Internal Impingement of the Shoulder

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Definition/Description

Background

         Historically, internal impingement syndrome has been described as impingement between the deep side of the supraspinatus tendon and the posteriosuperior edge of the glenoid bone seen in throwing athletes. It was thought to occur when the arm was placed in extreme ranges of abduction and external rotation. (drakos) To date there has been constant controversy as to exactly what internal impingement syndrome is and what causes it. The current understanding of internal impingement can be credited to Jobe and Walch, two investigators that have done extensive research on the topic. (heyworth) Jobe hypothesized that anterior instability of the shoulder complex caused by repetitive stretching of the anterior GH capsule led to this type of impingement in throwing athletes and also found that these athletes had an associated injury to one or more of the following structures; superior or inferior aspect of the glenoid labrum, rotator cuff tendons, greater tuberosity, inferior GH ligament, superior glenoid bone. (heyworth) Walch et al. also found that partial-thickness articular surface tears of the deep side of the rotator cuff tendons were associated with this syndrome. They reported on a series of 17 patients with internal impingement syndrome who were treated with arthroscopic debridement for under surface tears of the rotator cuff. This provided the first clinical evidence to support the concept of internal impingement. (heyworth) Although the debate continues as to the exact definition and etiology of this syndrome, the research done by these two investigators lays a foundational basis which can help clinicians gain a more clear understanding of the syndrome.

Description

          Today, internal impingement is commonly described as a condition characterized by excessive or repetitive contact between the posterior aspect of the greater tuberosity of the humeral head and the posterior-superior aspect of the glenoid rim when the arm is placed in extreme ranges of abduction and external rotation. This ultimately leads to impingement of the rotator cuff tendons (supraspinatus/infraspinatus) and the glenoid labrum. (heyworth) Although controversial, this described internal impingement condition has been referred to as both a normal and pathologic condition that is associated with throwing and other repetitive overhead activities. (drakos, heyworth) Cadaver, arthroscopic, and MRI studies have consistently shown that contact between the rotator cuff tendons and posteriosuperior aspect of the glenoid is a normal, physiologic occurrence. Burkart et al. asserted that a “loss of internal impingement” is actually the pathologic condition, and the absence of this normal restraint to hyperexternal rotation during throwing predisposes the shoulder complex to SLAP tears, rotator cuff fatigue failure, and “dead arm syndrome”. (heyworth) (drakos) There have been numerous investigators that hypothesized that the increased frequency and force with which abduction and external rotation occur in throwers is what leads to the development of the pathologic internal impingement syndrome. Along the same line of thinking, Jobe proposed that the extreme ranges of motion in both forward elevation and abduction and external rotation seen in throwers is what leads to the development of internal impingement. (Hayworth) The ongoing controversy of the etiology of this syndrome, along with the many different definitions described in the literature make it hard to gain an overall understanding of this syndrome without fully understanding the basic biomechanics of the shoulder complex. A general overview of the shoulder complex can be found in the resources section of this page.  With a basic understanding of this, it is much easier to conceptualize the basic underlying impairments seen in this syndrome. To add to the perplexity of this syndrome, Jobe et al. have identified 3 different types/stages of internal impingement which will be described in a later section.

Epidemiology /Etiology

Epidemiology

          Internal impingement typically affects young to middle aged adults; in most major series of internal impingement, patients are under 40 years of age and participate in activities involving repetitive hyperabduction and external rotation of the arm. The majority of patients who have been identified with internal impingement are elite overhead athletes. (heyworth) The majority of the research done on elite athletes with internal impingement has been on baseball players. However, non-elite athletes, as well as non-athletes may also be affected by internal impingement, highlighted by a recent case series done on 75 non-elite athletes.  (heyworth)  With this population, it is important to realize that older pts are more likely to have concurrent shoulder conditions such as subacromial impingement, SLAP tears, or glenohumeral arthrosis, which exhibits the need for a thorough examination to rule in/out diagnoses other than internal impingement. (Heyworth)

Etiology

          Although there is a relatively high concensus that the extreme ranges of GH abduction and external rotation are likely the culprit in the development of internal impingement, a precise biomechanical etiology has yet to be described. This is likely due to the fact that the pathobiomechanics of the syndrome are poorly understood and widely controversial. Orthopedic surgeons understanding of the biomechanics behind it have gradually evolved but remain incomplete. (heyworth) This is largely due to the limited patient population in which the syndrome is seen in as well as the myriad of pathologic findings that have been reported. It has been shown that unlike subacromial impingement, there is not a single pathomechanical process that is leading to internal impingement, making it more complex and multifactorial than subacromial impingement. Two potential biomechanical origins of internal impingement have been described in the literature by Jobe and Walch. The main difference between the two revolves around the role of GH translation in causing the rotator cuff changes and labral changes seen in throwing athletes. (heyworth) When reading through the literature on the biomechanics of internal impingement it is easy to get lost in all the different descriptions. The following summary serves as a general overview of the key concepts related to biomechanical deficiencies commonly seen in patients’ with internal impingement. The three most commonly reported impairments leading to the development of internal impingement are:

• Malpositioning of the scapula: Concurrent motions at the scapulothoracic and GH joints allow for optimal positioning of both the humeral head and scapula to allow for normal contact between the humeral head and the glenoid surface. Jobe et al. reported that malpositioning of the arm relative to the glenoid bone during throwing motions is what leads to impingement of the rotator cuff tendons between the glenolabral complex and the humeral head. (heyworth) Tyler et al., as well as numerous other authors, have also reported that scapular dyskinesia is a common finding in impingement patients. (tyler, drakos) During normal motion of the GH joint, the humeral head rolls posteriorly and glides anteriorly on the glenoid bone when the arm moves into abduction and external rotation, so one can see that if the scapula is unable to move through its’ full range of motion, dysfunction is going to occur.
• Weak scapular retractors and rotator cuff muscles: Coupled actions of the scapular upward rotators (serratus, lower trap) and humeral head depressors (RC mm’s), as well as the scapular retractor muscles (rhomboids, middle trap, lower trap) and GH ligaments also help ensure proper positioning of the GH joint during shoulder motion. Fatigue and/or weakness of the scapular retractors have been shown to cause a decreased force production in all four of the rotator cuff muscles. (tyler) Paley et al. cite "the combination of repetitive microtrauma and subsequent attenuation of the anterior glenohumeral ligament complex, and fatigue or desynchrony of the dynamic stabilizers of the glenohumeral and scapulothoracic articulations, as the precipitating mechanisms that allow abnormal anterior humeral head translation relative to the glenoid surface in some throwers."  This agrees with the findings of Andrews and Bigliani et al. who concluded that a finding of anterior laxity of the glenohumeral joint would allow for this increased translation of the humeral head ultimately leading to the entrapment of the posterior supraspinatus and anterior infrapsinatus tendons. (heyworth)  It is evident throughout the literature that these muscles are usually found to be weak in most patients studied with this syndrome. (heyworth)
• Tight posterior and lax anterior GH capsule: Several cases have reported that a contracture of the PIGHL seen in these patients shifts the contact position of the humeral head and glenoid posteriorly and superiorly, which allows for more external rotation during pitching, thus adding to the impingement condition as well. (heyworth)

Characteristics/Clinical Presentation

The diagnosis of internal impingement based on history alone is extremely difficult, and symptoms tend to be variable and fairly nonspecific. (heyworth) Because of the variable presentation, understanding the likely patient population and the clinical presentation of internal impingement is critical to identifying this disorder. A review of the literature does show several common symptoms that most internal impingement patients seem to share.

Internal Impingement patients present with:

Posterior Shoulder Pain 

• Chronic - diffuse posterior shoulder girdle pain is commonly the presenting complaint in the throwing athlete, but the pain may be localized to the joint line. (heyworth) The patient may describe the onset of posterior shoulder pain, particularly during the late-cocking phase of throwing, when the arm is in 90° of abduction and full external rotation. (Behrens)
• Acute – non-throwing athletes who also present with this syndrome have the chief complaint being acute shoulder pain following injury

Decrease in throwing velocity - a progressive decrease in throwing velocity or loss of control and performance in the overhead athlete.

Muscular asymmetry - Overhead athletes and throwers in particular often have muscular asymmetry between the dominant and the nondominant shoulder.

Increased Laxity - A patient with isolated internal impingement may have an increase in global laxity or an increase in anterior translation alone of the dominant shoulder. (drakos)

Instability - patients may have instability symptoms, such as apprehension or the sensation of Subluxation with the arm in a position of abduction and external rotation. (heyworth)

“Dead arm” - Some signs of the pathologic process include a so-called “dead arm,” the feeling of shoulder and arm weakness after throwing, and a subjective sense of slipping of the shoulder (behrens)

RC disease symptoms - patients may also present with symptoms similar to those associated with classic rotator cuff disease. Younger patients with such symptoms, particularly throwing athletes, should raise the clinician’s index of suspicion for internal impingement. In fact, some authors have identified internal impingement as the leading cause of rotator cuff lesions in athletes.

Jobe Clinical Classification of Internal Impingement
Jobe7 developed a classification scheme to further distinguish between the varying severities of internal impingement . (Behrens)The Jobe stage symptoms focuses on the primary patient population of overhead athletes.

1. Stage I: early Shoulder stiffness and a prolonged warm-up period; discomfort in throwers occurs in the late-cocking and early acceleration phases of throwing; no pain is reported with activities of daily living.
2. Stage II: intermediate Pain localized to the posterior shoulder in the late-cocking and early acceleration phases of throwing; pain with activities of daily living and instability are unusual.
3. Stage III: advanced Similar to those in stage II in patients who have been refractory to nonoperative treatment modalities.

Differential Diagnosis

Internal impingement can present as a constellation of pathologic processes, including but not limited to: (Behrens & Drakos)

• partial- or full-thickness rotator cuff tears
• anterior or posterior capsular injury
• labral tears
• glenoid chondral erosion
• chondromalacia of the posterosuperior humeral head
• biceps lesions

Each of these disorders can exist alone or as concomitant pathological condition.

Examination and Clinical Findings

          When evaluating a patient with suspected internal impingement syndrome, it is very important to get a thorough history, as it is an important element of the clinical diagnosis. (drakos) However, diagnosing internal impingement on the history alone is extremely difficult as symptoms tend to be variable and non-consistent. (heyworth) For this reason, along with the multitude of concominant conditions that can accompany internal impingement, a thorough, complete examination of the shoulder complex must be done to rule in/out any of these concominant or differential diagnoses.  The following section describes the clinical examination and most common findings seen in patients with internal impingement.  This should be viewed as a general overview and not all-inclusive.  All findings should be taken into consideration when developing a treatment plan for a patient.

The basic exam should include: 

Clinical Technique	Findings
Palpation of the shoulder complex	TTP posterior shoulder/joint line
Observation of muscle symmetry between shoulders	involved shoulder usually has increased muscle bulk and lies lower than unaffected shoulder abnormal scapulothoracic rhythm/scapular movement
Gross strength testing of the shoulder, rotator cuff, and scapular retractor/stabilizer muscles	weak rotator cuff muscles weak middle/lower trap, rhomboids weak serratus anterior
Joint accessory mobility: GH/ST/AC/SC joints	Decreased A/P glenohumeral glide due to posterior capsule tightness
Flexibility tests for the shoulder, thoracic, and cervical spine	Variable: General Considerations pec minor/major latissmus dorsi SCM, upper trap, levator scapulae thoracic rotation/extension
ROM: GH/scapulothoracic joints as well as the cervical and thoracic spine as it has been shown that dysfunction in any of these areas can directly impact the shoulder	decreased GH internal rotation: 10-15 degrees increased GH external rotation: 10-15 degrees

          Recently, a small number of tests were created to test specifically for internal impingement. (heyworth) Meister et al. investigated the “posterior impingement sign” for the ability to detect articular sided rotator cuff tears and posterior labral lesions. They reported a sensitivity and specificity of 75.5% and 85% respectively, and when patients who sustained contact injuries were taken excluded in a stratified analysis, the sensitivity improved to 95% and the specificity to 100%. They concluded that this test was extremely valuable in identifying operable internal impingement lesions in young throwers. (heyworth) Jobe and colleagues have reported that the relocation test can be used to identify internal impingement. The test is performed identical to the jobe subluxation/relocation test, however a positive test would be posterior shoulder pain that was relieved by a posterior directed force on the proximal humerus. (heyworth) Paley et al. reported similar findings and found that 100% of patients who had a positive relocation test on examination had evidence of a shoulder injury suggestive of internal impingement.

Testing for concominant and/or differential conditions

          It is critical to include tests for subacromial impingement and full/partial-thickness rotator cuff tendon tears as these are highly associated with internal impingement. The following tests were chosen due to the proven diagnostic accuracy that has been reported elsewhere in the literature. (drakos, heyworth) Impingement tests may or may not be (+).

• Hawkins-kennedy test
• Infraspinatus muscle test
• Painful arc sign
  
• Lag sign

          Although the validity of physical examination tests used to detect SLAP lesions is controversial, the fact that these lesions are a common finding with internal impingement warrants the need to perform at least some combination of the following tests: SLAP tests may be (+) or (-)

• Active compression test
• Crank test
• Speeds test
• Biceps load test II (heyworth)
  

Laxity of the anterior GH joint capsule is a common finding in patients with internal impingement, so tests for anterior GH instability should also be performed. The following have proven diagnostic accuracy: Generally (+) but may be (-) 

• The apprehension test
• Jobe subluxation/relocation test
• Anterior release test
  

           Burkhart et al. have reported that scapular protraction caused by SICK scapula syndrome is also a common finding in these patients. (heyworth) This is characterized by scapular malposition, a prominent inferior medial border, coracoid pain, and scapular dyskinesia, all of which can be picked up in the basic examination during palpation and observation of the scapula.  Tyler et al. reported that scapular retractor muscle fatigue led to an overall decrease in force production of the rotator cuff muscles as well as decreased strength of the scapular stabilizers. This overall decrease in strength of these muscles, which again are already usually weak, allows for an increased amount of superior/posterior humeral head migration which in turn leads to the internal impingement condition. (tyler) 

Medical Management (current best evidence)

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Physical Therapy Management (current best evidence)

Acquired glenohumeral anterior instability GIRD (Glenohumeral Internal Rotation Defecit) Scapular Dyskensia
Phase 1 – addressing any muscle imbalances (specifically, rotator cuff, LT, MT, & SA), restoring muscle endurance, addressing GH instabilities (usually anterior), as well as ROM deficits (decreased internal rotation), and gradually restoring proprioception and neuromuscular control. Closed kinetic chain exercises, strengthening of the rotator cuff as external rotators are often weak in overhead athletes. “Sleeper stretch” and “cross-body adduction stretch,” joint mobilisations to increase internal rotation can be used but use with caution especially with patients with anterior instability. Muscle imbalances must be addressed before beginning neuromuscular reeducation of abnormal scapular movements. For MT & LT to UT imbalances consider using these 4 exercises early in the rehab process. 1) side-lying forward flexion, 2) side-lying external rotation, 3) prone horizontal abduction with external rotation, and 4) prone extension in neutral position. For SA specific training consider variations of the push-up plus, which has been shown to decrease UT activation while increasing SA activation.
Phase 2 – Improving functional stability while progressing to more challenging and sport specific exercises to begin preparing for a return to play training program, strengthening shoulder musculature. More advanced closed-kinetic chain exercises and 2 handed plyo’s progressing to open chain and single-hand plyo’s, manual perturbations can be applied from all angles with the humerus in a variety of positions to encourage muscular stability. If mobilizations are to be employed, then they should be done in order to influence the posterior ligaments, with the pt’s shoulder placed in end-range internal rotation or horizontal adduction and then applying a grade III-IV mob in a dorsal direction. Begin neuromuscular rehab of abnormal movement synergies of the scapula in relation to the humerus. The scapula should be a stable base thus placing itself in the most optimal biomechanical position relative to the humerus, this can be initiated with manual PT encouragement when performing almost any exercise especially the diagonal and functional movement patterns and progressed to the patient “cueing” the scapula before beginning a movement.
Phase 3 – advanced phase, preparing the athlete to return to play, continue strengthening exercises, begin more advanced single hand plyometric drills, and more advanced whole body kinetic chain exercises. Continue strengthening shoulder musculature and challenging stabilizers in increasingly more difficult functional positions and begin advanced single arm plyos in full range of motion Continue stretching and mobs if necessary as well as initiating a maintenance program to continue stretching to maintain gains of internal rotation but continue to use caution if the pt still shows signs of instability Continue strengthening scapular stabilizes and begin functional sport specific exercises monitoring the scapula for correct kinematic movements and giving the pt verbal cues to remind them of scapular position.

Key Research

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Resources

Overview of the shoulder complex: Key elements

Clinical Bottom Line

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References

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