Illustration of typical observation of scapular dyskinesis
The clinical presentation of scapular winging can have multiple causes include neurologically based scapular winging, scapular muscle detachment, snapping scapula, and kinetic chain or muscle inhibition based scapular dyskinesis. Dyskinesis is found to be present in 67–100% of patients with shoulder injuries [26–28]. However, dyskinesis is best considered a potential impairment of optimum shoulder function, and if it is found in association with shoulder symptoms, it should be further evaluated.
Scapular dyskinesis is important as a component of the disabled throwing shoulder [4, 5]. It is associated with labral tears [4, 5, 29], internal impingement (the combination of partial rotator cuff injury and labral tears) [30, 31], and elbow injuries [32]. It is considered part of the shoulder at risk, and should be checked as part of the routine pre-participation evaluation. Common causative factors for shoulder pain in sports participation are the deficits in glenohumeral internal rotation (GIRD) or total range of motion. These range of motion alterations can result from capsular, muscular, and possible osseous alterations [33]. In addition to affecting shoulder joint function, they create scapular dyskinesis in the form of scapular protraction due to a wind-up effect as the arm, while continuing into forward flexion, internal rotation, and horizontal adduction in follow through, pulls the scapula into internal rotation and anterior tilt. Since optimised scapular function is a key factor in optimal sports participation, recognition of dyskinesis and restoration of scapular retraction capability should be a standard part of injury prevention strategies. Also, scapular dyskinesis resulting from fatigue was shown to be an important factor in producing errors of arm proprioception [34]. However, the exact relationship between scapular position and/or motion and injury is unclear. Abnormal scapular motion or scapular dyskinesis has been described as a non-specific response to a painful condition in the shoulder rather than a specific response to or a definite cause of specific glenohumeral pathology [25]. Various shoulder soft tissue pathologies including impingement (internal and external) [35], anterior capsular laxity [36], labral injury [4, 5], and rotator cuff weakness [12] have been found in association with scapular dyskinesis in overhead athletes complaining of shoulder pain. However, the confounding issue is that scapular asymmetries have been noted in overhead athletes that are asymptomatic as well as those injured. At this time, it is unknown if scapular dysfunction is a cause and/or an effect of shoulder injury in overhead athletes and is, therefore, most appropriately characterised as a physical impairment [37].
4.2.2 Causative Factors for Scapular Dyskinesis
Most scapular dyskinesis results from alteration in coupled muscle activation within the upper trapezius, lower trapezius, rhomboids, and serratus anterior. Neurogenic causes include injury to the long thoracic or spinal accessory nerves, which appear to be relatively rare in throwing athletes. More commonly, the alterations are due to inhibition of activation due to pain from glenohumeral joint injury [38], strength imbalance among the scapular stabilisers [39], fatigue of muscle activation [40], or change in activation pattern [17]. In virtually every case, the serratus anterior and lower trapezius have been shown to be weak, display less activation intensity, or to be late in activation timing, while the upper trapezius displays increased activation and abnormal activation timing [41]. This results in less posterior tilt, less external rotation, and less upward rotation motions, but increased elevation translation [21, 41]. These results have been found in throwers with impingement [42], instability [28], and labral tears [4, 5].
Bony causes in athletes relate to alteration in the strut stabilisation function of the clavicle. This would include malunited (shortened, angulated, or malrotated) or non-united fractures, high-grade (type V, some type III) acromioclavicular separations, or excessive (greater than 5 mm) distal clavicle excision.
4.2.3 Scapular Dyskinesis and Specific Shoulder Injuries
4.2.3.1 Labral Injury
Scapular dyskinesis has a high association with labral injury [43, 44]. The altered position and motion of internal rotation and anterior tilt changes glenohumeral alignment, placing increased tensile strain on the anterior ligaments [36], increases “peel-back” of the biceps/labral complex on the glenoid [4, 5], and creates pathological internal impingement [44]. These effects are magnified in the presence of GIRD, which creates increased protraction due to “wind-up” of the tight posterior structures in follow-through. The demonstration of dyskinesis in patients with suspected labral injury provides a key component of rehabilitation protocols. Correction of the symptoms of pain found in the modified dynamic labral shear test [45] can be frequently demonstrated by the addition of manual scapular retraction [46]. This indicates the presence of dyskinesis as part of the pathophysiology and the need for scapular rehabilitation to improve scapular retraction, including mobilisation of tight anterior muscles and institution of the scapular stability series of strengthening exercises.
Impingement
Impingement is frequently seen in throwing athletes. Most commonly in this group, impingement is secondary to other pathology such as instability, labral injury, or biceps pathology. Scapular dyskinesis is associated with impingement by altering scapular position at rest and upon dynamic motion. Scapular dyskinesis in impingement is characterised by loss of acromial upward rotation, excessive scapular internal rotation, and excessive scapular anterior tilt [22, 47]. These positions create scapular protraction, which decreases the subacromial space [21] and decreases demonstrated rotator cuff strength [20, 24].
Activation sequencing patterns and strength of the muscles that stabilise the scapula are altered in patients with impingement and scapular dyskinesis. Increased upper trapezius activity, imbalance of upper trapezius/lower trapezius activation so that the lower trapezius activates later than normal, and decreased serratus anterior activation have been reported in patients with impingement [21–23]. Increased upper trapezius activity is clinically observed as a shrug manoeuvre, resulting in a variation of the scapular dyskinesis pattern. This causes impingement due to lack of acromial elevation. Frequently, lower trapezius activation is inhibited or is delayed creating impingement due to loss of acromial elevation and posterior tilt. Serratus anterior activation has been shown to be decreased in patients with impingement, creating a lack of scapular external rotation and elevation with arm elevation [19].
The pectoralis minor has been shown to be shortened in length in patients with impingement. This tight muscle creates a position of scapular protraction at rest and does not allow scapular posterior tilt or external rotation upon arm motion, predisposing patients to impingement symptoms [48].
4.2.3.2 Rotator Cuff Injury
The rotator cuff is frequently clinically involved in throwers with shoulder symptoms and these symptoms can be exacerbated by dyskinesis. The dyskinetic position that results in an internally rotated and anteriorly tilted glenoid increases the internal impingement on the posterior superior glenoid with arm external rotation and increases the torsional twisting of the rotator cuff, which may create the under-surface rotator cuff injuries seen in throwers [4, 5, 35]. In addition, positions of scapular protraction have been shown to be limiting to the development of maximal rotator cuff strength. Recent work in laboratory models of rotator cuff disease has shown that surgically induced scapular dyskinesis results in changes in cell morphology, gene expression, and tendon characteristics that are similar to those seen in rotator cuff tendinopathy [49].
4.2.3.3 AC Joint Injuries
AC joint injuries are rare in throwing athletes except American football quarterbacks, but they can create major functional deficits due to the disruption of the important AC linkage. Dyskinesis is found in a high percentage of patients with high grade AC symptoms [26]. AC separations lessen, and high-grade AC separations remove, the strut function of the clavicle on the scapula. Loss of the strut function allows the “third translation” of the scapula, allowing it to move interior and medial to the clavicle, changing the biomechanical screw axis of scapulohumeral rhythm, allowing excessive scapular internal rotation and protraction and decreased dynamic acromial elevation when the arm is elevated. Iatrogenic AC joint injury due to excessive distal clavicle resection and detachment of the AC ligaments shortens the bony strut and allows excessive scapular internal rotation due to excessive anterior/posterior motion at the AC joint. The protracted scapular position creates many of the dysfunctional problems associated with chronic AC separations, including impingement and decreased demonstrated rotator cuff strength. However, scapular and shoulder dysfunction can also occur in type II injuries if the AC ligaments are torn. This creates an anterior/posterior AC joint laxity and can be associated with symptoms of pain, clicking, decreased arm elevation, and decreased shoulder function.
If dyskinesis is demonstrated on the clinical exam, then increased attention should be directed towards correcting the biomechanical abnormality rather than just placing the arm in a sling. Treatment should include, not only CC ligament reconstruction, but also AC ligament reconstruction to completely restore the screw axis mechanism.
4.2.3.4 Clavicle Fractures
Clavicle fractures may produce dyskinesis if the anatomy is not completely restored. The dyskinesis can be associated with alterations in shoulder function such as decreased strength and decreased arm motion in elevation [50]. Shortened mal-unions or non-unions decrease the length of the strut, and alter the scapular position towards internal rotation and anterior tilt. In addition to changes in length, changes in clavicle curvature or rotation will affect scapular position or motion. Angulated fractures result in functional shortening and loss of rotation. The distal fragment in midshaft fractures often internally rotates, decreasing the obligatory clavicle posterior rotation and scapular posterior tilt during arm elevation. Dyskinesis can be a clinical sign of potentially harmful alteration of clavicle anatomy, and can provide information to clarify indications for operative treatment in these fractures.
4.2.3.5 Scapular Muscle Detachment
Scapular muscle detachment is a relatively rare and poorly characterized injury, and the diagnosis is often delayed or missed [51]. The pathoanatomy appears to be detachment of the lower trapezius and rhomboids from the spine and medial border of the scapula. The scapula usually presents in a position of protraction and lateral translation. The majority of cases present after an acute traumatic tensile load such as seat-belt-restrained motor-vehicle accidents, catching or lifting a heavy object with the arm at full extension, or pulling against a heavy object. In athletes, it may occur after a fall, or from an acute tear in throwing. The presenting symptom cluster is very uniform with early post-traumatic onset of localised and intense pain along the medial scapular border. There is a weakness of the rhomboids and lower trapezius, with difficulty in retracting the scapula, with resulting major limitations of arm use away from the body in forward flexion or overhead positions. Increased upper trapezius activity and spasm, resulting from lack of lower trapezius activity, creates migraine-like headaches. Neck and shoulder joint symptoms may be present due to dyskinesis and will often become the focus of treatment, including surgery that may not properly address the underlying pathology.
Surgical exploration for repair of scapular muscle detachment is indicated after failure to improve symptoms following a specific protocol of scapular retraction and depression exercises [52, 53]. The operative technique has been previously described in detail as well as mid-term outcome results [51, 54].
4.3 Evaluation of the Scapula in the Throwing Athlete
The history is an important part of the evaluation. Specific questions should be asked regarding past or present trauma to the scapula, clavicle, or AC joint, chronic or acute spinal symptoms, recent or remote hip or leg injuries, or any surgical procedures. It is also important to establish if the patients have had physical therapy for any of these conditions, or for a scapular condition to document the exact extent of the therapy, and to document the results. Therapy that emphasises modalities, early open chain rotator cuff exercises with resistance, shoulder shrugs, and shoulder protraction exercises have not been found to be effective for scapular dyskinesis.
The goals of the scapular examination are to establish the presence or absence or dyskinesis, the effect on symptoms of corrective manoeuvres, and to investigate possible bony, joint derangement, or muscle strength/flexibility causes for the dyskinesis.
The scapular exam should largely be accomplished from the posterior aspect. The scapula should be exposed for complete visualisation. The resting posture should be checked for side to side asymmetry and obvious inferior medial or medial border prominence. If there is difficulty with determining the bony landmarks of the inferior medial or superior medial angles, marking the superior and inferior medial borders may help ascertain the position.
Visual dynamic assessment schemes of classifying the presence of scapular dyskinesis during shoulder motion have been developed in an attempt to resolve the issues with linear or static measures [8, 55, 56]. These methods are considered more functional and more inclusive with the ability to judge scapular movement in 3-dimensional patterns. Kibler et al. [55] were the first to describe a visually based system for rating scapular dysfunction that defined 3 different types of motion abnormality and one normal type. Reliability values for this system were too low to support clinical use and the test was subsequently refined [8, 56].
The scapular dyskinesis test [56] is a visual-based test for scapular dyskinesis that involves a patient performing weighted shoulder flexion and abduction movements while scapular motion is visually observed. This test consists of characterising scapular dyskinesis as absent or present and each side is rated separately. Good inter-rater reliability of this test (75–82% agreement; weighted kappa = 0.48–0.61) was achieved after brief standardised online training. Concurrent validity was demonstrated in a large group of overhead athletes, finding those judged as demonstrating abnormal motion using this system also demonstrated decreased scapular upward rotation, less clavicular elevation and less clavicular retraction when measured with 3-dimensional motion tracking [57]. These results support the assertion that shoulders visually judged as having dyskinesis utilising this system, demonstrate distinct alterations in 3-dimensional scapular motion, particularly during flexion.
Another dynamic test developed by Uhl et al. [8] used essentially the same criteria as the scapular dyskinesis test (winging or dysrhythmia) to classify an abnormality in scapular motion into the “yes” classification, and normal movement was classified as “no”. They studied both symptomatic patients with various soft tissue pathologies as well as an asymptomatic group. The “yes/no” test was found to have superior inter-rater reliability (79% agreement; kappa = 0.41), and demonstrated better specificity and sensitivity values when using asymmetry found with 3-dimensional testing as a gold standard [8]. An important finding in this study was a higher frequency of multiple-plane dyskinesis during shoulder flexion in patients (54%) compared with asymptomatic subjects (14%), while no differences between groups were detected during scapular plane elevation. It appears that the optimum position for evaluating scapular dyskinesis dynamically is in forward flexion.
The scapular assistance test
The scapular retraction test
Although these tests are not capable of diagnosing a specific form of shoulder pathology, a positive SAT or SRT shows that scapular dyskinesis is directly involved in producing the symptoms and indicates the need for inclusion of early scapular rehabilitation exercises to improve scapular control.
Coracoid based inflexibility can be assessed by palpation of the pectoralis minor and the short head of the biceps brachii at their insertion on the coracoid tip. The muscles will usually be tender to palpation, even if they are not symptomatic in use, can be traced to their insertions on the ribs as taut bands, and will create symptoms of soreness and stiffness when the scapulae are manually maximally retracted and the arm is slightly abducted to approximately 40–50°.
A major portion of the scapular exam is the evaluation of the proximal kinetic chain and distal glenohumeral joint structures that affect scapular position and motion. Kinetic chain screening can be accomplished by the one leg stability series—a combination of a standing balance test that assesses static control, and a single leg squat test that assesses dynamic control of the body over the planted leg [59]. In the standing balance test, the patient is asked to place their hands over their chest and stand on one leg with no other verbal cue. Deficits in balance and stability such as a Trendelenburg posture or internally or externally rotating the weight bearing limb indicates inability to control the posture and has been found to correlate with proximal core weakness especially in the gluteus medius [60–62]. The single leg squat is the next progressive evaluation. Assuming the same starting point as the standing balance test, the patient is asked to do repetitive partial half squats going down and returning to the standing position with no other verbal cues. Similar deviations in the quality of the movement are assessed as in the standing balance test. A Trendelenburg posture, which may not be noted on standing balance, may be brought out with a single leg squat. The patient may also use their arms for balance or may go into an exaggerated flexed or rotated posture—“corkscrewing”—in order to put the gluteal or short rotator muscles on greater tension to compensate for muscular weakness.
Standard glenohumeral exam techniques should be employed to evaluate for internal derangement and AC joint instability. Special attention should be paid to the examination for GIRD and the evaluation of labral injuries, both of which are associated with dyskinesis. To obtain accurate glenohumeral internal rotation measurements, the patient should be positioned supine on a flat level surface. A second examiner should be positioned behind the athlete in order to properly stabilise the scapula by applying a posteriorly directed force to the coracoid and humeral head to ensure that scapular movement does not occur [63, 64]. The humerus is supported on the surface with the elbow placed at 90° and the arm on a bolster in the plane of the scapula. A measurement is obtained using a standard bubble goniometer where the fulcrum is set at the olecranon process of the elbow, the stationary arm perpendicular to the table as documented by the bubble on the goniometer, and the moving arm in line with the styloid process of the ulna. The clinician passively moves the arm into internal and external rotation. Rotation is taken to “tightness”, a point where no more glenohumeral motion would occur unless the scapula would move or the examiner applies rotational pressure. This measurement should be taken bilaterally, and side-to-side differences are calculated. Side-to-side differences in internal rotation greater than 20° are considered clinical GIRD.
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