SHOULDER INSTABILITY

injury. There is increasing evidence that pain and pathology compromise the feed- forward processes influencing joint stiff- ness and the preparatory mechanisms enhancing joint stability (7). Furthermore there is evidence to show that the global stabilisers often become inappropriately facilitated in the presence of pain (8).

Earlier classification systems describing ‘voluntary’ or habitual instability resulted in many patients being labelled as having secondary gain issues and psychological problems preventing rehabilitation (9). The reality is that a lot of these patients will exhibit distress but this often results from their medical experience. In the polar type III group they often demon- strate bizarre movement patterns which are greeted with a shocked facial expres- sions and ‘I’ve never seen that before’, which unsurprisingly does not instil confi- dence! They are then often referred for physiotherapy which commonly emphasises strengthening which then fails because the resisted work merely reinforces the abnormal sequencing. It is essential not to write someone off as a voluntary dislo- cator. There are those patients who report doing a party trick for many years where they could actively dislocate the joint with a deliberate ‘trick movement’. However in some patients this abnormal muscle activation can become established as an involuntary movement pattern resulting in persisting muscle patterning instability.

Malone (3) reported that in a series of of patients with muscle patterning instability there were common patterns of inappropri- ate activation. In patients with anterior instability 58% of patients demonstrated a primary problem with pectoralis major. In posterior instability 74% of patients exhibited inappropriate activation of latis- simus dorsi or anterior deltoid.

Unfortunately patients do not always fit neatly into the polar groups. Bayley’s original series (10) reported that only a third of patients fitted into the polar groups. However in more recent reports it appears that up to two thirds of patients will fit into the polar groups (3). In con- sidering the sporting population there are specific subgroups we must identify. If we consider that patients can move around the triangle with time it is easy to appre- ciate how a first time dislocator who has

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a surgical repair can develop a patterning component in the presence of abnormal sequencing (type I/III). Similarly patients can develop the abnormal patterning after the initial dislocation which makes them unsuitable for surgery until this is addressed. This is a scenario we have identified in elite rugby players. Similarly in the patient with an acquired capsular laxity as a result of overhead throwing, repetitive microtrauma can also develop abnormal muscle patterning (Type II/III). Those patients with a deficient capsule as a result of connective tissue disorders or generalised hypermobility similarly can demonstrate a patterning component and the patterning can be the primary prob- lem. So why does this scenario develop?

WHAT CAUSES MUSCLE PATTERNING? The short answer to this is that we don’t really know. However, in the process of evaluating both our clinical experience and the available literature there appear to be significant factors that help guide appropriate rehabilitation. It is widely reported that patients with instability, whether traumatic or atraumatic, will demonstrate compromised proprioception. In type I and II instability, this appears to result from loss of the structural integrity of the capsular-labral structures whether by structural compromise ie. Bankart lesion or laxity/plastic deforma- tion (Fig.3).

Our increasing knowledge of the reflex loops that exist between the capsular-lig- amentous structures and the rotator cuff and other glenohumeral musculature, illustrate how cuff facilitation may be

Injury to articular ligaments/labrum Disruption to mechanoreceptors

Partial deafferentation of the glenohumeral joint

Inhibition of normal neuromuscular/ joint stabilisation/feedback loops to rotator cuff

Altered muscle sequencing Increase in instability

Figure 3: Possible process leading from injury to altered muscle sequencing and increased instability

compromised by insufficiency of these structures due to the loss of normal feed- forward and feedback mechanisms. It is conceivable to hypothesise that this abnormal sequencing is then compensated by the more superficial musculature.

Proprioceptive information transmitted from mechanoreceptors in the capsulo- ligamentous structures influence co- ordinated motor patterns, reflex activity and joint stiffness to provide enhanced joint stability (11). Sainburg demonstrat- ed that patients with proprioceptive deficits demonstrate loss of interjoint coordination (12). If we look at patients with type III instability (and the associat- ed subgroups) their ability to follow a target with their finger eg. a maze on a board, is often compromised. They com- monly have difficulty in following the line and controlling an efficient path of motion. This is consistent with the find- ings of Barden who showed that patients with atraumatic instability demonstrate a reduced ability to use proprioception to refine and control motor output of the upper limb (13).

The spinal stretch reflex has been used to evaluate elements of dynamic joint stabili- ty and function (14). It is the simplest and fastest stimulus-response paradigm in the vertebrate nervous system. It is an innate spinal segmental pathway and in the nor- mal subject evolves from a hyperexciteable and prominent state during infancy to a less prominent and quiescent state in adulthood. Patients with atraumatic insta- bility demonstrate a prominent reflex response which indicates decreased supraspinal reflex control processes. In contrast, the asymptomatic athletic popu- lation demonstrate a quiescent reflex response indicating enhanced reflex control mechanisms. This indicates an alteration in central processing as a result of developmental factors. Barret et al (15) used transcranial electromagnetic stimula- tion to investigate the corticospinal tract in patients with instability. Their early results suggest that patients with type III instability have altered corticospinal control with respect to the threshold for inhibition of voluntary contraction on the affected side. This was not demonstrated in a patient with traumatic Type I instability. This may indicate that the patient loses the ability at a cortical level to switch the muscles on and off.

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