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. 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

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) These muscles are usually found to be weak in patients with this syndrome which may facilitate the increased translation of the humeral head relative to the glenoid which ultimately leads to the impingement of the RC tendons. (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

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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 basic exam should include: 

Clinical Technique	Findings
•Palpation of the shoulder complex
• Observation of muscle symmetry between shoulders
• Gross strength testing of the shoulder, rotator cuff, and scapular retractor/stabilizer muscles
• Joint accessory mobility: GH/ST/AC/SC joints
• Flexibility tests for the shoulder, thoracic, and cervical spine
• 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

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
  

          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:

• active compression test
• crank test
• speeds test
• biceps load test. (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: 

• 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) 

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