03. the Rotator Interval. Anatomy, Pathology, And Strategies for Treatment

The Rotator Interval:Anatomy, Pathology, andStrategies for Treatment

AbstractOver the past two decades, it has become accepted that the rotatorinterval is a distinct anatomic entity that plays an important rolein affecting the proper function of the glenohumeral joint. The ro-tator interval is an anatomic region in the anterosuperior aspect ofthe glenohumeral joint that represents a complex interaction of thefibers of the coracohumeral ligament, the superior glenohumeralligament, the glenohumeral joint capsule, and the supraspinatusand subscapularis tendons. As basic science and clinical studiescontinue to elucidate the precise role of the rotator interval, under-standing of and therapeutic interventions for rotator interval pa-thology also continue to evolve. Lesions of the rotator interval mayresult in glenohumeral joint contractures, shoulder instability, orin lesions to the long head of the biceps tendon. Long-term clinicaltrials may clarify the results of current surgical interventions andfurther enhance understanding of the rotator interval.

In 1970, Neer1 coined the phrase“rotator interval” to describe the

anterosuperior space in the rotatorcuff between the supraspinatus andthe subscapularis tendons. One de-cade later, Neer and Foster2 offeredevidence that the rotator interval(RI) plays a significant role in shoul-der stability. Subsequently, Roweand Zarins3 presented evidence ofvariability in RI size in patients withglenohumeral instability. In 1987,Nobuhara and Ikeda4 reported onand classified the first large series ofpatients with RI lesions; these inves-tigators discussed RI involvement inboth glenohumeral instability andadhesive capsulitis. More recently,the complex support soft-tissuestructures compressing the RI havebeen found to play an important rolein stabilizing the long head of the bi-ceps tendon.

In the years since these early re-ports were published, the RI has be-come accepted as a distinct anatom-ic entity that plays an important rolein affecting the proper function ofthe glenohumeral joint. As basic sci-ence and clinical studies continue toelucidate the precise role of the RI,understanding of and therapeutic in-terventions for RI pathology alsocontinue to evolve.5

Anatomy

The RI is triangular in shape and lo-cated in the anterosuperior aspect ofthe glenohumeral joint. The base ofthe triangle is located medially at thecoracoid process. The transverse hu-meral ligament forms the apex later-ally at the intertubercular groove.The superior margin of the subscap-ularis tendon and the anterior mar-

Stephen A. Hunt, MD

Young W. Kwon, MD, PhD

Joseph D. Zuckerman, MD

Dr. Hunt is Attending OrthopaedicSurgeon, Bedminster, NJ. Dr. Kwon isAssistant Professor, Shoulder andElbow Services, Department ofOrthopaedic Surgery, NYU–Hospital forJoint Diseases, New York, NY. Dr.Zuckerman is Chairman, Department ofOrthopaedic Surgery, NYU–Hospital forJoint Diseases.

None of the following authors or thedepartments with which they areaffiliated has received anything of valuefrom or owns stock in a commercialcompany or institution related directly orindirectly to the subject of this article:Dr. Hunt, Dr. Kwon, and Dr. Zuckerman.

Reprint requests: Dr. Kwon, NYU–Hospital for Joint Diseases, 301 East17th Street, New York, NY 10003.

J Am Acad Orthop Surg 2007;15:218-227

Copyright 2007 by the AmericanAcademy of Orthopaedic Surgeons.

218 Journal of the American Academy of Orthopaedic Surgeons

gin of the supraspinatus tendon rep-resent the inferior and superiorborders of the RI, respectively. Thecontents of the interval include thecoracohumeral ligament (CHL), thesuperior glenohumeral ligament(SGHL), the glenohumeral capsule,and the biceps tendon4-7 (Figure 1).

Recently, Jost et al6 offered a morecomplex anatomic description of theRI in which the medial aspect iscomposed of two layers and the lat-eral RI is made up of four discretelayers. In the medial RI, the CHLcomprises the superficial layer,while the deep layer is composed ofthe SGHL and the joint capsule. Lat-erally, the superficial CHL fibers fanout to the insertional fibers of thesubscapularis and supraspinatus ten-dons in the superficial layer. Thesecond layer is composed of the sub-scapularis and supraspinatus fibers,with the subscapularis fibers creat-ing the roof of the bicipital groove.The third layer includes the deep

CHL fibers, and the fourth layer iscomposed of the SGHL and the later-al capsule.6

The CHL is a dense fibrous struc-ture connecting the base of the cora-coid process to the greater and less-er tuberosities at the bicipitalgroove. It has a thin and broad (al-most 2 cm) origin at the base of thecoracoid. Laterally, it contains twodiscrete bands. One of these bandsblends into the greater tuberosityand the supraspinatus tendon; theother merges into the lesser tuberos-ity, the subscapularis tendon, andthe transverse humeral ligament.7

Because of this blending, the inser-tion of the CHL ligament often can-not be clearly distinguished fromother structures. Electron micro-scopic analysis of the lateral inser-tion of the CHL has confirmed thiscomplicated intercalating of col-lagen fibers among the ligaments.8

Controversy exists as to whetherthe CHL is a separate entity or just a

thickening of the glenohumeral cap-sule. For example, Cooper et al9 re-ported that the CHL is a capsularfold that appeared more robust incertain glenohumeral positions andthat it was less functionally impor-tant than the SGHL. Boardman etal10 similarly reported that the CHLis a significant capsular thickeningthat can function as a ligament. Intheir cadaveric study, however, theyalso noted that the CHL cross-sectional is, on average, five timeslarger than that of the SGHL.10 Al-though some authors agree that theCHL most likely is a thickening ofthe anterosuperior glenohumeralcapsule similar to the glenohumeralligaments,7 others have argued thatthe CHL actually is a distinctligament.6,11-13

The SGHL originates from the la-brum adjacent to the supraglenoidtubercle. From this origin, it crossesthe floor of the RI deep to the CHLbefore inserting into the superior as-

Figure 1

Anatomy of the rotator interval. A, Frontal view. B, Sagittal view.

Stephen A. Hunt, MD, et al

Volume 15, Number 4, April 2007 219

pect of the lesser tuberosity knownas the fovea capitis.7 The remainingstructure of the RI is the long head ofthe biceps tendon, which originatesfrom the superior glenoid labrum. Ittraverses along the RI and exits theglenohumeral joint through the apexof the RI. The SGHL, CHL, and sub-scapularis tendon are all essentialcomponents of the biceps pulley sys-tem that maintains the anatomic po-sition of the tendon within the jointand the bicipital groove14 (Figure 2).

Function

In 1959, Basmajian and Bazant15 re-ported that the superior capsule andits related ligaments acted in concertto “lock” the glenohumeral jointand resist downward displacementwith the arm held in an adductedposition. Subsequently, multiple invivo and in vitro studies have beenperformed to determine the precise

function of the RI and its impact onthe glenohumeral joint.3,5-7,9,12,14,16

The SGHL and the CHL both ap-pear to possess similar roles in pro-viding resistance to inferior and pos-terior translation of the humeralhead.7 However, which of thesestructures is the more important sta-bilizer is a subject of scientific de-bate. Ovesen and Nielsen12 offeredexperimental data that supported theCHL as the predominant stabilizer.In their study, radiographs were ob-tained after sequentially sectioningthe supraspinatus tendon, the CHL,and the superoanterior capsule. Theyfound that sectioning of the CHLwas associated with the greatest in-ferior translation of the humeralhead on radiographs.12 Similarly,Boardman et al10 analyzed the tensileproperties of the two ligaments andfound that the CHL possessed signif-icantly greater stiffness and ultimateloads to failure than did the SGHL.

Thus, these authors also concludedthat the CHL is the main contributorto the glenohumeral stability con-ferred by the RI.10

Warner et al,16 however, conclud-ed that the SGHL was the more im-portant static restraint to inferiortranslation of the humeral head. Fur-thermore, based on their dissectionsand histologic analysis of fresh ca-daveric shoulders, Cooper et al9 pre-sented data against a key role for theCHL in glenohumeral stability. Al-though these investigators con-curred that the RI is important inlimiting inferior humeral head trans-lation, they concluded that thestructure most responsible for thisactivity is the SGHL.9 Thus, contro-versy remains as to the precise func-tion of the CHL and SGHL. Never-theless, both play a similar role inglenohumeral biomechanics becausemost surgical interventions treatboth ligaments.

Figure 2

The biceps pulley system. A, The two inset diagrams (a, b) illustrate the relationship of the coracohumeral ligament and superiorglenohumeral ligament, both medially and laterally, as they blend anterior to the biceps tendon to form a pulley. B, The superiorfibers of the rotator interval have been incised to illustrate the blending of the fibers and the lateral pulley system for the bicepstendon.

The Rotator Interval: Anatomy, Pathology, and Strategies for Treatment


In 1992, Harryman et al7 per-formed the first comprehensive ca-daveric study to examine the func-tion of the RI. Sectioning of the RIincreased the range of glenohumeralflexion, extension, adduction, andexternal rotation. In contrast, imbri-cation of the RI decreased these mo-tions. When the RI was relaxed byplacing the arm in abduction andinternal rotation, no significantchanges in motion were observedwith either sectioning or tighteningof the interval. These authors alsodemonstrated that the RI clearly in-fluenced humeral head translation inall directions. After sectioning of theRI, the humeral head tended totranslate in the posteroinferior direc-tion. The authors concluded that theoverall function of the RI included(1) “check-rein” restraint against ex-cessive flexion, extension, adduc-tion, and external rotation; (2) stabi-lization against inferior translationof the humeral head in the adductedshoulder; and (3) stabilization againstposterior translation of the humeralhead in the flexed or abducted andexternally rotated shoulder.7

Recently, several studies havedemonstrated that the different ana-tomic structures within the RI maybe independently responsible for dis-tinct functions. In addition to con-firming the data obtained by Harry-man et al,7 Jost et al6 showed thatthe medial portion of the CHL wasthe essential structure in resistinginferior translation of the humeralhead in the adducted arm. They alsodemonstrated that the lateral struc-tures of the RI were primarily re-sponsible for limiting external rota-tion in the adducted arm.6 In acadaveric study, Jazrawi et al17 ex-amined the effects of arthroscopic RIclosure and found that RI imbrica-tion resulted in a loss of about 11° ofexternal rotation. However, whenthe arthroscopic sutures were placedwithin 10 mm of the glenoid surfacethat the CHL could be tethered to,the result was a marked loss of exter-nal rotation. In addition, the data

also demonstrated that RI closurecaused a significant (P < 0.001) re-duction in anterior humeral headtranslation. In contrast with previ-ous studies, RI imbrication had min-imal effects on posterior humeralhead translation.17

Another subtle but importantrole of the RI in glenohumeral stabil-ity is maintaining negative intra-articular pressure. In addition to thecombination of static and dynamicstabilizers, negative intra-articularpressure provides a significant con-tribution to glenohumeral stabili-ty.18,19 Lesions in the capsular por-tion of the RI may result in a loss ofthis negative intra-articular pressureand lead to shoulder instability.20,21

These reports in the literaturesuggest that there is potential fortherapeutic interventions directed atthe RI to increase or decrease gleno-humeral motion. However, conflict-ing data and subtle differences in theexperimental methodology amongthe studies prevent forming a dis-crete conclusion that could be clin-ically applicable.6,7,17 In addition,many of the conclusions from thesein vitro studies have not yet beenconfirmed by in vivo scenarios.Hence, the exact role of the RI in gle-nohumeral stability has not yet beenestablished.

In addition to their role in gleno-humeral biomechanics, the struc-tures of the RI also are important inestablishing the stability of the ten-don of the long head of the biceps. Asstated, the long head of the bicepstendon exits the glenohumeral jointthrough the apex of the RI. TheSGHL, CHL, and subscapularis ten-don are all thought to be importantand essential components of the bi-ceps pulley system that maintainsthe anatomic position of the ten-don.14 Despite its location on the bi-cipital groove, the transverse humer-al ligament provides surprisinglylittle support to the biceps ten-don.14 Hence, the stability of theproximal biceps tendon appears to beintimately related to the integrity of

the RI structures at their lateral in-sertions.

Pathology

Pathology of the RI can be classifiedbased on several different schemes.For example, Nobuhara and Ikeda4

classified the RI lesion based on itsmechanical strength. In type I inju-ries, the RI is contracted and associ-ated with inflammatory changes,primarily in the superficial tissues.In type II injuries, the RI is lax andassociated with glenohumeral insta-bility. Type II lesions are thought toinvolve primarily the deeper tissuesof the RI.4

Another system of RI lesions isbased on the specific anatomic struc-ture involved.5 Classification thusincludes lesions to (1) the RI capsule,(2) the CHL, (3) the SGHL, (4) the an-terior aspect of the supraspinatustendon, (5) the superior aspect of thesubscapularis tendon, and (6) thelong head of the biceps tendon. Al-though these structures may be in-jured in isolation, more commonlythey are injured in conjunction withone another.

To date, no universally acceptedclassification system for RI patholo-gy has been established. Neverthe-less, several pathologies about theshoulder joint are closely associatedwith RI changes. These include rota-tor interval contractures, rotator in-terval laxity, biceps tendon instabil-ity, and coracoid impingement.

Rotator IntervalContractures

RI contractures vary in severity,ranging from mild contractures re-sulting in rotator cuff tendon im-pingement to severe contractures as-sociated with adhesive capsulitis.Although the pathogenesis of adhe-sive capsulitis is not completely un-derstood, some authors believe thata contracted RI capsule and, perhapsmore importantly, a contracted CHLare the “essential” lesions of adhe-sive capsulitis.11,22 Many patients



with this pathology report anteced-ent trauma followed by a variable pe-riod of disuse or immobilization.Injury, followed by inflammationand scarring of the RI, has been pro-posed as an etiology of RI contrac-tures.4,5,13 Nobuhara and Ikeda4 alsofound that RI contractures tended tooccur in older patients (average age,35.1 years) in comparison with RIlaxity (average age, 23.2 years).

Clinically, these patients presentwith painful and limited motion.They may also report pain at restand difficulty with nighttime sleep-ing. On physical examination, ab-normal scapulothoracic motion maybe noted as the patient attempts tocompensate for the lack of glenohu-meral mobility. Although disuse os-teopenia may be present in chroniccases, radiographs typically do notshow abnormalities. Arthrographyusually demonstrates decreased cap-sular volume and would not showany extravasation of the dye throughthe RI.4,5,13 A thickened and fibroticRI capsule and CHL are typicallynoted during diagnostic arthroscopy.There also may be significant in-flammation on the bursal side of theRI. Histologic examination of thesetissues typically demonstrates fibro-sis, hyalinization, and fibrinoid de-generation. Additionally, there maybe an absence of the synovial celllayer on the undersurface of the RIcapsule.13

For most patients, initial inter-vention comprises various nonsur-gical modalities, including painmedications, nonsteroidal anti-in-flammatory medications, local in-jections, and physical therapy. Mostcases of adhesive capsulitis are self-limited and resolve within a fewmonths with good to excellent clin-ical results.23 Because RI contrac-tures are part of adhesive capsulitis,one might surmise that isolated RIcontractures have a similar progno-sis; however, there is little evidenceto support this supposition. In casesof recalcitrant adhesive capsulitis,patients may require manipulation

under anesthesia or surgical soft-tissue release.

In 1989, Ozaki et al13 reported ontheir experience with 17 patientswho underwent isolated releases ofthe RI capsule and the CHL for recal-citrant adhesive capsulitis. The au-thors performed an open procedurethrough an anterolateral approach.After releasing the subacromial bur-sal tissue, the RI was identified be-tween the supraspinatus and sub-scapularis tendons. The humeruswas externally rotated to isolate theRI capsule and the CHL, which werethen released. Finally, the shoulderwas gently manipulated through afull range of motion. During the ma-nipulation, normal motion of the bi-ceps tendon was found to be restoredas it began gliding within the bicip-ital groove. The clinical outcome(average follow-up, 6.8 years) inthese 17 patients was reported to beexcellent. Pain was completely re-lieved in 16 of the 17 patients; thelast patient experienced pain onlywith overuse of the extremity. Sim-ilarly, all but one patient hadachieved full range of motion at lat-est follow-up. All patients had nor-mal muscle strength and were ableto perform normal activities of dailyliving. No patient demonstrated anysubjective or objective findings forinstability. Finally, postoperative ar-thrograms were performed on all pa-tients. Although the RI was left openduring the procedure, no extravasa-tion of contrast into the subacromi-al space was noted.13

More recently, arthroscopic cap-sular release procedures have beendescribed. These studies emphasizethe importance of releasing the RIcapsule and, more importantly, theCHL, in addition to other portions ofthe capsule.24-27 Tetro et al25 per-formed a cadaveric study to assessthe feasibility of completely releas-ing the RI capsule and CHL arthro-scopically. Their technique involvedbeginning the release just superior tothe superior border of the subscapu-laris, then proceeding superiorly un-

til the anterior edge of the bicepstendon is reached. The dissection isperformed from deep to superficial,cutting through the capsule first.The resection is then performed un-til the coracoacromial ligament is vi-sualized. Despite the fact that theCHL is an extra-articular structure,these surgeons noted that they wereable to reproducibly section the lig-ament using this technique.25

Other clinical studies have dem-onstrated improved motion andfunction in patients who underwentarthroscopic capsular release for re-calcitrant adhesive capsulitis, withminimal risk to nearby neurovascu-lar structures such as the musculo-cutaneous nerve.24-27

Rotator Interval LaxityAlthough the exact contribution

of the RI to glenohumeral stability isunclear, many studies have clearlydemonstrated that RI lesions canlead to excessive glenohumeral mo-tion and humeral head transla-tion.6,7,9,10,12,16 Thus, when the RIstructures are lax, patients may ex-perience instability and pain. Roweand Zarins3 first implicated the RI ashaving a significant role in shoulderinstability. In their study, 9% of the“normal” cadaveric shoulders dem-onstrated RI lesions, compared with54% of patients who required surgi-cal stabilization for recurrent shoul-der instability. The authors thereforeconcluded that the RI lesions wereassociated with recurrent glenohu-meral instability and should be ad-dressed during surgery.3

The patient with RI laxity maypresent with acute trauma, repeti-tive microtrauma, or an overuse in-jury superimposed on a shoulderwith underlying ligamentous laxity.Nobuhara and Ikeda4 demonstratedthat patients with RI laxity usuallywere younger than their counter-parts who were having RI contrac-tures. The patient with excessive RIlaxity typically reports an unstableshoulder as well as early fatigue. Onphysical examination, most of these



patients demonstrate inferior insta-bility that also may be associatedwith either anterior or posterior in-stability. When the RI is intact, theinferior sulcus sign disappears whenthe arm is externally rotated.4,5,7,28 Apersistent inferior sulcus sign withthe arm in external rotation strong-ly suggests RI laxity. Although mostradiographs may not show any focaldeformities, some may demonstratesubtle subluxation in the inferiorand/or posterior direction. Arthrog-raphy may demonstrate some con-trast extravasation through the RI or,more likely, contrast filling the RIspace when the arm is elevated andexternally rotated.4

Visualization of the RI duringopen surgical procedures is difficultbecause this region typically is ob-structed by the coracoid process andthe coracoacromial ligament. Roweand Zarins3 noted that the RI visual-ization can be improved with down-ward traction on the humerus. How-ever, they also had to perform cor-acoid osteotomies occasionally toimprove visualization of the defect.In general, better visualization canbe achieved during arthroscopy. Intheir study of normal cadavericshoulders, Tetro et al25 found thatthe distance between the anterioredge of the supraspinatus tendon andthe superior edge of the subscapu-laris tendon at the glenoid rim was21.6 mm; with joint distention, thisdistance could be increased to27.8 mm. These measurements offerguidelines for assessing significantlaxity or disruption of the RI duringarthroscopic procedures. Additional-ly, RI lesions may also be suspectedwhen one of the following changes isobserved: (1) capsular redundancybetween the subscapularis and thesupraspinatus, (2) fraying of the bi-ceps tendon as it exits the joint,(3) tearing of the SGHL, or (4) frayingof the superior border of the subscap-ularis tendon.29

After evaluating 76 of 106 shoul-ders (101 patients) that were treatedwith open RI repair for instability,

Nobuhara and Ikeda4 reported that40% of the patients had completepain relief and 56% had pain onlywith overuse of the shoulder. Theynoted that 91% of the patientsregained full motion and that 74%regained normal muscle strength.These authors also reported thatonly three patients had persistentand clinically significant shoulderinstability. Ultimately, 70% wereable to return to normal activities ofdaily living, whereas 26% had im-proved but were below their pre-symptomatic level of function.4

Similarly, Field et al28 reported aretrospective study of 15 patientswho underwent isolated closure ofthe RI for multidirectional instabil-ity. All of these patients originallyhad been scheduled for open capsu-lar shift procedures but were foundto have isolated RI lesions that mea-sured, on average, 27.5 mm. Afterthe RI interval was imbricated, thejoint was found to be stable, and nofurther procedures were performed.At an average follow-up of 3 years,these patients demonstrated statisti-cally significant improvements inpain, stability, and function (P < 0.01for all). All patients were able to re-turn to their presymptomatic levelsof function; 13 were able to partici-pate in sports. According to the au-thors, these findings suggest that tra-ditional capsular shifts may not benecessary for some patients with re-current multidirectional instabilityand that many patients may havehad their joints unnecessarily over-constrained.28

Although RI closure may be suffi-cient to stabilize some shoulders,Levine and colleagues30,31 have cau-tioned that, for many patients, RI le-sions are only part of the instabilitypattern. They also noted that isolat-ed RI interval closure should be per-formed only in selected patients. Ina group of 50 patients undergoing re-vision surgery for recurrent instabil-ity, 22% of the patients demon-strated asymmetrically tight antero-superior structures that included the

RI. Although these patients showedlimited external rotation with thearm in adduction, shoulder instabil-ity persisted when the arm wasplaced in abduction and external ro-tation. In addition, all patients hadlarge inferior capsular pouches thathad not been previously addressed.Thus, in the setting of anteroinferi-or capsular compromise, isolated RIclosure may be insufficient to stabi-lize the shoulder.31

Because RI defects may be bettervisualized arthroscopically, severalarthroscopic imbrication techniqueshave been described. These includetechniques to close the RI from thesubacromial space as well as those toimbricate the interval from theintra-articular space.29-31 In the firsttechnique, the knots are tied and cutunder direct visualization. In the lat-ter, however, the repair is directly vi-sualized while the knots are tied andcut indirectly on the subacromialspace. In 2004, Taverna et al32 de-scribed a technique that allowedintra-articular visualization of theinterval repair as well as knot-tyingand cutting. Regardless of technique,however, Gartsman et al29 recom-mended tensioning the sutures andtesting shoulder stability before finalknot-tying in order to optimize sta-bility without compromising mo-tion. They also recommended posi-tioning the arm in 30° of externalrotation before suture tightening toavoid excessively limiting externalrotation.29 However, clinical out-come studies for isolated arthroscop-ic RI closures for glenohumeral in-stability are still lacking. Therefore,the clinical efficacy of this procedurehas yet to be established.

“Hidden” Lesions: BicepsInstability

Biceps tendon instability was ex-tensively described by Meyer33,34 in aseries of case reports in the early20th century. In 1986, Petersson35

found that 3.3% of cadaveric shoul-ders demonstrated medial bicepstendon dislocation. More important-



ly, he described the biceps tendon asit dislocated medially under the sub-scapularis tendon and intimated therelationship between subscapularistendon tears and biceps tendon in-stability.35

These early descriptions laid thefoundation for the current under-standing of this pathology. Walch etal36 demonstrated that the pulley ofthe biceps tendon is a coalescence ofthe fibers of the CHL and the sub-scapularis tendon. Defects in the lat-eral aspect of the CHL, SGHL, andsuperior subscapularis tendon weredescribed as the “hidden” lesion thatoccurred in association with su-praspinatus tendon tears and usual-ly resulted in biceps tendon dislo-cation. These lesions were calledhidden because they can be easilymissed during both open and arthro-scopic evaluations. Although these

lesions were initially underappreci-ated, Walch et al36 reported a 16%incidence in symptomatic patients.

Similarly, a cadaveric study ofolder shoulder specimens (mean age,76.3 years) showed a high associa-tion between partial subscapularistendon tears at its superior borderand biceps tendon pathology.37 In ad-dition, the authors demonstratedthat these tears were associated withsupraspinatus tendon tears.

More recently, Bennett38,39 de-scribed an “anterosuperior” rotatorcuff tear that combined subscapu-laris, RI, and supraspinatus lesions.These lesions were thought to be as-sociated with pathologic and clini-cally significant injuries to the bicepstendon (tenosynovitis, tendinitis/fraying, subluxation, or dislocation)and required particular attention insymptomatic patients. Bennett39 also

proposed a classification system forthese lesions (Figure 3).

Patients with hidden lesions areoften difficult to evaluate becausethe symptoms can be diffuse andnonspecific. In the most patients, noclear association with trauma can befound. In the patient with subscapu-laris tendon tear, physical examina-tion may demonstrate positive belly-press and lift-off maneuvers.Similarly, positive biceps provoca-tive maneuvers may be indicative ofbiceps tendon pathology.40-42 Unfor-tunately, even with a discrete lesion,the examination findings can be sub-tle and difficult to delineate.

To better identify these lesions,Bennett38 described a provocativemaneuver that causes movement ofthe biceps tendon about the bicipitalgroove. This is accomplished by pas-sively moving the arm from ab-

Figure 3

Classification of biceps instability. A, The rotator interval capsule comprises the coracohumeral ligament, the superiorglenohumeral ligament, and the capsular fibers as they blend together at the insertions medial and lateral to the bicipital groove,maintaining the tendon in the groove. B, In type I lesions, a tear of the superior edge of the subscapularis tendon insertioncompromises the medial wall of the bicipital groove, allowing the tendon to shift medially within the groove. C, In type II lesions,a tear of the medial CHL insertion with an intact subscapularis insertion allows medial subluxation of the tendon. D, In type IIIinstability, both the subscapularis and the medial CHL insertions are torn, resulting in medial dislocation of the biceps tendon.E, In type IV lesions, the lateral insertion of the CHL is ruptured, allowing the biceps tendon to dislocate anteriorly over thesubscapularis tendon. F, In type V instability, all insertions are torn, and the biceps tendon is dislocated.



duction and external rotation tocross-body adduction and internalrotation. The arm should not be ele-vated beyond 90° because symptomsfrom impingement may present afalse-positive response. The maneu-ver is considered to be positive forinstability when the patient experi-ences a catching or clicking sensa-tion suggestive of tendon sublux-ation. When the maneuver isassociated with significant pain, thetest also can be considered positivefor tendon pathology such as teno-synovitis or partial tears.38

Similarly, imaging studies are notalways helpful in identifying hiddenlesions. Radiographs of these shoul-ders may demonstrate subtle cysticerosions of the lesser tuberosity.39 Inmost patients, however, imagingstudies are not particularly helpfulin diagnosing these lesions.36,39,43,44

Although Walch et al36 suggestedthat arthroscopic computed tomog-raphy may be helpful in some cases,Bennett45 found that no study, in-cluding magnetic resonance arthrog-raphy, allowed clear evaluation ofthese lesions. Therefore, he arguedthat these lesions can be reliablyidentified only during surgery. Whena subscapularis tendon tear is ob-served on a magnetic resonance im-age or during surgery, biceps tendoninvolvement is likely and should becarefully evaluated.44

Once identified, the lesions canbe surgically addressed, but resultsare mixed. Walch et al36 performedan open repair of the lesion in 21 pa-tients by reattaching the insertion ofthe subscapularis and reconstructingthe medial aspect of the sheath. In12 of the 21 patients, additionalwork on the bicipital groove, such asscar removal and/or deepening, hadto be performed to stabilize the en-larged tendon. Three of these pa-tients demonstrated postoperativerupture of the tendon within5 months of surgery. In addition,pain improvement was modest andunrelated to treatment, leading theauthors to postulate that tenodesis

may be the optimal treatment op-tion.36

In their experience with open re-pairs of massive anterosuperior rota-tor cuff lesions, Warner et al21 report-ed generally good results. Mostpatients had chronic rotator cuff ten-don tears and demonstrated severedamage to the biceps tendon. There-fore, rather than reconstruction ofthe pulley system and relocation ofthe tendon, all patients received bi-ceps tenodesis. The authors notedthat, although subscapularis func-tion was not restored in most pa-tients, the average Constant scoredid improve by 31 points. Althoughthis group of patients had more ex-tensive rotator cuff lesions, the au-thors suggest that biceps tenodesis isthe best option for dislocated bicepstendons.21

Bennett39 performed his repairsthrough an arthroscopic technique.When the lesion was not obvious, aprobe was used to pull the extra-articular portion of the biceps ten-don into the joint. When the bicepstendon dislocated inferomediallyduring this maneuver, a subscapu-laris and/or CHL lesion was suspect-ed. The author also noted that thevisualization of the subscapularistendon and the CHL insertions canbe improved by elevating and inter-nally rotating the shoulder and flex-ing the elbow.39 After restoring thebiceps pulley system, functionaloutcome of the treated patients dem-onstrated statistically significantimprovements in pain (P = 0.001) aswell as in American Shoulder andElbow Society (P = 0.001) and Con-stant (P = 0.001) scores. Additional-ly, at a minimum follow-up of2 years, the clinical symptoms re-solved in all patients. Thus, Bennettconcluded that this lesion should beaggressively sought and properlytreated.39 However, relocating the bi-ceps tendon remains a controversialsubject, and the literature appears tosupport biceps tenodesis.

Coracoid ImpingementCoracoid impingement has been

described as a potential etiology ofRI injury and shoulder pain.46-50 Al-though the clinical entity of cora-coid impingement is fairly well es-tablished, some authors have arguedthat this condition is a consequence,rather than cause, of RI and rotatorcuff lesions.51 One therefore must becognizant of the associated patholo-gy of coracoid impingement and RIlesions.

Summary

The RI is an important anatomic re-gion of the anterosuperior glenohu-meral joint. It is composed of a com-plex interplay of fibers of the CHL,the SGHL, the glenohumeral jointcapsule, and the tendons of the su-praspinatus and subscapularis mus-cles. The RI plays an essential role inglenohumeral joint and biceps ten-don stability. Pathology of the struc-tures of the RI can contribute to bothcontractures and instability of theglenohumeral joint. Furthermore, le-sions of the RI can contribute topathologic conditions of the bicepstendon. Results of recent in vitroand clinical trials have revealedmuch about the anatomy and func-tion of the RI. In the future, long-term clinical trials may clarify theresults of current surgical interven-tions and further enhance under-standing of the RI.

References

Evidence-based Medicine: There isone level II prospective study (refer-ence 23) on this subject. The remain-ing references are level III/IV, case-control cohort studies or casereports, or level V, expert opinion oranatomic studies.

Citation numbers printed in boldtype indicate references publishedwithin the past 5 years.

1. Neer CS II: Displaced proximal hu-merus fractures: I. Classification and



evaluation. J Bone Joint Surg Am1970;52:1077-1089.

2. Neer CS II, Foster CR: Inferior capsu-lar shift for involuntary inferior andmultidirectional instability of theshoulder: A preliminary report.J Bone Joint Surg Am 1980;62:897-908.

3. Rowe CR, Zarins B: Recurrent transientsubluxation of the shoulder. J BoneJoint Surg Am 1981;63:863-872.

4. Nobuhara K, Ikeda H: Rotator intervallesion. Clin Orthop Relat Res 1987;223:44-50.

5. Fitzpatrick MJ, Powell SE, Tibone JE,Warren RF: The anatomy, pathology,and definitive treatment of rotator in-terval lesions: Current concepts. Ar-throscopy 2003;19(suppl 1):70-79.

6. Jost B, Koch PP, Gerber C: Anatomyand functional aspects of the rotatorinterval. J Shoulder Elbow Surg 2000;9:336-341.

7. Harryman DT II, Sidles JA, Harris SL,Matsen FA III: The role of the rotatorinterval capsule in passive motionand stability of the shoulder. J BoneJoint Surg Am 1992;74:53-66.

8. Gohlke F, Essigkrug B, Schmitz F: Thepattern of the collagen fiber bundles ofthe capsule of the glenohumeral joint.J Shoulder Elbow Surg 1994;3:111-128.

9. Cooper DE, O’Brien SJ, Arnoczky SP,Warren RF: The structure and func-tion of the coracohumeral ligament:An anatomic and microscopic study.J Shoulder Elbow Surg 1993;2:70-77.

10. Boardman ND, Debski RE, WarnerJJP, et al: Tensile properties of thesuperior glenohumeral and coraco-humeral ligaments. J Shoulder ElbowSurg 1996;5:249-254.

11. Neer CS II, Satterlee CC, Dalsey RM,Flatow EL: The anatomy and poten-tial effects of contracture of the cora-cohumeral ligament. Clin OrthopRelat Res 1992;280:182-185.

12. Ovesen J, Nielsen S: Experimentaldistal subluxation in the glenohu-meral joint. Arch Orthop TraumaSurg 1985;104:78-81.

13. Ozaki J, Nakagawa Y, Sakurai G,Tamai S: Recalcitrant chronic adhe-sive capsulitis of the shoulder: Role ofcontracture of the coracohumeral lig-ament and rotator interval in patho-genesis and treatment. J Bone JointSurg Am 1989;71:1511-1515.

14. Slatis P, Aalto K: Medial dislocationof the tendon of the long head of thebiceps brachii. Acta Orthop Scand1979;50:73-77.

15. Basmajian JV, Bazant FJ: Factors pre-venting downward dislocation of the

adducted shoulder joint: An elec-tromyographic and morphologicalstudy. J Bone Joint Surg Am 1959;41:1182-1186.

16. Warner JJ, Deng XH, Warren RF, Tor-zilli PA: Static capsuloligamentousrestraints to superior-inferior transla-tion of the glenohumeral joint. Am JSports Med 1992;20:675-685.

17. Jazrawi LM, Plausinis D, Bravman JT,et al: Abstract: Arthroscopic rotatorinterval closure: Analysis of glenohu-meral motion and translation. 72ndAnnual Meeting Proceedings. Rose-mont, IL: American Academy of Or-thopaedic Surgeons, 2005, p 588.

18. Warner JJP, Deng X, Warren RF, Tor-zilli PA, O’Brien SJ: Superoinferiortranslation in the intact and ventedglenohumeral joint. J Shoulder El-bow Surg 1993;2:99-105.

19. Gibb TD, Sidles JA, Harryman DT II,McQuade KJ, Matsen FA III: The ef-fect of capsular venting on glenohu-meral laxity. Clin Orthop Relat Res1991;268:120-127.

20. Itoi E, Berglund LJ, Grabowski JJ, Nag-gar L, Morrey BF, An KN: Superior-inferior stability of the shoulder: Roleof the coracohumeral ligament andthe rotator interval capsule. MayoClin Proc 1998;73:508-515.

21. Warner JJP, Higgins L, Parsons IM IV,Dowdy P: Diagnosis and treatment ofanterosuperior rotator cuff tears.J Shoulder Elbow Surg 2001;10:37-46.

22. Bunker TD, Anthony PP: The pathol-ogy of frozen shoulder: A Dupuytren-like disease. J Bone Joint Surg Br1995;77:677-683.

23. Griggs SM, Ahn A, Green A: Idiopath-ic adhesive capsulitis: A prospectivefunctional outcome study of nonoper-ative treatment. J Bone Joint SurgAm 2000;82:1398-1407.

24. Harryman DT II, Matsen FA III, SidlesJA: Arthroscopic management of re-fractory shoulder stiffness. Arthros-copy 1997;13:133-147.

25. Tetro AM, Bauer G, Hollstien SB,Yamaguchi K: Arthroscopic release ofthe rotator interval and coracohumeralligament: An anatomic study in cadav-ers. Arthroscopy 2002;18:145-150.

26. Pollock RG, Duralde XA, Flatow EL,Bigliani LU: The use of arthroscopy inthe treatment of resistant frozenshoulder. Clin Orthop Relat Res1994;304:30-36.

27. Warner JJP, Allen A, Marks PH, WongP: Arthroscopic release for chronic,refractory adhesive capsulitis of theshoulder. J Bone Joint Surg Am 1996;78:1808-1816.

28. Field LD, Warren RF, O’Brien SJ, Alt-chek DW, Wickiewicz TL: Isolatedclosure of rotator interval defects forshoulder instability. Am J SportsMed 1995;23:557-563.

29. Gartsman GM, Taverna E, Hammer-man SM: Arthroscopic rotator inter-val repair in glenohumeral instability:Description of an operative tech-nique. Arthroscopy 1999;15:330-332.

30. Levine WN, Flatow EL: The patho-physiology of shoulder instability.Am J Sports Med 2000;28:910-917.

31. Levine WN, Arroyo JS, Pollack RG,Flatow EL, Bigliani LU: Open revisionstabilization surgery for recurrent an-terior glenohumeral instability. Am JSports Med 2000;28:156-160.

32. Taverna E, Sansone V, Battistella F:Arthroscopic rotator interval repair:The three-step all-inside technique.Arthroscopy 2004;20:105-109.

33. Meyer AW: Spontaneous dislocationand destruction of the tendon of thelong head of the biceps brachii: Fifty-nine instances. Arch Surg 1928;17:493-506.

34. Meyer AW: Spontaneous dislocationof the tendon of the long head of thebiceps brachii: Report of four cases.Arch Surg 1926;13:109-119.

35. Petersson CJ: Spontaneous medialdislocation of the tendon of the longbiceps brachii: An anatomic studyof prevalence and pathomechanics.Clin Orthop Relat Res 1986;211:224-227.

36. Walch G, Nove-Josserand L, LevigneC, Renaud E: Tears of the supraspi-natus tendon associated with “hid-den” lesions of the rotator interval.J Shoulder Elbow Surg 1994;3:353-360.

37. Sakurai G, Ozaki J, Tomita Y, KondoT, Tamai S: Incomplete tears of the sub-scapularis tendon associated with tearsof the supraspinatus tendon: Cadavericand clinical studies. J Shoulder El-bow Surg 1998;7:510-515.

38. Bennett WF: Subscapularis, medial,and lateral head coracohumeral liga-ment insertion anatomy: Arthroscop-ic appearance and incidence of “hid-den” rotator interval lesions. Ar-throscopy 2001;17:173-180.

39. Bennett WF: Arthroscopic repair ofanterosuperior (supraspinatus/sub-scapularis) rotator cuff tears: A pro-spective cohort with 2- to 4-yearfollow-up. Classification of bicepssubluxation/instability. Arthroscopy2003;19:21-33.

40. O’Brien SJ, Pagnani MJ, Fealy S, Mc-Glynn SR, Wilson JB: The active com-pression test: A new and effective test



for diagnosing labral tears and acro-mioclavicular joint abnormality. AmJ Sports Med 1998;26:610-613.

41. Yergason RM: Supination sign. JBone Joint Surg 1931;13:160.

42. Bennett WF: Specificity of the Speed’stest: Arthroscopic technique for eval-uating the biceps tendon at the levelof the bicipital groove. Arthroscopy1998;14:789-796.

43. Beall DP, Williamson EE, Ly JQ, et al:Association of biceps tendon tearswith rotator cuff abnormalities: De-gree of correlation with tears of theanterior and superior portions of therotator cuff. AJR Am J Roentgenol2003;180:633-639.

44. Li XX, Schweitzer ME, Bifano JA, Ler-

man J, Manton GL, El-Noueam KI:MR evaluation of subscapularis tears.J Comput Assist Tomogr 1999;23:713-717.

45. Bennett WF: Visualization of the anat-omy of the rotator interval and bicip-ital sheath. Arthroscopy 2001;17:107-111.

46. Dumontier C, Sautet A, Gagey O,Apoil A: Rotator interval lesions andtheir relation to coracoid impinge-ment syndrome. J Shoulder ElbowSurg 1999;8:130-135.

47. Paulson MM, Watnick NF, DinesDM: Coracoid impingement syn-drome, rotator interval reconstruc-tion, and biceps tenodesis in the over-head athlete. Orthop Clin North Am

2001;32:485-493.48. Le Huec JC, Schaeverbeke T, Moinard

M, et al: Traumatic tear of the rotatorinterval. J Shoulder Elbow Surg 1996;5:41-46.

49. Gerber C, Terrier F, Zehnder R, GanzR: The subcoracoid space: An anatom-ic study. Clin Orthop Relat Res1987;215:132-138.

50. Dines DM, Warren RF, Inglis AE, Pav-lov H: The coracoid impingementsyndrome. J Bone Joint Surg Br 1990;72:314-316.

51. Nove-Josserand L, Boulahia A, LevigneC, Noel E, Walch G: Coraco-humeralspace and rotator cuff tears [French].Rev Chir Orthop Reparatrice ApparMot 1999;85:677-683.



Documents

03. the Rotator Interval. Anatomy, Pathology, And Strategies for Treatment