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Hypermobility in Pole Dance

Updated: May 27

Today’s blog is undeniably a big one. It’s on a topic that’s quite important to our Pole Physio team, to numerous polers, patients and colleagues around us, so we hope you’re able to take time out of your day to join us on this journey and learn about the zebra (hypermobile) in the room.

If you’re a hypermobile aerialist out there, trust us when we say this is not a blog that you want to TL;DR. There’s a lot of new information in this blog so we suggest taking it in bit by bit and stepping away and coming back later if you feel overwhelmed at all. A reminder that The Pole Physio is here to help if you have any concerns or if this blog triggers you in any way.

Alright zebras and non-hypermobiles, let’s do this!

Hypermobility disorders are frustratingly hard to diagnose, let alone define. The lack of knowledge out there on these syndromes makes for a challenging time for patients and therapists alike. In fact, it usually takes on average 15-20 years for these disorders to be diagnosed from onset of symptoms, meaning most patients get diagnosed well into their 40s.

With the average age of a pole dancer/aerialist sitting in their late 20s, you can see why this can be a huge issue in our community. Most hypermobile aerialists are unaware they even have one of these disorders and really struggle through their artform due to their underlying problem until they are diagnosed much later on in life.

We are going to deep dive today and uncover what hypermobility really is, spanning from asymptomatic joint laxity to connective tissue disorders such as Ehlers-Danlos Syndrome (EDS).

Let’s start with a few definitions to get everyone up to speed…

Flexibility – Flexibility is one’s ability to change their joint’s position/range of motion into a pre-determined end range position, i.e. the ability to bend forward or reach overhead. The capacity of our body for flexibility comes from multiple structures including muscles, connective tissues, joints and nerves and is controlled almost entirely by the nervous system

. Joint Hypermobility (JH) – In the physio world joint hypermobility is defined as greater than average range of motion directly as a result of connective tissue laxity (i.e joint looseness). This is laxity of the ligaments and capsules that usually help to passively stabilise the joint and is NOT related to the flexibility of surrounding muscles.

So just to repeat: Flexibility is NOT hypermobility. They are very different things. You can be hypermobile and not flexible. And vice versa.

For many pole dancers and contortionists, hypermobility can be beneficial. An example of this in pole dancing is our hip range far exceeding the range of the normal population to produce those extreme range pole tricks and contorted positions that deceive the eye.

Another great example of joint hypermobility outside the pole studio, is actually in baseball where a pitcher’s shoulder external rotation can increase to 135 degrees when the normal is only 90 degrees. Baseball pitchers have trained to increase their range of motion to improve their sport specific skill of throwing. Incredible!

But remember the terms flexibility and hypermobility are not interchangeable! If your body is hypermobile, you’re not automatically guaranteed to be flexible. Our nervous system can and will step in to reduce range of motion as a protective response if it senses joint instability or lack of muscular support/control. It does this by activating the surrounding muscles to restrict range of motion. So, in certain cases of hypermobile shoulders, the body reduces the active range available to protect the shoulder from dislocation.

Fascinating right?! Now that we have that understanding, let’s focus more on hypermobility.

Hypermobility spectrum disorder

The focus of today’s blog is on Hypermobility Spectrum Disorders (HSD). Remember this abbreviation because we’ll use it a lot! HSD are in basic terms defined as conditions in people who present with joint hypermobility (greater than average range of motion) with additional symptoms/signs (we will discuss these shortly). In short HSD = JH (joint hypermobility) +/- symptoms.

The challenging part of this spectrum of hypermobile disorders is that symptoms may not present in people until their 30s, even 40s, and not even pose an issue for them until well into the future. So why do we worry about something when symptoms may not be present? Well the more educated the pole community are about these conditions, the quicker polers will be to pick up on symptoms if they occur, access help and prevent the commonly described ‘hitting the wall’ that athletes with HSD experience when their bodies start to feel like they just break down. And the more knowledgeable instructors are, the better they will be at assisting their hypermobile students and understanding their learning and physical needs.

The Hypermobility Spectrum From March 2017, a new classification system for hypermobility disorders was determined, with benign joint hypermobility syndrome (general hypermobility) now falling under the umbrella term of HSD.

To recognise the continuum of joint hypermobility, the hypermobility spectrum was created, ranging between, at one end, asymptomatic joint hypermobility —someone who has no symptoms apart from their joints’ capacity to move beyond normal limits—through to hypermobile Ehlers-Danlos Syndrome (hEDS), at the other end (another abbreviation to remember!).

The spectrum of joint hypermobility disorders now includes:

Asymptomatic joint hypermobility

  • Asymptomatic localised joint hypermobility (1 joint)

  • Asymptomatic peripheral joint hypermobility (hands and feet)

  • Asymptomatic generalised joint hypermobility (5 or more joints)

Symptomatic hypermobility spectrum disorder

  • Historical hypermobility spectrum disorder (H-HSD)

  • Localised hypermobility spectrum disorder (L-HSD) (1 joint)

  • Peripheral hypermobility spectrum disorder (P-HSD) (hands and feet)

  • Generalised hypermobility spectrum disorder (G-HSD) (5 or more joints)

It’s really important to note that this symptomatic spectrum does not infer any greater severity at one end of the spectrum compared to the other. A person with symptomatic HSD can have severe problems whilst a person with EDS can have minor problems. It simply is a spectrum of similar but distinguishable disorders based on diagnoseable traits.

Diagnosing hypermobility

Hypermobility is diagnosed typically via the Beightons score or five-point questionnaire.

Typically they are assessing for hypermobility of five key joints per the picture shown on the right:

  • 5th finger

  • Thumb

  • Elbow

  • Knee

  • Lumber/lower back

A maximum score of 9 is provided with a score > 5 definitively indicating joint hypermobility.

And now this is where things can get a tad confusing…

You don’t actually need to score > 5 or be symptomatic to be diagnosed as hypermobile.

As mentioned earlier, range of motion of a joint may be limited secondary to lack of flexibility of the soft tissues around a joint. Perhaps you had surgery at a young age and lost that joint’s mobility. Or your muscles have shortened as your body’s protective response to keep you from dislocating your joint. So you may only score 3/9 and still be diagnosed as hypermobile. The 5 point questionnaire can also be used to assess for hypermobility which asks the following questions:

  1. Can you now [or could you ever] place your hands flat on the floor without bending your knees?

  2. Can you now [or could you ever] bend your thumb to touch your forearm?

  3. As a child, did you amuse your friends by contorting your body into strange shapes or could you do the splits?

  4. As a child or teenager, did your kneecap or shoulder dislocate on more than one occasion?

  5. Do you consider yourself “double-jointed”?

The Beighton's scale and the 5 point questionnaire are both crude measurements and are useful in capturing majority of hypermobile individuals, but not everyone. It may often miss those with milder symptoms. So the diagnosis may come based on the experienced therapist's discretion.

Also another reminder for those that aren't typically flexible, not being flexible doesn't automatically rule out HSD or hEDS. Particularly if other symptoms are present which we'll be talking about shortly.

Understanding Asymptomatic vs Symptomatic Hypermobility

A great number of pole dancers, aerialists or contortionists have some level of hypermobility. In fact, some would say hypermobile people are drawn to this artform because of the way their body moves. But hypermobility is still very poorly understood in this world. When hypermobility is discussed with patients, common responses we receive are:

“I’m hypermobile – I always twinge my ankles” “I’m double jointed”

“Isn’t that a good thing for pole. I wish I was hypermobile”

For those who experience symptomatic hypermobility, these types of reactions can be quite frustrating, particularly as hypermobility can cause quite debilitating acute and chronic style pain. Just remember hypermobility is a spectrum with mild to extreme hypermobility and asymptomatic to severely symptomatic hypermobility. So, comparing your mobility levels with the next person doesn’t tell you whether you’ve got a HSD.

How does hypermobility/HSD occur? Joint hypermobility can be genetic in nature, can occur via joint trauma such as from injury, or from repetitive joint stress/load from training. However, HSDs are secondary to autosomal dominant hereditary connective tissue disorders that affect the connective tissue of a joint, specifically the collagen.

Understanding connective tissue, muscle and collagen Connective tissue is a type of tissue in the body that connects, separates and supports the joints. Examples of connective tissue are tendons, fascia, joint capsule and ligaments. Skeletal muscle is another type of tissue of the body that performs voluntary contractile actions under control of the somatic nervous system to move the body through space. Both connective tissue and skeletal muscle are built via the foundation blocks of collagen.

Collagen is the most represented protein in the human body (30% of the protein concentration). It is an incredibly important component of the extracellular matrix of our skeletal muscle and connective tissue and is mainly responsible for their functionality in terms of force transmission, flexibility, stiffness and adaptation.

Our skeletal system is actively and passively supported by our connective tissue so we can function day to day. In connective tissue disorders, there is an issue with the connective tissue (usually a lack of collagen), which then leads to laxity/hypermobility of that joint’s surrounding passive (and sometimes active) structures. Without our passive support system in place, joints become incredibly mobile and are able to access greater than usual range of motion, aka joint hypermobility – which is why HSD/EDS patients need to rely heavily on their active support system, aka the skeletal muscles, to stabilise their joints.

Asymptomatic HSD So you don’t have any symptoms other than hypermobility of a few joints? Then you will likely be classified under asymptomatic HSD. Why is hypermobility a disorder? Well if managed correctly, it’s not an issue! But it’s the genetic collagen deficiency which leads to the secondary hypermobility that’s the issue and why it’s classified as a disorder.

In fact, asymptomatic HSD is thought to occur in 4 to 13% of the population (Simpson, 2006), with a higher prevalence in women from an Asian, African and/or Middle Eastern background. Diagnosis of asymptomatic joint hypermobility is made via a process of exclusion and requires a battery of medical tests and physical exams.

Symptomatic HSD What’s more is that collagen and connective tissue is found all throughout the body (in the digestive tract, skin, heart and even eyes), so HSD does not just affect the joints, it can also affect skin elasticity, digestion, eye function and even heart function. And this is how a range of symptoms arise. So dependent on which protein is affected by the disorder, a person can experience a range of symptoms.

It’s important to distinguish asymptomatic hypermobility syndromes from other disorders out there such as symptomatic HSD, Ehlers-Danlos Syndrome (EDS), osteogenesis imperfecta, Rheumatoid Arthritis, Lupus Erythematosus and Marfan Syndrome as these syndromes do share similar features. These other conditions can be ruled out along with infection, inflammatory and autoimmune based disorders via blood tests, molecular/genetic tests and review by a specialist (usually a geneticist/rheumatologist).

Ehlers-Danlos Syndrome

Well done for getting this far – it’s a lot of information to take in. But I’m sure you’ll agree it’s all very important and relevant for all aerialists out there. We’re now moving on to discussing an important medical condition: Ehlers-Danlos Syndrome (EDS).

EDS are a group of inherited connective tissue disorders that are varied in how they affect the body and in their genetic causes. They are characterised by three key factors:

  1. Joint hypermobility

  2. Skin hyperextensibility (skin that can be stretched further than normal)

  3. Tissue fragility (ease of bruising)

The incidence of EDS, including all subtypes in the general population, is best estimated to be between 1 in 2500 and 1 in 5000 in the general population, and we imagine this number is closer to 1 in 250-500 in the pole and aerial community (no research to confirm).

Per the 2017 consensus, there are 13 different subtypes of EDS, but we now suspect there may be 14 subtypes (to be confirmed). Each EDS subtype has a set of clinical criteria that help guide diagnosis. A patient’s physical signs and symptoms will be matched up to the major and minor criteria to identify the subtype that is the most complete fit.

There is substantial symptom overlap between the EDS subtypes and the other connective tissue disorders including hypermobility spectrum disorders, as well as a lot of variability, so a definitive diagnosis for all the EDS subtypes (except for hypermobile EDS) requires genetic and molecular testing.

Types of EDS include:

  • Classical EDS (cEDS)

  • Classical-like EDS (clEDS)

  • Cardiac-valvular EDS (cvEDS)

  • Vascular EDS (vEDS)

  • Hypermobile EDS

  • Arthrochalasia EDS (aEDS)

  • Dermatosparaxis EDS (dEDS)

  • Kyphoscoliotic EDS (kEDS)

  • Brittle Cornea Syndrome (BCS)

  • Spondylodysplastic EDS (spEDS)

  • Musculocontractural EDS (mcEDS)

  • Myopathic EDS (mEDS)

  • Periodontal EDS (pEDS)

The most concerning of these diagnoses is the vascular EDS, which significantly reduces the last span of a person to an average of 48 years secondary to increased elasticity of the vascular structures which makes for an ineffective pumping system of blood vessels. This is why all hypermobile patients should be further assessed by their GP for cardiovascular issues, including assessment with an ECG and echocardiogram.

Hypermobile EDS Hypermobile EDS (hEDS) remains the only EDS without a confirmed cause/molecular marker. This means that this is the only form of EDS that currently cannot be diagnosed via testing, i.e there is currently no protein or molecular marker in the system to test for, so hEDS is a diagnosis made by ruling out all other possible diagnosis and ruling in certain hEDS criteria.

And the essential difference between the diagnosis of HSD and symptomatic hEDS lies in the stricter criteria for hEDS, i.e if all possible disorders are ruled out for the patient and they don’t tick all the boxes for hEDS but exhibit clear cut symptoms of hypermobility disorders then they are diagnosed with HSD.

Diagnosing hEDS

To confirm a diagnosis of EDS, specialist physicians will conduct a physical examination, and possibly skin biopsies, blood and urine tests, imaging tests, and genetic testing. Features clinicians will look for include:

  • Generalised joint hypermobility (diagnosed via Beighton’s or five-point questionnaire)

  • Unusually soft or velvety skin

  • Mild skin hyperextensibility (stretchiness)

  • Unexplained stretch marks without a history of significant gain or loss of body fat or weight

  • Spots on the heel (Bilateral piezogenic papules)

  • Recurrent or multiple abdominal hernia(s)

  • Poor wound healing/scarring

  • Pelvic floor, rectal, and/or uterine prolapse

  • Dental crowding and high or narrow palate

  • Long fingers

  • Arm span-to-height ≥1.05

  • Cardiovascular concern (via ECG/Echo)

  • Positive family history, with one or more first degree relatives independently meeting the current diagnostic criteria for EDS

  • Musculoskeletal pain in two or more limbs, recurring daily for at least 3 months

  • Chronic, widespread pain for ≥3 months

  • Recurrent joint dislocations or frank joint instability, in the absence of trauma

Not all of these are required for a diagnosis, only the first three. But it will often present with other symptoms too. If you think you exhibit any of these symptoms, it’s important you don’t try to diagnose yourself, but instead seek assistance from a healthcare professional that can assist. This may be a GP who has a specialist interest in hypermobility disorders, but usually is from a specialist such as a geneticist, rheumatologist, immunologist, sports physician or musculoskeletal physician.

Is there are cure for HSD/EDS? Unfortunately, no there is no silver bullet cure or drug for these disorders. However, holistic intervention from a symptomatic point of view can significantly improve a patient’s quality of life so they can continue doing everything they want to and need to do. More on this later.

Do we need a formal hEDS diagnosis? A lot of patients with hEDS have been given a primary diagnosis and have not undertaken formal testing with a geneticist. This may be due to a variety of reasons including the lack of access to clinicians that understand HSD/EDS conditions. And for many patients, they don’t feel they require a formal diagnosis as there is no medication to provide a simple cure for this disorder.

At the end of the day, regardless of the formal diagnosis, the focus remains on management of the condition.

Associated EDS conditions There is a range of conditions which can accompany EDS. While they’re associated with EDS, they’re not proven to be the result of EDS and they’re not specific enough to be criteria for diagnosis. These conditions may be even more debilitating than joint symptoms; they often impair daily life, and they should be considered and treated appropriately. Associated conditions include (but not limited to):

  • Anxiety

  • Cardiovascular problems – tachycardia, aortic root dilation and mitral valve prolapse

  • Cervico-cranial instability

  • Chiari malformation

  • Chronic degenerative joint disease

  • Chronic fatigue

  • Chronic pain syndrome

  • Depression

  • Dysautonomia

  • Functional gastrointestinal disorders – acid reflux and irritable bowel syndrome

  • Headaches

  • Hernias

  • Insomnia

  • Mast cell activation syndrome

  • Migraines

  • Neurodiversity – ADHD, Autism

  • Organ rupture

  • Orthodontia issues – crowding and high palate

  • Osteoporosis

  • Postural orthostatic tachycardia (POTS)

  • Pregnancy complications/Pre-term labour

  • Raynaud’s

  • Rectal or uterine prolapse/incontinence

  • Recurrent dislocations/subluxations

  • Respiratory and swallowing difficulties

  • Scoliosis

  • Skin scarring, stretching and slow wound healing

  • Small fibre neuropathy

The conditions listed in bold have been shown to have a very close link to EDS.

Did you know? A 2012 brain imaging study conducted by Dr Eccles and her colleagues found that individuals with joint hypermobility had a bigger amygdala? This is a part of the brain that is essential to processing emotion, especially fear. This is why hypermobility is highly linked to anxiety and depression.

In fact, research by Dr Eccles revealed that people with EDS are seven times more likely to be autistic, and six times more likely to have ADHD compared to the general population. There appears to be an incredibly important link between hypermobility and neurodivergence.

HSD/EDS and hormones The sex hormones, are divided into three types;

  • Androgens (mainly in males)

  • Oestrogens (mainly in females) and

  • Progestogens (also mainly in females)

The balance and change in levels of oestrogens and progestogens control the 28-day menstrual cycle in the female.

In hypermobile males the predominant androgen hormones have very little negative effect on collagen, with these hormones likely contributing to muscle bulking around the joints instead which is an ideal response.

In females though, it is quite a different story.

Whilst oestrogen tends to stabilise collagen levels, progestogens appear to destabilise or loosen them. Many hypermobile people, though not all, notice a worsening in symptoms including increased joint pain, clumsiness or a greater tendency to dislocate in the five days leading up to menstruation and in the few days after menstruation.

This is exactly the time when the progesterone compounds far exceed the stabilising oestrogen compounds and is particularly prevalent in collagen-based HSD/EDS.

Those females whose joints become worse at the time of menstruation often note that if their periods become irregular, for whatever reason, their joint symptoms not only become worse but, are worse for longer. This may be because in these people progesterone is present in high concentrations at times when it would not normally be present. Recurring irregularity of a period (<21 days and >35 days) requires assessment by a GP or gynaecologist.

Hypermobility and Contraceptives Please note that the following information is not medical advice or directives regarding contraception. But rather an expression of the current research and opinions of medical specialists in this field.

A variety of hormonal contraceptives are available for females. Many are ‘combined’ contraceptives, either a mixture of oestrogen or a progestogen given at the same time or sequentially (progestogen after the oestrogen) to mimic the normal female menstrual cycle. Others contain entirely progestogen. Injected contraceptives and intrauterine devices (coils) have become increasingly popular and are entirely progesterone based.

When careful gynaecological and rheumatological histories are taken together, it is surprising how frequently mildly symptomatic hypermobility becomes significantly worse with certain contraceptive pills, especially those containing progesterone alone. There appears to be a similar response with progesterone depo (intra muscular injection) contraception preparations and with mechanical devices impregnated with progesterone.

Oestrogens are not without their own adverse effects, one of the principal ones being a slight tendency to cause venous thrombosis (blood clots), a feature much less frequently seen with progestogens. Therefore, a progestogen-only preparation may have been prescribed for good and well-intentioned reasons, despite a possible tendency to increase hypermobility symptoms.

If you have hypermobile joints and have been taking hormones to modify menstruation or as contraceptives, you should discuss this further with your doctor and/or gynaecologist to determine what is the right form for you.

Management of all HSD and EDS conditions

Management of HSD/EDS requires a multi-pronged approach and often a multi-specialist approach dependent on the symptoms present.

Physiotherapy plays a key role in the management of all HSD, with the aim to improve any underlying muscle inhibition, muscle atrophy and reduced joint control.

A key part of treatment is education to the patient regarding normal joint range and how to keep within this range using local muscle control. This is quite a challenging concept and requires a great deal of proprioceptive control of the joint and surrounding musculature. Learning to access the smaller stabilising muscles helps to engage the larger muscles of the joint and improve the joint’s function. I.e stability of a joint will allow for greater mobility without injury/pain.

A perfect example of this is with hyperextending knees. Correctly accessing the stabilising muscles around the knee will improve control of the knee to avoid hyperextension and hypermobility. Staying away from this end of range is helpful in keeping the joint happy, healthy and strong.

So after all of this information are you curious to know why the zebras? Well in the medical world we have a saying "When you hear hoofbeats behind you, don't expect to see a zebra." Ie. doctors don’t look for an unlikely rare diagnosis when it’s most likely going to be a common diagnosis.

In fact, as mentioned earlier, EDS is not actually that rare, but it is still uncommon to find healthcare professionals who are knowledgeable about EDS due to the lack of information out there about these conditions. Which is why they have chosen the zebra as a way to educate healthcare professionals who may still be unaware of this condition. So, whilst a patient commonly is a ‘horse’, we still want to keep an eye open for that ‘zebra’!

And that’s a wrap Well we told you it was a big one, and hope we didn’t disappoint. It’s a complex topic with many areas to cover, so there’s more research to be had.

Additional resources we would recommend for anyone wanting to undertake further reading and research are:

Otherwise hit us up on the hypermobility socials on all your HSD/EDS related questions and I’ll do my best to answer!

Does your pole/aerial arts feel physically limited from your hypermobility spectrum disorder? Lacking control at your end range of motion?

Online telehealth appointments can be booked with the Pole Physio via our ‘Book Online’ page that can be found here. Assessment and tailored rehabilitation are provided in accordance with best practice and evidence-based treatment to help you unleash your 'poletential'.

Until next time, train safe.

The Pole Physio


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