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Magarey’s work indicates that it may be possible to identify ‘mas- sive tears’ through the perseverance of a ‘tricking’ manoeuvre on attempted elevation despite attempts at movement re-education combined with a severe weakness of medial or, more often, lateral rotation. Tricking is an excessive elevation of the scapular on attempted elevation of the shoulder - the scapular shrugs up as the arm is lifted. It is traditionally thought to indicate a supraspinatus tear but recent work indicates that it may indicate a tear involving infraspinatus.

To reiterate, we may be able to identify ‘massive tears’ but any attempts at differentiation to locate the site of the lesion or to dif- ferentiate between more minor tears and tendonitis are unlikely to be consistently accurate. As we shall see, this is good news.

The mechanism of rotator cuff injury Our apparent inability to identify either the site or, indeed, the nature of the lesion except in exceptional circumstances should per- haps persuade us that treatment interventions that attempt to specifically target the presumed source of symptoms are likely to be inaccurately applied. It may therefore be more appropriate to inves- tigate the mechanism by which the injury or damage occurred so that intervention can be structured around correction of these causal factors. This is obviously a complex task as glenohumeral function is intimately reliant upon the function of the scapular, trunk, spine, pelvis and lower limbs.

Three theories exist as to the mechanism of rotator cuff injury. They are: ● primary degeneration ● primary impingement ● secondary impingement

Primary tendon degeneration Primary degeneration is an in-substance tendon injury, theoretically due to tensile overstrain in an area of relative avascularity, the so-called critical zone. More recent vascular studies have thrown doubt on the critical zone concept. Symptomatic rotator cuff pathology gen- erally occurs in the more superficial layers of the cuff, the ’bursal’ surface. This area appears to have an intact vascular supply. There is some diminution of blood supply in the deeper, or ‘articular’ sur- face of the cuff, but pathology in this area is not usually sympto- matic and may be a natural occurrence of aging. So in the patho- genesis of most symptomatic cuff pathology, vascularity is not an issue. It appears that primary tendon degeneration as a cause of rotator cuff injury is exclusive to a particular population - young overhead-action athletes, as a result of massive loads and overuse. The rest have a component of impingement.

Impingement Impingement is a compressive injury, the rotator cuff being caught between the two unforgiving surfaces of the top of the humerus and the underside of the coraco-acromial arch. To effectively tailor treatment a distinction must be made between primary and sec- ondary impingement.

Primary impingement is an anatomical narrowing of the subacromi- al or subcoracoid space whereas secondary impingement is impinge-

ment secondary to some external influence that causes a function- al narrowing of the space. A primary impingement can relate to, for example, a hooked shape to the end of the underside of the acromion whereas a secondary impingement can relate to impover- ished control of the humeral head leading to excessive upward trav- el during movement. Hence a primary impingement often requires surgical intervention, in this case to decompress the subacromial space, whereas the patient with secondary impingement requires re- education of movement control. It would obviously be beneficial to be able to differentiate between these presentations. Unfortunately it is not straightforward and there is overlap.

Identifying the mechanism of injury Differentiating between tensile lesions of the rotator cuff (primary degeneration) and compressive lesions (impingement) is, however, relatively straightforward.

The procedure is to investigate the effect of manually decompress- ing the subacromial and/or subcoracoid space on the pain provoked by a painful resisted movement. If the pain reproduced by the resisted movement decreases or the power increases when the head of humerus is manually distracted the disorder has an element of impingement. If the pain and/or weakness remain constant despite the applied distraction, it is an in-substance tendon injury. This is called the Trott/Maitland test, among other things (see Fig.2). The effect of the distraction is to take the humeral head away from the lesion in impingement so that it no longer hurts and consequently the muscles work better.

Figure 2: The Trott/Maitland test

The differentiation is clinically relevant because in-substance tendon injuries will tend to improve faster. Intervention aims to reduce the underlying overuse that is irritating the tendon. This may involve a reduction in activity and pos- sibly a correction of faults in the biomechanics of the patient’s sporting activity.

Intriguingly, the so-called impingement tests do not identify impingement, in that they do not help differentiate compressive from tensile lesions of the rotator cuff. They aim to compress the subacromial and/or subcoracoid space and therefore they elicit pain in irritated tissues held within the space, irrespective of the mech- anism of injury of those tissues. Impingement tests help identify disorders of the subacromial space but do not indicate the nature of those disorders.

Unfortunately there is no clinical test to differentiate between pri- mary impingement and secondary impingement. Secondary impingement is due to poor control so can relate to glenohumeral instability, scapular instability, postural manifestations and inade- quacies of trunk, pelvic and lower limb control.

The differentiation between primary and secondary impingement is done retrospectively based on the effect on intervention.

A full

biomechanical assessment is performed and aberrations of move- ment control identified. If the symptoms ease when these aberra- tions of control are corrected it can be concluded that the impinge- ment was secondary to those factors. If the correction of faulty bio-

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