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   Impingement Syndromes: Subtypes

There are four (4) main types of “shoulder impingement syndrome” that have been identified today:

1) Primary Impingement

2) Secondary Impingement

3) Subcoracoid Impingement/Stenosis

a. TUFF’s (Tensile Under-Surface Fiber Failure) Lesion

4) Internal (Glenoid) Impingement

a. Posterior-Superior Glenoid Impingement (PSGI)

It is imperative that the shoulder diagnosis be as specific as possible. Each specific type of impingement syndrome requires it’s own type of treatment, rehabilitations and/or surgical procedure.

The History of Impingement Syndrome

1)     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.

2)     The concept was attributed to Charles Neer, MD, in 1972

3)     Neer Classified and named the disorder of shoulder impingement. He also gave structure to the diagnostic process.

Neer, JBJS(A) 1972

4)     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 1937;35:646-674.

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 Although this classification was an important step in understanding shoulder pathology for its time, it is now outdated.

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 impingement syndromes

Primary impingement

Primary impingement or external-Subacromial impingement is the closest thing to Neer’s original description of shoulder impingement syndrome.

The 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.

Andrews, 1994

1)     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.

2)     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.

3)     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 industrial population.

a.      Consequence of the aging process

b.      Mechanical compromise of the subacromial space

c.      DJD AC joint

d.      Subacromial spurring

e.      Rotator cuff atrophy

f.        Rotator cuff/scapular weakness (poor posture)

g.      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 III’s may or may not recover without surgery. Degenerative type III’s 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:

Acromial Morphology

Type I: Flat acromion low incidence of impingement

Type II: Curved acromion higher incidence of impingement

Type III: Beaked acromion very high incidence of impingement

1. May be a genetic anatomical variant
2. May be degenerative in nature (previous Type II that has degenerated)

Secondary Impingement

Secondary Impingement 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 impingement.

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 activities.

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 1993

Below is an example of the cascade of events that Dr. Frank Jobe first put together to explain secondary impingement.

Jobe’s Instability Continuum

1. RTC weakness generally occurs first.

2. Functional instability follows prolonged RTC weakness.

3. Capsular laxity, which develops (acquired) or becomes prominent      (preexisting congenital laxity).

4. Subluxation (inability of the humeral head to center in the glenoid during motion).

5. RTC/Labral tearing (late stage disease of secondary impingement).

Internal Glenoid Impingement

Introduction

1. 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 athlete

2. It is commonly misdiagnosed as rotator cuff (RTC) tendonitis.

3. It is also called posterior-superior glenoid impingement or PSGI for short.

                                    Jobe, Arthro 1995

a.      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 glenoid labrum

b. 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, etc.

c. 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.

                           Arroyo, 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

1. The glenohumeral joint (GHJ) is dependant on the RTC to provide dynamic stability during high velocity movements such as throwing.

2. Throwing also requires excessive ROM, especially external rotation. It is this excess ROM that predisposes the GHJ to instability.

3. 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.

4. Loss of the subscapularis force couple leads to anterior instability and hyper-angulation of the humerus in relationship to the scapula (shoulder blade).

5. This may happen prior to symptom onset in the throwing shoulder.

                                        Buchberger, MSSE 1999, 31:S26

6. Scapular Dyskinesia causes glenoid ante-version and also increases the hyper-angulation of the humerus in relationship to the scapula

7. Subtle anterior instability (micro-instability) of the GHJ is accentuated in the presence of scapular dyskinesia.

Symptom history and patient presentation

1. Posterior shoulder pain in the throwing shoulder during the cocking phase

2. 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.

3. Slow insidious onset; no history of trauma

4. 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

Stage I: Internal Glenoid Impingement

1. Symptomatology

a. Stiffness; slow to warm up

2. Treatment:

a. 2 weeks of throwing

b. Strengthen cuff muscles

c. Strengthen scapular rotators

Stage II:  Internal Glenoid Impingement

1. Symptomatology

a. Posterior shoulder pain

b. Positive Jobe’s relocation test

1) Indicates anterior instability as etiology

2. Treatment

a. 4-12 weeks of an interval throwing

b. Rehabilitation program

Stage III:  Internal Glenoid Impingement

1. Symptomatology

a. Posterior shoulder pain

b. Positive Jobe’s relocation test

c. Failure of an appropriate rehabilitation program

2. Treatment

a. Anterior capsulo-labral reconstruction

b. Thermal Capsulorraphy (TACS-Thermal Assisted Capsular Shrinkage)

Jobe CM, OCNA, 1997

Subcoracoid Impingement and Subcoracoid stenosis

Subcoracoid space: Interval between the tip of the coracoid and the humeral head (the coracohumeral interval).

Normal coracohumeral interval: 8.4-11.0mm

Subcoracoid stenosis:  Narrowing of the Subcoracoid space with a coracohumeral interval of less than 6mm. Subcoracoid stenosis may not be pathologic or symptomatic.

Subcoracoid Impingement: Impingement of the coracoid process against the humerus (usually the lesser tuberosity) in a coracoid impingement position (humerus is flexed, adducted and internally rotated).

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 TUFF’s  (Tensile under –surface fiber failure) lesion or an articular side tearing (inside the joint) of the Subscapularis tendon.

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 subscapularis tear.

Lo and Burkhart, Arthroscopy, 19;2003:1142-1150.