imagined), it triggers your
fight-flight-freeze response.

And that's when the physical symptoms show up:

Dizziness, breathlessness, chest tightness → Breathing quickens to send oxygen
to muscles

Heart pounding → Blood pressure increases to pump blood to muscles

Visual disturbance → Vision sharpens to see threats

Muscle tension → Muscles ready for action

Sweating → Body temperature maintenance

Tingling, numbness → Calcium discharged as part of activation

Feeling sick, dry mouth → Blood diverted to major muscles

Unable to concentrate → Mind focuses on threat detection

Need to use bathroom → Body prepares to be light for escape

EVERY SINGLE SYMPTOM IS DESIGNED TO HELP YOU SURVIVE.

Anxiety is like physical pain. Pain keeps you safe by telling you to pull your hand off a hot flame.

Anxiety keeps you safe by alerting you to psychological, social, or existential
threats.

Without anxiety, you wouldn't prepare for exams.
Without anxiety, you wouldn't practice for presentations.
Without anxiety, you wouldn't jump out of the way of oncoming traffic.

So it's not that you have anxiety, the problem is when your system perceives threat where there isn't one. When it's determined that something is dangerous that actually isn't. And then it's stuck in scanning mode.

And the more you fight it, the more it thinks: "We must be in danger (because
you're fighting)."

In PTSD, being overly critical is often a form of hypervigilance.

Your brain is scanning for danger.
Reading into tone, behavior, and small changes.
Trying to stay one step ahead.

The reaction can feel bigger than the moment…
because part of you is still trying to stay safe.

And that can turn inward.

You become critical of yourself.
Of others.
Of everything around you.

Not because you’re harsh…
but because you learned to be alert.

Understanding that is where healing starts.

Be patient with yourself.