May is EDS and HSD Awareness Month. It is a time to raise awareness of the Ehlers-Danlos syndromes (EDS), including hypermobile Ehlers-Danlos syndrome (hEDS) and hypermobility spectrum disorders (HSD). 

Recognition of these conditions is slowly growing. However, numerous misconceptions remain common in clinical practice and may contribute to delayed diagnosis and suboptimal management.

For many patients, the journey to diagnosis is long and frustrating. It often takes decades, involves multiple healthcare providers and includes numerous misdiagnoses. 

Along the way, patients may experience persistent pain, fatigue and a wide range of symptoms affecting different body systems.

We now understand that these are complex, multisystem conditions, not just ‘being flexible’.

For clinicians involved in diagnosis and management, addressing persistent misconceptions is essential, including the following.

Myth 1: hypermobility is simply joint laxity 

Clinical reality: hEDS and HSD are multisystem connective tissue disorders.

Joint hypermobility represents only one aspect of these conditions. Connective tissue abnormalities do affect ligaments, tendons and fascia but also skin, blood vessels, the nervous system and visceral organs (Hakim et al 2017, Hakim 2024, Francomano et al 2024).

Consequently, individuals with hypermobility disorders may exhibit an array of symptoms, which can vary from localised manifestations to systemic presentations, including (but not limited to):
•    joint instability and recurrent sprains or dislocations
•    chronic musculoskeletal pain
•    fatigue and exercise intolerance
•    gastrointestinal dysmotility
•    autonomic dysfunction
•    immune dysregulation
•    psychological comorbidities (including anxiety and depressive disorders).

These manifestations reflect the widespread role of collagen and extracellular matrix proteins in maintaining structural integrity across various tissues. 

Increasing evidence indicates that hEDS is a complex multisystem condition rather than an isolated musculoskeletal disorder (Wang et al 2025, Daylor et al 2024, Gensemer et al 2021, Petrucci et al 2024, Nicholson et al 2022).

Myth 2: hypermobility disorders are rare 

Clinical reality: hypermobility conditions are frequently under-recognised and misdiagnosed, often taking decades to reach correct diagnosis.

Population-based research suggests that diagnosed cases of EDS and HSD may occur in as many as one in 600–900 individuals, although the true prevalence is likely higher due to under-recognition (Demmler et al 2019, Ehlers-Danlos Society 2026).

Generalised joint hypermobility itself is considerably more common, though most in this category are asymptomatic. 

Pauline Slater.

Population studies estimate that 10–20 per cent of individuals demonstrate increased joint mobility, depending on age, sex and ethnicity (Blajwajs et al 2023, Singh et al 2017).

Clinically, the key distinction lies between asymptomatic hypermobility and symptomatic hypermobility disorders, where joint laxity contributes to instability, pain and functional impairment. Other related comorbidities may also exist.

International studies show that people with Ehlers-Danlos syndromes (especially hEDS and HSD) often wait 10–12 years for an accurate diagnosis, largely due to their varied and complex symptom presentation and limited clinician awareness (Halverson et al 2023). 

Australian research exploring the experiences of women with EDS similarly highlights a lengthy diagnostic journey, with many participants reporting symptoms for more than 15 years before diagnosis (Trudgian & Flood 2024). 

Recent global surveys show that the average diagnostic delay is even longer, with a mean of 22 years for hEDS and 17.5 years for HSD (Daylor et al 2024). 

This evidence highlights the fact that delays in recognition continue to be a major worldwide issue, due to varying presenting symptoms, coexisting conditions and insufficient clinical understanding.

Myth 3: normal investigations often exclude hypermobility or connective tissue disorders 

Clinical reality: routine tests often appear normal.

Many patients with hypermobility disorders present with significant symptoms despite normal imaging and laboratory findings.

Currently, hEDS remains a clinical diagnosis, based on the 2017 diagnostic criteria (Hakim et al 2010, Hermanns-Lê et al 2013).

Clinicians should therefore consider hypermobility disorders when patients present with multiple sprains and joint conditions, multisystem symptoms that may seem unrelated, chronic musculoskeletal pain, fibromyalgia and joint instability, even when routine investigations appear unremarkable.

A process is currently underway to update the diagnostic classifications for EDS and HSD through the Ehlers-Danlos Society’s international Road to 2026 initiative, aiming to improve diagnostic accuracy and recognition.

Myth 4: pain in hypermobility disorders results only from joint instability

Clinical reality: pain is multifactorial.

Pain in hypermobility disorders reflects a combination of biomechanical, neuromuscular, psychosocial and connective tissue factors. 

In a cohort study of individuals with EDS, pain was found to be both common and severe, frequently resulting in significant functional impairment (Voermans et al 2010, Börsch et al 2024, Kumar & Lenert 2017, Molander et al 2024, Pepe et al 2016).

Factors contributing to pain in hEDS, HSD and hypermobility include:
•    altered muscle structure and strength
•    joint instability and microtrauma
•    frequent subluxations and dislocations
•    muscle quality and intramuscular fat/fatty atrophy
•    muscle guarding (protective muscle tension)
•    impaired proprioception (reduced joint position sense)
•    poor motor control and coordination
•    biomechanical overload and compensation patterns
•    myofascial pain and fascial dysfunction
•    post-exertional symptom exacerbation
•    peripheral nerve compression or irritation
•    small fibre neuropathy
•    central sensitisation (amplified pain processing)
•    autonomic dysfunction, eg, postural orthostatic tachycardia syndrome (POTS)
•    local inflammation from repeated strain
•    deconditioning and reduced physical capacity
•    sleep disturbances
•    pain-related fear and movement avoidance
•    anxiety and depression (Hakim 2024, Wang et al 2025, Voermans et al 2010, Scheper et al 2015, Vlaeyen & Linton 2000, Rombaut et al 2015).

Altered muscle structure and strength

Muscle strength in hypermobility disorders has been reported to be 30–49 per cent lower than in healthy controls (Coussens et al 2022). 

Studies examining body composition in individuals with hEDS and HSD demonstrate important differences compared with healthy populations.

Imaging techniques such as peripheral quantitative computed tomography have revealed:
•    reduced muscle mass
•    smaller muscle cross-sectional areas
•    lower muscle density
•    reduced muscle strength (Coussens et al 2022).

Muscle quality and intramuscular fat

Reduced muscle density, often reflecting increased intramuscular fat infiltration, is associated with impaired muscle quality, reduced contractile efficiency and diminished force-generating capacity (Smith et al 2025, Wang et al 2024).

Muscle guarding and fascial involvement

In hEDS, HSD and generalised joint hypermobility, muscle tightness is often due not to true shortening but rather to a protective response (Murray & Sessle 2024). 

Ramona Chryssidis.

When joints lack passive stability, the body compensates by increasing muscle activity to create active stability around the joint – a process known as muscle guarding (Vlaeyen & Linton 2000). 

This ongoing contraction helps prevent excessive movement but can lead to the overwork cycle, with persistent feelings of
stiffness, fatigue and pain amplification (Murray & Sessle 2024, Broida et al 2021).

Fascia also plays an important role in force transmission and proprioception. 

In HSD, hEDS and EDS, altered connective tissue structure may affect fascial integrity, disrupting how forces are distributed through the body and reducing proprioceptive accuracy (Wang et al 2025). 

This can further drive compensatory muscle overactivity as the body attempts to maintain stability.

Together, these mechanisms help explain why people with HSD, hEDS and EDS often report tight, stiff muscles despite underlying joint laxity. 

Rather than being a problem to ‘stretch out’, muscle guarding is often a necessary, though sometimes maladaptive, strategy to protect unstable joints.

Myth 5: exercise should follow standard protocols, push through pain or focus on stretching

Clinical reality: exercise is beneficial but programs must be individualised, supervised and paced accordingly.

Key principles of exercise in hypermobility

Exercise is widely recognised as a core component of management for hEDS and HSD (Buryk-Iggers et al 2022). 

However, patients are often given conflicting advice, which can lead to increased pain and worsening of instability. 

Exercise programs must be tailored to the individual, understanding the factors that influence successful rehabilitation.

Avoiding exercise altogether, pushing through pain, following standard strengthening regimes or relying heavily on stretching to relieve stiffness are not productive strategies in this group of patients.

•    Avoiding exercise can lead to deconditioning, reduced muscle strength and increased joint instability.
•    Standard exercise or rehabilitation regimes, endurance or high-intensity exercise may increase the risk of injury and symptom exacerbation (Russek et al 2019).
•    Excessive stretching may worsen instability or symptoms rather than relieve them. Despite many individuals reporting significant stiffness, this is often protective muscle guarding, where muscles contract to stabilise unstable joints, rather than true tissue tightness.

Rehabilitation should instead prioritise:
•    strengthening
•    neuromuscular control
•    functional movement retraining.

Skeletal muscle plays a key role in joint stabilisation. Targeted exercise and motor control training can improve stability, function and quality of life (Coussens et al 2022, Smith et al 2025).

Closed-chain exercises are recommended as they promote joint stability and proprioceptive feedback with controlled loading across multiple joints.

Individuals with hypermobility also commonly experience altered pain perception, chronic pain and features of central sensitisation, alongside impaired proprioception and joint position sense (Kumar & Lenert 2017, Wang et al 2024).

These factors influence movement control and exercise tolerance, particularly in those with co-occurring sensory differences such as attention deficit hyperactivity disorder or autism spectrum disorder.

Rehabilitation programs must include:
•    gradual progression
•    individualised pacing
•    symptom-guided loading.

with an emphasis on:
•    balance and proprioceptive training
•    slow, controlled movement patterns that include strengthening
•    neuromuscular control and motor control retraining.

For individuals with associated conditions such as dysautonomia and POTS, exercise may need to begin in recumbent or low-orthostatic positions, with gradual progression as tolerance improves (Lau et al 2026, Fu & Levine 2018, Cortez et al 2025). As POTS is a common feature in EDS and hypermobility (over
60 per cent of the HSD and hEDS cohort) (Halverson et al 2023, Slater et al 2022, Daylor et al 2025), exercise prescription should also consider:
•    beginning with recumbent or semi-recumbent aerobic exercise
•    adding progressive resistance training
•    increasing duration before intensity
•    transitioning to upright exercise slowly
•    using individual pacing, symptom-guided progression and behavioural support.

Overall, evidence supports an individualised, multidisciplinary approach that prioritises strength, stability and functional capacity over flexibility or pain-based exercise models, improving long-term outcomes and quality of life (Engelbert et al 2017, Brittain et al 2024).

Myth 6: there are limited or no treatment options 

Clinical reality: multidisciplinary care can improve quality of life and symptoms.

Although no curative treatment currently exists, multidisciplinary management can significantly improve symptoms and quality of life.

Management strategies may include:
•    physiotherapy, hydrotherapy, exercise physiology and neuromuscular rehabilitation
•    multidisciplinary, neurodivergent-aware and trauma-aware pain management strategies
•    autonomic dysfunction treatment including POTS management
•    gastrointestinal and MCAS (mast cell activation syndrome) management
•    activity pacing and lifestyle adaptations
•    dextrose prolotherapy and regenerative injection therapies (such as platelet-rich plasma) to stabilise joints and fascia.

Recognising hypermobility disorders as multisystem connective tissue conditions is essential for guiding appropriate clinical care and improving outcomes.

Quick link: 

• References

Visit the Ehlers-Danlos Society, CTDNA, the EDS & Hypermobility Network Australia and Hypermobility Health Connect for more information.

>> Pauline Slater APAM is the principal physiotherapist and founder of Hypermobility and Health Connect, working nationally and internationally with children and adults living with hypermobility, EDS and POTS. She leads an Ehlers-Danlos Society’s CORE Network of Excellence and is a member of the Australian Dysautonomia (POTS) and Research Collaboration. Based in Adelaide, Pauline has over 35 years of clinical experience and is currently undertaking a PhD at the University of Adelaide. Her research focuses on the diagnostic journey and impact of EDS, hEDS and HSD in Australia.

>> Dr Ramona Chryssidis, a Fellow of the Royal Australian College of General Practitioners, has had a special interest in musculoskeletal medicine since 2002. She utilises a holistic approach and has extensive experience with sacroiliac joint and hypermobility disorders and advanced ultrasound-guided regenerative injections. Ramona is the immediate past president of the Australian Association of Musculoskeletal Medicine.