Module 1: Glenohumeral Joint Instability – Patho-anatomy, Diagnosis and Clinical Management Pathways

Welcome to the training modules

Glenohumeral joint (GHJ) instability is the inability to maintain the humeral head (HH) centered in the glenoid fossa
(Abboud & Soslowsky, 2002). It is associated with a pathological increase in the translational movement of the HH
that interferes with joint function and / or produces pain.
GHJ instability represents a spectrum of disorders with overlapping syndromes that range from complete dislocation
of the joint to excessive uncontrolled translation of the humeral head, leading to secondary shoulder symptoms.
Traditionally, the term GHJ instability implied dislocation (HH translation completely over the edge of the glenoid)
or subluxation (partial translation of the HH from the centre of the glenoid socket) of the humeral head.
In recent years it has been recognised that symptoms of instability (apprehension +/- pain) can result from excessive
or uncontrolled translations of the HH without frank dislocation or subluxation. These symptomatic translations can be
acquired through the stress of repeated microtrauma (such as throwing sports or repetitive gym) or due to congenital
alterations in anatomy or collagen type.
Instability differs from the term ‘laxity’, ‘hyperlaxity’ or ‘hypermobility’. Laxity refers to an asymptomatic hypermobile
joint with the ability to maintain centring of the humeral head in the glenoid fossa. The term instability is used when this
function is lost and results in symptoms of pain, discomfort, paraesthesia, apprehension, and/or fatigue. (ref)

The GHJ is a ball and socket joint.
The ‘ball’ refers to the humeral head which should sit in the ‘socket’ – the glenoid fossa.
The GHJ is inherently more mobile than other ball and socket joints (such as the hip). Its flexibility and large degree
of motion are advantageous to position the hand in space for multiple upper limb functions, such as throwing a ball,
scratching a back or doing up a bra.
Several anatomical structures are essential to maintain the passive stability in the shoulder

2.1.1 Boney stability

The Glenoid

The glenoid socket is smaller in radius of curvature than the humeral head (ref), which contributes to the inherent increased
translation of the GHJ compared to the hip
Glenoid depth is also an essential part of GHJ stability. Some people naturally have a smaller glenoid than others
(glenoid hypoplasia) or underdevelopment of the posterior/inferior glenoid rim (glenoid dysplasia).
These congenital alterations are part of normative population variability, though will result in these individuals
having greater translation of the humeral head on the glenoid compared to the average person.
This is one cause of GHJ hypermobility /laxity.
Hypermobility is asymptomatic laxity of the glenohumeral joint. (ref) This means that some people in the normative
population have greater translation of the humeral head in the glenoid fossa compared to others; typically inferiorly,
plus or minus excessive posterior and/or anterior translation. Hypermobility may be confined to the shoulder and
set up by individual variations in shoulder anatomy (such as smaller glenoid socket) or it can be associated with a
more generalized joint ligamentous laxity that is related to alterations in an individual’s collagen profile
(i.e. more systemic laxity). More about this later in the module. If hypermobility exists, it usually presents bilaterally (both sides).
The orientation of the glenoid is also relevant to an individual’s GHJ stability. The average orientation of the glenoid in the
coronal plane is approximately 6 ° retroversion(Hohmann & Tetsworth, 2015), meaning the glenoid normally faces
a slightly backwards. However, there is a wide variation in the orientation of the glenoid in the normal population with
some people facing a more forwards (ante-verted) and some facing more backwards (retroverted) (ref)
The changeable orientation of the glenoid is a part of normal foetal development. If the glenoid is
retroverted (faces more posteriorly) more than 10 °, then this predisposes to the development of posterior
instability (Hurley et al., 1992b).(Brewer, Wubben, & Carrera, 1986; Hurley et al., 1992a). Conversely,
If the glenoid is more anteverted,(-1.7° retroverted) this has been shown to contribute towards anterior instability
(Hohmann & Tetsworth, 2015). If one side is more
retro or anteverted then usually the other side follows a similar developmental pattern.
The best imaging modality to assess the orientation, size and any defects in the glenoid is a 3D coronal CT scan.
Damage to the glenoid classically occurs in traumatic shoulder dislocation or subluxation. Damage to the anterior glenoid
is known as a boney Bankart lesion. This lesion can be seen on plain radiographs (X-ray) but if further clarification of the size is
required then a CT scan is the best imaging modality.(Nolte, Elrick, Bernholt, Lacheta, & Millett, 2020)
While there is a paucity of evidence on how to classify the size of a bony Bankart, the recent classification by
Kim et al.,(Kim, Cho, Son, & Moon, 2014) possibly provides the most useful pathway for clinical decision making;
Small bony Bankart’s fragments ( < 12.5 % of the glenoid) generally have good outcomes with arthroscopic soft tissue repair with
suture anchors
Medium fragments (12.5 to 25 %) overall good outcomes with arthroscopic double-row repair (bony Bankart Bridge)
Large Fragments (> 25 %). If a large fragment is present and viable (in the absence of attritional or chonic glenoid bone loss),
then anatomic reduction should be obtained via fixation of the fragment with cannulated screws.
It is important to note that Bony Bankart fragments size is different to “attritional” glenoid bone loss (ie: erosion) percentage.
There are different treatment recommendations for attritional glenoid bone loss based on the percentage of the glenoid deficit
(Nolte et al., 2020)
Loss of glenoid bone stock will compromise GHJ stability and may be a cause of recurrent instability.
While damage to the anterior glenoid surface is typical in the setting of an anterior dislocation,
damage to the posterior glenoid surface during a posterior dislocation or subluxation can also occur,
which is known as a reverse Bankart lesion.
Whilst a boney Bankart lesion is an actual bony fragment, repetitive translation, subluxation or dislocation of the
humeral head can also cause corrosion of the anterior glenoid rim in anterior instability or posteriorly glenoid rim in
posterior instability. This is referred to as glenoid erosion and is one of the causes of recurrent instability.
(ref) After a traumatic, first-time anterior shoulder dislocation, the presence of glenoid erosion or glenoid bone
loss increases the risk of recurrence. (Dickens et al., 2019; Milano et al., 2011)As little as 10.2 % bone loss can
increase the risk of recurrence after a first-time dislocation. (Dickens et al., 2019)
Three-dimensional Computer Tomography (CT) imaging is the gold standard for assessing glenoid bone loss.
(Provencher et al., 2010; Sofu et al., 2014)
While there are some variations in the literature the general recommendations for the
treatment of glenoid erosion are as follows:
- In patients, with bone loss < 20 % a soft tissue reconstructive procedure (such as an arthroscopic anterior shoulder
 reconstruction / arthroscopic Bankart repair) can typically be performed with good outcomes.
- However, in patients with glenoid bone loss > 20 % , evidence supports the use of bone augmentation procedure such
 as a Latarjet Procedure or Eden-Hybbinette procedure(Provencher et al., 2010) as soft tissue reconstructive procedures
 in these patients result in a significantly higher rate of recurrence post-operatively and poorer
 Western Ontario Shoulder Instability (WOSI) scores.(Shaha et al., 2015) The WOSI is a patient reported
 instability specific outcome measures.
Although the traditional recommendation is that patients with < 20 % glenoid bone loss should have good outcomes with a
soft tissue repair, recent evidence suggests that the percentage of glenoid bone loss that tolerates a soft tissue repair with
good outcomes, continues to decrease.(Nolte et al., 2020) Shaha et al (Shaha et al., 2015) demonstrated that in an
active population, glenoid bone loss of just 13.5% led to a clinically significant decrease in the
Western Ontario Shoulder Instability score consistent with an unacceptable outcome, even without further recurrence,
when compared with patients with < 13.5% glenoid bone loss. Type of sport, career goals and risk of recurrence all
need to be considered in the context of treatment decisions
In the Latarjet procedure, a locally harvested coracoid autograft is positioned to become an extra-articular platform that
acts as an extension of the articular arc of the glenoid. The osseous block serves to extend the glenoid rim and enhances
the “safe arc” available for translation prior to dislocation. (Provencher et al., 2010; Ranalletta et al., 2018)
The Eden-Hybbinette procedure often uses an iliac crest bone graft to reconstitute glenoid bone loss.
It is typically indicated in the cases of a failed Latarjet procedure or severe glenoid bone loss > 40 %.
(Galvin, Zimmer, Prete, & Warner, 2019) the reported rates of recurrence and osteoarthritis are higher when
compared to the Latarjet(Longo et al., 2014)
Research evidence convincingly shows these procedures have a lower recurrence rate of instability compared to
arthroscopic stabilization procedures in contact athletes over a 10-year period. (Longo et al., 2014; Perret et al., 2021)
However they come with a higher complication rate than arthroscopic procedures in terms of loss of range of motion &
the implications to return to sport ( especially in an overhead athlete), long term increased exposure to arthritis risk
and an elevated infection incidence (Longo et al., 2014; Perret et al., 2021)
The amount of glenoid erosion or bone loss that is a significant factor for recurrence in posterior instability is less
well researched as posterior instability has traditionally been less well recognized clinically than anterior instability
In regards to treatment, the critical threshold for posterior glenoid bone loss (pGBL) remains controversial,
(Smith & Edwards, 2024) however a recent review suggests that a capsulolabral repair is inadequate in cases of
pGBL bone loss > 20 % in the primary surgical setting and > 10 % in revision cases(Dickens, Hoyt, Kilcoyne, & LeClere, 2023).
The threshold may also – depend on whether pGBL is isolated or present in combination with a horizontal orientated acromion
(Check numbers – more about this below)
There are various surgical procedures available for posterior glenoid erosion ranging from using bone putty or chips
to reinforce any deficit present to utilizing a J Graft – where a piece bone from the tibia or the iliac crest is utilized to fashion a
bone segment to fill in the deficit in the posterior glenoid (ref)

The Humeral Head

The anterior or posterior surface of the humeral head can also be injured in shoulder dislocation or subluxation.
If the HH dislocates or subluxes anteriorly, it can create a compression fracture on its posterior aspect,
as it abuts into the anterior glenoid while exiting the joint. This is known as a Hills-Sachs lesion. A Hill- Sach’s lesion may be
“engaging and off-track” or non-engaging and “on track”.
The glenoid track refers to the contact zone between the humeral head and glenoid and is defined as approx. 83% of
glenoid width(Yamamoto et al., 2007) (Figure X) During shoulder motion, if the hill sachs lesion stays on the glenoid track,
it is determined an ‘on track’ hill sachs lesion and there is little risk of engagement and dislocation (Figure X).
If the HSL is outside of the glenoid track, it is determined an ‘off track’ hill sachs lesion and there is risk of engagement
and dislocation. (Itoi, 2017) An engaging Hill-Sachs lesion is one that is off track and has engaged with the glenoid rim (Figure X).
An engaging Hill Sachs is more likely to occur with a concurrent bony Bankart lesion(Itoi, 2017).
- - Figure aX. (Glenoid Track) Figure xb. The glenoid track width imposed on the posterior humeral head.
    As the hill sach’s lesion remains within the track, it is an ‘on track’ HSL.(Itoi, 2017)Figure X ( An “off track “Engaging HSL) (Itoi, 2017)
An “engaging” Hills Sachs can cause frank instability with innocuous activities of daily living– not just with contact injury.
This occurs in approximately 7% of Hill Sachs lesions. (Itoi, 2017)
Engaging HLS more likely in combination with concurrent glenoid bony deficit (Itoi, 2017)
The follow recommendations(Itoi, 2017) have been made for the treatment of Hill Sach’s lesions;
- On track lesions with glenoid bone loss < 25 % may be managed aged with a soft tissue arthroscopic stabilization
 procedure (such as a Bankart repair), whilst “off-track” lesions may require further augmentation surgery.
- Off-track lesions with glenoid bone loss > 25 % typically requires a Latarjet procedure to address the
 glenoid deficit(Itoi, 2017)
For off-track lesions with < 25 % glenoid bone loss, the Remplissage and Latarjet procedures have been
reported as treatment options.
Remplissage is a French word meaning “To fill the defect.” Therefore, in this technique, a pair of anchors are
introduced into the Hill-Sachs lesion and the infraspinatus rotator cuff tendon is repaired into the defect to fill the defect.
Studies (ref) looking at the effect of the Remplissage report “good” function on ASES scores however this score
is not specific or sensitive to measuring change in the instability population and does not detect deficits in overhead function,
which occur post Remplissage as patients typically lose a significant amount of overhead ER.
Therefore in the case of the overhead throwing athlete that requires near full overhead ER ROM or contact/collison
athlete the Latarjet proceure may be the most appropriate treatment option as it can convert an off track HSL to an
on track HSL as the platform of the glenoid is extended. (Itoi, 2017)
If the humeral head dislocates posteriorly (out the back of the joint) then a compression fracture will occur on the
anterior superior aspect of the HH – this is called a “reverse Hills Sachs” deformity
This is a less common injury than anterior Hills Sachs and less likely commonly described in the literature –
similar principles of management apply to posterior Hills Sachs as anterior.

The Acromion

Until recently much of the interest around the acromion was related to it’s potential role in GHJ impingement syndrome.
Recently research and clinical interest has turned to its potential role in predisposing patients to some forms of posterior instability.
Normally, when looking at it in the coronal plane on imaging such as a radiograph or CT scan (True lateral view)
(Meyer et al., 2019)the acromion should be posteriorly tilted relative to the inferior angle of the scapula and centre
of the glenoid (Figure X)
- - Figure X Myers et al., 2019.
This gives a natural bony buttress to preventing posterior translation of the HH – if the acromion is angled more
horizontally ( check figure) then the humeral head is able to translate more posteriorly due to a lack of bony support
(Meyer et al., 2019)
Recent evidence has shown that patients with posterior instability have a more horizontally angled (flatter)
acromion (increased posterior tilt angle, increased posterior acromial height and decreased post acromial
coverage) compared to those with anterior instability and controls without PSI (Figure X). (Akgün et al., 2024; Arner et
al., 2023; Meyer et al., 2019)
- Figure X – a) Flatter, higher acromion in PSI. b) Low and more vertical acromion in anterior instability and
  control patients (Arner et al., 2023)
Experts have hypothesised that a more horizontal acromion is a potential predisposing factor to developing posterior
instability (Akgün et al., 2024; Meyer et al., 2019) . In addition, a flatter, higher acromion with less posterior coverage
relative to the centre of the glenoid is associated with increased posterior glenoid bone loss in patients with posterior
glenohumeral instability. (M. Livesey et al., 2022)
A more horizontal acromion in PSI may also /- contributing to failure of posterior soft tissue arthroscopic
stabilization procedures(Hochreiter et al., 2023; M. G. Livesey et al., 2023) – especially if present with co-existing
posterior glenoid erosion(Nacca, Gil, Badida, Crisco, & Owens, 2018; Wolfe et al., 2020).
The amount of posterior glenoid erosion considered to be relevant and require surgical correction is 10%.
(ref) However if a horizontal acromion is present then glenoid erosion of 5% or above is relevant for recurrence
of posterior instability.
If present some form of glenoid bony augmentation should be considered ( whether it be check what Shane is using
– I am unsure if it is a putty or chips or something more substantial such as a J graft which is a piece of the tibia
that is screwed into the posterior glenoid deficit (ref)

2.1.2 The Glenoid Labrum

The glenoid labrum is a fibrocartilaginous structure that deepens the glenoid socket. The labrum increases the radius
of curvature so that the total glenoid socket depth further approximates the humeral head radius of curvature.
Via negative intra-articular pressure, the labrum creates a “suction seal” effect that contributes to the inherent
stability of the GHJ. The labrum also acts as a buttress to control or prevent excessive humeral head translation (ref).
Anatomical variations in the glenoid labrum exist, including absent labral tissue or focal detachment of the
anterior-superior labrum from the underlying glenoid rim (sublabral foramen). These variations can increase
translation of the humeral head and are another contributing factor to GHJ hypermobility (ref).
The labrum can be damaged through trauma or repetitive microtrauma. If the labrum is damaged traumatically
and torn away from the underlying bone, they do not typically heal, resulting in ongoing feelings of apprehension,
pain or clicking sensations with specific GHJ positions. Micro-trauma to the labrum typically occurs with
repetitive overhead activity wuch as throwing, swimming, tennis, overhead weights in the gym or manual labour.
Labral lesions are known to occur anteriorly, posteriorly and superiorly, known as a superior labrum anterior
posterior (SLAP) lesion. Anterior labral tears are typical of a traumatic anterior inferior dislocation/subluxation or
through the repetitive stress of microtrauma with the arm in a position of abduction, extension & external rotation
at 90 ° elevation (such a pitching in baseball).
Posterior labral tears are typical of a traumatic posterior dislocation/subluxation or through the repetitive stress
of microtrauma with the arm in a combined position of flexion, horizontal flexion and internal rotation such as the
follow through position in pitching. The location of the posterior labral tear is dependent on the shoulder position that
contributes to the injury. If the shoulder is in 90° of flexion, then a posterior labral tear is likely to occur. If the arm
above 90 degrees of flexion (eg: overhead press in the gym) then a posterior inferior labral tear is more likely.
SLAP tears are more controversial, with some authors considering them to be clinically relevant whilst others
suggest they are over-diagnosed. (ref) The general consensus is that traumatic superior labral tears that extend both
anteriorly and posteriorly are considered clinically relevant. Though not common, they can occur either from a from
a fall or collision (such as a tackle) while the arm is adducted (with impact occurring to the superior aspect of the GHJ,
or the patient falls on the point of the elbow with the arm adducted, driving the humeral head superiorly,
creating the SLAP lesion.
The gold standard for labral imaging is a 3T MRI. An MR arthrogram may be required to better visualise the labral
deficit if only 2T imaging is available(Soldatos, Shah, & Chhabra, 2024)
Evidence from high quality trials supports that for traumatic anterior labral tears, surgery is the recommended
treatment choice for optimal patient outcomes in a large majority of cases (Handoll & Al‐Maiyah, 2004; Jakobsen,
Johannsen, Suder, & Søjbjerg, 2007)
The evidence is less prolific in traumatic posterior and traumatic superior labral (SLAP) lesions although there
is emerging evidence that surgery is also the most predictable solution for return to higher level activity
(such as overhead sports and occupations) for both patient populations.(Jang, Seo, Jang, Jung, & Kim, 2016)
However, this evidence and the decision for surgical management needs to be considered in the
context of patient sporting level and type, age, occupation, and type of health care access.
(more detail to be provided later in the module).
If the labrum is damaged as a result of micro-trauma, then 6 months of conservative management is considered
the first line of management, with surgical repair considered if conservative management fails(LeVasseur et al., 2021).
Micro-traumatic SLAP lesions are typically treated conservatively, as surgical management has been
associated with poor healing rate, high rate of stiffness post operatively and difficulty in anchor placement in the
surgical technique (ref)
An important side issue to consider is that if labral tears are present for a period of time – especially posteriorly or
with SLAP lesions – then a cyst or ganglion may develop whereby leakage of intra-articular fluid into
the area of the suprascapular or spinoglenoid notch may create pressure on the suprascapular nerve +/- its
surrounding blood supply. (Baums et al., 2006) Compression to this neurovascular bundle will create atrophy,
fatty infiltration and eventually denervation of the infraspinatus +/- the supraspinatus muscle. If the compression
is more proximal (at the suprascapular notch) then both supraspinatus and infraspinatus are affected, were as
more proximal lesions (at the spinoglenoid notch) effects the infraspinatus only.(Leider et al., 2021)
Patients typically present with significant weakness of abduction and external rotation, atrophy of the infraspinatus
+/- supraspinatus muscles and sensory loss and pain in the posterior-lateral aspect of the shoulder.(Leider et al., 2021)
If a ganglion is present this should be addressed surgically before too much pressure on the nerve results in
compromise to the supraspinatus or infraspinatus muscles(Leider et al., 2021).

2.1.3 Ligaments

Stability of the GHJ is highly dependent on its ligament architecture. The GHJ ligaments are comprised of thickened
fibrous bands connecting the humeral head to the glenoid fossa and are a reinforcement of the GHJ capsule.
Anteriorly, there are three primary ligaments that contribute towards stability of the GHJ; the superior glenohumeral
joint ligament (SGHL) (complex), middle glenohumeral ligament (MGHL) and inferior glenohumeral joint ligament
(MGHL).
Posteriorly, the posterior inferior glenohumeral joint ligament and the posterior glenohumeral joint
capsule provide passive support to the posterior aspect of the shoulder.
Each of the GHJ ligaments becomes taut in varying positions of abduction and humeral rotation. Each ligament
also has specific branches of the axillary nerve that act as an afferent feedback mechanism to the
central cortex. This provides information to the brian on joint position sense , which creates a feed forward
mechanism to generate specific patterns of muscle activation to support shoulder stability (ref).
The gold standard for imaging the GHJ ligaments is a 3T MRI scan. (ref)

Inferior Glenohumeral Ligament (IGHL) Complex

The IGHL complex is considered the most important stabilizer of the GHJ (ref). It is the prime passive controller
of external rotation and abduction in the shoulder. Significant tension in the IGHL doesn’t develop until approximately
45 ° of shoulder elevation and reaches its maximum at approximately 90° abduction external rotation
(O’Connell, Nuber, Mileski, & Lautenschlager, 1990)
The IGHL is the commonly damaged during a shoulder dislocation or subluxation. Damage to the anterior
portion of the IGHL (+/- the anterior/inferior glenoid labrum) where it attaches to the glenoid is called a
soft tissue Bankart Lesion (Figure X) Damage to the IGHL where it attaches to the
humerus it is called a Humeral Avulsion of the Glenohumeral Ligament (HAGL) lesion (ref)
A glenoid avulsion of the glenohumeral ligament (GAGL) lesion occurs when the labrum remains attached to
the glenoid while the inferior glenohumeral ligament complex detaches from the labrum and glenoid
(O’Reilly, Andrews, & Siparsky, 2019)(Figure X)
An anterior labro-ligamentous periosteal sleeve avulsion (ALPSA) lesion occurs when the anterior IGHL
complex is stripped off the bone. And anterior labral tear associated with anterior inferior glenoid cartilage injury is
called a GLAD (Glenolabral Articular Disruption) lesion.
Damage to the anterior inferior GHL complex usually comes from a traumatic injury with the arm in an overhead
position and being forced backwards; such as a tackle in contact sport with the arm in an overhead position or
falling onto the arm. Typically, the shoulder will dislocate or sublux and the patient will be conscious that a
shoulder injury has occurred. The patient will either need to seek medical assistance to re-locate the shoulder or
in some cases, may be able to manoeuvre it themselves which results in a relocation.
After the acute event the patient is usually left with symptoms of pain, avoidance or apprehension with
use of the arm in the abduction and ER at 90° elevation (“stop sign”) position.
The posterior IGHL placed under most tension in a combination of 90° shoulder flexion, horizontal flexion and
internal rotation.(Dashottar & Borstad, 2012) Hence trauma to the shoulder in these combined positions
(e.g. fall with the arm in front of the body) may damage the posterior IGHL. (ref)
The patient with trauma to the posterior IGHL typically presents with pain, guarding, apprehension and/or
avoidance in positions of shoulder flexion, horizontal flexion and internal rotation. (ref)
An injury of the posterior IGHL where it attaches to the glenoid it is called a reverse Bankart Lesion (ref)
Injury to the posterior IGHL at the humeral attachment is called a posterior or reverse humeral avulsion of
the glenohumeral ligament (PHAGL or reverse HAGL)(Martetschläger, Ames, & Millett, 2014)
The estimated incidence according to data from emergency and trauma settings suggests that PSI
accounts for 2 and 3% of all shoulder instabilities.(Xu et al., 2015) This is likely underestimated
since only 23 % of traumatic posterior instabilities require reduction. (Goubier, Iserin, Duranthon, Vandenbussche,
& Augereau, 2003; McIntyre, Caspari, & Savoie, 1997; R. J. Williams, Strickland, Cohen, Altchek, & Warren, 2003)
Recurrence rates (a subsequent dislocation after a first-time dislocation) after damage to the posterior IGHL are
much lower compared to damage to anterior glenoid structures. (ref) This may be due to an under-reporting of
recurrence rates due to spontaneous relocation in PSI. (ref) In addition, it may be that the posterior muscles of the
GHJ can guard and compensate against posterior instability to a greater extent than anterior instability (ref).
Compared to anterior instability, PSI patients often present with secondary soft tissue overload due to the
uncontrolled humeral head translation creating stress and strain around the rotator cuff and capsule tissue (ref).
Like anterior instability, PSI related structural lesions do not typically heal (ref). The extent of the structural lesion,
patient activity participation, age, and response to conservative management are just some of the factors all
need to be considered when making decisions around the need for surgical referral (see Module X).

Middle Glenohumeral Ligament

The middle GHL has maximum tensional control around 45 – 60 ° of abduction and external rotation.
(O’Connell et al., 1990) The middle GHL is primarily an anterior stabilizer as it controls and restricts external
rotation with the IGHL.(O’Connell et al., 1990)
The middle GHL has a high level of anatomical variation (Caspari & Geissler, 1993) with 12% of the normative
population not having one(DePalma, Gallery, & Bennett, 1949). An absent middle GHL results in increased
external rotation ROM; another contributing factor to GHJ hypermobility. This may be advantageous for some
sports (i.e. increased external rotation correlates with increased ball velocity in a throw (Manzi et al., 2022))
though may predispose to an increased risk of injury in overhead repetitive sports due to a lack of passive support. (ref)
The middle GHL can be damaged due to trauma or over-stretched through repetitive overload; If the middle
GHL it is absent, damaged in a trauma or over-stretched through repetitive overload; typically, with use of the
arm in abduction and ER combinations at 45 to 60° abduction (such as the wind-up phase of the forehand in tennis).
Absence of or damage to the middle GHL typically results in excessive translation of the HH anteriorly and
symptoms of anterior cuff overload (anterior supraspinatus, LHB and subscapularis), rather than symptoms of frank instability.
Patients with isolated damage to the middle GHL usually respond well to rehabilitation with surgery only
being considered if the patient fails a 6-month conservative rehabilitation program. If damage to the middle
GHL is part of a broader shoulder ligament injury, then surgical intervention may be required (Ref).

Superior Glenohumeral Ligament

The superior GHL (SGHL) is compromised of the Coracohumeral Ligament (CHL) superiorly and the
SGHL inferiorly. These complex forms part of the biceps pulley mechanism where the CHL forms the roof,
the superior SGHL the floor, the supraspinatus the lateral border and the subscapularis tendon the medial
border; all of which stabilise the LHB.
The SGHL helps prevent inferior translation of the HH and is the primary stabilizing structure to prevent
the HH going either anterior or inferior in the adducted arm (arm by the side).(O’Connell et al., 1990)
The SGHL can be damaged by trauma or overload in lower ranges of abduction (0 – 45°) plus or minus shoulder
external rotation and/or an inferior traction force (e.g. dropping a heavy object with it still in your hands, catching a
patient falling down, losing control of a very heavy incline bench press or dead lift)
Damage to this ligament will result in pain, apprehension, and/or guarding in positions that create traction
on the arm inferiorly and/or force the arm back into external rotation in lower ranges of abduction.
Symptoms are still likely to exist at 90° abduction as the SGHL continues to contribute towards stability in
higher ranges of abduction (i.e. throwing a ball).
Patients with isolated damage to the middle SGHL usually respond well to rehabilitation with surgery only
being considered if the patient fails a 6-month conservative rehabilitation program. If damage to the middle
SGHL is part of a broader shoulder ligament injury, then surgical intervention may be required (Ref).

2.1.4 Glenohumeral Joint Capsule

The GHJ capsule is a fibrous sheath that encapsulates the GHJ. It is a continuous supportive structure
that wraps around the anatomic neck of the humerus and connects it to the glenoid rim
It characterised by distinct thickened bands which are GHJ ligaments (see above)
The inner surface is lined by a synovial membrane which produces synovial fluid to reduce friction between
the articular surfaces.
As with the ligaments, varying positions of the GHJ in elevation and rotation specifically places different areas
of the capsule under tension
With the arm by the side the superior aspect of the GHJ capsule is under maximum tension – in external
rotation the anterior superior (rotator cuff interval) section of the capsuloligamentous complex is further
tightened whilst the posterior superior aspect is tightened in internal rotation
With abduction & external rotation the anterior capsule is tightened – the further up into elevation range the
movement progresses the tension in the anterior capsule increases, starting with anterior superior capsule
tightness in lower ranges of abduction and progressing to more anterior inferior capsule tightness once the
arm progresses up into higher ranges of elevation
The posterior capsule is tightened with internal rotation and horizontal flexion – in lower ranges of elevation
the primary tension is on the posterior superior capsule but as the motion progress up into further range of
flexion the tension increases around the posterior inferior capsule
The capsule tissue will be damaged in conjunction with the ligaments in the varying positions described for
ligament injury (above)
However depending on the individual, in some patients more of a capsular injury occurs where the capsule is
pulled off the bone (name of injury) and in others most of the damage occurs to the ligament component
or a combination of both can occur
Younger patients tend to sustain more of a ligament injury whilst older patients tend to damage more the
capsular tissue
If a ligament is avulsed off the bone it is not likely to heal or re-attach and can be a source of ongoing symptoms
of instability
Capsular tissue often heals up with a “plug” of fibrous tissue – this can lead to capsular restriction and
tightening which will create altered positioning of the humeral head
If the anterior capsule is injured as a result of a dislocation or subluxation– this area of the capsule has a high
level of a protein called verbatin which creates a thickening or tightening response to injury. (ref)
The increased fibrous scar tissue then creates a restriction of range of abduction / external rotation,
especially in higher ranges of elevation. The anterior capsule tightness will create a posterior translation
of the HH when abduction / external rotation movements are performed which can lead to posterior compression
pain in the GHJ as the HH is articulating off centre.

2.1.5 Negative Intraarticular Pressure

The final passive stabilising structure is the inherent negative intraarticular joint pressure which creates a
suction seal effect if all the passive stabilizing structures are intact
Disruption of any of the capsulolabral or ligament structures will disrupt the negative joint pressure and
result in increased translation of the HH on the glenoid
GHJ capsular venting (introducing additional air into the capsular space and hence opening it to the
atmosphere) has been shown to lead to a 50% increase in anterior displacement, a 19% increase in posterior
displacement and a significant inferior displacement (Wülker, Rössig, Korell, & Thren, 1995)

When the term Instability is utilized in relation to the GHJ, normally this implication is that there has been damage to one
or several of the passive stabilizers of the GHJ

However, it should be acknowledged that there are Active or Dynamic stabilizers or Muscles that also are inherently
involved in GHJ stability

2.2.1 The Rotarator Cuff

The rotator cuff (RC) comprises of 4 muscles – the subscapularis (anteriorly) the supraspinatus superiorly
and the infraspinatus and teres minor posteriorly
The RC muscles surround the shoulder joint – coming off their muscular attachments to the varying points
of the scapula proximally and forming tendon structures distally that insert into the tuberosities of the
humerus and blend with the GHJ capsule. The resting tone of these muscles act to compress the humeral
head into the glenoid fossa (concavity compression mechanism)
The RC act as physical buttresses to prevent excessive translation of the humeral head (subscapularis anteriorly
and supraspinatus and infraspinatus posteriorly) (ref). When an external displacement force is applied
experimentally to a shoulder in elevation, a reduction of rotator cuff force of 50% has been shown to
create an increase of 46% in the anterior displacement and an increase of 31% in posterior displacement
(Wülker et al., 1995)
The RC also contribute to GHJ range of motion; all in varying degrees depending on the plane of motion.
Supraspinatus acts in abduction, flexion, external rotation, extension and horizontal extension
Infraspinatus acts in abduction, in later degrees of flexion (> X ), external rotation, extension &
horizontal extension
Subscapularis acts in flexion, abduction, internal rotation, horizontal flexion and in later ranges of extension
(> X degrees)
Teres minor has a role in external rotation and abduction (M. D. Williams, Edwards, & Walch, 2018)
The RC tendon can be injured during a traumatic shoulder dislocation or subluxation with the subscapularis
or supraspinatus typically injured during an anterior dislocation and infraspinatus, a posterior dislocation.
These RC injures can include detachment of the RC tendon from its bony insertion, which typically needs
repairing surgically (ref).
Partial thickness tears or tendinopathy of the RC is a more common finding in association with
shoulder instability as dislocations, subluxations and uncontrolled translation of the humeral head can
injure the surrounding active soft tissue structures (ref).
Injury to the RC often results in pain, leading to muscle inhibition and loss of the concavity compression
mechanism of these muscles, further propagating uncontrolled translations of the humeral head.
As a result, the GHJ often displays proprioceptive deficits, weakness and aberrant functional movements,
impacting on motor control and performance.
Traditionally, the subscapularis muscle is considered to be a primary stabiliser anteriorly to prevent excessive
anterior translation of the HH (ref), whilst posteriorly, the posterior cuff (i.e. supraspinatus,
infraspinatus and teres minor) prevent excessive posterior translation of the humeral head. However in reality,
when a patient dislocates their shoulder either anteriorly or posteriorly, both sides of the joint are impacted
to varying degrees, (ref) hence clinically, most patients will have deficits in both their anterior and posterior cuff.
Therefore, rotator cuff rehabilitation is an integral part of any rehabilitation programme for instability whether
it be conservative or post operative.

2.2.2 The Long Head of Biceps

The long head of biceps (LHB) contributes towards GHJ stability.
It inserts superiorly inside the GHJ into the superior tubercle and the superior labrum.
Contraction of the LHB sets provides a suction seal effect through its tightening of the superior labrum (ref)
and has been considered a minor humeral head depressor (ref).
Research has demonstrated that if it detached there is a significant increase in translation in
several directions depending on which motion is being performed (Alexander, Southgate, Bull, & Wallace, 2013;
Rauck et al., 2022)

2.2.3 The Deltoid Muscle

If the rotator cuff is the inner muscular group to stabilize the HH, the deltoid comprises the outer sleeve of
stability. (ref)
All three components of deltoid (anterior, middle and posterior) are essential for varying motions of the
shoulder, but also provide a physical muscle mass to protect the shoulder girdle and limit unwanted HH translations.
The anterior deltoid assists in providing a buttress for the front of the shoulder to limit anterior instability,
the posterior deltoid to the back of the shoulder to limit posterior instability, and the middle deltoid assists in
stabilizing and protecting the HH laterally (ref)
The deltoid creates superior translation of the HH and, with the RC, contribute to the concavity compression
mechanism of the HH into the glenoid fossa. (ref)
If the axillary nerve (which runs in close proximity to the shoulder joint) is damaged during an anterior shoulder
dislocation, then paralysis of the deltoid can occur. (ref)
This will result in the HH sitting inferiorly at rest in glenoid socket and severely impacts on the patients ability
to elevate their arm depending on the extent of the nerve injury.

2.2.4 Scapula Stabilizers and Scapula Orientation

The position of the scapula is integral to the concept of GHJ stability.
Wherever the scapula is orientated (anteriorly or posteriorly titled, upward or downward rotation) this will
affect the orientation of the glenoid fossa and therefore in turn the position of the HH.
For example, if the scapula is anterior tilted, the HH will sit anterior from its centre on the glenoid fossa.
A common scapula movement error that occurs in GHJ instability is excessive downward rotation of the
scapula (or insufficient upward rotation of the scapula) during elevation of the arm.
Normally the scapula should provide approximately 60 ° of upward rotation during elevation of the arm.
This allows the socket to rotate superiorly ( facing upwards) to enable the HH to stay centred within
the glenoid socket (like balancing and egg in a spoon). (ref)
If scapula upward rotation is insufficient, the bony contact between the HH and the glenoid is reduced,
which typically results in inferior translation of the HH (ref).
This alteration in scapulo-humeral biomechanics will result in increased translations of the HH, attenuate
(or stretch) the surrounding capsular structures and predispose an individual to macro-traumatic,
micro-traumatic and atraumatic instability (ref).

GHJ Proprioception and Central Control

Glenohumeral joint proprioception is the ability of the individual’s GHJ to be able to perceive the location,
type, and position of motion as well as the muscle force and effort required for a movement strategy.
Normal proprioception replies on a complex interaction between the varying mechanoreceptors
(sensory receptors ) in the muscles and capsuloligamentous structures of the shoulder sending afferent
feedback to the sensorimotor cortex. The sensorimotor cortex, in combination with other brain areas then
generates the appropriate efferent response to determine the characteristics of the motor output. (ref)
This mechanism is significantly impacted by structural and non-structural instability.
Patients with structural damage to the capsuloligamentous structures (such as those with traumatic anterior
instability), display reduced proprioception and altered firing in the sensorimotor cortex(Haller et al.,
2014; Shitara et al., 2014)compared to those with normal shoulders.
Similarly, patients with atraumatic shoulder instability, with no structural damage to the capsuloligamentous
structures, but signs of hypermobility and poor motor pattering (such as those with multidirectional
instability); also have altered joint position sense (J. Barden, Balyk, Raso, Moreau, & Bagnall, 2004;
Jari, Boyd, Neumann, & Wallace, 2002; Kirkley, Adlington, Edmonds, & Griffin, 2001) and altered function
of the sensorimotor cortex compared to those with normal shoulders.(Howard et al., 2019; S. Warby et
al., 2024)
Both definitive structural damage and hypermobility associated with microtrauma, may damage the neural
receptors in the shoulder joint capsule, disrupting afferent signalling to the central nervous system
(J. M. Barden, Balyk, Raso, Moreau, & Bagnall, 2005). Consequently, efferent neuromuscular
control of the scapular and humeral muscles is altered(Lephart & Jari, 2002)
Proprioception deficiencies result in altered timing and amplitude of muscle contraction, increased
movement at a joint segment, and an inability to correct motion errors for placing of distal segments
(J. Barden et al., 2004); all of which affect joint function.
Given that cortical processes, shoulder proprioception and movements patterning is altered in
shoulder instability, addressing these issues is an important part of any rehabilitation programme.
(L. Watson, Pizzari, Balster, Lenssen, & Warby, 2022)
It is essential that the correct movement control signalling or movement strategy is retrained prior
to commencing strength work if effective movement performance is going to be achieved(Warby et
al., 2017; Lyn Watson, Balster, Lenssen, Hoy, & Pizzari, 2018; L. Watson et al., 2022) (See Rehabilitation
Module (x))

Glenohumeral joint instability can be classified in a variety of ways, including:

aetiology (traumatic versus atraumatic onset)
degree of instability (subluxation versus dislocation)
grades of instability
direction of instability (unidirectional or multidirectional)
the presence or absence of generalised ligament laxity
or the presence of volitional I or voluntary – instability

There are a number of shoulder instability classifications systems that attempt to encompass one or many of
these instability traits, however no system has gained universal acceptance.

Thomas & Matsen

Some early systems used aetiology to classify instability, which is an important consideration
as the presence or absence of trauma can assist with perceived direction of instability and treatment
selection. (ref)
Patients who have a significant history of trauma (such as a fall with resulting full glenohumeral
joint dislocation) are more likely to sustain a structural lesion resulting in a predominantly unidirectional
instability; at least initially.
Instability with an atraumatic onset is less likely to have structural damage to the joint, and more
likely to have signs of poor muscle patterning, including scapula dyskinesis, and multiple directions of
instability (ref)
Thomas and Matsen used Acronyms to distinguish these two polar groups;
TUBS (Traumatic Unidirectional Instability with a Bankart Lesion requiring Surgery) and AMBRI
(Atraumatic Multidirectional Bilateral requiring Rehabilitation (and if fails) an Inferior Capsular Shift).
The disadvantage of this system is that using the presence of absence of trauma as a primary
classification method dichotomises patients into the extreme poles of instability, with no allowance for
mixed or shifting pathologies. (Lewis, Kitamura, & Bayley, 2004)

Gerber & Nyffeler; Moroder et al.

Other systems(Gerber & Nyffeler, 2002; Moroder et al., 2020) that have added hyperlaxity and volitional
instability to their classification systems.
Hyperlaxity is defined as s defined as a condition in which most of the individual’s synovial joints
have a range of motion beyond normal limits(Boyle, Witt, & Riegger-Krugh, 2003). Hyperlaxity can be
confined to the shoulder or can be general throughout the body and is therefore termed generalised
ligament laxity.
Generalised ligament laxity may pre-disposed to traumatic instability in an active or sporting population
(Cameron et al., 2010; Chahal, Leiter, McKee, & Whelan, 2010) and the incidence of generalised
ligament laxity is high in patients with MDI(Ma et al., 2012).
Authors have speculated that generalised ligament laxity could precipitate a decreased stimulation of
proprioceptive afferents in the shoulder, reducing efferent muscle control(J. M. Barden et al., 2005; Blasier,
Carpenter, & Huston, 1994) which may contribute to the development of atraumatic instability through
a lack of dynamic stability(Illyés & Kiss, 2006).
It is important to distinguish between the terms laxity and instability. Laxity of the glenohumeral
joint refers to an asymptomatic hypermobile joint with the ability to maintain centring of the humeral head
in the glenoid fossa. The term instability is used when this function is lost and results in symptoms of pain,
discomfort, or apprehension
Most glenohumeral joint instability is involuntary(Beasley, Faryniarz, & Hannafin, 2000) however a small
subgroup of patients can voluntarily sublux their glenohumeral joint by selective activation and relaxation of
certain muscles. Some authors associate this with emotional disorders or secondary gain, which
really in our experience is an extremely small group of patients. Regardless, patients with volitional
instability should be educated to cease the habit. (ref)

FEDS Classification

The Frequency, Etiology, Direction and Severity or FEDs classification system is the only system that
has been tested and shown to have preliminary validity and reliability. (Kuhn, 2010)
The FEDS system categorises shoulder instability based on patient perceived Frequency,
Etiology, Direction and Severity of their symptoms. The FEDS system eliminates the concept of MDI
all together, with the rationale that MDI is difficult to define and that patients reporting symptoms in
multiple directions will have a primary direction of instability. And This elimination has been criticised
(Shea, 2013).
The FEDS system fails to acknowledge that pain could be a secondary sign of subtle instability in some
patients, disregards voluntary instability, and does not take into account the presence of structural lesions
in the shoulder, which could significantly alter management (ref).

Stanmore Triangle

The Stanmore classification(Lewis et al., 2004) is the only system that allows for the often multifactorial
and sometimes shifting nature of shoulder instability by classifying patients anywhere between three
distinct poles of a triangle (traumatic structural, atraumatic structural and muscle patterning
non-structural).
While there is a consensus on the subgroups of traumatic structural and motor patterning
non-structural, the subgroup of atraumatic structural instability can be misleading as it implies that
patients with acquired structural lesions have no seemingly obvious mechanism of injury or cause of
onset; though in reality there is likely to be a history of microtrauma that contributed to the development
of these structural lesions.(Sadi et al., 2020)
The Stanmore classification also does not include specific directions of instability.

The Delphi Classification (for Posterior Shoulder Instability)

The important differentiation between micro-traumatic and atraumatic shoulder instability has been recently
agreed up in a large Delphi Study, where a panel of 70 shoulder experts convened to classify posterior
shoulder instability and came to a consensus (98% agreement)(Sadi et al., 2020) of 3 subgroups:
including traumatic, and atraumatic instability micro-traumatic.
These sub-groups are defined by etiology or likely cause: but are related to a cluster of associated
factors that contribute to the presentation of that sub-group.
Traumatic instability, as discussed above, involves an incident of significant trauma to the shoulder,
associated with a GHJ dislocation, structural lesion- and typically unidirectional instability.
Atraumatic is instability has no seemingly obvious mechanism of injury or cause of onset but is often
associated with very poor scapula and HH motor control, multiple directions of instability and congenital
factors such as generalized ligament laxity. This group are less likely to have structural lesions.
Micro-traumatic instability is caused by tasks with repetitive or increased load, such as months of
back to back tennis sessions with a heavier than usual racquet. The associated factors are more
varied for this group, though the main differential factor is that, compared to the atraumatic group,
they have a higher likelihood of acquired structural lesions that have developed due to the repetitive
microtrauma.
The differentiation between the atraumatic and microtomic groups is important because it can alter your
management plan (see more below and module X).

Watson Instability Program (WIP) CLassification

Classifying shoulder instability is extremely challenging as many systems attempt to fit shoulder instability
into a defined category, which ignores the (often) multifactorial nature of a patient’s presentation.
Given these challenges, in conjunction with the previously published literature(Lewis et al., 2004;
Sadi et al., 2020) and our research collaborators (ref), the Melbourne Shoulder Group has developed the
Watson Instability Program (WIP) classification system. The WIP classification system further builds
on the work of the Stanmore and Delphi systems as it defines three subgroups (like the Delphi study),
headed by etiology, but allows for the often evolving and shifting mature of shoulder instability
(like the Stanmore classification system). These sub-groups are related to a cluster of associated
factors, which guide evidence-based treatment selection

(Figure X) – WIP FIGURE

While the sub-groups and their associated factors are typical, they are not completely ridged in their
place on the system and different clusters of associated factors can still exist. For example, your
atraumatic instability patient (with congenital hypermobility and scapula dyskinesia) can still over and
sustain a traumatic structural lesion and head into the macro-traumatic group, which can change your
management strategy. Alternatively, they may pick up a heavy racquet and start playing tennis five
times a week and move into the micro-traumatic group.
Understanding the etiology and associated factors that contribute to a patient’s presentation
relies on the thorough assessment by the clinician. In this way, treatment can address all these factors for
optimal patient outcomes.

3.6.1 Macro-traumatic Instability

Macro-traumatic instability typically refers to instability that has resulted in structural damage to
the passive stabilizing structures of the shoulder such as bone, ligament, and/or labral tissue.
Instability is from a traumatic onset such as a fall or collision in contact sport or it can be due to a
sudden increase in overload leading to a moment in time when a structural lesion develops
(such as the last repetition of a bench press after an overloaded session in the gym or the last few
serves after doubling training duration in a tennis session).
Person may or may not have a background Hypermobility / Laxity of the shoulder due to anatomical
or collagen anomalies, then trauma or overload applied to develop a symptomatic structural lesion
Evidence supports that the majority of these patients have the most optimal outcomes from surgical
stabilization to restore passive integrity of the joint (refs). However, a number of factors need to be
considered when directing patients towards surgical options, such as such as lifestyle, age,
occupational and sporting participation and insurance cover (see below)

3.6.2 Micro-traumatic Instability

Instability caused by a gradual or acute overload of musculature +/- capsuloligamentous structures (ref)
This type of instability is common in gym or repetitive overhead sports such as swimming
and tennis.
The instability may be anterior, posterior, posterior-inferior, or anterior-inferior due to failure of the
passive and/or active stabilizing mechanisms
While subluxations of the HH may be evident, it is more common for this group to have pathological
translations of the HH. Because these HH translations are often less perceptible than subluxations,
these patients are often misdiagnosed as having RC related pain, acromioclavicular joint pathology and
impingement (either sub-acromial or intra-articular), though it is the instability that is setting up these
secondary issues. (ref)
This group have a higher likelihood of structural lesions in both passive and active structures
due to the repetitive micro-trauma.
The initial treatment for these patients is typically conservative management as re-building
the active restraints may be able to compensate for any acquired structural lesion (ref). If 6 months of
evidence-based rehabilitation fails, the patient may require surgical stabilization to achieve their
functional goals (ref).

3.6.3 Atraumatic Instability

Instability with an atraumatic onset (no obvious mechanism of injury or cause of onset of atraumatic
onset).
This instability is associated with a congenitally lax or hypermobile GHJ (see hypermobility
section below).
Patients may or may not have generalised ligament laxity (GLL) however the incidence of GLL is higher
in this group(Saccomanno, Fodale, Capasso, Cazzato, & Milano, 2013)
These patients have a higher rate of congenital anomalies such as:
- Glenoid retroversion (glenoid facing more posteriorly > 10 deg)
- Glenoid hyperplasia (underdevelopment of the posterior-inferior glenoid rim)
- Alterations in the capsulo-labral structures (i.e. Buford complex, labral cleft)
- Collagen and connective tissue disorders (hypermobility syndrome, Ehler’s Danlos
  Syndrome, Marfan’s Syndrome)
Symptoms typically arise through loss of scapula and humeral head motor control superimposed
on a background of congenital capsular laxity (ref).
EMG studies show they have altered rotator cuff and scapula- thoracic function when compared to
normal controls (ref) In particular these patients have scapula that sit in excessive downward
rotation at rest and have a lack of upward rotation through range which is one of the major factors
that contributes to the pathological humeral head translations seen in atraumatic instability (ref)
Preliminary evidence from functional MRI studies have shown that these patients have altered function
in the primary motor cortex when compared to controls. Specifically, these patients have reduced activation
in primary motor cortical areas and increased activation in pre-frontal cortical areas when performing a
shoulder motion, which may indicate that these patients are exerting greater cognitive effort to plan,
control and execute a shoulder motion. (ref) These findings indicate a central component to atraumatic
shoulder instability.
There is also emerging evidence that there is an associated between joint hypermobility and functional
neurological disorder (FND). FND is a sensory and motor neurological disorder characterised
by functional rather than structural deficits. (ref). Joint hypermobility is more frequently observed in
patients with FND compared to a non-clinical comparison group(Koreki et al., 2022) and patients with
FND have altered brain connectivity (changes in neutral processing) compared to controls.
(Drane et al., 2020) Researchers hypothesise that that differences in interoception (the ability to
sense and understand your body’s internal state), autonomic control, and brain structure, associated
with joint hypermobility,(Koreki et al., 2022) may predispose patients to FND. Given FND is associated
with hypermobility and altered brain connectively, a small number of patients with atraumatic
shoulder instability may present with FND.
Due to their atraumatic onset, these patients typically have no structural lesion on MRI
Neer and Foster (Neer & Foster, 1980) originally described this condition as Multidirectional
Instability (MDI) which is extreme form of atraumatic instability. The original definition for MDI was GHJ
instability in three directions (anterior posterior and inferior), with a symptomatic sulcus sign
(for inferior instability) being the quintessential finding for diagnosis (ref)
The definition has evolved to include instability in two directions as well as three, with one of those
directions needing to be inferior for diagnosis (ref)
Evidence from multiple systematic reviews show that the majority of these patients have good
outcomes with an evidence-based rehabilitation program; with the rationale that restoring motor control
then strength of the scapula and RC compensates for their lack of passive stability and assists in
active control of the shoulder (ref). Patients with autramtic instability and MDI may have poor outcomes
with surgical stabilization as the primary driver is the motor patterning dysfunction (ref). (See module X)

Glenohumeral Joint Hypermobility

The topic of glenohumeral joint hypermobility warrants additional information as it is a large
consideration in many shoulders presenting with instability.
Instability by definition means an increased or uncontrolled translation of the HH that is associated with
pain, apprehension or functional loss of glenohumeral joint motion (ref).
Hypermobility refers to a congenitally lax joint, with an increase in translation of the HH that is
asymptomatic. Hypermobility is part of the normative population spectrum (ref) There is an increased
prevalence in the post-pubertal population due to a complex interaction of hormonal factors (ref),
lagging muscular development (ref), and variations in the underlying anatomy (ref), combined with
opportunity for increased activity. (ref)
While hypermobility is not pathological, it is risk factor for a traumatic shoulder dislocation or subluxation
in contact sports (ref) and may predispose patients to developing micro-traumatic and atraumatic
shoulder instability, particularly in the context of repetitive, overhead activity (Castori, Camerota,
Celletti, Grammatico, & Padua, 2010)
Patients with hypermobile shoulders have an increased incidence of bilateral shoulder problems (ref).
A hypermobile shoulder is often associated with other anatomical anomalies of the GHJ such as
a voluminous or redundant capsule, a large rotator interval, absent labral tissue and/or glenoid bone
alterations (e.g. glenoid hypoplasia or retroversion)
Hypermobility can be confined to the shoulder but can also be generalized throughout the entire body;
then the term generalized ligamentous laxity is used. (ref). GLL is present when an individual’s
synovial joints have a range beyond normal limits (ref). The Beighton Score assesses GLL. Patients
scoring > 4 /9 are said to have the condition (ref).
Not all patients with MDI have GLL. Some MDI trials (ref) report that 50 % of their cohort had GLL,
while other authors have reported varying rates (40% – 70 %)(Saccomanno et al., 2013)
Beighton Score (ref)
Hypermobility has a reported incidence of between10- 42% reported in sporting populations
(Nathan, Davies, & Swaine, 2018) and has an increased prevalence in certain sports such as
swimming, gymnastics, ice skating , cheerleading , diving , yoga (refs) Females sportspeople
have a higher reported incidence (up to 48%) compared to male sports people (up to 20%)
(Borsa, Sauers, & Herling, 2000; Kocher, Waters, & Micheli, 2000; Nathan et al., 2018; Wessel,
Eliasberg, Bowen, & Sutton, 2021).
It is unknown if hypermobility self-selects athletes for certain sports or if it is acquired due to the nature
of the sporting participation of the athlete (ref). One theory is that an athlete may be naturally good
at certain overhead sports due to their increased range of shoulder motion (such as pitchers with
increased external rotation in baseball). Alternatively, the athlete may acquire the shoulder hypermobility
due to the increased amount of time in training and play required at high-level competition (attenuating
the capsulolabral structures(ref)) especially in repetitive overhead sports such as swimming
(Wessel et al., 2021) For example, overhead loading > 3 hours week prior to 10 years of age increases
the chance of elongating collagen or changing bone alignment(Wessel et al., 2021)
Patients with hypermobility don’t necessarily “grow out of it” as is sometimes alluded to in the literature
(ref). Rather, over time, patients are likely to reduce, modify or avoid their participation in their
symptom-provoking activity (Kitamurra 1991)
If a hypermobile athlete sustains a macro-traumatic structural lesion, they will often require surgery
as per the non-hypermobile patient (ref). However, their post operative rehabilitation must cater for their
underlying hypermobility (See module X)
Hypermobility has been shown to have a negative effect on return to sport rates in soccer,
Australian Rules Football, Rugby, Cricket and Handball; with rates for hypermobile players at
37.5% vs 64 % to 92% for non-hypermobiles (Wessel et al., 2021)

3.7.1 Management Strategies in the Hypermobile Patient
<ul>
<li style=”font-weight: 400;” aria-level=”1″>There are certain management strategies that can be employed to reduce the risk of a hypermobile
shoulder sustaining or developing shoulder instability in the setting of contact or repetitive overhead sports.
For example:
<ul>
<li style=”list-style-type: none;”>
<ul>
<li style=”font-weight: 400;” aria-level=”1″>Encourage the athlete to develop more muscle mass before they are exposed/returned
to their contact sport, especially at higher levels of competition. Often the hypermobile
patient can be really slow to put on muscle bulk due to a complex interaction between
capsuloligamentous laxity, altered proprioceptive input and often altered muscle fiber type
combinations with less slow twitch muscle fibers (ref) (type IIC ??) (refs+)</li>
<li aria-level=”1″>Technique variation; such as avoiding putting heavier resistance at the distal end of the limb
(hand) which will stress proximal stability (i.e.: avoiding paddles in swimming, heavier
racquets in tennis)</li>
<li aria-level=”1″>Given hypermobiles have higher fatiguability levels than non-hypermobiles(Liaghat et al., 2018;
To, Strutton, & Alexander, 2019), extra consideration should be given to load management
and progression, especially once returning to sport after injury. For example , a contact athlete
should avoid tackling drills in training after a heavy weight lifting session in the gym
(see more in module X)</li>
</ul>
</li>
</ul>
</li>
</ul>

<hr />

3.7.2 Clinical Representation of the Hypermobile Patient

Subjectively; 
<ul>
<li style=”list-style-type: none;”>
<ul>
<li style=”list-style-type: none;”>
<ul>
<li style=”font-weight: 400;” aria-level=”1″>Patients are often unaware of their hypermobility, especially if they have an asymptomatic side.</li>
<li aria-level=”1″>Patient may report that they have always felt “loose” or “clunky” in their shoulder/s
but do not perceive this as an issue.</li>
<li aria-level=”1″>Patients have often avoided certain exercises in the gym. For example, they may not “ feel right”
with a bench press or overhead press if they have posterior translations.</li>
<li aria-level=”1″>Patients often present to a clinic with symptoms of rotator cuff overload, or acromioclavicular
joint pain which are secondary to the underlying uncontrolled HH translations.</li>
</ul>
</li>
</ul>
</li>
</ul>
Objectively: 
<ul>
<li style=”list-style-type: none;”>
<ul>
<li style=”list-style-type: none;”>
<ul>
<li>Increased inferior translation of the HH at rest – Sulcus Sign.</li>
<li>The sulcus test stresses the superior glenohumeral ligament and can be a test for inferior
instability or laxity(Tzannes & Murrell, 2002)</li>
<li>It was originally described by Neer and Foster as the quintessential sign for multidirectional
instability(Neer & Foster, 1980)</li>
<li>The test is performed at rest with the arm by the patient’s side. The elbow is grasped and pulled
inferiorly by the examiner.</li>
<li>The distance between the acromion and the HH is noted</li>
<li>It has been reported that a resting sulcus up to 1 cm is normal(Tzannes & Murrell, 2002)
(check figure) (video)</li>
<li>There is a lack of consensus in the literature on what criteria constitutes a positive sulcus test
(McFarland, Kim, Park, Neira, & Gutierrez, 2003) as some authors use the size of the sulcus to
diagnose multidirectional instability (> 2 cm) with no mention of symptom reproduction
(Tzannes & Murrell, 2002), while others(Warby et al., 2016; S. A. Warby et al., 2024) require
instability symptoms on testing (apprehension and/or muscle guarding) in addition to inferior
translation > 1 cm. This results in discrepancies in how many patients are diagnosed with MDI in
instability groups.(McFarland et al., 2003)</li>
<li>Given that laxity is asymptotic translation, our philosophy is that inferior instability should produce
symptomatic inferior translation.</li>
<li>Asymptomatic inferior laxity should still be noted on examination as it could pre-dispose to inferior
instability and hence MDI(Illyés & Kiss, 2006; Saccomanno et al., 2013).</li>
<li>An increased inferior translation in neutral rotation which is asymptomatic represents inferior laxity
(check figure with Dan) and is part of the presentation of a hypermobile shoulder</li>
<li>The sulcus test being performed in external rotation tests more the anterior superior capsuloligamentous
complex net translational control (video)</li>
<li>Whilst the test being performed in internal rotation tests more posterior superior capsuloligamentous
complex (video)</li>
<li>Anterior / Posterior draw tests in the adducted shoulder test for anterior and posterior laxity and
either may be increased in the hypermobile shoulder (video)</li>
<li>The hypermobile shoulder at rest often sits with the an anterior inferior position due to scapula
resting position which is often in depression + /- downward rotation +/- anterior tilt ( All below will need 
video shoot list or photo shoot list – Simon to sort )</li>
<li style=”font-weight: 400;” aria-level=”1″>But not all excessive HH translation is anterior!</li>
<li>It more common to have posterior inferior laxity vs anterior – 60% vs 40% (Panayiotou Charalambous,
2019; Warby et al., 2017)</li>
<li>While assessing resting position is important, given hypermobile and MDI patients typically
have aberrant motion patterns, it is important to look at active motion strategies.</li>
<li>Often these patients will have increased translation of the HH at the end of range in several
motions that can be anterior, inferior, posterior or all of the above.</li>
<li>In anterior -inferior hypermobility the HH will translate excessively anteriorly in abduction and ER
rotation combination at 90 ° elevation.</li>
<li>↑ Anterior translation of the HH – after 20 ° HE at 90° elevation (Simon please check this )</li>
<li>> 110° ER 90 ° ( Itoi personal communication – Simon please ref)</li>
<li>In posterior-inferior hypermobility the HH typically translates posteriorly in flexion, horizontal
flexion, internal rotation and combinations thereof. These translations often commence around 90 °
of shoulder flexion (especially if the patient is symptomatic ) but can also occur much later in range
with horizontal flexion at 160 ° elevation ( Itoi – Personal communication – Simon please ref)</li>
<li>Posterior HH translation is often missed due to a low level of clinical suspicion. Therapists
are more often trained to look for anterior rather than posterior HH translations.</li>
<li>Due to anatomical variations (such as increased glenoid retroversion) in hypermobile patients,
the HH is often off center posteriorly: articulating off the posterior glenoid.</li>
<li>In all categories of hypermobility there is often insufficient upward rotation of the scapula in later ranges
of elevation : especially the last 20°. It can appear that the scapula ceases upward rotation,
or the patient struggles and has to work harder to get into full elevation with a lag of upward
rotation of the scapula occurring</li>
<li>In association with poor scapula upward rotation, the HH often slides posterior-inferior at the end of
range of elevation due to failure of the scapula UR to keep the HH centered</li>
<li>This may be associated with clunking or clicking in the GHJ.</li>
<li>Shoulder findings are usually bilaterally as there is often similar anatomy or collagen make up in
both shoulders, though dysfunction may be more obvious on the symptomatic side.</li>
</ul>
</li>
</ul>
</li>
</ul>

<hr />

Clinical Examination of Instability

Before we look at examining for Instability there are a couple of questions that need to be discussed:

How much translation is normal in the GHJ and what is considered abnormal translation?

- - The GHJ naturally is quite lax with varying translations of the HH occurring within the glenoid
    depending on the motion being performed
  - Del Maso et al (ref) have estimated that a maximum of 7.5mm of upward translation of the HH
    may occur during range of motion movements
  - Traditional arthrokinematics models have determined the pattern of HH translation in varying
    GHJ motions:
  - Flexion > 55° HH slides anterior
  - Extension > 35° HH slides posterior
  - External rotation / HH slides posterior
  - Internal rotation / HH slides anterior
  - Abduction – superior translation(Saha, 1971)
  - Other authors have found that with active elevation of the arm the HH also goes anteriorly as well as
    superiorly(Wuelker, Schmotzer, Thren, & Korell, 1994)
  - In reality the translation of the HH and where it occurs will vary from individual to individual depending
    on several anatomical factors such as size & orientation of the glenoid, depth of the labrum and
    normal variation of the capsuloligamentous structures of the GHJ
  - Once pathology is superimposed, such as damage to the IGHL, normal translational patterns
    will alter. For example a study by Matsumara et al (2019), found that dysfunction of the anterior band
    of the IGHL caused decreased posterior (increased anterior), increased inferior and decreased
    medial translation of the HH during abduction and ER
  - Sarah not sure if can get some more information & figures in here

Can we clinically assess GHJ translation?

- - Clinically it has been found that therapists can reliably assess the HH position with arm by the side
    (adducted) for both anterior and inferior translation but Ultrasound scanning has much higher inter
    and intra rater reliability through greater ranges of motion ( Konieczka, 2017) (Double check this
    article in Journal of Hand Therapy please Sarah to get the actual figures or get Dan to help you
    with this)
  - More research is require to look at posterior translation
  - In looking at what is abnormal HH translation :
  - The average resting acromial humeral distance (AHD) is 1cm (Check with Dan) on ultrasound scan
  - Spanhove et al.,(2020) found that an increase in acromial humeral distance (AHD) or inferior
    translation of as little as 0.7mm was abnormal in MDI compared to controls
  - This is in line with the MDC values of 0.6mm found in a systematic review by Konieczka in 2017
  - Less research has been conducted around measuring the glenohumeral distance (GHD)-
    anterior or posterior position of the HH – under ultrasound and this is probably reflected in the lower
    inter and intra- rater reliability around this measure
  - New research underway by Dan Verdon (Melbourne Shoulder Group) will hopefully shed greater
    knowledge and date around this measure
  - Currently as it stands the MDC for GHD to be considered to be significant is 1.7mm (Konieczka 2017)
    (Sarah please check with D)

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Module 1: Glenohumeral Joint Instability – Patho-anatomy, Diagnosis and Clinical Management Pathways

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