If you have hypermobility and your head is a regular problem, you’ve probably had it explained to you in one of two ways. Either it’s “just tension, try to relax”, or it’s “just migraines, here’s a leaflet”. And then you’re sent off with the same advice everyone gets, which does nothing, because the advice was never built for a head like yours. Maybe your headache changes depending on how you’re holding your neck. Maybe it’s worse the longer you’re upright and eases the second you lie flat. Maybe it comes bundled with the dizzy spells, the racing heart, the mental fog that so many describe, but none of that fits neatly into “just tension”.
Here’s the thing though, headaches in those of us with hypermobility, often get lumped into one bucket, and treated as one problem, but they aren’t. There are several very different mechanisms that can cause head pain when you’re hypermobile, and they wear the same coat. They feel similar from the inside, a headache is a headache when you’re the one with it, but underneath they’re driven by completely different things. Migraines are not the same as a headache thats coming from your neck. A headache from low spinal fluid pressure, is not the same as one coming from your jaw. And the reason so much advice fails is simple: people keep treating the wrong mechanism.
So, this article is going to split them apart, and we’re going to go through migraines, cervicogenic headaches, the unstable upper necks, the headache that’s worse when you stand up, spontaneous CSF leaks, craniocervical instability (the controversial one), the jaw connection, and the medication overuse trap that catches so many people out. For each one, how to spot it, and honest first moves that actually match the mechanism.
Quick word on scope before we start, this is not a diagnosis, and it’s not a substitute for a proper assessment with a neurologist. We’re education and movement led here at The Fibro Guy. Some headaches are red flags: a sudden thunderclap headache that hits maximum in seconds, a headache with new weakness, numbness, vision loss, confusion, or a fever and stiff neck, needs urgent medical attention, today, not after you’ve finished reading a blog. If that’s you, stop here and go get seen.
Why one label never fits a hypermobile head
The first thing to get straight is that “hypermobility headache” is not a diagnosis. It’s a description of who’s getting the headache, not what’s causing it. And when it comes to those with hypermobility, the causes stack up in a way they don’t for most people.
Part of it is anatomy, as the upper part of your neck and the sensory nerves of your face share a relay station in the brainstem. The nerves from the top three levels of the neck feed into the same nucleus as the trigeminal nerve, which handles sensation for most of your head and face. So, a problem in the neck doesn’t always feel like a neck problem. The brain can read it as head pain, because the wiring genuinely overlaps down there. This is why “it’s coming from your neck” and “my head hurts” are not contradictions. They’re the same signal, arriving at the same place.
Then there’s the wider system, as hypermobility rarely appears alone. Dysautonomia, the umbrella term for a wonky autonomic nervous system, turns up a lot for those with hypermobility, and it’s been reported in as many as 78% of people with EDS in the literature [1]. Now, that doesn’t mean 78% of people with hypermobility have it, the figure comes from clinic populations and the real number in the wider community is lower, but it tells you the link is strong. POTS sits under that umbrella too, and POTS brings its own flavour of headaches. Then there is the Mast cell issues, which can easily pile in on top, and when the mast cells are twitchy, they can add their own flushing, their own headaches, and their own general sense of the volume being turned up. So, you get a person whose head pain might be a migraine, might be neck driven, might be autonomic, might have a jaw component, and quite often enough, is more than one of those all at once, layered on top of each other.
That layering is the bit that trips most people up though. If you only ever had one mechanism, you’d probably have worked it out by now. The reason so many people go round in circles is that they’ve got two or three running at the same time, so a treatment aimed at one of them helps a bit, which is confusing, because it doesn’t touch the other two. When it comes to unpicking a hypermobile head, you have to be willing to accept that the answer might not be a single tidy label, It might be a stack.
And there’s the bit that most explainers skip: what your nervous system is actually doing while all this is going on. When you’ve been in pain for a while, or when your joints feel unreliable, the body tends to guard, or in other words, It braces. The muscles around the neck and jaw quietly ratchet up their tone and they stay there, because on some level, the system has decided that holding everything tight is safer than letting it move. That bracing is protective in the short term, but a bit of a problem in the long term, because a permanently gripped neck, is a tired, sensitised, headache prone neck. Add the anxiety that living with unpredictable pain understandably brings, and you’ve got an arousal loop: worry feeds bracing, bracing feeds pain, pain feeds worry. We’ll come back to that loop, because it runs underneath nearly every headache type on this list.
So when we talk about hypermobility headaches, we’re really talking about a cluster of overlapping mechanisms sitting on top of a nervous system, that’s often already wound a bit tight. Sorting out which mechanism is doing the most is the whole game. Let’s take them one at a time, starting with the most common.
Migraine, the most common one
If you’re hypermobile and you get headaches, migraine is statistically the most likely culprit. The numbers are striking. Depending on which study you look at, migraine estimates in symptomatic hypermobility run anywhere from about 40% up to three quarters [1]. In one large EDS clinic group, 42.5% had migraine and 13.8% had chronic migraine [1]. And if fibromyalgia was in the mix as well, those figures jumped: 63.8% had migraine, 34.1% of them chronic [1]. In another hypermobile group, migraine made up 82.5% of all the headache diagnoses, and around a third of people had a head or neck symptom as their main complaint [1].
It’s not just adults, either, a study of children found that headaches were about 3.7 times more likely in kids with hypermobility, than in those without. And migraine specifically, about 4.5 times more likely [5]. So this seems to start early.
There’s also a pattern to how migraines behave in hypermobile population as well. It tends to start younger, hit more often, and be much more disabling than migraines in the general population [1]. That last part matters, because it means “just migraines” is doing a lot of dismissive lifting for something that can genuinely wreck a week.
What migraine actually is, versus a bad headache
A migraine isn’t just a severe headache, It’s a whole neurological event unto its self. The brain becomes temporarily hyperexcitable, a wave of altered activity spreads across the surface, and the trigeminal system, that same head and face sensory network we mentioned earlier gets dragged into it. That’s why migraines so often comes with the extras: the nausea, the sensitivity to light and sound, the visual aura for some people, the feeling that your whole head and gut have gone offline. A tension headache is a band around the head. A migraine is a system wide storm.
A little side note here, back in 2009 when I was having migraines everyday, I swear I could smell an open can of Pringles in the next room! I still can’t stomach them to this day.Migraines also tends to move in phases, and knowing them helps you recognise your own patterns. There’s often a prodrome in the hours or day before, subtle stuff like yawning, mood shifts, food cravings, or a stiff neck. Some people get an aura, usually visual (zigzags, blind spots) but sometimes sensory or speech related, lasting under an hour before the pain. Then the headache itself, then a postdrome: the washed out, hungover day afterwards that most people forget to count as part of the attack. That neck stiffness in the prodrome is worth flagging, because it’s one of the reasons migraine and neck driven headache get muddled: the neck symptom can be part of the migraine rather than the cause of it.
Why hypermobile brains seem more prone to migraine isn’t fully pinned down yet, but no surprise there really. The autonomic overlap is most likely, probably, part of it. Migraines and dysautonomia share a lot of the same machinery. That overaroused and overbraced state we talked about earlier is likely a part of it too, because a sensitised nervous system is an easier one to tip into a migraine. Warts and all, the honest read is that we know migraine is more common here, and we have good guesses as to why, but the full mechanism is still being worked out.
Managing migraine when you’re hypermobile
The good news however, is that migraines are one of the better understood headaches, and there’s a real toolkit for them. The general approach, in line with standard guidance [10] has three parts. First, trigger management: working out what reliably sets yours off (sleep debt, dehydration, skipped meals, hormones, specific foods for some people) and heading it off. Secondly, abortive treatment for when one hits: typically a triptan paired with an anti-sickness drug and an anti-inflammatory, or one of the newer gepant drugs. And thirdly, preventives if the attacks are frequent, which is essentially medication taken daily to reduce how often they come.
Something to keep your eye on though, and it’s the bit a General Practitioner/Primary Care Physician may miss. Some of the most common migraine preventives lower your blood pressure. Beta blockers and candesartan are classic examples. If you’re hypermobile with orthostatic intolerance or POTS, your blood pressure regulation is already struggling, introducing a preventive that drops it further can leave you dizzier, foggier and worse off overall. So, in hypermobility with orthostatic symptoms, those blood pressure lowering preventives are usually avoided [1][11]. It’s not a hard rule for everyone, but it’s a conversation worth having with whoever’s prescribing for you, because the standard first choice preventive might be exactly the wrong one for your body.
Beyond the medication, the framework side still applies. Down regulating that background arousal, breathing work, pacing, keeping sleep steady, does not cure migraine, but it lowers the excitability that makes attacks easier to trigger. Think of it as raising the threshold rather than flipping a switch.
Cervicogenic headache and the unstable upper neck
This is the one where hypermobility really shows its hand, and it’s where our framework earns its place, so we’re going to spend proper time here.
Cervicogenic simply means “coming from the neck”. Because of that brainstem overlap we covered, problems in the top of the neck refer pain up into the head, usually starting at the base of the skull and spreading forward, sometimes behind one eye [1]. It’s often one sided, often worse with certain neck positions or after holding your head still for too long, and it doesn’t usually come with the full migraine circus of aura and severe nausea.
In hypermobility, a big driver of this is instability at the upper neck. Now, “instability” is a loaded word, so let’s be precise. Mild upper cervical instability appears to be relatively common in symptomatic hypermobility, with estimates in the region of 52 to 66% [2]. Severe upper cervical instability, the genuinely serious kind, is uncommon, around 5% [2]. That gap matters enormously. Most people worried about their neck have the mild, manageable end. A small minority have the severe end that needs specialist input. The symptom picture for upper cervical involvement includes suboccipital headache (that base of skull ache), coat-hanger pain across the shoulders and up the neck, general neck tension, brain fog, a heavy head that feels hard to hold up, and symptoms that shift depending on neck position [2].
Instability is a control problem, not just loose ligaments
Here is the single most important idea in this whole section, and it’s the one that changes what you do about it.
When people hear “unstable neck”, they picture stretched out ligaments, floppy connective tissue, and they conclude there’s nothing to be done short of surgery to bolt it all together. That’s the wrong model though, as instability at the neck is driven by insufficient neuromuscular control and poor recruitment patterns, as well as lax ligaments [2]. In plain English: it’s not only that the passive structures are loose, it’s that the muscles aren’t switching on at the right time, in the right order, to control the joint through movement. The ligaments hand more of the job to the muscles, and if the muscles aren’t doing that job well, the joint feels unstable.
And that is very good news, because muscle control can be trained. You can’t tighten a ligament with exercise. You can absolutely improve how well your nervous system controls a joint. This is where the framework lives. Sensory clarity: the brain needs an accurate map of where the neck is in space, and in hypermobility that map is often fuzzy, so training joint position sense sharpens it. Tone regulation: teaching the constantly braced neck and jaw to let go, so the muscles aren’t burning themselves out holding a defensive grip all day. Motor learning: rebuilding control gradually, in a graded way, so the system learns to trust the movement again instead of guarding against it.
There’s a genuinely counterintuitive finding here too. Training motor control away from the neck, at the lower back and the shoulder blades, can improve neck control [3]. It sounds odd, but the neck doesn’t work in isolation. If your trunk and shoulder girdle give it a stable base to work from, the neck has less to fight against. So neck rehab often doesn’t start at the neck at all.
What actually helps
The recommended approach for upper cervical instability is conservative and physiotherapy first, graded to how irritable your neck is on any given day [2]. That means starting where the neck is comfortable and building from there, not charging in with aggressive end range work that flares everything up for a week. A neuroplasticity based approach has been described for exactly this: proprioception and motor control training with feedback on how accurately you’re moving, combined with breathing and graded exposure to movement [3].
I want to be honest about the evidence here, because that honesty is the whole point of this site. The neuroplasticity approach comes from a very small case series, just three people, and the outcomes varied a lot. One returned to full function. One improved but eventually needed a fusion. And one was left disabled after surgery. So this is not a guaranteed fix, and anyone telling you a specific protocol cures neck instability in hypermobility is definitely overselling it [3]. What it does tell us though, is that the control based approach is a reasonable, low risk first move that helps some people meaningfully, and it should come well before anyone reaches for surgery.
Now, on the braces and collars front: they have a place, dont get me wrong, but it’s a small one. The guidance is to use them for short rest breaks, travel, or for a flare, not to wear them constantly [2]. A collar worn all day tells your neck muscles they don’t need to work, and they’ll happily oblige by getting weaker, which makes the underlying control problem worse. Use it as a crutch for a bad hour or two, not as a lifestyle. However, this is dependent on things like Craniocervical Instability, where you may not have a choice.
One caveat on diagnosis as well. Cervicogenic headaches themselves are a bit controversial in neurology, as there’s no perfect test for them, and even a greater occipital nerve block giving relief doesn’t definitively confirm the headache is coming from the neck [1]. So, the label is useful as a working idea, but don’t treat it as a hard fact stamped on your forehead.
The headache that’s worse when you stand up
If there’s one clue worth learning to spot, it’s definitely this one. A headache that’s clearly worse when you’re upright and better when you lie down (an orthostatic headache), is a signal your body is trying to give you a heads up. It should raise suspicion of several things: a CSF leak, POTS or dysautonomia, a craniocervical problem, migraine, or raised pressure inside the skull [1][9]. Each of those needs a different response, which is exactly why the pattern is worth flagging to whoever’s assessing you.
In hypermobility, the autonomic route is common. When you stand, gravity pulls blood down into your legs, and a healthy autonomic system clamps the vessels and nudges the heart rate to keep blood flowing to your brain. In dysautonomia, that regulation is sloppy, so standing up becomes a small crisis every time. POTS is the best known version. It’s diagnosed by a sustained heart rate rise of more than 30 beats per minute in adults, or more than 40 in adolescents, within ten minutes of standing [1]. The headache that comes with it, is part of the same picture of the brain not getting a steady blood supply when you’re vertical, often alongside the coat hanger ache, the lightheadedness, and the fatigue.
For orthostatic headaches driven by autonomic problems, there isn’t a good evidence base for headache specific drugs [1]. The management aims at the underlying POTS instead: getting fluid volume up with plenty of water (in the region of two to three litres a day) and a genuinely high salt intake (often ten to twelve grams a day), pacing activity so you’re not constantly crashing, building tolerance to being upright with graded exercise, and using compression garments to stop blood pooling in the legs [1]. It’s unglamorous I know, and it’s a slow build, but it targets the actual mechanism rather than chasing the symptom with pills.
The framework overlaps heavily here as well. That same overaroused nervous system that braces the neck also struggles to regulate the autonomic side. Breathing work matters more than people expect also, partly because how you breathe influences your carbon dioxide levels and, in turn, how your blood vessels behave. And that instinct to “push through” an orthostatic crash is usually counterproductive, because it drives the arousal loop harder. Steady, graded, and patient work wins here: heroics don’t.
When to think CSF leak and low pressure
This one is a lot less common, but much more serious, and it’s a mechanism that hypermobile folk are genuinely more prone to, so it’s worth knowing the signs.
Your brain floats in cerebrospinal fluid, sealed inside a tough membrane called the dura. A spontaneous CSF leak is a tear in that membrane that lets fluid escape, dropping the pressure around your brain. The classic sign is a positional headache that is bad when you’re upright and eases when you lie flat, often within minutes of lying down [4][1]. It tends to come with other things too: nausea, neck stiffness, ringing in the ears, blurred vision, and sometimes cognitive changes [4]. Now, notice the overlap with orthostatic headache from POTS, both are worse upright, which is exactly why the standing up clue needs proper assessment rather than a guess.
The dura is made of connective tissue, and in hEDS the same collagen issues that affects the rest of the body can affect it too. It can thin and balloon out in places (dural ectasia), and this is thought to raise the risk of a spontaneous leak [4]. I’ll flag the hedge honestly here: the collagen issues to leak link is a “thought to” and “may”, not a nailed down definitively, and CSF leaks are widely reckoned to be underdiagnosed [4].
Spontaneous intracranial hypotension, the low pressure state a leak causes, is uncommon overall, roughly 5 cases per 100,000 people a year, and it turns up more often in women [1]. Crucially, a normal brain MRI does not rule it out: the scan comes back normal in up to one in five cases [1]. So if you’ve had a clear MRI and been told it’s therefore not a leak, that isn’t the whole story. And the connective tissue link shows up in the data from the other direction too. In one group of people with these leaks, 18% had a diagnosed heritable connective tissue disorder and another 16% had connective tissue features or a positive hypermobility score [1]. That’s a pretty meaningful chunk.
There’s one small study worth mentioning carefully here as well. Among eleven people with postural headaches who were investigated, a CSF leak was found in all of them [4]. Now, that’s a tiny, selected group who were referred precisely because a leak was suspected, so you can’t read it as “postural headache always means a leak”. But it does underline that when the positional pattern is strong, a leak deserves to be on the table.
On management, and again these are figures for the general leak population rather than hypermobility specifically: conservative measures like bed rest, fluids and caffeine help only a minority, around 28% in one analysis [1]. The next step up, a first epidural blood patch (where a little of your own blood is injected to seal the leak), resolves symptoms in around 64% [1]. The takeaway isn’t to self diagnose, it’s to know that a strongly positional headache is a “get this properly investigated” situation, not a “push through it” one.
Craniocervical instability, the controversial one
Now we come to the section that needs the most careful handling, because it’s the one the internet gets most excited and most wrong about, all at the same time.
Craniocervical instability (CCI), is the idea that excess ligament laxity right at the junction between the skull and the top of the neck lets the head settle down onto the structures below, potentially compressing things near the brainstem [1]. In theory it can cause headache, along with a long list of other symptoms. And if you spend any time in hypermobility spaces online, you’ll have seen CCI discussed as though it’s a common, obvious diagnosis with an obvious surgical fix.
Here’s the honest picture though, CCI remains highly controversial in the medical literature [1]. There’s no agreed way to reliably tell ordinary hypermobility apart from genuine instability on imaging, there’s no solid set of normative data to measure a scan against, and the evidence base for both diagnosis and surgery is weak [1][8]. The research that exists is low quality, mostly small case series and retrospective reviews, the kind of evidence that can suggest a signal but can’t confirm one [8].
That doesn’t mean CCI isn’t real. Severe, genuine instability at the skull neck junction exists and can be devastating. But, when it comes to surgery, the bar is, and should be, crazy high. Surgical fusion is reserved for cases with clear radiographic instability that matches the person’s symptoms, and even then, it’s a genuine last resort, not a first move [8][1]. Fusing the top of the neck is major, irreversible surgery with real risks, and doing it on the strength of a contested scan and a hopeful theory, is not something the evidence supports.
So, if you’re worried about CCI, the sensible path is the same conservative, control based work we covered in the cervicogenic section first, done properly and given real time, with specialist assessment if severe signs are present. Be very wary of any clinic that reaches for a scan and a surgical or injection solution early. The framework answer here is not exciting, but it’s the honest one: control before cutting, always.
The jaw connection
The jaw gets overlooked in headache conversations, which is a shame, because it’s genuinely connected.
In people who have both EDS and jaw problems, the most common jaw disorders are joint pain, muscle pain, disc displacement, and subluxation of the jaw joint, and the most frequent companions to those jaw problems are headache and neck pain [7]. That’s a direct EDS finding, so it carries weight for this audience. The jaw joint is a small, hard working, often hypermobile joint, and when it’s unhappy, the pain doesn’t stay politely local. It spreads into the temples, the side of the head, and down the neck.
There is supporting evidence from the wider headache world too, though it needs a caveat. Across the general population literature, jaw (temporomandibular) disorders are notably more common in people with migraines, with an odds ratio of 3.79, and in people with tension type headache, an odds ratio of 4.45 [6]. In plain terms, that’s roughly three to four and a half times more likely. But I have to be straight about what that does and doesn’t tell us. Those figures come from general populations, not EDS specific groups, the studies are cross-sectional, so they’re snapshots rather than anything that can prove cause and effect, and a link between two things is not proof that one causes the other [6]. So read it as “jaw problems and headaches travel together a lot”, not “your jaw is definitely causing your headaches”.
The framework thread runs through the jaw as well, as the jaw is a classic site for overbracing. Clenching, especially at night, especially under stress, cranks the tone in the jaw and the muscles that share territory with the neck, and it feeds the same arousal loop that’s driving so much of the rest. So jaw work often isn’t just about the jaw, it’s about teaching a wound up system to unclench.
Medication overuse headache, the trap
This one catches good people out constantly, and it’s rather cruel, because it’s caused by trying to treat the pain.
Medication overuse headache is exactly what it sounds like: taking acute painkillers too often actually causes more headaches. The thresholds are fairly specific too. Taking triptans or opioids on ten or more days a month, or paracetamol and NSAIDs on fifteen or more days a month can drive it [1]. And here’s the nasty part: it can turn episodic migraines, the kind that comes and goes, into chronic migraines, the kind that’s there most days [1]. So, the very act of reaching for the painkillers, more and more often because the headaches are getting worse, is what’s making them worse.
If you’re hypermobile with frequent headaches, you’re at real risk of stumbling into this, simply because you’ve got more reasons to take painkillers than most people from the general population.
Managing it is very straightforward to describe, yet difficult to do. You have to stop the overused painkiller, and usually start a preventive at the same time, to catch the fallout [1]. The honest warning: the headache often gets worse for a few days first, before it gets better [1]. That withdrawal period is grim, which is why it’s worth doing it with support from your prescriber, rather than going cold turkey on your own. But, it’s one of the more fixable headache problems once you spot it, and spotting it is half the battle. If you’re taking something for your head more days than not, this is the mechanism to consider first.
How to work out which one you’ve got
Right, let’s pull this together into something usable, because knowing the mechanisms only helps if you can start to place your own headache among them. None of this replaces a proper assessment, but it gives you a much better set of notes to walk in with.
Start with position. Is the headache clearly worse when you’re upright and better lying down? That points toward the orthostatic group: CSF leak, POTS, or raised pressure. Does it change with neck position, or come on after holding your head still, or sit at the base of the skull? That leans cervicogenic. Does it come with aura, severe light and sound sensitivity, nausea, and knock you out for hours? That’s migraine territory.
Then look at the company it keeps. Coat hanger pain across the shoulders and neck, lightheadedness on standing, racing heart: think autonomic. A jaw that clicks, locks, or aches, especially with morning headaches: think about the jaw. Fogginess, ringing ears, and a strongly positional pattern: keep a CSF leak in mind.
Then look at your painkiller pattern. If you’re taking acute medication on more days than not, medication overuse could be layered on top of whatever started it, and it may need dealing with first.
A couple of practical, low stakes cues that come up again and again from people living with this, offered as things to try rather than rules: many find that cold tends to suit a migraine, an ice pack on the head or neck, while gentle heat tends to suit a neck driven headache by easing the muscle tension. And a lot of people find that a thinner, firmer pillow that keeps the neck better aligned reduces the morning headaches and the overnight neck grief. These won’t diagnose anything, but they’re cheap to try and they can tell you something about which mechanism is in play.
The most useful thing you can do before an appointment is keep a simple diary for a few weeks. When it comes to getting the right help, a clear record beats a vague memory every time, and most people massively underestimate their own painkiller use until they see it written down. You don’t need anything fancy. For each headache, jot down: when it started and how long it lasted, what you were doing and what position you were in when it hit, whether it was better or worse lying down, what else your body was doing (dizzy, nauseous, fogged, jaw sore, heart racing), and exactly what you took for it and how much. Do that for three or four weeks and patterns fall out of it that you’d never spot in the moment. A cluster of positional headaches, or a run of days where the painkillers stack up, or a link to your cycle, or a link to bad nights, whatever it is, that single sheet of paper will do more to get you the right help than any amount of guessing in a ten minute appointment.
What actually helps, across the board
For all the differences between these mechanisms, there’s a common thread in what helps, and it’s the opposite of what a lot of people expect.
The first move, for almost all of these, is conservative and mechanism matched. Not “here’s a stronger painkiller”, but “let’s work out what’s driving this and address that”. For the neck driven and instability related headaches, that means the control work we’ve talked about: sensory clarity to sharpen the brain’s map of the neck, tone regulation to unwind the constant bracing, and graded motor learning to rebuild trust in movement, often starting away from the neck itself [2][3]. For the autonomic and orthostatic side, it means the fluids, salt, compression, and graded exposure to being upright [1]. For migraines, it’s trigger management, sensible acute treatment, and preventives chosen with your body in mind [1][10].
Underneath all of it sits the nervous system, and this is where the biggest general gains often hide. That arousal loop, worry feeding bracing feeding pain feeding worry, is doing real work in almost every headache type here. Breathing work helps, both because it directly influences the autonomic side and because it’s one of the few reliable ways to talk a wound up system down. There’s a physiological reason it matters, too. When you’re anxious or in pain, you tend to over breathe without noticing, which blows off carbon dioxide and, in turn, tightens up your blood vessels. Given how much of the hypermobile headache picture involves blood flow to the brain, that’s not a small detail. Learning to breathe slower and lower, through the nose, letting the carbon dioxide come back up to where it should sit, is one of the more useful skills you can build. It’s free, it’s always available, and it targets the arousal side and the autonomic side at the same time.
Pacing also helps, because boom and bust cycles keep the whole system on high alert. When it comes to a sensitised nervous system, the worst thing you can do is smash a good day and then pay for it with three bad ones, because that pattern teaches the system that activity is dangerous. Steady beats spiky. Sleep helps too, because a tired nervous system is a sensitised one, and sensitised systems produce more headaches. None of this is a cure, and I’m not going to pretend it is. What it does is lower the background excitability that makes every mechanism on this list easier to trigger and harder to shift. Think of it as lowering the water level so fewer rocks stick out.
A word on braces, collars and gadgets. They’re tools, not lifestyles. A collar for a bad flare or a long journey, fine. A collar worn all day, every day, teaches your muscles to stop working and makes the underlying control problem worse [2]. The same logic applies to leaning on any passive fix: use it to get through a rough patch, but keep building the active side underneath it.
And on escalation: there’s a place for medication, for specialist assessment, for imaging, and occasionally for surgery. But the order matters. Conservative, control based work first, given real time to work, escalating only when the mechanism genuinely demands it. Surgery for neck instability is a last resort with weak supporting evidence, not a shortcut [8]. If a clinic is selling you the shortcut, be careful.
This is the bit that makes our approach ours. Not a leaflet, not a sales pitch, but a map of what’s actually going on and a plan that matches it. If you want to work on the control and tone side properly, that’s exactly what we teach in the studios.
Frequently Asked Questions
Yes, clearly so. In symptomatic hypermobility, migraine estimates run from about 40% up to three quarters, and in one EDS clinic group 42.5% had migraine [1]. It starts young, too: in children with joint hypermobility, headache was about 3.7 times more likely and migraine about 4.5 times more likely than in those without [5]. So if it feels like your head is a bigger problem than it is for the people around you, that’s not in your imagination.
The clues for a neck driven (cervicogenic) headache are that it often starts at the base of the skull and spreads forward, it’s frequently one sided, and it tends to change with neck position or after you’ve held your head still for a while [1]. Upper cervical involvement can also bring coat-hanger pain across the shoulders, brain fog, and a heavy head [2]. It’s worth knowing that neck stiffness can also be part of a migraine rather than the cause of it, and that even neurologists find cervicogenic headache tricky to confirm [1], so treat it as a working idea to explore with a good physio, not a certainty.
A spontaneous cerebrospinal fluid leak is a tear in the membrane around the brain that lowers the pressure inside your skull. The giveaway is a headache that’s clearly bad when you’re upright and eases within minutes of lying flat, often with nausea, neck stiffness, ringing in the ears, blurred vision, or fogginess [4]. The connective tissue weakness in hEDS is thought to raise the risk [4]. Importantly, a normal MRI does not rule it out, the scan is normal in up to one in five cases [1], so a strongly positional headache deserves proper investigation even if a scan has come back clear.
Severe craniocervical instability is real, but it’s uncommon and the whole area is genuinely controversial [1]. There’s no agreed way to reliably separate ordinary hypermobility from true instability on a scan, no solid normative data to compare against, and the evidence for diagnosis and surgery is weak [1][8]. So a scan is not a first step for most people, and be wary of any clinic that jumps quickly to imaging and surgery. Conservative, control based work comes first, with specialist assessment reserved for genuine severe signs.
It can, but the key isn’t raw strength, it’s control. Neck instability in hypermobility is driven more by insufficient neuromuscular control than by loose ligaments alone [2], and control can be trained even though ligaments can’t be tightened. The recommended approach is conservative and graded, with proprioception and motor control work, and interestingly, training the lower back and shoulder blades can improve neck control too [3]. The honest caveat: the direct evidence is small and outcomes vary [3], but it’s a low risk, sensible first move that helps a lot of people.
If you’ve got this far, you’ll have noticed the theme. There isn’t one hypermobility headache, and there isn’t one fix. There’s a handful of different mechanisms, they overlap, they hide behind each other, and the whole job is working out which one (or which ones) is doing the most in your particular head. Get that right and the management follows. Get it wrong and you’ll spend years on advice that was never built for the problem you’ve actually got.
None of this is quick, and I won’t pretend otherwise. But it is knowable, and it is workable, and understanding your own headache is the first proper step toward doing something useful about it. You’re not stuck with “just tension” and a shrug. You’ve got a mechanism, and mechanisms can be worked with.
Take it steady, keep the diary, and start with the conservative side.
– Adam –
References
- Mehta D, Simmonds L, Hakim AJ, Matharu M. Headache disorders in patients with Ehlers-Danlos syndromes and hypermobility spectrum disorders. Front Neurol. 2024;15:1460352. doi: 10.3389/fneur.2024.1460352
- Russek LN, Block NP, Byrne E, Chalela S, Chan C, Comerford M, et al. Presentation and physical therapy management of upper cervical instability in patients with symptomatic generalized joint hypermobility: International expert consensus recommendations. Front Med (Lausanne). 2023;9:1072764. doi: 10.3389/fmed.2022.1072764
- Chalela S, Russek LN. Presentation and physical therapy management using a neuroplasticity approach for patients with hypermobility-related upper cervical instability: a brief report. Front Neurol. 2024;15:1459115. doi: 10.3389/fneur.2024.1459115
- Severance S, Daylor V, Petrucci T, Gensemer C, Patel S, Norris RA. Hypermobile Ehlers-Danlos syndrome and spontaneous CSF leaks: the connective tissue conundrum. Front Neurol. 2024;15:1452409. doi: 10.3389/fneur.2024.1452409
- Jari M, Alesaeidi S. Correlation between benign joint hypermobility syndrome and headache in children and adolescents. BMC Musculoskelet Disord. 2024;25:347. doi: 10.1186/s12891-024-07473-3
- Bizzarri P, Manfredini D, Koutris M, Bartolini M, Buzzatti L, Bagnoli C, Scafoglieri A. Temporomandibular disorders in migraine and tension-type headache patients: a systematic review with meta-analysis. J Oral Facial Pain Headache. 2024;38(2):11. doi: 10.22514/jofph.2024.011
- Di Giacomo P, Celli M, Ierardo G, Polimeni A, Di Paolo C. Evaluation of temporomandibular disorders and comorbidities in patients with Ehler-Danlos: clinical and digital findings. J Int Soc Prev Community Dent. 2018;8(4):333-338. doi: 10.4103/jispcd.JISPCD_103_18
- Lohkamp LN, Marathe N, Fehlings MG. Craniocervical instability in Ehlers-Danlos syndrome, a systematic review of diagnostic and surgical treatment criteria. Global Spine J. 2022;12(8):1862-1871. doi: 10.1177/21925682211068520
- Fermo OP. Evaluation and management of orthostatic headache in hypermobility disorders. Front Neurol. 2023;14:1321350. doi: 10.3389/fneur.2023.1321350
- National Institute for Health and Care Excellence. Headaches in over 12s: diagnosis and management (CG150). 2012 (updated 2021). https://www.nice.org.uk/guidance/cg150
- Matharu M. Management of Headache in EDS and HSD. The Ehlers-Danlos Society. 2021. https://www.ehlers-danlos.com/wp-content/uploads/2021/04/PDF_pain_management_matharu_manjit.pdf
