What Causes chronic pain in Fibromyalgia and Hypermobility

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Jonny Young

Jonny Young is an award-winning PT with a focus on hypermobility, fibromyalgia, and motor mapping. Having lived with fibromyalgia for seven years, Jonny brings both personal insight and experience to his work at The Fibro Guy. After going through the programme himself, he now helps others reduce pain and regain control using tailored, evidence-based strategies aimed at improving quality of life.

Latest posts by Jonny Young (see all)

• What Causes chronic pain in Fibromyalgia and Hypermobility - 27 June 2025
• Mast Cells and Fibromyalgia: The Hidden Connection - 19 June 2025

Fibromyalgia and hypermobility both produce pain that’s real, widespread, and completely out of proportion to anything a scan is going to show, which is a large part of why the two get handed to you as one problem with two names. There’s a fair chance you’ve had both of them explained to you in the same appointment, by the same person. They don’t get there the same way though. In fibromyalgia the best supported explanation is that the nervous system itself is amplifying what it receives, so ordinary input arrives louder and the body’s own dampening system doesn’t do its job as well as it should ^[1]. In hypermobility the pain usually starts somewhere a great deal more ordinary than that, at a joint that’s gone further than it was meant to, in tissue that gives a bit more easily, and then it spreads over the years as that same amplification builds on top of it ^[2][3].

That changes quite a lot for you: which explanation actually fits your own history, what your flares are made of, and where your fairly limited energy is best spent.

What’s Actually Going On in Fibromyalgia

The term you’ll meet in a clinic letter is nociplastic pain, and it’s a useful one once somebody bothers to explain it to you. Nociception is the signalling that comes from tissue when something’s been damaged or threatened, and it isn’t pain. Nociplastic pain means the pain is being produced by altered processing of that input rather than by tissue damage sitting there driving it, and it’s a formal category with published criteria behind it ^[4]. If it’s ever been handed to you as a polite way of saying nothing’s wrong, that isn’t what it means. Fibromyalgia is more or less the condition the category was built around ^[1][5].

What turns up when somebody measures it is fairly consistent, and you may recognise both halves of it. Repeated pressure that a nervous system is supposed to get bored of instead builds, so each one lands harder than the last, and the descending system meant to turn the volume down partway through doesn’t do a great deal ^[6]. That second part is the brake, and it explains something women with fibromyalgia describe constantly: pain that doesn’t settle on its own the way it used to.

Now, the older version of this story stopped there, and it was too tidy. Small fibre damage turns up in roughly half the fibromyalgia groups that have been looked at with skin biopsies ^[7]. Small fibres are the thinnest nerve endings in the skin, the ones carrying temperature, burning sensations and a lot of the body’s automatic housekeeping. It doesn’t line up neatly with how much pain somebody reports though, which is why it reads more like a marker for one subgroup than the cause of the whole thing ^[8]. Purified antibodies from people with fibromyalgia, most of them women, have been injected into mice, and the mice became more sensitive to pressure and to cold and lost grip strength ^[9]. It is a mouse study, so what it shows is what those antibodies can do to a mouse, and whether the same thing happens in you is a question it does not answer. Inflammatory messengers run higher on average as well, although none of them is specific enough to be used as a test ^[10].

So it isn’t purely central, and it isn’t purely peripheral either. Different women appear to be arriving at the same syndrome from different directions, which is genuinely awkward for a healthcare system that likes one diagnosis to mean one mechanism.

Where Hypermobility Pain Starts

Hypermobility pain has a far more boring beginning, and that’s precisely why it gets dismissed for years. Early on it’s mechanical: sprains, subluxations, full dislocations, tendons taking load they were never built for, spinal segments moving more than they should, and repeated microtrauma from tissue that simply deforms further under the same force ^[11][2]. The joints that tend to go first are the ones doing the most work in the most directions, so knees, hips, ankles, shoulders, the spine and the jaw ^[2].

The muscles around those joints also end up doing a job the ligaments normally do for free (and muscles are not a registered charity), which is tiring, and a real source of pain in its own right, whatever you’ve been told over the years about not trying hard enough.

Underneath all that, the tissue isn’t sitting there passively either. Changes in the extracellular matrix, which is the scaffolding holding everything in place between the cells, appear to change how fascia behaves, with sliding surfaces gliding less well and areas of connective tissue stiffening even while the joints themselves stay lax ^[12]. Those stiffened areas sit directly on top of free nerve endings, so you get a source of low grade irritation with nothing obvious to see on a scan ^[12][3]. Most of you could recite that sentence from memory by now.

Then there’s the nerve side of it. Burning pain, numb patches, pins and needles, and skin that hurts to be touched are common enough in hypermobility to matter clinically ^[13]. Some of that is entrapment and compression from lax tissue moving where it shouldn’t, and some of it is genuine small fibre neuropathy, with reduced nerve fibre density showing up on skin biopsy across a large subset ^[14][15].

None of that needs central amplification to explain it, as it’s ordinary tissue and nerve pain in a body where perfectly ordinary loads are landing somewhere they shouldn’t.

Position Sense, and How Much It Explains

Proprioception is your sense of where your joints are without looking at them, and it genuinely is less precise in hypermobility. Put your hand back on a target you can’t see, which is how it gets measured in a lab, and those with Ehlers-Danlos syndrome hit it about as accurately as anybody else on average, but with roughly twice the scatter around it ^[16]. Think of an old SatNav, in that it gets you to the right street and is then fairly vague about which bit of it. Pooled across the hypermobility work, joint position sense comes out reduced ^[17], and it turns up in the way balance and postural sway behave too ^[18].

That part everybody gets right, and it’s the next step where it goes wrong.

Proprioceptive scatter tracks how hypermobile somebody is. It doesn’t track how much pain they’re in ^[16]. So the version of this you’ll read almost everywhere, the one where poor position sense is what generates the pain, is running well ahead of what’s been measured. The more defensible reading is an indirect one: a joint being controlled off imprecise information gets put into positions it can’t defend, which produces the microtrauma, which produces the constant low level input that keeps the whole system busy ^[3].

The reason that matters to you, and not only to a journal, is simple enough, as if poor position sense were the pain then better position sense would be the cure, and it isn’t. Physical therapy aimed at retraining that feedback does bring reported pain down in hypermobile Ehlers-Danlos syndrome ^[19], which is a decent reason to do it, but it’s one input into a system with several, and anybody selling it to you as the answer is ahead of the evidence.

How Local Pain Turns Into Everywhere Pain

Keep a nervous system fed with constant low level input from unstable joints, irritated fascia and repeated small injuries, and the spinal cord neurons receiving all of it become easier to fire. Their thresholds drop and the area of body they respond to widens, so pain stops staying politely where the injury was ^[20][21]. You’ll know that one. Measured in hypermobile adults, that shows up as lower pressure thresholds all over the body, more of that building under repeated stimulation, and a descending brake that’s blunted in much the same way it is in fibromyalgia ^[3][22]. It’s been found in hypermobile adolescents as well, which puts a fairly unwelcome timescale on all of it ^[23], and if you were the teenager who kept getting sent home with a shrug, that will be familiar enough.

Pain genuinely does change character over the years because of this: localised, injury linked pain in childhood and adolescence, widespread chronic pain by adulthood, and more overlap with fibromyalgia as it goes ^[13][2][3].

Now, the balance between peripheral and central drivers in hypermobility isn’t settled, and some of the better recent thinking argues that small fibre dysfunction is doing primary work in a subset of people rather than turning up afterwards as a consequence ^[24]. Which is another way of saying this is one route in, and not the route in.

Three Kinds of Pain, and Most People Have More Than One

Pain gets sorted into three types, and the sorting is genuinely useful to you, because the three of them don’t respond to the same things. You’ll almost certainly have a mix of all three, and what differs between the two conditions is the proportions ^[25][21].

The first is the pain that comes from tissue being damaged or threatened, so a sprained ankle, a shoulder that’s come partway out, a tendon you’ve asked to hold something for two hours. In hypermobility that accounts for most of the early years ^[11][2]. In fibromyalgia that sort of input still exists, but it doesn’t account for how much pain there is, or for where it’s spread to ^[1].

The second is nerve pain, which is what you get when the nerves themselves are damaged or compressed. Burning, electrical, pins and needles, numb patches, skin that objects to being touched. In hypermobility it comes from entrapment, from nerves sitting where they shouldn’t in lax tissue, and from small fibre damage ^[13][14].

The third is the amplified kind, where the processing has changed and the pain no longer maps onto anything you could point at on a scan. That’s the dominant one in fibromyalgia, and it’s increasingly recognised in the group with hypermobility who’ve ended up with widespread pain, fatigue and sensory sensitivity sitting on top of the joint problems ^[4][2][3].

That sorting is the bit clinics skip. If your pain is mostly the first kind, and somebody else’s is mostly the third, the two of you get handed the same advice, constantly, and only one of you was ever going to get anything out of it. You’ll have a fair idea which of the two you’ve been.

What Turns the Volume Up

Neither condition sits still, and both have amplifiers running alongside them, which is usually where your day to day variation comes from. They’re also the parts most likely to be handed back to you as separate complaints by somebody who has ten minutes.

Sleep is the big one, and it isn’t only a consequence of hurting. You’ll have been told to wind down before bed and stay off screens by now (which is roughly where that advice tends to stop). Poor sleep quality goes with weaker pain inhibition in fibromyalgia ^[26], and when sleep is deliberately disrupted under controlled conditions, the inhibitory machinery measurably changes along with inflammatory signalling ^[27]. Across broader pain populations that link holds up consistently in direction, while how big it is varies between studies and may differ between women and men ^[28]. A bad night raises tomorrow’s pain, and a bad pain day wrecks tomorrow night’s sleep, which is a loop that closes very quietly and takes months to spot.

Autonomic symptoms are the second one. The automatic side of the nervous system, the part quietly running heart rate, blood pressure, digestion and sweating, misbehaves often in hypermobile Ehlers-Danlos syndrome and hypermobility spectrum disorders, and postural tachycardia syndrome, where the heart rate climbs hard on standing, is the version most people meet by name ^[29]. In women with these conditions the autonomic symptom burden tracks with worse quality of life rather than sitting off to one side as an unrelated problem ^[30]. Standing up badly all day is a physiological stressor, and stressors feed the same system that’s already amplifying.

Mast cells come up constantly in this space (and you’ve met the subject whether you went looking for it or not). The evidence is thinner than the internet would have you believe. Mast cells can plausibly activate nerve endings, and mast cell symptoms cluster with hypermobility often enough that people keep asking about it. A shared mechanism tying hypermobility, postural tachycardia syndrome and mast cell activation together hasn’t been established ^[31], and current gastroenterology guidance doesn’t support testing everybody with hypermobility for it either ^[32]. None of which is a reason to ignore it if you’ve got clear mast cell symptoms, it’s a reason to be wary of anybody handing you the three of them as one tidy package.

Pain somewhere else in the body counts as an amplifier too, and this one you can do something about. In women with fibromyalgia alongside irritable bowel, period pain or endometriosis, the more pain there was coming from the internal organs the worse the fibromyalgia was, and treating that condition brought the fibromyalgia symptoms down with it ^[33]. In hypermobility the same spread shows up as headaches, abdominal pain, pelvic pain, period pain, bladder symptoms and vulval pain joining the joint pain ^[21][34]. All of it is load on the same system rather than a separate list of complaints that happen to be yours as well, and taking one of them off can move the rest.

When You’ve Got Both

The overlap between the two is substantial, and having both isn’t the same as having either one on its own. Women diagnosed with hypermobile Ehlers-Danlos syndrome or hypermobility spectrum disorder who also meet the criteria for fibromyalgia report a heavier burden across pain, fatigue, autonomic symptoms and quality of life than those carrying the hypermobility diagnosis alone ^[35].

Which, in practice, is a lot of you. You’ve probably got a mechanical problem at the joints, a sensitised system sitting on top of it, and a couple of amplifiers ticking over in the background. All three need addressing, and they don’t respond to the same things.

What Helps

None of what follows is exciting, and you’ll have heard of most of it before. The average effects of the ones that genuinely do work are moderate, and no single intervention works for everybody ^[36].

Exercise, at the right dose: Exercise has the strongest repeated support of anything tested for fibromyalgia pain without a prescription pad ^[37]. The programmes that did best were aerobic and ran for at least eight weeks. Pushing the weekly volume much past three hours didn’t buy anything extra ^[37], which is a lower bar and a much longer timescale than most people assume.

Retraining the feedback before adding the load: In hypermobile Ehlers-Danlos syndrome, physical therapy targeting position sense and joint control reduces reported pain ^[19]. This is the part our own work sits in, so read it with that in mind, and the order matters as much as the content: a joint being controlled off a poor signal doesn’t need more load piled onto it, it needs a clearer signal first, and then the load.

Treating sleep as part of the pain problem: Given what disrupted sleep does to pain inhibition ^[27][26], sleep isn’t the thing you sort out once the pain has settled. It’s one of the levers on the pain itself, and for most people it’s the lever with the most room left in it.

Not one of the candidate blood markers put forward so far is specific enough to diagnose fibromyalgia or to sort people into treatment groups ^[38]. So the sorting still gets done by history, which means your own matters a great deal more than anything you’ll be sent for. Pain that started at one joint after an injury, in a body that’s always been mobile, is telling a different story from pain that arrived everywhere at once with fatigue and broken sleep, and being able to say which of those you are is more useful than the scan.

What you do with that is deal with the mechanical problem where there is one, take the amplifiers seriously instead of parking them as somebody else’s department, and give the system better information before you ask more of it.

The Fibro Guy

References

[1] Carneiro, B.D., Torres, S., Costa-Pereira, J.T., Pozza, D.H. and Tavares, I. (2025) ‘Descending Pain Modulation in Fibromyalgia: A Short Review of Mechanisms and Biomarkers’, Diagnostics. https://doi.org/10.3390/diagnostics15212702

[2] Morlino, S. and Castori, M. (2023) ‘Placing joint hypermobility in context: traits, disorders and syndromes’, British Medical Bulletin. https://doi.org/10.1093/bmb/ldad013

[3] De Wandele, I., Colman, M., Hermans, L., Van Oosterwijck, J., Meeus, M., Rombaut, L. et al. (2022) ‘Exploring pain mechanisms in hypermobile Ehlers‐Danlos syndrome: A case–control study’, European Journal of Pain. https://doi.org/10.1002/ejp.1956