Glasgow - Scotland


The terms "laxity" and "instability" as applied to the shoulder are often the cause of confusion. I prefer to refer to such shoulders as being "loose" and to consider the issues of laxity and instability separately. As will be seen instability often has a subtle presentation and its diagnosis can present a challenge to the clinical acumen of the Orthopaedic Surgeon.

In this article I would like to consider:

  • Shoulder laxity
  • The factors influencing shoulder stability
  • Pathology
  • Clinical assessment
  • l'évaluation clinique
  • Management


The term SHOULDER LAXITY refers to the physiological motion of the glenohumeral joint that allows a normal range of motion. It is asymptomatic. A shoulder is usually referred to as being lax when the range of external rotation with the arm by the side exceeds 80 degrees and a sulcus sign (vide infra) can be demonstrated.

Shoulder laxity may be part of generalised ligamentous laxity, typically characterised by Beighton's five signs of hyperflexibility of the wrist (Fig 1), hyperextensibility of the MCP joint of the middle finger, hyperextension of the elbows, hyperextension of the knees and the ability to bend forward and place the hands flat on the floor without bending the knees. In most patients there is a genetic element to this which, in its most extreme form, is represented by the Ehlers-Danlos syndrome.

Figure 1. Hyperflexion of the wrist in a patient with generalised ligamentous laxity.

Beighton (1973) found that females were more mobile than males at any age. However, Emery and Mullaji (1991) found no difference between men and women in terms of laxity of the shoulders.

Biochemical abnormalities have been suggested as a cause of laxity. Tsutsui (1991) found no difference in the collagen types or their quantities in the shoulder but did find a significant reduction in the cross linkages that were present. Bell and Hawkins (1991) found a significant increase in the rate of collagen formation in the shoulder capsule in these patients.

More than half of all patients who demonstrate laxity of the shoulder have no evidence of generalised laxity. It has been suggested that laxity of the shoulder can occur as a result of functional adaptation and Bigliani (1997) has found that baseball pitchers have more external rotation at 90 degrees abduction and more internal rotation than position players. Similarly Zekek and McGee (1996) have shown that elite swimmers have a greater degree of glenohumeral laxity than recreational swimmers. However, these findings may not reflect an adaptation to function. They may be the consequence of individuals with laxity being better suited to being, for example, baseball pitchers or elite swimmers. The fact that laxity is almost always demonstrable in both shoulders further emphasises this point.



Shoulder INSTABILITY is defined as the abnormal symptomatic motion of the glenohumeral joint which results in pain, subluxation or dislocation.

My own concept of shoulder instability is that there is a loss of control of the position of the humeral head relative to the glenoid during dynamic functional activities. Instability is therefore the consequence of the loss or failure of those factors which contribute to controlling the position of the humeral head.



The stabilisers of the glenohumeral joint can be considered as being STATIC or DYNAMIC. Static stabilisers function at the extremes of the range of motion where as Dynamic stabilisers function throughout the range of motion.

· The capsule and ligaments
· The shape of the humeral head

The glenohumeral ligaments have been well described by a number of authors. The advent of arthroscopic shoulder surgery resulted in a better understanding of their structure and function. (Fig 2).

Figure 2. Glenohumeral ligaments

The tendency to anterior translation of the humeral head is resisted by the anterior band of the inferior glenohumeral ligament when the arm is in abduction and external rotation. With lesser degrees of abduction the middle glenohumeral ligament and the bulk of the subscapularis tendon and muscle provide the resistance.

In cadaveric studies even the complete division of the posterior capsule will not allow posterior dislocation. This will only occur if there is loss of the anterosuperior capsule. This area of the capsule is referred to as the rotator interval and contains the tendon of the long head of biceps as well as the coracohumeral ligament. Its inferior border is formed by the superior glenohumeral ligament and the upper border of subscapularis.

This same area is responsible for resisting the tendency of the humeral head to displace inferiorly. Considerable variation in the size and extent of the rotator interval has been described. Individuals with lax glenohumeral joints will have a large interval. Traumatic conditions of the interval predisposing to instability have also been reported.

The shape of the humeral head together with the capsulolabral structure and the associated intra-articular subatmospheric pressure combine to stabilise the glenohumeral joint, especially when the limb is relaxed by the side. The cavity compression effect produced by the rotator cuff muscles (vide infra) enhances this effect.

The DYNAMIC STABILISERS involve muscle action around the shoulder girdle and proprioception.

The trunk and upper limb can be considered as an open kinetic chain with the trunk, scapula and humerus linked and entirely dependent upon muscle action for stability and control.

The scapulae provide proximal stability for the upper limb and enable quality distal segment mobility. The scapula's only firm attachment to the axial skeleton is via the ligaments of the acromioclavicular joint otherwise it is entirely attached by muscles and is therefore extremely vulnerable to conditions which result in the impairment of any of these muscles.

The motion of the scapula on the chest wall is such that it provides support for the humerus (Figure 3) and maintains the length-tension relationship of the scapulohumeral muscles

Figure 3. Motion of the scapula during abduction of the arm

The muscles of the rotator cuff provide both static and dynamic control of the humeral head. Supraspinatus resists superior and inferior translation of the humeral head and subscapularis resists anteroinferior translation (vide supra).

During motion deltoid and the rotator cuff muscles are active throughout. Infraspinatus, subscapularis and teres minor produce an inferior shear force to counteract the deltoid action. Supraspinatus generates a compressive force across the glenohumeral joint. The force couple resulting from these actions maintains the humeral head centred on the glenoid to within 1mm throughout the range of motion.

The tendons of the rotator cuff muscle blend with the glenohumeral capsule and it is felt that they can adjust its tension. This is referred to as DYNAMIC LIGAMENT TENSION. However, if the capsule is extremely lax it can be seen that dynamic ligament tension may have very little effect upon the control of the humeral head.

Proprioceptors have been found in the capsule of the glenohumeral joint as in other major joints. It is felt that they may have a role in modulating the cuff forces as part of the mechanism of dynamic ligament tension. Abnormalities of proprioception have been demonstrated in patients with recurrent anteroinferior dislocation but, to date, no abnormalities have been demonstrated in the lax shoulder.

Overhead repetitive activities require synchronising of the musculotendinous units around the shoulder in combination with the capsulolabral structures (figure 4). A humeral head which is fully controlled during these activities can be said to have functional stability. This functional stability is dependent upon the ability of muscle action to centre the head on the glenoid, to the contribution of dynamic ligament tension and to proprioceptive impulses.

Figure 4. Interactive motion of the joints of the shoulder complex



Pathology can be considered as failure of the static and/or dynamic stabilisers of the glenohumeral joint. A symptomatic loose shoulder is unstable by definition.

The best recognised form of shoulder instability is that of recurrent anterior dislocation. This is associated with a failure of the capsulolabral complex. The so-called Bankart lesion is an avulsion of the glenoid labrum at the point of insertion of the anterior band of the inferior glenohumeral ligament (Fig 5). However, it has been shown that the Bankart lesion is not merely the labral detachment (Yamaguchi and Flatow 1995). In cadaveric studies detaching the labrum did not produce instability but sectioning of the anterior band of the glenohumeral ligament allowed dislocation to take place. It was therefore felt that the pathology is stretching of this anterior band together with detachment of the labrum.

Figure 5. Illustration of a Bankart lesion

The posterior head indentation fracture referred to as the Hill-Sach's lesion rarely causes problems with instability. However, when large (Fig 6) it can engage on the anterior rim of the glenoid with only small degrees of external rotation causing dislocation to take place.

Figure 6. A large Hill-Sach or Broca lesion as seen on a CT arthrogram

Failure of the dynamic stabilisers can occur in several ways. The mechanisms probably apply in all shoulders but are more significant in lax joints where the stability of the glenohumeral joint is critically dependant upon muscle action.

Muscle imbalance is considered to be one of the major reasons for instability in the lax shoulder. The actions of the internal rotators (subscapularis) and external rotators (infraspinatus) are usually balanced but the internal rotation action is enhanced by the action of pectoralis major. If an individual and especially a sportsman, over-uses the shoulder, fatigue is likely to take place in the external rotators before the internal rotators resulting in an imbalance. This will cause the control of the humeral head position to be lost. This loss of control allows the humeral head to impinge against the coracoacromial arch with resultant irritation/compression of the subacromial bursa and pain in the epaulette region and the upper arm. This type of impingement syndrome is referred to as INSTABILITY IMPINGEMENT and must be distinguished from other types of impingement which are more usually degenerative in origin.

The external rotators act as humeral head depressors when the arm is being used at or above shoulder level. Repetitive activity at this level resulting in fatigue of the external rotators is therefore likely to allow the humeral head to rise up and to impinge against the coracoacromial arch, again resulting in INSTABILITY IMPINGEMENT.

This is usually only a problem in the lax shoulder where the degree of humeral head translation is such that impingement can take place. This is the way in which laxity (asymptomatic) can be converted to instability (symptomatic) with over-use or fatigue or mild injury being the stimulus.

Muscle imbalance around the scapula can also result in instability of the shoulder. EMG studies in elite swimmers have shown that subscapularis and serratus anterior, which are scapular stabilisers, are active throughout the freestyle stroke and thus are more likely to fatigue resulting in a loss of scapular control. This is reflected in an abnormality of scapular motion as the arm is lifted and results in the greater tuberosity not being able to clear the acromion during elevation, leading to impingement. It appears that loss of scapular control can also occur late in patients with instability impingement and it is surmised that this is due to failure of the scapular stabilisers that are having to over-work to cope with the loss of control of the humeral head.

It has been suggested that once instability impingement has become established, stretching of the anterior capsule takes place and a tightening of the posterior capsule occurs. This so-called capsular tightening predisposes to further anterior translation of the humeral head during movements and thus contributes to impingement.



The condition referred to as multidirectional instability (MDI) is badly named. Most of these patients have excessive glenohumeral translation in more than one direction but have symptoms when the humeral head moves in one direction only. It would be more correct to think of them as having multidirectional laxity with unidirectional (anterior, posterior or inferior) instability.
This condition is most commonly seen in patients in their third decade but can be seen from the mid-teens to the fifth decade. The majority are athletic but a number are sedentary. The sex instance is equal. The main clinical feature is usually pain. Occasionally the patient will complain of "the shoulder going out" and this will be the result of minimal trauma. Self reduction is the norm. However, the features of instability are usually subtle. The history is often the most informative part of the assessment.

The description of symptoms may be vague but the account of how the symptoms came about and the description relating to pain or subluxation and its relationship to the position of the arm can be very helpful. For example, a patient who develops symptoms when carrying heavy bags is likely to have predominantly inferior instability whereas a patient who experiences symptoms when the arm is in an overhead abducted and externally rotated position probably has anterior instability. Patients with predominantly inferior instability are likely to complain of intermittent and transient episodes of paraesthesiae in the upper limb which may be non-anatomical in distribution.

Since these symptoms are the result of failure of the dynamic stabilisers, the instability should be regarded as functional instability and its effects are therefore seen throughout the range of motion and not only at the ends of the range of motion. Accordingly, this type of instability creates much more disability than the physical signs would suggest.

The sign that is felt to be pathognomic of multidirectional instability is the sulcus sign (Fig 7). This produced by downward traction on the limb in a relaxed patient. The sulcus will appear beneath the acromion. This sign reflects laxity in the capsule and usually indicates that there is a large rotator interval.

Figure 7. Sulcus sign demonstrated by applying longitudinal traction on the arm

Excessive anterior and posterior shift of the humeral head against the glenoid can be demonstrated by stabilising the scapula and moving the humerus anteriorly and posteriorly. This can be done either with the patient in the seated or the supine position (Fig 8). The generally accepted classification is that the humeral head which moves but does not reach the rim is grade I whilst a head which reaches the rim is graded II and a head which can be completely subluxated is grade III. It can be difficult to appreciate the grade II in particular.

Figure 8. A technique of demonstrating anteroposterior shift of the humeral head in the seated patient

Posterior laxity can be demonstrated by the posterior load shift test where the arm is flexed to 90 degrees with the elbow at 90 degrees and internally rotated across the body. Longitudinal compression is then applied to the humeral head and maintaining this pressure the arm is then brought into abduction and down to the side (Fig 9). If there is excessive laxity the humeral head will have subluxated posteriorly with the longitudinal pressure and will be felt "clunking" back into joint.

Figure 9. Posterior load-shift test. The longitudinal force subluxates the humeral head which relocates as the arm is brought back to the patient's side.

The above are tests of laxity. They are only of significance if they are symptomatic. However, when a shoulder is painful it may be difficult or impossible to demonstrate these tests. Indeed, it may not be possible to show any motion between the humeral head and the glenoid. If the laxity signs are present in the other shoulder, then I regard the lack of movement at the symptomatic shoulder as being "pseudostability". This is a very important sign and indicates that there is significant pathology within that shoulder. Examining the contralateral shoulder first is good practice and allows the patient to appreciate what is going to be done to the symptomatic shoulder.

Several other signs can be demonstrated in patients with instability.

Loss of scapular control is detected by demonstrating scapular dyskinesis or scapular winging. Scapular dyskinesis or loss of control of scapular motion during arm elevation is seen by observing the patient from behind and asking then to elevate and lower the arm slowly. The motion of the scapulae on the chest wall is then observed for asymmetry. Several repetitions may be necessary before this is seen. Scapular winging can be demonstrated by asking the patient to push against a wall or, preferably, to push against the examiner's hands. This allows the amount of force being applied to be better assessed. In a positive test scapular winging can be seen (Fig 10). Occasionally this can be so marked as to suggest the possibility of a neurological lesions.

Figure 10. Scapular winging in a patient with instability-impingement. EMG studies were normal

Laxity in the anterior capsule can be demonstrated using the Jobe anterior relocation test. This is done with the patient in the supine position. The arm is abducted to 90 degrees and externally rotated to 90 degrees. This will allow the humeral head to slide anteriorly and stretch the anterior capsule thus producing pain. Once pain is demonstrated posterior pressure is applied to the shaft of the humerus moving the head posteriorly. This should relieve the pain. If further external rotation is applied and the hand is then removed. In a positive test further pain should be experienced. The classical anterior apprehension test done with a seated or standing patient (Fig 11) also tests the anteroinferior capsule and will be positive - producing pain or the feel the shoulder may dislocate - where the anteroinferior capsule labral strutures are deficient.

Figure 11. Anterior apprehension sign. I prefer to place my thumb behind the humeral head to increase the sensitivity of the test.

A restriction of cross body adduction is not infrequently encountered in patients with instability impingement. It is often referred to as being a tight posterior capsule (Fig 12). However there is little evidence to show that the pathology is actually in the posterior capsule. Nevertheless, tightness posteriorly would be expected to produce an anterior translation of the humeral head during elevation motion and to therefore exacerbate any tendency to impingement.

Figure 12. Tight posterior capsule. The flexed arm is adducted across the body.

Muscle imbalance can be difficult or impossible to detect manually and in this situation Isokinetic testing of the shoulder musculature can be of value. Warner (1990) has shown that in patients with impingement the internal rotator to external rotator ratio is 200% and in patients with instability the ratio is 100%. However, it is not clear from this study whether there is external rotation weakness or excessive internal rotation strength in patients with impingement.

Imaging is not usually necessary in these patients although it must be remembered that it is possible for these patients to sustain a Bankart lesion or significant capsular injury.

Mention should be made of the patient with "voluntary dislocation". Although extensive reference is made to this type of patient they are infrequently encountered. Psychological problems are often present but may be difficult to detect. Dislocations are always atraumatic and may take place in situations where there is a clear element of secondary gain. It is sometimes possible to demonstrate asymmetric muscle contraction. It is usually recommended that these patients are managed with "skilful neglect". However, it should be emphasised that diagnosis may be difficult and several interviews with the patient may be necessary to establish the correct diagnosis.



The management of the patient with recurrent anterior dislocation is well established in the literature and is beyond the scope of this particular article. The same consideration applies to the much rarer situation of recurrent posterior dislocation. I will confine my comments to the management of instability impingement and multidirectional instability.

Rehabilitation is the most important element of management. However, the rehabilitation must be appropriate.

The Jobe and Pink have classified the muscle balance of the shoulder into four groups, the so-called 4 P's. These are the glenohumeral Protectors, the scapular Pivoters, the humeral Positioners and the Propellor muscles. The glenohumeral protectors are the rotator cuff muscles, the scapular pivoters are the trapezius, serratus anterior and the rhomboids, the humeral positioners are the three parts of deltoid and the propellor muscles are represented by the pectoralis major and latissimus dorsi.

A careful assessment of the patient is required to identify the areas in which failure has taken place but in a typical situation the approach would be to strengthen the glenohumeral protectors and scapular pivoters first and to then incorporate the glenohumeral positions (the deltoid), strengthening the propellor muscles last of all. Typically the exercises are carried out initially in an isotonic fashion and then in an isokinetic fashion. Any limitation of motion such as a tight posterior capsule should be stretched up before muscle rehabilitation is commenced.

It is important to stress to the patients that this type of rehabilitation regime takes a long time. The longer the period the symptoms have been present prior to treatment, the longer the regime will last. In most cases such treatment is required for a minimum of 6 months and one years' treatment is not unusual. Patients should not move onto the second stage incorporating the glenohumeral positioners until the scapular muscles and rotator cuff muscles have been rehabilitated sufficiently to regain control of the humeral head. Supplementary treatments using biofeedback machines or isokinetic machines can be of value.



Surgery should not be considered in this group of patients until there has been at least 6 months of appropriate rehabilitation. It should be remembered that even patients with lax shoulders can sustain mechanical lesions within the shoulder such as a Bankart lesion and if the history is suggestive then some means of detecting this eg. CT arthrogram, MRI arthrogram or arthroscopy, should be used at an early stage. The presence of such a lesion means that even the most appropriate rehabilitation is unlikely to be effective. Although it is possible to regain control of patients who have recurrent posterior dislocations in association with laxity, this group is very difficult to manage and surgery is more commonly required. The same consideration applies to those patients who have recurrent dislocations which occur during sleep.

In my practice surgery will be used mostly for patients with symptoms of dislocation or subluxation rather than those presenting with pain. In the latter group rehabilitation is almost always successful.

The principle of surgery is to reduce the volume of the capsule and therefore provide some capsular restraint to the humeral head, reducing the load on the shoulder musculature. This can be achieved by procedures such as the open inferior capsular shift operation described by Neer and Foster (Fig 13), the arthroscopic capsular shift described by Snyder and Stafford (1993) or by the use of laser or thermal capsular shrinkage.

Figure 13. Inferior capsular shift procedure. Note that the rotator interval must be closed.

The inferior capsular shift operation was first described by Neer and Foster in 1980. In their series 31 out of the 32 patients had successful results. More recent reports by Cooper and Brems in 1992 showed good results in 39 out of 43 patients whilst Yamaguchi and Flatow reported that 66 of their 75 patients did well in a paper published in 1995. Savoie and Field (2000) have shown in a comparative study that at least 90% satisfactory results can be achieved using either an arthroscopic suturing technique or the arthroscopic technique using thermal capsular shrinkage. Structured rehabilitation is necessary following surgery and usually commences after 4 to 6 weeks of immobilisation.

No long-term results concerning the use of capsular shrinkage have yet been published. Clinical reports suggest good early outcomes but basic science studies (Hayashi et al 2001) have expressed concern about the varying degree of tissue damage produced because of the difficulty in knowing exactly how much energy is being delivered by the probe. This is a promising technique but careful long-term follow up is required with further development of the thermal probes.


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Maîtrise Orthopédique n°111 - 2002; Febuary.