Wednesday, May 25, 2011

GIRD- Glenohumeral internal rotation deficit

Definition of GIRD:
GIRD is a 20° or greater loss of internal rotation of the dominant shoulder compared with the non-dominant shoulder.

Glenohumeral internal rotation deficit, often diagnosed in players of overhead sports, has been associated with the development of secondary shoulder lesions. Conditions such as labral and rotator cuff injuries have been linked with decreases in glenohumeral internal-rotation and increases in external-rotation motion. This group also shows a loss of horizontal or cross-body adduction in the throwing shoulder when compared with the non-throwing shoulder. GIRD is also strongly associated with scapular dyskinesis.

Tennis players, swimmers & athletes in throwing sports are commonly affected by GIRD. Deficit in dominant shoulder of tennis players is about twice the deficit found in swimmers. Data suggest that GIRD and scapular position change worsens as the level of competition increases in overhead sports. Pathologic conditions in the shoulder of a throwing athlete frequently represent a breakdown of multiple elements of the shoulder restraint system, both static and dynamic, and also a breakdown in the kinetic chain.

GIRD a structural adaptation for good or bad
Altered shoulder mobility reported in overhead athletes and is thought to develop secondary to adaptive structural changes resulting from the extreme physiological demands of overhead activity. Debate continues as to whether these altered mobility patterns arise from soft-tissue or osseous adaptations within and around the shoulder.

People who support the onset through osseous adaptations argue humeral retroversion are thought to develop over time in young pre-adolescent throwers when the proximal humeral epiphysis is not yet completely fused. Retroversion is thought to account for changes in the rotational ROM in overhead athletes. This may lead to superimposition of soft tissue adaptations i.e. capsulo-ligamentous adaptations such as anterior-inferior stretching (accountable for increased ER) or posterior-inferior contracture (accountable for increased IR) upon the osseous changes. This may ultimately lead to pathological manifestations such as secondary impingement, type II superior labrum from anterior to posterior (SLAP) lesions and/or internal (glenoid) impingement.

Internal impingement & GIRD
GIRD and posterior shoulder tightness (capsule, rotator cuff) have been linked to internal impingement. Increased posterior shoulder tightness and glenohumeral internal rotation deficit that exceeds the accompanying external rotation gain, are suggested contributors to throwing-related shoulder injuries such as pathologic internal impingement. On the contrary Mayers et al found throwing athletes with internal impingement demonstrated significantly greater glenohumeral internal rotation deficit and posterior shoulder tightness in the absence of significant differences in external rotation gain.

However it is very clear now that repetitive forces in overhead sports cause adaptive soft tissue and bone changes that initially improve performance but ultimately may lead to shoulder pathologies.

The cardinal lesions of internal impingement, articular-sided rotator cuff tears and posterosuperior labral lesions, have been shown to occur in association with a number of other findings, most importantly GIRD and SICK scapula syndrome, but also with posterior humeral head lesions, posterior glenoid bony injury and, rarely, with Bankart and inferior glenohumeral ligament lesions.

GIRD is difficult to treat by physiotherapy
Physical therapy and rehabilitation should be, with only a few exceptions, the primary treatment for throwing athletes before operative treatment is considered. According to Myers JB shoulder internal impingement management should include stretching to restore flexibility to the posterior shoulder. However Tyler TF et al reported resolution of symptoms after physical therapy treatment for internal impingement is due to correction of posterior shoulder tightness but not correction of GIRD. But Braun S et al reported throwing athletes who have a glenohumeral internal rotation deficit have a good response, in most cases, to stretching of the posteroinferior aspect of the capsule.

Wilk KE reported compared with pitchers without GIRD, pitchers with GIRD appear to be at a higher risk for injury and shoulder surgery.

1. Wilk KE et al; Am J Sports Med. 2011 Feb;39(2):329-35. Epub 2010 Dec 4.
2. Torres RR et al; Am J Sports Med. 2009 May;37(5):1017-23. Epub 2009 Mar 4.
3. Thomas SJ et al; J Athl Train. 2010 Jan-Feb;45(1):44-50.
4. Tyler TF et al; Am J Sports Med. 2010 Jan;38(1):114-9. Epub 2009 Dec 4.
5. Myers JB et al; Am J Sports Med. 2006 Mar;34(3):385-91. Epub 2005 Nov 22.
6. Braun S et al; J Bone Joint Surg Am. 2009 Apr;91(4):966-78.
7. Kirchhoff C et al; Int Orthop. 2010 Oct;34(7):1049-58. Epub 2010 May 19.
8. Borsa PA et al; Sports Med. 2008;38(1):17-36.

Monday, May 9, 2011

Radiological interpretation of joint space narrowing & Kellgren-Lawrence (K-L) scale

Grade 0 = Normal

Grade 1 = Doubtful narrowing of the joint space & possible osteophytic lipping

Grade 2 = Definite Osteophytes & definite narrowing of joint space

Grade 3 = Moderate multiple Osteophytes, definite narrowing of joint space, some sclerosis & possible deformity of bone contour

Grade 4 = Large Osteophytes, marked narrowing of joint space, severe sclerosis & definite deformity of bone contour

Saturday, May 7, 2011

Internal impingement of shoulder: A simple overview

The impingement in shoulder can clearly be classified into internal & external varieties.

Internal impingement:

The internal impingement syndromes result from the impingement of the soft tissues of the rotator cuff and/or joint capsule on the glenoid or between the glenoid and the humerus.

External impingement:

The external impingement syndromes result from the impingement of the soft tissues of rotator cuff and bursa on the structures of the coracoacromial arch.

External shoulder impingement and rotator cuff disease has been corroborative despite of research arguments. Attempts have been made to identify objective imaging criteria that confirm the diagnosis of impingement, but at present external impingement remains primarily a clinical diagnosis.

Mainly shoulder impingement is caused by compression of the supraspinatus tendon underneath the coracoacromial arch, mostly in forward flexion of the arm.

Stages of external impingement:
Different stages of impingement syndrome are described.
Stage I: There is edema and hemorrhage of the supraspinatus tendon.
Stage II: There is characterized by bursal inflammation and fibrosis, as well as tendinopathy.
Stage III: there is a tear of the rotator cuff.

It is important to remember that clinical signs may overlap in these described stages.

The internal impingement syndrome:

Internal impingement was first described by Walch in 1992 and defined as contact between the supraspinatus tendon and posterior-superior glenoid rim with the shoulder in the cocked, throwing position of 90 degrees of abduction and maximum external rotation.

It is debatable whether internal impingement syndromes truly the result of impingement. Internal impingement seems to be a normal physiological occurrence with the shoulder in certain positions. Imaging findings in internal impingements reveals that these conditions there are 3 different pathologies: undersurface partial-thickness cuff tears, superior labral pathology, and bone changes. According to Paley et al’s study (N=41) in overhead throwing athletes suffering from internal impingement; undersurface cuff fraying was found in 93%, posterosuperior labral fraying was found in 88%, and anterior labral fraying was found in 36% of the subjects.

Theory explaining the internal impingement in overhead athletes:

In athletes where position of extreme abduction and external rotation (ABER position) are repeatedly taken this type of internal impingement occurs. However in simple ABER position also showed physical contact between the undersurface of the rotator cuff and the posterior superior glenoid. In athletes repeated contact between the undersurface of the rotator cuff and the posterosuperior glenoid rim leads to articular-sided partial-thickness rotator cuff tears and superior labral lesions. Hence the "kissing lesions" of undersurface rotator cuff tears and posterosuperior labral damage may be explained by mechanisms other than "internal impingement."

Interestingly Kim et al (2004) have demonstrated flexion as a cause of internal impingement as it affects the labrum. Labral pathologies lead to internal impingement. This study showed that internal impingement in flexion may contribute to the development of Type II SLAP lesions and rotator cuff disease.

Shoulder laxity & instability also has been incriminated as a source of internal impingement but McFarland et al have reported otherwise.

However even the non athletes also suffer from internal impingement. According to McFarland et al contact of the rotator cuff to the posterosuperior glenoid with the arm in abduction and external rotation can occur in a wide spectrum of shoulder disease and is not limited to the throwing athlete.

According to Halbrecht et al internal impingement is also seen in asymptomatic population.


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