Articular surfaces

Changes in the articular surfaces may restrict the movement of the joint. Deterioration of cartilage and formation of osteophytes on the joint surface in osteoarthritis limits ROM.

Loose body

A loose body within the joint can block the movement of the articular surfaces; the degree of limitation may vary as the loose body moves within the joint.

Bone

Fracture of a bone is likely to limit movement due to the altered mechanics of the fractured bone providing an unstable surface and disrupting the muscle action.

Ligaments

Damage to the joint ligaments can disrupt movement by failing to limit movement, hence producing an abnormal increase in ROM. They may also limit the movement through the loss of the ability to direct the movement of the articular surfaces.

Imposed restriction of movement

Immobility may be due to an imposed restriction at a specific joint or joints secondary to injury or surgery. For example a period in plaster following a fracture, or deliberate restriction of movement following skin grafting.

Muscle

Immobility may also be due to the inability of the patient to access full ROM actively due to muscle weakness. This may be due to specific muscle weakness following local injury. Muscle weakness may also be the result of general deconditioning, as seen in some long-term intensive-care patients.

Tear or rupture of a muscle will disrupt the muscle filaments and the ability of the muscle to contract.

Neurological disorders

Absence of or change in neural control, due to upper or lower motor neurone disorders or brain injury or pathology, may cause a muscle to become denervated or have altered muscle innervation and therefore restrict the ROM available actively. An example of this is the loss of range of dorsiflexion secondary to foot drop.

Imbalance of muscle activity secondary to neurological disorders, such as that seen in spasticity, may also limit the ability to move through range resulting in the loss of range.

Decreased functional range

Immobility may also be due to a person not using the full normal ROM during their daily activities and therefore losing the extremes of movement; for example an older person who may spend a lot of time sitting and walks with a stooped posture is likely to lose some range of hip extension.

Articular structures

After prolonged immobilization, 32 weeks, the articular structures become the main limiting factor to movement (Trudel 2000). The mechanism of intra-articular limitation is not clear, although the proliferation of intra-articular connective tissue, increase in collagen cross-linking and adaptive shortening of the capsule have all been suggested (Trudel 2000).

Muscle

The lack of longitudinal force through a muscle during immobilization leads to tissue remodelling to accommodate the new shortened resting length. Muscles immobilized in a shortened position over a period of time demonstrate a reduction in sarcomeres (Goldspink et al 1974), and an increase in the proportion of connective tissue which results in a decrease in joint ROM and compliance of the muscle (Williams 1988). These changes in sarcomeres can be seen as early as 24 hours after immobilization (McLachlan 1983). There is evidence from animal studies demonstrating that after a period of 2 weeks of immobilization the main factor limiting movement is muscle shortening.

Collagen

After a period of immobilization there is a change to the organization of the collagen within the muscle, leading to an increase in the number of perpendicularly orientated collagen fibres, which connect two adjacent muscle fibres (Jarvinen et al 2002). Chains of collagen molecules contain cross-links which weld them into a strong unit. It has been suggested that during immobilization there is a change in chemical structure and loss of water within the collagen which leads to the fibres coming into close contact with one another. This close contact is thought to lead to the formation of abnormal crossbridges, leading to an increase in tissue stiffness (Alter 2004).