Study Group – the shoulder non-pathology DD’s
The shoulder – Non- pathology Differential Diagnosises
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1010712/pdf/westjmed00198-0104a.pdf
http://www.shoulderdoc.co.uk/article.asp?article=760&section=497
The study concluded that "the best test" was a combination of tests. For the diagnosis of
impingement disease the best combination of tests were a positive: Hawkins-Kennedy impingement
sign, a positive painful arc sign, and weakness in external rotation with the arm at the side.
J Bone Joint Surg Am. 2005 Jul;87(7):1446-55.
Diagnostic accuracy of clinical tests for the different degrees of subacromial impingement syndrome.
Park HB, Yokota A, Gill HS, El Rassi G, McFarland EG.
Supraspinatus tendinitis
Patient presents with a vague history of anterior shoulder region pain, no clear reason as to when,
why, and how it occurred. May be a direct blow, lifting without extending the upper body. May be
caused by fatigue or overuse.
Painful arc may be demonstrated, may be tender to palpate. Limited active range of abduction,
weakness, pain on active resisted or eccentric loading – or may be apprehension.
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Study Group – the shoulder non-pathology DD’s
Painful arc is 60 degrees > 90 degrees going up or coming down – it is during this movement that the
greater tuberosity passes under the acromion and the coracoacromial ligament. The greater
tuberosity needs to be externally rotated on abduction.
Rotator cuff tear
Cuff tears have a increasing tendency with age. It is usually related to ischaemia, and degeneration.
Two types; acute (trauma) chronic (degenerative). Acute are associated with sudden traumatic
incidents whereas chronic are associated with altered biomechanics / muscle imbalances. Poor
blood supply is also associated with chronic should injuries. Acute injuries are less common than
chronic shoulder issues.
Acute tear may be after a weight lifting competition lifting weight above head. Tear can develop
from tendinitis
To diagnose a full-thickness rotator cuff tear, the best combination of tests, when all three are
positive: were the painful arc, the drop-arm sign, and weakness in external rotation.
Biceps tendon / transverse lig
Yergasons test: Yergason's was designed to assess for pathology in the long head of biceps tendon in
its sheath.
Test
The patient's elbow is flexed and their forearm pronated. The examiner holds their arm at the wrist.
Patient actively supinates against resistance.
Positive
Pain located to bicipital groove area suggests pathology in the long head of biceps in its sheath.
Research
Holtby and Razmjou performed a prospective blinded study of 152 consecutive patients with a wide
spectrum of shoulder problems. The validity of the Yergason's and Speed's tests was evaluated
against fmdings at surgery. Surgical fmdings included bicipital tendonitis, 10 biceps partial tears and
2 complete ruptures. 15 patients had SLAP lesions.
Sensitivity
Specificity
PPV
NPV
Yergason's
43%
79%
60%
65%
Speed's
32%
75%
50%
58%
The authors concluded that clinicians should understand that clinical examination tests do not
perform consistently and have variable predictive values in different patient populations and
settings.
Speeds Test
Jo Gibson
Speed's test was originally designed to assess for pathology of the long head of biceps in its groove
but has also been utilised in the assessment for SLAP lesions.
Test
The patient's elbow is extended, forearm supinated and the humerus elevated to 60°. The examiner
resists humeral forward flexion.
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Study Group – the shoulder non-pathology DD’s
Positive
Pain located to bicipital groove. This is commonly interpreted as suggestive of inflammation or
lesions related to the long head of biceps or biceps/labral complex.
Research
Bennett's prospective study of all patients who presented with shoulder pain between Oct 1 sI 1994
- February 28 1995 correlated the clinical results of the Speed's test with biceps/labral pathology by
direct arthroscopic visualisation.
46 shoulders in 45 patients were operated on during this time. Speed's test was positive in 40
shoulders. Biceps/labral pathology was present in 10 of these patients.
He concluded that the Speed's test is a non-specific but sensitive test for macroscopic biceps/labral
pathology. However it is positive with a various number of other shoulder pathologies.
Specificity
Sensitivity
PPV
NPV
13.8%
90%
23%
83%
Superior Labral Antero-Posterior lesion - Abbreviated term for an injury to the superior labrum of
the glenoid.
The labrum is a firm, white structure that forms a ring around the glenoid cavity (the cup of the ball
and socket shoulder joint). It deepens the socket, providing stability to the joint.
bone of the upper arm - connecting the shoulder to the elbow
'key-hole' surgery. Surgery performed via small incisions, using special instruments and a viewing
scope..
OBriens Test
O'Brien's active compression test was primarily developed for assessment of Acromioclavicular joint
pathology following a patient's demonstration of what reproduced their shoulder pain. O'Brien
noted in a series of patients it was also excellent for detecting labral pathology.
Test
The patient is instructed to flex their arm to 90° with the elbow fully extended and then adduct the
arm 10-15°medial to sagittal plane. The arm is then maximally internally rotated and the patient
resists the examiner's downward force. The procedure is repeated in supination. The O'Brien Test is
designed to maximally load and compress the ACJ and superior labrum. For maximal results the
authors stress that the patient should resist the examiner's downward force rather than the
examiner resisting forward flexion.
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Study Group – the shoulder non-pathology DD’s
Positive
Pain elicited by the fIrst manoeuvre is reduced or eliminated by second.
ACJ pain =ACJ
Pain or clicking deep in the GHJ = labral
Arthroscopy revealed that the test position (90° forward flexion, 10-15° adduction and maximum
internal rotation) displaces the biceps tendon medially and inferiorly therefore putting tension on
the bicipitallabral complex. A secondary shear is created in the glenoid and labrum. In an unstable
SLAP lesion tension from the biceps tendon from this shear, compression from capsular windup, or
both creates an internal mechanical derangement and displacement that accounts for the painful
clicking that patients experience. For a positive test the patient MUST report a significant decrease in
symptomology in the supination test position. Cadaver studies (Parentis et al 2004) have clarified
contact between the lesser tuberosity, subscapularis tendon and superior aspect of the glenoid and
labrum in the internally rotated position.
Cadaver studies examined the anatomical basis of the ACJ component of the test. They revealed that
the highest compressive pressure was generated in the test position. The greater tuberosity elevates
the relatively depressed acromion and locks and loads the ACJ. Full supination relaxed the joint by
virtue of the greater tuberosity moving out of the way.
The following results are based on O'Brien's prospective study of 268 patients.
Sensitivity
Specificity
NPV
labral
100%
98.5%
100%
ACJ
100%
96.6%
100%
PMR
Several sets of criteria for diagnosing polymyalgia rheumatica have been proposed, principally to aid
research by ensuring uniformity within trials and to allow comparison of results from different
studies. However, the criteria have also been used for clinical purposes.
One report examined the performance of individual criteria and sets of criteria for making a
diagnosis of polymyalgia rheumatica . The set of criteria proposed was found to be most useful
(sensitivity 92%, specificity 80%, likelihood ratio 5).
Polymyalgia rheumatica is diagnosed by the Bird criteria if three or more of the following are
present:
Bilateral shoulder pain or stiffness.
Onset of illness less than 2 weeks previously.
Initial erythrocyte sedimentation rate (ESR) greater than 40 mm per hour.
Morning stiffness lasting longer than an hour.
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Study Group – the shoulder non-pathology DD’s
65 years of age or more.
Depression and/or weight loss.
Bilateral tenderness in the upper arms.
Diagnostic criteria drafted at the Third International Conference on Polymyalgia Rheumatica and
Giant Cell Arteritis (July 2005) have also been published, and are currently being tested in a clinical
trial.
Symptoms

Onset — the onset of polymyalgia rheumatica is usually rapid, but may be insidious. However,
symptoms may have been present for weeks or months before the diagnosis is made .

Muscle pain — shoulder pain is the presenting feature in 70–95% of people, with the hips and
neck being less frequently involved (50–70%). The pain usually radiates distally towards the
elbows and knees. It can begin in one shoulder or hip but soon becomes bilateral. Pain is more
severe with movement and interferes with sleep at night.

Stiffness — stiffness after periods of rest, and morning stiffness of more than 45 minutes are
typical. The stiffness may be so profound that the person may have great difficulty turning over in
bed, rising from a bed or a chair, or raising their arms above shoulder height (for example to comb
their hair).

Low-grade fever, fatigue, anorexia, weight loss, and depression (systemic symptoms) occur in up
to 40% of people.

Headache, scalp tenderness, and visual disturbances, (symptoms indicative of giant cell arteritis)
may be present in 10–20% of people with polymyalgia rheumatica.
o
For more information see the section on Symptoms in the PRODIGY topic on Giant cell arteritis.
Signs

Bilateral upper arm tenderness is sometimes present. Shoulder abduction is often uncomfortable
and may be limited by pain.

Muscle strength is not usually impaired, but muscle pain may make testing difficult. If symptoms
are protracted, disuse atrophy of muscle can occur, leading to muscle weakness.

Peripheral musculoskeletal signs are seen in approximately 50% of people. They include:
o
Carpal tunnel syndrome.
o
Peripheral arthritis (predominantly affecting the knees and wrists), which is asymmetric, nonerosive, and self-limiting.
o

Swelling with pitting oedema of hands, wrists, feet, and ankles.
Scalp tenderness and visibly thickened and tender temporal arteries are signs indicative of giant
cell arteritis, and may be present in 10–20% of people with polymyalgia rheumatica.
o
For more information see the section on Signs in the PRODIGY topic on Giant cell arteritis.
Burner / Stinger
Burners and stingers are common injuries in contact or collision sports. A burner or a stinger is an
injury to the nerve supply of the upper arm, either at the neck or shoulder. The injury is named for
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Study Group – the shoulder non-pathology DD’s
the stinging or burning pain that spreads from the shoulder to the hand. This can feel like an electric
shock or lightening bolt down the arm.
In most cases, burners and stingers are temporary and symptoms quickly go away.
Symptoms
Burner and stinger symptoms typically occur in one arm only. They usually last seconds to minutes,
but in 5% to 10 % of cases, they can last hours, days, or even longer. The most common symptoms of
a burner or stinger include:
 A burning or electric shock sensation
 Arm numbness and weakness immediately following the injury
 A warm sensation
Neck related
Cervical facet / axillary post dislocation / C4 / C5 neuropathy – disc, stenosis, lig flavum, osteophyte
Scapulocostal
2:1 ration of humerous to scapular during abduction
For every 15 degrees og abduction – 10 degrees at humorous and 5 degrees @ scapular. = 90
degrees of humerus abduction = 60 degrees of scapular movement.
Winging and hitching – importance of serratus anterior
Initial 20-30 degrees of abduction of humerous should be without scapular movement.
AC disease
Osteoarthritis Ligament damage
Gleno-humeral disease
RA / septic
Calcific tendinitis
Calcium crystals are often deposited in the tendon. Usually present in people over 35. Associated
with periods of compression and traction, hyperemia of the critical zone and ischaemia. Calcium
deposit greater than 1.5cm in diameter will cause pain. On active ROM the calcium deposit acts as a
mechanical obstacle to abduction and elevation.
Presents as a chronic aching aggravated by flexion, abduction and external rotation
Bursitis: subdeltoid / subacromial
Usually rare. Lack when, how and why. Can come about from abnormal strain on joint, normal strain
on abnormal joint, poor joint performance
Subluxation / dislocation
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Study Group – the shoulder non-pathology DD’s
Often a progression of instability > usually anterior displacement > forced abduction with external
rotation or fall onto shoulder > acromion appears more prominent >
Impingement syndrome
Painful arc, swimmers shoulder, lifters shoulder, tennis shoulder.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3395987/
Subacromial space is defined by the humeral head inferiorly, the anterior edge and under surface of
the anterior third of the acromion, coracoacromial ligament and the acromioclav-icular joint
superiorly. The height of space between acromion and humeral head ranges from 1.0 to 1.5
centimeters as seen on radiographs. Interposed between these two osseous structures are the
rotator cuff tendons, the long head of the biceps tendon, the bursa, and the coracoacromial
ligament. Any abnormality that disturbs the relationship of these subacromial structures may lead to
impingement
Structures under the acromial arch become irritated – subacromial bursa, supraspinatus tendon, GH
capsule. Irritation / inflammation condition. Larger buttress of the greater tuberosity impacts.
Thickening or calcification of the coracoacromial ligament can also cause impingement. Tests: neers
hawkins, painful arc. . For the diagnosis of impingement disease the best combination of tests were
a positive: Hawkins-Kennedy impingement sign, a positive painful arc sign, and weakness in external
rotation with the arm at the side.
Subacromial impingement syndrome (SAIS) is the most common disorder of shoulder, accounting for
44–65% of all complaints of shoulder pain during a physician's office visit.1 SAIS encompasses a
spectrum of subacromial space pathologies including partial thickness rotator cuff tears, rotator cuff
tendinosis, calcific tendinitis, and subacromial bursitis. The main consequences of SAIS are functional
loss and disability.
Neer described three stages of impingement.4 Stage-I impingement is characterized by edema and
hemorrhage of the subacromial bursa and cuff. It is typically found in patients who are less than
twenty-five years old. Stage-II impingement represents irreversible changes, such as fibrosis and
tendinitis of the rotator cuff, and is typically found in patients who are twenty-five to forty years old.
Stage-III impingement is marked by more chronic changes, such as partial or complete tears of the
rotator cuff, and usually is seen in patients who are more than forty years old.
Translation of the humeral head in the magnitude of 1–3 mm in the superior direction occurs in the
first 30–60° of active glenohumeral scapular plane elevation.
Superior humeral translation that occurs during the initial phase of elevation appears to be due in
part to the cranially directed pull on the head of the humerus by the deltoid muscle
SAIS is an encroachment of the subacromial tissues as a result of narrowing of the subacromial
space. Mechanisms of rotator cuff (RC) tendinopathy have been classically described as extrinsic,
intrinsic or a combination of both. Intrinsic impingement, theorizes that partial or full thickness
tendon tears occur as a result of the degenerative process that occurs over time with overuse,
tension overload, or trauma of the tendons.5 An alternative theory is that of extrinsic impingement,
where inflammation and degeneration of the tendon occur as a result of mechanical compression by
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Study Group – the shoulder non-pathology DD’s
structures external to the tendon.4 A unique subset of extrinsic impingement, internal impingement
occurs due to compression of the articular side rather than the bursal side of the RC tendons,
between the posterior superior glenoid rim and humerus when the arm is in full external rotation,
abduction, and extension. Although internal impingement can be considered an extrinsic
mechanism, narrowing of the subacromial space is not a hallmark finding.12
Extrinsic Impingement
Extrinsic mechanisms of RC tendinopathy that result in bursal sided RC tendon compression due to
narrowing of the subacromial space include anatomical factors, biomechanical factors, or a
combination. The acromiohumeral distance (AHD), a linear measure between the acromion and the
humeral head used to quantify the subacromial space, has been studied in patients with RC disease
using magnetic resonance imaging,13 ultrasonography,14 and radiographs.13 AHD is normally between
7 and 14 mm in healthy shoulders. It is reduced in SAIS patients with the muscles at rest or during
muscle activation which functionally narrow the subacromial space. Furthermore, AHD less than 7
mm with the arm at rest is a predictive indicator of less favorable surgical outcome.15
Biomechanical mechanism of extrinsic SAIS is based on dynamic narrowing of the subacromial space
leading to RC tendon compression secondary to superior translation of the humeral head or
aberrant scapular motion that causes the acromion to move inferiorly. These include shortening of
the posterior-inferior glenohumeral joint capsule and decreased RC muscle performance
Posterior capsule
Posterior capsular tightness may cause changes in glenohumeral kinematics leading to SAIS. When
posterior capsular tightness was surgically induced in cadavers, there was an in increase in superior
and anterior humeral head translations during passive glenohumeral flexion. Excessive superior and
anterior humeral head translations can decrease the size of the subacromial space, leading to
increased mechanical compression of the subacromial structures.9 Glenohumeral internal rotation
range of motion and horizontal adduction at 90° of elevation are reliable clinical measures that
potentially assess posterior capsule length. Furthermore, stretching to address impairments of
posterior shoulder tightness has been identified as an important component to rehabilitation for
patients with RC tendinopathy.17
Scapular musculature
Aberrant scapular muscle activity has been identified in patients with SAIS and been directly linked
to abnormal scapular kinematics. Of particular interest are the relative contributions of the upper
and lower serratus anterior muscles and trapezius muscles, found to stabilize the scapula and induce
scapular upward rotation, external rotation, and/or posterior tilt to potentially allow the humeral
head to clear the acromion with elevation.18 These individuals have decreased muscle performance
of the trapezius and serratus anterior in terms of force output,19 muscle balance/ ratios,19
electromyographical activity,18 and latencies in activation.20
Relatively small changes in the muscle performance of the scapulothoracic muscles can alter the
position of the scapula at a fixed angle of humeral elevation and, in theory, affect the length-tension
relationship (point on the length-tension curve) of the RC muscles and the subacromial space.12
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Study Group – the shoulder non-pathology DD’s
Spine
A relatively small increase in thoracic spine flexion has resulted in a more elevated and anteriorly
tilted scapula at rest, and less upward rotation and posterior tilt during glenohumeral elevation. An
increase in thoracic spine flexion has also resulted in a decrease in the amount of elevation of the
glenohumeral joint and a decrease in the amount of force generated at 90° of glenohumeral
scapular plane abduction.21
Rotator cuff musculature
The supraspinatus along with the other rotator cuff muscles of teres minor, infraspinatus, and
subscapularis serve to maintain the congruent contact between the humeral head and the glenoid
fossa by producing a compressive force during glenohumeral movements.5 Weakness or
dysfunctional rotator cuff musculature can lead to changes in glenohumeral and scapulothoracic
kinematics. Excessive superior translation of the humeral head resulting from rotator cuff weakness
can lead to a decrease in the subacromial space during elevation, and thus increased mechanical
compression of the subacromial contents.22
Clinical Evaluation
History
Although impingement symptoms may arise following trauma, the pain more typically develops
insidiously over a period of weeks to months. The pain is typically localized to the anterolateral
acromion and frequently radiates to the lateral mid-humerus. Patients usually complain of pain at
night, exacerbated by lying on the involved shoulder, or sleeping with the arm overhead. Normal
daily activities such as combing one's hair or reaching up into a cupboard become painful. Weakness
and stiffness may also be encountered, but they are usually secondary to pain.2
Physical examination
In their systematic analysis, Papadonikolakis et al.23 concluded that the physical findings used to
diagnose the impingement syndrome, i.e., the Neer sign (pain on forced flexion), the Hawkins sign
(pain on internal rotation with the arm elevated to 90_), and the Neer injection test (relief of pain on
the Neer sign after subacromial injection of local anesthetic) may be sensitive, but are not specific.
The average sensitivity (and standard deviation) of the Neer sign was 76±11%, while the average
specificity was 36±22%. The respective values for the Hawkins sign were 80±11% and 41±19%. In
their meta-analysis, Hegedus et al.24 concluded that neither the Neer nor the Hawkins sign had
diagnostic utility for impingement.
INTERESTINGLY – if the supraspinatus muscle has ruptured or has decreased in activity the 1cm space
sub-acromial space will decrease by as much as 50%, due to the unopposed pull of the deltoid.
Changes in microvascular supply – possible ringing out mechanism > avascular zone . repeated
microtrauma may lead to odema / and increased tissue volume.
WEAK ROTATOR CUFF ALLOWS FOR THE HUMERAL HEAD TO RIDE UP.
Erbs / klumpkes
Erbs palsy:
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Study Group – the shoulder non-pathology DD’s
Brachial plexus stretch / clavicle fracture – neuronotomy!
Nerve effected: musculocutaneous, suprascapular, axillary
The signs of Erb's Palsy include loss of sensation in the arm and paralysis and atrophy of the deltoid,
biceps, and brachialis muscles.[8] "The position of the limb, under such conditions, is characteristic:
the arm hangs by the side and is rotated medially; the forearm is extended and pronated. The arm
cannot be raised from the side; all power of flexion of the elbow is lost, as is also supination of the
forearm".[6] The resulting biceps damage is the main cause of this classic physical position commonly
called "waiter's tip."
Klumpke:
Symptoms include claw hand, paralysis of intrinsic hand muscles, and ulnar nerve distribution
numbness. Involvement of T1 may result in Horner's syndrome, with ptosis, and miosis
Usually C8 T1 effected.
The subsequent paralysis affects, principally, the intrinsic muscles of the hand (notably the
interossei, thenar and hypothenar muscles)[10] and the flexors of the wrist and fingers (notably flexor
carpi ulnaris and flexor digitorum).[1][6][10][11] Forearm pronators and wrist flexors may be involved, as
may dilators of the iris and elevators of the eyelid (both of which may be seen in the case of
associated Horner's Syndrome). The classic presentation of Klumpke's palsy is the “claw hand”
where the forearm is supinated and the wrist and fingers are flexed. If Horner syndrome is present,
there is miosis (constriction of the pupils) in the affected eye.
Adhesive capsulitis
MRI can be used to show characteristic findings in diagnosing AC. Thickening of the CHL and the
capsule at the rotator cuff interval and complete obliteration of the fat triangle under the coracoid
process have been shown to be the most characteristic MR findings seen with AC.
Risk factors
It is not fully understood why frozen shoulder occurs and, in some cases, it is not possible to identify
a cause. However, a number of things can increase your risk of developing it. These are outlined
below.
Shoulder injury or surgery
Frozen shoulder can sometimes develop after a shoulder or arm injury, such as a fracture, or after
having surgery to your shoulder area.
This may partly be a result of keeping your arm and shoulder immobile (still) for long periods of time
during your recovery. Your shoulder capsule may tighten up due to a lack of use.
For this reason, it is very important you do not ignore a painful shoulder injury and always seek
medical advice.
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Study Group – the shoulder non-pathology DD’s
Diabetes
If you have diabetes, your risk of developing a frozen shoulder is increased. The exact reason for this
is unknown.
It is estimated that people with diabetes are twice as likely to develop a frozen shoulder compared
with those who do not have diabetes.
If you have diabetes, your frozen shoulder symptoms are likely to be more severe. You are also more
likely to develop the condition in both shoulders.
Other health conditions
Your risk of developing a frozen shoulder may also be increased if you have other health conditions
including:






Dupuytren's contracture - where small lumps of thickened tissue form in the hand, causing
the fingers to bend into the palm of the hand
heart disease
stroke
lung disease
thyroid disease
breast cancer
Other shoulder conditions
Frozen shoulder can also sometimes develop in association with other shoulder conditions such as:


calcific tendonitis - where small amounts of calcium are deposited in the tendons of the
shoulder
rotator cuff tear - the rotator cuff is a group of muscles that control shoulder movements
Immobility
Not moving for long periods of time is another risk factor for frozen shoulder. This can sometimes
occur if you have to spend time in hospital - for example, after having a stroke or a car accident.
Stages of frozen shoulder
The symptoms of a frozen shoulder usually progress gradually over a number of months or years.
There are three separate stages to the condition (see below), which can sometimes be difficult to
distinguish. The symptoms may also vary greatly from person to person.
Stage one
During stage one, often referred to as the 'freezing' phase, your shoulder will start to ache and
become very painful when reaching.
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Study Group – the shoulder non-pathology DD’s
The pain is often worse at night and when you lie on the affected side. This stage may last 2-9
months.
Stage two
Stage two is often known as the 'frozen' phase. Your shoulder may become increasingly stiff, but the
pain does not usually get worse and may decrease.
Your shoulder muscles may start to waste away slightly because they are not being used. This stage
lasts 4-12 months.
Stage three
Stage three is the 'thawing' phase. During this period, you will gradually regain some movement in
your shoulder. The pain will begin to fade, although it may recur from time to time as the stiffness
eases.
Although you may not regain full movement of your shoulder, you will be able to carry out many
more tasks. Stage three can last from five months to many years.
Physical exam: Pain during range of motion may be the only physical finding. Passive and active
glenohumeral motions are decreased, often accompanied by pain and associated muscle spasms.
Usually moving the arm away from the body (abduction) and outward (external) rotation are most
severely affected. Motion between the scapula and the chest wall (scapulothoracic motion) is not
affected by this condition. Diagnostic criteria include loss of 30° of external rotation and less than
130° of flexion (both actively and passively). Tenderness that is often generalized rather than
localized usually is noted about the rotator cuff. Physical examination may include assessment of
signs of illness or injury.
Ligament sprain – A/C – C/C
Trigger point
12