SHOULDER INSTABILITY
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.
FACTORS CONTROLLING THE STABILITY
OF THE GLENOHUMERAL JOINT
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 STATIC
STABILISERS comprise:
· 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
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.
CLINICAL FEATURES
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.
MANAGEMENT
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.
INDICATIONS FOR SURGERY
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.
