This article needs additional citations for verification. (April 2026) |
Hypermobility, also known as double-jointedness, describes joints that stretch farther than normal.[2] For example, some hypermobile people can bend their thumbs backwards to their wrists, bend their knee joints backwards, put their leg behind the head, or perform other contortionist "tricks". It can affect one or more joints throughout the body.
| Hypermobility | |
|---|---|
| Other names | hyperlaxity, benign joints hypermobility syndrome (BJHS), hypermobility syndrome (HMS)[1] |
| Hypermobile fingers and thumb | |
| Specialty | Rheumatology, Medical genetics |
Hypermobile joints are common and occur in about 10 to 25% of the population.[3] Most have no other issues. In a minority of people, pain and other symptoms are present. This may be a sign of hypermobility spectrum disorder (HSD). In some cases, hypermobile joints are a feature of connective tissue disorders. One of these, Ehlers-Danlos Syndrome, was classified into several types which have been found to be genetic. Hypermobile Ehlers–Danlos syndrome (hEDS), formerly called EDS Type 3, remains the only EDS variant without a diagnostic DNA test.
In 2016 the diagnostic criteria for hEDS were re-written to be more restrictive, with the intent of narrowing the pool of hEDS patients, in the hope of making it easier to identify a common genetic mutation and create a diagnostic DNA test.
At the same time, joint hypermobility syndrome was renamed as hypermobility spectrum disorder, and redefined as a hypermobility disorder that does not meet the diagnostic criteria for any heritable Connective Tissue Disorder (such as hEDS, other types of Ehlers–Danlos Syndrome, Marfan Syndrome, Loeys–Dietz Syndrome, or osteogenesis imperfecta). Sometimes called "non-genetic EDS," hypermobility spectrum disorder can have the same signs as hEDS, but be caused not by a heritable genetic mutation but by problems in fetal development, such as pre-natal exposure to toxins like agricultural chemicals, drugs, or alcohol. Fetal Alcohol Spectrum Disorders affect at least 1 in 20 people in the U.S.,[4] and joint hypermobility with other symptoms is common.[5]
Signs and symptoms
editPeople with joint hypermobility syndromes may develop conditions caused by their unstable joints.[6][7] These conditions include:
- Subluxations or dislocations
- Sprains, tendinitis, or bursitis from activities. However, a 2018 study reports that while hypermobile individuals are more likely to suffer dislocations doing sports than non-hypermotile individuals, they are less likely to suffer muscle and tendon sprains. The overall chances of sports injury are not significantly different.[8]
- Joint pain[6]
- Fatigue due to muscle weakness[9]
- Back pain, prolapsed discs or spondylolisthesis
- Joints that make clicking noises
- Susceptibility to whiplash
- Temporomandibular joint dysfunction, also known as TMD
- Chance of nerve compression disorders in the joints (such as carpal tunnel syndrome)
- "Growing pains" (as described in children in late afternoon or night)[citation needed]
Associated conditions
editJoint hypermobility may be associated with other conditions. These include ADHD, autism, dyspraxia, fibromyalgia, hereditary connective tissue disorders, mitral valve prolapse, and anxiety disorders such as panic disorder.[10][11][12][3][13] Joint hypermobility does not cause these other conditions. Most people with joint hypermobility do not have them. In people who do, the underlying cause can be a general syndrome that affects the whole body and brain (such as Autism or Fetal Alcohol Spectrum Disorders), or a genetic condition or disease that affects certain tissues (such as Ehlers-Danlos syndrome or lupus).
Medical conditions that can cause joint hypermobility include FASDs, Stickler syndrome, Ehlers–Danlos syndrome,[14] Marfan syndrome,[14] Loeys–Dietz syndrome, rheumatoid arthritis, osteogenesis imperfecta,[14] lupus, polio, Fragile X syndrome, Down syndrome,[14] Morquio syndrome, cleidocranial dysostosis and myotonia congenita. All have other diagnostic criteria as well.
Causes
edit
Hypermobility generally results from one or more of the following:
- Unusually-shaped ends of one or more bones where they form a joint, or an increased angle of the bone, such as in coxa valga.[15]
- A mutation in collagen or collagen-related genes (as found in certain types of Ehlers-Danlos syndrome) or other connective tissue (as found in Loeys–Dietz syndrome and Marfan syndrome) resulting in weakened ligaments/ligamentous laxity. Ligaments hold bones together at the joints.[16][17]
- Abnormal joint proprioception (an impaired ability to locate body parts in space and/or monitor an extended joint)[18]
Any of these causes can increase the level of mechanical stress on a joint. Chronically stressed joints may experience higher or faster than usual levels of wear, leading to osteoarthritis.[19]
Hypermobility tends to run in families, suggesting a genetic basis for at least some forms.[20] The term double jointed is often used to describe hypermobility; however, the name is a misnomer and should not be taken literally, as people with hypermobile joints do not have any extra joints, or any extra bones or parts in the joint.
Most people with hypermobile joints do not have a hypermobility spectrum disorder. Approximately 5% of the healthy population has one or more hypermobile joints. However, people with symptomatic hypermobility are subject to many difficulties. For example, their joints may be easily injured, be more prone to complete or partial dislocation due to the weakly stabilized joint,[21] and they may develop problems from muscle fatigue[22] (as muscles must work harder to compensate for weakness in the ligaments that support the joints). Hypermobility syndromes can lead to chronic pain or even disability in severe cases.[23]
Hypermobility has been associated with myalgic encephalomyelitis (chronic fatigue syndrome) and fibromyalgia. Hypermobility syndromes can cause physical trauma, pain, and stress (in the form of joint dislocations, joint subluxations, joint instability, sprains, etc.), and chronic stress from repeated trauma is a possible trigger for chronic conditions such as fibromyalgia.[24]
Symptoms are often exacerbated during pregnancy. During pregnancy, the body releases relaxin and certain hormones that alter ligament physiology, easing the stretching needed to accommodate fetal growth as well as the birthing process.[25] The combination of hypermobility and pregnancy-related pelvic girdle during pregnancy can be debilitating. The pregnant person with hypermobile joints may be in significant pain as muscles and joints adapt to the pregnancy. Pain makes standing or walking difficult during pregnancy, so some women who have one of these disorders find they need to use a wheelchair during pregnancy.[25] They are also at risk for excessive bleeding during and after childbirth, and the baby is at risk of dislocated joints, especially of the clavicle, hip, and neck.[25]
Syndromes
edit


Hypermobility syndrome is generally considered to comprise hypermobility together with other symptoms, such as myalgia and arthralgia.[22] Hypermobility is reported more often in females than males.[26] Hypermobile joints are also relatively common among children, though this is often benign.[27]
Current thinking suggests four causative factors:
- The shape of the ends of the bones — Some joints normally have a large range of movement, such as the shoulder and hip. Both are ball-and-socket joints.[28] The joint ends of bones finish their growth last, so children tend to have more flexible joints than adults; children may "grow out of" hypermobility as their bone ends fully develop.[citation needed] A shallow socket will lead to a relatively large range of movement. If the hip socket is particularly shallow, then the hip may dislocate easily.[28]
- Ligament problems— Ligaments are made of several types of protein fiber, including elastin and collagen. Gymnasts and athletes can voluntarily acquire hypermobility in some joints[28] by stretching healthy ligaments over time. However, weak or abnormally long ligaments can cause unstable hypermobile joints.[citation needed] Protein deficiencies may weaken ligaments. Some hormones may alter the structure of collagen proteins. For example, in late pregnancy, relaxin allows the ligaments of the pelvis to lengthen so the head of the baby can pass.[28]
- Muscle tone—Opposing sets of muscles are attached to bones to move joints in various directions. The tone of muscles—a mild basic level of contraction that protects joints and organs—is controlled by the nervous system. Neuromuscular problems can cause loss of muscle tone, increasing the range of movement possible and removing the muscles' protection of the joint. Lack of exercise also weakens the muscles that support and anchor highly flexible joints such as the shoulder, hip, wrist, and ankle.[citation needed]
- Proprioception—Disorders such as dyspraxia affect the brain's communication with the sensors that detect the motion and position of the body in space.[citation needed] A person with poor proprioception may habitually hyperextend joints during normal activities such as walking and sitting, because they can't internally sense where the joint is.[28] If stress/pain perception is also affected, they may not experience hyperextension as uncomfortable until an injury occurs.[citation needed]
Hypermobility can also be caused by genetic or developmental disorders that reduce the strength of the connective tissue the body can make. Commonly, hypermobility is dismissed by medical professionals as nonsignificant, though it may be a sign of a systemic problem.[29]
Ehlers–Danlos syndrome hypermobility type
editJoint hypermobility is often correlated with hypermobile Ehlers–Danlos syndrome (hEDS, known also by EDS type III or Ehlers–Danlos syndrome hypermobility type (EDS-HT)). Ehlers–Danlos syndrome is a genetic disorder caused by mutations or hereditary genes, but the genetic defect that produces hEDS is largely unknown. In conjunction with joint hypermobility, a common symptom for hEDS is smooth, velvety, and stretchy skin. When diagnosing hEDS, the Beighton Criteria are used, but are not always able to distinguish between joint hypermobility syndrome and hEDS.[30]
Ehlers–Danlos hypermobility type can have severe musculoskeletal effects, including:
- Jaw laxity that may make an individual's jaw open and close like a hinge, as well as open further than the average.
- Neck pain that can lead to chronic headaches and is usually associated with a crackling or grinding sensation (crepitus).
- The spine may end up in a "round back" or inversely may extend too much into hyperlordosis. Individuals may also experience scoliosis.
- Joints commonly associated with hypermobility (wrists, knees, ankles, elbows, shoulders) may be at more severe risk to dislocate or strain.
Diagnosis
editJoint hypermobility syndrome shares symptoms with other conditions such as Marfan syndrome and Ehlers-Danlos Syndrome. Hypermobility syndrome and Hypermobile Ehlers-Danlos syndrome are difficult to diffentiate, and the boundaries between them may be arbitrary.[31] Hypermobility syndrome and hypermobile Ehlers-Danlos syndrome are both likely to have a variety of genetic causes. Generalized hypermobility is a common feature in hereditary connective tissue disorders and many features overlap, but often features are present that enable differentiating these disorders. Ehlers-Danlos Syndrome was defined based on its observable symptoms in the skin and joints.[32]
The inheritance pattern of Ehlers-Danlos syndrome varies by type. The arthrochalasia, classic, hypermobility and vascular forms usually have an autosomal dominant pattern of inheritance. Autosomal dominant inheritance occurs when one copy of a gene in each cell is sufficient to cause a disorder. In some cases, an affected person inherits the mutation from one affected parent. Other cases result from new (sporadic) gene mutations. Such cases can occur in people with no history of the disorder in their family.
It is impossible to tell whether a person has EDS symptoms due to an inherited EDS gene, a spontaneous mutation that causes identical symptoms, or a problem in fetal development causes identical symptoms, without both knowing the genetic family history and performing a specialized genetic test. The results do not matter to clinical treatment of the symptoms.
The dermatosparaxis and kyphoscoliosis types of EDS and some cases of the classic and hypermobility forms, are inherited in an autosomal recessive pattern. In autosomal recessive inheritance, two copies of the gene in each cell are altered. Most often, both parents of an individual with an autosomal recessive disorder are carriers of one copy of the altered gene but do not show signs and symptoms of the disorder.[citation needed]
Beighton criteria
edit
As of July 2000, hypermobility was diagnosed using the Beighton criteria. In 2017, the criteria changed, but still involve the Beighton score.[34] The Beighton criteria do not replace the Beighton score but instead use the previous score in conjunction with other symptoms and criteria. HMS is diagnosed in the presence of either two major criteria, one major and two minor criteria, or four minor criteria.[citation needed] The criteria are:
Major criteria
edit- A Beighton score of 5/9 or more (either current or historic)
- Arthralgia for more than three months in four or more joints
Minor criteria
edit- A Beighton score of 1, 2 or 3/9 (0, 1, 2 or 3 if aged 50+)
- Arthralgia (> 3 months) in one to three joints or back pain (> 3 months), spondylosis, spondylolysis/spondylolisthesis.
- Dislocation/subluxation in more than one joint, or in one joint on more than one occasion.
- Soft tissue rheumatism. > 3 lesions (e.g. epicondylitis, tenosynovitis, bursitis).
- Marfanoid habitus (tall, slim, span/height ratio >1.03, upper: lower segment ratio less than 0.89, arachnodactyly; positive Steinberg finger / Walker wrist signs).
- Abnormal skin: striae, hyperextensibility, thin skin, papyraceous scarring.
Beighton score
editThe Beighton score is an edited version of the Carter/Wilkinson scoring system which was used for many years as an indicator of widespread hyper-mobility. Medical professionals varied in their interpretations of the results; some accepting as low as 1/9 and some 4/9 as a diagnosis of HMS. Therefore, it was incorporated, with clearer guidelines, into the Beighton Criteria.[citation needed] The Beighton score is measured by adding 1 point for each of the following:
- Placing flat hands on the floor with straight legs
- Left knee bending backward
- Right knee bending backward
- Left elbow bending backward
- Right elbow bending backward
- Left thumb touching the forearm
- Right thumb touching the forearm
- Left little finger bending backward past 90 degrees
- Right little finger bending backward past 90 degrees[35]

The Beighton score has been widely used among athletes for screening purposes. It does not appear to be a valid scale when used for this purpose: there exists a statistically significant correlation between the score and the athlete's passive shoulder and hip ranges of motion, but the difference is small enough to be buried by measurement error.[36]
Treatments and management
editExercise
editIt is recommended that hypermobile individuals remain fit, to prevent pain and fatigue.[9] Regular exercise and exercise that is supervised by a physician and physical therapist can reduce symptoms because strong muscles increase dynamic joint stability. Low-impact exercise such as closed kinetic chain exercises are usually recommended as they are less likely to cause injury when compared to high-impact exercise or contact sports.[37]
Strength training can be used to stabilise muscles around hypermobile joints. Hydrotherapy can be a beneficial medium for muscle training.[38] Some isometric exercises can also be beneficial.[39] Coordination may be improved through balance exercises.[38]
High impact sports are not recommended.[9]
Medication
editMedication is used in a similar way as for other chronic pain conditions,[39] and can be used as a treatment for related joint pain.[40] Nonsteroidal anti-inflammatory drugs and acetaminophen are used to treat pain.[39] Opioids are often used, and prescribed for many with hypermobile Ehlers-Danlos syndrome.[41]
Lifestyle modification
editFor some people with hypermobility, lifestyle changes decrease symptom severity. Regular movement is recommended, and support devices can be used. These include shaped keyboards to assist posture, insoles to support flat feet, and wide grip pens. Pillows and cushions can be used to support joints.[42]
Other treatments
editEpidemiology
editHypermobile joints occur in about 10 to 25% of the population, but do not define hypermobility syndromes.[3]
See also
editReferences
edit- ↑ Federman CA, Dumesic DA, Boone WR, Shapiro SS (1990). "Relative efficiency of therapeutic donor insemination using a luteinizing hormone monitor". Fertil Steril. 54 (3): 489–92. doi:10.1016/S0015-0282(16)53767-4. PMID 2204553.
- ↑ Kirk, J. A.; Ansell, B. M.; Bywaters, E. G. (September 1967). "The hypermobility syndrome. Musculoskeletal complaints associated with generalized joint hypermobility". Annals of the Rheumatic Diseases. 26 (5): 419–425. doi:10.1136/ard.26.5.419. ISSN 0003-4967. PMC 1031347. PMID 6039590.
- 1 2 3 Garcia-Campayo, J; Asso, E; Alda, M (February 2011). "Joint hypermobility and anxiety: the state of the art". Current Psychiatry Reports. 13 (1): 18–25. doi:10.1007/s11920-010-0164-0. PMID 20963520. S2CID 24237928.
- ↑ May, Philip A.; Chambers, Christina D.; Kalberg, Wendy O.; Zellner, Jennifer; Feldman, Haruna; Buckley, David; Kopald, David; Hasken, Julie M.; Xu, Ronghui; Honerkamp-Smith, Gordon; Taras, Howard; Manning, Melanie A.; Robinson, Luther K.; Adam, Margaret P.; Abdul-Rahman, Omar (2018-02-06). "Prevalence of Fetal Alcohol Spectrum Disorders in 4 US Communities". JAMA. 319 (5): 474–482. doi:10.1001/jama.2017.21896. ISSN 1538-3598. PMC 5839298. PMID 29411031.
- ↑ Givetash, Linda. "Adults with fetal alcohol syndrome appear prone to health conditions, survey says". Canadian Broadcasting Corporation. Retrieved August 14, 2025.
- 1 2 "Joint hypermobility syndrome". NHS. 2023-08-30. Retrieved 2025-09-15.
- ↑ "Clinician's Guide to JHS". hypermobility.org. Hypermobility Syndromes Association. Archived from the original on 2016-11-15. Retrieved 2016-12-02.
- ↑ Nathan, JA; Davies, K; Swaine, I (2018). "Hypermobility and sports injury". BMJ Open Sport & Exercise Medicine. 4 (1) e000366. doi:10.1136/bmjsem-2018-000366. PMC 6196975. PMID 30364440.
- 1 2 3 Castori, Marco; Morlino, Silvia; Celletti, Claudia; Celli, Mauro; Morrone, Aldo; Colombi, Marina; Camerota, Filippo; Grammatico, Paola (11 July 2012). "Management of pain and fatigue in the joint hypermobility syndrome (a.k.a. Ehlers–Danlos syndrome, hypermobility type): Principles and proposal for a multidisciplinary approach". American Journal of Medical Genetics. 158A (8): 2055–2070. doi:10.1002/ajmg.a.35483. PMID 22786715. Retrieved 26 April 2026.
- ↑ Glans, Martin R; Nils, Thelin (8 February 2022). "The Relationship Between Generalised Joint Hypermobility and Autism Spectrum Disorder in Adults: A Large, Cross-Sectional, Case Control Comparison". Frontiers in Psychiatry. 12 803334. doi:10.3389/fpsyt.2021.803334. PMC 8861852. PMID 35211037.
- ↑ Glans, Martin R; Nils, Thelin (November 2021). "Association between adult attention-deficit hyperactivity disorder and generalised joint hypermobility: A cross-sectional case control comparison". Journal of Psychiatric Research. 143: 334–340. doi:10.1016/j.jpsychires.2021.07.006. PMID 34560594.
- ↑ Piedimonte, Caterina; Penge, Roberta (September 2018). "Exploring relationships between joint hypermobility and neurodevelopment in children (4-13 years) with hereditary connective tissue disorders and developmental coordination disorder". American Journal of Medical Genetics Part B: Neuropsychiatric Genetics. 177 (6): 546–556. doi:10.1002/ajmg.b.32646. PMID 30070022. S2CID 51895371.
- ↑ Araújo, C. G. S.; Chaves, C. P. G. (23 September 2005). "Adult women with mitral valve prolapse are more flexible". British Journal of Sports Medicine. 39 (10): 720–4. doi:10.1136/bjsm.2004.014324. ISSN 0306-3674. PMC 1725042. PMID 16183767.
- 1 2 3 4 Simpson, MR (September 2006). "Benign joint hypermobility syndrome: evaluation, diagnosis, and management". The Journal of the American Osteopathic Association. 106 (9): 531–6. PMID 17079522. Archived from the original on 2013-03-02.
- ↑ Viehweger, Elke; Kläusler, Michèle; Loucheur, Naima (2022-02-01). "Paralytic dislocation of the hip in children". Orthopaedics & Traumatology: Surgery & Research. 2021 Instructional Course Lectures (SoFCOT). 108 (1, Supplement) 103166. doi:10.1016/j.otsr.2021.103166. ISSN 1877-0568. PMID 34871796.
- ↑ Omar, Ramla; Malfait, Fransiska; Van Agtmael, Tom (2021-12-01). "Four decades in the making: Collagen III and mechanisms of vascular Ehlers Danlos Syndrome". Matrix Biology Plus. 12 100090. doi:10.1016/j.mbplus.2021.100090. ISSN 2590-0285. PMC 8609142. PMID 34849481.
- ↑ Kothari, Neel; Shannon, Nora; Erhayiem, Bara; Suri, Mohnish; Yu, Jing; Pagnamenta, Alistair T.; Dixit, Abhijit (2026-03-17). "Refinement of Connective Tissue Disorder Diagnosis From Marfan to Loeys-Dietz Syndrome Type 4—End of a 30-Year Diagnostic Odyssey". American Journal of Medical Genetics Part A ajmg.a.70130. doi:10.1002/ajmg.a.70130. ISSN 1552-4825. PMID 41844566.
- ↑ Langevin, Helene M (7 July 2021). "Fascia Mobility, Proprioception, and Myofascial Pain". Life. Vol. 11, no. 7. p. 668. Bibcode:2021Life...11..668L. doi:10.3390/life11070668. PMC 8304470. PMID 34357040 – via MDPI.
- ↑ He, Yuchen; Li, Zhong; Alexander, Peter G; Ocasio-Nieves, Brian D; Yocum, Lauren; Hang, Lin; Tuan, Rocky S (28 July 2020). "Pathogenesis of Osteoarthritis: Risk Factors, Regulatory Pathways in Chondrocytes, and Experimental Models". Biology. 9 (8): 194. doi:10.3390/biology9080194. PMC 7464998. PMID 32751156.
- ↑ Akhiiarova, Karina; Tyurin, Anton; Khusainova, Rita (6 October 2025). "Molecular Pathogenesis of Joint Hypermobility: The Role of Intergenic Interactions". Medical Sciences. 13 (4): 223. doi:10.3390/medsci13040223. PMC 12550910. PMID 41133505.
- ↑ Gensemer, Cortney; Burks, Randall; Kautz, Steven; Judge, Daniel P.; Lavallee, Mark; Norris, Russell A. (March 2021). "Hypermobile Ehlers-Danlos syndromes: Complex phenotypes, challenging diagnoses, and poorly understood causes". Developmental Dynamics. 250 (3): 318–344. doi:10.1002/dvdy.220. ISSN 1058-8388. PMC 7785693. PMID 32629534.
- 1 2 Akkaya, Kamile Uzun; Burak, Mustafa; Erturan, Sinem; Yildiz, Ramazan; Yildiz, Ayse; Elbasan, Bulent (2022-12-01). "An investigation of body awareness, fatigue, physical fitness, and musculoskeletal problems in young adults with hypermobility spectrum disorder". Musculoskeletal Science and Practice. 62 102642. doi:10.1016/j.msksp.2022.102642. ISSN 2468-7812. PMID 35973358.
- ↑ Meulenbroek, Thijs van; Huijnen, Ivan P. J.; Simons, Laura E.; Conijn, Arnoud E. A.; Engelbert, Raoul H. H.; Verbunt, Jeanine A. (2021-01-01). "Exploring the underlying mechanism of pain-related disability in hypermobile adolescents with chronic musculoskeletal pain". Scandinavian Journal of Pain. 21 (1): 22–31. doi:10.1515/sjpain-2020-0023. ISSN 1877-8879. PMID 32862151.
- ↑ "Fibromyalgia: Possible Causes and Risk Factors". Webmd.com. 2008-05-21. Retrieved 2014-03-06.
- 1 2 3 Pezaro, Sally; Brock, Isabelle; Buckley, Maggie; Callaway, Sarahann; Demirdas, Serwet; Hakim, Alan; Harris, Cheryl; High Gross, Carole; Karanfil, Megan; Le Ray, Isabelle; McGillis, Laura; Nasar, Bonnie; Russo, Melissa; Ryan, Lorna; Blagowidow, Natalie (2024). "Management of childbearing with hypermobile Ehlers-Danlos syndrome and hypermobility spectrum disorders: A scoping review and expert co-creation of evidence-based clinical guidelines". PLOS ONE. 19 (5) e0302401. Bibcode:2024PLoSO..1902401P. doi:10.1371/journal.pone.0302401. ISSN 1932-6203. PMC 11095771. PMID 38748660.
- ↑ Castori, Marco; Camerota, Filippo; Grammatico, Paola; Padua, Luca (3 August 2010). "Ehlers–Danlos syndrome hypermobility type and the excess of affected females: Possible mechanisms and perspectives". American Journal of Medical Genetics. 152A (9): 2406–8. doi:10.1002/ajmg.a.33585. PMID 20684008. Retrieved 25 April 2026.
- ↑ Coles, William; Copeman, Annabel; Davies, Karen (February 2018). "Hypermobility in children". Paediatrics and Child Health. 28 (2): 50–6. doi:10.1016/j.paed.2017.12.001. Retrieved 26 April 2026.
- 1 2 3 4 5 "Joint hypermobility". Arthritis Research UK. Archived from the original on 2009-04-08.
- ↑ Levy, Howard (2004). "The Ehlers Danlos Syndrome, Hypermobility Type." Archived 2013-10-19 at the Wayback Machine University of Washington: NIH. Retrieved from
- ↑ Tinkle, Brad T. (2010). Joint hypermobility handbook: a guide for the issues & management of Ehlers-Danlos syndrome hypermobility type and the hypermobility syndrome. Greens Fork, IN: Left Paw Press. ISBN 978-0-9825771-5-8. OCLC 672037902.
- ↑ Castori, Marco; Tinkle, Brad; Levy, Howard; Grahame, Rodney; Malfait, Fransiska; Hakim, Alan (1 February 2018). "A framework for the classification of joint hypermobility and related conditions". American Journal of Medical Genetics. 175 (1): 148–57. doi:10.1002/ajmg.c.31539. PMID 28145606. Retrieved 26 April 2026.
- ↑ Zweers MC, Kucharekova M, Schalkwijk J (March 2005). "Tenascin-X: a candidate gene for benign joint hypermobility syndrome and hypermobility type Ehlers-Danlos syndrome?" (PDF). Ann. Rheum. Dis. 64 (3): 504–5. doi:10.1136/ard.2004.026559. PMC 1755395. PMID 15708907.
- ↑ File:Hiperlaxitud.jpg
- ↑ Grahame R, Bird HA, Child A (July 2000). "The revised (Brighton 1998) criteria for the diagnosis of benign joint hypermobility syndrome (BJHS)". J Rheumatol. 27 (7): 1777–9. PMID 10914867.
- ↑ "Assessing Joint Hypermobility". ehlers-danlos.com. The Ehlers Danlos Society. Retrieved 29 April 2026.
- ↑ Parks, A; Kazemi, M; Frost, D; Howarth, SJ (December 2023). "Assessing construct validity of the Beighton Score as a measure of generalized joint hypermobility in varsity athletes". The Journal of the Canadian Chiropractic Association. 67 (3): 269–278. PMC 10814702. PMID 38283156.
- ↑ "The Evidence-Based Rationale for Physical Therapy Treatment of Children, Adolescents, and Adults Diagnosed With Joint Hypermobility Syndrome/Hypermobile Ehlers-Danlos Syndrome (for Non-experts)". The Ehlers Danlos Society. Retrieved 2025-08-14.
- 1 2 Palmer, Shea; Bailey, Samuel; Barker, Louise; Barney, Lauren; Elliott, Ami (September 2014). "The effectiveness of therapeutic exercise for joint hypermobility syndrome: a systematic review". Physiotherapy. 100 (3): 220–7. doi:10.1016/j.physio.2013.09.002. PMID 24238699. Retrieved 28 April 2026.
- 1 2 3 4 Carroll, Matthew (July 22, 2023). "Hypermobility spectrum disorders: A review". Rheumatology and Immunology Research. 4 (2): 60–68. doi:10.2478/rir-2023-0010. PMC 10457547. PMID 37637226.
- 1 2 3 Whalen, Kiley; Crone, Wilson (6 September 2022). "Multidisciplinary Approach to Treating Chronic Pain in Patients with Ehlers–Danlos Syndrome: Critically Appraised Topic". Journal of Pain Research. 15: 2893–2904. doi:10.2147/JPR.S377790. PMC 9482467. PMID 36124037.
- ↑ Schubart, Jane; Schilling, Amber; Schaefer, Eric; Bascom, Rebecca; Francomano, Clair (9 January 2019). "Use of prescription opioid and other drugs among a cohort of persons with Ehlers–Danlos syndrome: A retrospective study". American Journal of Medical Genetics. 179 (3): 397–403. doi:10.1002/ajmg.a.61031. PMID 30624009. Retrieved 28 April 2026.
- 1 2 "Pain Management". hmsa.org. Hypermobility Syndromes Association. Retrieved 28 April 2026.
External links
edit- Eccles, Jessica A.; Cadar, Dorina; Quadt, Lisa; Hakim, Alan J.; Gall, Nicholas; Bowyer, Vicky; Cheetham, Nathan; Steves, Claire J.; Critchley, Hugo D.; Davies, Kevin A. (2024). "Is joint hypermobility linked to self-reported non-recovery from COVID-19? Case–control evidence from the British COVID Symptom Study Biobank". BMJ Public Health. 2 (1) e000478. doi:10.1136/bmjph-2023-000478. PMC 11812800. PMID 40018183.