Fibromyalgia and Central Sensitisation, What Is It in Plain English?

• About
• Latest Posts

Adam Foster

Director at The Fibro Guy

Adam Foster is the founder of The Fibro Guy and one of the leading voices in hypermobility, EDS, and chronic pain rehabilitation. A former Reconnaissance Soldier, he developed chronic pain after an IED blast in Afghanistan and built his approach from the ground up when the medical system had no answers. Since 2009 he has worked with thousands of people across eight countries, drawing on pain neuroscience, motor learning, and sensorimotor rehabilitation. He co-authored "No Pain, No Pain" with trauma psychologist Dr Mairi Harper, directed the documentary "Invisible Monster," and has been featured in Forbes, BBC Radio 4, ITV News, LiveScience, and The Telegraph.

Latest posts by Adam Foster (see all)

• Fibromyalgia and Central Sensitisation, What Is It in Plain English? - 8 October 2026
• Which supplements are worth taking when you’re hypermobile - 4 October 2026
• Hypermobile Wrists: Why They Hurt, Which Brace to Use, and How to Build Control - 4 October 2026

Central sensitisation means your spinal cord and your brain are amplifying the signals arriving from your body. The signals themselves haven’t got any bigger. What’s changed is how loud they are by the time they come out the other end.

That single change produces four things at once. Things that were always going to hurt….. now hurt more. Things that shouldn’t hurt at all…. start to. The pain spreads out past wherever it began. And the whole thing carries on long after whatever set it off has gone ^[4][5][6][7].

Which is why fibromyalgia looks, from the outside, like a pile of unrelated problems that all happened to turn up in the same bad year.

You will have almost certainly been told some version of this already. That your nervous system has turned the volume up, the dial is stuck or that your pain system is oversensitive. And it’s true as far as it goes, but it gets handed over as though it explains it fully and more importantly, simply……., but it doesn’t. Nobody tells you where that dial is, what it’s attached to, or what turns it.

So, this article is the middle bit. Where the amplifying actually happens, what physically changes when it does, and why that accounts for the specific, strange and genuinely infuriating way your pain behaves. The reason it’s explained so badly everywhere else, is that everyone gives you the summary and skips the mechanism, and the mechanism is the part that makes it make sense.

No, this isn’t a polite way of saying it’s psychological

The nervous system isn’t the mind, and sensitisation isn’t just another word for you’re imagining it. The reason that’s known rather than asserted is a reflex in your leg.

You have a reflex that pulls your leg away from something sharp or hot. It’s handled entirely inside your spinal cord, and it fires before the information has gotten anywhere near the part of you that produces a conscious thought. You don’t choose to do it, and you can’t talk yourself out of it. It also has a threshold that can be measured in actual units, which makes it about as far from a self report as a measurement in a pain clinic gets.

In fibromyalgia, that threshold is lower ^[1].

That’s really the whole argument. A reflex sitting down in the cord, with no access whatsoever to your mood, your beliefs or how you feel about your diagnosis, goes off sooner than it should. Go up a level and the same thing shows up in how much stimulation it takes to produce pain at all. People with fibromyalgia often need around half the stimulus before they report pain, and they show exaggerated responses to painful and even low intensity input ^[2][3].

So when somebody tells you this is a nervous system problem, they are not being tactful about something else. There are actual measurements.

Nociception isn’t pain

You don’t have pain detectors. There’s no such thing, which surprises most people the first time they hear it.

What you have are nociceptors. They’re nerve endings that fire when something crosses a threshold that might mean trouble for the tissue they’re sitting in: too much pressure, too much stretch, too much heat, cells in distress. The signal they send upwards is called nociception, and nociception is information rather than pain. It’s a shout that something somewhere may be in danger of actual, or potential, harm or threat.

Pain is what your nervous system produces at the end of that process. And between a nociceptor firing and you feeling anything at all, the signal passes through two places where it can be turned up, turned down, spread about or thrown away entirely. The first is a junction in your spinal cord. The second is your brain.

Those two places are where the volume knob everybody keeps mentioning actually lives. Central sensitisation is what happens when both of them start amplifying.

The first place it gets turned up: the junction in your spinal cord

The nerve carrying the signal up from your knee does not run all the way to your brain. Most people assume it does. It doesn’t. It gets as far as the back of your spinal cord and stops, and there it hands over to a second nerve cell, which carries the message the rest of the way up. That handover is where the first decision about your pain gets made, and it happens long before you’re aware of anything.

The mechanism is simpler than it sounds though. The receiving cell has a particular kind of gate on it that sits plugged up with magnesium. While not much is going on, the plug stays in and the junction stays quiet. Strong or repeated incoming traffic knocks that plug out. Calcium then floods in through the gate it was blocking, the incoming side starts releasing more of its excitatory chemicals and more substance P, which is another messenger that stokes the receiving cell, and the receiving cell changes. What you’re left with is a cell that fires more easily than it used to ^[8].

None of that is damage. It’s the same machinery your nervous system uses to learn anything at all, which is exactly why it’s so good at it. It’s learning. It’s just learning something you’d rather it hadn’t bothered with.

You can watch it happen in a lab. Give somebody short pokes of heat at a steady interval and the pain climbs with every poke, even though the heat itself hasn’t changed at all. Everybody does this. It’s perfectly normal. Twenty six people with fibromyalgia and 23 people without had exactly that done to them, and the fibromyalgia group reached the wound up state at lower intensities and at lower frequencies, held it there, rated it higher, and their after sensation ran longer once the poking had stopped ^[9]. An aftersensation is pain that carries on after the thing causing it has been taken away, and you’ll have met plenty of those without having had a word for them.

Nothing during your day is a single poke. It’s a few hundred of them. Standing up, carrying things, sitting too long in an uncomfortable chair, a long drive, a cold morning. What’s changed for you isn’t any one of those on its own. It’s how they stack on top of each other, and how long they take to settle again, once you stop. Which is why the thing that finally finished you off, was so often something completely trivial. It wasn’t the trivial thing. It landed on a junction that still hadn’t come back down from the days or weeks before.

The second place it gets turned up: your brain

Your brain doesn’t simply receive sensation. It’s constantly working out what the incoming information means, how urgent it is and what you ought to do about it, using what’s arriving right now, plus everything it has learned to expect. Pain is what comes out of that process.

You already know this part works, even if nobody has ever put it to you in those terms. Catch your hand on something in the garden, and the first thing you do is look at it, and what you see changes the next few seconds completely. Same hand, same information coming up the arm, entirely different conclusion.

Put people with fibromyalgia in a scanner, give them the same stimulus you’d give anybody else or a weaker one, and the pain related response that comes back is exaggerated ^[10][11]. Those are scans taken while something is actually being done to the person, and they hold up better when other researchers repeat the work than the resting state scans do, taken while you lie there doing nothing, or the structural ones measuring shape and size ^[10][11].

In ordinary terms: the same knock, the same cold, the same arm of the same chair, arriving louder and more urgent for you, than it does for the person sitting next to you.

Most of this imaging though, is a snapshot, and the authors say so themselves, which means it can’t tell us whether the brain side of this came first or whether it followed years of being in pain ^[11]. Probably some of both, in different proportions in different people, but that isn’t settled yet.

The wiring that’s meant to turn it back down

So far everything has only gone one way, and a volume knob that only goes up isn’t a volume knob.

You do have wiring that runs the other way. It comes down from your brain, through your brainstem, into your spinal cord, and arrives back at that same junction, and its entire job is to damp the handover down. It’s why you can keep walking on a rolled ankle until you’re somewhere safe to sit down, and why the same cut hurts differently in a hospital and in a car park. The name for it is descending inhibition, which is exactly what it says on the tin. Something coming down, and holding something else back.

In fibromyalgia, that damping tends to arrive weaker than it should, or the traffic that comes down alongside it and turns the junction up rather than down arrives too strong ^[12]. Imaging of the spinal cord and brainstem during wind up shows abnormal control signals ^[13]. So there’s something off with the brake, as well as with the junction it’s supposed to be holding back.

It isn’t universal, though. Some experimental work finds the heightened sensitivity sitting right next to pain modulation that tests perfectly normally ^[12], so a failure of the damping is common, without being present in everybody. Two people with the same diagnosis can genuinely have the trouble in different places. Which is one reason the thing that transformed somebody’s life in a Facebook group, can do absolutely nothing for you, and it isn’t because you did it wrong.

Hyperalgesia

Hyperalgesia is too much pain from something that was always going to hurt a bit ^[21][22].

A knock on the shin that ought to be one swear word and a quick pirate impressions. Having bloods taken. A firm massage. Getting into cold water. The input is already in the painful category, and what comes out the other end is nowhere near the size of what went in.

Measured against people without fibromyalgia, pressure, heat and cold all start hurting at lower levels, and they do it at body sites well away from the worst of it, as well as at the obvious ones ^[23][24]. Your sore shoulder isn’t extra sore because of something specific going on in the shoulder. It’s the setting on the whole system.

Allodynia

Allodynia is pain from something that shouldn’t hurt at all ^[21][22].

A waistband. A bedsheet. The shower. A hand on your arm from somebody who loves you. None of that is in the painful category to begin with, and it hurts anyway. It’s what people are describing when they say my skin hurts, or my skin is burning, which is what most people type into a search bar long before anybody says the word Allodynia.

Touch is carried on its own separate fibres, nothing to do with the nociceptors, and they were never in the business of producing pain at all. In Allodynia, that touch input gets recruited into the nociceptive machinery regardless ^[21][22]. Antibodies taken from people with fibromyalgia have been shown to sensitise those touch fibres to pressure and to cold ^[25].

How common it is depends a great deal on how you ask the question. In large symptom surveys, around 20% of people with fibromyalgia reported touch evoked allodynia, while clinically relevant pressure pain came out far higher at around 58% ^[26][27]. Formal brushstroke testing comes out lower again, at around 14% to 15% ^[28]. So pain from light brush or touch sits in a subgroup, rather than in everybody with the diagnosis ^[29].

Telling the two words apart takes one question, and you can run it on your own experience. Was the thing that hurt going to hurt anyway? If it was, and it was far worse than it had any business being, that’s hyperalgesia. If it was never going to hurt in the first place, a sleeve, a breeze, a cuddle, that’s allodynia.

Naming it doesn’t stop it, obviously. What it does do, is stop you explaining it badly to a GP who’s already running fifteen minutes late, and it stops you lying there at two in the morning wondering whether you’re the only person in the country whose dressing gown hurts.

Why it spreads to places that were never injured

It started in your neck, or after an operation, or after a virus, and now it’s in your hips and your forearms and the soles of your feet, and nobody has found a single thing wrong with any of them.

Go back to that second nerve cell at the junction. As it sensitises, its receptive field widens ^[8]. Its receptive field is simply the patch of you it answers for. A junction that used to cover an area the size of a coin now covers an area the size of a hand, and it’s easier to set off than it was a year ago. Do that at a lot of junctions and the map of where you hurt gets bigger without a single new thing having gone wrong anywhere.

And when people go and measure it, what turns up is a setting. Hands and feet behaved much the same as each other under wind up testing, which is very hard to pin on any one bit of tissue ^[9]. Broad hypersensitivity, to temperature and to pressure, turns up outside the painful regions ^[14], and the pattern is widespread rather than confined to one segment of the body ^[15].

Which, I suspect, explains the folder most of you are carrying around. The clear MRI, the clear bloods, the clear ultrasound, each one handed back as though it had put something to bed finally, then a referral for whichever bit is new or the most sores, and round you go again. Those scans weren’t missing anything. They were looking at the tissue, and what changed isn’t in the tissue.

Why it carries on after the thing that started it has gone

Two things are keeping it going, and they work differently.

The first is that the amplified state partly keeps itself going. A junction that fires more easily, covering a wider area, with the damping from upstairs arriving weak, doesn’t need a great deal to stay roughly where it is.

The second is that it’s also being fed, and from more than one direction. Some of that feed comes from your body. Numbing a painful muscle with local anaesthetic can reduce hyperalgesia at sites well away from the injection, and broader fibromyalgia pain measures along with it ^[16], which is quite hard to explain if the central state were running entirely under its own steam.

Sleep is another feed, and a big one. Poor sleep increases the risk of developing chronic widespread pain later on, measured by following people forwards in time, rather than asking them to remember backwards, and it weakens exactly the descending inhibition we went through above. Deliberately depriving people of sleep can bring on fibromyalgia like pain, tenderness, and fatigue ^[17]. That takes sleep out of the column marked general lifestyle advice and puts it in the mechanism itself.

Then there’s stress, trauma, low mood, anxiety and catastrophising. Catastrophising is the word for the mind going to the worst version of what the pain might mean. These do go with greater pain severity and worse function, and the evidence supports them as amplifiers, as vulnerability factors, and as chronifiers, meaning things that help turn a short problem into a long one. What the evidence doesn’t support though, is them explaining the pain on their own ^[18].

So, if you’ve spent months trying to isolate the one thing that did this to you, that’s why it’s been such hard going. You aren’t looking for one input into one system. You’re looking at several of them, loaded in proportions that are yours and nobody else’s.

It isn’t identical in everybody

Small fibre pathology, meaning a measurable change in the smallest nerve fibres in the skin, is found in about half of people with fibromyalgia ^[19]. And somewhere between 30% and 70% of people carrying a clinical fibromyalgia diagnosis, come back without the classic sensory testing evidence of central sensitisation on any given battery of tests ^[20]. Sensory testing there means an afternoon in a lab scoring what hurts and at what level.

So this is a mechanism that’s present in a great deal of fibromyalgia, that sits alongside other things in some people, and that doesn’t show up on every test in everyone (the should probably start taking the hypermobile cohort out first, before testing).

What to do with this

A mechanism isn’t a treatment, and this article was only ever meant to explain what central sensitisation is. There’s a lot to say about what actually helps, and it doesn’t fit in here.

But knowing it does three things for you straight away.

It explains why your pain behaves the way it does. The spread, the delay, the days where everything is louder for no reason you can point at, the symptom that outlasted the injury by a decade. Those are the predictable output of a system with the gain turned up and the damping turned down, and not one of them is you reporting badly.

It explains the clear scans. If the problem were sitting in the sore bit, the sore bit would show something, and the fact that it doesn’t has been used against you more than once. It was never going to show anything, because that isn’t where it is.

And it gives you something to say at the next appointment. My pain is being amplified in my spinal cord and my brain, the measurements of that don’t depend on what I report, and I’d like us to work from there. That’s a very different conversation from the one that opens with you trying to convince somebody you aren’t exaggerating.

You’ve carried this around for a long time without anybody naming it properly. It has a name, it has a mechanism, and not one part of it requires you to be imagining a single thing.

Adam

References

[1] Desmeules, J.A., Cedraschi, C., Rapiti, E., Baumgartner, E., Finckh, A., Cohen, P. et al. (2003) ‘Neurophysiologic evidence for a central sensitization in patients with fibromyalgia’, Arthritis & Rheumatism. https://doi.org/10.1002/art.10893

[2] Clauw, D.J., Arnold, L.M. and McCarberg, B.H. (2011) ‘The Science of Fibromyalgia’, Mayo Clinic Proceedings. https://doi.org/10.4065/mcp.2011.0206

[3] Gyorfi, M., Rupp, A. and Abd-Elsayed, A. (2022) ‘Fibromyalgia Pathophysiology’, Biomedicines. https://doi.org/10.3390/biomedicines10123070