Internal Impingement of the Shoulder

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Original Editors

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Search Strategy

Databases: CINAHL, Cochrane, EBSCO, Google Scholar, JOSPT, Medline with full text, PEDro, PubMed, ProQuest & Rehab reference center, Science Direct

Keywords: Shoulder Internal Impingement, internal impingement, shoulder impingement syndrome, impingement, dead arm syndrome, posterior shoulder tightness, posterior shoulder pain, scapular dyskinesia

Search Timeline: September 27, 2010 – November 27, 2010

Definition/Description

          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.   (heyworth, behrens, drakos, jobe) This ultimately leads to impingement of the rotator cuff tendons (supraspinatus/infraspinatus) and the glenoid labrum. To date there has been constant controversy as to exactly what causes internal impingement syndrome. The current understanding of internal impingement can be credited to Jobe and Walch, two investigators that have done extensive research on the topic.  Their research helps to lay a foundational basis which can help clinicians gain a more clear understanding of this complex syndrome.

Epidemiology /Etiology

Epidemiology

          The majority of patients who have been identified as having internal impingement are overhead athletes. Understanding this patient population, it is not surprising that it typically affects young to middle aged adults. In most major case 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 the research on internal impingement has been done on elite 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 the non-elite athletic population, it is important to realize that older patients are more likely to have concurrent shoulder conditions such as subacromial impingement, SLAP tears, and glenohumeral arthrosis, which exhibits the need for a thorough examination to rule in/out diagnoses other than internal impingement. (Heyworth)

Etiology

          The understanding of the etiology behind internal impingement has gradually evolved but remains incomplete. The lack of a common biomechanical model is largely due to the limited patient population in which the syndrome is seen in as well as the myriad of associated pathologic findings that have been reported.  (heyworth) (drakos) Although many different biomechanical explanations have been proposed by numerous investigators, there is a relatively high consensus that the repetitive, extreme ranges of GH (glenohumeral) abduction and external rotation are likely the prime culprit leading to the development of internal impingement. 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.  (heyworth, drakos) There are three common factors aside from the repetitive motion mentioned previously that have been shown to contribute to this disorder.     (heyworth, drakos, jobe, Burkhart, tyler)

• Anterior GH instability: Jobe et al. 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 found that these athletes commonly 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) This agrees with the results of later studies done by Walch et al. that found partial-thickness articular surface tears of the deep side of the rotator cuff tendons to be associated with this syndrome. A case series on 17 patients with internal impingement syndrome who were treated with arthroscopic debridement for under surface tears of the rotator cuff provided the first clinical evidence to support the concept of internal impingement. (heyworth) Andrews and Bigliani et al. also concluded that a finding of anterior laxity of the glenohumeral joint would allow for increased translation of the humeral head ultimately leading to the entrapment of the posterior supraspinatus and anterior infrapsinatus tendons.
• Muscle imbalance and/or improper neuromuscular control of the shoulder complex: 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 help ensure proper positioning of the GH joint during shoulder motion. If the scapula is unable to move through its’ full range of motion, or it moves abnormally, optimal positioning of the GH joint is hard to achieve. 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) Furthermore, 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, which would also lead to abnormal positioning of the GH joint. (tyler) Paley et al. cited that "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. (heyworth) It is evident throughout the literature that patients with internal impingement have imbalances in many of the muscles mentioned above. (heyworth)
• Tight posterior GH capsule: Several cases have reported that a contracture of the PIGHL (posterior-inferior GH ligament) 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) The PI capsule is hypothesized to become hypertrophied in the follow-through tensile motion of throwing. After ball release, the elbow is nearly extended, with the forearm pronated. The resultant force on the glenohumeral joint is one of distraction. Such a force can reach up to 750 N. The posterior shoulder musculature responds by providing a compressive force (decelerating). However, such a force may be too much for the musculature to resist fully, especially when it is fatigued. Therefore, the PI capsule is subjected to high tensile forces, resulting in hypertrophy over time. (preston) Posterior capsule tightness also leads to GIRD (glenohumeral internal rotation deficit), which is a key clinical finding associated with this syndrome that will be discussed in a later section. 
  

           A basic understanding of the biomechanics of the shoulder complex can make it much easier to conceptualize the underlying impairments seen with this syndrome. A general overview of the shoulder complex can be found in the resources section of this page.

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 nature of internal impingement, understanding the patient population and the clinical presentation 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 the chief complaint in the throwing athletes with internal impingement, but the pain may also 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 present with this syndrome, have a chief complaint of 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.
“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)
Muscular Asymmetry - Overhead athletes and throwers in particular often have muscular asymmetry between the dominant and the nondominant shoulder.
Muscular/Neuromuscular Imbalance – A common finding is muscle imbalances in the shoulder complex as well as improper neuromuscular control of the scapula. (Cools)
Increased Laxity - A patient with isolated internal impingement may have an increase in global laxity or an increase in anterior laxity alone of the dominant shoulder. (drakos)
Anterior 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)
Rotator Cuff Pathology - Patients may also present with symptoms similar to those associated with other rotator cuff pathologies (tears, other impingements). 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. (heyworth)
Jobe Clinical Classification of Internal Impingement
 - Jobe developed a classification scheme to further distinguish between the varying severities of internal impingement. The Jobe classification system focuses on the primary patient population of overhead athletes. (Jobe & Behrens)
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 not responded to nonoperative treatments.

Differential Diagnosis

Internal impingement is truly a diagnosis of exclusion. Suspicion should be raised when patients present with signs of numerous pathologies, yet do not fit any one pathology exclusively. This should lead the clinician to consider internal impingement as a possible diagnosis. Internal impingement also has a similar presentation to numerous pathologic shoulder conditions, including but not limited to: (Behrens & Drakos)
• Partial- or full-thickness rotator cuff tears
• Anterior or posterior capsular pathologies
• SLAP (Superior Labrum Anterior to Posterior) lesion
• Subacromial Impingement
• Glenoid chondral erosion
• Chondromalacia of the posterosuperior humeral head
• Anterior GH instability
• Biceps tendon lesion
• Scapular Dysfunction
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) A thorough, complete examination of the shoulder complex must be done to rule in/out any concomitant shoulder pathologies.  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.

The basic exam should include: 

Clinical Technique	Findings
Palpation of the shoulder complex	TTP (tender to palpation) 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 dorsal glenohumeral glide 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

Tests for Internal Impingement     

Recently, a small number of tests were created to help rule in/out the presence of 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, meaning a negative test is extremely accurate in ruling out posterior rotator cuff tears.  They concluded that a positive test was extremely valuable in identifying operable internal impingement lesions in young throwers. (heyworth)
• Jobe and colleagues have reported that the relocation testcan 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

Tests for other shoulder pathologies may be (+) or (-) due to the variable clinical presentation of internal impingement.  Understand that there is no proven combination of test findings that identify internal impingement.    

           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)

• 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:

• 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)

          Surgery for internal impingement may be indicated if improvements have not been seen with a prolonged rehab protocol specifically designed to correct any impairments, imbalances, deficiencies and/or pathologic findings. Based on recent literature, arthroscopic interventions are listed as the preferred type of surgery. Prior to any surgical procedure it is highly recommended that a thorough exam under anesthesia (EUA) is done, as well as a diagnostic arthroscopy. Due to the often-confusing physical findings that may be associated with internal impingement, the final therapeutic surgical plan should be aimed at specific pathologic lesions related to patient symptoms that have been identified from an EUA and diagnostic arthroscopy. It’s recommended that the EUA specifically assess for GH ROM, any kind of subluxation, as well as a meticulous analysis for the presence of any instability. (Heyworth, 2008)

          Non-surgical interventions for internal impingement that are recommended in the literature are rest, ice (cryotherapy), and NSAIDS (or other oral-anti-inflammatory meds). However, physical therapy is the cornerstone of non-surgical interventions and should always be extensively tried before considering surgical interventions.

Physical Therapy Management (current best evidence)

One of the early signs of internal impingement, which should be carefully monitored for, is a decrease in pitching ability and quality. In addition to the signs and symptoms previously mentioned, the pitcher or overhead athlete may report feelings of tightness, stiffness, or not loosening up (Jobe, 2000). If these signs or symptoms are observed the pitcher should be removed from participation and started in a rehab program. (Jobe, 2000) In this early stage, treatment is typically stretching to increase ROM and decreasing posterior capsule tightness, strengthening to rebuild the soft tissue support, and then neuromuscular reeducation and retraining to prevent recurrence (Jobe, 2000).

With the findings from a thorough clinical exam, the clinician should design an individualized impairment based treatment plan with an initial focus on correcting muscle imbalances, instabilities and ROM deficits before beginning more complex dynamic exercises. (Cools, Burkhart, Jobe)

• Anterior GH Instability: It’s been reported that if anterior instability is present and not improved through strengthening of the supporting shoulder musculature then operative management reconstructing the anterior capsulolabral area may be warranted. The good news is that many of the exercises used to treat instability are already being employed in many shoulder rehab protocols. One example is closed kinetic chain (CKC) exercises, which can have several therapeutic benefits including the ability to engage the rotator cuff musculature as a single stabilizing unit
• Tight Posterior GH Capsule: GIRD (Glenohumeral Internal Rotation Deficit) is highly correlated with a tight posterior capsule and is another common finding in all over-head athletes. As an injury prevention measure, research has shown that 90% of throwers could reduce GIRD to an acceptable level in 2 weeks after beginning a posterior capsule stretching program.
• Muscle Imbalance and/or improper neuromuscular control of the shoulder complex: Scapular dyskinesia caused by these imbalances of the shoulder complex are also associated with internal impingement as well as any kind of shoulder injury, especially in over-head athletes. Research looking at 96 overhead athletes with isolated SICK scapula, showed a 100% return to pre-injury level of throwing after engaging in a 4 month scapular stabilization program aimed at strengthening the periscapular musculature and the rotator cuff. The subscapularis, the only internal rotator of the 4 rotator cuff muscles, is often over looked but strengthening this muscle has been suggested in order to prevent over-angulation in the late cocking phase of throwing. (Burkhart et al, & Jobe et al, 2000).
  

Cools, et al, 2008 provides guidelines for rehabbing internal impingement in tennis players based on clinical literature & clinical experience, therefore, many of the treatments discussed have not been validated with medical research, so until that research is conducted these guidelines may provide a foundational starting point for clinicians treating internal impingement. The guidelines below are geared toward rehabbing the three main shoulder dysfunctions seen with this syndrome; anterior instability (caused by weak RC), GIRD (posterior tightness), and scapular dyskinesia. Again, it is critical to realize that overhead athletes with internal impingement often have concomitant pathologies for which an individualized treatment plan is needed to address all impairments. This custom treatment plan should incorporate a deliberate order of execution aimed at restoring the shoulder in phases.

Phase one:

• For treatment of GIRD, see additional considerations section after phase 3
• Restore proper muscle balance and endurance: Focus should be on correcting muscle imbalances between the rotator cuff muscles and periscapular muscles. Due to the reduced external rotation to internal rotation ratio, restoring muscle control and muscle strength of the external rotators (internal as well) is critical. Gradually start to incorporate proprioceptive training and dynamic stability exercises.
• Address instability: Closed chain exercises are suggested because axial compression exercises that put stress through the joint in a weight-bearing position result in joint approximation and improved co-contraction of the rotator cuff muscles, thus helping to combat instability.
• Neuromuscular Re-education: Scapular dyskinesia is largely due to decreased activation of the middle trap (MT), lower trap (LT), and serratus anterior (SA) when compared to the upper trap (UT). Therefore, exercises should be chosen that emphasize MT, LT, & SA activation while decreasing UT activation. 4 exercises aimed specifically at the MT and LT are referenced in the table below. For SA activation, variations of the push-up plus can be used, which is a closed-chain exercise that further helps to restore stability. These exercises should be done early in rehab before functional patterns are employed in order to normalize the activation ratios of the LT, MT & SA to the UT, thus providing a stable base for which select functional exercises can work to impose proper kinematic movements into the scapular musculature (Cools, et al, 2008)

Phase two:

• Improve dynamic stability: Done with progressively more complex and activity specific exercises. With muscle imbalances already addressed, the therapist can begin to add dynamic movements into rehab using “tactile cueing” to ensure patient is engaging the scapular musculature before beginning a movement. Progress to verbal cueing.
• Strengthening exercises: Target all shoulder and scapular musculature. Start introducing eccentric and open kinetic chain exercises in order to begin preparing for specific athletic overhead movements. (Cools, et al, 2008)

Phase three:

• Functional rehabilitation plan: Designed to prepare the athlete to return to full athletic activity. Strengthening exercises are continued and plyometrics are initiated using both hands and limiting external rotation at first, progressing to one handed drills and gradually working into increasing velocity and resistance.

Additional Considerations:
Rehabbing the GIRD component: Started immediately upon 1st treatment and continue throughout. Numerous RCT’s have shown that this internal rotation deficit can be decreased by performing stretches aimed at the posterior capsule; namely the “sleeper stretch” and the “cross body adduction stretch.”

• The sleeper stretch is performed with the patient lying on their injured side with the shoulder in 90° forward flexion, the scapula manually fixed into retraction, while glenohumeral internal rotation is performed passively. The patient should feel a stretch in the posterior aspect of the shoulder and not in the anterior portion, if they do, then reducing intensity and rotating the trunk slightly backwards can reduce the intensity of the stretch.
• The “cross-body stretch,” is another popular stretch for the posterior capsule and can be performed by moving the arm into horizontal adduction. This stretch has been shown to be superior for stretching the posterior capsule and for increasing internal ROM (McClure, 2007).

Joint mobilizations (mobs): GH anterior-posterior joint mobs can be used to help stretch the posterior capsule and increase internal rotation, however, if posterior instability is noted on the initial exam, joint mobs should be avoided as to not increase this instability. Grade IV, end range, dorsal-glide mobilizations performed with the patient supine with shoulder placed into 90 abduction, and either in neutral or end range internal rotation of the humerus (refer to pictures). (Cools, et al, 2008)

Whole body kinetic chain exercises: Incorporating this early in rehab has been recommended in order to prepare the athletes whole body for return to activity. Core stability, leg balance, and diagonal movement patterns can be used to incorporate the entire kinetic chain while simultaneously involving the shoulder as well. One example of this is simply adding a degree of instability to an exercise; doing external rotation exercises while sitting on an exercise ball or while performing a single leg stance by standing on the opposite leg of the arm you are working. (Cools, 2008)

Rehab guidelines for overhead athletes with internal impingement

Key Research

 case study template

 Bang & Deyle, RCT, 2000

Resources

Overview of the shoulder complex: Key elements

Burkhart S, Morgan C, Kibler W. The Disabled Throwing Shoulder: Spectrum of Pathology. Part III: The SICK Scapula, Scapular Dyskinesis, The Kinetic Chain, and Rehabilitation. Arthroscopy. (2003) 19:641-661

Halbrecht J, Tirman P, Atkin D. Internal Impingement of the Shoulder: Comparison of Findings Between the Throwing and Non-Throwing Shoulders of College Baseball Players. Arthroscopy. (1999) 15:253-258

Edelson G, Teitz C. Internal Impingement In The Shoulder. Journal of Shoulder& Elbow Surgery. (2000) 9:308-315

Figure 1. Line drawing illustrates impingement of the greater tuberosity on the posterosuperior glenoid rim, with the interposed articular side of the rotator cuff and the posterosuperior labrum, which are prone to inflammation, fraying, or tears.

Figure 1. Line drawing illustrates impingement of the greater tuberosity on the posterosuperior glenoid rim, with the interposed articular side of the rotator cuff and the posterosuperior labrum, which are prone to inflammation, fraying, or tears.

Clinical Bottom Line

           Internal impingement can come across as a very difficult diagnosis to evaluate and treat. However, it is important to realize that this diagnosis, just like most shoulder conditions, is really impairment-based; it just happens to have a name attached to it. That said, an impairment-based treatment approach aimed at the individual clinical findings should be the treatment of choice. The three most common impairments that have been found to contribute to internal impingement, and that need to be addressed from day 1 include:

• Anterior GH instability
• Tight posterior GH capsule
• Muscle imbalance and/or improper neuromuscular control of the shoulder complex

          Furthermore, understand the importance of a thorough and complete shoulder examination including the cervical and thoracic spine in assessing for any impairments/concurrent conditions that may be also be contributing to this condition. As mentioned earlier, these can include SLAP tears, rotator cuff tendon tears, and anterior GH instability, although this list is not all inclusive. As with other types of shoulder impingement, the primary conservative treatment techniques should include manual therapy and exercise, which will help get patients’ better results in a shorter time period. When conservative treatment fails, surgery is warranted. Manual therapy techniques should be used to address any movement dysfunctions found on exam in combination with the exercise program mentioned previously. Manual techniques may include joint mobilizations/manipulations and manual stretching.

Recent Related Research (from Pubmed)

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References

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