REHABILITATION

elevation (1), and modalities (eg. ice, elec- trotherapy etc.) (1,3,6). Some clinicians also recommend the use of ‘gentle’ joint mobilisation (eg. grade II) to assist ‘clear- ance’ of effusion fluid (29), presumably by means of fluid ‘agitation’ and venous lym- phatic drainage. This is not an unreasonable recommendation since passive movement certainly causes changes in intra-articular pressure, movement of intra-articular fluid, and changes in synovial fluid volume (30).

PROTECT HEALING TISSUE Any injury results in the affected tissue’s ability to tolerate both tensile, compres- sive, and shear forces. The extent of this loss is directly related to the severity of injury and the magnitude of tissue dam- age (1). Early in the healing process (eg. 0-21 days), excessive tissue forces can re- rupture healing blood vessels and disrupt fibrin matrices resulting in re-injury of the damaged tissues (1,12). Consequently injured tissues must be protected to min- imise patient discomfort and regression of rehabilitation. Protection of injured tissue can be achieved using crutches, compres- sion bandage, taping, bracing, splinting, casting etc. (1). Protection of injured tis- sues is also achieved by a judicious pro- gression of passive and active rehabilita- tion techniques as a result of implement- ing evaluation-based progression-criteria (10). In other words, the duration of pro- tection techniques is dictated not only by the severity of injury, but also by the time-line of pain resolution as demon- strated by patient tolerance of rehabilita- tion techniques (1).

RESTORE JOINT MOBILITY There are two reasons why restoration of joint mobility is critical for effective rehabilitation. 1) From a biomechanical perspective ‘nor- mal’ human movement cannot exist without adequate physiological joint movement and intact accessory joint movement (18,23). 2) From a neurophysiological perspective, since the capsuloligamentous tissue of syn- ovial joints is densely innervated with mechanoreceptor nerve endings (31) which polysynaptically project to the cell body of the muscle spindle’s motorneurone in the spinal cord (32) as well as the somatosenso- ry cortex (33), normal joint mobility is criti- cal for normal afferent feedback to the CNS.

Therefore, joint mobilisation is able not only to restore actual joint mobility (23,24), but also to normalise and enhance sensorimotor function of the patient (17,34).

RESTORE NERVE MOBILITY Since an injury rarely results in damage to a single tissue, nerve mobility is often reduced as a consequence of fibrosis of the injured epineurium (9,15,35), fibrosis of the adjacent injured musculoskeletal tis- sues (9,15,35,36), or both. All of these result in nerve entrapment (15,35,36). Since muscle overactivity (37) and repeti- tive muscle injury (38) are associated with reduced nerve mobility, restoration of nerve mobility using the appropriate neur- al mobilisation techniques (15) appears essential for normalising sensorimotor function via decreased muscle overactivity, as well as reducing the risk of repetitive

TABLE 2. CLINICAL IMPLICATIONS OF INJURY REHABILITATION

■ Safe and effective rehabilitation is dependent on appropriate clinical reasoning ■ Multiple physiological and behavioural factors affect the duration of rehabilitation ■ Injury rarely results in damage to a single structure or tissue-type ■ Pain results in significant patient discomfort, impaired proprioception, muscle inhi- bition, and guarded movements

■ Effusion results in significantly impaired proprioception and muscle inhibition ■ Healing tissue is fragile and easily re-injured ■ Reduced joint mobility results in abnormal normal human movement due to decreased range-of-motion and impaired afferent feedback to the CNS

■ Reduced nerve mobility results in perineural muscle overactivity and an increased risk of injury to perineural muscles

■ Isolated muscle weakness is a common clinical complication following injury ■ CKC muscle strength tests demonstrate a stronger relationship to lower limb function than OKC muscle strength tests

■ Proprioceptive acuity is greater in a CKC versus an OKC ■ Optimal sensorimotor control is important for normal human movement and functional joint stability

8 injury to overactive perineural muscles.

RESTORE ISOLATED MUSCLE STRENGTH Reduced muscle strength (ie. muscle weak- ness) is a common complication following neuromusculoskeletal injury (3,5,6,39), which is typically due to muscle inhibition and/or disuse atrophy (3,5,28,39). Isolated muscle weakness is a major clinical problem because it results in: ■ increased local joint reaction forces in the joint for which the weak muscle is the agonist (40) ■ decreased whole limb force absorption (41) ■ decreased whole limb stability (42). All of these increase the risk of both re- injury and the onset of degenerative joint disease (ie. osteoarthritis). For example, fol- lowing knee injury, isolated quadriceps weakness results in increased knee joint reaction forces (40) and a decreased ability to maintain hip-knee-ankle alignment (42) during single leg stance. Since multi-joint exercise (eg. squat, step-up etc.) results in compensation by proximal and/or distal muscle groups adjacent to the ‘weak’ muscle group (43), CKC is ineffective at restoring isolated muscle strength following neuro- musculoskeletal injury (43). Consequently, single-joint (ie. open kinetic chain (OKC)) strength training is always indicated in the presence of isolated muscle weakness. Once isolated muscle strength has been restored to ≥ 80% of ‘normal’, multi-joint (ie. CKC) exercise may be commenced (10,42,44).

RESTORE FUNCTIONAL MUSCLE STRENGTH Functional muscle strength refers to whole limb force expression during multi-joint, multi-muscle group movements specific to a person’s unique activity or purpose. For example with regard to the lower limb, since force production predominantly occurs in a CKC (13), functional muscle strength of the lower limb is expressed dur- ing the concentric phase of CKC activities such as sit-to-stand, stair ascent and jump- ing. Consequently, it is not surprising that CKC muscle performance tests (eg. leg press 1RM) demonstrate a stronger relationship to lower limb function defined by hopping, jumping, and running than OKC muscle per- formance tests (eg. knee extension 1RM) (10). This is attributed to neurophysiologi- cal mechanisms and the preferential recruit- ment of ‘task-specific’ motor units (45). Therefore, with regard to optimising whole

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