Shoulder pain affects up to 67% of the population at some point in their lifetime.¹ Although the etiology of shoulder pain is multifactorial, specific impairments such as posterior shoulder tightness have been associated with many of the more common conditions. Generally speaking, PST may be defined as soft tissue restrictions of the posterior shoulder structures. These restrictions may be the result of adaptive shortening, contractile tissue stiffness, and/or contracture of the posterior capsuloligamentous structures. While the concept of posterior capsule tightness is not new to physical therapists, the term “capsule” is a misnomer because the impairments associated with PST may be attributed to both contractile and inert tissue.

PST has received considerable attention in the literature because it has been associated with and implicated in the etiology of numerous shoulder disorders, such as rotator cuff pathology and impingement syndromes (subacromial and internal), as well as labral tears.^2-6 Overhead athletes in particular are prone to PST because of repetitive microtrauma at the posterior capsule and articular surface of the rotator cuff during the follow-through phase of throwing, which eccentrically stresses these tissues. It has been presumed that these stresses may induce hypertrophy (thickening and contracture of the soft tissue), thus leading to PST. In the weight-training population, it has been postulated that the lack of internal rotation during common exercises permits the posterior tissues to adaptively shorten. Moreover, it is not common practice for weight-training participants to stretch the posterior shoulder tissues.⁷ Although overhead athletes and weight-training participants are prone to developing PST, this impairment has been reported in the general population as well. Trauma, post-operative fibrosis, and idiopathic explanations have been offered for the pathogenesis of PST in the general population. Irrespective of sports participation or etiology, evidence suggests that exercise programs designed to reduce PST may be effective in preventing shoulder pain among athletes as well as reducing pain among symptomatic individuals who have existing shoulder pain.^8-10

Given the evidence implicating PST as both a causative and a perpetuating factor for shoulder disorders, rehabilitation professionals must have an understanding of evidence-based procedures that may accurately identify and treat this condition.

Anatomical and Biomechanical Considerations

A brief discussion of the relevant posterior shoulder anatomy is required to understand the structures that may be responsible for PST. The shoulder complex includes the glenohumeral, acromioclavicular, and sternoclavicular joints, along with the scapulothoracic articulation. An individual’s shoulder mobility is dependent upon numerous factors, including joint mobility, flexibility of soft tissues (such as the shoulder capsule and muscles), and synchrony of the shoulder complex musculature. PST primarily affects the glenohumeral joint and has been associated with impaired mobility of the posterior glenohumeral joint capsule^11-13 and posterior-inferior glenohumeral ligaments,¹² as well as stiffness of the infraspinatus, teres minor, and posterior deltoid musculature.^14,15 PST may result from any combination of the aforementioned soft-tissue structures and should not be considered as only arising from the posterior capsule.

From a biomechanical perspective, PST has been directly linked to altered shoulder biomechanics such as abnormal humeral head translation, which may lead to subacromial impingement, internal impingement, and the ensuing mobility impairments of internal rotation (when arm is abducted to 90°) flexion, and horizontal adduction.⁵ Specifically, PST induces “obligate translation,” which means the humeral head translates away from the region of tightness. Thus, in the normal functioning shoulder, posterior translation is required during glenohumeral internal rotation; however, in the presence of PST, the humeral head may inadvertently translate anteriorly. This anterior translation not only compromises normal arthrokinematics and impairs mobility, but it may place the humeral head in close proximity to the acromion process, leading to impingement. Another example is horizontal adduction, which requires lengthening of the posterior tissues to allow both osteokinematic motion and the posterior translation of the humeral head. In the case of PST, the posterior soft tissue will not lengthen, and thus the humeral head will have an obligatory anterior translation that compromises normal mobility. Moreover, the loss of horizontal adduction may be clinically occult during standard goniometric measurements as a result of compensation from scapular protraction. Scapular protraction as a compensatory movement may allow full horizontal adduction.

In the throwing population, PST causes abnormal humeral head translation during the late-cocking phase of throwing (when arm is cocked back prior to release). During the late-cocking phase of throwing, the humeral head is purported to translate posterior and inferior to allow the necessary external rotation. In the presence of PST, the humeral head shifts superior in the late-cocking phase as a result of posterior-inferior glenohumeral ligament tightness. This superior shift has been implicated as a causative source of internal impingement (impingement of the articular surface of the posterior rotator cuff and posterosuperior labral tissue between the humerus and glenoid neck). Individuals with internal impingement have a propensity to develop articular surface rotator-cuff tears as well as posterior and poster-superior labral tears.

Physical therapists should recognize that PST is an impairment, not a diagnosis per se. Although PST has been associated with certain diagnoses, the clinical presentation will represent the actual diagnosis. However, clinical characteristics such as pain in the posterior shoulder and a specific pattern of mobility loss are associated with PST. Individuals with PST often will present with a loss of internal rotation, flexion, and possibly horizontal adduction. Evidence exists from both in vivo (living patients) and in vitro (cadavers) studies that suggest this loss of mobility may be directly attributed to PST. Specifically, researchers have reported that surgically releasing the posterior shoulder capsule and posterior-inferior glenohumeral ligaments leads to restoration of internal rotation, whereas surgical tightening of the capsule and ligaments directly impairs internal rotation mobility and leads to subacromial impingement during flexion. Clinically, a loss of horizontal adduction is often less obvious, owing to compensatory scapular protraction. Despite the fact that PST is characterized by a loss of internal rotation, flexion, and horizontal adduction, current measurements may not be sufficient to quantify the contribution of PST to these mobility impairments. Although internal rotation loss has been directly linked to PST through surgical exploration^16,17 and imaging studies,^2,18 its use as a sole measurement may be confounded by joint pathology such as osteophytes¹⁹ and increased humeral retroversion,^20,21 which is often present among overhead athletes. Retroversion is a structural change of the humerus that results from torsion during the ossification phase of growth and leads to a structural loss of internal rotation as well as increased external rotation.²⁰ Retroversion is common among throwing athletes²² who began competitive training at an early age when the growth plates were not completely ossified. Thus, the presence of retroversion may prevent clinicians from gathering an accurate depiction of PST from internal rotation measurements alone. While it is beyond the scope of this course to discuss retroversion in depth, it should be noted that clinicians with experience in treating throwing athletes will often use total range of motion (internal rotation + external rotation) and compare the affected to unaffected sides to gain a more accurate assessment of the extent to which PST is contributing to the loss of IR with respect to retroversion. In regard to total range of motion, if the loss of IR is a result of retroversion and not PST, the total range of motion would be nearly equal on both sides. The reason for this nearly equal measurement despite a loss of IR lies in the osseous changes that produce increased ER. When measuring osteokinematic horizontal adduction, there are shortcomings as well if the goal is to identify PST. The techniques described in traditional joint measurement textbooks do not isolate the glenohumeral joint, thus allowing the scapula to protract as a means of compensation. As a result, measurements have been specifically designed to quantify PST that prevent scapular compensation and are not necessarily affected by humeral retroversion or osteophytes.

Quantifying PST

The measurement procedure used to identify PST has been found to possess good reliability (consistent reproducibility) and validity for quantifying PST among individuals both with and without shoulder disorders.²³ The procedure requires a treatment table and either a gravity-based dial or bubble inclinometer (Figures 1A and B), which may be obtained at a local hardware store or through a medical supply company. The inclinometer illustrated in Figure 1A costs approximately $10 at a hardware store. For simplicity, the technique will be described using the inclinometer in Figure 1A because it is gravity based and has a set zero-point. Other inclinometers such as the one illustrated in Figure 1B require the tester to set the dial to zero at a “true-zero” point prior to use. Digital inclinometers may also be used, however, at a substantial cost compared to the aforementioned models.

                          
Figure 1: A) Gravity-based dial inclinometer        B) Gravity-based bubble inclinometer

The procedure for measuring PST is performed with the individual in side-lying position on his or her non-tested side (Figure 2) with the tested arm up. The individual being measured should be close to the edge of the table to allow the tested arm to possibly move past the table (although unlikely) during the test. The non-tested extremity is placed under the head to support a neutral neck position; the trunk should be directly perpendicular to the plinth with hips and knees flexed to 45°. It is important that the individual being measured is in a strict side-lying position and that his or her trunk is not rotated, otherwise the tester may get an inaccurately high or low measurement angle result. The tester stands facing the individual at the level of his or her shoulders and grasps the flexed elbow with one hand while passively abducting the humerus to 90° (maintaining 0° of rotation at the humerus) as illustrated in Figure 2. Arm positioning is maintained with the initial contact hand while the other hand manually contacts the participant’s lateral scapular border and places it in a fully adducted (retracted) position toward the spine as illustrated in Figure 2. This fully retracted scapular position is to be maintained by the tester throughout the procedure. Failure to maintain strict scapular retraction during the measurement may compromise the reliability and validity of the measurement. Recent evidence suggests that even a neutral non-protracted position may be insufficient to stress the posterior capsule.²⁴

Figure 2: Side-lying position illustrating start position for measurement. Individual being measured is lying on non-tested side with arm abducted to 90° and the humerus in neutral rotation. Examiner retracts scapula toward table (arrow).

The next step in the measurement requires the tester to passively lower the arm (toward the table) across the individual’s chest in the transverse plane (Figure 3). It is important that during this step the humerus is lowered in the strict horizontal plane at 90°. Also, the tester must maintain neutral humerus rotation and scapular stabilization in the retracted position for the duration of the measurement. The movement is ceased once the tester determines that the scapula or humerus is unable to be further stabilized and/or movement stops.  Once end range is obtained, a trained assistant places the inclinometer flat on the distal arm (Figure 3) and the measurement angle is recorded in degrees. A normal angle for this measurement among asymptomatic individuals who do not participate in overhead sports or weight training is approximately 83°.^9,25 A change of greater than or equal to 8° would be required to exceed the threshold of measurement error for this  technique (minimal detectable change)²⁶ when the same tester repeats the measurement or 9° when the measurement is obtained by two different testers.²³ Thus, if the same clinician repeats the measurement at a subsequent session to determine improvement, a change of 8° or greater would be needed to indicate true change. A change of 5°, for example, may be the result of the expected error in the measurement technique.

Figure 3: End measurement position for PST. Examiner achieves end-range while maintaining scapular retraction (arrow). A trained assistant places inclinometer on distal arm to be recorder.

Interventions

Clinicians may use various interventions to address PST, including but not limited to joint mobilization, muscle energy techniques and stretching exercises.^10,27,28 Application of posterior glides has been efficacious among patients with internal impingement10; however, some individuals may have hypermobile posterior translation of the humeral head on the glenoid despite having PST.

Evidence exists to support the inclusion of PST exercises as both a preventive and a corrective intervention. Specifically, exercises designed to address PST have been associated with symptom resolution among individuals with shoulder disorders from both the athletic and the general population.^9,10,15,16  Moreover, preventive interventions designed to address PST have been reported as reducing injury rates among both baseball and tennis players.⁸

Numerous exercises have been advocated to improve PST, and it is not unreasonable to assume that any position that achieves end-range horizontal adduction or internal rotation would be effective. Although this may be the case, all exercises are not created equal and an understanding of both biomechanics and compensatory patterns may assist the clinician in choosing the most effective exercises. Movements of the shoulder complex, which are often prescribed to stretch the posterior structures, such as horizontal adduction (cross-arm stretch), may be less effective as a result of compensatory movement from the scapulothoracic articulation if the scapula is not stabilized. During horizontal adduction, the posterior shoulder tissues are engaged; however, the freely moving scapula will often compensate and limit the stretch’s effectiveness to isolate the posterior shoulder structures. Similarly, during internal rotation, the scapula may tip forward, thus limiting the movement’s ability to engage the posterior shoulder structures. Effective stretching exercises must incorporate both movements that engage the posterior shoulder structures and stabilize the scapula to prevent compensation. The sleeper and cross-arm stretches have been recommended to decrease PST. Both stretches have been found efficacious in research investigations and are relatively simple to perform.^9,27,29 Moreover, these exercises may be performed in both injured and asymptomatic individuals.

The sleeper stretch is performed with the body in the side-lying position. Participants lie on the side to be stretched with their arm in a position of just below 90° of abduction with the forearm flexed to 90°. Once in position, the opposite arm is used to push (proximal to the wrist) the stretched arm toward the table (Figure 4). With the side-lying cross-arm stretch, the individual lies on the side to be stretched with the arm in a 90° abducted position. Once in position, the opposite arm is used to pull the arm (proximal to the elbow) across the chest (Figure 5). An advantage of performing the cross-arm stretch in the side-lying position is the ability to stabilize the scapula and prevent compensatory scapular protraction.

Figure 4: Sleeper stretch to improve PST. Individual lies on the side to be stretched with arm abducted to just below 90° with elbow flexed. Once in position, the non-stretched arm grasps the wrist of the arm to be stretched and pushes it toward the table (arrow).

Figure 5: Cross-arm stretch with scapular stabilization. Individual lies on the side to be stretched with arm abducted to just below 90° with elbow straight or slightly bent. Once in position, the non-stretched arm grasps the elbow of the arm to be stretched and pulls it across the chest (arrow).

Flexibility exercises should be performed on a daily basis. The exercises recommended in this program should be held for 30 seconds and repeated three to five times (similar to the duration and frequency used in the studies that have identified efficacy of the stretches).^27,29 Individuals are advised to bring each stretch to the point of mild discomfort and then hold it. If the discomfort level increases during the stretch, they should release the position to a steady level. Participants should be advised that the strain felt during the stretch should resolve immediately upon completion. If the strain persists, participants should reduce the intensity in future sessions. Because individuals may lose mobility following resistance training sessions, timing of stretches should be considered; it would not be unreasonable for participants to perform the stretches after resistance training in addition to their daily routine if they have PST. When PST is improved, the clinician would recognize an increase of internal rotation mobility and PST using the previously mentioned measurement technique. Finally, it is important to prescribe exercises within an individual’s available range of motion. As participants improve, the posterior shoulder mobility exercises should be prescribed within the new range.

Conclusion

PST has been identified in the literature as an impairment that is both predictive of and associated with shoulder disorders. Therefore, it is essential for clinicians to possess an understanding of measurements designed to quantify PST. The measurement technique described in this program is relatively simple, has portability, and does not require expensive equipment. A disadvantage lies in the need to recruit an assistant to record the measurement, which may make the technique undesirable for some.

Although many individuals engage in stretching, the posterior shoulder structures may often be overlooked or ineffectively addressed. The stretching exercises recommended are designed to isolate the posterior structures while preventing compensatory scapular movements. These exercises have been found efficacious in the literature. Individuals involved in prescribing exercises must be cognizant of proper form in order to isolate the desired structures, as illustrated above. Finally, individuals with previously diagnosed shoulder disorders may perform these exercises, provided they do not experience pain or discomfort at the conclusion of the stretch. 

Gannett Education guarantees this educational activity is free from bias.