Shoulder Treatment – Rehabilitation versus Surgery

European Musculoskeletal Review, 2008;3(2):72-74

In shoulder treatment, as in medicine in general, accurate diagnosis is essential in order to increase the chances of a successful clinical outcome. It is important to think of the shoulder as a joint whose function depends on a complex kinetic chain composed of other joints that must be co-ordinated by the neuromuscular system. In this way it is clear that dysfunction of a ‘proximal’ (or distal) ring can have a negative impact on the workings of the shoulder as a whole,1 resulting in symptoms of a clinical (pain or restricted movement) or anatomical/ pathological nature (subacromial bursitis, cuff tears, disinsertion of the labrum, osteochondral defects and so on).2–4

A careful review of the most reliable specialist literature shows that new aetiopathogenetic explanations of frequent lesions of the rotator cuff have evolved in recent years. Pioneering work by Bigliani and Morrison5 named reduction of the subacromial space due to a hooked acromion as the most frequent cause of inflammation/degeneration of the subacromial bursa and tendinous tissue. Other authors have pointed to the tendinous structures of the rotator cuff of the locus minoris resistentie, represented by hypovascularised areas subject to particular strain, especially on the articular side.6,7 Our clinical and surgical experience, backed up by the growing body of orthopaedic, psychiatric, neurophysiological and biomechanical literature, suggests more dynamic aetiopathogenetic theories highly suited to what might be considered the most mobile joint in the human body.

We have noticed how many authors place great emphasis on diagnostic tests or diagnostic investigations (Jobe, Yocum, Impingement test/sign, etc.), which, when properly executed, can reveal latent clinical conditions caused by tears or inflammation that permit diagnosis. A functional examination of the joint must include an accurate and systematic assessment of both active and (especially) passive joint motion. Passive function must be assessed on various levels, in particular in abduction and adduction with internal and external shoulder rotation. Any reduction of range of motion (ROM) due to capsular contraction must be given serious consideration since this can significantly alter the specificity and sensitivity and therefore the result of the above tests.

An elegant study by Uhthoff and Boileau8 describes cases of global capsular contraction (easy to diagnose) and cases localised to just some areas of the glenohumeral capsule. These are very tricky to identify in that the symptoms and positive clinical tests perfectly match the better known ‘subacromial impingement syndrome’. However, rehabilitative and surgical treatment of impingement is based on quite different assumptions from that of capsulitis. The physician must therefore be instructed and trained to identify and discriminate between these two pathologies that have the same symptoms but require different treatment. 9

An example may make this clearer. In a ‘localised’ capsular contraction of the postero-inferior region, elevation of the arm produces a ‘yo-yo’ effect,10,11 i.e. antero-superior motion of the humeral head. This establishes dynamic contact with the coracoacromial joint, causing inflammation of the bursa and the tendons (long head of the biceps, rotator cuff, etc.). Thus, bursitis and tendinitis are the end of a chain of effects triggered by the posterior capsular contraction, requiring targeted rehabilitative treatment designed to stretch the posterior capsule. In patients suffering from capsulitis, the ideal surgical treatment for subacromial impingement – acromionplasty – is at best useless and at worst counterproductive.12–15 We must stress that in cases of frozen shoulder specific and well executed tests are essential, such as a true antero-posterior X-ray view that is able to discriminate between the onset of capsular damage and symptoms of arthrosis/degeneration, which require a quite different response. An interesting area of investigation, both now and in the future, will be to try to understand the intrinsic (or apparently intrinsic) causes of primary capsular contractions, which are today generically attributed to genetic, immunological and metabolic factors or to mechanical adaptation. 16

Lesions may occur not only as a result of capsular inflammation or contracture, but also due to disturbances in the kinetic chain. This is a highly complex mechanism in which force is generated and transmitted in a proximal–distal direction. It is extremely important in professional athletes, for example those taking part in throwing events; it is less important, but not negligible, in everyday patients, in whom articulation of the shoulder must be seen as formed not only by the humerus and the scapula, but also by the sliding of the scapula on the chest. Thus, good shoulder function depends not only on the rotator cuff but also on scapulothoracic stability, whose effectiveness in turn depends on lumbar–pelvic stability. Fluid and functional shoulder movement therefore depends on the synchrony of the kinetic chain. 17,18

Happee and Van der Helm19 have clearly shown how the thoracoscapular muscles deliver around 40% of the energy required for acceleration of the arm during anteflexion and how, if the scapula is used incorrectly, the metabolic cost of the cuff is increased by 13%. In a dyskinetic shoulder, if the sporting task (e.g. throwing) or functional scope remains the same, the organism tends to compensate (catch up) for a limited period through arthro-kinematic (humerus out of the safe zone) or biofunctional mechanisms (cuff overload). In time, unless a proper balance is restored, this overload may produce symptoms caused by anatomical changes that develop slowly depending on the type of activity, the ‘quality’ of movement and the genetic profile, which influences both the characteristics of the tissues and the morphotype of the patient. 20 The kinetic chain is co-ordinated by the sensorimotor system, which is defined as all of the sensory, motor and central integration and processing components involved in maintaining joint stability and co-ordination. It consists of the visual system, the vestibular system and the somatosensory (in particular proprioceptive) system. 21–23 The proprioceptive mechanism is defined as the afferent information arising from peripheral areas of the body (including receptors in the static and dynamic restraints), and contributes to joint stability, posture control and motor control. 24–26