Over the past 20 years, there has been an increasing interest in and number of studies investigating the biomechanics of the scapula and its role in shoulder pathologies. In 2003, the “scapula summit” (1) was founded, where leading entities in this field meet to discuss the biomechanical and clinical factors attributed to the scapula in causing shoulder pathologies, in particular, “scapula dyskinesis.”
Scapula dyskinesis is defined as “the alteration of normal scapula kinematics” (1). It has been argued that the alternative term of scapula dyskinesia, meaning abnormally active movements of the scapula secondary to neurological mechanisms, such as tardive dyskinesia, should be phased out. This is because there are many other mechanical factors that can cause altered kinematics of the scapula, such as clavicle fractures and acromioclavicular (AC) ligament ruptures. Therefore, the term scapula dyskinesis is preferred as the term is more inclusive (2).
Scapula dyskinesis can be asymptotic or symptomatic and is largely recognized in athletes who perform repetitive overhead hand movements, as in tennis, volleyball, and baseball. The 2001 Wimbledon winner, Goren Ivenisovich, is one of a few famous examples of high-performance athletes to have either ended or taken a break from their sports careers as a result of scapula dyskinesis (3).
To understand the pathophysiology of this condition, it is essential for clinicians to have a grasp on the normal biomechanics of the scapula.
The triangular shaped scapula is a highly mobile bone. Its full mobility is unlikely to be initially appreciated due to its coverings of muscles. The scapula’s only bony articulation is with the clavicle at the AC joint which acts as a bony strut for the shoulder. There is no articulation with the posterior thoracic wall. This lack of congruency allows the scapula to be mobile, allowing movements of elevation, depression (superior translation [ST]/inferior translation), retraction, protraction (PRO), internal rotation (IR)/external rotation, anterior/posterior tilt, and upward rotation (UR)/downward rotation. These movements occur via a gliding motion of the scapula on the thoracic cage secondary to contraction of serratus anterior and subscapularis (4). Figure 1 depicts the rotary movements of the scapula.
There are a number of muscles that surround and insert to the scapula, which can be divided functionally into three groups (5). First, muscles that contribute to scapula stability and rotation-trapezius, rhomboids, levator scapulae, and serratus anterior. Second, the extrinsic muscles of the glenohumeral joint, deltoid, biceps, and triceps; and a third group of intrinsic muscles, or the “shoulder protectors” comprising the rotator cuff muscles, supraspinatus, infraspinatus, teres minor, and subscapularis. The next section will focus on this first group of muscles.
Originating from ribs 1 to 8, it travels posterosuperiorly along the rib cage to insert to the medial border of the scapula with the inferior fibers attaching into the inferior angle of the scapula. These multiple sites of attachment give the muscle a pivotal role in scapula stabilization during elevation and to protract the scapula on the thoracic cage. Three-dimensional (3D) orientation studies and electromyography (EMG) reading have shown that serratus anterior has a role in posterior tilting, external rotation, and UR of the scapula (6).
Rhomboids (major and minor)
Rhomboid minor originates from the spinous processes of C7 to T1, and rhomboid major originates from T2 to T5. They insert to the medial border of the scapula near the base of the scapula spine and inferior to this, respectively. These muscles are powerful retractors of the scapula. Full retraction is imperative for sporting actions, such as throwing or a tennis serve. The EMG studies on baseball players during the action of pitching a ball also have shown eccentric contraction of the rhomboids during the follow-through action of a baseball pitch, where the rhomboids help reduce the velocity of the arm once the ball has been thrown. Therefore, rhomboid integrity is essential for rapid overhead arm movements (8).
Originating from the medial third of the nuchal line, external occipital protuberance, nuchal ligament, and spinous processes of C7 to T12, it attaches to the lateral third of the clavicle, acromion, and spine of the scapula. The large trapezius muscle, depending on the orientation of the fibers, aids the elevation of the scapula and UR (superior fibers), retraction (middle fibers), and UR and depression (inferior fibers). The EMG studies highlight that the downward and medially directed inferior fibers of trapezius may have a role in posterior tilting and external rotation of the scapula (6).
Originating from the transverse processes of C1 to C4 and is inserted to the medial border of the scapula at the level of the scapula spine. The function of the levator is to elevate the scapula and rotate the scapula downward. The EMG studies have found it difficult to isolate levator scapulae activity as the probes may be influenced by crosstalk from the upper trapezius given their close proximity. Nevertheless, Ludewig et al. (6) showed an increase in muscle activity in 72% of subjects during humeral elevation.
Normal Biomechanics of the Scapula
During the first 30° to 50° of humeral abduction, the scapula moves laterally on the thoracic cage. As abduction continues past 50°, the scapula undergoes UR of approximately 65° as the shoulder reaches full abduction. This scapula-humeral rhythm has an average ratio of approximately 2:1 between the glenohumeral rotation and scapulothoracic rotation. This varies according to the arms angle. Some authors report variations in this ratio from 1:1 to 4:1.
Retraction of the scapula depends on the size of the subject’s thoracic cage for the scapula to translate on and also the type of activity conducted. Studies have shown that distance from full retraction to full PRO can be between 15 cm and 18 cm. PRO is usually a lateral movement which follows the anterior curve of the posterior thoracic cage and is usually nonlinear in the transverse plane with movement superiorly or inferiorly, depending on the activity undertaken. Retraction is usually linear in the transverse plane, curving around the thoracic cage.
The moments described are resultant forces from muscle activation of the muscles around the shoulder in addition to passive forces from momentum and inertia of the movements of the upper limbs and trunk. Most of the movements of the scapula are secondary to contraction of the scapula stabilizers group of muscles described above. These muscles generally act in pairs to exert their effects. Generally, the upper trapezius is paired with the lower trapezius and serratus anterior; this is accepted to be the most important force couple in arm elevation (9).
Causes of Dyskinesis
Scapula dyskinesis can occur as a result of any injury or alteration to the bony or soft tissue anatomy, such as labral injuries, biceps injuries, instability and adhesive capsulitis. Bony causes include clavicle fractures leading to shortening or nonunion, excessive thoracic kyphosis, AC joint disruption, and abnormalities in the glenohumeral joint.
Soft tissue abnormalities causing dyskinesis can involve any pathology related to the rotator cuff. PRO and anterior tilt of the scapula can be caused by pulling of the coracoid process anteriorly by pectoralis minor and the short head of biceps (10). Shoulder impingement can cause pain, which in turn can lead to voluntary underuse of serratus anterior, which can reduce the posterior tilt and UR of the scapula, leading to dyskinesis (11). As mentioned, the upper and lower trapeziuses are coupled to instigate certain movements and any alteration in this pairing, such as delayed activation of lower fibers, can augment posterior tilting and upward scapula rotation (1).
Neurological injuries involving cranial nerve 11, the long thoracic nerve, or cervical radiculopathy also will result in decreased power of the surrounding musculature, resulting in scapula dyskinesis.
Clinical Features of Scapula Dyskinesis
In 2003, Burkhart et al. (12) coined the “SICK syndrome,” which is an acronym for the clinical symptoms displayed by patients with clinically obvious scapula dyskinesis, because it is not a specific diagnosis but a collection of symptoms. The acronym equates to S-scapula malposition, I-inferior medial border prominence, C-coracoid pain and malposition, and K-dyskinesis of scapula motion. Patients with this syndrome classically present with a dropped scapula (13), as shown in Figure 2.
Scapula dyskinesis can be asymptomatic; however, symptomatic patients most commonly report pain in the medial scapular border. Other areas of pain are either in the anterior or posterior aspects and sometimes laterally, inferior to the acromion. Patients may rarely complain of pain radiating throughout the superior portion of the trapezius. The most common complaint is anterior pain in the coracoid process due to a tight pectoralis minor causing a downward tilt and retraction of the scapula. This can easily be mistaken for anterior instability; therefore, thorough examination of the coracoids for tenderness is required (12).
Scapula dyskinesis is best observed with the patients facing forward. If the patient shows one or more asymmetrical positions, this is generally regarded as a dyskinesis. In 2002, Kibler et al. (14) classified altered scapula kinematics into four recognizable patterns shown in Figure 3; type I, inferior medical scapula border prominence; type II, medial scapula border prominence; type III, prominence of the superomedial border of the scapula; and type IV, normal.
How to Assess Scapula Dyskinesis
This section of the review is going to cover the various ways of assessing scapula dyskinesis using clinical tests, objective measurements, direct 3D kinematic measurements, and 3D wing computer tomography.
Clinical Observational Tests
Scapula dyskinesis test
The patient is asked to flex and abduct their shoulder while carrying light weights (15). The practitioner then observes to see if there is any protrusion of the medial/inferior borders of the scapula away from the thorax sometimes referred to as winging; however, it is not a true winged scapula as seen in a long thoracic nerve palsy. Uncoordinated movements, such as early/late scapula elevation and stuttering, also are noted. This test uses the visually altered 3D kinematics of the scapula in dyskinetic shoulders. A second group of authors (16) modified the same test, by assessing defined parameters, recording any positive findings as a yes, and normal findings as a no. This is currently the gold standard for observational testing (1,2).
Lateral scapula slide test
Bilateral measurements are made from the inferior angle of the scapula to the closest spinous process while the arms are elevated. The difference between the measurements from both sides indicates the severity of the dyskinesis (8).
Scapula assistance test
This test attempts to reduce the abnormal lie of a dyskinetic scapula. During shoulder elevation, the clinician applies lateral pressure to the inferior portion of the medial border of the scapula while stabilizing the upper medial border with the free hand (Fig. 4). A test is deemed positive if the maneuver relieves pain caused by impingement or painful arc, making it useful in these situations; however, it is not useful in asymptomatic individuals (17).
Scapula repositioning test
This involves the clinician attempting to realign the scapula by stabilizing its medial edge and simultaneously posteriorly tilting the scapula while it is marginally retracted on the thoracic cage (18). A positive result is counted if this maneuver reduces the pain and there is an increase in strength during isometric contraction of the affected arm during elevation (19).
It is possible to assess scapula dyskinetic movements, in particular in SICK scapula syndrome (Fig. 5) using a goniometer. Three objective static measurements are taken (12).
This is the difference in height (cm) between the superomedial scapula edge of the affected and contralateral scapulae. Despite the measurement being taken in the linear, vertical axis, the measurement is actually of the rotational displacement created by forward tilting and PRO. Nevertheless, the difference in height enables evaluators to measure the extent of recovery during rehabilitation.
Measurements are taken from the superomedial scapula angle to the midline. This is done bilaterally, and the measurement is given as the difference between the left and right side (cm).
This is measured as the angle between the medial scapula border and the plumb midline. This is measured on the unaffected side also; the result is the difference between the two sides (cm).
Most patients with SICK scapula will have positive results in all three categories. A scoring system has been devised by imputing the data attained from the goniometry into a table to give a quantitative assessment of scapula dyskinesis (Fig. 6).
3D Kinematic Analysis
Studies have mapped the movement of the scapula using 3D electromagnetic tracking devices. Coordinates are interpreted by placing transmitters aligned with the chief body planes; the subject’s position can be maintained by getting them to stand on demarcated lines parallel to the transmitters. Receivers are then placed on the body on the thorax, humerus, and scapula. Receivers are electromagnets that can be mounted either by bone pins inserted under local anesthetic (19) or adhesive tape (16). Subjects are asked to maintain a resting position with arms extended and by their side. Repetitive movements, such as abduction, rotation, and flexion of the humerus, are carried out, and the transmitter and receivers interact to map the movements of the scapula in all three dimensions (Fig. 7). Anterior tilting (AT) and posterior tilting of the scapula are represented by rotation of the clavicle. Studies have been done to map the normal movements of the scapula (19) as well as in patients with dyskinetic scapula (16).
3D Wing Computer Tomography
In 2013, Park et al. (20) published an article highlighting the use of 3D wing computed tomography (CT) in mapping dyskinetic movements of the scapula. The study was conducted by trained investigators on 89 subjects (178 shoulders) with known scapula dyskinesis, grouped into one of the four types of scapula dyskinesis described by Kibler.
In order to calculate the magnitude of abnormal movements on CT, three bony landmarks were used; the inferior medial angle of the scapula (IMA), the AC joint, and the root of the spine of the scapula (RSS). From these landmarks five movements of the scapula were recorded: UR, IR, AT, ST, and PRO. Measurements were taken while the patient was laid supine on the CT scanner (Fig. 8).
UR was measured from the posterior coronal view and taken as the angle between the line joining the AC joint to the RSS and the vertebral axis. IR was taken from a superior-axial view; the angle measured was from the line joining the bilateral AC joints and the line between the AC joint and RSS. AT was taken from the lateral sagittal view; the angle was measured from the line between the IMA to the medial border of the scapula and the vertebral axis. ST was measured in the posterior coronal view; the measurement was between the AC joint to the vertebra prominence of C7 and the vertebral axis. PRO was measured in the superior-axial view and taken as the line of the vertebral axis and the line from the AC joint to the middle of the C7 vertebral body. The above values can then be compared with normal reference values as shown in Figure 9.
In order to enable appropriate rehabilitation of patients with scapula dyskinesis, it is essential that practitioners are able to accurately assess the extent of their dyskinetic movements. The simplest way of doing this is by using observational methods.
The lateral slide test introduced by Kibler has come under scrutiny for a number of reasons; the study was conducted on symptomatic athletes only, and it has been suggested that asymptomatic athletes have symmetrical stabilizers. Subsequent studies have therefore applied the lateral slide test to asymptomatic athletes with dyskinesis and found at least a 1.5 cm difference from the inferior angle to the adjacent spinous process (21). Therefore, because both asymptomatic and symptomatic patients display asymmetry the validity of this test is questionable. Furthermore, this test would be invalidated in a patient with pathological symmetrical dyskinesis, as measurements would be similar bilaterally. The specificity has been calculated at 28% and sensitivity at 57% (22). The last criticism of this test is that it only measures the abnormal lie of the scapula in a two-dimensional axis and neglects the ability of the scapula to move in three dimensions.
The scapula dyskinesis test using the yes/no method described by Uhl et al. (16) has been deemed as the gold standard for observational testing, demonstrating an inter-rater agreement of 79% and sensitivity of 76%. This test takes into account the 3D movements of the scapula and the observer is no longer restricted to recording 1 plane movement, as in the lateral slide test. However, the specificity of this method was 30% leading to a large number of false positives. The scapula dyskinesia test is, therefore, likely to be best used as a screening tool.
Scapula assistance test has been shown to provide adequate levels of reliability deeming it appropriate for clinical use (17) with kappa coefficients of 0.51 and percentage agreements between investigators shown to be 76%. Due to the nature of the test, it fails to distinguish whether it is shoulder malposition or scapula dyskinesis that is propagating the symptoms. A study on the scapula repositioning test (23) provided equivocal results; 98 athletes with shoulder impingement were tested, and 46 of them showed a positive result whereby there was a reduction in pain following the maneuver. Furthermore, an increase in strength was found in impingement groups (P = 0.001) as well as nonimpingement groups (P = 0.012).
The global pitfalls with using clinical evaluation are that it relies on operator reliability and their expertise in assessing dyskinetic movements. Even with standardization of operators, it is still very much a subjective assessment. This is exacerbated by the fact that the scapula has a deep layer of overlying tissue making it difficult to visualize abnormalities and create exact clinical criteria for categorizing the extent of dyskinesis. Goniometry can go some way to help overcome this by quantifying the extent of the abnormality. However, this technique is unlikely to give an accurate measurement of the actual extent of the scapula malposition as it is yet to be determined if the movement of the skin is an accurate representation of the movement of underlying bone. This is something that will need to be assessed in the future.
To overcome some of the pitfalls of clinical evaluation, 3D kinematics using electromagnets can be used. Difficulties here lie in the choice of appropriate bony landmarks used to create coordinates, methodology used to calculate the different angles, and choice of a fixed landmark. Unsurprisingly, there is a large amount of variability in data from the literature in healthy subjects (19). Furthermore, these tests require the drilling of bone pins into the subjects which is unlikely to be acceptable to many subjects, and it is also likely that bone pins themselves will alter the kinematics of the scapula. This can be overcome by applying adhesive electromagnets to the bony landmarks; however, movements of the overlying skin are unlikely to be representative of the underlying bone rendering it inappropriate for large dynamic movements. One study showed a positive predictive value for detecting scapula asymmetry of 79% similar to that of the yes/no version of the scapula dyskinesia test.
The study by Park et al., which investigated 179 shoulders, is the first to describe scapula dyskinesis using CT and is one of the largest studies conducted. It compared the use of CT and observational assessment. The interclass correlation coefficient for observational methods was 0.78 (using the scapula dyskinesis test) whereas the interclass correlation coefficient for 3D wing measurements was 0.972, rendering this method of assessment the most accurate in diagnosing scapula dyskinesis, and also the type of scapula dyskinesia present (statistical value given previously). The downfall with this study is the patients were examined in the supine position while on the CT scanner; this is likely to alter the biomechanics of the joint due to gravity and the weight of the body compressing the joint against the CT bed. However, a subsequent study by the same group (24) has recently been published with the patients in a prone position. Results were again statistically significant; however, they showed an increase in IR and PRO angle when compared to the previous supine study. The major limitations with this study are the fact that these facilities are not widely available, the expense involved, and the irradiation subject’s encounter. Furthermore, these studies only quantify dyskinesis in static movements with the arms adducted and give no indication to the extent of aberrant scapula movements in important motions such as shoulder abduction or flexion. More work will have to be done in the future on how these static positions correlate to dynamic motions.
3D wing CT followed by 3D kinematic mapping is the most accurate way of qualifying scapula dyskinesis. However, the inability to map dynamic motions using CT and the invasive nature of 3D kinematics, in addition to their expense and lack of availability, make them impractical to use. These tests should be reserved for high-performance athletes where precise dyskinetic movements need to be assessed for appropriate rehabilitation. Therefore, clinical observation should remain the mainstay of evaluation for scapula dyskinesis. The most accurate test for this, as evidenced in the literature, is the scapula dyskinesia test using the yes/no methodology; however, users must be cautious of the high false positive rate.
Observational tests are certainly useful for identifying dyskinesis at initial assessment, but none of these tests are effective at identifying successful treatment and this is an area which requires more evaluation.
The author declares no conflict of interest and does not have any financial disclosures.
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