the disabled throwing shoulder: spectrum of pathology...

Current Concepts

The Disabled Throwing Shoulder: Spectrum of PathologyPart III: The SICK Scapula, Scapular Dyskinesis, the Kinetic

Chain, and Rehabilitation

Stephen S. Burkhart, M.D., Craig D. Morgan, M.D., and W. Ben Kibler, M.D.

We use the acronym SICK to refer to the findingsone sees in this syndrome (Scapular malposi-

tion, Inferior medial border prominence, Coracoidpain and malposition, and dysKinesis of scapularmovement). This recently recognized overuse muscu-lar fatigue syndrome is yet another cause of shoulderpain in the throwing athlete who presents with deadarm complaints.1 The hallmark feature of this syn-drome is asymmetric malposition of the scapula in thedominant throwing shoulder, which usually appearson examination as if one shoulder is lower than theother. This statically observable position is suggestiveof underlying muscle activation alterations that pro-duce altered kinematics of the scapula upon dynamicuse. The altered kinematics fall into 3 clinically rec-ognizable patterns of scapular dyskinesis, 2 of whichare most commonly associated with labral pathology:type I, inferior medial scapular border prominence,and type II, medial scapular border prominence.

The type III pattern, which is associated with im-pingement and rotator cuff lesions rather than labrallesions, displays prominence of the superomedial bor-der of the scapula. In the SICK scapula syndrome,scapular asymmetry is measured statically, but ac-tively produces scapular dyskinesis as the shouldergoes through the throwing cycle. The malpositioneddyskinetic scapula, in turn, dynamically produces al-tered kinematics of the glenohumeral and acromiocla-vicular joints and the muscles that insert on the scap-

ula. Because of these complex interrelationships,scapular dyskinesis, including the SICK scapula syn-drome, can cause a spectrum of clinical complaintsoriginating from any or all of these anatomic loca-tions.

A thrower with this syndrome presents with anapparent “dropped” scapula in his dominant symptom-atic shoulder compared with the contralateral shoul-der’s scapular position. In actuality, the scapula ini-tially protracts, rotating about a horizontal axis, withthe upper scapula rotating anteroinferiorly. However,the clinical appearance, with the arms relaxed in ad-duction at the side, is that the involved scapula islower than the scapula on the uninvolved side (Figs 1and 2). Viewing from behind, the inferior medialscapular border appears very prominent, with the su-perior medial border and acromion less prominent.When viewed from the front, this tilting (protraction)of the scapula makes the shoulder appear to be lowerthan the opposite side. The pectoralis minor tightensas the coracoid tilts inferiorly and shifts laterally awayfrom the midline, and its insertion at the coracoidbecomes very tender.

Symptomatic patients with an isolated SICK scap-ula may complain of anterior shoulder pain, postero-superior scapular pain, superior shoulder pain, proxi-mal lateral arm pain, or any combination of the above.In addition, posterosuperior scapular pain may radiateinto the ipsilateral paraspinous cervical region or thepatient may complain of radicular/thoracic outlet typesymptoms into the affected arm, forearm, and hand orany combination of the above. The onset of symptomswith the SICK scapula syndrome is almost alwaysinsidious. By far, the most common presenting com-plaint is anterior shoulder pain in the region of thecoracoid, which can easily be confused with anterior

Address correspondence and reprint requests to Stephen S.Burkhart, M.D., 540 Madison Oak Dr, Suite 620, San Antonio, TX78258, U.S.A.

© 2003 by the Arthroscopy Association of North America0749-8063/03/1906-3489-3$30.00/0doi:10.1016/S0749-8063(03)00389-X

641Arthroscopy: The Journal of Arthroscopic and Related Surgery, Vol 19, No 6 (July-August), 2003: pp 641-661

pain associated with anterior instability if the coracoidis not meticulously examined for tenderness. Postero-superior scapular pain with or without radiation intothe paraspinous neck region is next in frequency.Proximal lateral arm pain (subacromial) and superiorshoulder pain (acromioclavicular joint) are less fre-quent, and radicular symptoms (thoracic outlet) arerare.

Of 96 overhead-throwing athletes diagnosed andtreated for this isolated syndrome by one of the au-

thors (C.D.M.), 58 were baseball pitchers, 6 werebaseball catchers, 20 were tennis players, and 12 werevolleyball players. In this series, presenting pain lo-cation was as follows: approximately 80% anterior(coracoid) pain, 70% anterior (coracoid) and postero-superior scapular pain, 10% isolated anterior (cora-coid) pain, 20% proximal lateral arm (subacromial)pain, 5% acromioclavicular joint pain, and 5% radic-ular (thoracic outlet) pain radiating into the arm, fore-arm, and hand.

In throwers presenting with the SICK scapula syn-drome, static scapular malposition versus the non-

FIGURE 2. (A) A professional right-handed baseball pitcher witha SICK right scapula viewed from posterior. (B) Viewed from theanterior, the apparent inferior position of the lateral clavicle causedby scapular protraction can be seen.

FIGURE 1. (A) A severe SICK right scapula viewed from poste-rior. The right shoulder appears more than 1.5 inches lower thanthe left shoulder despite the absence of scoliosis, limb lengthdiscrepancy, or pelvic tilt. (B) A SICK right scapula viewed fromanterior in a multisport high school overhead athlete.

642 S. S. BURKHART ET AL.

throwing shoulder is objectively measured in 3 cate-gories: (1) infera, which is the visual appearance of adropped scapula due to scapular tilting or protraction;(2) lateral displacement; and (3) abduction. All mea-surements are made statically with the patients stand-ing erect with arms relaxed in adduction at their side.The measurement of infera is the difference in verticalheight of the superomedial scapular angle of thedropped scapula in centimeters compared with thecontralateral superomedial angle (Figs 3 and 4). Thismeasurement is most accurately performed with abubble goniometer that uses the same bubble chamberas a carpenter’s level. Although the measuring processwould appear to quantify linear displacement of the

scapula inferiorly, the malposition is actually a rota-tional displacement (forward tilting, protraction).Even so, the linear measurements are useful in esti-mating how severe the dysfunction is and allowingobjective measurement of recovery during rehabilita-tion. Scapular lateral displacement is the difference incentimeters of the superomedial scapular angle fromthe midline between the SICK and contralateral scap-ula (Figs 3 and 4). Scapular abduction is the differencein angular degrees of the medial scapular margin fromplumb midline between the SICK and contralateralscapula measured with a goniometer (Fig 5).

FIGURE 3. Three categories of static scapular malposition seenwith the SICK scapula syndrome. (A) All 3 malpositions—infera,lateral protraction, and abduction—are illustrated in a high schoolquarterback’s right shoulder. (B) One or any combination of the 3malpositions may occur, as seen in the right shoulder of a collegebaseball pitcher with an isolated abduction component of the SICKscapula syndrome.

FIGURE 4. (A) A high-level woman tennis player with a SICKright scapula. (B) Note that the severity of the problem is moreevident when the scapular margins are outlined.

643THE DISABLED THROWING SHOULDER

Most throwers with the SICK scapula syndromepresent with static scapular malposition in all 3 cate-gories, but single or dual combinations of any of the 3have been seen. Although one of the authors (C.D.M.)has devised a grading system for the severity of scap-ular malposition based on these measurements, werecognize that the use of superficial landmarks canmake these measurements less reliable and less repro-ducible than we would like. Nonetheless, they give usa qualitative sense of the severity of this dyskineticsyndrome and a method of measuring progress with arehabilitation program (Table 1).

On physical examination, patients with anteriorshoulder complaints and a SICK scapula are found tohave marked coracoid tenderness, more medial thanlateral on the coracoid tip, at the point of insertion ofthe pectoralis minor tendon. Throwers with anteriorcoracoid pain can easily be confused with throwerswith other causes of anterior shoulder pain, such asanterior instability or SLAP lesions, unless the cora-coid is meticulously examined. SICK scapula patientswith coracoid pain usually lack full forward flexion onthe affected side and have accentuated coracoid painwith attempts at gaining maximum passive forwardflexion by the examiner (Fig 6). With manual reposi-tioning of the scapula in retraction and posterior tilt bythe examiner (the scapular retraction test), full for-ward flexion without coracoid pain is usually attained,which is diagnostic of this syndrome (Fig 6B).

The pathophysiology behind why the dropped SICKscapula presents with coracoid pain is explained bythe coracoid static malposition and the dyskinesis thatit produces. Because of the ellipsoid shape of thethorax, as the scapula tilts anteriorly, protracts, andabducts, it tends to ride “up and over” the top of thethorax.2,3 As it does, the coracoid tilts anteroinferiorlyand moves laterally from the midline. The pectoralisminor and short head of the biceps become adaptivelytight. This tightness increases the scapular malposi-tion, lowers the leading edge of the acromion, anddecreases the ability to achieve full forward flexion ofthe arm. Impingement-like symptoms result from theanteroinferior angulation of the acromion because ofscapular protraction.

Overhead athletes with SICK scapulas who presentwith posterosuperior periscapular and lower paracer-vical pain are usually found to have marked tender-ness at the superomedial angle of the affected scapulain the area of insertion of the levator scapulae muscle.As the scapula tilts and rotates laterally, traction onthe levator scapulae creates pain and muscle spasm(Fig 7). This can often be relieved on physical exam-ination by correcting the tilted scapula by means of thescapular retraction test.

TABLE 1. SICK Scapula Rating Scale: StaticMeasurements: 0–20 Points

FIGURE 5. Scapular abduction is measured with a goniometer onthe affected medial scapular margin in reference to vertical midlineversus the uninvolved medial scapular margin.


Subacromial origin pain in the SICK throwingshoulder will present with positive subacromial im-pingement tests that bring out proximal lateral armpain. However, the true cause of these findings is amalpositioned dyskinetic acromion resulting fromscapular protraction during all phases of the throwingcycle, rather than true mechanical subacromial im-pingement produced by a type III acromion with ananterior osteophyte. Likewise, acromioclavicular jointpain is caused by a relatively discongruous position ofthe distal clavicle in reference to the acromion as aresult of scapular malposition. As the scapula tilts andprotracts, its acromion process moves anterior, de-creasing the acromioclavicular angle and increasingcompressive stress to the acromioclavicular joint.4

The altered kinematics at the acromioclavicular joint(and occasionally the sternoclavicular joint) causepain with repetitive overhead use.

Finally, the rare thrower with radicular or thoracicoutlet symptoms associated with a malpositionedSICK scapula develops these symptoms due to a shift

in position of the clavicle in reference to the upperchest wall, particularly the first rib. As the scapulashifts, the lateral clavicle also drops anteroinferiorly,resulting in a decreased subclavian chest wall space.This space restriction may impinge the brachial plexusas it crosses this zone resulting clinically in the pictureof thoracic outlet syndrome.

A 20-point clinical rating scale for the SICK scap-ula syndrome has been developed by one of the au-thors (C.D.M.) to statically assess the severity of thesyndrome at the time of presentation and to objec-tively monitor clinical improvement during the treat-ment phase (Table 1). The rating scale awards pointsfor subjective complaints and objective findings in thecategories previously discussed, as well as points forthe presence and severity of static scapular malposi-tion in the 3 modes (“apparent” infera, lateral trans-lation, and abduction). A healthy symmetrical asymp-

FIGURE 6. The scapular retraction test. (A) SICK scapula patientswith infera and abduction components and resultant coracoid painpresent with lack of full forward flexion because of pseudotight-ness of the pectoralis minor caused by coracoid malposition. (B)With manual repositioning of the scapula (retraction) the coracoidpain resolves and full forward flexion is attained.

FIGURE 7. Levator scapulae insertional pain caused by a SICKscapula. As the scapula abducts and protracts, the insertion of thelevator scapulae at the superomedial angle of the scapula becomesovertensioned and produces a painful tendinopathy in this area.


tomatic scapula receives a score of 0, and the worstSICK malpositioned scapula with all the pathologicclinical components is scored as 20.

In an attempt to determine if components of scap-ular malposition could be a normal adaptive phenom-enon in the throwing athlete, a group of asymptomaticprofessional baseball pitchers who denied previousshoulder problems were prospectively evaluated forpresence or absence of SICK scapulas and scored onthe SICK scapula rating scale (Table 1) during springtraining and at the end of 2 consecutive pain-freebaseball seasons (P. Donley, J. Cooper, personal com-munication, 2000). Nineteen pitchers meeting thesecriteria were studied and found to have scores of 0during the entire testing period (P. Donley, J. Cooper,personal communication, 2000). These findings sup-port the concept that the healthy throwing shoulderexhibits no component of the SICK scapula syndrome(no scapular asymmetry), and that this syndrome isabnormal and predisposes the throwing shoulder topathologic symptomatology as previously discussed.

Treatment for the SICK scapula syndrome regard-less of presenting symptoms or severity of scapularmalposition is nonoperative and focused on scapularmuscle rehabilitation. Initially, the thrower is re-stricted from all throwing and begun on a regimenteddaily strengthening and re-education program for allthe scapular stabilizer muscles (P. Donley, J. Cooper,personal communication, 2000). Details of a scapularrehabilitation program are discussed in the sectiondealing with rehabilitation. During the treatment pe-riod, scapular position is monitored on a weekly basis.When the affected scapula is 50% or more improvedin position from its initial pathologic position, thethrower is begun on an interval throwing program, ifasymptomatic, and continues the scapular programuntil the scapula is symmetric with the other side (Fig8). At that time, return to sport and unrestricted throw-ing is allowed and the thrower is strongly encouragedto maintain an every-other-day scapular muscle-strengthening program to prevent recurrence of thesyndrome.

In general, most throwers with symptomatic SICKscapulas present with scores between 10 and 14. In-terval throwing usually begins with scores in the 4 to6 range, and return to sport at the thrower’s previouslevel of performance is attained when the score dropsbetween 0 and 2.

In an adherent patient who commits to doing therehabilitation exercises 3 times per day, the 50% re-positioned scapula can be routinely attained within 2to 3 weeks. Completion of the interval throwing pro-

gram usually takes 3 to 4 weeks, and complete sym-metrical scapular repositioning usually takes 3months. In general, the anterior tilt (apparent infera)component is the first to resolve, the lateral translationgoes away second, and the abduction component (lossof protraction control) is the last and most difficult toresolve. Of the 96 overhead athletes treated for thissyndrome and followed up for more than 1 year, allsuccessfully returned to asymptomatic throwing attheir preinjury level of performance by 4 months.

Resolution of symptoms during the treatment periodwas directly proportional to the rehabilitation pro-gram’s ability to reposition the scapula symmetrical tothe other side. In addition, compliance with an every-other-day scapular stabilizer muscle-strengtheningprogram prevented recurrence of the syndrome. Nineof the 96 patients developed recurrence of the syn-drome after 3 to 4 months of symptom-free throwing.However, all 9 of these throwers admitted to totalnonadherence with the maintenance scapular programfor more than 3 months before developing symptomsrelated to recurrent SICK scapula syndrome.

PRE-SLAP PRODROME AND THE“SHOULDER AT RISK”

On persistent questioning, most throwers with ar-throscopically proven posterior type II SLAP lesionsand the picture of internal impingement admit to apre-SLAP prodrome of ill-defined symptoms that theyignored. During the early prodromal phase, thethrower senses tightness in the back of his or herdominant shoulder, oftentimes described as an inabil-ity to “get loose.” As the player tries to “play through”these prodromal symptoms and continues to throw,the posteroinferior capsular contracture that causedthe tight symptomatology gets worse, to a point whereposterosuperior discomfort is now present with thesense of tightness or stiffness. As the magnitude of thecapsular contracture continues to increase with con-tinued throwing in the face of these prodromal symp-toms, the SLAP event will then occur at which timethe shoulder develops sudden onset of mechanicalsymptoms that were absent during the prodrome.Once mechanical symptoms are present, treatmentbecomes a surgical issue directed toward SLAP repairand correction of the internal rotation deficit as dis-cussed in the section dealing with posterior inferiorcapsular contracture.

The “shoulder at risk” of developing dead armcomplaints is the asymptomatic shoulder that exhibitssmall to moderate amounts of either a throwing-ac-


quired glenohumeral internal rotation deficit (GIRD),a malpositioned SICK scapula, or both.

In our experience, if the athlete with a shoulder atrisk keeps throwing, the magnitude of the shoulderdysfunction will increase to a point at which intra-articular structural damage occurs and the patient be-comes symptomatic. Unfortunately, at this point theproblem has usually become a surgical issue. Theshoulder most at risk is one with a SICK scapula andGIRD. This combination is particularly dangerous tothe posterosuperior labrum, the undersurface of the

posterior supraspinatus tendon, and the anterior infe-rior capsular structures. The reason for this is that bothproblems cause the thrower to abduct in extension(toward second base), rather than in the plane of thescapula, and hyperangulate in external rotation with alow arm body angle (below the horizontal) during thelate cocking phase of throwing (Fig 9). This hyperan-gulation is made more acute if the dyskinetic scapulais in a position of protraction and glenoid antetilting,thereby bringing the posterior edge of the glenoidtoward the humerus. More proper mechanics seen in

FIGURE 8. The SICK scapula before and after treatment. A professional right-handed baseball pitcher with a symptomatic SICK rightscapula seen (A) at the time of initial presentation and (B) 6 weeks after scapular rehabilitation. The 1999 National League All Star startingpitcher and 2001 World Series Most Valuable Player seen in the late 1999 season with a (C) symptomatic SICK right scapula and (D) 6 weeksafter scapular rehabilitation.


healthy shoulders consist of abduction in the plane ofa well-positioned scapula and a greater arm–bodyabduction angle during the late cocking and earlyacceleration phases of the throwing cycle (Fig 10).

Early recognition of the shoulder at risk and insti-tution of internal rotation stretching and scapular sta-bilizer strengthening protocols have been shown to behighly effective in converting the shoulder at risk tothe shoulder not at risk and, in so doing, avoiding theshoulder at surgery. For these reasons, we encourageand recommend screening examinations to find theseproblems at the beginning and during each season forall overhead athletes. In addition, these athletes needto be educated by their respective athletic trainers anddoctors regarding these issues so that they are willingto commit to the stretching and strengthening that willkeep their shoulders healthy.

THE ROTATIONAL UNITY RULE

The healthy throwing shoulder has normal rota-tional kinematics without any form of glenohumeralinstability throughout the throwing cycle as long as itsGIRD is less than or equal to its external rotation gain.However, if the GIRD exceeds the external rotationgain (ERG) with a GIRD/ERG ratio greater than 1, theshoulder then becomes headed for trouble because ofa posterosuperior shift of the glenohumeral rotationpoint with abduction and external rotation during thelate cocking phase of throwing as previously dis-cussed. The risk of structural injury is directly propor-tional to the increase in the GIRD/ERG ratio pastunity. Although the absolute rotational numbers indegrees will vary from patient to patient because ofvariability in congenital laxity, GIRD that exceeds10% of the contralateral shoulder’s total rotation arcwill usually produce a GIRD/ERG ratio significantlygreater than 1. It is important to stabilize the scapulawith the arm at 90° abduction when measuring inter-nal and external rotation.

KINETIC CHAIN CONTRIBUTIONS TODEAD ARM

Shoulder function in throwing requires contribu-tions from all body segments to generate the forcesnecessary to propel the ball and position the bones ofthe joints to minimize the loads each joint structuremust bear, and pass the forces and loads to the distalsegments.5 This coordinated sequencing of the seg-ments is termed the kinetic chain. In the normal ki-netic chain of throwing, the ground, legs, and trunk act

as the force generators; the shoulder acts as a funneland force regulator; and the arm acts as the forcedelivery mechanism. The labrum is a key structure inproviding glenohumeral stability in this sequence andmay be injured by excessive or imbalanced forces thatmay occur at the shoulder if regional or distant areasof the kinetic chain are abnormal.

Clinical studies have shown that alterations in flex-ibility or muscle imbalance are common in patientswith shoulder injury. Kinetic chain alterations havebeen documented in shoulder impingement,6,7,8 rota-tor cuff injury,6,9 and instability.9,10 One study specif-ically evaluated distant findings that were present inthrowers with arthroscopically proven posterosuperiorlabral tears.11 Of 64 patients, 38 had isolated postero-superior labral tears, and 26 had combined anteriorand posterior lesions. On physical examination, 64 of64 (100%) had restricted goniometrically measuredinternal rotation (with the shoulder at 90° abduc-tion and the scapula stabilized) of more than 25°compared with the opposite side (mean, 32.6°;range, 26° to 58°). A total of 60 of 64 (94%) hadpatterns of dynamic scapular dyskinesis, or asymmet-ric motion or position of the scapula on rest or abduc-tion motion.6,12

The SICK scapula is an extreme form of scapulardyskinesis. A total of 41 subjects had the type Idyskinetic pattern of winging of the inferomedialscapular border and depression of the acromion withrest or motion, whereas 19 showed the type II patternof true lateral slide, in which the entire medial scap-ular border is winged with the scapula protracted andlaterally translated with rest or motion.13 The meanlateral slide asymmetry measurement12 in 60 patientswas 2.2 cm (range, 0.7 to 3.1 cm). A total of 46 of 64patients (72%) showed weakness of the infraspinatusor teres minor on resisted external rotation. A total of31 of 64 (48%) exhibited lower-back inflexibility,with reach deficits of greater than 5 cm on sit-and-reach examination. A total of 28 of 64 (44%) wereunable to complete a nondominant leg stability se-quence of one-legged stance with no Trendelenburgsign, 1-legged squat with pelvic stability, and 1-leggedstep-up and step-down with pelvic stability. Finally,25 of 64 subjects (39%) had asymmetric decreasedinternal rotation on the nondominant hip.

These alterations in normal kinetic chain motionsand positions affect the shoulder by altering proximalforce generation and altering distal joint positioning.These alterations are especially important at the shoul-der, which does not have a large force-generating


capability and whose bony anatomy is dependent onbody positioning and muscular activation to controlexcessive joint translations.

Leg and Trunk

The leg and trunk are important to provide a stablebase for arm motion,13,14 provide rotational momen-tum for force generation,14,15 and generate 50% to55% of the total force and kinetic energy in the tennisserve.3 Inflexibility of the nondominant hip or of trunkrotation, or weakness of hip abductors or trunk flexors“breaks the kinetic chain.” This breakage increaseslumbar lordosis in acceleration, which places the armbehind the body. This “slow arm” creates a hyperab-duction/external rotation position at the shoulder andincreases posterior compression loads on the struc-tures including the labrum. It moves the arm out of thesafe zone of glenohumeral angulation that has beenadvocated by Jobe et al.16 and shown by Happee17 tobe the most stable angle for the joint.

Scapula

The scapula plays many roles in throwing or servingthat may affect labral injury.9 First, the glenoid mustbe positioned and stabilized in 3-dimensional space toact as a congruous socket for the humeral head as itrotates at the high velocities necessary for throwing orserving. Second, it must smoothly retract and protractaround the thoracic wall as the arm moves from cock-ing through full cocking and then into acceleration andfollow-through. The scapula must move in relation to

FIGURE 9. This pitcher shows abduction in extension, with angu-lation of the arm posterior to the plane of the scapula rather than inthe plane of the scapula. Note the “dropped elbow” in this pitcher,causing the arm-body angle to drop below the horizontal.

FIGURE 10. Ideal mechanics involve abduction in the plane of thescapula (A, dotted line) with the elbow high enough to keep theupper arm at or above the horizontal plane. (B) With a “droppedelbow” (solid line), the upper arm hyperangulates posterior to theplane of the scapula. (C) This pitcher has excellent mechanics, withthe arm abducted in the plane of the scapula and positioned abovethe horizontal plane.


the moving humerus to maintain a safe zone of gle-nohumeral angulation and avoid hyperangulation ofthe humerus on the glenoid.16 Finally, it acts as astable base for origin of the extrinsic and intrinsicmuscles that control arm motion and provide gleno-humeral compression. These roles require active po-sitioning and active motion by the periscapular mus-cles. Alterations of normal position or motion, whichhave been termed scapular dyskinesis,13 can be causedby inflexibility, weakness, or activation imbalance ofthe muscles.

Two patterns of dynamic scapular dyskinesis areassociated with posterosuperior labral lesions. Thetype I pattern consists of inferomedial scapular border

prominence at rest, with increasing prominence, lackof acromial elevation, and lack of full retraction oncocking (Fig 11). It is associated with inflexibility ofthe pectoralis major and minor, and weakness of thelower trapezius and serratus anterior. The type II pat-tern consists of entire medial border winging at rest,which becomes more prominent with cocking or ele-vation (Fig 12). It is associated with upper and lowertrapezius and rhomboid weakness, with little anteriorinflexibility. Both patterns create an abnormal positionof excessive scapular protraction at rest and an abnor-mal motion of decreased scapular retraction and de-creased acromial elevation during cocking and earlyacceleration. The type III pattern, which is not asso-ciated with superior labral lesions, displays promi-nence of the superomedial border of the scapula. It isassociated with impingement and rotator cuff symp-toms.

Scapular dyskinesis that creates excessive protrac-tion and decreased cocking and elevation alters nor-mal scapular biomechanics and plays a role in pos-

FIGURE 11. Type I scapular dyskinesis, with prominence of theinferomedial scapular border.

FIGURE 12. Type II scapular dyskinesis, with prominence of theentire medial border.

FIGURE 13. Scapular assistance test. The examiner stabilizes theupper scapular border and assists upward rotation of the inferome-dial border.


terosuperior labral injuries. Excessive protractionincreases glenohumeral angulation outside of the safezone, creating excessive anterior tension and posteriorcompression. Increased glenohumeral angulation alsomay increase humeral external rotation in cocking andacceleration as the arm lags behind the body, increas-ing the peel-back effect. Decreased retraction in-creases the posterior glenohumeral compression onthe labrum and rotator cuff and decreases the scapularrole as a stable base for muscle origin, thereby effec-tively decreasing muscle strength. Decreased acromialelevation due to scapular protraction creates rotatorcuff impingement in cocking and acceleration as thearm is abducted.

Clinical Implications

Evaluation of athletes with suspected superior gle-noid labral lesions should include tests to check ki-netic chain functioning. History taking should includequestions about previous leg or back problems, espe-cially on the nondominant side. A screening exami-

FIGURE 14. Scapular retraction test. The examiner stabilizes theretracted scapula against the thorax.

FIGURE 15. One-leg stance, trunk rotation, and scapular retraction combined movements.


nation for the legs and trunk should include a postureexamination for legs and trunk, seated range-of-mo-tion examination of both hips and knees, the one-legstability series (i.e., 1-legged stance with no Tren-delenburg sign and 1-legged squat with no pelvic tiltor rotation), low back flexion and extension and side-bending, and situps and back extensions. Further test-ing is indicated for patients with positive tests.

The screening scapular examination should include aposture check for cervical and thoracic areas, scapularsymmetry at rest and on ascending and descending armmotion in flexion and abduction, active scapular retrac-tion and elevation, lateral slide measurements, and gle-nohumeral internal rotation measurements.

Special scapular tests include the scapular assis-tance test (SAT) and the scapular retraction test(SRT). The SAT (Fig 13) involves assisting scapularupward rotation by manually stabilizing the uppermedial border and rotating the inferomedial border asthe arm is abducted. The test is positive when it givesrelief of symptoms of impingement, clicking, or rota-tor cuff weakness.13 The scapular retraction test (Fig14) involves manually positioning and stabilizing theentire medial border of the scapula. This test is helpfulin 2 groups of patients. The first group has decreasedretraction and apparent rotator cuff weakness. The testis positive when retesting reveals increased musclestrength with the scapula in the stabilized position.The second group has a positive Jobe relocation testfor posterosuperior labral injury. The test is positivewhen scapular retraction decreases the pain or im-pingement associated with the Jobe relocation test.When positive, these tests show that specific scapularalterations are present and should be addressed as partof the rehabilitation.

REHABILITATION OF THE OVERHEADATHLETE

Rehabilitation of patients with superior glenoid la-bral lesions and scapular dyskinesis should also in-clude the kinetic chain. This aspect of the rehabilita-tion may be started early, even while shoulderevaluation and treatment is being done. Leg, back, andtrunk flexibility and strength should be normalized,and exercises that emphasize kinetic chain activationof the leg, trunk, and scapula should be instituted.13,18

Useful combinations of movements to allow activa-tion include trunk extension and scapular retraction,trunk rotation and scapular retraction, and 1-leggedstance and diagonal trunk rotation and scapular retrac-

tion (Fig 15). All of these exercises facilitate lowertrapezius muscle activation.

Scapular exercises start with scapular punches andisometric scapular retractions. A very safe exercise isthe “low row” (Fig 16), an exercise that involves trunkextension, scapular retraction, and arm extension asthe patient pushes against resistance in a posteriordirection. More advanced closed-chain exercises in-clude the scapular clock (Fig 17), in which the hand isplaced on the wall, eliminating the weight of the arm,and moving the scapula in elevation and depression(the 12 and 6 o’clock positions) and retraction andprotraction (the 9 and 3 o’clock positions). Theseexercises are generally safe and do not seem to in-crease labral injury. All preoperative patients may beplaced on this program, similar to knee exercisesbefore anterior cruciate ligament reconstruction. Bystabilizing the kinetic chain and scapular base, the

FIGURE 16. The “low-row” trunk extension, scapular retraction,and arm extension. This can be initially done as an isometricexercise, progressing to an isotonic movement.


patient can move more rapidly through the earlystages of rehabilitation, regain the normal patterns oftrunk-scapula-arm integration, eliminate the “shrug”that is common when arm abduction is attempted, andmove more rapidly into rotator cuff strengthening.

Rotator cuff exercises can be integrated into therehabilitation program after the proximal base hasbeen established.18,19 Maximal rotator cuff activationrequires a stable scapular base, since all the rotatorcuff muscles have their origin on the scapula; ade-quate scapular elevation, to eliminate impingement;closed-chain activation to eliminate excessive shear inthe early stages of rehabilitation; and coordinated ac-tivation of all of the components in force couples,rather than isolated activation of individual muscles.Closed-chain rotator cuff exercises include humeralhead depressions and rotations on a ball (Fig 18),

FIGURE 17. Scapular clock: The hand is placed on the wall or aball, with varying degrees of abduction and flexion.

FIGURE 18. Humeral head depressions and rotations with thehand on a ball.

FIGURE 19. “Wall washes”: (A) Starting position and (B) move-ment pattern. The arm is then brought back to the starting position.


“wall washes,” which combine trunk and scapula ac-tivation with rotator cuff activations (Fig 19), andpunches, which combine closed-chain shoulder acti-vation with open-chain arm motion (Fig 20). Thisprogression of exercises creates a progression of chal-lenge to the rotator cuff, and a resulting progression ofmuscle activation (Table 2).20,21 Closed-chain exer-cises require less activation than open-chain exercises,

and vertical patterns with the arm closer to the body,creating a shorter lever arm, requires less activationthan diagonal patterns, with a long lever arm. Thisprogression allows a more rapid but safe progressionof rehabilitation that can be characterized as “accel-erated,” similar to the accelerated anterior cruciateligament programs that take advantage of the samephysiologic and biomechanical principles of stablefixation, early protected range of motion, closed-chainactivation of cocontraction force couples, and earlyactivation of muscles in their physiologic positions.22

Rehabilitation for the SICK Scapula

The SICK scapula, as well as other types of scap-ular dyskinesis, must be aggressively treated with afocused scapular rehabilitation program. Rehabilita-tion consists of both stretching and strengthening.

The 2 areas of tightness that accompany the SICKscapula are (1) pectoralis minor tightness anteriorlyand (2) posteroinferior capsular tightness with GIRD.

FIGURE 20. Punches: (A) Punch out. The motion may be varied-diagonal, upward, or downward. (B) Return position should always be“elbows in the back pocket” to facilitate scapular retraction.

TABLE 2. Progression of Muscle Activation

Exercise

Percent of MaximalMuscle Activation

Supraspinatus Infraspinatus

Humeral head rotations(Codman exercise on a ball) �10 �10

Vertical wall wash 12.8 8.6Diagonal wall wash 18.0 10.4Vertical punch 16.9 9.8Diagonal punch 21.6 14.6


The anterior tightness is treated by placing a rolledtowel between the shoulder blades of the supine pa-tient and steadily pushing posteriorly on the shouldersto stretch the pectoralis minor (Fig 21). The postero-inferior capsular tightness is treated by “sleeperstretches” in which the athlete lies on his side with theshoulder in 90° flexion and the elbow in 90° flexion.The shoulder is passively internally rotated by pushingthe forearm toward the table around a fixed elbow,which acts as the pivot point (Fig 22).

Strengthening for the SICK scapula patient consistsof exercises to regain control of scapular protraction,retraction, depression, elevation, and rotation. Closed-chain exercises without weight are initiated to regainscapular control (Fig 23). Open-chain forward andlateral lunges and diagonal pulls are added, first with-out weights and then with 2- to 3-lb wrist weights ordumbbells (Fig 24). Blackburn retraction exercises areused to strengthen the scapular retractors and posteriorrotator cuff (Fig 25). Seated push-ups strengthen scap-ular depressors or retractors, triceps, latissimus dorsi,and teres major (Fig 26). Rowing exercises, bothstandard row and low row, strengthen scapular retrac-tors and the posterior rotator cuff. The low row ismore specific for strengthening the serratus anterior(Fig 27).

SUMMARY OF THE ENTIRE CURRENTCONCEPTS: PARTS I, II, AND III

The disabled throwing shoulder comprises a spec-trum of pathology. At the most dramatic and severeend of this spectrum is the dead arm, a pathologicshoulder condition in which the thrower is unable tothrow with preinjury level velocity and control. Themost common cause of the dead arm syndrome is atype II SLAP lesion, although the SICK scapula maycause a reversible type of dead arm with differentclinical findings from those of the SLAP lesion.

FIGURE 21. Pectoralis minor tightness is treated by placing arolled towel between the shoulder blades of the supine patient andpushing posteriorly on the shoulders.

FIGURE 22. Sleeper stretch: (A) The patient lies on the side with the involved arm against the table and perpendicular to the body. The elbowis flexed 90°. (B) The patient pushes the forearm toward the table, stretching the posteroinferior capsule. (See Fig 4 in Part I of this CurrentConcepts in the April issue for other variations of the “sleeper stretch.”)


FIGURE 23. Closed-chain scapular control exercises are best done in front of a mirror so that the patient can observe that he is performingthe proper maneuver with his scapula. (A) Protraction, (B) retraction, (C) elevation and retraction, (D) depression and retraction, (E) internalrotation and elevation, and (F) external rotation and depression.


FIGURE 24. Open-chain scapular strengthening exercises. (A, B) Forward lunges to strengthen scapular protractors and retractors. (C, D)Lateral lunges to strengthen scapular retractors and upward rotators (upstroke) as well as scapular depressors and downward rotators(downstroke). (E, F) Diagonal pulls (lawnmower pulls) to strengthen scapular protractors and depressors as well as retractors and elevators.


The culprits in development of the dead arm are:

1. A tight posterior-inferior capsule causing GIRDand a posterosuperior shift in the glenohumeralrotation point, with a resultant increase in theshear stress applied to the posterosuperior gle-noid labrum;

2. Peel-back forces in late cocking that add to thealready-increased labral shear stress to cause theSLAP lesion;

3. Hyperexternal rotation of the humerus relativeto the scapula caused by the shift in the gleno-humeral rotation point that increases the clear-ance of the greater tuberosity over the glenoidand reduces the humeral head cam effect on theanterior capsule; and

4. Scapular protraction.

The ultimate culprit that initiates the pathologiccascade to the SLAP lesion is the tight posteroinferiorcapsule, which probably develops in response to the

loads that act on it during follow-through. The me-chanics responsible for this pathologic cascade can berepresented by means of a reciprocal cable model.

Hyperexternal rotation causes a hypertwist phenom-enon that can, over time, result in (1) fatigue failure ofposterosuperior rotator cuff fibers due to tensile, tor-sional, and shear overload, overshadowing any dam-age caused by direct abrasion of the cuff against theposterosuperior glenoid (internal impingement); and(2) torsional overload of the inferior glenohumeralligament, causing elongation of anterior stabilizingstructures. It should be emphasized that fatigue failureof the inferior glenohumeral ligament occurs mainlyin veteran elite pitchers and that anterior instability asa part of the dead arm syndrome is very unusual,particularly in younger athletes.

We believe that microinstability is not a cause of thedead arm and that pseudolaxity from SLAP lesionscoupled with a reduction in the cam effect (as a resultof the posterosuperior shift of the glenohumeral con-

FIGURE 24 (Continued).


FIGURE 25. Blackburn exercises to strengthen scapular retractors and posterior rotator cuff. (A) Position 1, (B) position 2, (C) position 3,(D) position 4, (E) position 5, and (F) position 6.


tact point) has been misinterpreted as microinstability.Furthermore, we believe that internal impingement isa normal phenomenon that is not usually pathologic inthe throwing shoulder.

For a thrower with a dead arm and a SLAP lesion,repair of the SLAP lesion combined with an ongoingstretching program of the posteroinferior capsule isusually curative, returning the thrower to his preinjury

level of competition in 87% of cases.23 For successfulSLAP repair, the surgeon must arthroscopically con-firm elimination of the peel-back sign and eliminationof the drive-through sign. For throwers who have been“stretch nonresponders,” the surgeon may considerperforming an arthroscopic release of the posteroinfe-rior capsule. If there is greater than 130° of externalrotation with the scapula stabilized, one should con-sider electrothermal shrinkage versus arthroscopiccapsular plication of the anterior band of the inferiorglenohumeral ligament.

The SICK scapula syndrome, an extreme form ofscapular dyskinesis, can be a cause of dead arm.Extreme protraction and anterior tilting of the scapulagives the impression that it is inferiorly displaced.This syndrome has unique clinical characteristics andgenerally responds to a focused rehabilitation of theshoulder.

Scapular biomechanics are vitally important to thethrowing athlete and can be adversely affected byderangements at any point in the kinetic chain, includ-ing lower extremity function. The surgeon who treatsthrowing athletes must have a thorough understandingof the kinetic chain as well as an appreciation for theneed for a well-focused rehabilitation program in re-storing these athletes to the high level of function thattheir sport demands. In addition, closed-chain exer-cises can restore function while decreasing stresses todamaged tissues, resulting in more rapid rehabilita-tion.

The biomechanical and anatomic factors responsi-

FIGURE 26. Seated push-ups: (A) Strengthening scapular retractors and elevators. (B) Strengthening scapular retractors and depressors.

FIGURE 27. The low row is performed with the patient pullingposteriorly (shoulder extension and retraction) with the elbowlocked in full extension. This exercise strengthens scapular retrac-tors, particularly the serratus anterior.


ble for the dead arm have only recently been identi-fied. As a result, appropriate surgical and nonsurgicaltreatments, including rehabilitation, can now be moreprecisely directed at specific pathophysiologic ele-ments. The dead arm syndrome, so mysterious and soelusive for so long, is finally giving up its secrets.

Editor’s Note: This concludes this three-part Cur-rent Concepts series published in Vol. 19, Nos. 4, 5,and 6 of Arthroscopy.

Acknowledgment: The authors wish to thank Jeff Coo-per, P.T., A.T.C. (Head Athletic Trainer, Philadelphia Phil-lies baseball team), and Phil Donley, P.T., A.T.C., M.S.(Consultant, Philadelphia Phillies) for their assistance in thepreparation of this manuscript.

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