Hypermobility Part 1

For many, hypermobility does not cause a problem and can even be seen as an asset. For others, their hypermobility brings with it numerous, widespread and longstanding musculo-skeletal symptoms, which may have been mismanaged in the past.

A large percentage of physical therapists deal with restricted movement, and when faced with a patient who has good range of movement, there is a danger that it can lead to their condition being misunderstood; which is essentially excessive range of movement within the context of disordered connective tissue. Because of the ubiquitous nature of connective tissue proteins, the possible consequences of tissue trauma are legion. Every patient will need a treatment plan tailored to their particular set of problems.

Few people recognise hypermobility as a pain syndrome. There is no range to improve on and easy to make symptoms worse with incorrectly prescribed stretching and exercise. Generally, there exists a greater prevalence of Hypermobility Syndrome in females, Asian populations, then Africans and least in Europeans. Joint laxity is usually greatest at birth, decreasing during childhood and continues to decrease during adolescence and adult life. Ligament laxity is determined by the individual’s genetic makeup and hormones, and the genes that encode collagen, elastin and fibrillin are important in influencing joint flexibility. Other factors that impact range of motion include shape of joint surfaces, muscle length and mobility of neural structure.


Likely mechanisms involved in the development of pain symptoms;

-lack of muscular control in the hypermobile joint range / transferring loads ineffectively and causing subsequent microtrauma to tissues. Decreased muscle tone and tensile strength which decreases the overall efficiency in the active support system (Panjabi 1992).

– less restraint and control offered by inherently weaker ligaments, capsules and fascia leading to a deficiency in the passive support system.

-Deficient proprioception may lead to problems in the neural feedback and feedforward system, leading to abnormal motor control. Individuals with Hypermobility Syndrome have altered proprioception, kinaesthesia, or sense of their body position in space. Therefore, not only is there less support for any given movement offered by the muscles, ligaments, fascia and tendons, there is a reduced ability to sense what is good posture and correct positioning or exercise technique.

Bergmark (1989) proposed there are 2 muscle systems involved in the maintenance of spinal stability;

  • Local Muscle System : smaller, deep muscles which attach to the lumbar vertebrae and provide segmental stability and control rather than movement.
  • Global Muscle System : large, superficial muscles which directly produce spinal movement without attaching directly to the spine.

There tends to be a cycle of overactivity/underactivity involved with the pain, therefore the individual needs pacing.

A common test to identify the possibility of Hypermobility, (although with some limitations in that not all joints are included) is the 9 point Beighton Hypermobility score;

– (2pt) passively dorsiflex 5th metacarpal joint greater or equal to 90deg

– (2pt) passively flex thumb to wrist

– (2pt) passively hyperextend elbow greater or equal to 10deg

– (2pt) passively hyperextend knee greater or equal 10deg

hypermobility 9pointhypermobility sydneystrengthconditioning


Photographs of real hypermobilty cases can be seen below.Hypermobility-sydneystrengthconditioning-beightonhypermobilityscore-min

Additional questions to aid recognition of Hypermobility Syndrome:

  • Did they have pain as a child / growing pains?
  • Did they participate in Gymnastics or Ballet in their youth?
  • Did they feel better or worse in pregnancy? It is common to report a considerable change in their wellbeing during pregnancy (seems that pregnancy was the start of their problems) with more relaxin being produced the joints become more mobile.
  • Have they had any dislocations or subluxations or fractures?
  • How have they responded to analgesia (usually little effect)?
  • Do they dislike sustained postures such as sitting and standing?
  • Do they dislike too much activity?
  • Do they bruise easily?
  • Do they have stretchy skin?
  • Do they have any hernia, varicose veins or prolapses (connective tissue is involved systemically)?
  • Do they have any neuropathies?
  • Do they have Raynaud’s phenomenon?

The individual will often;

  • Fidget with hands
  • Have skin that is thinner, stretchier or subject to striae which are not due to large weight changes
  • Have a sway back or kyphosis-lordosis
  • Hyperextend knees*
  • Hyperextend hips (sway back – weak hip flexors, weak glutes)*
  • *attempt to gain more stability end-range
  • End-range for passive range of motion testing has a soggy, empty, saggy feel. When resistance is encountered it is often hard and springy, suggesting muscle spasm rather than restriction due to a tight or fibrosed tissue.
  • Not all joints are mobile. Eg thoracic and cervicothoracic junction tend to stiffen. These areas have the potential to increase stress on mid cervical and lumbar spine.
  • Have increased healing time

It is probable that individuals with average flexibility have better protection from injury by their normal tissues (except those who require greater range of motion for their specific sport, eg. Kickboxing), and those who have developed a hypermobile range can enhance joint stability through good muscle strength and control.

Management of Hypermobilty Syndrome include various modalities – general advice, reassurance, passive mobilisations, exercise to improve posture, muscle balance and endurance, joint stabilisation, proprioception and joint awareness, rehabilitation, lifestyle modifications and chronic pain management are the mainstay of treatment. Good muscle tone, particularly the deep postural muscles, help protect against injury and improve joint stability.

In ‘Hypermobility’ Part Two, we’ll look at training foundations and progressions.


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