Research Review by Dr. Shawn Thistle©


May 2008

Study Title:

The disabled throwing shoulder: Spectrum of pathology Part 1: Pathoanatomy and Biomechanics


Burkhart SS, Morgan CD, Kibler B

Authors’ Affiliations: Not listed (all authors are American orthopedic surgeons)

Publication Information:

Arthroscopy: The Journal of Arthroscopic and Related Surgery 2003; 19(4): 404-420.


Overhead sports participation is very common, as are associated shoulder injuries. This important paper (Part 1 of a 3 part series) provided an overview of a unifying theory of shoulder pathology (for throwing athletes), representing years of clinical and surgical observation by three of the leading shoulder experts in the United States. Although published a few years ago (2003), it still represents the most comprehensive explanation of these concepts that will change the way you view and assess shoulder mechanics, pathology, and injuries in throwing or overhead athletes (and I would argue the general population as well).

An executive summary of this paper follows, and a review of Part 3 of the series is upcoming. That review will clarify their methods of diagnosing and labeling scapular dysfunction as it pertains to shoulder function – useful information that can be applied clinically to any population.

It is a great athletic achievement to throw a ball 90+ mph with accuracy, one that has fascinated sports fans for years. The sudden loss of this ability, commonly referred to as the dreaded “dead arm”, is nothing short of a sporting tragedy. “Dead arm” is defined as any pathologic shoulder condition which renders the athlete unable to throw with pre-injury velocity and control due to a combination of pain and subjective “unease” in the shoulder. The pain is usually related to the late cocking phase of throwing, as the arm begins to accelerate forward. The thrower then reports sudden sharp pain, and an inability to attain top velocity.

Historically, the exact cause of the “dead arm” has eluded clinicians and surgeons alike. A number of etiological theories exist, including: psychopathology, posterior glenoid calcifications, coracoacromial ligament impingement, acromial osteophytosis, rotator cuff pathology, biceps tendinopathy, acromioclavicular joint dysfunction, internal impingement, labral (SLAP) lesions, or microinstability. The authors state that although SLAP lesions are most commonly associated with this syndrome, a number of other factors can be involved, each discussed below.

Changes in Internal/External Rotation:
  • throwing shoulders acquire increased external rotation and abduction compared to non-throwing shoulders
  • this adaptation is postulated to result in repetitive microtrauma to the anterior aspect of the glenohumeral (GH) capsule – if excessive, this may result in “dead arm” syndrome
  • the authors however, believe that the most important pathological consequence of repetitive throwing is a loss of internal rotation while the arm is in an abducted position
  • this loss of internal rotation far exceeds the gain in external rotation, and has been documented in painful throwing shoulders
  • this loss of internal rotation has been termed GIRD: Glenohumeral Internal Rotation Deficit, which is defined as the loss (in degrees) of GH internal rotation in the throwing shoulder compared to the non-throwing shoulder – conventionally measured with the patient supine, and the arm in 90° or abduction in the plane of the body, and the scapula stabilized on the treatment table
  • GIRD is thought to occur from posterior-inferior GH capsular contracture (which the authors also propose secondarily causes the gain in external rotation – see below) – remember that the posterior capsule would come under tension as the arm moves into internal rotation
SLAP Lesions:
  • the authors state that SLAP lesions are most commonly associated with the “dead arm”
  • pseudolaxity that is often associated with SLAP lesions may lead to the erroneous diagnosis of anterior microinstability in these patients
Internal Impingement:
  • generally thought to occur in most shoulders in an abducted and externally rotated position (90°/90°), as the undersurface of the posterior-superior rotator cuff may become pinched between the greater tuberosity and the glenoid labrum
  • there is controversy as to whether increased anterior laxity (whether real or perceived) would increase or alleviate internal impingement symptoms
  • the authors believe that internal impingement is normal in all shoulders, and is not part of the disabled throwing shoulder
The “Tethered Shoulder”: The Reciprocal Cable Model and Cam Effect:
  • the inferior glenohumeral ligament (IGHL) complex is bound by an anterior and posterior band, acting like a hammock to support the humeral head while the arm is abducted
  • in a simplified model, these two bands (anterior and posterior) can be thought to exert tension reciprocally and equally as the shoulder internally and externally rotates in a 90° abducted position
  • the position of the IGHL complex shifts during the throwing motion (for example: in full external rotation and abduction, the posterior band of the IGHL is directly below the humeral head – if it were shortened/contracted in this position, it would exert a posterior-superior force on the humeral head)
  • this reciprocal cable model defines the allowable “envelope of motion” of the shoulder
  • if one of the cables is shortened, it acts as a tether, shifting the glenohumeral contact point
  • in the case of external rotation/abduction: if the shortened posterior cable reaches its maximum length before the anterior cable, the anterior cable will still permit external rotation even though the posterior cable is tethering the humeral head from underneath, resulting in motion of the greater tuberosity shifting posterosuperiorly, eliminating the abutment against the posterior glenoid and permitting greater external rotation – this is the proposed mechanism for this adaptation
Hyperexternal Rotation of the Humerus:
There are two mechanisms proposed by which a tightened posterior-inferior capsule allows hyperexternal rotation of the humerus:
  1. the tethering effect as discussed above
  2. the shift in the glenohumeral contact point minimizes the cam effect on the anterior capsule, allowing greater external rotation due to redundancy in that part of the capsule
The authors argue that true anterior instability is generally not part of the disabled throwing shoulder. Apparent increased laxity may be due to a reduction of the cam effect and functional lengthening of the anterior capsule (perhaps in conjunction with pseudolaxity from a posterior SLAP lesion, as mentioned above). They feel true instability takes time to develop, and hence would normally only appear in veteran players.

The authors propose that hyperexternal rotation of the humerus may also pose a risk of repetitively hypertwisting the fibres of the rotator cuff, leading to torsional overload and tissue failure. This would occur on the articular side of the cuff, the most common location for cuff failure in throwers.

The External Rotation Set Point:
  • in elite throwers, the maximum internal rotation velocity is ~ 7000°/second
  • the best way to maximize internal rotation velocity is to maximize the arc of rotation by means of hyperexternal rotation in the late cocking phase
  • high level throwers have a certain set point of external rotation that they require to attain peak velocity – they refer to this as the “slot”
  • throwers with tightness in the posterior capsule and GIRD will often reach their set point, or “slot” through deranged mechanics, placing them at risk for increased peel-back forces on the superior labrum (or injury at other sites) – the authors postulate that these athletes are always on the brink of injury
  • Peel-back mechanism: occurs when the arm is in the cocked backed position of abduction and external rotation – the biceps tendon then assumes a more vertical and posterior angle, which when combined with a twist at the base of the attachment, transmits a torsional force to the posterior superior labrum. If the superior labrum is not well anchored, it may rotate medially over the corner of the glenoid, onto the posterior/superior scapular neck.
Acceleration Versus Deceleration Labral Injuries:
  • the authors feel labral injuries are more commonly an acceleration injury – as throwers report the sudden onset of pain in the position of late cocking
  • the other theory suggests that the biceps must contract eccentrically to slow the rapidly extending elbow on follow-through – this high tensile load is thought to pull the labrum from the glenoid
Instability Versus Laxity: The Circle Concept:
  • as mentioned above, the authors disagree with the premise that anterior instability is the primary cause of the “dead arm” syndrome
  • Circle Concept: disruption of the labral attachment on one side results in laxity on the opposite side of the glenoid (i.e. if the pivot point shifts posterosuperiorly, the cam effect on the humeral head and anterior capsule is reduced, producing a relative capsular redundancy that can be misinterpreted as instability)
Summary – The Pathological Cascade:
  1. an acquired posteroinferior capsule tightness is thought to be the first essential abnormality
  2. this results in a shift in the glenohumeral contact point, causing maximum shear stress on the postero-superior labrum at the exact time when the peel-back force is maximal
  3. the presence of a contracted or shortened posterior band of the IGHL complex alters the cradling effect of the structure, acting as a bowstring to tether the humeral head, exerting a posterosuperior force which shifts the rotation point – allowing excessive external rotation
  4. the shoulder is now abducted and excessively externally rotated, leading to a number of adverse consequences:
    • increased shear forces to the biceps tendon anchor via the peel-back mechanism
    • anterior capsular structures become functionally lax due to the shift in pivot point, leading to hyperexternal rotation, and abnormal tension on the IGHL
    • excessive external rotation caused by GIRD increases shear and torsional stress in the porterosuperior rotator cuff, which may lead to tissue failure
All of the above consequences are worsened by a protracted scapula. This entire cascade begins with a tightened posterior capsule, which may have been clinically silent.

What causes a tight posterior capsule?

The authors believe that the most likely explanation is that the soft tissue changes are induced by forces acting on the structure during repetitive follow-through. After ball release, a large distraction force of up to 750N is applied at the shoulder. As the arm is in an internally rotated position at this point, the posterior capsule would be in a central position on the humeral head, a position that would allow it to directly resist this distraction force.

Although the rotator cuff acts eccentrically to resist this motion, it stands to reason that the posterior capsule may take a significant portion of this demand. Any deficiency in the rotator cuff would only enhance this effect, which may also contribute to the overall pathology.

Conclusions & Practical Application:

This paper outlined a unifying theory of pathology in elite throwing shoulders, which can be summarized by identifying the following “Culprits”:
  • tight posterior capsule (that is often clinically silent)
  • excessive peel-back forces leading to a SLAP lesion
  • hyperexternal rotation causing a shift in the pivot point and a reduction in the cam effect on the anterior capsule (which may be mistaken for anterior instability)
  • scapular protraction, and poor scapular stability
The second review on the third paper in this series will outline SICK Scapula syndrome, scapular dyskinesis, and rehabilitation concepts for this spectrum of disorders.

Additional Resources:

  • Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: Spectrum of pathology Part III: The SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy: The Journal of Arthroscopic and Related Surgery 2003; 19(6): 641-661.
  • Kibler WB. The role of the scapula in athletic shoulder function. American Journal of Sports Medicine 1998; 26(2): 325-337.