There are four (4) main
types of shoulder impingement syndrome that have been identified
1) Primary Impingement
2) Secondary Impingement
3) Subcoracoid Impingement/Stenosis
TUFFs (Tensile Under-Surface Fiber Failure) Lesion
4) Internal (Glenoid) Impingement
Posterior-Superior Glenoid Impingement (PSGI)
It is imperative that the
shoulder diagnosis be as specific as possible. Each specific type of impingement
syndrome requires its own type of treatment, rehabilitations and/or surgical
The History of Impingement Syndrome
By definition shoulder impingement syndrome was considered,
Subacromial outlet obstruction resulting in irritation of the supraspinatus
tendon. In other words the supraspinatus tendon of the rotator cuff (RTC) would
be pinched against the undersurface of the acromion portion of the scapula
during elevation of the arm overhead.
The concept was attributed to Charles Neer, MD, in 1972
Neer Classified and named the disorder of shoulder impingement. He also
gave structure to the diagnostic process.
Neer, JBJS(A) 1972
However the process itself was first described but not named by
Meyer as early as 1931.
Meyer AW JBJS 1931;13:341-348
Meyer AW Arch Surg
The Neer Classification of
Impingement Syndrome is listed below. Although this classification was an
important step in understanding shoulder pathology for its time, it is now
Neer Classification of Shoulder Impingement
Type I: <25 years old, Reversible,
swelling, tendonitis, no tears, conservative treatment
Type II: 25-40
years old, Permanent scarring, tendonitis, no tears, SAD
Type III: >40
years old, Small RTC tear, SAD with debridement/repair
Type IV: >40
years old, Large RTC tear, SAD with repair
Current classification of shoulder
or external-Subacromial impingement is the closest thing to Neers original
description of shoulder impingement syndrome.
area of the RTC that is torn or irritated in primary impingement is typically
the superior or bursal side of the RTC. This is referred to as
Extra-articular RTC pathology. This means the source of pathology is outside
of the glenohumeral joint itself and confined to the Subacromial space.
These patients are typically older than 50 years of age (age is a poor
criteria for diagnosis. There can be significant overlap of disease processes
between age populations) although it is not uncommon to see this type of
impingement in patients as young as 22.
Age can be a good place to START suspicions however. In an older patient
population degenerative processes are higher on the list than in younger
patients. Patients generally experience pain in the anterior or front of the
shoulder during overhand activities. They may experience pain at night when they
roll onto that shoulder.
This may be due to the pathologic changes in the coracoacromial arch
(e.g. acromial and AC joint spurs, bursal scarring). This is most common in the
Consequence of the aging process
Mechanical compromise of the subacromial space
DJD AC joint
Rotator cuff atrophy
Rotator cuff/scapular weakness (poor posture)
Increased thoracic kyphosis
4) Because primary
impingement is usually do to degenerative changes and spurring in the joint area
X-rays are mandatory if primary impingement is suspected. Patients should
request them and doctors should expect them!
The shape of the acromion
process of the scapula or shoulder blade plays an important role in recovery and
treatment from primary impingement. Types I and II usually recover with
conservative care while congenital types IIIs may or may not recover without
surgery. Degenerative type IIIs absolutely require surgical debridement before
the spur causes a RTC tear and the need for a RTC repair. Patients who undergo
debridement without repair do much better post operatively. Patients who undergo
debridement with repair do not do as well.
A description of the
acromion types and incidence of impingement is listed below:
Flat acromion low incidence of impingement
Curved acromion higher incidence of
Beaked acromion very high incidence
- May be a genetic
- May be degenerative in
nature (previous Type II that has degenerated)
by definition implies that there is a problem with keeping the humeral head
centered in the glenoid fossa during movement of the arm. Generally is caused by
weakness in the RTC muscles (functional instability) combined with a
glenohumeral joint capsule and ligaments that are to loose (micro-instability).
The impingement generally
occurs at the coracoacromial space secondary to anterior translation of the
humeral head as opposed to the Subacromial space that is seen in primary
Tearing of the RTC is again
Extra-articular however intra-articular tearing is also seen in these patients.
Patients are typically
younger and the pain is located in the anterior or anterolateral aspect of the
shoulder. The symptoms are usually activity specific and involve overhand
It is important to treat
the underlying micro-instability in patients with secondary impingement.
Arroyo et al, Orth Cl North Am 1997
Kvitne et al, Clin Orthop
Jobes Instability Continuum
RTC weakness generally occurs first.
Functional instability follows prolonged RTC weakness.
3. Capsular laxity, which
develops (acquired) or becomes prominent
(preexisting congenital laxity).
Subluxation (inability of the humeral head to center in the glenoid during
RTC/Labral tearing (late stage disease of secondary impingement).
Internal Glenoid Impingement
Internal Glenoid Impingement is probably the most common cause of posterior
shoulder pain (pain in the back of the shoulder) in the throwing or overhead
It is commonly misdiagnosed as rotator cuff (RTC) tendonitis.
is also called posterior-superior glenoid impingement or PSGI for short.
Jobe, Arthro 1995
PSGI is caused by the impingement of the articular surface
(intra-articular) of the RTC (posterior edge of the supraspinatus and the
anterior edge of the infraspinatus) against the posterior-superior-glenoid and
It mainly seen in overhead athletes but occurs at an alarming rate in weight
lifters do to poor lifting technique (and
utilize high-risk exercises) and patients
involved in occupational overhand activities such as mechanics, electricians,
stocking shelves, or steering tow motors,
The mechanism of injury is shoulder extension, abduction and ER mechanism. This
is the exact mechanism the arm is in when you try and throw a ball overhand.
Orth Clin North Am 1997
d. Humeral retro-version (the bone structure of the humerus is developed
rotated back into external rotation as an adaptation to repetitive throwing) may
be present as an underlying etiology to reduced Internal rotation.
1. Riand, et al. results of derotational humeral osteotomy in posterior-superior
glenoid impingement. Am J Sports Med 1998; 26:454
2. Davidson PA, et al. Rotator cuff and posterior-superior glenoid labrum injury
associated with increased glenohumeral motion: A new site of impingement. J
Shoulder Elbow Surg 1995;4:384-390.
Instability as a cause of PSGI
The glenohumeral joint (GHJ) is dependant on the RTC to provide dynamic
stability during high velocity movements such as throwing.
Throwing also requires excessive ROM, especially external rotation. It is
this excess ROM that predisposes the GHJ to instability.
Chronic repetitive eccentric loads on the subscapularis muscle (the RTC muscle
that is on the front of the shoulder) during the cocking motion lead to
micro-trauma and weakness.
Loss of the subscapularis force couple leads to anterior instability and
hyper-angulation of the humerus in relationship to the scapula (shoulder blade).
This may happen prior to symptom onset in the throwing shoulder.
Buchberger, MSSE 1999, 31:S26
Scapular Dyskinesia causes glenoid ante-version and also increases the
hyper-angulation of the humerus in
relationship to the scapula
Subtle anterior instability (micro-instability) of the GHJ is accentuated in the
presence of scapular dyskinesia.
Symptom history and patient presentation
Posterior shoulder pain in the throwing shoulder during the cocking phase
Posterior shoulder pain during the cocking phase that worsens
during early acceleration is by itself an indication that the
subscapularis is eccentrically weak and/or scapular dyskinesia is present.
Slow insidious onset; no history of trauma
Pain is primarily associated with the athletic activity
5. Pitching mechanics
should be evaluated for faults in the balance leg and plant leg. Usually there
is weakness of the gluteus maximus and gluteus medius.
Buchberger JSCR 2000
Stages of Internal Glenoid Impingement
Internal Glenoid Impingement
Stiffness; slow to warm up
a. 2 weeks of throwing
b. Strengthen cuff muscles
c. Strengthen scapular rotators
Stage II: Internal Glenoid Impingement
a. Posterior shoulder pain
b. Positive Jobes relocation test
Indicates anterior instability as etiology
a. 4-12 weeks of an interval throwing
b. Rehabilitation program
Stage III: Internal Glenoid Impingement
a. Posterior shoulder pain
b. Positive Jobes relocation test
c. Failure of an appropriate rehabilitation program
a. Anterior capsulo-labral reconstruction
Thermal Capsulorraphy (TACS-Thermal Assisted Capsular Shrinkage)
Jobe CM, OCNA, 1997
Interval between the tip of the coracoid and the humeral head (the coracohumeral
Narrowing of the Subcoracoid space with a coracohumeral interval of less than
6mm. Subcoracoid stenosis may not be pathologic or symptomatic.
Impingement of the coracoid process against the humerus (usually the lesser
tuberosity) in a coracoid impingement position (humerus is flexed, adducted and
Subcoracoid impingement may cause undersurface Subscapularis tears via the
Roller-Wringer Effect. This is caused by the bowstringing of the
Subscapularis across the prominent coracoid process.
The Coracoid process causes an indenting of the superficial surface of the upper
Subscapularis tendon while stretching (tensile loading) of the deep surface of
the Subscapularis. This leads to a TUFFs (Tensile under surface fiber
failure) lesion or an articular side tearing (inside the joint) of the
Intrinsic tendon degeneration may also be an
important etiologic factor in tears of the Subscapularis tendon. If the tendon
degenerates do to overuse or disuse it will be susceptible to tearing.
Patients will have anterior shoulder pain with
coracoid tenderness especially on flexion, adduction and internal rotation
(Hawkins Impingement sign). The pain is characterized as deep inside and medial
to the coracoacromial ligament. Instability signs such as the Jobe relocation
maneuver are usually absent.
This is usually resistant to conservative care
and surgical treatment is usually warranted.
Surgical treatment involves a coracoplasty
(removing a portion of the coracoid process) with debridement or repair of the
Lo and Burkhart,