Anatomical and Functional Relationship Between SLAP Lesions and the Supraspinatus Muscle
SLAP lesions are anatomically and functionally connected to the supraspinatus muscle through their proximity at the superior aspect of the glenohumeral joint, with SLAP lesions often coexisting with supraspinatus pathology, particularly in patients over 40 years of age.
Anatomical Relationship
The superior labrum anterior to posterior (SLAP) lesion and the supraspinatus muscle share important anatomical connections:
- The supraspinatus muscle is positioned superiorly in the rotator cuff, attaching to the greater tuberosity of the humerus 1
- SLAP lesions affect the superior labrum where it connects to the biceps tendon anchor, which is in close proximity to the supraspinatus insertion 2
- The supraspinatus occupies a narrow space between the humeral head and the coracoacromial arch during normal shoulder abduction 1
- The intraarticular portion of the long head of the biceps tendon (LHBT) has anatomical variants that affect its relationship with the supraspinatus and can influence SLAP lesion development 3
Pathophysiological Connection
Several key pathophysiological relationships exist:
- Adherent-type variants of the long head biceps tendon to the supraspinatus significantly increase the risk of developing Type II SLAP lesions (p=0.0001) 3
- Supraspinatus tears are significantly associated with Type I SLAP lesions (p=0.001) 4
- In patients over 40 years of age, Type II SLAP lesions are commonly associated with supraspinatus tears 4
- Chronic superior instability from SLAP lesions can lead to secondary lesion-location-specific rotator cuff tears, including supraspinatus tears 5
Clinical Implications
The relationship between SLAP lesions and supraspinatus has important clinical implications:
Diagnostic Considerations
- MR arthrography is the gold standard for detecting both SLAP lesions and associated supraspinatus pathology 2
- Standard MRI without contrast can be highly effective with optimized imaging equipment 2
- Ultrasound can evaluate the supraspinatus but has limitations in detecting labral pathology 2
Physical Examination
- Hawkins' test (92% sensitive) and Neer's test (88% sensitive) can help identify supraspinatus impingement that may coexist with SLAP lesions 1
- Speed and O'Brien tests are useful for predicting anterior SLAP lesions, while the Jobe relocation test helps predict posterior SLAP lesions 5
Treatment Considerations
Non-operative management:
- Scapular exercises and balanced musculature restoration can provide symptom relief in approximately 2/3 of patients 6
Surgical management:
- For traumatic SLAP lesions with instability: SLAP repair without biceps tenotomy/tenodesis (age <40) or with biceps tenotomy/tenodesis (age >40) 6
- For overuse-related SLAP lesions without instability: biceps tenotomy or tenodesis 6
- For throwing athletes: specialized physical therapy focused on hip, core, and scapular exercise 6
Special Considerations
- Repeated impingement of the coracoacromial arch onto the supraspinatus tendon can contribute to both supraspinatus tendinopathy and associated SLAP lesions 1
- Hypovascularity in the region proximal to the supraspinatus insertion may have implications for both rotator cuff tendinopathy and SLAP lesion healing 1
- SLAP lesions with a posterior component can develop posterior-superior instability that affects the biomechanics of the supraspinatus 5
- Isolated SLAP lesions without associated pathology (including supraspinatus pathology) are uncommon 4
Common Pitfalls
- Attributing symptoms solely to a SLAP lesion when supraspinatus pathology is also present may lead to incomplete treatment 4
- Failing to recognize that different types of SLAP lesions have varying associations with supraspinatus pathology based on patient age 4
- Not considering that anatomical variants of the biceps tendon can predispose to both SLAP lesions and associated supraspinatus pathology 3
The relationship between SLAP lesions and the supraspinatus muscle is complex and multidirectional, with each potentially contributing to the development or exacerbation of pathology in the other structure.