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May 2003 (Vol. 11, Issue 2)

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PrefaceMR imaging of sports-related injuriesby Steinbach LSpages xi-xiiFull Text | PDF (41 KB)Review articleJoint MR imaging: Normal variants and pitfalls related to sports injuryby Pfirrmann CWA, Zanetti M, Hodler Jpages 193-205Full Text | PDF (539 KB)Review articleMR imaging of sports injuries to the rotator cuffby Tuite MJpages 207-219Full Text | PDF (724 KB)Review articleMR imaging of shoulder instability injuries in the athleteby Beltran J, Kim DHMpages 221-238Full Text | PDF (649 KB)Review articleSports injuries of the elbowby Chung CB, Kim HJpages 239-253Full Text | PDF (605 KB)Review articleMR imaging of sports-related hip disordersby Boutin RD, Newman JSpages 255-281Full Text | PDF (629 KB)Review articleMR imaging of meniscal and cruciate ligament injuriesby Fritz RCpages 283-293Full Text | PDF (861 KB)Review articleImaging sports injuries of the foot and ankleby Zoga AC, Schweitzer MEpages 295-310Full Text | PDF (756 KB)

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Magnetic Resonance Imaging Clinics of North America

Review articleWinter sports injuries: The 2002 Winter Olympics experience and a review of the literatureby Crim JRpages 311-321Full Text | PDF (659 KB)Review articleImaging of stress fractures in the athleteby Spitz DJ, Newberg AHpages 323-339Full Text | PDF (791 KB)Review articleImaging of sports-related muscle injuriesby Boutin RD, Fritz RC, Steinbach LSpages 341-371Full Text | PDF (999 KB)Indexpages 373-378PDF (44 KB)View Selected Abstracts Display:

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Preface

MR imaging of sports-related injuries

Guest Editor

I have been fortunate enough to have edited

two issues of the Clinics that focus on sports-

related injuries. This topic is very popular, and

with good reason. Our society is more fitness-con-

scious than ever. Children and adolescents, espe-

cially females, are more involved in sports than

they were in my generation. Elite athletes expect

imaging to be interpreted instantly with the cor-

rect diagnosis and to be provided with a prognosis

that determines the appropriate therapy and ex-

pected recovery period. Baby boomers are work-

ing out for their own health in record numbers

but, because of their age, are also more prone to

injury. On top of this, new knowledge and devel-

opments in MR imaging technology are difficult

to find in books, which take years to write and

publish. Clinicians are demanding that radiolo-

gists know the material so that they may provide

helpful and accurate MR imaging interpretations.

This compendium of articles focuses on the use of

MR imaging in sports injury.

To play a useful role in diagnosis and therapy

of sports injuries, it is important for the imager to

be familiar with normal musculoskeletal anatomy,

in addition to the potential pitfalls. Drs. Pfirr-

mann and colleagues have put together a review

of normal variants and pitfalls in MR imaging

that relate to sports imaging. This article is being

republished from the March 2002 issue of the

Radiologic Clinics of North America on sports

imaging because it provides a good baseline for

decision-making. Athletic injuries to the shoulder

are discussed in two separate articles by three

well-regarded authors who have published exten-

sively on this material: Dr. Tuite, Dr. Beltran,

and Dr. Kim. Drs. Chung and Kim bring new

concepts in elbow anatomy and MR imaging elo-

quently to light. Drs. Boutin and Newman present

a cutting edge report on sports imaging of the hip,

discussing areas such as impingement and snap-

ping hip. Dr. Fritz elucidates some important

new concepts regarding meniscal and cruciate

ligament injuries, including the flap tear of the

posterior lateral meniscus and injuries to the dif-

ferent bands of the cruciate ligaments. Drs. Zoga

and Schweitzer use their extensive experience to

enrich our knowledge of sports injuries to the foot

and ankle. Dr. Crim, who was in charge of radiol-

ogy in the polyclinic at the Salt Lake City Olym-

pics, shares a unique, well-researched background

and interesting cases from that event. Drs. Spitz

and Newberg have done an admirable job of

reviewing the different types of stress fractures in

the athlete and how they are viewed by different

Lynne S. Steinbach, MD

1064-9689=03=$ - see front matter � 2003, Elsevier Inc. All rights reserved.

doi:10.1016=S1064-9689(03)00030-8

Magn Reson Imaging Clin N Am

11 (2003) xi–xii

imaging techniques, which was originally pub-

lished in the Radiologic Clinics of North America.

In an encore from the most recent issue of the

Radiologic Clinics of North America, Dr. Boutin

comprehensively reviews imaging of sports-related

muscle injuries, with special attention given to

specific common musculotendinous injuries.

I want to thank this group of highly regarded

authors who contributed articles to this issue in

such an accomplished and timely manner. The

efforts of these leaders in the field have resulted

in a presentation of fresh concepts in another out-

standing overview of sports imaging.

Lynne S. Steinbach, MD

Department of Radiology

University of California–San Francisco

505 Parnassus, San Francisco

CA 94143-0628, USA

E-mail address:

[email protected]

xii L.S. Steinbach / Magn Reson Imaging Clin N Am 11 (2003) xi–xii

Joint MR imagingNormal variants and pitfalls

related to sports injuryChristian W.A. Pfirrmann, MD*, Marco Zanetti, MD,

Juerg Hodler, MDDepartment of Radiology, Orthopedic University Hospital, Balgrist, Forchstrasse 340, CH-8008 Zurich, Switzerland

Knowledge of normal anatomic variants and

other diagnostic pitfalls is the first but crucial stepfor accurate analysis of MR images of the joint.Such variants and pitfalls are commonly found

as coincidental findings on MR images performedafter sport injuries and may easily be misdiag-nosed as relevant abnormality. The consequences

may be overtreatment, such as unnecessary reduc-tion of sports activities, plaster casts, or evenarthroscopy or surgery. This article starts witha short discussion of artifacts as far as relevant for

musculoskeletal imaging, followed by a descrip-tion of commonly found anatomic variants andpitfalls for all major joints.

Artifacts

Artifacts may simulate pathologic conditionson MR images. Aliasing occurs when the field of

view does not include all of the anatomic struc-tures present in the imaged section. Aliasingartifacts can be eliminated by increasing the fieldof view, by oversampling, by applying saturation

pulses outside the region of interest, or by usingsurface coils. Chemical shift artifacts can be foundat the interface between fat and other structures.

Chemical shift artifacts increase with field strength

and are more pronounced in images acquired with

narrow bandwidth. Motion artifacts arise fromseveral sources, including respiration, flow inblood vessels, and motion caused by pain or

reduced levels of patient cooperation. Artifactscaused by a nonuniform magnetic field may bethe cause of inhomogeneous fat saturation. Such

problems are more pronounced in frequency-selective T2-weighted spin echo images than onSTIR images [16]. They are commonly found inthe presence of metallic implants and in peripheral

regions, such as the forefoot. Shimming of themagnet is another important aspect. Magneticsusceptibility artifacts are more severe in images

acquired with gradient echo sequences or fat-suppressed sequences, when compared with stan-dard or turbo (fast) spin echo images.

Truncation artifacts

Truncation artifacts result from the use of

Fourier transform methods to reconstruct MRimages. Ringing artifacts (Gibbs phenomenon)occurring near highly contrasting interfaces rep-resent one manifestation of truncation artifacts

[1]. Truncation artifacts appear as a series of highand low signal intensity lines, adjacent andparallel to these boundaries. Such a line of high

signal intensity within the low signal intensity ofthe meniscus may simulate the appearance ofa meniscal tear (Fig. 1) [35]. When superimposed

on the meniscus, truncation artifacts tend to besubtle, uniform in thickness, and parallel to thesurfaces of the menisci. They may extend beyond

Reprinted with permission from Radiologic Clinics

of North America 2002;40(2):167–180.

* Corresponding author.

E-mail address: [email protected]


doi:10.1016=S1064-9689(03)00020-5


11 (2003) 193–205

the boundaries of the meniscus. Truncation

artifacts can be reduced with data extrapolationalgorithms, image filtering, or equal in-planeresolutions [8].

Magic angle

The presence of magic angle effect contributesto the difficulty of interpretation of MR imagesof the joints. This effect is commonly found in

ligaments and other ordered structures when theyare oriented approximately 55� to the main mag-netic field (B0). This orientation leads to shorten-

ing of the apparent T1 time, resulting in anincrease in signal intensity of the tendon, whichmay simulate the appearance of a tear or tendi-

nosis [13]. This phenomenon is most pronouncedwhen a short echo time is used [24]. Increasedsignal intensity within the distal portion of thesupraspinatus tendon or within the long tendons

of the ankle (submalleolar and retromalleolarregion) is frequently observed and are probablycaused by the magic angle effect (Fig. 2).

Shoulder

Labral variability

The normal glenoid labrum is highly variable.

Most of the anatomic variants are found at theanterosuperior aspect of the shoulder joint, be-tween the 11- to 3-o’clock position [18]. Zanetti

et al [38] investigated the MR arthrographic

variability of the arthroscopically normal glenoid

labrum. One hundred twenty-one (50%) of 241 ar-throscopically normal labral parts demonstratednormal (low) signal intensity and normal form on

MR arthrograms. Increased linear or globularsignal was seen in 31% of normal labral parts. De-formed or fragmented labra were found in 12%.

Complete separation of the labrum from theglenoid was found in 2%, a cleft in 2%, andcomplete absence in 2%. Because the MR imag-ing appearance of the arthroscopically normal

glenoid labrum varies considerably with regardto signal intensity, form, and size, other signs forglenohumeral instability, such as capsular abnor-

malities, lesions of the glenohumeral ligaments,Hill-Sachs impression fractures, or osseous abnor-malities of the glenoid rim, should be considered

in the evaluation of the labrum. Several specificsituations are discussed in the following sections.

Sublabral hole versus labral tear

The sublabral hole is an anatomic variant

located anterosuperiorly at the 2-o’clock position,anterior to the biceps insertion. A sublabral holeis seen in 12% of individuals [37]. A sublabral hole

Fig. 2. Magic angle phenomenon: sagittal T1-weighted

spin-echo image (TR 473 ms, TE 11 ms) through the

medial malleolus. The flexor digitorum longus tendon

(white arrowheads) demonstrates hypointense signal. The

posterior tibialis tendon (black arrowheads) is slightly

hyperintense because of the magic angle phenomenon,

which may simulate the appearance of tendinopathy or

even a tear.

Fig. 1. Truncation artifact: sagittal proton-density turbo

spin-echo image (TR 3610 milliseconds [ms], TE 14 ms)

at the level of the lateral condyle. Note the line of high

signal intensity (white arrowhead) within the low-signal

intensity of the meniscus, which may simulate the

appearance of a meniscal tear. This is an example of

a truncation artifact, which usually is subtle, uniform in

thickness, and parallel to the surface of the meniscus or

the femoral condyle. The line extends beyond the bound-

aries of the meniscus (black arrowheads).

194 C.W.A. Pfirrmann et al / Magn Reson Imaging Clin N Am 11 (2003) 193–205

may be misinterpreted as a labral tear (Fig. 3) [9].

The craniocaudal diameter of a sublabral holeshould probably not exceed 15 mm, is located atthe labral base, and is not associated with

traumatic abnormalities of the joint capsule andthe glenohumeral ligaments.

Buford complex versus labral tear

The Buford complex is an anatomic capsulola-bral variant that can be misdiagnosed as a lesionof the anterior labrum. The Buford complex con-

sists of a cord-like middle glenohumeral ligamentand absent anterosuperior labrum. In a series of200 shoulder arthroscopies this unusual variant

was noted in 3 (1.5%) shoulders. In the presenceof a Buford complex the thickened middle gleno-humeral ligament originates from the superior

labrum at the biceps tendon origin, crosses under-neath the subscapularis tendon, and inserts on thelesser tuberosity the humerus. The anterosuperiorlabrum is missing (Fig. 4). This anatomic varia-

tion has to be differentiated from a sublabral holeand from true labral detachment. In the presenceof a Buford complex the labral tissue of the re-

maining three glenoid quadrants is normal, andno abnormalities, such as a Hill-Sachs lesion orcapsular insertion abnormality, are found [37].

Sublabral recess versus superior labrumanteroposterior lesion

The attachment of the superior glenoid labrumdeserves special attention because normal variants

have to be differentiated from superior labrumanteroposterior (SLAP) lesions. There commonly

is a physiologic sublabral recess, which is locatedin the anterior part of the bicipitolabral complex.There is an overlapping appearance between the

physiologic sublabral recess and a type 2 superiorlabrum anteroposterior lesion. A sublabral recessis found in approximately 70% of patients [17].The sublabral recess is a smooth line that follows

the surface of the glenoid. This line is not usuallyoriented laterally toward the substance of thelabrum (Fig. 5). Lesions of the superior labral

complex commonly can be differentiated fromthe normal sublabral recess because they extendposterior to the biceps tendon insertion. More-

over, tears often have a frayed appearance, theycan have a branching pattern, and they tend toinvolve the labral substance.

Os acromiale versus acromial fracture

The os acromiale is an acromial apophysisthat has not united with the main part of the

acromion. The os acromiale is bilateral in approxi-mately 60% of patients. The connection betweenthe os acromiale and the main bone is commonly

sagittal but may also have an oblique course. Theos acromiale may contribute to shoulder im-pingement syndrome. It can easily be detected onroutine MR images of the shoulder. The diagnosis

is best made on axial images. Angled coronal andsagittal images may also be adequate, depending

Fig. 4. Buford complex: axial T1-weighted spin-echo

MR arthrogram (TR 600 ms, TE 12 ms) in a shoulder

with a Buford complex. The Buford complex is an ana-

tomic capsulolabral variant that can be misdiagnosed as

a lesion of the anterior labrum. The Buford complex

consists of a ‘‘cord-like’’ middle glenohumeral ligament

(arrow) and absent anterosuperior labrum (arrowhead).

Fig. 3. Sublabral hole: axial T1-weighted spin-echo MR

arthrogram (TR 600 ms, TE 12 ms) demonstrating

a sublabral hole (arrow). This anatomic variant is

located antero-superiorly at the 2 o’clock position, and

anteriorly to the biceps insertion. A sublabral hole may

be misinterpreted as a labral tear.

195C.W.A. Pfirrmann et al / Magn Reson Imaging Clin N Am 11 (2003) 193–205

on the orientation of the attachment. The os

acromiale can simulate an acromial fracture [11],although such diagnosis is rare. It has beendescribed in patients with shoulder prosthesis

where altered biomechanics may lead to a fatiguefracture.

The postoperative shoulder

Imaging the postoperative shoulder is challeng-ing. Zanetti et al [40] found residual defects orretears in the rotator cuff in 21% and bursitis-like

abnormalities in 100% of asymptomatic patientsafter rotator cuff repair (Fig. 6). The size of theresidual defects or retears was significantly smallerin the asymptomatic group (mean, 8 mm; range, 6

to 11 mm) than in the symptomatic group (mean,32 mm; range, 7 to 50 mm) (t-test, P ¼ 0.001).Subacromial bursitis-like MR abnormalities are

almost always seen after rotator cuff repair. Theymay persist for several years after rotator cuffrepair and seem to be clinically irrelevant. Small

residual defects or retears (<1 cm) of the rotatorcuff are not necessarily associated with clinicalsymptoms and are probably also unimportant [40].

Elbow

The pseudodefect of the capitellum

The pseudodefect of the capitellum is one of

the most commonly encountered diagnostic pit-falls in MR imaging of the elbow. The pseudode-fect is found at the junction of the capitellum and

lateral (radial) epicondyle of the distal humerus. Itis seen on cross-sectional images partially cuttingthrough the irregular surface of these bonystructures. The pseudodefect of the capitellum

may simulate an osteochondral lesion on sagittal(Fig. 7) and coronal MR images [26].

Fig. 5. Sublabral recess: sagittal o-blique proton�den-

density turbo spin-echo MR arthrogram with fat satu-

ration (TR 3300 ms, TE 14 ms) of a right shoulder. Note

the sublabral recess, which is located in the anterior part

of the bicipitolabral complex. This normal recess should

be differentiated from a superior labrum anteroposterior

(SLAP) lesion. The sublabral recess (arrowhead) is a

smooth line that follows the surface of the glenoid. SLAP

lesions can commonly be differentiated from the normal

sublabral recess because they extend laterally, have a

complex form, or extend posterior to the biceps tendon

insertion.

Fig. 6. Postoperative pseudobursitis: (A) coronal oblique T2-weighted turbo spin-echo (TR 3500 ms, TE 98 ms), and (B)

corresponding short–tau inversion recovery (STIR) (TR 4800 ms, TE 30 ms, TI 180 ms) images of a 53-year-old man 2

years after rotator cuff repair (supraspinatus tendon, arrows). The patient is completely asymptomatic and has regained

complete shoulder function. Note the bursitis-like high signal at the site of the subacromial bursa (arrowheads).


Variations of the trochlear groove

The proximal portion of the ulna is formed bythe olecranon and the coronoid process. They

form the trochlear groove, which articulates withthe distal humerus. The groove is constricted atthe junction of the olecranon and the coronoid

process. A thin, transverse, nonarticular ridge in-tersects the groove at this junction. Both theconstriction at the periphery of the groove and thenonarticular ridge may simulate disease on MR

imaging of the elbow. The nonarticular ridge isoften not covered by articular cartilage [27].

Synovial plicae

Synovial plicae are frequently found during

MR imaging of the elbow. They are most oftenlocated at the posterior part of the joint. Synovialplicae may be misdiagnosed as intra-articular

bodies on cross-sectional images. Plicae are usuallyasymptomatic. Rarely, they present with lockingsensations or pain [7]. The lateral synovial fringeis a particular synovial plica located between the

radial head and the capitellum of the humerus.Rarely, the lateral synovial fringe leads to animpingement between the radial head and the

capitellum during repeated elbow flexion andextension, particularly with the forearm in pro-nation [7].

Wrist and hand

Pseudo dorsal intercalated segment instability(DISI) seen on sagittal MR images

Lunar tilt is an important diagnostic sign of

a static carpal instability. It is usually diagnosedon standardized lateral radiographs of the wrist.Theoretically, such diagnosis can also be made on

sagittal MR images. Zanetti et al [39] have shown,however, that on sagittal images the lunate ap-parently is more dorsally tilted than on standard

lateral radiographs. A DISI configuration can bemimicked (Fig. 8). In neutrally positioned wrists,the authors found that the mean capitolunate,

scapholunate, and radiolunate MR imagingangles were 13.6�–14.5�, 4�–9.9�, and 18�–20.3�

larger, respectively, than those measured on lateralradiographs. In 15� radially deviated wrists, the

mean MR imaging angles were similar to those onlateral radiographs. In 15� ulnarly deviated wrists,the mean MR imaging angles were 32.3�, 16.6�,and 37.1� larger than those on lateral radiographs.At MR imaging, a DISI configuration would havebeen diagnosed in 4 of 10 subjects with neutrally

positioned wrists and in 8 of 10 subjects withulnarly deviated wrists. It may be difficult toobtain a perfectly neutral position of the wristduring MR imaging. When the patient is exam-

ined with the hand above the head, ulnar tiltingis very common. Analysis of a DISI or volar in-tercalated segment instability (VISI) configuration

should only be performed on standard lateralradiographs to avoid this pitfall.

Asymptomatic triangular fibrocartilage andinterosseous ligament lesions

With increasing age, defects and communi-

cation within the triangular fibrocartilage andthe interosseous ligaments increase in frequency.Many of these defects have no clinical signifi-

cance. Zanetti et al [41] have shown that radial-sided communicating triangular fibrocartilagedefects described in the literature as post-trau-

matic (Palmer classification type IA and ID)are commonly seen bilaterally and in asymp-tomatic wrists. In a population of 56 patients (age,16 to 52 years; mean, 32 years) with isolated

triangular fibrocartilage lesions communicating

Fig. 7. Pseudodefect of the capitellum: sagittal T2-

weighted fat-saturated turbo spin-echo image (TR 3600

ms, TE 96 ms) at the level of capitellum of the humerus.

Note the pseudodefect (arrowheads) at the posterior

aspect of the capitellum. The pseudodefect of the

capitellum may simulate an osteochondral lesion.


defects were noted in 36 (64%) of 56 symptomaticand in 26 (46%) of 56 asymptomatic wrists.

Twenty-five (69%) of 36 communicating defectswere bilateral (Fig. 9). Almost all communicatingdefects were noted radially. Noncommunicatingdefects were noted in 28 (50%) of 56 symptomatic

wrists and in 15 (27%) of 56 asymptomatic wrists.Eleven (39%) of 28 noncommunicating defects

were bilateral. Noncommunicating and commu-nicating defects of the triangular fibrocartilage

near its ulnar attachment have a more reliableassociation with symptomatic wrists than theradial communicating defects.

Hip

Labrum

In MR imaging of asymptomatic hips, abnor-

mal shape and signal intensity of the labrum arefrequent. Abe et al [43] investigated 73 asymp-tomatic hips. They found a triangular shape in80% of labral segments. The labrum was round in

13% and irregular in shape in the remaining 7%.The labrum was not identified in 1% of labralsegments. Homogeneous low signal intensity was

observed in 56% of labral segments. Signalchanges were a frequent finding (Fig. 10). Thefrequencies of labral irregularity or its absence

and of high signal intensity increased both withsubject age and with a more anterior anatomiclabral location. The fact that the findings vary

according to age and labral portion should beconsidered in interpreting MR images in patientssuspected of having a labral lesion. MR arthrog-raphy may be required to differentiate zones of

degenerated tissue from detachments.

Fig. 9. Communicating defect of the triangular fibro-

cartilage (TFC): coronal T1-weighted image (TR 500

ms, TE 15 ms) of the wrist, demonstrating a communi-

cating defect (arrowheads) of the TFC near its radial

attachment. Communicating defects are a frequent

finding (46%) in asymptomatic writsts and are often

(69%) bilateral.

Fig. 8. Pseudo DISI configuration: sagittal T1-weighted spin-echo image (TR 435 ms, TE 21 ms) at the level of the

lunate- (A) and corresponding lateral radiograph of the wrist (B) in an asymptomatic subject without history of trauma.

The lunate usually appears to be tilted more dorsally on sagittal MR images than on standard lateral radiographs. On

sagittal MR images, a DISI configuration can easily be misdiagnosed.


Knee

Asymptomatic meniscal tear

Not all meniscal tears are symptomatic. In an

investigation by Boden et al [3] in asymptomaticvolunteers meniscal tears were found in 16% ofknees. The prevalence of MR imaging findings of

a meniscal tear increased from 13% in individualsbelow the age of 45 years to 36% in those olderthan 45. An additional 30% of the volunteers had

meniscal abnormalities consisting of a linear areaof increased MR imaging signal not communicat-ing with a meniscal surface. The authors con-cluded that the high prevalence of abnormal MR

imaging findings in asymptomatic subjects under-scores the danger of relying on a diagnostic testwithout careful correlation with clinical signs and

symptoms. These findings also emphasize the im-portance of access to relevant clinical data wheninterpreting MR imaging scans of the knee [3].

Pitfalls mimicking meniscal tears

Many anatomic structures and variations may

simulate a meniscal tear. Increased signal intensityat the anterior horn of the lateral meniscus nearits central attachment site is frequent and usually

does not represent a meniscal tear [32]. The syno-vial recess of the popliteus tendon is locatedbetween the posterior horn of the lateral meniscusand the popliteus tendon at the posterolateral

aspect of the knee. This recess may have a linear

appearance and simulate a tear of the posteriorhorn of the lateral meniscus [15].

Meniscofemoral ligamentsThe meniscofemoral ligaments are accessory

ligaments of the knee that extend from the pos-

terior horn of the lateral meniscus to the lateralaspect of the medial femoral condyle. As theyextend across the knee, they are intimate with

portions of the posterior cruciate ligament. Theanterior meniscofemoral ligament, or ligament ofHumphry, passes in front of the posterior cruci-

ate ligament, and the posterior meniscofemoralligament, or ligament of Wrisberg, passes behindthe posterior cruciate ligament. The meniscofem-

oral ligaments are highly variable in size andmay even be absent (both or one of them). Bothligaments are visualized in about one third of MRimaging examinations. The meniscofemoral liga-

ments are seen both on coronal and sagittal MRimages. They may simulate a tear of either the pos-terior cruciate ligament or the posterior horn of

the lateral meniscus (Fig. 11). On sagittal images,the meniscofemoral ligaments can be mistaken forosteochondral or meniscal fragments [6,36].

The transverse ligamentThe transverse ligament connects the convex

portions of the anterior horns of the medial andlateral menisci. Its diameter is variable, and it may

be absent in some persons. This ligament is iden-tified on sagittal MR images of the knee as ahypointense structure close to the anterior horns

of the menisci. On coronal and axial images it maynot be visible or appears as a linear structure. As itseparates from the menisci, particularly the medial

meniscus, the space filled by fat between theligament and the meniscus may be misinterpretedas a meniscal tear (Fig. 12) [15]. The transverseligament has a reported prevalence of about 58%

on sagittal MR images [33].

Chondrocalcinosis versus meniscal tearCrystal deposition diseases, particularly those

related to calcium pyrophosphate dihydrate andcalcium hydroxyapatite crystal accumulation, af-fect the menisci. Both of these disorders lead to

cartilage calcification. Both the calcium depositsand the usually present surrounding zones of men-iscal degeneration lead to signal changes in themeniscal substance, which may simulate meniscal

tears [4]. Correlation of MR images with plainradiographs may help to diagnose this condition.Occasionally, calcification of articular cartilage

Fig. 10. Acetabular labrum variability: coronal T1-

weighted spin-echo MR arthrogram (TR 512 ms, TE

14 ms) demonstrating a slightly rounded labrum (arrow)

and signal changes in the substance. Signal changes and

form variations are a frequent finding in asymptomatic

patients.


can be identified as small foci of low signal on MRimages [2].

Meniscocapsular separation

The diagnostic performance of MR imagingin meniscocapsular separation is low (positive

predictive value 9% medially and 13% laterally);the reported MR imaging signs correlate poorlywith arthroscopic findings [28]. The junctional re-

gion between the posterior portion of the medialmeniscus and the joint capsule contains peripheralvessels whose signal intensity can mimic the ap-

pearance of a meniscocapsular detachment [14].The differential diagnosis of ameniscocapsular sep-aration includes normal recesses that may appearabove or below the peripheral portion of the pos-

terior horn of the medial meniscus. A bursa of the

medial collateral ligament is present in more than

90% of cadaveric knees. This bursa separates theperipheral region of the midportion of the medialmeniscus and the medial collateral ligament.

Bursitis may lead to increased signal intensity inthis junctional region that simulates the appear-ance of meniscocapsular separation [36].

Postoperative meniscus

Imaging the postoperative meniscus is chal-lenging. Frequently, signal changes in the menis-

cal substance are seen, which may simulate tears.It seems that grade 3 signal from both conserva-tively treated and repaired menisci may persist

long after the tear has become asymptomatic andhas presumably healed. Moreover, signal associ-ated with degeneration of the meniscal substance

may reach the meniscal surface after partial men-iscectomy but does not represent a tear. Increasedsignal of the meniscus, which is interpreted as atear in nonoperated knees, should be interpreted

with caution after surgery [10]. MR arthrographymay help to distinguish between healed or scarredmenisci and retears.

Meniscal ossifications

Meniscal ossicles are rare. Radiographically,these ossicles often are mistaken for intra-articu-

lar bodies. Meniscal ossicles have a character-istic MR imaging appearance that may help todistinguish them from loose bodies. They appear

Fig. 12. Transverse ligament: sagittal proton-density

turbo spin-echo image (TR 3610 ms, TE 14 ms) through

the medial condyle of a knee in a 34-year-old man.

Transverse ligament (straight arrow) is shown in close

relationship to the anterior horn (curved arrow) of the

medial meniscus simulating a meniscal tear (arrowhead).

Fig. 11. Meniscofemoral ligament (ligament of Wris-

berg): (A) sagittal proton-density trubo spin-echo image

(TR 3610 ms, TE 14 ms), and (B) coronal T1-weighted

spin-echo image (TR 450 ms, TE 14 ms) demonstrating

a meniscofemoral ligament (ligament ofWrisberg, arrow-

heads) extending from the posterior horn of the lateral

meniscus (arrow). A tear of the posterior horn of the

lateral meniscus (arrow) may be simulated.


as a circumscribed ossification with fatty bonemarrow in the center. They are usually locatedwithin the posterior horn of the medial meniscus[30].

High signal in the patellar tendonversus jumper’s knee

Thickening of the patellar tendon and foci ofincreased tendon signal intensity have been de-

scribed as characteristic features of jumper’s knee(chronic patellar tendinitis). The presence of in-creased signal in asymptomatic subjects, however,

has been described by Reiff et al [25]. They foundsuch signal on T2*-weighted gradient echo imagesin 45 (75%) of 60 patients without anterior knee

pain (Fig. 13). They stated that the asymptomaticpatellar tendon usually shows uniform thicknessthroughout most of its length, but some thicken-

ing is present at both the proximal and distalinsertions. The patellar tendon usually demon-strates low signal intensity on MR images, butmay contain foci of increased signal intensity at

either or both ends. Such signal is most pro-nounced on gradient echo sequences. With regardto the diameter, Schmid et al [29] found a sig-

nificant difference in the anteroposterior diameterof the proximal patellar tendon (symptomatic, 7.1mm; asymptomatic, 5.5 mm [P ¼ 0.005]). Cutoffvalues are unreliable, however, because of a signif-

icant overlap between symptomatic and asymp-tomatic subjects.

Joint effusion versus iliotibial bandfriction syndrome

The iliotibial band friction syndrome is clini-cally characterized by poorly defined pain in thelateral and distal aspects of the thigh or lateralknee pain just proximal to the joint line. This

syndrome is most commonly seen in long-distancerunners, cyclists, football players, and weightlifters. It is believed that the pain is caused by

friction of the iliotibial tract over the lateralfemoral epicondyle and a resultant inflammatoryresponse. There is a close anatomic relationship

between the iliotibial tract and the lateral recessesof the knee joint and the lateral femoral epicon-dyle. On MR images, increased signal intensity onT2-weighted images, representing bursal fluid or

synovial hypertrophy, is identified deep to theiliotibial band adjacent to the lateral femoralepicondyle. This fluid must be distinguished from

fluid located intra-articularly in the lateral para-patellar recess (Fig. 14). There is no normallydetectable bursa between the lateral femoral epi-

condyle and the iliotibial tract [22].

Ankle and foot

Normal fluid collections

Tenosynovial fluid collections are frequentlyfound about the foot and ankle. The presence ofsmall or even moderate amounts of fluid within

a tendon sheath by itself is not diagnostic of anabnormality because such fluid is seen in asymp-tomatic persons [31]. Tenosynovial fluid is morefrequent in flexor tendons (as compared with

extensor tendons) and may be particularly prom-inent about the flexor hallucis longus tendon [19].The extensor tendons are usually not surrounded

by fluid. Schweitzer et al [31] have shown thatfluid in the articulations and tendon sheaths of theankle is common in asymptomatic patients, and

the amounts of fluid are not significantly differentfrom the amounts in patients with symptoms.There also seem to be complex interrelationshipsbetween fluid seen in the joint and in tendon

sheaths.

Fig. 13. Psuedo jumper knee: sagittal proton-density fast

spin-echo (TR 3610 ms, TE 14 ms) image of the patellar

tendon. Hyperintensity (white arrowheads) occurs at the

proximal insertion of the patellar tendon (black arrow-

heads). This is a frequent finding and is present in up to

75% of asymptomatic patients without anterior knee

pain. This finding should not be misinterpreted as a sign

for a patellar tendinopathy or jumper’s knee.


Asymptomatic findings about ligamentsand tendons

Noto et al [23] analyzed 30 asymptomaticankles with MR imaging. They found severalasymptomatic conditions. The posterior talofibu-

lar ligament frequently demonstrated an irregularand frayed superior edge, which could simulatea tear. The navicular insertion of the posteriortibial tendon showed heterogeneous signal in-

tensity (47% of cases). The deltoid ligament wasalso frequently (70%) inhomogeneous [23].

Imaging findings after physical activity

Recreational sports may lead to a number ofpositive MR imaging findings without correlationwith clinical findings. Small amounts of fluid in

the retrocalcaneal bursa are common (prevalenceis 53% to 68% [Fig. 15]). Peritendinous joint fluidis found in 22% of ankle tendons, most ofteninvolving the tendon sheath of the flexor hallucis

longus tendon. An increased amount of joint fluidis noted in 18% to 34% of the joints. Even bonemarrow edema may be found as an occasional

finding after physical activity [20].

Accessory muscles

Anomalous muscles occur in the ankle, in-cluding accessory soleus, peroneus quartus, and

flexor digitorum longus accessorius muscles. These

can be seen on routinely obtained MR images and

must not be mistaken as soft tissue masses. Theperoneus quartus muscle, also called the peroneusaccessorius, peroneus externus, or peroneus cal-

caneus externus muscle, has been associated with

Fig. 14. Iliotibial band friction syndrome and its pitfalls: (A) coronal STIR (TR 4980 ms, TE 35 ms, TI 160 ms) and (B)

axial T2*-weighted (TR 905 ms, TE 26 ms, flip angle 30�) images in a patient with a iliotibial band friction syndrome.

There is a close anatomical relationship between the iliotibial (curved arrow) and the lateral recesses of the knee joint

(straight arrow). Note increased signal intensity (arrowheads) deep to the iliotibial band (curved arrow) adjacent to the

lateral femoral epicondyle. This fluid must be distinguished from fluid located intraarticularly within the lateral

parapatellar recess (arrow).

Fig. 15. Retrocalcaneal bursa: sagittal T2-weighted fat-

saturated turbo spin-echo image (TR 4000 ms, TE 64 ms)

demonstrating small fluid colletion in the retrocalcaneal

bursa (arrow).This is a commonfinding (prevalence: 53%–

68%) in asymptomatic physically active individuals.


chronic pain and swelling about the ankle. Itsreported frequency, based on results of cadavericdissections, has varied from approximately 12%to 22% [34]. The peroneus quartus originates at

the distal lateral portion of the fibula and theperoneus brevis or longus muscle. The insertion islocated at the phalanges or metatarsal bone of the

fifth toe, the calcaneus, the cuboid bone, and thelateral retinaculum of the ankle. Accurate di-agnosis is provided by MR imaging [5]. The

accessory soleus muscle is an unusual anatomicvariant that may present as a mass in the distalcalf or medial ankle region. The accessory soleus

muscle arises from the anterior surface of thesoleus or from the fibula and tibia. It inserts eitheronto the Achilles tendon or the calcaneus poster-omedially. The diagnosis is not difficult based on

the typical location and the MR imaging signalpattern corresponding to that of normal striatedmuscle [12].

The pseudodefect of the talar dome

The pseudodefect of the talar dome is a normal

groove at the posterior aspect of the talus (Fig. 16).

The groove contains the posterior talofibularligament. This defect should not be misinter-preted as an articular erosion or osteochondraldefect [21].

Accessory ossicles and sesamoid bones

Accessory ossicles and sesamoid bones arefrequently encountered about the ankle and foot.

They rarely cause diagnostic difficulties. Their ap-pearance is rather typical, with rounded shape,intact cortical bone, and typical location. It is

important, however, to recognize these ossicles asnormal variant to prevent their misdiagnoses asfractures and loose bodies [19].

MR imaging of the forefoot: asymptomatic findings

Fluid collections in the first three intermeta-tarsal bursae are a frequent finding (prevalence

20% to 49%) in asymptomatic subjects (Fig. 17).In addition, Zanetti et al [42] found Morton’sneuromas in 30% of asymptomatic volunteers.Symptomatic Morton’s neuromas tend to be

larger (range, 4 to 8 mm; mean, 5.6 mm) comparedwith asymptomatic ones (range, 3 to 7 mm; mean,4.5 mm). Morton’s neuroma may be relevant only

when the transverse diameter is 5 mm or more.The diagnosis should be correlated to clinicalfindings [42].

Fig. 17. Inermetatarsal bursae: coronal T2-weighted

turbo spin-echo image (TR 4500 ms, TE 91 ms) of the

distal forefoot. Note fluid in the intermetatarsal bursae

(arrowheads). Fluid collections in the first three inter-

metatarsal bursae are a frequent finding with a preva-

lence of 20%–49% in asymptomatic subjects.

Fig. 16. Pseudodefect of the talar dome: sagittal T1-

weighted spin-echo MR arthrogram (TR 473 ms, TE 11

ms) of the hindfoot. Pseudodefect (arrow) at the pos-

terior aspect of the talar dome. This defect should not be

misinterpreted as an articular erosion or osteochondral

defect.


Summary

MR imaging abnormalities, such as increasedsignal within normally hypointense structures,

form and attachment abnormalities, fluid collec-tions in joints, tendon sheaths and bursa, or eventumors, such as Morton’s neuromas, are commonin asymptomatic volunteers. They may be ex-

plained by normal physiology, anatomic variabil-ity, MR imaging artifacts, or true abnormalitieswithout clinical importance. Although it is not

always possible to differentiate such variants orartifacts from clinically relevant findings, it isimportant to know their potential cause and

clinical importance and not to over-report themas abnormality requiring additional imaging ortreatment. Thorough knowledge of normal anat-omy is crucial in this situation.

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MR imaging of sports injuries to the rotator cuffMichael J. Tuite, MD

Department of Radiology, University of Wisconsin Hospital and Clinics, Clinical Science Center-E3/311,

600 Highland Avenue, Madison, WI 53792-3252, USA

Shoulder pain is a common complaint of

people active in sports, and can be due to a varietyof causes, including glenohumeral joint instabilityor injury to the acromioclavicular joint. Impinge-

ment and rotator cuff injury are also commoncauses of shoulder pain in athletes, particularly inoverhand throwers and swimmers.

Athletes with rotator cuff symptoms can haveseveral findings on MR, including a normal cuff,tendonitis (more properly termed tendonosis), or

a rotator cuff tear. Although it is helpful todiagnose tendonosis on MR, the primary role ofMR in imaging athletes with impingement pain isto identify or exclude a rotator cuff tear. In this

article, we will review the mechanisms that canlead to rotator cuff pathology in sports enthusi-asts. We will then focus on the MR appearance

of cuff injuries in athletes, various tear locationsin younger and older individuals, and how toimprove your accuracy for detecting cuff tears on

MR images in athletes.Correctly identifying a rotator cuff tear on

conventional MR images in young, athletic

individuals can be difficult for two reasons. Thefirst is that these tears are usually small andshallow and therefore do not appear like the largefluid-filled defects commonly seen in older pa-

tients. The second is that these tears often occur inatypical locations. When evaluating the rotatorcuff on MR images in older individuals with

chronic impingement pain, it is important toconcentrate on the anterior half of the supra-spinatus tendon in the ‘‘critical zone’’ 1 cm medial

to the insertion where 89% of cuff tears occurin people over the age of 35 [1]. Accurately

diagnosing cuff tears in athletes involves looking

carefully for these small tears and knowing whento recommend an MR arthrogram with abductionand external rotation (ABER), particularly for

throwers.MR can be beneficial to orthopedic surgeons

treating athletes with impingement pain because it

can reveal unsuspected cuff tears and alter thetreatment plan [2]. Although the treatment ofimpingement pain begins with physical therapy

and strengthening exercises, athletes who haveeven a partial thickness tear may require arthro-scopic debridement of the tear to become pain free[3,4]. In addition, MR provides information on

the status of the labrum and glenohumeralligaments that can also be injured in athletes withshoulder pain.

To understand why cuff tears occur in differentlocations in athletes, it is necessary to review themechanisms of shoulder injuries that occur during

athletics. Sports trauma to the rotator cuff can bedivided into six main categories:

1. Primary impingement2. Secondary impingement from instability3. Posterosuperior (internal) impingement in

throwers4. Tensile overload (overuse)5. Macrotrauma from contact sports

6. The older athlete

Primary impingement

Primary impingement refers to pain caused by

contact between the rotator cuff and the coracoa-cromial arch. The pain is believed to be causedprimarily by compression of the well-innervated

subacromial bursa between the cuff and thecoracoacromial arch. Although it is an importantE-mail address: [email protected]

1064-9689/03/$ - see front matter � 2003, Elsevier Inc. All rights reserved.

doi:10.1016/S1064-9689(03)00025-4


11 (2003) 207–219

cause of cuff pain in older patients, primaryimpingement is fairly uncommon in young indi-viduals. When seen, it is often the result of a

congenital or posttraumatic abnormality of thecoracoacromial arch, such as a down sloping ofthe anterior acromion (Fig. 1) or a mobile osacromiale [5]. Because the acromial apophysis

may not completely fuse until individuals are intheir early twenties, a careful physical examina-tion may be necessary in some young individuals

to distinguish a normal physis from a painfulfibrocartilaginous union [6]. As in older patientswith primary impingement, the cuff pathology will

usually be in the anterior portion of the supra-spinatus tendon adjacent to the inciting osseousstructure.

Primary impingement can also result from

a congenitally thickened coracoacromial ligament[4], a ligament that is particularly well seen onMR images. In addition, coracoid impingement

can occur in throwing athletes where there isdecreased distance between the tip of the coracoidprocess and the humerus, although the rotator

cuff itself is usually not torn in this condition [7].

Secondary impingement from instability

Secondary impingement from instability is themost common cause of impingement pain in

athletes [8]. This is considered a secondary im-pingement because the root cause is instability ofthe humeral head within the glenoid fossa, and the

abnormal motion of the humeral head leads torotator cuff tendonosis or tearing, which thenbecomes the main complaint of the athlete. Thecuff pain results from either contact between the

cuff and the coracoacromial arch or frommicroscopic or macroscopic tearing of the cufffrom secondary tensile forces [8].

Although the primary problem is instability,this type of impingement rarely presents aftera glenohumeral joint dislocation. The instability is

usually minor and by itself asymptomatic, andresults from a lax capsule or stretched glenohu-meral ligaments that develop over time. This isparticularly common in swimmers and in athletes

who use an overhead motion, such as throwers ortennis players. In swimmers, the pull-throughphase against resistance leads to disproportion-

ably strong internal rotators and adductors. Thismuscle imbalance, combined with the extremeranges of motion during the swimming stroke, is

felt to be the cause of the instability in swimmers[8]. In the cocking phase of throwing, the arm isrepeatedly placed in 90 degrees of abduction and

maximal external rotation, which can graduallystretch the anterior capsuloligamentous complex.As the anterior capsule and ligaments becomemore lax, the cuff is increasingly overworked and

more likely to contact the coracoacromial arch. Inathletes who have a SLAP tear or weak long head

Fig. 1. A 51-year-old man with impingement pain.

Oblique sagittal FSE proton density weighted image

shows a severely down-sloped acromion process (arrow)

indenting and causing increased signal in the supra-

spinatus tendon.

Fig. 2. A 15-year-old with impingement pain and

multidirectional instability. MR arthrogram axial T1-

weighted image with fat suppression demonstrates a lax

anterior capsule (arrow). No rotator cuff abnormality

was seen.

208 M.J. Tuite =Magn Reson Imaging Clin N Am 11 (2003) 207–219

of the biceps tendon, the humeral head canmigrate superiorly and lead to cuff impingement.

Cuff tendonosis or tears can occur anywherein the supraspinatus or infraspinatus tendon in

athletes with secondary impingement, dependingon the arm motion that is used during their sport.Instability is the most important condition for the

orthopedist to diagnose because these patients aretreated by addressing the capsuloligamentouslaxity and not by performing a decompression of

the coracoacromial arch. MR arthrography canbe particularly useful in showing a capaciouscapsule and lax ligaments (Fig. 2).

Posterosuperior (internal) impingement

One of the major developments in treating

impingement pain in athletes over the past 10years has been recognizing the entity called

posterosuperior, or internal, impingement. Walchand colleagues [9] and Jobe [10] were some of thefirst to notice that the cuff tears in overheadathletes were often at the posterior aspect of the

supraspinatus tendon or top of the infraspinatustendon. They also noted that the cuff tears wereoften associated with fraying or tears of the

adjacent posterosuperior labrum. In a cadaverstudy, Jobe found that during the cocking phaseof throwing there can be contact between the cuff

in the region of the supraspinatus and infra-spinatus tendon interval and the posterosuperiorlabrum [10]. They postulated that this repetitive

contact might lead to injuries to these twostructures, and termed this condition ‘‘internalimpingement’’ to distinguish it from the extrinsicimpingement caused by the coracoacromial arch.

Some authors consider posterosuperior im-pingement a subset of secondary impingementfrom instability. In normal throwers there is no

Fig. 3. A 31-year-old woman with a greater tuberosity fracture after a fall while snow skiing. (A) AP internal rotation.

(B) Neer AP external rotation radiographs were interpreted as no fracture. (C ) T1-weighted and (D) T2-weighted with

fat suppression oblique coronal MR images demonstrate the greater tuberosity fracture (arrows).

209M.J. Tuite /Magn Reson Imaging Clin N Am 11 (2003) 207–219

significant contact between the posterior cuff andthe adjacent glenoid, but in many athletes withposterosuperior impingement there is mild in-

stability that allows repetitive impaction to occur[10–12]. Some of these throwers have a combina-tion of a tight posterior capsule and anteriorcapsuloligamentous laxity. The instability may be

difficult to demonstrate, however, even at exam-ination under anesthesia [10]. Most researchersbelieve that the posterosuperior cuff tears in

throwers belong in a separate category becausethey can occur in athletes without any evidence ofinstability, and because of the unique pattern of

injuries [9,13].In addition, there is some debate as to whether

the posterosuperior cuff tear is caused by repetitive

contact between the cuff and the glenoid rim. Onegroup has reported that the cuff tear may resultfrom the shearing forces from differences in the

direction of pull between the supraspinatus andinfraspinatus tendons near their insertions [13].These authors also found in their population ofthrowing athletes that the posterior cuff tears were

not as often associated with any adjacent labralpathology, and that at arthroscopy in these patientsthey could not simulate contact between the cuff

and the adjacent glenoid rim. Regardless of theetiology, posterosuperior impingement is an im-portant injury to recognize because it is common in

throwers and because MR arthrography in theABER position is crucial in helping make thediagnosis before arthroscopy.

Fig. 4. A 22-year-old man with an articular surface partial thickness cuff tear at surgery. (A) Oblique coronal

T2-weighted image with fat suppression shows faint increased signal along the articular surface of the cuff (arrow).

(B) Oblique sagittal T2-weighted image with fat suppression also shows the subtle area of increased signal (arrow).

(C ) Angled oblique sagittal sections localized on an oblique coronal image. (D) Angled oblique sagittal T2-weighted

image with fat suppression demonstrates clearly the obliquely oriented cuff tear (arrow).


Tensile overload (overuse)

Tensile overload, a primary overuse injury,refers to repetitive traction forces on the rotatorcuff leading to collagen fiber failure. This is seen

mainly in overhead throwing athletes who sud-denly increase their intensity or duration ofthrowing [11]. If the soreness or muscle fatigue

leads to altered throwing mechanics, mild in-stability can exacerbate the situation further bycausing secondary tensile overload.

There is still some controversy regarding thismechanism as a cause of tendonosis or cuff tearsin athletes. Jobe showed that the supraspina-

tus muscle never exceeds 60% of its maximumactivity during the throwing cycle, and thereforethat primary tensile overload should be rare [14].Others have also noted that in young healthy

individuals the tensile strength of the supra-spinatus tendon is greater than bone [4], andtherefore a fracture might be more likely to occur

than a cuff tear. Other authors have reported,however, that during the deceleration phase ofthrowing, which occurs immediately after the ball

is released, the eccentric traction force on therotator cuff is massive as it keeps the humeralhead properly situated within the glenoid fossa

[11,13,15]. They propose that the forces are greatenough, especially with the additional shear forcesas the humeral head rotates during the throwingmotion, to lead to tensile overload and cuff tears.

Most authors now include overuse injury asa potential etiology of tendonosis and cuff tearsin throwing athletes.

Macrotrauma from contact sports

The rotator cuff can be injured by an acute

traumatic event during athletics, although this isuncommon [11]. The cuff can be contused or tornby an impaction injury where the tendon is caught

between the humeral head and the coracoacromialarch. Acute traction injuries to the cuff in youngathletes are rare, again because the tensile strength

of the normal cuff is greater than bone. Zanettiand colleagues reported that greater tuberosityfractures following acute shoulder trauma aremore

common in young patients, and may be occulton radiographs and thus first detected at MR im-aging (Fig. 3) [16].

The older athlete

Because the supraspinatus tendon is weakenedby age-related myxoid and eosinophilic degener-

ation, the rotator cuff in older patients is vul-nerable to tearing while playing sports. Chronic

cuff tendonosis can be aggravated by activitiessuch as golf or tennis, and gradual-onset cuff tearscan result [11]. As in occupational overuse or

non–sports-related trauma, the cuff tears tend tooccur in the anterior supraspinatus tendon in theso-called ‘‘critical zone.’’ Another location for

tears seen in middle-aged individuals is the rimrent-type tear, an articular surface partial thick-ness tear just at the insertion onto the greater

tuberosity [1]. The already somewhat weakenedcuff is also more likely to tear after acute athletictrauma, such as a glenohumeral joint dislocation.Fortunately, current rehabilitation and surgical

techniques can often help older individuals returnto their previous level of athletic ability [17].

Conventional MR technique

Although conventional MR is accurate fordetecting rotator cuff tears in older patients, itsaccuracy is less in young athletic patients [1,18].

We therefore usually recommend MR arthrogra-phy for these patients, particularly for throwingathletes. If a conventional MR is obtained, for

example in older individuals with a sports-relatedinjury or an athlete after acute macrotrauma, wetypically perform the following pulse sequences:

1. Oblique coronal fast spin-echo (FSE) T2 with

fat suppression.2. Oblique sagittal FSE T2.

Fig. 5. A 17-year-old man with a SLAP tear (arrowhead)

but no impingement symptoms and a normal cuff at

surgery. Note the low signal bursal (white arrow) and

articular (black arrow) surfaces of the cuff on either side

of intermediate signal within the tendon.


3. Axial FSE mid-echo time (TE[eff]=30) withfat suppression.

4. Angled oblique sagittal FSE T2 with fat

suppression.

We prefer fat-suppressed FSE T2-weighted

images for evaluating the rotator cuff withconventional MR because most authors havefound that these are the most accurate for de-

tecting cuff tears [19–24]. They report a sensi-tivity of 84% to 100% and a specificity of 77%to 97% for full-thickness tears, although the

accuracy is lower for the partial thickness tearsthat are more common in athletes. We alsoobtain angled sagittal images perpendicular to

the lateral aspect of the supraspinatus tendon,which are sometimes better at showing smallpartial tears (Fig. 4) [25].

MR arthrography

MRarthrography ismore accurate for detecting

articular surfacepartial thickness tears, particularlythe posterior cuff tears seen in throwers [18,26–29].MR arthrography is also better at showing theposterosuperior labral fraying seen in internal

impingement, as well as SLAP tears or a lax inferiorglenohumeral ligament that may be contributingto the patient’s shoulder pain. Our standard

MR arthrography protocol follows:

1. Oblique coronal T1 with fat suppression.2. Oblique sagittal T1 with fat suppression.3. Axial T1 with fat suppression.

4. Oblique coronal FSE T2 with fat suppression.5. ABER position coronal localizer.6. ABER position oblique axial T1 with fat

suppression.

If the patient cannot abduct the arm into the

ABER position, we obtain instead an additionalaxial T1-weighted set of images with the arm inmaximum external rotation. Full external rotation

tightens the anterior capsuloligamentous structuresand may demonstrate better some anterior labraltears that can be associated with secondary

impingement.

Normal MR appearance of the rotator cuff

in athletes

To recognize cuff pathology on MR images, it

is helpful to be familiar with the appearance ofthe normal rotator cuff in young individuals.Histologically, there are five layers that make up

the rotator cuff [30]. The two layers forming thebursal one-third of the tendon contain closelypacked, well-organized tendon fibers, as does the

layer forming the articular surface of the cuff. Inthe center of the cuff are two layers that containless-organized fibers mixed with loose connectivetissue. On fat-suppressed T2-weighted MR im-

ages, this central third of the tendon can haveintermediate signal even in young healthy indi-viduals. The articular and bursal portions of

the cuff should be low signal in a normal cuff(Fig. 5).

Fig. 6. A 15-year-old male gymnast with shoulder pain and a normal-appearing cuff at surgery. (A) Oblique coronal and

(B) oblique sagittal T2-weighted images with fat suppression show high signal within the posterior cuff (arrow) but with

intact articular and bursal tendon surfaces. The patient was believed to have tendonosis and did well with physical

therapy.


Several authors have found that intermediatesignal may involve the cuff surfaces in asymptom-atic athletic individuals, and that this may be

difficult to distinguish from subtle partial tears[31,32]. Because of this, we do not interpret a tearunless the signal intensity is greater than hyaline

articular cartilage on fat-suppressed FSE T2-weighted images. Although high signal on FSET2-weighted images disrupting the surface of the

cuff is the most accurateMR sign of a cuff tear, thisfinding has been reported in asymptomatic pro-fessional baseball pitchers [31]. Some have specu-lated that this may represent an asymptomatic (or

unacknowledged) partial tear in these athletes.Finally, the signal intensity of the rotator cufftendon does not change after exercise, although the

supraspinatus muscle itself may have increasedsignal intensity immediately after exercise [33].

One of the pitfalls in interpretingMR images of

the cuff is themagic angle effect seen laterally wherethe tendon is oriented at 55 degrees to the mainmagnetic field B0. The well-organized collagenfibers in the outer portions of the cuff are organized

longitudinally, and therefore these normally low-signal fibers have increased signal on short-TEimages as they curve and become oriented at the

‘‘magic angle’’ [34]. This is usually not a problemonthe fat-suppressed T1-weighted images obtainedduring MR arthrography because of the high

contrast resolution between the gadolinium solu-tion and the soft tissues of the shoulder, or on the

long-TE FSE T2-weighted images used in conven-tional MR imaging of the cuff.

MR imaging of impingement and rotator cuff

injuries

There is a continuum of injuries that occur tothe rotator cuff of athletes, from mild tendonosisto full-thickness tears. In this section, we reviewthe variety of MR appearances of cuff pathology

Fig. 7. An 18-year-old male baseball pitcher with mild instability and impingement pain, and an articular surface

partial-thickness tear in the anterior supraspinatus tendon at surgery. (A) Oblique coronal and (B) oblique sagittal T1-

weighted with fat-suppression images show contrast extending into the cuff (arrows) at the site of the tear.

Fig. 8. A 48-year-old man with a rim-rent tear. Oblique

coronal T2-weighted image with fat suppression shows

high signal at the enthesis disrupting the insertion of the

articular surface cuff fibers (arrow).


and the unique locations where tears can occur inathletes.

Tendonosis, cuff strain, and cuff contusion

The most common MR finding in the athlete

with mild impingement pain is a normal cuff. Someof these patients may have mild subacromial-subdeltoid bursitis at arthroscopy even thoughthey do not have significantly increased bursal

fluid or thickened high-signal synovium on MRimages.

With increasing severity, the cuff develops in-

trasubstance fissures, edema, and myxoid changethat is often termed ‘‘cuff tendonitis’’ [35]. Bi-opsies of the cuff in patients with this condition

reveal no inflammatory cells and thereforemost authors now prefer a term such as ‘‘ten-donosis.’’ There are three main MR findingsthat we like to see before we will interpret cuff ten-

donosis: fluid-signal fissures; high and not justintermediate signal within the cuff; or a swollencuff with increased signal (Fig. 6) [36].

The cuff may also have a focal area ofincreased signal after an acute traumatic eventwithout a tear involving the cuff surface, which

depending on the mechanism represents eithera hyper stretch injury or contusion. The signalabnormality of a rotator cuff strain is often in the

posterior cuff and may be associated with a bone

contusion [37]. A cuff contusion resulting froma direct blow to the shoulder is often associatedwith an edematous high signal subacromial bursa,

which over time can become thickened and lowsignal from fibrosis [11].

Rotator cuff tears

Most cuff tears in athletes are small, articular

surface partial-thickness tears [3,8,11,13]. Thetears tend to be small because the high tensilestrength of the tendon in young people makes the

cuff resistant to extensive tearing at the time ofinjury. Because the cuff in a young person doesnot have preexisting myxoid degeneration, thetears tend to stay small instead of enlarging by

extending through weakened portions of the cuffas often occurs in older individuals. There arethree main reasons why the partial thickness tears

also typically involve the articular surface: (1) theeccentric forces on the cuff that occur in athletesare greater on the articular side [15], (2) the

articular side fibers are weaker than the bursalside, and (3) when injured, the articular surface isless well vascularized and therefore does not heal

as well [13].There are three main locations where rotator

cuff tears occur in athletes: standard (criticalzone), rim-rent tears, and posterosuperior tears.

Standard (critical zone)Cuff tears in the anterior half of the supra-

spinatus tendon 0.5 to 1 cm from the insertion are

common in athletes. In one study, 79% of the cufftears in patients under 36 years old were centeredin the anterior half of the supraspinatus tendon

[1]. These tears can occur either from acutetrauma or impingement by the coracoacromialarch. Partial thickness tears even in this standardarea can be difficult to diagnose, so the articular

surface should be carefully inspected for disrup-tion by high signal in the athlete with impinge-ment pain (Fig. 7) [22,25,38].

Rim-rent tears

The rim-rent tear is an articular surface partial-thickness tear that occurs right at the insertion ofthe tendon onto the humerus (Fig. 8). Althoughnot specific for athletes, several authors have

shown this tear to be more common in youngerindividuals and may be the tear site in a middle-aged person with pain while playing sports

[1,39,40]. The cuff is vulnerable to tearing in thisregion because the collagen fibers make an abrupt90-degree turn as they approach the greater

Fig. 9. A 22-year-old man with multidirectional in-

stability and a normal cuff at surgery. Oblique coronal

T2-weighted image with fat suppression shows an

intrasubstance fissure near the enthesis (arrow) but

intact articular (arrowhead) surface cuff fibers down to

the insertion on the greater tuberosity.


tuberosity, and this may be one of the weakerpoints in an otherwise young healthy cuff.

The main issue with rim-rent tears is distin-guishing them from intrasubstance fissures at the

enthesis. Fissures within the cuff that do notextend to the cuff surface are part of the spectrumof findings seen in tendonosis, and fissures com-

monly occur adjacent to the greater tuberosity.The important feature is to determine if the arti-cular surface cuff fibers are intact down to their

attachment on the greater tuberosity, indicating

simply tendonosis (Fig. 9), or if there is highsignal between the articular surface of the cuffand the humerus consistent with a tear. Like allpartial-thickness tears, rim-rent tears are typically

debrided at arthroscopy.

Posterosuperior (internal) impingement cufftears

These cuff tears are seen in overhead athletes,such as throwers and tennis players, and involve

the posterosuperior cuff about 0.5 to 1 cm from

Fig. 10. A 23-year-old man with a posterior supraspinatus tendon articular surface partial thickness tear at surgery. (A,

B) Two consecutive oblique coronal T2-weighted images with fat suppression show unusually extensive subcortical cysts

in the posterior greater tuberosity, and increased signal disrupting the articular surface of the cuff (arrow). (C) Oblique

sagittal T2-weighted image with fat suppression shows faint disruption of the low signal articular surface at the tear

(arrow). A, anterior; P, posterior.


the insertion on the greater tuberosity. Internalimpingement tears are difficult to see on conven-tional MR images for two reasons. First, like all

tears in athletes they are usually small, articularsurface partial-thickness tears that can be easily

overlooked [22,25,38]. Second, the orientation ofthe posterosuperior cuff in this region is obliquerelative to the standard imaging planes. Partial

averaging can obscure tears as the high signal ofa small rotator cuff tear is averaged with the

Fig. 11. ABER imaging. (A) Coronal localizer image with the right arm in the ABER position and showing the

orientation of the oblique axial images. (B) Orientation of the oblique axial images relative to the glenohumeral joint

during ABER imaging, as seen en face. A, anterior; P, posterior.

Fig. 12. A 29-year-old man with posterosuperior impingement. (A) Oblique coronal MR arthrogram T1-weighted with

fat suppression shows intraarticular contrast extending into a humeral head notch (arrow). No definite labral or cuff

abnormality was seen. (B) ABER position oblique axial T1-weighted image with fat suppression shows a small articular

surface partial thickness tear of the infraspinatus tendon (arrow) and fraying of a blunted posterosuperior labrum

(arrowhead).


adjacent low signal intact cuff within the samevoxel. When these tears are seen on conventionalMR images, they appear as increased signaldisrupting the articular surface of the cuff near

the supraspinatus–infraspinatus tendon junction(Fig. 10).

The most accurate way to diagnose postero-

superior impingement tears is with MR arthrog-raphy, including images obtained with the armin abduction and external rotation (ABER) [18].

The images obtained by localizing oblique axialimages off a coronal localizer with the arm in the

ABER position have two main advantages. First,the ABER position simultaneously relaxes theposterosuperior cuff as the anterior labroligamen-tous complex is placed under tension. The de-

creased tension on the posterosuperior cuff maymean that small, shallow, partial-thickness tearswith smooth gradual margins are not as stretched

and therefore the edges of the tear are moreconspicuous. Second, because of the arm position,the oblique axial images are oriented from ante-

roinferior to posterosuperior and are thereforeorthogonal to the posterosuperior cuff and labrum

Fig. 13. An 18-year-old man with posterosuperior impingement and a focal notch in the posterior greater tuberosity. (A)

Oblique coronal T2-weighted image with fat suppression shows a focal indentation in the cortex (arrow) and adjacent

high signal in the bone marrow (arrowhead). (B) Axial T1-weighted and (C ) fat-suppressed mid-TE images show the

notch (black arrow) and adjacent marrow edema (white arrow).


(Fig. 11). There is less partial averaging of the highsignal from tears in the posterosuperior cuff, andtherefore the tears are more conspicuous.

When evaluating the ABER images, it isimportant to inspect the front and the back ofthe joint. The anteroinferior side displays theanteroinferior labrum and anterior band of the

inferior glenohumeral ligament, and subtle inju-ries to these structures are common in patientswith posterosuperior impingement [26]. On the

posterosuperior side, the articular surface of thecuff should be inspected for contrast extendinginto an articular surface partial thickness tear

(Fig. 12). Although these are often small cufftears, there may be a horizontal component withinthe tendon associated with deeper tears [27]. Apitfall when evaluating the posterior cuff in the

ABER position is that because the cuff is notunder tension, it can develop a fold that shouldnot be confused with a tendon tear. Unlike a cuff

tear, a fold in the tendon does not cause a focalthinning of the cuff or disrupt the low signalarticular surface layer of densely packed collagen

fibers.There are several findings associated with

posterosuperior impingement tears that can help

make the diagnosis on MR images. The mostimportant is associated fraying of the postero-superior labrum, although when mild this can bedifficult to see, particularly on conventional MR

images. MR arthrography with the arm in theABER position is the most sensitive technique foridentifying posterosuperior labral fraying and

should be looked for in any overhead athlete(Fig. 12). Several studies have reported that actualtears of the posterosuperior labrum are also fairly

common in these athletes. In one study of 38overhead athletes with posterosuperior impinge-ment cuff tears, there were 21 SLAP tears and27 tears of the posterosuperior labrum [13]. In

another study of 41 professional athletes, 93%had cuff tears and 88% posterosuperior labralpathology [12].

In addition, many of these athletes will haveunusually large subcortical cysts in the posteriorgreater tuberosity, although these can be difficult

to distinguish from the enthesopathic cysts, whichare common in people with shoulder pain [13,18].A more specific finding of posterosuperior im-

pingement is a focal indentation in the cortex ofthe posterior greater tuberosity, which is seen insome overhead throwers (Fig. 13) [13,18]. Someathletes may have just focal marrow edema in the

posterior greater tuberosity, presumably from

repetitive contact [18]. This marrow edema is notwell seen on fat-suppressed T1-weighted imagesand is one of several reasons why T2-weighted or

inversion recovery images should be obtainedduring an MR arthrogram study. Finally, al-though spinoglenoid or suprascapular notchganglion cysts are often associated with postero-

superior labral tears in patients with a priorhistory of trauma, paralabral cysts are uncommonin athletes with chronic posterosuperior impinge-

ment labral tears [13,29].

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MR imaging of shoulder instabilityinjuries in the athlete

Javier Beltran, MD*, David Hyun-Min Kim, MDDepartment of Radiology, Maimonides Medical Center, 4802 Tenth Avenue, Brooklyn, NY 11219, USA

During the past few decades, the use of sophis-

ticated technology, such as arthroscopy and MRimaging, combined with a better knowledge of theshoulder anatomy, biomechanics, and clinicalevaluation, has provided an improved understand-

ing of the pathology of the shoulder in theathlete.

Because of its remarkable degree of mobility,

the glenohumeral joint is inherently prone to in-stability. Functional stability of the glenohu-meral joint can be defined as the maintenance of

alignment of the center of the humeral head withinthe glenoid fossa during shoulder motion and isachieved through precise synchronization of static

(or passive) mechanisms and dynamic (or active)mechanisms. The static mechanisms include neg-ative intraarticular pressure; adhesion and co-hesion of the articular surfaces; size; and shape and

orientation of the glenoid fossa and the capsulo-labral complex. Dynamic mechanisms include therotator cuff and the long bicipital tendon.

The throwing action places high stress loads onthe capsulolabral complex and rotator cuff, andeven minor degrees of injury to these structures

can become symptomatic and produce significantfunctional impairment. Joint laxity may developas a consequence of the injury to the tissues, lead-ing to even more damage and further instability.

It is now understood that in the throwing athletethese injuries are not the consequence of a singleevent of dislocation but are the result of multiple

episodes of microtrauma, producing gradual in-crease of shoulder pain at some point in thethrowing position.

This article will discuss the basic normal

anatomy, biomechanics, and pathophysiology ofshoulder instability in the athlete, with specialemphasis on the overhead-throwing athlete, andwill review the MR imaging findings in some of

the instability patterns seen in these patients.

MR imaging strategies

In the past, nonenhanced MR imaging of theshoulder for the detection of capsulolabral lesions

has been reported to have variable results by dif-ferent researchers [1–3]. Different types of surfacecoils, field strength, and imaging parameters

may all have contributed to the differences.More recently, better knowledge of the anatomyand normal variants, as well as improved imagingtechniques has led to improved accuracy [4]. The

presence of a joint effusion provides capsulardistension and aids in defining the anatomy of theintracapsular structures [4,5]. Although nonen-

hanced MR imaging has been demonstrated tohave high accuracy rates for the demonstration oflabral tears [6], MR arthrography with intrar-

ticular injection of gadolinium has gained pop-ularity during the past few years because of itsability to depict not only the labrum but also the

glenohumeral ligaments and the undersurface ofthe rotator cuff when the joint capsule is distended[2,7–13]. The main disadvantage of direct MRarthrography is the need to schedule the patient

for fluoroscopy for needle positioning, althoughsome authors have used ultrasound-guided in-jection [14] and open MR needle positioning [15].

Indirect MR arthrography has also been pro-posed as an alternative to direct intraarticularinjection of gadolinium [16,17]. Contrast material

is injected intravenously, and images of the* Corresponding author.

E-mail address: [email protected] (J. Beltran).


doi:10.1016/S1064-9689(03)00023-0


11 (2003) 221–238

shoulder are obtained following a short period ofgentle exercise of the joint. Pathology is visualizedby way of enhancement of hyperemic soft tissues

and small amount of contrast material accumu-lated in the joint. This technique does not requirefluoroscopy or intraarticular needle placement,thereby making it less invasive and ensuring

greater patient acceptance. Additionally, it hasthe advantage of being faster and less expensivethan direct arthrography. The main disadvantage

is that joint distension is not achieved unless apreexisting joint effusion is present. In two differ-ent series, Sommer et al [16] and Maurer et al [17],

comparing nonenhanced MR imaging with in-direct MR arthrography in patients with suspectedlabral tears, achieved significant improvement insensitivity and specificity with the latter technique.

Additional imaging strategies to improve de-tection of lesions in patients with microinstabil-ity have been described recently. These include

imaging in the abduction and external rotationposition (ABER) following intrarticular injectionof gadolinium [18,19] for improved visualization

of the anterior capsuloligamentous structures,posterosuperior labrum, and undersurface of therotator cuff and imaging in the oblique coronal

plane with arm traction to better visualize lesionsof the superior labrum (SLAP lesions) [20].

Hodge et al [21] described recently dynamicMR imaging and stress testing in patients with

glenohumeral instability using an open configura-tion 0.5 Tesla magnet. These authors evaluatedthe position of the humeral head on the glenoid in

11 subjects, comparing the symptomatic shoulderwith the asymptomatic one. They performedimaging in abduction=adduction and in internal

and external positions. They also performed stresstesting during imaging. They found that dynamicevaluation without stress testing underestimatedthe abnormalities in symptomatic shoulders, and

when imaging during stress testing was per-formed, there was a strong correlation with clin-ical grading of instability.

Normal MR imaging anatomy and biomechanics

The glenohumeral joint is the joint of thehuman body with the greatest range of motion(over 180 degrees in several planes). The relativelylarge articular surface of the humeral head

compared with the small articular surface of theglenoid cavity explains the extended mobility ofthe joint. Because of its wide range of motion, the

glenohumeral joint is also more susceptible to

dislocations, subluxations, and lesions related tochronic stress in the surrounding soft tissues.

The superior, middle, and inferior glenohu-

meral ligaments reinforce the joint capsule anteri-orly (Fig. 1). The labrum is a fibrous structuresurrounding the edge of the osseous glenoid andincreases the depth of the glenoid fossa by about

50% in all directions and hence the stability of theglenohumeral joint [22]. On MR imaging the la-brum is seen as a low signal intensity structure ad-

jacent to the glenoid margin. The labrum is mostoften triangular in shape on axial and obliquecoronal images (Fig. 2). Articular cartilage is

Fig. 1. Schematic rendering of the glenoid fossa,

capsuloligamentous structures, rotator cuff, and scapula.

SSP, supraspinatus muscle and tendon; SSC, subscapu-

laris muscle and tendon; IS, infraspinatus muscle and

tendon; TM, teres minor muscle and tendon; BT,

intracapsular long bicipital tendon and tendon anchor;

SGHL, superior glenohumeral ligament; MGHL, mid-

dle glenohumeral ligament; IGHL, inferior glenohu-

meral ligament; A, anterior band of the IGHL; P,

posterior band of the IGHL; AR, axillary recess; CCL,

coracoclavicular ligament; CAL, coracoacromial liga-

ment; CHL, coracohumeral ligament. The space be-

tween the anterior margin of the SSP and the superior

margin of the SSC is the rotator cuff interval (between

the two arrowheads). The joint capsule, BT, SGHL, and

CHL, occupies this space.

222 J. Beltran, D. Hyun-Min Kim / Magn Reson Imaging Clin N Am 11 (2003) 221–238

often seen between the fibrous, low signal inten-sity labrum and the subchondral cortex of the gle-noid margin.

The glenoid labrum also helps in preventing

translational forces, especially in the lower half ofthe joint were the labrum is more firmly attachedto the bony glenoid margin. However, the more

important function of the labrum is to serve as theanchoring structure for the glenohumeral liga-ments and the long head of the biceps tendon,

superiorly. The normal labrum is attached to theglenoid margin of the scapula and the scapularperiosteum. However, the anterior superior la-brum may be partially detached, creating a space

between the glenoid and the labrum called thesublabral foramen or sublabral hole, not to beconfused with an anterior superior labral tear

when performing arthroscopy or MR imaging(Fig. 3) [4]. A second potential space or recess mayexist between the superior labrum and the glenoid

and it is termed the sublabral recess, often con-fused with a superior labral tear (Fig. 4) [4].

The glenohumeral ligaments are infoldings of

the capsule and each one contributes to a differentdegree to the stability of the glenohumeral joint,depending on the position of the arm.

The superior glenohumeral ligament (SGHL) isa fairly constant structure that arises in the shouldercapsule just anterior to the insertion of the longhead of the bicep tendon (LHBT) and it inserts

into the fovea capitis line just superior to the lessertuberosity. It varies in thickness and it is present90% to 97% of the time in cadaver dissections.

The coracohumeral ligament (CL) is an extracap-sular structure located superior to the LHBT.

The middle glenohumeral ligament (MGHL)

has been described arthroscopically as beingattached to the anterior surface of the scapula,medial to the articular margin. It then liesobliquely, posterior to the superior margin of the

subscapularis muscle and blends with the anteriorcapsule. Distally, it is attached to the anterioraspect of the proximal humerus, below the attach-

ment of the superior glenohumeral ligament[23,24]. Using MR arthrography, the scapular in-sertion of theMGHL is seenmore often at the level

of the superior anterior labrum than at the levelof the scapula as was suggested arthroscopically[23,24].

The MGHL presents the largest multiplicityof normal variants. In one anatomic study, theligament was absent in 30% of the specimens [25].

Fig. 2. (A, B) Normal glenoid labrum. Axial (A) and oblique coronal (B) T1-weighted fat-suppressed images obtained

following intrarticular injection of gadolinium. The most frequent appearance of the glenoid labrum is a triangular, low

signal intensity structure attached to the glenoid margin (long arrows in A and B). Frequently there is intermediate signal

intensity articular cartilage interposed between the labrum and the cortical bone. The distension of the capsule allows

visualization of the undersurface of the rotator cuff (short arrow in B). Note the flat appearance of the MGHL

(arrowhead in A) and the axillary recess (arrowhead in B). (Fig. A from Beltran J, Bencardino J, Padron M, et al. The

middle glenohumeral ligament: normal anatomy, variants and pathology. Skeletal Radiol 2002;5:253–62; with

permission.)

223J. Beltran, D. Hyun-Min Kim / Magn Reson Imaging Clin N Am 11 (2003) 221–238

Using MR arthrography, Chandnani et al [24]identified the MGHL in 85% of their cases. Other

frequent variants include common origin of theMGHL with the SGHL, common origin with theSGHL and long biceps tendon, common origin

with the inferior glenohumeral ligament (IGHL),cordlike thickening, with or without associated

absence of the anterior superior portion of thelabrum (Buford complex), and split or duplicateligament [26–30].

The IGHL is composed of an anterior band,a posterior band and the axillary recess of thecapsule located in between the two bands. Itinserts in a collar-like fashion in the inferior

aspect of the anatomical neck of the humerus. TheIGHL is considered the most important stabilizerof the glenohumeral joint, especially with the arm

in abduction and external rotation (the throwingposition). In this position the anterior band isunder tension. If the arm is placed in abduction

and internal rotation, the posterior band is inmore tension than the anterior band.

The relative contribution of each individualglenohumeral ligament to joint stability has been

the subject of debate. Matsen et al [31] and Caspariet al [23] indicated that the SGHL and MGHL areabsent in a high percentage of individuals and

therefore must not be important structures inmaintaining joint stability. Turkel et al [32] studiedthe contribution of each one of the glenohumeral

ligaments by means of selectively cutting thesestructures in cadavers and then assessing thestability of the joint at different degrees of ab-

duction and external rotation. They concludedthat the IGHL is the most important structure inthe prevention of dislocation with the arm at 90degrees of abduction and external rotation.

In another classic experiment, O’Connell et al[33] measured the tension of the glenohumeralligaments in cadavers after application of a con-

trolled external torque. They concluded that at90 degrees of arm abduction, the IGHL and theMGHL developed the most strain, whereas with

the arm at 45 degrees of abduction, the most strainwas also developed by the IGHL and MGHL,though some strain also occurred at the SGHL.

The different ligaments contribute to the

stability of the glenohumeral joint in a diversefashion, depending on the position of the arm.The SGHL and the CL in concert limit inferior

translation of the adducted shoulder and posteriortranslation of the flexed, adducted, and internallyrotated shoulder. The MGHL limits anterior

translation of the humeral head when the arm isabducted between 60 degrees and 90 degrees. TheIGHL complex prevents increased translation of

the humeral head on the glenoid. With the arm inabduction, the entire complex moves beneath thehumeral head and becomes taut. With internalrotation the complex moves posteriorly and limits

posterior translation. With external rotation the

Fig. 4. Sublabral recess. Oblique coronal T1-weighted

image obtained following intraarticular injection of

gadolinium. The sublabral recess (long arrow) extends

about halfway into the base of the labrum (arrowhead ).

The labrum is continuous with the long bicipital tendon

(short arrow). Note that the direction of the sublabral

recess is toward the head of the patient. This feature

distinguishes the sublabral recess from a superior labral

tear (SLAP lesion). Superior labral tears tend to be

oriented in the opposite direction, toward the shoulder

(see Fig. 14A).

Fig. 3. Foramen sublabrum. Axial T1-weighted image

obtained fsollowing intraarticular injection of gadoli-

nium through the superior aspect of the glenohumeral

joint. The anterior superior labrum (arrowhead ) is

separated from the glenoid margin (short single arrow)

and the space is filled with gadolinium, representing the

foramen sublabrum (long arrow). The normal MGHL is

anteriorly located (double short arrows). (From Shank-

man S, Bencardino J, Beltran J. Glenohumeral in-

stability: evaluation using MR arthrography of the

shoulder. Skeletal Radiol 1999;7:365–82; with permis-

sion.)


complex moves anteriorly and limits anteriortranslation.

The long head of the biceps tendon and thecoracohumeral and coracoacromial ligaments are

also important structures contributing in differentways to the normal biomechanics of the joint. Thecoracohumeral ligament helps maintain the sta-

bility of the long head of the biceps tendon, andthe coracoacrial ligament is an important part ofthe acromial arch. The long head of the biceps

tendon has an intracapsular portion and an ex-tracapsular portion. The intracapsular portionextends from its insertion into the superior labrum

to the bicipital groove. The insertion of the tendonmay be in a broad base or in a thin area.

The capsular mechanism provides the mostimportant contribution to the stabilization of the

glenohumeral joint. The anterior capsular mech-anism includes the fibrous capsule, the glenohu-meral ligaments, the synovial membrane and its

recesses, the fibrous glenoid labrum, the subsca-pularis muscle and tendon, and the scapularperiosteum. The anterior capsular insertion can

be divided into three types, depending on theproximity of the capsular insertion to the glenoidmargin [30]. In general, the further the anterior

capsular insertion from the glenoid margin (typeIII), the more unstable will be the glenohumeraljoint.

The posterior capsular mechanism [34] is

formed by the posterior capsule, the synovialmembrane, the glenoid labrum and periosteum,and the posterosuperior tendinous cuff and

associated muscles (supraspinatus, infraspinatus,and teres minor). The long head of the bicepstendon inserting in the superior aspect of the

labrum and the triceps tendon inserting in theinfraglenoid tubercle inferiorly constitute addi-tional supportive structures of the glenohumeraljoint.

The rotator cuff is composed of the supra-spinatus, infraspinatus, subscapularis, and teresminor muscles and their corresponding tendons.

The space between the anterior margin of thesupraspinatus muscle and the superior margin ofthe subscapularis muscle is called the rotator cuff

interval (Fig. 5). The joint capsule covers thisspace and it contains the long head of the bicepstendon, the coracohumeral ligament, and the

superior glenohumeral ligament. Haryman et al[35] have shown that sectioning the rotator cuffinterval in cadaver shoulders significantly in-creases anterior, posterior, and inferior humeral

head translation. They concluded that the func-

tion of the rotator cuff interval is to limit inferior

translation of the glenohumeral joint in the ad-ducted shoulder and to provide stability againstposterior dislocation in flexion or abduction and

external rotation. In addition, this structure limitsthe range of flexion, extension, adduction, andexternal rotation.

The muscles around the shoulder are impor-tant contributors to the stability of the shoulderjoint. The rotator cuff muscles and perhaps toa lesser degree the long bicipital tendon provide

dynamic compression of the humeral head intothe glenoid fossa, centering the humeral head andcountering the oblique translational forces gener-

ated during the act of throwing [36–39]. Warneret al [40] demonstrated that this concavity-com-pression mechanism provides greater stability to

the glenohumeral joint in the inferior directionthan negative intraarticular pressure or ligamenttension in all degrees of abduction and rotation.

Fig. 5. Normal rotator cuff interval. Oblique sagittal

T1-weighted fat-saturated image following intraarticular

injection of gadolinium. The rotator cuff interval is

located between the asterisks, from the anterior margin

of the supraspinatus tendon to the superior margin of

the subscapularis tendon (compare with schematic

representation in Fig. 1). The long bicipital tendon

(single arrowhead) and the striated CHL and SGHL

(short arrow) are seen within the rotator cuff interval.

Note the capsule containing the fluid within the joint

(long arrow). The CAL is seen superficial to the rotator

cuff interval (double arrowhead). (From Beltran J,

Bencardino J, PadronM, et al. The middle glenohumeral

ligament: normal anatomy, variants and pathology.

Skeletal Radiol 2002;5:253–62; with permission.)


Another significant factor contributing to thestability of the glenohumeral joint is the scap-ulothoracic coordination during throwing. This is

achieved mainly through synchronization with thelatissimus dorsi, pectoralis major, and serratusanterior muscles [41,42]. In a classic study, Inmanet al [43] demonstrated that there is 2:1 ratio of

glenohumeral to scapulothoracic motion duringabduction. More recent studies indicate that thisratio is even higher and it is more significant

during the early degrees of abduction [44]. Failureof the scapulothoracic coordination may placeadditional stress on the capsulolabral complex,

hence increasing the risk for soft tissue damage. Ithas been shown that patients with shoulderinstability have increased scapulothoracic asym-metry [45].

To understand the pathophysiology of theglenohumeral instability in the throwing athlete itis important to know the normal joint motion

during the act of throwing. With minor differ-ences, overhead throwing, the volleyball spike, thegolf swing, and the tennis serve all have similar

throwing mechanics [42–45]. There are six phasesin the overhead throwing motion: wind-up, earlycocking, late cocking, acceleration, deceleration,

and follow-through (Fig. 6) [42]. During the wind-up phase there is minimal stress loading andmuscular activity of the shoulder. At the end ofthis phase the shoulder is in minimal internal

rotation and slight abduction (positions 1 and 2,see Fig. 6). During the second phase of earlycocking the shoulder reaches 90 degrees of

abduction and 15 degrees of horizontal abduction(elbow posterior to the coronal plane of the torso)(position 3, see Fig. 6). During this phase there is

early activation of the deltoid muscle and lateactivation of the rotator cuff muscles, with theexception of the subscapularis muscle. During the

third phase of late cocking the shoulder ends inmaximum external rotation of 170 degrees to 180degrees, maintaining 90 degrees to 100 degreesof abduction. The 15 degrees of horizontal ab-

duction changes to 15 degrees of horizontaladduction (position 4, see Fig. 6). The scapularetracts to facilitate this position and provide

a stable base for the humeral head. The combi-nation of abduction and external rotation forcesposterior translation of the humeral head on the

glenoid. The activity of the deltoid muscle de-creases, while the rotator cuff muscles reach theirpeak. During the terminal portion of the latecocking phase, the subscapularis, latissimus dorsi,

pectoralis major, and serratus anterior musclesincrease their activity. During the fourth phase ofacceleration, abduction is maintained while the

shoulder rotates to the ball release (position 5, seeFig. 6). The scapula protracts as the body movesforward and the humeral head recenters in the

glenoid fossa, decreasing the stress on the anteriorcapsule. During the early acceleration phase thetriceps muscle shows marked activity, while the

latissimus dorsi, pectoralis major, and serratusanterior muscles increase their activity during thelate acceleration phase. During the fifth phase ofdeceleration the energy not imparted to the ball is

dissipated. It begins at the moment of ball releaseand it ends with cessation of humeral rotation to0 degrees. Abduction is maintained at 100 degrees,

and horizontal adduction increases to 35 degrees.All muscle groups contract violently, with eccen-tric contraction, allowing the arm to slow down.

Fig. 6. The six basic positions of a baseball pitch. Positions 1 and 2 are the wind-up phase. Note that the shoulder is in

internal rotation and mild abduction at the end of the wind-up phase, in position 2. Position 3: Early cocking phase. The

shoulder is in 90 degrees of abduction and 15 degrees of horizontal abduction. Position 4: Late cocking phase. Shoulder

in maximum external rotation at 90 degrees of abduction and 15 degrees of horizontal adduction. Position 5:

Acceleration phase. Shoulder in 90 degrees of abduction, rotating from external rotation to internal rotation. The ball is

released. Position 6: Deceleration and follow-through phases. Shoulder in internal rotation, horizontal adduction, and

moving from abduction to adduction.


During this phase, joint loads and compressiveforces are high posteriorly and inferiorly throughstrong contraction of the biceps muscle. Duringthe sixth phase of follow-though the body moves

forward with the arm until the motion ceases.Shoulder rotation decreases to 30 degrees, hori-zontal adduction increases to 60 degrees and ab-

duction is maintained at 100 degrees while jointloads decrease, ending in adduction (position 6,see Fig. 6).

Pathophysiology and MR imaging manifestations

Glenohumeral instability can be classified ac-cording to the etiology or according to the direction

of the instability. Based on the etiology, three maintypes of shoulder instability are recognized: trau-matic, atraumatic, and microtraumatic [45,46].

Traumatic and atraumatic instability are not fre-quently seen in the overhead-throwing athletes.These athletes usually complain of gradually in-creasing shoulder pain at some position during the

throwing motion, and the symptoms are theconsequence of multiple episodes of microtraumarather than a single episode of injury (traumatic

instability) or generalized joint laxity (atraumaticinstability) [47]. The acronyms TUBS (traumatic,unilateral, Bankart lesion, surgery) and AMBRI

(atraumatic, multidirectional, dilateral, rehabilita-tion, inferior capsular shift) have been used as asimple guide to classification and treatment ofshoulder instability [46]. The acronym AIOS (ac-

quired, instability, overstress, surgery) may beadded to include the microtraumatic instabilitydeveloping in the throwing athlete.

According to the direction of laxity testing,shoulder instability can be classified in anterior,posterior, and multidirectional instability (MDI).

Traumatic instability

Traumatic instability evolves following an

acute episode of shoulder dislocation, more oftenanterior inferior dislocation resulting from anabrupt abduction and external rotation force.

Recurrence rates of dislocation and subluxationsfollowing the first episode are high [48]. Theresulting injury to the anterior inferior capsulola-bral complex is the most frequently encountered

lesion, the so-called ‘‘classic Bankart lesion’’(Fig. 7) [49], often accompanied by an impac-tion fracture of the posterior superior aspect of

the humeral head, the Hill-Sachs lesion [50,51].This circumferential pattern of injuries was first

described by Perthes [52] and latter redefined byWarren [53] in his circle concept of capsuloliga-mentous instability of the shoulder. This concept

indicates that a significant lesion anywhere in thecapsule affects motion of the humeral head on theside of the lesion and also in other directions,resulting in MDI.

Variants of the Bankart lesion have been de-scribed and include the Perthes lesion [54] (Fig. 8;see also Fig. 11), the anterior labral periosteal

sleeve avulsion (ALPSA lesion) (Fig. 9) [55], thehumeral avulsion of the glenohumeral ligaments(HAGL lesion) (Fig. 10) [56,57], the bony avulsion

of the inferior glenohumeral ligament (BAGHLlesion) [58], the combined Bankart and HAGLlesion (Floating AIGHL lesion) [59–61], and sometypes of lesions involving the superior labrum

(SLAP lesions) [62–65]. Any of these lesions canalso be seen associated with a lesion of the articularcartilage at the edge of the glenoid, resulting in the

glenolabral articular cartilage disruption (GLADlesion) (Fig. 11) [66]. A summary description ofthese lesions is provided in Table 1.

Anterior inferior glenohumeral dislocationmay also produce damage to the axillary nerveor its branches, leading to atrophy of selected

muscle groups. In a series of 77 cases, Visser et al[67] found 43% incidence of axillary nerve damagein patients with history of glenohumeral jointdislocation.

Injuries to the posterior capsulolabral complexoccur following acute traumatic posterior dislo-cations, particularly in patients with seizures or

during electroshock therapy. The injury frequently

Fig. 7. Classic Bankart lesion. Axial T1-weighted image

following intrarticular injection of gadolinium. The

labrum is completely separated from the glenoid margin

(long arrow), still attached to the capsule and MGHL

(short arrow). The capsule is separated from the scapular

neck. Note the partially stripped periosteum (arrow-

head).


includes a posterior labral tear (Fig. 12), a disrup-tion of the posterior capsule and periosteum andan anterior impacted fracture of the humeral head

(McLaughlin lesion or reverse Hill-Sachs lesion).In the throwing athlete, posterior traumatic in-stability resulting from an injury to the posterior

capsulolabral complex in isolation has beenquestioned [45]. For a posterior dislocation totake place with the arm in flexion, adduction and

internal rotation, in addition to injury to theposterior capsule, an injury to the rotator cuff

interval has to occur, as described by Harrymanet al [35].

Atraumatic instability

Atraumatic instability of the shoulder is seen inpatients associated with generalized joint laxityoften presenting with classical stigmata such asgenu recurvatum, hyperextensibility of the elbows

and metacarpophalangeal joints, and ability topassively abduct the thumb to the forearm [45].Atraumatic instability includes MDI [68]. These

patients often have a patulous inferior pouch,attenuation of the capsuloligamentous structures,and redundancy of the rotator cuff interval [69]. It

is possible that atraumatic instability is secondaryto repetitive microtrauma because bilateral laxityis often present [45].

Microinstability

Microtraumatic instability or microinstability

is seen typically in the overhead athletes involvedin events such as throwing, swimming, and ten-nis. Injuries to any number of dynamic or static

Fig. 8. Perthes lesion and posterior superior impinge-

ment. T1 fat-suppressed image in the ABER position,

following intraarticular injection of gadolinium. The

anterior inferior labrum is detached from the glenoid

(black arrow), without associated capsuloperiosteal

stripping. Normally the labrum is well attached to the

glenoid at this level. This feature distinguishes the

Perthes lesion from the Bankart lesion on MR imaging.

The separation of the labrum in the Perthes lesion is

better seen on MR imaging using the ABER position,

placing tension in the anterior capsule. The failure of the

anterior labrum and capsule allows anterior subluxation

of the humeral head, producing impingement of the

rotator cuff between the humeral head and the posterior

superior aspect of the glenoid (white arrow). Note the

fragmentation of the labrum at this level (arrowhead).

See text for description of the posterior superior im-

pingement syndrome. (From Shankman S, Bencardino J,

Beltran J. Glenohumeral instability: evaluation using

MR arthrography of the shoulder. Skeletal Radiol

1999;7:365–82; with permission.)

Fig. 9. ALPSA lesion. Axial T1-weighted image through

the lower margin of the glenoid (arrowheads), following

intraarticular injection of gadolinium. The anterior

inferior aspect of the labrum (long arrow) is detached

from the glenoid and displaced medially. Note the large

gap between the labrum and the glenoid. In a chronic

ALPSA lesion this gap fills with ‘‘synovialized’’ tissue.

Note also that the labrum remains attached to the

capsuloperiosteal complex medially (short arrow). The

medial displacement of the labrum in relationship with

the glenoid defines the characteristics of ALPSA lesion

on MR imaging. (From Beltran J, Rosenberg ZS,

Chandanani VP, et al. Glenohumeral instability: evalu-

ation with MR arthrography. Radiographics 1997;

3:657–73; with permission.)


shoulder stabilizers can occur [69]. Kvitne andJobe [70] developed a classification system based

on various signs and symptoms seen in thesepatients. Group I includes patients generally overthe age of 35 years, with impingement syndrome,

without instability. Group II includes patientswith primary instability and secondary internalimpingement. Group III includes patients with

increased ligamentous laxity and signs and symp-toms of instability, and Group IV includes pa-tients with classic anterior instability.

More recently, Meister [42] modified this

classification to include additional factors contrib-uting to the pathomechanics of injury.

Fig. 11. GLAD lesion and Perthes lesion. Axial T1-

weighted fat-suppressed image obtained following intra-

articular injection of gadolinium. There is a tear of the

anterior inferior labrum without capsuloperiosteal strip-

ping (Perthes lesion) (arrow). The intermediate signal

intensity articular cartilage is partially detached from the

glenoid fossa (arrowhead). This is the characteristic MR

imaging finding in GLAD lesion.

Table 1

Bankart lesion and variants

Lesion Definition References

Classic Bankart Tear of the anterior inferior labrum with capsuloperiosteal stripping 49–51

Perthes Tear of the anterior inferior labrum without capsuloperiosteal stripping 54

ALPSA Anterior labrum periosteal sleeve avulsion: anterior labral tear with posterior

medial displacement and capsuloperiosteal stripping

55

HAGL Humeral avulsion glenohumeral ligaments: avulsion of the humeral insertion

of the anterior band of the IGHL

56,57

BAGHL Bony avulsion glenohumeral ligament: same as HAGL with humeral body

avulsion

58

Floating AIGHL Floating anterior inferior glenohumeral ligament: combined Bankart and

HAGL

59–61

SLAP Superior labrum anterior posterior: tear of the superior labrum extending in

different directions (10 types described)

19,62–65,83–99

POLPSA Posterior labrocapsular periosteal sleeve avulsion: same as ALPSA but

located in the posterior labrum

101,102

SLAC Superior labrum anterior cuff: superior labral tear associated with partial tear

of the articular surface of the supraspinatus tendon

100

GLAD Glenoid labrum articular cartilage disruption: labral tear with associated

avulsion of articular cartilage

66

Fig. 10. HAGL lesion. Axial gradient echo sequence

obtained at the level of the surgical neck of the humerus.

The patient had a joint effusion. The MGHL is

thickened (arrow) and detached from its humeral

insertion (arrowhead).


Primary disease

Primary disease includes the lesions takingplace in the throwing shoulder, related to normaloveruse. In this group, minimal or no laxity is

found and no significant instability is present. Theinjuries may involve any or several of the followingstructures: the rotator cuff (primary tendinosis,

subacromial impingement, coracohumeral im-pingement), biceps tendon (tendinosis), posteriorcapsule (Bennett lesion), and superior labrum

(some SLAP lesions). In this group, lesions ofthe superior labral complex are mostly related topulling forces by the biceps tendon [42]. Anothercause for superior labral tears in this group is

related to the ‘‘grinding factor’’ described byAndrews et al [71]. Displacement of the humeralhead combinedwith compression and internal rota-

tion during deceleration can cause the humeralhead to grind on the base of the biceps tendonand anterosuperior labrum. Injuries to the rotator

cuff, latissimus dorsi, and subscapularis musclehave also been well documented in overheadthrowers [41].

Coracoid impingement syndrome is a well-de-

scribed cause of anterior shoulder pain in thethrowing athlete [72]. The syndrome is producedby impingement of the anterior rotator cuff be-

tween the lesser tuberosity of the humeral head andthe lateral aspect of the coracoid process. Thenormal distance between these two structures was

determined to be 8.6 mmbyGerber et al [73], basedon computed tomography studies. The distancedecreases to 6.7 mm in patients with coracoid im-

pingement. The causes for the decreased cora-cohumeral distance include idiopathic long orlaterally based coracoid, posttraumatic deformity,or postsurgical deformity [72].

Bennett described a lesion related to repetitivetraction posterior shoulder in the throwing athlete

Fig. 12. Posterior labral tear. Axial T1-weighted fat-

suppressed image obtained following intraarticular in-

jection of gadolinium. There is a tear of the posterior

labrum (arrow) associated with posterior periosteal

stripping (arrowhead ).

Fig. 13. (A, B) Bennett lesion. Axial CT (A) and axial gradient echo MR imaging (B) in two different patients

demonstrate the characteristic ‘‘spur’’ adjacent to the posterior glenoid (arrows in A and B). The patient in (A) has also

developed osteoarthritis of the glenohumeral joint, with osteophyte formation. The Bennett lesion is difficult to

distinguish form a posterior labral tear on MR imaging due to the low signal intensity of both, the labrum and the

calcified lesion. (Courtesy of Lynne Steinbach, MD, San Francisco, CA.)


[74–76]. The lesion consists of an extraarticulardeposit of calcium or bone along the posteriorinferior aspect of the glenoid rim in a subperi-osteal location, well seen on CT and MR imaging

(Fig. 13). This traction ‘‘exostosis’’ is located atthe insertion of the posterior capsule and the longhead of the triceps muscle. The Bennett lesion has

been attributed to an excessive pull on the pos-terior capsule and is often associated with tears ofthe infraspinatus and teres minor tendons [75,76],

posterior labral tears, and instability [75,77].Other investigators believe that the Bennett lesionoccurs from traction of the posterior band of the

inferior glenohumeral ligament during decelera-tion [78].

Primary instabilityRepeated microtrauma leads to instability as

a result of laxity and failure of the anterior

capsular complex, producing lesions in the rotatorcuff (secondary impingement, tendinosis, partialtears, and rotator cuff interval tears), anterior

labral tears, and SLAP lesions. Athletes withgeneralized joint laxity (see discussion of atrau-matic instability) and secondary capsulolabralinjuries are also included in this group.

Tears of the rotator cuff interval can lead toshoulder instability, as described by Harrymanet al [35]. As many as 50% of patients undergoingshoulder surgery for rotator cuff interval tears in

one series had instability [79]. Lesions associatedwith rotator cuff interval tears include injuries ofthe biceps tendon (tendinosis, tears, dislocation),

SLAP lesions, glenohumeral ligament lesions, andcoracohumeral ligament lesions (Fig. 14) [80,81].Chung et al [81] evaluated the normal anatomy of

the rotator cuff interval using MR imagingarthrography in 20 cadaver specimens and con-cluded that MR arthrography is useful in evalu-

ating the rotator cuff interval, crossing structures,and the rotator cuff interval capsule.

Superior labral anterior and superior lesions(SLAP lesions) are rare (3.9% of patients un-

dergoing arthroscopy), although more frequentuse of MR arthrography has led to higher rates ofdiagnosis of this lesion. These lesions involve the

superior part of the labrum with varying degreesof biceps tendon involvement. Pain, clicking,and occasional instability in a young patient are

the typical clinical manifestations. Four types ofSLAP lesions were originally described based onarthroscopic findings [82–85]. Type I is a partial

Fig. 14. (A, B) Rotator cuff interval tear with associated SLAP lesion. Oblique sagittal (A) and oblique coronal (B) T1-

weighted fat-suppressed images obtained following intravenous injection of gadolinium (indirect MR arthrogram).

There is extravasation of contrast material at the level of the rotator cuff interval (white arrow in A). Compare with the

normal, well-demarcated rotator cuff interval shown in Fig. 5. The CHL (arrowhead ) and the SGHL (short arrow) are

thickened, irregular, and partially torn. Compare with the MR imaging appearance of the normal fine striation of the

CHL and SGHL shown in Fig. 5. The oblique coronal image (B) of the same patient demonstrates a tear of the superior

labrum (SLAP lesion) (black arrow). (From Beltran J, Bencardino J, PadronM, et al. The middle glenohumeral ligament:

normal anatomy, variants and pathology. Skeletal Radiol 2002;5:253–62; with permission.)


Fig. 15. (A–C) SLAP lesions in three different patients. (A) Oblique coronal T1-weighted fat-suppressed image obtained

following intraarticular injection of gadolinium. Note the ‘‘arrowhead’’ configuration of the superior labrum, pointing

toward the shoulder of the patient (arrow). This is the hallmark of SLAP lesions on MR imaging. In this case, the tear of

the superior labrum is partial and represents a type II lesion. (B) Oblique coronal T1-weighted fat-suppressed image

obtained following intraarticular injection of gadolinium. In this case, the SLAP lesion is like a bucket-handle tear of the

knee meniscus, with a displaced fragment (arrow) located between the articular surfaces of the humeral head and the

superior glenoid. This case represents a type III lesion. (C ) Oblique sagittal T1-weighted fat-suppressed image obtained

following intraarticular injection of gadolinium. SLAP lesion (type VII) extending from the superior labrum (arrow) to

the MGHL (arrowheads). (Fig. A from Shankman S, Bencardino J, Beltran J. Glenohumeral instability: evaluation using

MR arthrography of the shoulder. Skeletal Radiol 1999;28:265–382; Fig. C from Beltran J, Bencardino J, Padron M,

et al. The middle glenohumeral ligament: normal anatomy, variants and pathology. Skeletal Radiol 2002;5:253–62;

with permission.)


tear of the superior part of the labrum withfibrillation of the LHBT. Type II is an avulsion ofthe LHBT with tear of the anterior and posteriorlabrum. Type III is a bucket-handle tear of the

labrum, and type IV is a bucket-handle tear ofthe labrum with longitudinal tear to the LHBT.Maffet et al [86] expanded the classification to

seven types. More recently, up to 10 types havebeen described, representing a combination ofsuperior labral tears with extension into different

areas of the labrum and glenohumeral ligaments[19] (Fig. 15).

Causative mechanisms for the development of

SLAP lesions include repetitive overhead activity[87], internal impingement [88,89], ‘‘peel-back’’[90], falling on an outstretched arm with theshoulder in abduction, and slight forward flexion

(see ref. 7 in Musgrave and Rodosky [65]) andforced eccentric contraction of the biceps [91].In the ‘‘peel-back’’ mechanism, described by

Burkhart and Morgan [90], the labrum is peeledback from the superior glenoid by the posteriordominant biceps attachment which undergoes tor-

sional force generated by extreme abduction andexternal rotation (the cocking phase). Differentmechanisms of injury are likely to be operationalin different patients.

Some types of SLAP lesions are associatedwith Bankart lesions and shoulder instability[86,91,92]. Cordasco et al [93] reported 70%

prevalence of instability in patients with SLAPlesions regardless of the presence of a Bankartlesion, suggesting that the biceps anchor contrib-

utes to the stability of the glenohumeral joint.Other reports [94–96] indicate that SLAP lesionsalso occur without associated instability.

Patients with SLAP lesions and other types of

labral tears often develop ganglion cysts adjacentto the labrum or at some distance form the labrum,especially at the spinoglenoid notch and supra-

scapular notch, causing compressive neuropathyand resulting in atrophy of the supraspinatusmuscle, infraspinatus muscle, or a combination of

both, depending on the location of the cyst [97,98].Savoie et al [99] recently described a specific

combination of anterior superior labral tear

(SLAP lesion) and partial tear of the undersurfaceof the supraspinatus tendon in a group of patientswith anterosuperior instability. Other lesionsfound in this group included the anterior part of

the biceps anchor and the superior glenohumeralligament. They coined the term ‘‘superior labrumanterior cuff’’ or SLAC lesion. MR imaging and

MR arthrography was used in their series forpreoperative diagnosis of the lesions (Fig. 16).

A variant of the posterior labral injury has

been described by Simons et al [100] in a patientsustaining posterior dislocation of the shoulderthat was locked in position by an impactedfracture of the humerus. They coined the term

‘‘posterior labrocapsular periosteal sleeve avul-sion’’ (POLPSA), owing to the similarity withthe ALPSA lesion described by Neviaser et al

[55]. Yu et al [101] described the findings in sixathletes with POLPSA lesions (four footballplayers, one wrestler, and one weightlifter), with

Fig. 16. (A, B) SLAC lesion. (A) Oblique coronal T2-weighted fat-suppressed image demonstrate a tear of the superior

labrum (SLAP lesion) (white arrow). There is an incidental large cyst in the greater tuberosity. (B) Oblique coronal

section of the same series obtained in a more ante0rior plane, at the level of the supraspinatus tendon, demonstrating

a tear (black arrow).


clinical posterior shoulder instability, withouthistory of posterior shoulder dislocation. Theydescribed the POLPSA lesion as an avulsion ofthe attachment of the capsule and the periosteum,

without capsular tear, creating a patulous recessposteriorly. Although Yu et al [101] found lesionsto the infraspinatus tendon in all of their six cases,

lesions of the rotator cuff interval were notdescribed in their series, as one would expectaccording to the theory of Harryman et al [35].

The SLAC and POLPSA lesions can be in-cluded in the group of primary instability, becauseoverhead activity, instability, and absence of acute

trauma are the common denominators in thesepatients.

Acute traumatic instabilityAs indicated above, shoulder instability sec-

ondary to an acute injury is frequent in athletes

but unusual in the overhead-throwing athlete [42].Pathology and MR imaging manifestations aredescribed in the section of traumatic instability.

Posterosuperior glenohumeral instability

In the overhead-throwing sports, repeatedmovements of abduction and external rotation ofthe shoulder during the late cocking phase result in

contact of the posterosuperior glenoid margin,labrum, and the greater tuberosity, producingimpingement of the supraspinatus and infraspina-

tus tendons, especially in patients with anteriorcapsuloligamentous laxity and subsequent in-creased anterior translation of the humeral head.The syndrome was described originally by Walsh

et al [102] and subsequently confirmed by otherresearchers [103,104]. The injuries resulting fromthis mechanism include cyst formation in the

greater tuberosity, tear of the posterior superiorlabrum, and undersurface tearing of the rotatorcuff.

MR imaging of the shoulder in the ABERposition has contributed greatly in identifying thelesions occurring in patients with posterosupe-

rior impingement syndrome (Figs. 8, 17) [18,105,106]. A recent study by Halbrecht et al [107] inasymptomatic throwing and nonthrowing athletes,using indirect MR arthrography in the ABER

position, demonstrated that contact between theundersurface of the rotator cuff and the poster-osuperior glenoid occurred in all shoulders. No

clinical or MR imaging abnormalities were seenin the nonthrowing athletes. The images of thethrowing athletes demonstrated superior labral

tears, paralabral cysts, and signal changes in therotator cuff tendons. Contact between the un-dersurface of the rotator cuff and the poster-osuperior labrum was seen normally in the

ABER position.

Summary

Lesions leading to glenohumeral instability

may result from acute trauma, atraumatic laxity,or repetitive microtrauma. Athletic activities,especially overhead throwing, may lead to a series

of lesions involving the stabilizing structures ofthe shoulder. The resultant injuries and pathome-chanics leading to shoulder symptoms can beclassified as primary disease, primary instability,

acute traumatic instability, and posterosuperiorimpingement syndrome. MR imaging with orwithout intrarticular or intravenous injection of

contrast material, along with clinical examination

Fig. 17. Posterior superior impingement syndrome. T1-

weighted image in the ABER position, obtained

following intraarticular injection of gadolinium. There

is abnormally high signal intensity of the anterior

inferior labrum (short arrow), an impacted fracture at

the level of the grater tuberosity (arrowhead), and a tear

of the superior posterior labrum (long arrow).


and stress testing, provides valuable preoperativeassessment.

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Sports injuries of the elbowChristine B. Chung, MD*, Hyun-Jin Kim, MD

Department of Radiology, University of California San Diego and Veterans Affairs Healthcare System,

3350 La Jolla Village Drive, La Jolla, CA 92161, USA

The elbow is a complex joint comprised ofthree components: the humeroradial, humeroul-nar, and proximal radioulnar articulations. As isoften the case in the architecture of the body,

structural complexity parallels functional com-plexity. In the elbow, though the primary motionof flexion and extension explains its designation as

a hinge joint, it also is capable of axial rotation.Perhaps most importantly, the elbow serves as thefunctional link between the glenohumeral joint

and the hand, facilitating remarkable accessibilityof the fine motor and sensory abilities of the handand fingers for the performance of the activities ofdaily living so commonly take for granted.

Elbow injuries in the athlete are common andcan be classified into acute or chronic injuries.The following discussion of sports injuries of the

elbow will address the complex anatomy of theelbow, variations in normal anatomy that representpitfalls in imaging diagnosis, and commonly en-

countered osseous and soft tissue pathology.

Osseous anatomy and pathology

The elbow articulation is comprised of threeosseous (distal humerus, proximal ulna, andradius) structures that fit together like the pieces

of a three-dimensional jigsaw puzzle to form threearticulations. At the distal aspect of the humerus,the bone widens into a fanlike configuration. The

medial most extent, the medial epicondyle, is anosseous projection that serves as the attachmentsite for the superficial flexor group of the forearm

and the ulnar collateral ligament complex. Thelateral epicondyle is the osseous projection thatserves as the attachment site for the superficialextensor muscles of the forearm and parts of the

radial collateral ligament complex. The medialthird of the humeral articular surface is referredto as the trochlea, is intimate with the ulna, and

forms the humeroulnar articulation. The lateralarticulating surface of the humerus is formed bythe capitellum, a smooth, rounded prominence

that arises from its anterior and inferior surfaces.From its anterior margin with the distal hu-meral shaft, the capitellum curves downward andposteriorly. As it does so, its width decreases

from anterior to posterior. This morphology ofthe capitellum (smooth surface), in conjunctionwith the knowledge that the adjacent lateral epi-

condyle (rough surface) is a posteriorly orientedosseous projection of the distal humerus, explainsthe pseudodefect of the capitellum (Fig. 1) [1].

The pseudodefect is encountered in coronal MRimages, when an apparent interruption in thecapitellar surface occurs at the posterior aspect

of the joint. This appearance can be mistakenfor an osteochondral lesion of the capitellumwhen it is simply the junction between the ante-rolateral capitellum and posterolateral lateral

epicondyle.The articular surface of the proximal ulna is

formed by the combination of the posterior

olecranon and the anterior coranoid processeswith the articular surfaces taking the configura-tion of a figure of eight. At the waist of the eight,

or junction between anterior and posterior aspectsof the ulna, the articular surface is traversed bya cartilage-free bony ridge (Fig. 2). This trochlearridge is 2 to 3 mm wide and is at the same height

as the adjacent cartilaginous surface, resulting in* Corresponding author.

E-mail address: [email protected] (C. Chung).


doi:10.1016/S1064-9689(03)00024-2


11 (2003) 239–253

no impediment to smooth motion of the joint [2].Knowledge of this anatomic detail avoids themistaken diagnosis of central osteophyte forma-tion, or articular surface irregularity on sagittal

MR images of the elbow.The figure-of-eight morphology of the ulnar

articular surface results in an additional imaging

pitfall in diagnosis that of the trochlear groove(Fig 3). The waist of the figure of eight is formedby the tapered central surfaces of the coronoid

and olecranon processes medially and laterally,forming small cortical notches devoid of cartilage.On sagittal MR images, these focal regions devoid

of cartilage could be mistaken for a focal chondrallesion [2].

The proximal end of the radius consists ofhead, neck, and tuberosity. The radial head is

shaped like a mortar with a cupped articularsurface. The neck is the constricted portion of thebone distal to the articular surface. The tuberosity

is beneath the medial aspect of the neck and servesas the attachment site for the biceps tendon.

Osteochondral lesions

In the case of acute medial elbow injury, theinvolvement of a valgus force is usually described

as one of the most common mechanisms of injury[3]. Subchondral bone and cartilage injuries thatoccur in this setting result from impaction and

shearing forces applied to the articular surfaces(Fig. 4). The overall configuration of the humero-radial articulation, in this case, can be likened to

a mortar and pestle with the capitellar articularsurface impacting that of the radius to result ina chondral or osteochondral lesion of the cap-itellar surface. These acute posttraumatic lesions

are manifested on MR images as irregularity ofthe chondral surface, disruption or irregularity ofthe subchondral bone plate, or the presence

of a fracture line (Fig. 5). The acuity of the lesionand posttraumatic etiology are implied by thepresence of marrow edema and joint effusion.

Close inspection of the location of the lesion oncoronal and sagittal MR images is of the utmost

Fig. 1. (A) Coronal T1-weighted MR image of the elbow demonstrated irregular contour (arrow) in the region of the

capitellum. (B) Corresponding sagittal T1-weighted MR image verifies the coronal image was obtained at the junction of

the anterior capitellum and the posterior lateral epicondyle (arrow), the pseudodefect of the capitellum.

240 C.B. Chung, H.-J. Kim /Magn Reson Imaging Clin N Am 11 (2003) 239–253

importance to distinguish a true osteochondrallesion from the pseudodefect of the capitellum.Correlation with presenting clinical history is alsohelpful in determining the etiology of imaging

findings.The entity of osteochondritis dissecans remains

controversial, primarily because of debate over its

etiology. The precise relationship of osteochon-dritis dissecans and an osteochondral fracture isunclear, but many investigators regard the former

as a posttraumatic abnormality that may leadto osteonecrosis. Osteochondritis dissecans isbelieved to occur in immature athletes between

11 and 15 years of age, rarely in adults [4]. Os-teochondritis dissecans of the elbow involvesprimarily the capitellum, but reports have de-scribed this process in the radius and trochlea [5].

Regardless of the etiology of the osteochondralinjury, the role of imaging is to provide infor-mation regarding the integrity of the overlying

articular cartilage, the viability of the separatedfragment, and the presence of associated intra-articular bodies. CT and MR imaging with and

without arthrography can provide this informa-tion to varying degrees, although no scientific in-vestigation has been performed to date thatestablishes specific indications for each study.

MR imaging, with its excellent soft tissue con-trast, can directly visualize the articular cartilageand the character of the interface of the osteo-

chondral lesion with native bone. The presence ofjoint fluid or granulation tissue at this interface,manifested as increased signal intensity on fluid-

sensitive MR images, generally indicates an un-stable lesion. The introduction of contrast intothe articulation in conjunction with MR imagingcan be helpful in two ways: (1) to facilitate the

identification of intraarticular bodies (Fig. 6) and(2) to establish communication of the bone-fragment interface with the articulation by fol-

lowing the route of contrast, providing evenstronger evidence for an unstable fragment [6,7].

Capsule anatomy and pathology

The osseous structures of the elbow are in-vested in a two-layer capsule. The synovial capsule

or membrane comprises the deep layer and linesthe more superficial fibrous capsule and theannular ligament. The fat pads of the elbow are

located between the synovial and fibrous capsules.

Fig. 2. A gross anatomic section in the sagittal plane

obtained through the midportion of the ulnar articular

surface demonstrates a focal area (arrow) between the

coronoid articular surface (Co) and the olecranon

articular surface (Ol) devoid of cartilage. This region is

called the trochlear ridge and should not be mistaken for

a central osteophyte.

Fig. 3. This sagittal MR arthrogram image in a cadaveric

specimen at the margin of the ulnar articular surface

demonstrates a focal area (arrow) between the coronoid

articular surface (Co) and the olecranon articular surface

(Ol) devoid of cartilage that is referred to as the trochlear

groove. This normal anatomic appearance can be easily

confused with an osteochondral lesion.

241C.B. Chung, H.-J. Kim /Magn Reson Imaging Clin N Am 11 (2003) 239–253

As there are normal variations in osseousanatomy that can simulate pathology for the in-

experienced reader, so there are similar variationsin capsular anatomy.One such variation is a tongueof synovial tissue that projects into the joint

between the radius and ulna, partially dividingthe articulation into humeroulnar and humero-radial portions (Fig. 7). This has been referred to asthe synovial fold [8]. Embryologically, the elbow

joint space is formed by mesenchymal cavitationsin three regions (humeroradial, humeroulnar, andproximal radioulnar) that ultimately become

confluent. The synovial fringe is believed to bea septal remnant, or incomplete plica [8]. It canbecome compressed between the radial head and

the humerus, resulting in pain and inflammation.

In addition, if viewed en face in the sagittalimaging plane, it could be misdiagnosed as anintraarticular body.

The second variation in elbow anatomy thatoccurs in the elbow articulation is that of theplica. As previously mentioned, plica are believedto be the remnants of embryonic septae. These

structures can become inflamed and thickened,resulting in impingement, snapping, and the sen-sation of intraarticular bodies. The diagnosis of

a painful snapping plica can be confirmed if theplica snaps back and forward over the radial headin flexion and extension. This entity is often as-

sociated with focal areas of synovitis and cartilagelesions in the radial head [9]. The most commonlocation for an abnormal plica is in the postero-lateral joint space (Fig. 8) [10].

Ligament anatomy and pathology

Classic descriptions of the ligamentous anat-omy of the elbow emphasized radial and ulnarcollateral ligaments, characterized as regions of

focal thickening of the fibrous capsule that servedto reinforce and stabilize the joint. Though thecharacterization and function of the ligaments hasremained constant in the literature, the concept of

their exact structural designation has becomemore complex [11].

Ulnar collateral ligament complex

The medial collateral ligament of the elbow iscomprised of three components, an anterior,posterior, and transverse bundle. The ligamentoriginates from the central 65% of the antero-

inferior surface of the medial epicondyle. Theanterior band is taut from full extension to 60degrees of flexion, whereas the posterior compo-

nent is taut from 60 to 120 degrees of flexion. Theanterior band is the strongest and stiffest compo-nent of the medial or ulnar collateral ligament

complex. Its distal attachment is to the mostmedial portion of the coronoid process, also calledthe sublime tubercle, in close proximity to the

attachment of the anterior capsule and brachialistendon. The posterior bundle of the medial col-lateral ligament is a less discrete structure orthickening of the posterior elbow capsule and

attaches in a broad fashion along the peripheryof the medial ulna. The transverse bundle, alsoknown as Cooper’s ligament, is comprised of

fibers that bridge the base of the anterior andposterior bundles of the ligament complex.

Fig. 4. This diagram demonstrates the shearing and

compressive forces associated with a valgus stress at

the elbow. The compression at the humeroradial artic-

ulation can result in osteochondral injury to the

capitellar articular surface and radial head or neck

fractures. Compression at the lateral elbow results in

opening of the medial joint space and potential in-

sufficiency of the medial supporting structures (capsule,

ulnar collateral ligament complex, and common flexor

tendon).


Valgus instability

The principle function of the ulnar collateralligament complex is to maintain medial joint

stability to valgus stress. The anterior bundle isthe most important component of the ligamentouscomplex to this end, as it serves as the primary

medial stabilizer of the elbow from 30 to 120degrees of flexion. The most common mecha-nisms of ulnar collateral ligament insufficiency

are chronic attenuation, as seen in overhead orthrowing athletes, and posttraumatic, usually aftera fall on the outstretched arm. In the case of thelatter, an acute tear of the ulnar collateral (Fig. 9)

may be encountered.With throwing sports, high valgus stresses are

placed on the medial aspect of the elbow. The

maximum stress on the ulnar collateral ligamentoccurs during the late cocking and accelerationphases of throwing [12]. Repetitive insults to the

ligament allow microscopic tears that progress to

significant attenuation or frank tearing within itssubstance. Though MR imaging allows directvisualization of the ligament complex, in chroniccases, the development of heterotopic calcification

along the course of the ligament has beendescribed [13].

Valgus instability is examined with the patient

seated and his or her hand and forearm securedbetween the examiner’s torso and arm. The pa-tient’s elbow is flexed to 25 degrees to unlock the

olecranon process from its fossa, and the medialcollateral ligament is palpated while a valgusstress is applied. Studies have shown that acquired

valgus laxity does not exist in asymptomaticathletes, and that furthermore, there is nothreshold value of measurement indicated for thediagnosis of acquired valgus laxity [14].

Treatment for ulnar collateral ligament injuryin the throwing athlete includes rest with cessationof throwing, physical therapywithmuscle strength-

ening, and nonsteroidal antiinflammatories.

Fig. 5. (A) Coronal fat-suppressed T2-weighted fast spin echo MR image of the elbow demonstrates irregularity of the

capitellar articular surface with bone marrow edema in the capitellum (arrow) and in the radial head (curved arrow). (B)

Corresponding fat-suppressed T2-weighted fast spin echo MR image verifies the anterior articular location of the

findings. The location, in conjunction with the bone marrow edema in the radius, suggests a posttraumatic etiology to

this abnormality.


Operative repair is typically reserved for compet-

itive athletes or those involved in heavy manuallabor because valgus laxity has been shown to causeminimal functional impairment in normal activitiesof daily living [11].

Radial collateral ligament complex

Similar to the medial side of the elbow, on the

lateral side, a radial collateral ligament complex ispresent. The radial, or lateral, collateral ligamentcomplex consists of four components: radial col-

lateral ligament, annular ligament, lateral ulnarcollateral ligament, and accessory lateral collat-eral ligament. The radial collateral ligament is less

distinct and more variable than its counterpart onthe medial side. It is a thick, rough, triangularband of fibrous tissue that attaches superiorly tothe lateral epicondyle of the humerus, beneath the

origin of the common extensor tendon and in-feriorly to the annular ligament. This ligamentremains taut through the normal range of flexion

and extension of the elbow.

The annular ligament is circular in shape andextends around the radial head neck junction toattach at the anterior and posterior margins of the

radial notch of the ulna. It serves as a restrainingligament, maintaining the radial head in contact

Fig. 6. Sagittal MR arthrogram image in a 34-year-old

patient with a history of locking elbow shows a large

intraarticular body (arrow) in the coronoid fossa out-

lined by contrast material.

Fig. 7. Gross anatomic specimen oriented in the coronal

plane in the region of the humeroradial articulation

demonstrates a tongue of synovial tissue (arrow), the

synovial fold, extending between the radial and the

capitellar articular surfaces.

Fig. 8. Gross anatomic specimen oriented in the axial

plane shows a fold of synovial tissue (arrow), the

posterior plica, extending into the posterolateral joint

space.


with the ulna and preventing inferior displace-ment of the radius.

The lateral ulnar collateral ligament originatesfrom the lateral epicondyle and blends with

the fibers of the annular ligament proximally.It extends posteriorly to cradle the head–neckjunction of the radius as it moves to its distal

attachment at the supinator crest of the ulna (Fig.10). This structure is one of the primary stabilizersof the elbow and is taut in flexion and extension.

The accessory lateral collateral ligament is notuniformly present but represents discrete fibersthat extend from the annular ligament to the

supinator crest. When present, it may serve tostabilize the annular ligament during varus stress.

Varus instability

Lateral elbow instability related to isolated

abnormalities of the lateral collateral ligamentcomplex is not as well described as that on themedial side of the elbow. If it were to occur, the

mechanism would be a stress or force applied to

the medial side of the articulation, resulting incompression on that side, with opening of thelateral articulation and subsequent insufficiency of

the radial collateral ligament (Figs. 11, 12). As theradial collateral ligament attaches on and isintimately associated with the annular ligament,

an abnormality discovered in one of the structuresrequires careful inspection of the other.

Varus stress applied to the elbow may occur as

an acute injury, but rarely as a repetitive stress asencountered on the medial side. Though lateralcollateral ligament injuries rarely occur as theresult of an isolated varus stress, other causes can

commonly result in this injury, including disloca-tion, subluxation and overly aggressive surgery(release of the common extensor tendon or radial

head resection).Varus instability is also tested with the elbow

in full extension and 30 degrees of flexion to

unlock the olecranon. A varus stress is applied tothe elbow while palpating the lateral joint line.

Posterolateral rotary instability and elbow

dislocation

The subject of elbow instability is complex andhas been a challenge because of the difficulty es-tablishing a mechanism of injury and reliable

clinical tests for diagnosis. With the realizationthat elbow instability is more common thanpreviously thought, marked advances in the un-

derstanding of this entity are occurring.

Fig. 9. Coronal inversion recovery MR image in a 27-

year-old patient shows abnormal signal intensity and

morphology of the ulnar collateral ligament. There is

focal discontinuity of the ligament just distal to the

humeral attachment consistent with a full thickness tear.

Fig. 10. Coronal MR arthrogram image in a 40-year-old

patient demonstrates the normal appearance and course

of the lateral ulnar collateral ligament (arrows). It

extends from the undersurface of the lateral epicondyle

and around the posterior head neck junction of the

radius as it courses distally to its insertion on the

supinator crest of the ulna.


A simple classification for elbow instabilitydoes not exist. The literature points to five criteria

that should be considered to produce a usefulclassification system for treatment: (1) timing(acute, chronic, recurrent), (2) articulation in-

volved (elbow versus radial head), (3) direction ofdisplacement (valgus, varus, anterior, posterolat-eral rotary), (4) degree of displacement (sub-luxation or dislocation), and (5) presence or

absence of associated fractures [15].For recurrent instability, posterolateral rotary

instability is the most common pattern. This type

of instability represents a spectrum of pathologyconsisting of three stages according to the degree ofsoft tissue disruption. In stage 1, there is postero-

lateral subluxation of the ulna on the humerus thatresults in insufficiency of the lateral ulnar collateralligament (Fig. 13) [15–17]. In stage 2, the elbow

dislocates incompletely so that the coronoid is

perched under the trochlea. In this stage, the radialcollateral ligament, and anterior and posteriorportions of the capsule, are disrupted in addition to

the lateral ulnar collateral ligament. In stage 3, theelbow dislocates anteriorly so that the coronoidrests behind the humerus. Stage 3 is subclassifiedinto three categories. In stage 3A, the anterior band

of the medial collateral ligament is intact and theelbow is stable to valgus stress after reduction. Instage 3B, the anterior band of the medial collateral

ligament is disrupted so that the elbow is unstablewith valgus stress. In stage 3, the entire distalhumerus is stripped of soft tissues, rendering the

elbow grossly unstable even when a splint or cast isapplied with the elbow in a semiflexed posi-tion. This classification system is helpful becauseeach stage has specific clinical, radiographic, and

pathologic features that are predictable and haveimplications for treatment [15].

Traditional teaching dictated that the mecha-

nism of injury for elbow dislocation included hy-perextension. More recently, it is believed that thismechanism is the result of a fall on the out-

stretched hand. The elbow experiences an axialcompressive force during flexion as the bodyapproaches the ground. As the body rotates in-

ternally on the elbow (forearm rotates externallyon the humerus), a supination moment occursat the elbow. This combination of valgus andsupination with axial compression during flexion

results in the posterolateral rotary subluxationor dislocation of the elbow. The correspond-ing pathoanatomy previously described can be

thought of simply as the disruption of a soft tissuering that progresses from posterolateral to medialin three stages [15].

Subluxation or dislocation of the elbow can beassociated with fractures. Fracture dislocationsmost commonly involve the coronoid and radialhead, a constellation of findings referred to as the

‘‘terrible triad’’ of the elbow because the injurycomplex is difficult to treat and prone to un-satisfactory results [15]. Radial head fractures do

not cause clinically significant instability unlessthe medial collateral ligament is disrupted. Animportant feature of elbow injuries to recognize is

that the small flake fracture of the coronoid,commonly seen in elbow dislocations, is not anavulsion fracture. Nothing attaches to the tip of

the coronoid, rather the capsule attaches on thedownward slope of the coronoid, the brachialiseven more distal. This fracture is a shear frac-ture and is likely pathognomonic of an episode

of elbow subluxation or dislocation (Fig. 14).

Fig. 11. This diagram demonstrates the shearing and

compressive forces associated with a varus stress at the

elbow. The compression at the medial elbow results in

opening of the lateral joint space, and potential in-

sufficiency of the lateral supporting structures (capsule,

radial collateral ligament complex, and common exten-

sor tendon).


A second consideration with respect to elbowdislocation is that as the ring of soft tissues

is disrupted from posterolateral to medial, thecapsule is torn and insufficient. In the absence ofan intact capsule, joint fluid dissects through the

soft tissue planes of the forearm, negating anindirect radiographic sign of trauma in the elbow,that of the joint effusion.

Tendon anatomy and pathology

The many muscles about the elbow can bedivided into four groups: posterior, anterior,

medial, and lateral. The muscles of the posteriorgroup are the triceps and anconeus. The musclesof the anterior group are the biceps brachii and

brachialis. The muscles in the medial group arethe pronator teres, the palmaris longus, and theflexors of the hand and wrist. The muscles in the

lateral group include the supinator, brachioradia-lis, and extensor muscles of the hand and wrist.Specific anatomic considerations and tendon

pathology commonly encountered in the elbowwill be addressed.

The classification of tendon injuries about theelbow can be organized by location, acuity, anddegree of injury. Tendon injury related to a single

isolated event is uncommon, although exceptionsto this rule do occur. More commonly, tendinousinjuries in this location relate to chronic repetitive

microtrauma. MR imaging, with its excellent softtissue contrast, is particularly well suited todiagnose tendon pathology. This is done primarily

by close inspection of signal intensity and mor-phology of the tendons. As elsewhere in the body,the tendons about the elbow should be smooth,linear structures of low signal intensity. Abnormal

morphology (attenuation or thickening) canbe seen in tendinosis or tear. If signal intensitybecomes bright or increased on fluid sensitive

sequences within the substance of a tendon, a tearis present. Tears can be further characterized aspartial or complete. A complete tear is diagnosed

by a focal area of discontinuity.

Fig. 12. (A) Coronal T1-weighted MR image of the elbow in a 47-year-old man shows discontinuity of the radial

collateral ligament (arrow) at the humeral attachment. The ligament also demonstrates somewhat abnormal morphology

with thickening. The overlying common extensor tendon is normal. (B) Corresponding axial fat-suppressed proton

density weighted MR image shows abnormal morphology and signal intensity (arrow) of the posterior attachment of the

annular ligament, consistent with a high-grade partial tear.


Common flexor tendon and medial muscles

The muscular anatomy about the medial elbowis complex and includes three separate layers. Themost superficial layer includes the pronator teres,

flexor carpi radialis, palmaris longus, and flexorcarpi ulnaris. The middle layer is comprised of theflexor digitorum superficialis, and the deep layer ismade up of the flexor digitorum profundus. Only

the flexor digitorum profundus does not takea part of its origin from the common flexortendon. In rare cases, it may be necessary to lo-

calize pathology to a specific muscle group;however, the majority of pathology will occur inthe common flexor tendon near its distal humeral

attachment.

Common extensor tendon and lateral muscles

The lateral extensor muscles include theextensor carpi radialis longus, extensor carpi

radialis brevis, extensor digitorum, extensor digitiminimi, and extensor carpi ulnaris muscles. Only

the extensor carpi radialis longus does not takea part of its origin from the common extensor

tendon. As with the medial muscles, the vastmajority of pathology encountered in this regionis associated with the common extensor tendon

rather than specific muscles.

Epicondylitis and overuse syndromes

Chronic stress applied to the elbow is the mostfrequent injury in athletes, and a spectrum ofpathology can exist with varying degrees of

severity. The frequency of involvement of the com-mon flexor and extensor tendons to the medial andlateral epicondyles, respectively, has led to the

designation of ‘‘epicondylitis’’ as a general termapplied to these overuse syndromes. Anatomically,these overuse syndromes are classified by location

and are further associated with sports that incite

Fig. 13. Inversion recovery coronal MR image of the

elbow in a 52-year-old man shows abnormal high signal

intensity (arrows) in the expected position of the lateral

ulnar collateral ligament, with no visualization of a

normal ligament.

Fig. 14. Sagittal fat-suppressed proton density weighted

MR image demonstrates several findings of acute dis-

location: (1) anterior subluxation of the humerus, (2)

coronoid process fracture (arrow), (3) irregularity of the

articular surface of the olecranon (curved arrow), and (4)

disruption of the anterior and posterior capsule (double

arrow). The corresponding coronal image (not shown

here) further demonstrated complete disruption of the

radial and ulnar collateral ligament complexes.


the pathology. The injury is believed to result fromextrinsic tensile overload of the tendon, which, overtime, produces microscopic tears that do not healappropriately.

Although these overuse entities about theelbow have been termed ‘‘epicondylitis’’ for thepurpose of clinical diagnosis, inflammatory osse-

ous changes rarely occur. The imaging findingsare those reflecting chronic change in the tendonas evidenced by tendinosis alone or in conjunction

with partial or complete tear. The distinction be-tween types of pathology is made by considerationof morphology and signal intensity changes.

Medial epicondylitis involves pathology of thecommon flexor tendon and is associated primarilywith the sport of golfing. It also has been reportedwith javelin throwers, racquetball and squash

players, swimmers, and bowlers. The pronatorteres and flexor carpi radialis tendons are involvedmost frequently resulting in pain and tenderness

to palpation over the anterior aspect of the medialepicondyle of the humerus and origin of thecommon flexor tendon. The mechanism of injury

includes repetitive valgus strain with pain result-ing from resisting pronation of the forearmor flexion of the wrist [18]. The imaging findingsencountered can include tendinosis or tendi-

nosis with superimposed partial or full thicknesstear (Fig. 15). When assessing the tendon, itis necessary to closely scrutinize the underly-

ing ulnar collateral ligament complex to ensureintegrity.

Lateral epicondylitis is the most common prob-

lem in the elbow in athletes and has been termed‘‘tennis elbow.’’ This term may be somewhat in-appropriate as 95% of cases of the clinical entity of

lateral epicondylitis occur in non–tennis players[18]. Moreover, it has been estimated that 50% ofpeople partaking in any sport with overhead armmotion will develop this process [19].

Lateral epicondylitis is associated with repeti-tive and excessive use of the wrist extensors. Thepathology most commonly affects the extensor

carpi radialis brevis at the common extensor ten-don (Fig. 16). A number of investigators havedescribed the pathology encountered in the

Fig. 15. (A) Frontal view of the elbow shows subtle irregularity (arrow) of the medial aspect of the distal humerus. (B)

Coronal fat-suppressed T2-weighted fast spin echo image shows a focal full-thickness tear (arrow) of the attachment of

the common flexor tendon to the medial epicondyle.


degenerated tendon of this disease process. Histo-

logically, necrosis, round cell infiltration, focalcalcification, and scar formation have been shown[20]. In addition, invasion of blood vessels,

fibroblastic proliferation, and lymphatic infiltra-tion, the combination of which are referred toas angiofibroblastic hyperplasia, occur and ulti-mately lead to mucoid degeneration as the pro-

cess continues [21,22]. The absence of a significantinflammatory response has been emphasized re-peatedly and may explain the inadequacy of the

healing process.The imaging findings in this process are exactly

those encountered in the clinical entity of medial

epicondylitis. As on the medial side, when pa-thology is encountered in the tendon, closescrutiny of the underlying ligamentous complexis necessary to exclude concomitant injury. In

particular, thickening and tears of the lateralulnar collateral ligament have been encounteredwith lateral epicondylitis [23].

Biceps tendon

The biceps brachii muscle consists of twoheads, the short head and long head. The shorthead arises from the tip of the coracoid process, in

common with the coracobrachialis. The long headarises from the supraglenoid tubercle of thescapula. The two muscles join to form a commontendon 6 to 7 cm above the elbow joint line. This

common tendon traverses the antecubital fossa todive to its attachment at the radial tuberosity. Anaponeurosis, the bicipital aponeurosis or lacertus

fibrosus, arises from the musculotendinous junc-tion, passes across the brachial artery, and mergeswith the fascia that covers the pronator teres and

superficial flexors of the forearm. The distal bicepstendon does not have a tendon sheath, rather thereis a bursa (cubital bursa) intimately associatedwith its attachment to the radial tuberosity [24].

Distal biceps tendon rupture

Rupture of the tendon of the biceps brachiimuscle at the elbow is rare, and constitutes less than

5% of all biceps tendon injuries [25]. It usuallyoccurs in the dominant arm ofmales. Injuries to themusculotendinous junction have been reported,

but themost common injury is complete avulsionofthe tendon from the radial tuberosity.Although theinjury often occurs acutely after a single traumaticevent, the failure is thought to be the result of

preexisting changes in the distal biceps tendoncaused by intrinsic tendon degeneration, enthesop-athy at the radial tuberosity, or cubital bursal

changes. The typical mechanism of injury relates toforceful hyperextension applied to a flexed andsupinated forearm. Athletes involved in strength

sports, such as competitive weightlifting, football,and rugby, often sustain this injury.

Clinically the patient gives a history of feelinga ‘‘pop’’ or sudden sharp pain in the antecubital

fossa. The classic presentation of a complete distalbiceps rupture is that of a mass in the antecubitalfossa caused by proximal migration of the biceps

muscle belly. Accurate diagnosis is more difficultin cases of the rare partial tear of the tendon,or more common complete tear of the tendon

without retraction. The latter case can occur withan intact bicipital aponeurosis, which serves totether the ruptured tendon to the pronator flexor

muscle group (Fig. 17).MR imaging diagnosis of biceps tendon pathol-

ogy becomes important in patients who do notpresent with the classic history or mass in the

antecubital fossa, or for evaluation of the integrity

Fig. 16. Coronal fat-suppressed T2-weighted fast spin

echo image of the elbow in a 50-year-old tennis player

demonstrates abnormal morphology of the common

extensor tendon with superimposed intrasubstance high

signal intensity (arrow) consistent with a partial tear of

the tendon. These imaging findings support the clinical

diagnosis of tennis elbow.


of the lacertus fibrosus. MR imaging diagnosis oftendon pathology, as previously mentioned, islargely dependent on morphology, signal intensity,

and the identification of areas of tendon dis-continuity. In the case of the biceps tendon, animportant indirect sign of tendon pathology is the

presence of cubital bursitis (Fig. 17).With delayed diagnosis, chronic pain can

ensue, as well as weakness in flexion, supination,and with grip strength. Treatment options fa-

vor surgical reattachment because nonoperativelytreated ruptures have been reported to result inloss of 20% of elbow flexion strength and 40% of

supination strength. If operative treatment ischosen, early repair is desirable, particularly whenthe lacertus fibrosus is ruptured and there is

muscle retraction. If the lacertus fibrosus is intact,delayed primary repair is feasible [25].

Triceps tendon

The triceps consists of three muscle bellies: thelong head, the lateral head, and the medial head.

The long head of the triceps arises by a strong

tendon from the infraglenoid tubercle of thescapula near the inferior margin of the glenoidcavity. It descends into the arm between the teres

major and teres minor muscles. The lateral headoriginates from the posterior and lateral surfacesof the humerus and from the lateral intermuscular

septum. The medial head arises from the posteriorsurface of the humerus, medial and below theradial groove, and from the medial and lower partof the lateral intermuscular septum. The tendon of

the triceps descends to attach to the upper surfaceof the olecranon process of the ulna and to theantebrachial fascia near the laterally located

anconeus muscle and tendon.Rupture of the triceps tendon is rare. The

mechanism of injury has been reported to result

from a direct blow to the triceps insertion ora deceleration force applied to the extended armwith contraction of the triceps as in a fall. Similar

to pathology encountered in the distal bicepstendon, most ruptures occur at the insertion site,although musculotendinous junction and musclebelly injuries have been reported. Complete

Fig. 17. (A) Axial T1-weighted MR image shows abnormal morphology of the distal biceps tendon (arrow). The

thickened lacertus fibrosus is intact (curved arrow). (B) Oblique coronal fat-suppressed T2-weighted MR image

demonstrates a small stump of residual tendon (arrow) coursing toward the radial tuberosity. The high signal intensity

around the tendon remnant is fluid within the cubital bursa.


ruptures are more common than partial tears.Associated findings may include olecranon bursi-tis, subluxation of the ulnar nerve, or fracture of

the radial head. Accurate clinical diagnosis relieson the presence of local pain, swelling, ecchymo-sis, a palpable defect, and partial or complete lossof the ability to extend the elbow. With more than

2 cm of retraction between the origin and theinsertion, a 40% loss of extension strength canresult [25].

For MR imaging diagnosis of triceps tendonpathology, it is imperative to be aware that thetriceps tendon appearance is largely dependent on

arm position. The tendon will appear lax andredundant when imaged in full extension, whereasit is taut in flexion. MR imaging features of a tearare similar to those associated with any other

tendon.The treatment of a complete rupture is surgical

repair; partial tears are often treated conserva-

tively.

Summary

There is a wide spectrum of pathology thataffects the elbow in the athlete. This is furthercomplicated by the complex anatomy of this

articulation and the numerous normal anatomicvariations that can serve as pitfalls in imagingdiagnosis. A detailed knowledge of the anatomy

and pathology that commonly affect this articu-lation can facilitate the ease and accuracy ofimaging diagnosis.

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MR imaging of sports-related hip disordersRobert D. Boutin, MDa,*, Joel S. Newman, MDb

aMed-Tel International, 3713 Lillard Drive, Davis, CA 95616, USAbDepartment of Radiology, New England Baptist Bone and Joint Institute,

New England Baptist Hospital, 125 Parker Hill Avenue, Boston, MA 02120, USA

Physical activity is associated with betterphysical and mental health [1,2]. Indeed, physicalactivity reduces the risk of dying prematurely in

general, and of coronary heart disease, hyperten-sion, colon cancer, diabetes mellitus, and, inparticular, feelings of depression and anxiety in

particular [2]. The potential national medical costsavings if all inactive American adults becamephysically active has been estimated at $76.6

billion annually [3]. Consequently, it comes asno surprise that major public health campaignshave been aimed at promoting better healththrough physical activity and sport [4]. For

example, the United States Surgeon General callsfor incorporating at least 30 minutes of physicalactivity into most, if not all, days of the week [2].

The benefits of exercise, however, come with thepotential for orthopedic injury, including injuriesin and about the hip.

Injuries to the hip and pelvis generally accountfor 5% to 6% of athletic injuries in adults and10% to 24% of such injuries in children [5]. Some

athletes are particularly prone to such injuries,including soccer players (13%), runners (11%),and ballet dancers [5]. Among disabled and blindathletes, the prevalence of hip and thigh injuries is

reportedly as high as 14% to 21% [6].This article focuses primarily on MR imaging

as the radiological test of choice for evaluating

sports-related hip injuries. From our perspective,MR imaging is the most versatile and robustimaging method for examining injured athletes

after radiography. After briefly discussing hiparthroscopy and MR techniques, the most com-

mon hip injuries in athletes are reviewed, in-cluding labral tears, ligament injuries, osteo-chondral injuries, fractures, bursitis, and selected

musculotendinous injuries.

Hip arthroscopy

Hip arthroscopy is an increasingly used alter-native to arthrotomy for the treatment of internalderangements in athletes [7,8]. For example, in

a recent study of 42 athletes undergoing arthros-copy (with an average follow-up of over 2 years),there was a general postoperative improvement in

hip pain and function, most prominently forathletes with ligamentum teres tears, loose bodies,and avulsed bone fragments [7]. Labral tears

and chondral lesions also were addressed arthros-copically.

Indications and contraindications

Proper patient selection is a fundamentaldictum for ensuring successful outcomes afterarthroscopic surgery [9]. Although there is debate

over the indications and contraindications forroutine therapeutic arthroscopy [9–11], potentialindications in athletes include labral tears, liga-

mentum teres tears, joint instability, focal chon-dral injuries, loose bodies, septic arthritis, andsynovial disease [9]. Potential contraindicationsidentified with imaging may include advanced

osteonecrosis, advanced arthritis, ankylosis, andipsilateral lower extremity fracture or osseousneoplasm. It is our belief that hip arthroscopy and

MR imaging often are complementary techniques,each compelling the other to a more accurateunderstanding of hip disorders that previously

went unrecognized and untreated.* Corresponding author.


doi:10.1016/S1064-9689(03)00029-1


11 (2003) 255–281

Technique and complications

Arthroscopy is performed commonly withthree portals (anterior, anterolateral, and postero-lateral) that are established with the aid of

fluoroscopy [9,12]. Between 25 and 75 lbs oftraction typically are applied to distract the hipjoint approximately 1 cm to permit the introduc-tion of arthroscopic instrumentation [9,13,14].

Iatrogenic complications are infrequent (prev-alence: 1.3% [13] to 5% [15]) but not insignificant[9]. Most complications result from hip traction

(eg, transient sciatic, pudendal, or peroneal nerveneuropraxis) and fluid extravasation [15]. Un-commonly, iatrogenic injury to the labrum,

articular cartilage, or periarticular neurovascularstructures may occur from insufficient traction orunintended portal placement.

MR imaging—technical considerations

Hip MR imaging protocols vary from institu-

tion to institution, depending on the patient popu-lation, the physicians’ experiences with variouspulse sequences, and the MR imaging equipment.

Two different types ofMR imaging protocols oftenare employed in athletes, depending on whetherthe primary clinical concern relates to (1) an in-

ternal derangement (eg, labral tear, ligamentumteres tear, osteochondral injury, loose body) or (2)nonspecific pain or an extra-articular abnormal-ity (eg, osseous injury, bursitis, musculotendinous

injury).

Internal derangement protocol

Detailed assessment for internal derange-

ments in the adult hip requires unilateral imaging(with a commensurate field of view), analogous tothat used routinely for MR imaging of other

appendicular articulations. Relatively high spatialresolution can be achieved by imaging the symp-tomatic hip using a surface coil (eg, flexible shoul-der phased array coil), a 14 to 18 cm field of view,

and a 3 to 4 mm section thickness. Image qualityis optimized further by the presence of joint fluidfrom an effusion or arthrography, since fluid

under pressure tends to outline pathologic areas(eg, labral tears, chondral defects, loose bodies).

To perform MR arthrography, a 20-gauge

spinal needle is commonly used to inject 8 to 12mL of fluid intra-articularly (eg, sterile saline ordiluted gadolinium [0.1 mL in 15–25 mL of sterilesaline solution]). In our practices, MR imaging is

commenced within 30 minutes of fluoroscopically

guided injection of diluted gadolinium. (With MRarthrography, the peak contrast-to-noise ratioand joint distention occurs at 30 minutes in the

hip; the contrast-to-noise ratio decreases by morethan 50% by 2 hours [16].) T1-weighted spin-echoor three-dimensional gradient-echo images (withor without fat suppression) then are performed in

the coronal, sagittal, and axial planes that may beobliqued. (The oblique-sagittal plane is prescribedperpendicular to a line drawn between the

superior labrum and the transverse ligament[generally parallel to the femoral neck] on a mid-coronal localizer hip image.) Finally, coronal fast

spin-echo (FSE) T2 and axial fat-suppressedproton density images help to evaluate for extra-articular abnormalities that are inconspicuous onT1-weighted spin-echo and gradient-echo images,

such as soft tissue edema or bone marrowpathology. (If saline is used as the intra-articularcontrast agent [eg, because the injection is not

image guided], the MR imaging protocol usuallyincludes fat-suppressed proton density or T2-weighted images in three planes.)

An additional benefit of the arthrographyprocedure is that local anesthetic (eg, 1–5 mL oflidocaine or bupivacaine) or cortocosteroid (eg,

1 mL [80] mg of depomedrol) may be injectedconcurrently with the contrast material under fluo-roscopic control [17]. A positive response to thepresence of intra-articular anesthetic confirms

that the patient’s ‘‘pain generator’’ is in the hip(eg, labral tear). Conversely, if no pain relief isachieved, the examiner must consider that the hip

pain may be referred from another site (eg, thelumbar spine). Local anesthetic can be injectedbefore introducing contrast material into the joint

or, alternatively, amixture of contrast material andanesthetic from the same syringe can be injectedtogether. (Such an injectate may be prepared bymixing gadolinium contrast material (0.8 mL) and

normal saline (100 mL), and then combining 10mL of this mixture with 5 mL of 60% iodinatedcontrast material and 5 mL of 1% lidocaine [18].)

MR arthrography is a widely used, well-tolerated, safe procedure [19–21]. In a report of13,300 such procedures [19], there were no severe

reactions to intra-articular gadolinium injections,and the rate of minor reactions was significantlylower than that associated with intravenous gado-

linium injection. Still, MR arthrography is min-imally invasive, and gadolinium contrast agentshave not been approved for intra-articular use bythe United States Food and Drug Administration.

An alternative to MR arthrography for evaluating

256 R.D. Boutin, J.S. Newman /Magn Reson Imaging Clin N Am 11 (2003) 255–281

internal derangements uses intravenous gadolin-ium administration or leg traction during MRimaging [22–24]. Traction is believed to be usefulbecause distraction of the relatively tight hip joint

allows synovial fluid to outline abnormalities inthe labrum and articular cartilage. Recent reportsalso have described the prescription of ‘‘radial’’

images (centered at the mid-point of the acetab-ulum) that diminish volume-averaging artifacts bydisplaying the acetabular rim in tangent [25–29].

Extra-articular derangement protocol

When the primary clinical concern is an extra-articular abnormality or if the patient complainsof nonspecific hip pain, a relatively large field of

view is appropriate for at least part of the exam.An example of a screening hip MR examinationbegins with coronal T1 and coronal FSE inversionrecovery images of the pelvis that include both

hips. Then sagittal T1, axial FSE T2, and coronalfat-suppressed proton density–weighted images ofthe affected hip are obtained using a 16- to 22-cm

field of view. Other protocols also are commonlyused [30].

Labrum and labral tears

Anatomy and function

The acetabular labrum is a rim of fibrocarti-lage that deepens the acetabular fossa for the

femoral head, thus promoting hip joint congru-ency and stability [31]. Recent studies also suggestthat the labrum helps seal a layer of pressurized

synovial fluid between the articulating surfaces ofthe femur and acetabulum during weight-bearing,thus distributing loads, decreasing contact pres-

sures, and protecting articular cartilage [31,32]. Itis noteworthy that the labrum is innervated bynerves that play a role in proprioception and painproduction [33,34]. Unfortunately, blood vessels

reportedly only penetrate the labrum to a depth of0.5 mm, leaving most of the labrum avascular andlimiting the potential for an injured labrum to

heal [8,35].

Clinical features

The cause of a labral tear may be trauma-tic, degenerative, dysplastic, or idiopathic. In ath-

letes sustaining a labral tear, the mechanism ofinjury may include hyperrotation, hyperextension,hyperflexion, or hyperabduction [8]. For example,anterior labral tears may occur with a hyperex-

tension-external rotation injury, whereas poste-

rior labral lesions typically occur as a result ofaxial loading of the hip in a flexed position[8,17]. Athletes also may sustain tears in the set-ting of femoroacetabular impingement (see later

discussion).Patients with labral tears typically complain of

hip or groin pain, often associated with painful

clicking, transient locking, or ‘‘giving way’’ of thehip [36,37]. Although the onset of symptoms maybe acute (eg, after a modest twisting injury), clin-

ical manifestations often are insidious and may in-tensify over time [8].

On physical examination, several signs are

considered typical of a torn acetabular labrum[36,38,39], including pain elicited by the anteriorimpingement position (ie, flexion, adduction, andinternal rotation) or the posterior impingement

position (ie, hyperextension, abduction, and ex-ternal rotation) [37,40,41]. However, in a recentstudy of 60 arthroscopically-proven labral tears

[42], the maximum flexion-internal rotation ma-neuver was positive in only 39% of patients. Inparticular, this maneuver predicted incomplete

(but not complete) detaching tears in the postero-superior labrum in this report.

Association with hip osteoarthritis and dysplasiaLabral derangements are associated with ar-

ticular cartilage lesions and may be a cause ofosteoarthritis [43–46]. The hypothesis that labraltears contribute to early hip joint degeneration is

supported by the observation that lesions of thelabrum and articular cartilage often are contigu-ous. In a study of 170 hips with mild or moderate

dysplasia evaluated arthroscopically [44], 113patients with anterior labral tears commonly hadadjacent articular cartilage lesions in the anterior

acetabulum (69%) and anterior femoral head(39%). In another study of 436 hip arthroscopies[45], 73% of patients with fraying or a tear in thelabrum also had articular cartilage degenerative

changes. Labral tears may predispose the hip toadjacent chondral lesions, because weight-bearingloads are no longer distributed appropriately and

subsequent (repetitive or episodic) impactionforces tend to overload adjacent articular carti-lage.

Individuals with even mild degrees of hipdysplasia are at increased risk for labral tears,because decentering of the femoral head generateshigh loads at the acetabular rim. Certain types of

athletic activities, such as gymnastics and dance,may self-select for athletes with greater arcs of hipmotion [8]. Although diminished femoral head

257R.D. Boutin, J.S. Newman /Magn Reson Imaging Clin N Am 11 (2003) 255–281

containment due to mild hip dysplasia theoreti-

cally might enhance performance of certain activ-ities, increased forces on the labrum can result inbiomechanical overload and injury.

MR imaging

Diagnostic criteriaThe clearly normal labrum is a triangular

structure of homogeneous low signal intensity onall pulse sequences. The principal criterion fora labral tear is linear hyperintense signal contact-

ing the labral surface (on the articular side [45]),either at the labral-acetabular junction or thelabrum itself (Figs. 1–3) [37]. Blunting or absenceof the labrum also can suggest a tear, but these

two criteria may be insufficient for definitivelydifferentiating a labral lesion from normal varia-tion, particularly in the anterosuperior quadrant

[47,48]. Labra are considered to be degenerated

when they appear enlarged, have indistinct mar-gins, or demonstrate substantial intrasubstanceintermediate signal intensity.

Tear classificationLabral tears may be categorized according to

location and morphology. With respect to loca-tion, a tear may be in one or more of the quad-

rants of the horseshoe-shaped labrum – anterior,anterosuperior, posterosuperior, and posterior[49]. Most tears occur in the anterior or ante-

rosuperior portion of the labrum [36,37,50–53].Sports-related tears typically target the antero-superior quadrant [54]. In hips with mild to

moderate dysplasia undergoing arthroscopy,labral tears can be found at the articular surfacefree margin in 72% (specifically affecting theanterior labrum in 66%) [45].

Fig. 1. A 59-year-old female with left hip pain and

anterior labral tear. Sagittal fat-suppressed T1-weighted

MR arthrogram demonstrates gadolinium extending

across the base of the labrum (arrow), indicating a tear.

Fig. 2. A 30-year-old athletic female with superior labral

tear. Coronal fat-suppressed T1-weighted MR arthro-

gram shows gadolinium extending into a defect at the

undersurface of the superior labrum (arrow), adjacent to

the labrum-articular cartilage junction.

Fig. 3. A 37-year-old female marathon runner with hip pain and anterior labral tear. Oblique-sagittal (A) and sagittal

(B) fat-suppressed T1-weighted MR arthrogram images show a complex tear of the anterior labrum (arrow). There is

a transverse component cleaving the base of the labrum and a longitudinal tear within the substance of the labrum.


Regarding morphology, two basic types oflabral lesions are recognized: (1) a ‘‘tear’’ orcleavage plane in the substance of the fibrocarti-lage, and (2) a ‘‘detachment’’ or avulsion of the

fibrocartilaginous labrum from its attachmentto the adjacent articular cartilage [46]. Labraldetachments (sometimes referred to as ‘‘detaching

tears’’ [42]) are more common than tears isolatedto the labral substance [37,47]. Some investigatorsdifferentiate between labral tears that are ‘‘par-

tial’’ and ‘‘full-thickness’’ and suggest that thesetwo types of tears have distinctive symptoms andtreatment outcomes [55]. Four types of tear

morphology have been described at arthroscopy[49,56]: radial flap (57%); radial fibrillated (22%);longitudinal peripheral (16%); and unstable (5%).

Secondary findingsLabral lesions may be associated with several

abnormalities in the adjacent bone and soft tissue[57,58]. In the adjacent bone, common associatedfindings are subchondral bone marrow edema,

subchondral cystic changes, and osseous fragmen-tation, especially at the superior acetabulum.

In the adjacent soft tissue, paralabral cysts arenot uncommon and are considered highly specificsecondary signs of labral tears (Fig. 4) [58]. In onerecent study of 87 hips using conventional MR

imaging [58], paralabral cysts were present in 13patients (15%). All 10 patients who went on tosurgery had a labral tear adjacent to the

paralabral cyst, but the labral tear itself could beseen only on three nonarthrographic MR exams.At pathologic inspection, a paralabral cyst may be

either a ganglion cyst (defined by a connective-tissue lining, thick mucinous fluid contents, andrarely a patent communication with the joint) or

a synovial cyst (defined by a synovial cell lining,fluid contents, and often a patent communicationwith the joint).

An anterior paralabral cyst should not be

mistaken for fluid in the adjacent iliopsoas bursa(which may arise through the hiatus between thepubofemoral and iliofemoral ligaments). A pos-

terior paralabral cyst rarely may impinge upon thesciatic nerve, thus causing sciatica [59]. Effectivetreatment of a paralabral cyst usually involves

therapy for the underlying joint derangement,

Fig. 4. A 30-year-old female with painful right hip, extensive labral tearing, and large paralabral cyst demonstrated by

MR arthrography. Axial proton-density fat-suppressed (A) and coronal FSE T2-weighted (B) images show a high signal

intensity mass along the lateral articular margin (arrows). Oblique-sagittal fat-suppressed T1-weighted image (C) shows

degeneration and a tear of the anterior labrum (arrow). Coronal T1-weighted fat-suppressed image (D) shows the

superior labrum (arrow) completely replaced by abnormal signal, indicating the presence of severe degeneration and

a tear.


because these cysts commonly recur if the onlytreatment is cyst aspiration.

Imaging accuracy

MR arthrography generally is considered moreaccurate than conventional MR imaging for thediagnosis of labral tears. In one recent studycomparing the two techniques for the diagnosis of

labral lesions [60], sensitivity and accuracy were80% and 65% for conventional MR imaging, re-spectively, versus 95% and 88% for MR arthrog-

raphy. Reported results for both MR techniquesvary considerably (with sensitivity reported ashigh as 95% for conventional MR imaging [61]

and sensitivity/specificity reported as low as 49%/28% for MR arthrography [62]). The size ofa labral lesion affects the likelihood it will be

detected, and small detachments are diagnosedless reliably than large detachments [63].

Anatomic variations

Diagnostic accuracy may be limited by variousfactors, including the variability in labral signalintensity, shape, and size in asymptomatic persons[48,64,65]. Intermediate signal intensity in the

labrum may result from magic angle artifact (onshort echo-time images) or early myxoid degen-eration. Alterations in both labral signal and

shape have been correlated with age in asymptom-atic volunteers [66].

It is not uncommon for the shape of the labrum

to be altered by a cleft, or sulcus [9,17,47,50,52,67].The sublabral sulcus in the hip characteristicallyoccurs at the junction of the articular cartilage withthe superior or anterosuperior labrum. This

normal variant may be recognized by its location,smooth edges, and the absence of adjacent de-generative or traumatic changes.

The size of the labrum also can vary. Al-though some authorities have found that thelabrum is thinner anteriorly and thickest poste-

riorly [8,47], others have concluded that thelabrum is wider anteriorly and superiorly than itis posteriorly (average width, 5.3 mm; standard

deviation, 2.6 mm) [68]. An elongated appear-ance has been described in degenerated andnondegenerated labra of adult dysplastic hipsanteriorly and superiorly [69]. Absence of the

labrum should be considered abnormal, otherthan in the anterosuperior quadrant [47]. Giventhe many variations in the acetabular labrum,

MR findings are appropriately correlated withclinical presentation and the response to intra-articular anesthetic injection.

Treatment and prognosis

The rationales for excision of the torn labrumare to alleviate pain and mechanical symptoms,prevent propagation of tearing to the adjacent

labrum, and—some surgeons believe—slow anysubsequent degenerative process [67]. Afterarthroscopic partial labrectomy in hips withoutarthritis, results are good to excellent in approx-

imately 70% of patients after a mean follow-up of3 years [70,71]. However, in hips with arthritis,only 21% of patients have good to excellent

results [71].

Ligaments and ligament injuries

Although the contribution of ligaments to the

stability of other joints has been studied sedu-lously, relatively little attention has been paid toimaging of the ligaments that support the adult

hip. Recently, the imaging of intrinsic andextrinsic hip ligaments in adults has been studied[72] and is summarized in this section.

Ligamentum teres

Anatomy and functionThe two intrinsic ligaments of the hip are the

ligamentum teres and the transverse acetabular

ligament. The ligamentum teres (also referred toas the ligament of the femoral head) passes fromthe acetabular notch to the fovea of the femoral

head. Although the ligamentum teres generally isnot thought to contribute to hip joint stability inadults [73,74], it does carry the artery of the liga-

mentum teres that supplies blood to the femoralhead in children. The ligamentum teres alsocontains free nerve endings that are thought totransmit signals to the spine and brain, enabling

normal reflexive muscle actions that help protectthe hip joint from excessive motion [75].

ClinicalThe presence of free nerve endings could

explain both altered proprioception and hip painin patients with ligamentum teres derangements.Recent investigations [7,76,77] have emphasized

that derangements in the ligamentum teres cancause pain (that may be referred to the thigh) andmechanical symptoms (eg, clicking, catching). In

particular, a ligamentum teres injury with hemor-rhage can be confused clinically with a labral tear[53]. However, only approximately 5% of hipswith ligamentum teres tears are diagnosed clinic-

ally (preoperatively).


MR imagingWith MR imaging and MR arthrography, the

spectrum of ligamentum teres derangements is notwell publicized [78]. It has been suggested that the

ligament is best visualized on axial MR images,while coronal images mistakenly may suggestligament discontinuity and sagittal images are

the least helpful [78]. Thin-section, three-dimen-sional gradient-echo images along the course ofthe ligamentum teres also may be helpful in as-

sessing fiber continuity [72].

ArthroscopyWith hip arthroscopy, ligamentum teres de-

rangements are classified generally into threegroups: (1) complete ligament tear; (2) partialligament tear; and (3) ligament degeneration [77].

The ligamentum teres also may become avulsed ateither the acetabular or femoral attachments[76,79–81], become ossified [82], or act as a pref-

erential route for transarticular spread of tumor[83,84]. Ligamentum teres derangements are diag-nosed in approximately 8% [76] to 25% [7] of hipsexamined arthroscopically, and the postoperative

outcome for isolated derangements is regarded asgood or excellent [7,76].

Transverse acetabular ligament

The transverse acetabular ligament traversesthe acetabular notch at the inferior aspect of theacetabulum. The function of this ligament is

debated, particularly with respect to its possiblerole as a tension band that stabilizes the labrumand resists the anteroposterior widening of theacetabular notch during loading [85,86]. Clinically,

hypertrophy of the transverse acetabular ligamentand the ligamentum teres may interfere withconcentric reduction of dysplastic hips in pediatric

patients [87]. On MR images, the cleft formed bythe confluence of the transverse acetabular liga-ment and the labrum should not be mistaken for

a labral tear [88].

Extrinsic ligaments

Anatomy and functionThe three principal extrinsic ligaments are

external to the hip joint capsule and pass from

the pelvis to the femur. These ligaments—the ilio-femoral, pubofemoral, and ischiofemoral liga-ments—are named according to the bones to

which they are attached [85,89]. The circular fibersof the zona orbicularis, seen as a collar surround-ing the femoral neck with arthrography, partially

blend with the extrinsic ligaments superficially anddo not attach directly to bone.

ClinicalPatients with hip instability may present with

substantial hip pain, mechanical symptoms, andan antalgic gait. Hip instability is well recognizedin patients with generalized ligamentous laxity

(eg, Ehler-Danlos syndrome), with hip dysplasia,and after major trauma (eg, hip dislocation,subluxation). More recently, hip instability alsohas been recognized in high-level athletes who

subject their hips to episodes of trauma orrepetitive microtrauma [90]. Ligamentous insuffi-ciency possibly may predispose patients to sub-

sequent hip dislocation and may result insubclinical joint instability that hastens the onsetof osteoarthritis. Hip instability reportedly may

be treated effectively with promising surgicaltechniques, such as arthroscopic thermal capsu-lorrhaphy [90]. However, accurate preoperative

diagnosis of ligament insufficiency patterns re-mains challenging clinically.

MR imagingWith MR imaging, injuries to the extrinsic

ligaments may be diagnosed using the criteria

commonly used for ligaments elsewhere in thebody. For example, injury to the iliofemoral liga-ment is common (89%) after traumatic disloca-

tion of the femoral head and is diagnosed readilywith MR imaging [91]. After hip dislocation,a displaced iliofemoral ligament can play a role

in inhibiting reduction of the dislocated fem-oral head [92]. The small foci of intra-articular gascommonly seen immediately after a hip dis-location may be less conspicuous by MR imaging

than CT. With an effusion or arthrography, thereis improved delineation of the ligament under-surfaces that might be useful in displaying a partial

undersurface tear or fiber laxity [72].

Joint effusion, osteochondral injury,

and osteoarthritis

Joint effusion

A joint effusion is considered an early—albeitnonspecific—sign of an internal derangement.MR imaging is more sensitive than other imaging

techniques—including ultrasound—in detectingsmall joint effusions in adults [93]. In a studyof hip joint fluid [94], the average fluid volumein asymptomatic hips was 2.7 mL (range, 0.7–

5.6 mL) versus 6.1 mL (range, 1.7–11.6 mL) in


symptomatic hips [94]. These investigators alsofound that, when at least 5 to 10 mL of intra-articular fluid is present, the joint capsule is dis-

tended by at least 5 mm along the length of thefemoral neck. They concluded that this findingcan be used to define a hip joint effusion with MRimaging [94].

Osteochondral injury

Just as in other joints, osteochondral injuriesmay occur in the hip. Such osteochondral lesionscharacteristically are seen in young adults who are

avid athletes and present with groin pain [95].Osteochondral injuries may be caused by a spec-trum of injury, ranging from overt hip dislocation

[91,96] to subclinical shearing or impaction injury[95]. Although osteochondral lesions are thoughtto be due to trauma, these patients may not recall

a distinct traumatic event.On MR images of the hip, osteochondral

lesions in athletes often target the superomedial

femoral head and are characterized by chondralirregularity and subchondral bone marrow edemasignal [95]. More extensive osteochondral injuries

also can occur in athletes and may be accompa-nied by joint effusion, joint capsule injury, ace-tabular rim fracture, or loose bodies (Fig. 5).

Osteoarthritis

Clinical

Osteoarthritis is a well-known source of painand disability. The prevalence of hip osteoarthritisis approximately 3% to 6% in white populations

[97]. Interestingly, hip osteoarthritis is much lessprevalent in Asian and black populations in theirnative countries [97]. For example, hip osteoar-

thritis in China is 80% to 90% less frequent thanin white persons in the United States, presumablydue to genetic or environmental factors [98].

The relationship between exercise and sub-sequent osteoarthritis has been the subject of long-standing debate. Although the debate continues,

Fig. 5. A 21-year-old National Collegiate Athletic Association Division I football linebacker, injured during a tackle,

with consequent osseous and chondral injury. Axial fat-suppressed T2-weighted (A) and coronal FSE inversion recovery

(B) images of the pelvis show posterosuperior acetabular rim fracture (arrows) with marked surrounding edema and

hemorrhage in the soft tissues accompanying a capsular injury. Sagittal FSE T2-weighted image (C) shows a chondral

defect (arrows) in the superior femoral head. The patient experienced continued pain following the injury and a MR

arthrogram was performed. Axial FSE fat-suppressed proton density (D) and coronal T1-weighted (E) images show two

discrete intracapsular chondral fragments (arrows) near the fovea. This case illustrates the value of MR arthrography in

the detection of loose bodies.


recent studies offer some compelling insights [97].Several studies [99–107] have concluded that one ormore of the following factors contribute to hiposteoarthritis: obesity; joint injury; occupational

activities involving heavy lifting; and prolonged,intense activity in certain sports. While moderateactivity has not been shown convincingly to be

a cause of osteoarthritis, certain activities mayexacerbate the disease once degenerative changesare present. A specific biomechanical cause of hip

pain, labral tears, and osteoarthritis propoundedin athletes is femoroacetabular impingement.

Femoroacetabular impingement

Femoroacetabular impingement occurs withhip flexion, adduction, and internal rotation (the‘‘anterior impingement position’’) in individuals

who have subtle predisposing anatomic features[40,108–112]. These anatomic features result indecreased clearance between the anterior acetab-ular rim and the anterior femur at the head–neck

junction. In the anterior impingement position,these two anatomic sites ‘‘impinge’’ upon eachother, potentially resulting in injury to the labrum

and adjacent articular cartilage. This impingementcan be seen intraoperatively and can be demon-strated with open MR imaging of the hip [112].

The proposed anatomic features predisposing hipsto this femoroacetabular impingement include:reduced concavity (‘‘shallow tapering’’) at the

femoral head-neck junction; reduced femoralhead-neck offset; reduced femoral anteversion;acetabular retroversion; a wide femoral neck; andacetabular protrusion. A decreased anterior fem-

oral head–neck offset can be demonstrated byspecific orientation of the MR imaging planecoaxial to the femoral neck [112].

Because reduced femoroacetabular offset canonly cause anterior impingement with flexion (es-pecially with internal rotation), some authoritiessuggest that a patient’s level of activity can play

a role in this process becoming clinically signif-icant [40,112]. Early treatment may potentiallyalleviate impingement microtrauma and preserve

the hip joint. Indeed, for young to middle-agedadults with anterior femoroacetabular impinge-ment and mild to moderate cartilage lesions,

surgeons may debulk the anterior femoral head–neck region and perform a periacetabular osteot-omy [112] or perform cartilage debridement [111].

ImagingWith radiography, the presence of osteoarthri-

tis is inferred by several ‘‘secondary’’ signs, in-

cluding the presence of joint space narrowing,subchondral eburnation, subchondral cyst forma-tion, and osteophytosis [113]. These secondarysigns also should be sought when interpreting MR

examinations of the hip, although MR imagingpotentially allows direct inspection of articularcartilage (Fig. 6).

Compared with the knee, MR imaging assess-ment of articular cartilage in the hip is challengingowing to several factors, including: (1) articular

cartilage in the hip is relatively thin, measuringno more than about 3 mm in thickness [114];(2) the thickness of the acetabular and femoral

head cartilage varies normally, depending on thelocation in the joint [114]; (3) miscalculation ofcartilage thickness may occur owing to use oftwo-dimensional image display for evaluating

cartilage on curving surfaces [115,116]; and (4)the hip is relatively deeply located, resulting ina relatively diminished signal to noise ratio.

Fig. 6. A 30-year-old athletic female with right hip pain and premature osteoarthritis demonstrated on MR

arthrography. Sagittal fat-suppressed T1-weighted image (A) demonstrates superior femoral cartilage loss with a small

cortical rent and a large acetabular geode (arrow). Coronal FSE T2-weighted image (B) again shows the large acetabular

geode.


In a recent study on the detection of cartilagelesions in the hip, the sensitivity, specificity, andaccuracy of MR arthrography were 50% to 79%,

77% to 84%, and 69% to 78%, respectively [111].The accuracy of MR imaging tends to be morefavorable for high-grade or large cartilage de-fects; however, chondral softening, fibrillation, or

partial-thickness defects less than 1 cm in diam-eter are detected inconsistently by MR imaging.Furthermore, small intra-articular osteochondral

fragments often are not demonstrated well by MRimaging [117].

Treatment

Treatment of hip osteoarthritis is influencedmost by the severity of the disease. Managementof mild osteoarthritis typically includes adminis-

tration of nonsteroidal anti-inflammatory medi-cations and activity modification, while profounddisease usually is treated with total hip arth-roplasty [118,119]. Other treatments that have

gained attention for their potential role includeglucosamine sulfate, chondroitin sulfate, hyal-uronic acid, microfracture, and osteochondral

allografting.

Differential diagnosis

When signs of arthritis are recognized, thedifferential diagnosis in athletes occasionally

may include inflammatory arthropathies, septicarthritis, synovial (osteo)chondromatosis, andpigmented villonodular synovitis. Inflammatory

arthropathies can exhibit a proclivity for synovial-lined joints, tendon sheaths, and bursae about thehip [120,121].

Septic arthritisSeptic arthritis is less common in adults than in

younger individuals. Risk factors for septic arthri-

tis include septicemia, prior injection into the joint,and an immunocompromised state. Patients typi-cally present with considerable hip pain, oftenaccompanied by fever. Radiographs may be nor-

mal or demonstrate soft tissue swelling, periartic-ular osteopenia, osseous erosion, and eventuallyjoint space narrowing. MR imaging findings of

septic arthritis include joint effusion with internaldebris, marginal erosions, cartilage destruction,and periarticular contrast enhancement. Prompt

diagnostic aspiration of joint fluid in patients withsuspected septic arthritis, of course, is imperative.

Idiopathic synovial (osteo)chondromatosisIdiopathic synovial (osteo)chondromatosis is

an uncommon synovial metaplastic disorder that

may occur in joints, bursae, or tendon sheaths[122]. It is most likely to be discovered in the thirdto fifth decades of life. Men are affected twice as

often as women [123]. Clinical symptoms includepain, swelling, and locking of the affected joint[123]. The hip may be the second most commonly

affected joint, after the knee [124].Radiographs may be normal, because the

chondromata are not mineralized in one third ofcases [123,125]. In the remaining cases, radio-

graphs may show multiple calcified or ossifiednodules within a joint, classically with erosion ofadjacent bone. The MR imaging appearance of

synovial (osteo)chondromatosis reflects nodulecomposition (Fig. 7). Purely cartilaginous nodulesare isointense with articular cartilage on all pulse

Fig. 7. A 37-year-old male with a history of synovial chondromatosis and previous synovectomy presented with

recurrent hip pain and limited range of motion. Axial FSE proton density fat-suppressed (A) and coronal FSE T2-

weighted (B) MR arthrogram images show erosions of the margins of the femoral neck (arrows). Note the innumerable

filling defects within the joint capsule indicative of tiny chondral bodies.


sequences. Calcified nodules are seen as signalvoid foci on all pulse sequences. Ossified noduleshave a peripheral rim of low signal intensity on allpulse sequences and a central area of high T1

signal intensity (corresponding to medullary fat)[125–127].

Pigmented villonodular synovitisPigmented villonodular synovitis is an idio-

pathic proliferative disorder of the synovium [122,128–130]. This uncommon entity (annual inci-dence: 1.8 cases per million) most often occurs in

young to middle-aged adults, and is more com-mon in men. Clinically, patients experience me-chanical pain and a limited range of motion [131].

Radiographically, pigmented villonodular sy-

novitis may be detected as lobulated soft-tissueswelling without calcification. MR imaging allowsthe diagnosis of pigmented villonodular synovitis

to be suggested because of hemosiderin, jointeffusion, and hyperplastic synovium, generallywithout prominent joint destruction [132,133].

Hemosiderin has a characteristic appearance,and is displayed as very low signal intensity onboth T1- and T2-weighted images [134]. Although

hemosiderin typically is present, it is not in-variably detected by MR imaging [133,135–138].

Osseous injuries

MR imaging facilitates the diagnosis of frac-tures, stress reactions, and bone contusions, andhelps rule out other uncommon osseous derange-ments in athletes (eg, transient bone marrow

edema, osteonecrosis). Although the majority offractures adjacent to the hip joint are diagnosedby radiography, the diagnosis of nondisplaced

fractures may be difficult with radiography alone.Fractures adjacent to the hip in athletes usuallyare observed in characteristic clinical settings, most

commonly occurring in the setting of chronicrepetitive microtrauma (stress fracture), indirecttrauma (avulsion fracture), and direct trauma.

Stress fracture

ClinicalBone is a dynamic tissue that continually

responds to the stresses placed on it. Stress

fractures result from insufficient degrees of bonedeposition and bone resorption in the setting ofrepetitive loading. Fatigue-type stress fracturescharacteristically occur in serious endurance

athletes, dancers, or military recruits. Women

are at statistically increased risk for stress injury(eg, owing to amenorrhea, disordered eating, lowcalcium intake [139]).

The initial symptom of an osseous stress injury

is activity-related pain that is relieved with rest.With continued activity, the pain is progressive,and may become more constant or nocturnal.

With femoral neck stress fractures in athletes,physical examination occasionally reveals tender-ness to palpation, but heel strike and other

percussive tests have poor predictive value [140].Stress fractures occur at several locations

about the hip, including the femur, acetabulum,

and sacrum [141,142]. Of all stress fractures adja-cent to the hip, those located at the femoral neckare the most common and clinically important.Exercise-induced stress injuries to the femur also

may occur in the femoral head, intertrochantericregion, or shaft [143–146]. Acetabular stressfractures may occur in the roof or in the anterior

column (usually with fracture of the inferior pubicramus) [147].

MR imaging

Fractures are characteristically hypointense onT1-weighted images (owing to trabecular impac-tion) [148], with surrounding T2 hyperintensity

(from variable amounts of edema and hemor-rhage) (Fig. 8). The diagnostic value of fastspin-echo inversion recovery and fat-suppressedT2-weighted images is generally superior to

T1-weighted images in detecting and staging stressinjury to bone [149].

MR imaging is the most accurate and rapid

method of diagnosing stress fractures, whileradiographs may not show abnormalities (eg, sub-tle callus formation, irregular or disrupted cortical

margin) for 4 to 6 weeks [150]. For example, ina study of 340 consecutive conscripts with hip,groin, or buttock pain, MR imaging effectively

displayed 174 bone stress injuries in 137 patients(40%) [145]. In this series, radiography was 37%sensitive, 79% specific, and 60% accurate. Inaddition to facilitating the diagnosis of stress

fracture, MR imaging also allows the diagnosisof prefracture bone remodeling, termed stressreaction (before a macroscopic fracture develops).

MR imaging is also more sensitive and specificthan bone scintigraphy for assessing stress injuriesto bone [151]. In a prospective study of 22 hips in

endurance athletes [152], MR imaging was 100%accurate in diagnosing femoral neck stress frac-tures. By contrast, radionuclide bone scans had an

accuracy of 68% for stress fractures, with 32%


false-positive results. MR imaging also allowedthe specific diagnosis of other derangements,including synovial herniation pits, iliopsoas in-jury, and osteonecrosis.

Synovial herniation pits of the femoral neckfrequently are considered normal variants butmay be symptomatic in athletes [153]. Symptoms

may occur as these pits enlarge, and the overlyingcortex even may fracture. These pits reportedlyare caused by the changing relationship between

the joint capsule and the iliopsoas muscle.Although the natural history of these signal

intensity abnormalities varies with the clinical

setting, 90% of young patients with stress frac-tures of the femoral neck show resolution of signalintensity abnormalities on inversion recoverysequences within 6 months [154]. Conversely,

when high signal intensity persists on inversionrecovery images 6 months after the initial di-agnosis of fracture, this indicates the presence of

a residual or recurrent injury.

TreatmentThe treatment of stress fractures is influenced

by the cause and location. In the femoral neck,for example, nondisplaced compression-type stress

fractures (affecting the medial cortex) may bemanaged nonoperatively with protected weight-bearing and frequent radiographic follow-up.

Conversely, tension-type stress fractures (affectingthe lateral cortex) are potentially unstable andoften are stabilized internally to prevent the ad-

verse consequences of fracture displacement [155].Fracture displacement is associated with a highrate of complication, including osteonecrosis and

nonunion [156]. For femoral neck fractures thatare treated operatively with cannulated screws,there is increasing use of nonferromagnetic tita-nium screws, facilitating subsequent MR imag-

ing evaluation for hip derangements such asosteonecrosis [157–159]. Treatment of pelvic stressfractures includes rest and gradual return to ac-

tivity; healing may take 3 to 5 months [150].

Fig. 8. A 14-year-old athletic male with right hip pain and stress fracture in the femoral neck. Coronal T1-weighted

image of the pelvis (A) shows abnormal low signal intensity in the bone marrow of the right femoral cortex (arrow) with

low signal intensity line perpendicular to medial femoral neck, an appearance and location typical for stress fracture. On

coronal STIR image (B) bone marrow edema (arrow) is conspicuous. A frontal radiograph of the right hip (C) shows

a linear, transversely-oriented radiodense focus (arrow), compatible with callus associated with fracture healing.


Apophyseal avulsion injuries

ClinicalIn children and adolescents, injuries involving

the physis and apophysis are common. The pelvis,with its many apophyses, is a common location ofavulsion injuries. In a recent study of 203 apo-physeal avulsion fractures seen on radiographs of

adolescent athletes [160], the most commonly in-jured sites in the pelvis were (in order offrequency): (1) the ischial tuberosity (the origin

of the hamstrings and adductor magnus); (2)the anterior inferior iliac spine (the origin of thestraight head of the rectus femoris); (3) the ante-

rior superior iliac spine (the origin of the sartoriusand the tensor fascia lata); and (4) the superiorcorner of the pubic symphysis. The most com-

monly implicated sports in this study were soccerand gymnastics. Football, baseball, and trackathletes also are prone to avulsion injury [161].

Avulsion injuries may be due to sudden force-

ful (often eccentric) contraction of the mus-culotendinous unit during running, jumping, orkicking a ball. Alternatively, repetitive micro-

trauma from intensive training can cause bio-mechanical failure at the physeal plate (at the baseof the apophysis).

ImagingA displaced avulsion fracture fragment gener-

ally can be recognized with ease on radiographs

[161]. However, radiographs may be interpretedas negative in children when an apophysealavulsion essentially is nondisplaced. In such cases,cross-sectional imaging may prove helpful by

showing subtle asymmetry or edematous changes(Fig. 9). In the subacute or chronic setting, an

avulsion injury potentially may resemble a neo-plastic or infectious process, especially when nohistory of trauma is provided [161]. Knowledge ofthe major tendinous attachments to bone is

indispensable in arriving at a correct diagnosis.

TreatmentNondisplaced apophyseal avulsive injuries usu-

ally heal with conservative therapy. Surgery maybe considered for a recent apophyseal avulsiondisplaced more than 2 cm. With old avulsions,surgical excision of a malunited or hypertrophic

fragment may provide relief of pain in somepatients [162].

Hip bursae and bursitis

Bursae are sacs of synovial tissue that mitigatefriction between bones and tendons or between

bones and skin. Although bursae normally facil-itate the gliding of one musculoskeletal structureon another, they can become dysfunctional and

painful when inflamed [163]. In athletes, bursalderangements are typically secondary to repetitivemicrotrauma or acute trauma, but rarely may berelated to other causes (eg, infection, inflam-

matory arthritides, metabolic disease).The hip is surrounded by 15 to 20 bursae

[164,165]. Although most cases of bursitis are

diagnosed clinically and treated conservatively,MR imaging can be helpful in definitively in-cluding or excluding the diagnosis of bursitis. MR

imaging has proved sensitive for detecting andlocalizing fluid collections in several bursae atcharacteristic sites, including in the iliopsoas [166]

and trochanteric [167] bursae.

Fig. 9. A 17-year-old male after a soccer injury that resulted in sartorius avulsion. Coronal (A) and axial (B) FSE T2-

weighted images of the pelvis using a 0.3-T open MR unit show absence of the proximal left sartorius (arrow), which has

been avulsed from the anterior superior iliac spine, as well as adjacent soft tissue edema.


Iliopsoas bursa and bursitis

AnatomyThe iliopsoas bursa (also termed the iliopecti-

neal bursa) is the largest bursa in the human body.When distended, intrabursal fluid can extend fromthe region of the lesser trochanter (inferiorly)upward into the iliac fossa (superiorly). The

clinical differential diagnosis of a soft tissue massin this anatomic region may include such diversederangements as bowel herniation, hematoma,

abscess, lymphadenopathy, and neoplasm.

ClinicalIliopsoas bursitis is believed to be caused most

commonly by irritation of the iliopsoas as it movesover the iliopectineal eminence or femoral head.Athletes commonly present with anterior hip or

groin pain, although patients with rheumatoidarthritis and other conditions are known to presentclinically with a nonpainful soft-tissue mass that

may compress adjacent structures [168–172]. Thispain tends to be exacerbated during hip extension(which stretches the iliopsoas) and relieved duringhip flexion with external rotation. Iliopsoas bursi-

tis, iliopsoas peritendinitis, and iliopsoas tendoninjury have been associated with running, resis-tance training, soccer, gymnastics, and dance.

MR imagingIn approximately 15% of normal individuals,

there is a hiatus between the pubofemoral and

iliofemoral ligaments that allows connection be-tween the iliopsoas bursa and the hip joint [173].In the presence of this connection, the iliopsoas

bursa may contain fluid that has decompressedfrom the hip joint of patients with a joint effusionor synovitis (eg, owing to osteoarthritis). Alterna-tively, pathologic changes may arise from within

the iliopsoas bursa itself (eg, owing to iliopsoasbursitis, synovial (osteo)chondromatosis, or pig-

mented villonodular synovitis) [174]. In a recentstudy on iliopsoas bursitis, communication be-tween the bursa and the hip joint was observed in

all patients by MR imaging and at surgery [175].With MR imaging, iliopsoas bursitis is displayedas a well-defined, thin-walled cystic mass alongthe iliopsoas that enhances peripherally [175].

Cross-sectional imaging also can define the ex-tent of the bursal derangement if surgery is indi-cated (eg, iliopsoas bursectomy via an iliofemoral

approach).

Trochanteric bursae and lateral hip pain

AnatomyA complex of three bursae has been described

over the four facets of the greater trochanter(Fig. 10) [165].

� The trochanteric bursa is located between the

gluteus medius muscle and the posterior facetof the greater trochanter. No tendon fibersattach to the posterior facet, which is best seen

on sagittal images when the lower extremity ismildly externally rotated. On axial T1-weight-ed images, the nondistended trochanteric

bursa may be seen as a thin, inconspicuousband of intermediate signal intensity immedi-ately posterior to the greater trochanter.

� The subgluteus medius bursa lies between the

gluteus medius tendon and the lateral facet ofthe greater trochanter. The gluteus mediustendon inserts into the lateral and supero-

posterior facets, which generally are best dis-played on coronal and sagittal images.

� The subgluteus minimus bursa is located

between the gluteus minimus tendon and theanterior facet of the greater trochanter. Themain tendon of the gluteus minimus tendon

inserts into the anterior facet, which is bestseen on transaxial images.

Fig. 10. Trochanteric bursa and adjacent anatomy. (A) Schematic of the anatomy on sectional images. Sagittal,

transverse, coronal images through the anterior part of the greater trochanter, and coronal image through the posterior

part of the greater trochanter (a, b, c, d, respectively). The dotted lines display the needle paths for bursography. AF,

anterior facet; G. Medius, gluteus medius; G. Minimus, gluteus minimus; LF, lateral facet; oe, obturator externus; oi,

obturator internus; p, piriformis muscle; PF, posterior facet; SPF, superoposterior facet. (B) Axial T1-weighted image

shows the trochanteric bursa (white arrowheads) and subgluteus minimus bursa (black arrowheads) as thin hypointense

lines, the gluteus minimus tendon (curved arrow), and the iliotibial tract (straight arrow). (C) Coronal T1-weighted image

through the posterior part of the greater trochanter displays the lateral facet (arrowheads), the lateral part of the gluteus

medius tendon (curved arrow), and the iliotibial tract (straight arrow). (D) Coronal T1-weighted image through the

anterior part of the greater trochanter shows the anterior facet (arrowheads) with the gluteus minimus tendon (curved

arrow) attached to it. (From Pfirrmann CW, Chung CB, Theumann NH, Trudell DJ, Resnick D. Greater trochanter of

the hip: attachment of the abductor mechanism and a complex of three bursae–MR imaging and MR bursography in

cadavers and MR imaging in asymptomatic volunteers. Radiology 2001;221:469–77; with permission.)

c


ClinicalPain at the lateral aspect of the hip commonly

is attributed to trochanteric bursitis. However,

clinical misdiagnosis may occur because the symp-toms of trochanteric bursitis can be nonspe-cific, with pain potentially referred to the groin,thigh, or buttock. Furthermore, a spectrum of ab-

normalities may occur at the lateral aspect of thehip besides trochanteric bursitis, including tendi-nosis, tendon tear, tendon avulsion, and various

muscle derangements [176–179]. This spectrumof abnormalities—and the MR imaging find-ings—are similar to those observed in the shoulder,

and thus the hip’s abductor mechanism has beenreferred to as the ‘‘rotator cuff of the hip.’’ Justas in the shoulder, accurate diagnosis is impor-tant because the treatment for bursitis and

tendon tears can be quite different (see detailsin later discussion).

Trochanteric bursitis is a well-described athletic

injury. In runners, it has been associated withtightness of the iliotibial tract, leg length discrep-ancy, pelvic obliquity, and running on banked

surfaces. Trochanteric bursitis also may occur withother activities as an overuse injury (eg, balletdancers) or secondary to blunt trauma (eg, football

and hockey players). The colloquial term hippointer has been used in athletes to describe softtissue contusions over the greater trochanter andiliac crest. Hematoma, scarring, and heterotopic

ossification may be observed after such injuries.

MR imagingAccurate diagnosis may be accomplished with

MR imaging, particularly when the relevant anat-

omy is understood and examined with sufficientspatial and contrast resolution. For example, ina recent study of 24 women (age range: 36–75

years) with ‘‘greater trochanteric pain syndrome’’for more than 1 year [180], MR imaging showeda variety of abnormalities: gluteus medius tear

(46%); gluteus medius tendinosis without a tear(38%); trochanteric bursal distension (8%); andfemoral head osteonecrosis (4%). The best phys-

ical examination test in predicting a gluteusmedius tendon tear in this population (a positiveTrendelenburg sign) was only 73% sensitive and77% specific. Other authors have reported young

or athletic patients who were misdiagnosed clini-cally with ‘‘trochanteric bursitis,’’ but later weredetermined to have other conditions, including

muscle strain, stress fracture, lumbar radiculop-athy, entrapment neuropathy, and neoplasm[181–184].

Treatment

Treatment of bursitis generally consists ofconservative measures, such as activity modifica-tion (including protective padding, as appropri-

ate), ice, nonsteroidal inflammatory medications,stretching, specific exercises, and therapeuticsonography [185]. Percutaneous injection of localanesthetic and corticosteroid medications are

second-line therapeutic alternatives that may helpconfirm the clinical diagnosis [186]. Complicationsafter percutaneous injections are uncommon, but

even a single steroid injection of the trochantericbursa has been reported to cause necrotizingfasciitis and death [187].

Surgical procedures to address recalcitrantbursitis are well described [163]. For treatmentof recalcitrant trochanteric bursitis, surgical pro-cedures include open bursectomy with surgical

release of the iliotibial band over the greater tro-chanter [188] and arthroscopic trochanteric bur-sectomy [189]. Endoscopic treatment also has

been successful in the treatment of chronic lateralhip pain owing to trochanteric bursitis with cal-cific tendinitis involving the gluteus medius and

minimus tendons [190]. MR imaging may be help-ful in preoperative planning, because trochantericbursitis clinically may mimic gluteus medius

tendon tears [178]. The surgical treatment forsuch tears is accomplished by reattaching thegluteus medius tendon to the greater trochanter.

Musculotendinous injuries

The myotendinous unit may be avulsed,

strained, fatigued, contused, lacerated, or de-nervated [191]. Several sequelae may be observedafter musculotendinous injury, including hemor-

rhage, fibrosis, atrophy, heterotopic ossification,muscle herniation, and compartment syndrome.The various athletic injuries to muscle are dis-cussed in detail in the article by Boutin et al

elsewhere in this issue [192]. We have chosen tofocus on musculotendinous and adjacent hipinjuries emphasized in the recent medical litera-

ture, including the snapping hip, pubalgia, osteitispubis, and adductor insertion avulsion syndrome.

Snapping hip

Coxa saltans, commonly referred to as ‘‘snap-ping hip syndrome,’’ is characterized by audiblesnapping that usually occurs with hip flexionand extension [193–196]. Such snapping is seen

commonly in athletes, and may or may not be


symptomatic. For example, snapping hip syn-drome can represent 44% of hip problems inballet dancers, with about one third of casesassociated with pain [197]. Three types of coxa

saltans are recognized: external, internal, andintra-articular.

External type

The external (or lateral) type of coxa saltans isby far the most common. It occurs when thetypically thickened iliotibial tract or gluteusmaximus snaps forward over the greater trochan-

ter with hip flexion. Because the greater tro-chanteric bursa lies just superficial to the greatertrochanter, it may become inflamed and cause pain

in patients with the external type of snapping hip.

Internal typeCompared with the external variety of snap-

ping hip, the internal type is less prevalent but may

be more difficult to diagnose clinically [195].Consequently, patients with this condition maymore commonly be referred to radiologists for

diagnostic evaluation. The internal (or anterior)type is usually caused during hip extension whenthe iliopsoas tendon snaps medially over the

iliopectineal eminence or femoral head. Inflamma-tion of the iliopsoas bursa has been implicated asa potential pain generator in these patients [198].

Intra-articular type

The intra-articular type of snapping is due toan internal derangement within the joint, such asa loose body, labral tear, or redundant synovial

fold. These patients may complain of a clickingsensation (rather than audible snapping), and painis generally the chief complaint.

Imaging

For evaluating extra-articular causes of thesnapping hip, advanced imaging options includeiliopsoas bursography, sonography, and MR

imaging. Iliopsoas bursography is performed bypercutaneous injection of iodinated contrast usingfluoroscopic guidance. The iliopsoas tendon can

then be seen as a cord-like filling defect adjacent tothe opacified iliopsoas bursa. By reproducing therange of motion that elicits the snapping hipduring fluoroscopy, sudden jerking of the iliop-

soas tendon may be documented. Disadvantagesof this technique include that it is invasive, requirescontrast material, and exposes patients (who are

often of childbearing age) to pelvic radiation.Sonography facilitates noninvasive, dynamic

visualization of abrupt tendon displacement over

a bony prominence coincident with an audiblesnap. Sonography also permits assessment forpain elicited by transducer pressure, even whenthe tendons have a normal sonographic appear-

ance [195]. Although sonography is the bestimaging technique to demonstrate extra-articularsnapping dynamically, sonography does not eval-

uate optimally intra-articular structures.MR imaging generally is performed without

dynamic maneuvers. Secondary findings associ-

ated with coxa saltansmay include synovitis, bursi-tis (affecting the greater trochanteric or iliopsoasbursa), and tendinopathy or fibrosis (affecting the

iliotibial tract, iliopsoas, rectus femoris, or gluteusmaximus) [199]. For the internal type of snappinghip, MR imaging or MR arthrography may bethe single best imaging test. In a recent study

comparing various imaging techniques [200], MRimaging identified the cause of internal snapping inall cases. By comparison, the causative pathology

was identified less commonly by radiography(37%), sonography (46%), combined radiographyand CT (88%), and combined radiography and

sonography (94%).

Treatment

Conservative management of the extra-articu-lar types of snapping hip commonly includes restfrom aggravating activities, nonsteroidal anti-

inflammatory medications, physical therapy (eg,iliotibial tract stretching), and, occasionally, per-cutaneous injection of corticosteroid. For rare

cases of persistently painful extra-articular snap-ping hip, surgery may be indicated (eg, iliopsoastendon lengthening [193], greater trochantericbursa excision with Z-plasty of the iliotibial tract

[201,202]). For the intra-articular type of snappinghip, arthroscopy may be indicated to remove loosebodies or resect labral tears.

Athletic pubalgia

ClinicalGroin injuries are said to comprise 2% to 5%

of all sports injuries [203]. Acute groin pain in

athletes is caused most commonly by musculo-tendinous injuries involving the hip adductors(Fig. 11). However, pain referable to the groin canbecome chronic, and accurate clinical diagnosis

may be difficult because of vague or referredsymptoms involving the groin, medial thigh, lowerabdominal, perineal, and hip regions. Conse-

quently, pubalgia in athletes can have an extensiveclinical differential diagnosis that potentially in-cludes: osteitis pubis; adductor tendinopathy and


enthesitis; lower abdominal musculofascial de-rangements; hernias (eg, inguinal, femoral); geni-tourinary tract abnormalities (eg, ureteral calculi);fractures (eg, apophyseal avulsion, femoral neck

stress fracture); entrapment of the obturator nerveby soft tissue fibrosis; and, rarely, other conditionssuch as infection and neoplasm [198,203–221].

This section discusses athletic pubalgia in general,as well as osteitis pubis in particular.

MR imaging

In a large, blinded, prospective study, a historyof groin pain in athletes was associated signifi-cantly with pubic bone marrow edema [209]

(Fig. 12). However, chronic groin pain (which maybe defined as lasting longer than 3 months) com-monly has two or more etiologies in athletes [222,

223]. In a recent study of 30 athletes with pubalgiacaused primarily by abdominal musculofascialabnormalities, the authors concluded that pubal-gia is a complex process that is frequently multi-

factorial [208]. CommonMR findings in this seriesincluded:

� Attenuation or bulging of the lower abdom-inal wall musculofascial layers (93%)

� High T2 signal in one or both pubic bones(70%)

� High T2 signal in one or more groin muscles,

particularly the adductor muscles (60%)

Stress-related reactive marrow changes in thepubic bones often are not seen in isolation, andtherefore should prompt a search for associatedmusculotendinous, musculofascial, or osteoartic-

ular abnormalities. For example, athletes withstress injuries involving the pubic symphysisoften may have an associated stress injury in the

sacrum and degeneration in the sacroiliac joints[224].

Treatment

Although treatment of most musculotendinousinjuries is conservative (eg, with rest, ice, andnonsteroidal anti-inflammatory drugs), surgery

may be indicated for certain causes of pubalgiaif nonoperative measures fail after 6 to 8 weeks,particularly in high-level athletes [198]. Severalsurgical techniques are variations on a standard

hernia repair, sometimes with musculotendinousreattachment (eg, rectus abdominis muscle) orrelease (eg, adductor muscle). Postoperative prog-

nosis is generally good [198,215], with rates ofreturn to full athletic activity reported to be87% [207,219], 93% [220], 97% [210], and 100%

[218].

Fig. 11. A 32-year-old professional basketball player with acute right groin pain after a fall during a game. Axial FSE

fat-saturated proton density (A) and coronal FSE inversion recovery (B) MR images show high signal intensity indicating

edema within the right adductor muscles (arrows) compatible with a mild (grade 1) muscle strain.

Fig. 12. A 20-year-old college football linebacker with

midline lower abdominal pain and pubalgia. The MR

imaging examination was ordered to exclude a rectus

abdominus muscle tear. An axial FSE fat-saturated T2-

weighted image shows bone marrow edema within the

symphysis pubis (arrows) correlating with symptoms. No

muscle tear was appreciated.


Osteitis pubis

ClinicalThe pubic symphysis is a nonsynovial am-

phiarthrodial joint containing hyaline cartilageand a central fibrocartilaginous disk. Inflamma-tion, degeneration, and posttraumatic changes atthe pubic symphysis have been termed osteitis

pubis and may cause substantial pain [198,204,205,211,225–228]. In athletes, the pubic symphysisonly rarely is affected by septic arthritis and

osteomyelitis [206,217].

ImagingRadiographs may show variable degrees of

osteophytosis, subchondral cysts, subchondral

osteosclerosis, subchondral irregularity, and peri-articular demineralization. Symphyseal joint lax-ity or disruption also may be observed, which hasbeen defined as a joint space measuring more than

7 mm in width or malalignment of the uppermargins of the superior pubic rami measuringmore than 2 mm on flamingo radiographic views

[204,211].Bone scintigraphy characteristically shows in-

creased accumulation of radiopharmaceutical in

the parasymphyseal subchondral bone. Uptake istypically bilateral, but may be unilateral [204,226].This technique is imperfect in differentiating para-symphyseal stress reaction from stress fracture

and in diagnosing nonosseous causes of pubalgia.MR imaging findings of osteitis pubis include

osteophytosis, subchondral cysts, irregularity of

the pubic symphysis, juxta-articular pubic bonemarrow edema, and intraarticular fluid signal.Additional findings that may be seen with this

technique are joint incongruity (either in theanteroposterior or superoinferior plane) andextrusion of the fibrocartilaginous disk (most

frequently posteriorly or superiorly) [204,229].

Treatment

Treatment initially involves conservative mea-sures (eg, rest, nonsteroidal anti-inflammatorymedications, physical therapy). In some patients,

imaging-guided percutaneous injection of thesymphyseal cleft may be an effective minimallyinvasive treatment. In a recent study of 16 athletes

with debilitating groin pain and osteitis pubis,symphyseal cleft injection was accomplished withan aqueous suspension composed of 20 mg ofmethyprednisolone acetate and 1 mL of 0.5%

bupivacaine hydrochloride local analgesic [204].Eighty-eight percent of patients experienced im-mediate relief of some symptoms and were able to

resume athletic activities 2 days after the pro-cedure. At 2-month follow-up, 31% of the pa-tients were completely symptom-free. In casesrefractory to conservative management, surgery

may be performed (eg, symphyseal curettage[205], arthrodesis with bone grafting and com-pression plate [211], wedge resection of the pubic

symphysis [227]).

Adductor insertion avulsion syndrome

ClinicalSports-related injuries at the femoral shaft

entheses have been well demonstrated by MR

imaging in children [230] and adults [231].Adductor insertion avulsion syndrome, also re-ferred to as ‘‘thigh splints,’’ presents clinically aspain and tenderness in the hip, groin, or proximal

to mid-thigh. Similar to ‘‘shin splints,’’ this con-dition is thought to be due to repetitive avulsionstresses at the tendinous insertions into bone,

resulting in traction periostitis. With thigh splints,the periosteal changes occur at the medial aspectof the proximal to mid-femur because of the pull

of the adductor longus and brevis tendon in-sertions. Adductor insertion avulsion syndrome isthought to represent one end of a continuum thatranges from accelerated tissue remodeling to overt

stress fracture.

ImagingRadiographs are expected to be normal when

symptoms begin. Later, radiographs typically showsubtle periosteal new bone or cortical thickening atthe medial aspect of the proximal to mid-femo-

ral shaft. Bone scintigraphy shows an elongatedarea of increased tracer accumulation in the sameregion. MR imaging characteristically shows a

segment of high T2 signal along the medial perios-teum of the femoral shaft. The underlying cortexand medullary canal also may display hyperin-

tense T2 signal, but no osseous destruction ormass.

Treatment

Treatment consists of rest from inciting activ-ities. Short-term follow-up imaging may be usefulto document appropriate healing, but symptoms

typically resolve within 1 to 2 months with con-servative management.

Summary

Hip arthroscopy is being used increasingly forthe diagnosis and treatment of hip disorders. MR

imaging performed with appropriate technical


considerations may aid not only in preoperativeplanning but in the appropriate selection of pa-tients, which tends to lead to better postopera-

tive results. Although the painful hip is imagedmost commonly by radiography, MR imaging isconsidered the next imaging test of choice forevaluation of most common hip abnormalities in

athletes, including labral injuries, ligament inju-ries, osteochondral injuries, fractures, bursitis, andmusculotendinous injuries. MR arthrography can

be a particularly useful technique for dedicatedassessment of hip joint internal derangements.

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MR imaging of meniscal and cruciateligament injuriesRussell C. Fritz, MD

National Orthopedic Imaging Associates, 1260 South Eliseo Drive, Greenbrae, CA 94904, USA

Knee pain is a common sports-related clinicalcomplaint that may be caused by abnormalities of

the cruciate ligaments and menisci as well asvarious other pathologic conditions. An accuratediagnosis is an essential element of a successfultreatment plan in patients that present with knee

pain. Diagnostic imaging is especially importantwhen there is significant uncertainty regarding thecause of knee pain, and the outcome may be

improved by timely implementation of varioustreatment options.

MR imaging provides clinically useful infor-

mation by detecting and characterizing pathologicconditions of the knee. MR imaging is currentlythe premier imaging technique for evaluatingthe knee and may help establish the cause of

a patient’s signs and symptoms by accurately de-picting the presence and extent of bone and softtissue pathology about the knee. The information

provided by MR imaging is a useful piece of thepuzzle in a diagnostic workup and can helpestablish an anatomic diagnosis. In this article,

we focus on evaluation of the menisci as well asthe anterior cruciate ligament (ACL) and poste-rior cruciate ligament (PCL) with MR imaging.

MR imaging techniques

The knee is typically scanned with the patientin a supine position with the leg fully extended.

The patient should be scanned in a comfortableposition to avoid motion artifact. Excellentimages may be obtained with midfield and high-

field MR systems; however, the best images are

currently obtained on 1.0 and 1.5 Tesla machines.Experience is now accumulating with dedicated

1.0 Tesla extremity scanners that provide im-proved image quality when compared with thefirst generation of low field strength extremityscanners. Experience also is currently accumulat-

ing with 3.0 Tesla systems; however, problemswith chemical shift artifact on the images thatare not fat suppressed make evaluation of the

chondral surfaces problematic. Moreover, theincreased cost of these systems and the need todevelop compatible surface coils have limited the

orthopedic applications of 3.0 Tesla systems todate. A surface coil is essential for obtaining high-quality images regardless of the field strength ofthe MR imaging system. Ongoing improvements

in surface coil design and newer pulse sequenceshave resulted in higher-quality MR images of theknee that can be obtained more rapidly when

compared with older MR systems. Phased-arrayand quadrature surface coils are examples ofnewer coil configurations that allow faster, higher-

quality images of the knee.We typically image the knee in the axial, oblique

coronal, and oblique sagittal planes. The axial

images typically extend from the quadricepstendon, proximal to the epicondyles, to the patellartendon insertion on the tibial tuberosity. Theoblique coronal images are prescribed from the

axial images and are oriented parallel to a linedrawn though the epicondyles. The oblique coronalimages extend from the patella anteriorly into the

musculature posteriorly. The oblique sagittal im-ages are prescribed from the axial images andoriented perpendicular to the oblique coronal

images. The oblique sagittal images are obtainedfrom themedial to the lateral subcutaneous tissues,extending just beyond the collateral ligaments.E-mail address: [email protected]


doi:10.1016/S1064-9689(03)00028-X


11 (2003) 283–293

We use various pulse sequences to evaluate the

knee depending on the available software and thefield strength of the particular MR imaging sys-tem. In general, we rely on fast spin-echo pro-

ton density and fast spin-echo fat-suppressedT2-weighted images in the oblique coronal, obliquesagittal, and axial planes to diagnose internal

derangement of the knee [4]. The images with andwithout fat suppression are obtained in the samelocations to facilitate analysis of the anatomy.Anatomic structures such as the menisci and the

cruciate ligaments are identified on the protondensity images and evaluated for their relativewater content on the fat-supressed T2-weighted

images (Fig. 1). It is essential to have properlydisplayed and photographed fat-suppressedT2-weighted images that allow differentiation

between tissue and fluid. We have found thathaving control of the greyscale used for im-age display is useful when reading MR scans;

therefore, we typically interpret the images oncomputer workstations rather than using thehard-copy film for diagnosis.

Meniscal tears

MR imaging can be used to accurately di-agnose meniscal tears and has been the standard

imaging technique in clinical practice for approx-imately 15 years. Degenerative meniscal tears are

Fig. 1. A 44-year-old skier with an acute ACL tear. There is increased signal delineating a midsubstance rupture of the

ACL on these proton density (A) and fat-suppressed T2-weighted (B) sagittal images. The distal fibers of the ligament are

balled up and have a lax appearance (arrows). An edematous stump of the ligament remains attached to the femur

further proximally.

Fig. 2. A 54-year-old tennis player with a lateral

meniscal tear and cyst. There is a horizontally oriented

tear of the body segment of the lateral meniscus

communicating with the free edge (curved black arrow)

on this fat-suppressed T2-weighted coronal image. There

is an intrameniscal cyst displacing the superior leaf of

the meniscus superiorly. This cyst extends into a septated

lobular parameniscal cyst (white arrow). A small surface

tear was found at surgery, resulting in a one-way valve

mechanism between the superior and inferior leaf tissue

of the lateral meniscus.

284 R.C. Fritz / Magn Reson Imaging Clin N Am 11 (2003) 283–293

common in the general population and in athletes.Although intrameniscal signal that extends to anarticular surface is the hallmark of a meniscal

tear, this finding has been overemphasized relativeto the alteration of meniscal morphology. Carefulattention to the size and shape of the menisci is

necessary to recognize displaced meniscal tearsand discoid menisci on MR imaging. Buckethandle tears, flap tears, and displaced radial tears

may be subtle and can be missed if the menisciare only evaluated for intrasubstance signalalteration.

Fig. 3. Small radial tear of the lateral meniscus in a 25-year-old basketball player with an acute ACL tear. A proton

density coronal image (A) reveals a small radial tear of the lateral meniscus at the junction of the anterior horn and body

segments (arrow). A fat-suppressed T2-weighted axial image (B) also shows this small tear (arrow) that is limited to the

free edge of the meniscus.

Fig. 4. A 72-year-old woman with meniscal dysfunction secondary to a displaced radial tear of the medial meniscus.

There was no acute injury in this case. Interruption of the circumferential hoop fibers of the medial meniscus has resulted

in load transfer to the medial femoral condyle, contributing to a stress fracture. There is bone marrow edema (large white

arrows) in the medial femoral condyle surrounding a subchondral insufficiency fracture (small black arrows) on these fat-

suppressed T2-weighted coronal images (A, B). A displaced radial tear in the posterior horn segment (small white arrows

in A) has interrupted the meniscal hoop. There is associated peripheral displacement of the body segment of the meniscus

when its position is compared with the medial margin of the medial tibial plateau.

285R.C. Fritz / Magn Reson Imaging Clin N Am 11 (2003) 283–293

The information provided by MR imaging canhelp establish an anatomic diagnosis of a meniscaltear and depict intrameniscal and parameniscal

cysts that may develop through the substance ofthe meniscus (Fig. 2) [4]. The cross-sectional

Fig. 5. A 25-year-old man with an acute ACL tear and

lateral meniscal tear. There are ACL-associated con-

tusions (white arrows) of the posterolateral aspect of the

proximal tibia and more anterior aspect of the lateral

femoral condyle caused by rotatory subluxation of these

bones at the time of ACL rupture. This fat-suppressed

T2-weighted sagittal image also reveals a vertical pe-

ripheral tear of the posterior horn of the lateral meniscus

(black arrow). This small tear did not communicate with

an articular surface on other adjacent images and was

considered stable upon arthroscopic probing.

Fig. 6. A 23-year-old soccer player with an ACL-

deficient knee and a bucket-handle tear of the medial

meniscus. There is absence of the proximal ACL fibers in

the superior lateral aspect of the intercondylar notch

(large arrow) on this proton density coronal image. A

displaced bucket-handle fragment of the medial menis-

cus is seen along the superior margin of the medial tibial

spine (curved arrow). There is also a vertical tear in the

nondisplaced peripheral remnant of the body segment

(small arrow).

Fig. 7. ACL tear and associated displaced flap tear of the posterior horn of the lateral meniscus in a 35-year-old skier.

Fat-suppressed T2-weighted coronal (A) and axial (B) images reveal a flap tear of the far medial aspect of the posterior

horn of the lateral meniscus that is displaced superiorly and medially into the lateral aspect of the intercondylar notch.

This meniscal fragment (curved arrow) remains connected to the tibia by way of the posterior root attachment and is

displaced into the substance of the torn ACL.


morphology of a meniscal tear is well seen withMR imaging and may be horizontal, oblique, orvertical on a sagittal or coronal MR scan through

the meniscus. A radial tear is a vertically orientedtear that may be limited to the free edge of themeniscus and may be subtle on MR imaging (Fig.3). These radial tears may progress out to the

periphery of the meniscus and gradually tearthrough the circumferential hoop fibers of themeniscus. As the radial tear widens in response to

weight bearing, the remainder of the meniscusextrudes out to the periphery and the meniscusbecomes more dysfunctional in transmitting

compressive load across the knee. The articularcartilage and underlying trabecular bone aresubjected to increased load when the meniscus isdysfunctional and may fail in response to this

stress. MR imaging can depict the meniscal tearand reveal the underlying biomechanics and thestress response that can result from meniscal

Fig. 8. Normal fibers bundles of the ACL. Proton density sagittal images (A, B) depict the anteromedial bundle (black

arrows) and the posterolateral bundle (white arrows) of the intact ACL. A fat-suppressed T2-weighted axial image (C)

through the mid to proximal aspect of the ACL reveals the femoral attachment of the posterolateral bundle (white

arrows) and the midsubstance fibers of the anteromedial bundle (black arrows) further anteriorly. These bundles

normally diverge and become more discrete on distal axial images (not shown). The fibers within the ACL reciprocally

tighten and loosen to stabilize the knee throughout the arc of flexion and extension. The anteromedial bundle is tight in

flexion, and the posterolateral bundle is tight in extension.


dysfunction. Chondral defects or stress fracturesof the subchondral bone may develop in thesetting of meniscal dysfunction unless there is

reduced demand on the knee from patient weightloss or activity modification to allow time for therestoration of tissue homeostasis. This phenome-non of meniscal hoop dysfunction resulting in

load transfer to the articular cartilage and un-derlying bone is more commonly seen with MRimaging in the medial compartment where there is

more compressive load relative to the lateralcompartment (Fig. 4). The subchondral bonewithin these stress fractures typically seen in the

medial femoral condyle with MR imaging are atrisk to develop osteonecrosis with subsequentcollapse or fragmentation.

The information provided by MR imaging can

also help to establish if a tear is unstable bydetermining the extent and complexity of the tear(Fig. 5). Vertical longitudinal tears become more

Fig. 9. Selective sprain of the posterolateral bundle of the ACL in a 22-year-old skier. A fat-suppressed T2-weighted

sagittal image (A) reveals a normal anteromedial bundle of the ACL (black arrows). A fat-suppressed T2-

weighted sagittal image (B) reveals a mildly lax posterolateral bundle of the ACL (white arrows). A fat-suppressed

T2-weighted axial image in the superior aspect of the intercondylar notch (C) reveals a normal anteromedial bundle of

the ACL (black arrows). A fat-suppressed T2-weighted axial image further distally (D) reveals normal anteromedial

bundle fibers (black arrows); however, there is increased signal and mild laxity of the posterolateral bundle fibers (white

arrows) caused by a selective sprain of this portion of the ACL.


unstable as they propagate along the circumfer-ence of the meniscus and may ultimately result in

a displaced bucket-handle tear. Vertical longitu-dinal tears are well seen with MR imaging andshould be carefully looked for in the ACL-

deficient knee (Fig. 6). A specific type of flap tearof the posterior horn of the lateral meniscus ishighly associated with a torn or dysfunctional

Fig. 10. ACL rupture in a 42-year-old skier. A fat-

suppressed T2-weighted axial image reveals fluid (arrow)

extending across the mid to proximal aspect of the ACL.

Fig. 11. Three-week-old sprains of the ACL and medial collateral ligament (MCL) in a 25-year-old basketball player. A

proton density sagittal image (A) reveals increased signal within the ACL fibers; however, there is no evidence of laxity

(arrows). A fat-suppressed T2-weighted axial image (B) reveals increased signal, poor definition of the fiber bundles, and

irregular thickening of the ACL (solid arrows) and the MCL (open arrow). The appearance is compatible with a subacute

sprain with developing scar formation.

Fig. 12. Conservatively treated midsubstance ACL

rupture that was documented by physical exam and

MR imaging after a ski injury in a 42-year-old physician.

MR imaging at the time of injury (not shown) revealed

a typical ACL rupture without gross separation of the

torn fibers. This fat-suppressed T2-weighted axial image

was performed 2 years after the ACL rupture and reveals

mild fiber thickening and poor delineation of the fiber

bundles compatible with scarring (arrows).


Fig. 13. ACL ganglion cyst in a 28-year-old golfer who suffered a twisting injury 10 months before this MR scan. Fat-

suppressed T2-weighted axial (A) and sagittal (B) images reveal a mildly lax-appearing ACL with expansion and

peripheral displacement of the ligament fibers by dissecting cyst fluid (small arrows). A septated, lobulated component of

the cyst is seen within the proximal ACL (curved arrow). There also is an intraosseous component of the ganglion cyst

within the tibia (large arrow) with mild surrounding marrow edema.

Fig. 14. Proximal avulsion of the PCL in a 23-year-old

football player. There is edema within the mid to

proximal portion of the PCL (solid arrows) on this

proton density sagittal image. There is detachment of the

entire PCL from the femur (open arrow). The ligament

has a lax appearance and there is posterior translation of

the tibia relative to the femur.

Fig. 15. Distal avulsion of the PCL in a 16-year-old

football player. There is increased signal at the site of an

avulsion fracture of the PCL from the tibia (open arrows)

on this fat-suppressed T2-weighted sagittal image. The

growth plate is almost closed (solid arrows) and is well

seen just distal to the avulsion fracture. The ligament has

a lax appearance and there is posterior translation of the

tibia relative to the femur.

ACL and may be detected with MR imaging.

This flap typically arises from the free edge ofthe posterior horn of the lateral meniscus anddisplaces into the posterior aspect of the inter-

condylar notch. The displaced flap of meniscaltissue typically rotates up just posterior to theruptured ACL fibers (Fig. 7).

Horizontal tears that communicate with a ra-

dial tear may also result in displaced flap tearsthat are commonly seen with MR imaging. Theseflaps tears are most commonly seen arising from

the body segment of the medial meniscus anddisplacing peripherally just inferior to the jointline. Superiorly displaced flap tears that arise from

the superior leaf tissue are less common but mayalso be seen with MR imaging. Medial meniscalflaps also are commonly seen at the posteriormargin of the medial tibial spine where they may

also be difficult to detect arthroscopically throughstandard portals.

ACL tears

MR imaging can be used to accurately diagnoseACL tears and has been the standard imagingtechnique in clinical practice for the last 15 years [8].

The information provided byMR imaging can helpestablish the anatomic diagnosis of a completeligament rupture or less severe degree of sprain

injury. MR imaging also can help distinguish anacute ACL rupture from a chronic deficiency basedon the morphology of the ligament. Rupture of the

ACL is a common sports-related injury that isusually a straightforward diagnosis with MRimaging. The ACL is composed of anteromedial

and posterolateral bundles that reciprocally tightenin flexion and extension. The anatomy of thesebundles may be seen with MR imaging (Fig. 8).Although an acute complete tear is the most

commonly encountered situation in clinical prac-tice, partial tears and lesser degrees of ACL spraininjury may occur and may be limited to the an-

teromedial or posterolateral bundle (Fig. 9). Themidproximal fibers of the ACL most commonlyrupture, leading to a proximal stumpof theACLon

the femur, posterior sloping of the distal ACL onthe sagittal MR images, and a fluid-filled gap at thesite of the tear on the axial images (Fig. 10).

Axial, sagittal, and coronal T2-weighted im-ages are useful in evaluating the status of the ACLbecause of its oblique course through the inter-condylar notch [3]. The axial and coronal planes

are especially useful for differentiating femoralavulsion of the ACL and lesser degrees of spraininjury from the more typical midsubstance rup-

ture. Coronal and sagittal images are useful fordetecting avulsion of the tibial attachment of theACL, which is more common in skeletally

immature patients. Evaluation of the ACL onfat-suppressed T2-weighted images in all threeplanes also facilitates detection of scarring of theligament fibers from previous injury that may be

more subtle when looking at the ACL only on thesagittal images. Injury of the ACL, as in otherligament injuries, is followed by a healing re-

sponse and eventual scarring of the ligament(Figs. 11, 12). This healing response is character-ized by a gradual resolution of ligament edema

with the development of ligament thickening andpoor definition of the fiber bundles that is vari-able in extent. There also may be hypertrophy of

the bony attachment sites adjacent to the siteof ligament injury and subsequent scarring.The ligament may scar to the PCL or to theintercondylar notch in an area inferior to the

Fig. 16. Conservatively treated midsubstance PCL

rupture that was documented by physical exam and

MR imaging after a soccer injury in a 32-year-old

woman. MR imaging at the time of injury (not shown)

revealed a typical PCL rupture without gross separation

of the torn fibers. This proton density sagittal image was

performed 4 years after the PCL rupture and reveals

moderate fiber thinning and a lax appearance of the

ligament (arrows). There is also mild posterior trans-

lation of the tibia relative to the femur that suggests

partial insufficiency of the PCL.


normal femoral attachment site resulting indysfunction.

A ganglion cyst of the ACL may be confused

with rupture of the ACL on MR imaging. Aganglion cyst of the ACL may develop after injuryand is characterized onMR imaging by a septated,lobulated fluid collection that displaces the liga-

ment fibers, though the ligament fibers remain incontinuity and are intact (Fig. 13). Intraosseouscyst components and reactive marrow edema are

common at the ACL attachment sites in patientswith ganglion cysts of the ACL [2].

Acute injuries of the ACL are often accompa-nied by injury to the posterolateral capsule andadjacent muscles in the posterolateral corner of

the knee as well as lateral compartment bonecontusions. These contusions are caused by im-paction of the anterior weight-bearing portion ofthe lateral femoral condyle with the posterior

aspect of the lateral tibial plateau that occurswhen the ACL ruptures [7]. Anterior subluxationof the lateral tibial condyle relative to the lateral

femoral condyle occurs at the time of injury andexplains the location of these bone contusions.

Fig. 17. Selective rupture of the posteromedial bundle of the PCL in a 28-year-old football player who suffered

a hyperextension injury during a game that was documented by review of the videotape. Proton density sagittal images

(A, B) and a fat-suppressed T2-weighted axial image (C) reveals a normal anterolateral bundle of the PCL (curved

arrows); however, there is increased signal and poor definition of the posteromedial bundle compatible with a selective

rupture of this portion of the PCL.


Anterior tibial translation relative to the lateralfemoral condyle can be observed on sagittal MRimages as a sign of ACL insufficiency [1]. Anteriortibial translation and other secondary signs may

be helpful in prompting a more careful analysis ofACL morphology, especially when a chronicallytorn ACL has scarred to the PCL or the femur

and is not obviously disrupted or sloping poste-riorly on the sagittal images.

PCL tears

PCL injuries are less common than ACL andmeniscal injuries. Midsubstance rupture of the

PCL as well as proximal and distal avulsions ofthe ligament from the tibia and the femur mayoccur and seen easily with MR imaging (Figs. 14,

15) [5,6]. Scarring of the PCL is characterized bythickening of the ligament fibers and the absenceof edema as well as a somewhat lax appearance

(Fig. 16). The PCL is composed of anterolateraland posteromedial bundles that reciprocallytighten in flexion and extention. The postero-

medial bundle is tight in extension and theanterolateral bundle is tight in flexion. Isolatedposteromedial bundle tears have been occasion-ally seen with MR imaging in our experience.

We have read approximately 10 clinical cases withhyperextension injuries of the knee that appear toselectively injure the physiologically taut fibers of

the posteromedial bundle of the PCL before fullytearing the entire PCL (Fig. 17).

When combined rupture of both cruciate

ligaments along with collateral ligament injury isidentified with MR imaging, the possibility of kneedislocation and associated dissection of the pop-liteal artery should be considered. An intraluminal

flap or thrombus in the popliteal artery may beseen on the routine MR images. MR angiographycan sometimes be performed after the standard

MR study of the knee without moving the patientand is more accurate than the routine MR imagesfor detecting injuries of the popliteal artery.

Summary

MR imaging provides clinically useful infor-mation in detecting and characterizing sports-related pathology of the menisci and cruciate

ligaments in a noninvasive fashion. Meniscal tearscan also be detected and characterized with regardto extent and tear stability with MR imaging.

Acute and chronic tears of the anterior andposterior cruciate ligaments can be accuratelyidentified and evaluated with MR imaging.

References

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tibia. AJR Am J Roentgenol 1994;162:355.

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Intraligamentous ganglion cysts of the anterior

cruciate ligament: MR findings with clinical and

arthroscopic correlations. J Comput Assist Tomogr

1996;20:80.

[3] Fitzgerald SW, Remer EM, Friedman H, et al. MR

evaluation of the anterior cruciate ligament: value of

supplementing sagittal images with coronal and axial

images. AJR Am J Roentgenol 1993;160:1233.

[4] Munk B, Madsen F, Lundorf E, et al. Clinical

magnetic resonance imaging and arthroscopic find-

ings in knees: a comparative prospective study of

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lesions. Arthroscopy 1998;14:171.

[5] Patten RM, Richardson ML, Zink-Brody G, et al.

Complete vs partial-thickness tears of the posterior

cruciate ligament: MR findings. J Comput Assist

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Posterior cruciate ligament injury: MR imaging

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[7] Speer KP, Spritzer CE, Bassett FH, et al. Osseous

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Imaging sports injuries of the foot and ankleAdam C. Zoga, MD*, Mark E. Schweitzer, MDDepartment of Radiology, Musculoskeletal Division, Thomas Jefferson University,

111 South 11th Street, Philadelphia, PA 19147, USA

As health care evolves in the early twenty-firstcentury, a combination of factors has increased

the demand for accurate diagnosis and efficienttreatment of sports injuries in high-level athletesand throughout the general populous. Patient

populations are gradually aging while simulta-neously becoming increasingly fitness conscious,with older patients living a more athletic lifestyleand younger generations participating in a more

diverse array of traditional and ‘‘extreme’’ sports.Patient education continues to improve with ever-expanding media and internet resources. Growing

patient demands compounded by a trend awayfrom specialization by health care providers createa greater role for the science of imaging in injury

diagnosis and assessment of pathology evolutionand therapeutic response.

Foot andankle structures bearmassive amounts

of force during athletic activities and are naturallysusceptible to a vast and ever-expanding array ofinjuries. MR imaging continues to become morewidely available with a growing number of systems

and shorter scan times, while technologic improve-ments allow for better anatomic detail and anincreased sensitivity for pathology. Often the exact

location and nature of an injury is governed by theprinciple of failure at the weakest point alonga musculo-teno-osseous axis. This point of failure

then varies with patient age and physical condition.Adolescents and young adults are most susceptibleto bony growth plate or apophyseal injury, whereastendinous and musculotendinous injuries are more

prevalent in the middle aged [1,2]. Additionally,

tendons themselves demonstrate a varying pro-pensity for injury based on their anatomic course

and stresses. Tendons that change direction at somepoint along their course employ a synovial sheath,which is protective but susceptible to inflammation.

Others are subject to hypoxic degeneration andtearing at predictable locations when exposed torepetitive abnormal stresses. These locations aredetermined in large part by regional tendinous

vascularity, with degeneration beginning in therelatively hypovascular portions of the tendon [3].Ligaments are injured with one-time high-velocity

traction or impaction stresses and can be sprainedor ruptured. Bony injury can occur with highvelocity one-time injuries or repetitive overuse

stresses with resulting contusion and or fracture[4]. Symptomatology presenting a significanttime after a trauma is often a manifestation of

previous injury, such as articular cartilage andosteochondral defects or instability syndromes(Fig. 1) [5].

When imaging the foot and ankle after an

athletic injury, we employ pathology-sensitive andanatomy-specific MR sequences in multiple imag-ing planes. In most cases, a pathology-sensitive

sequence in the form of a T2-weighted sequencewith fat suppression or STIR is obtained in planessagittal, axial and coronal to the long axis of the

body and anatomic T1-weighted or proton densitysequences are performed in a short axis plane(coronal for foot, axial for ankle) and a long axisplane (axial for foot, and coronal for ankle). It is

important for one bone marrow-specific sequence,usually T1 weighted, to be obtained without fatsuppression. Intravenous gadolinium contrast in

the form of an indirect MR arthrogram can behelpful in postoperative joints and in specificdifferential considerations, such as stenosing


E-mail address: [email protected] (A. Zoga).


doi:10.1016/S1064-9689(03)00026-6


11 (2003) 295–310

tenosynovitis. In our institution, intraarticular

contrast (direct MR arthrography) in the foot andankle is generally reserved for cases of suspectedoccult ligament injury or articular cartilage andosteochondral defects (Table 1) (Fig. 2) [6].

The Achilles tendon may be the most com-monly injured tendon in athletic activities. Pa-tients with chronic symptoms are often given

a diagnosis of Achilles tendonitis. This is a clinicalsyndrome but not a histologic entity, and MRimaging most often demonstrates paratendinitis.With Achilles paratendinitis, the tendon main-

tains its normal size and shape with abnormalsemicircumferential T2 hyperintensity peripher-ally at its paratenon. It is important to remember

that a synovial sheath is absent in the majority oftendons that do not change direction along theiranatomic course. Conservative, symptom-guided

therapy is effective in alleviating pain associatedwith Achilles paratendinitis (Fig. 3). In contrast,hypoxic tendinosis, another cause of clinical Achil-les tendonitis, usually occurs in a region from

2 cm to 7 cm proximal to its calcaneal insertion.The Achilles is enlarged in a fusiform configura-tion on sagittal images with an abnormal anterior

convexity but without focal signal abnormality onboth T1-weighted and T2-weighted sequences. Onhistologic examination, this is a degenerative

process, as opposed to an inflammatory one andsymptoms can be long-standing (years) withpersistent activity. Mucoid degeneration is more

often asymptomatic. In this entity, the tendon isagain at least mildly enlarged, but there is focalintratendinous signal abnormality in the form ofrelative hyperintensity on T2-weighted, and some-

times T1-weighted sequences. Mixed results havebeen reported with aggressive and conservativetherapies, but failure of therapy can ultimately

lead to complete tendon rupture. A final cause ofclinical Achilles tendonitis symptomatology is

Fig. 1. This professional football player suffered an

extreme eversion stress on an artificial surface. The

coronal short tau inversion recovery image shows an

unusual high-grade deltoid ligament tear (arrow).

Table 1

Foot and ankle sports protocols (1.5T)

Sagittal Coronal Axial

Routine ankle T1 non–fat suppressed T2-TSE fat suppressed Proton density fat suppressed

STIR T2-TSE fat suppressed

Biphasic indirect

ankle arthrogram

Early T1 non–fat

suppressed

Early proton density fat

suppressed

T2-TSE fat suppressed T2-TSE fat suppressed T2-TSE fat suppressed

Delayed T1 fat

suppressed

Delayed T1 non–fat

suppressed

Delayed T1 fat suppressed

Routine foot STIR T1-weighted non–fat

suppressed

T1-weighted non–fat

suppressed

T2-TSE fat suppressed T2-TSE fat suppressed

Routine sports imaging protocols employed at our institution when MR imaging is performed on a 1.5 Tesla system.

We obtain pathology-sensitive and anatomy-specific sequences of commonly injured structures. When performing

a biphasic indirect arthrogram, we obtain early sequences immediately after IV contrast administration followed by T2-

TSE sequences in three anatomic planes and then a set of delayed sequences to allow for accumulation of contrast within

the joint.

296 A.C. Zoga, M.E. Schweitzer /Magn Reson Imaging Clin N Am 11 (2003) 295–310

localized edema in Kager’s fat pad, anterior to

the tendon. In this case, symptoms are generallyself-limited, and specific therapy is rarely indicated(Fig. 4) [7–9].

In contradistinction to clinical Achilles ten-

donitis, symptoms localized to the region of thecalcaneal insertion of the Achilles are associatedwith etiologies such as insertional Achilles ten-

donitis and Haglund’s syndrome. There is con-siderable overlap in the symptomatology and MRcharacteristics of these two entities, as insertional

paratendonitis and retrocalcaneal bursitis occur inboth. The retrocalcaneal bursa is a physiologicone, and bursitis in this location is defined asa cranial-caudad span greater than 14 mm and

measurements greater than 2 mm anterior-poste-rior and 6 mm transverse [10]. The sine quo non ofHaglund’s syndrome is an enlarged calcaneal

tuberosity. Employing parallel pitch lines, thisHaglund’s deformity can be identified on lateralradiographs and sagittal MR images. Congenital

enlargement of the calcaneal tuberosity causesrepeated compression of the retrocalcaneal bursaand impaction on the insertional aspect of the

Achilles. The result is bony proliferation at the

already enlarged tuberosity (Haglund’s deformity)

and a cycle of accelerated injury. The diagnosis ofHaglund’s syndrome can often be confirmed bythe presence T2-weighted hyperintensity indicat-

ing bone marrow edema in the enlarged calcanealtuberosity (Fig. 5). Insertional Achilles tendonitis,on the other hand, is a classic runner injury often

with intratendinous T2-weighted hyperintensityin a flame-shaped or comet tail configurationextending to the calcaneal periosteum (Fig. 6)

[7,9,11–14].In the medial compartment of the ankle, the

majority of tendon disorders are degenerative andfall outside the scope of this article. However, a

subtype of posterior tibial tendon injury occur-ring distally near its insertion is seen occasion-ally in athletes. These partial or interstitial tears

Fig. 2. A coronal (short axis) fat suppressed indirect

arthrographic image at the level of the fifth metatarsal

base demonstrates intense soft tissue enhancement at the

site of a peroneus brevis avulsion (large arrow) and the

enlarged, retracted tendon (small arrow).

Fig. 3. T2-weighted fat-suppressed image through the

ankle demonstrating abnormal fluid signal at the Achil-

les paratendon (arrows). Note the loss of the normal

anterior concave border of the Achilles, in this case of

paratendinitis.

297A.C. Zoga, M.E. Schweitzer /Magn Reson Imaging Clin N Am 11 (2003) 295–310

are often subtle and best demonstrated on coronalT2-weighted sequences with a small field of view.

Any fluid in or around the distal posterior tibialtendon is suggestive of pathology, as there is noanatomic bursa in this location. Fluid signalaround the tendon implies tenosynovitis and

proliferative metaplastic synovium, whereas ten-dinous enlargement and fluid signal within thetendon itself indicates tendinosis and interstitial

tendon tear. Other medial tendons are uncom-monly involved in sports injuries [3,14,15].

The deltoid ligament, though commonly

sprained, is rarely torn completely. More com-monly, one or two of the five fascicles is partiallyor completely torn with an eversion injury. With

an inversion trauma, MR in the subacute settingcommonly demonstrates edema within the deltoidligament and in the medial malleolus at itsinsertion. This pattern is likely due to impaction

trauma at the time of the inversion stress andsubsequent medial contusion [16].

At the lateral ankle, the peroneal tendons

function as dynamic stabilizers working in con-junction with static ligamentous stabilization.

Fig. 4. An axial T1-weighted image of hypoxic Achilles tendinosis (A). Intratendinous signal is homogeneous, but the

tendon is enlarged and has lost its normal concave anterior margin (arrows). In contradistinction, the fat suppressed T2-

weighted image (B) demonstrates abnormal intratendinous high signal typical of mucoid Achilles degeneration.

Fig. 5. A T2-weighted fat-suppressed sagittal image of

Haglund’s syndrome demonstrating the prominent

calcaneal tuberosity (arrowhead ), an enlarged and

fluid-filled retrocalcaneal bursa (large arrow) and ab-

normal fluid in the retroachilles bursa (small arrow).


Understanding of this interrelationship is essential

for accurate assessment of sports-related pathol-ogy. With an acute lateral injury, most often froman inversion stress but occasionally related to

axial loading, there is a tendency for hemorrhageinto the peroneal tendon sheath. With subsequentactivity and repetitive stress, a complex synovitis

lends to the evolution of fibrous bands withinthe hemorrhagic synovium, ultimately leading tostenosing tenosynovitis. On MR imaging, boththe excessive fluid and complex fibrous bands are

often visible within the tendon sheath. If theclinical picture is unclear, intravenous gadoliniumcontrast (indirect arthrography) can be helpful in

making the diagnosis of stenosing tenosynovitisbecause the fibrous bands and surrounding softtissues tend to enhance intensely (Fig. 7) [17].

Tendinous injury is least common in theanterior compartment of the ankle, but partialand complete tears of the tibialis anterior tendon

occur infrequently with an acute plantar flex-ion force. High-level kicking athletes, usually insoccer or American football, are predisposed totibialis anterior tendon rupture, and the location

of injury is invariably at the level of the talar

dome. With complete tears, the remnant proximal

tendon can retract significantly, and a large fieldof view sequence may be necessary for localizationbefore operative repair (Fig. 8).

Lateral ankle ligamentous injury is common,and the anterior talofibular ligament (ATFL) ismost commonly involved. With ATFL disruption,

the primary lateral ankle stabilizer is missing, andthe calcaneofibular ligament is susceptible tosprain or rupture. The posterior talofibular liga-ment is rarely torn. Edema anterior to one or

more of these structures on fluid-sensitive se-quences is indicative of ligamentous sprain. Anenlarged ligament without surrounding edema

suggests a chronic injury or scarring. When thereis ligamentous disruption, fluid signal violates thenormal anatomic course of the ligament, most

often at its talar insertion. Lateral ankle ligamenttears evolve rapidly, and a subacute tear mayappear identical to a ligament sprain on MR

imaging, so secondary signs of pathology arehelpful. Fluid dissecting around the distal fibulaon coronal T2-weighted or STIR sequences isa strong indicator of ligamentous disruption. If

the fluid tracks cephalad, the anterior talofibular

Fig. 6. A sagittal T1-weighted image of the ankle (A) demonstrating fusiform Achilles enlargement approximately 4 cm

from its calcaneal insertion, typical of hypoxic Achilles degeneration. In contrast, this fat suppressed fluid-sensitive

T2-weighted image (B) calls attention to intratendinous edema at the calcaneal insertion diagnostic of an often pain-

ful condition, insertional Achilles tendonitis.


ligament is likely torn, whereas caudal extension

suggests a calcaneofibular ligament disruption(Fig. 9) [1].

The term ‘‘high ankle sprain’’ is often used tocommunicate a tibiofibular syndesmotic injury.

This entity can be difficult to identify on MRbecause of normal fenestrations within the liga-ments and the obliquity of their anatomic course.

Axial MR sequences with high anatomic resolu-tion (proton density or T1-weighted non–fatsuppressed) are usually the most useful in eval-

uation of the syndesmotic ligaments. Helpful sec-ondary signs of syndesmotic ligament disruptioninclude an increased syndesmotic recess height

and strain of the adjacent flexor hallicus longusmuscle belly immediately posterior to the syndes-mosis. Tears of one or both syndesmotic liga-ments can occur in isolation without other

ligamentous injury, but often the anterior syndes-motic ligament is ruptured while the posteriorsyndesmotic ligament remains intact (Fig. 10).

Ossification at the syndesmosis suggests a chronicor remote ligament injury.

With insufficient lateral ligamentous struc-

tures, the peroneal tendons are prone to sub-luxation. The morphology of the peroneal-fibulargroove plays a role as well, with hypoplastic,

convex, and externally rotated groove configura-

tions predisposing the tendons to repeated sub-

luxation. This diagnosis should be made only atthe distal-most aspect of the fibula, as the normalanatomic position of the tendons is lateral to thefibula at its distal metaphysis. Sequelae of re-

current peroneal subluxation include a syndromeof disorders ranging from attritional wear of theperoneus brevis tendon to peroneus brevis split-

ting, which manifests on MR as an enlarged,boomerang-shaped peroneus brevis at the level ofthe distal fibula (Fig. 11).

Though posttraumatic bony contusion afterinversion stresses are more commonly seen in themedial ankle structures because of compressive

tensile forces, lateral bone marrow edema in thefibula, talus, and cuboid also occur, likely owingto the rotational component of ankle sprains[4,18]. Acute lateral tendon tears are less common

than the above disorders in sports-related inju-ries but occasionally involve the peroneus longustendon at the level of the calcaneal-cuboid ar-

ticulation or the peroneus brevis tendon at itsinsertion.

Plantar fasciitis is a common overuse injury

frequently related to athletic activities. MR imag-ing is generally not essential in establishing thediagnosis at initial presentation but plays a role in

the evaluation and management of prolonged

Fig. 7. Axial T2-weighted fat-suppressed image (A) demonstrating fibrous bands (arrow) within the peroneal tendon

sheath. A sagittal indirect arthrographic image (B) confirms the diagnosis of stenosing tenosynovitis. Note the extensive

enhancement of the peritendinous soft tissues (arrows).


symptoms, or those refractory to conservative

therapy. Acute plantar fasciitis is visible onunenhanced MR of the foot or the ankle asperifascial edema at the proximal aponeurosisnear or at its calcaneal insertion. An entheso-

phytic calcaneal spur may be present but does notnecessarily correlate with symptoms. Simple acuteplantar fasciitis with perifascial edema only is

treated conservatively based upon symptomatol-ogy. When intrinsic fluid signal is present withinthe plantar fascia on T2-weighted or STIR

sequences, a partial plantar fascia tear should beconsidered, and more aggressive treatment may bewarranted. With recalcitrant plantar fasciitis,

bone marrow edema and reactive bony changesat the anteroinferior calcaneus are common andindicate microavulsive trauma at the insertionalfibers. Often this marrow edema is apparent on

T1-weighted and T2-weighted sequences, andthere will be correlative increased radiotraceruptake on bone scintigraphy. In such cases, the

microavulsive plantar fascial injury can be treatedas a typical fracture with a long leg boot. A

thickened plantar fascia without intrinsic or

perifascial edema may indicate chronic plantarfasciitis or scar from previous plantar fasciitis andcan be asymptomatic (Fig. 12). A subgroup ofpatients with clinical plantar fasciitis will have

a normal plantar fascia by MR imaging. Intrinsicmuscle tears, most often involving the flexordigitorum brevis, can mimic plantar fasciitis and

are identifiable on MR imaging by contrastingT2-weighted signal in adjacent muscle bellies.Linear high signal within a muscle belly suggests

an intrinsic muscle tear. For this reason, a field ofview should be chosen in clinical plantar fasciitisadequate to visualize the regional flexor muscle

insertions [19].There is a clinical overlap between plantar

fasciitis and plantar nerve impingement disorders.The majority of nerve impingement disorders

of the foot are occult to conventional imagingexaminations. However, a diagnosis of either me-dial or lateral plantar nerve impingement can be

suggested by the presence of muscle edemalocalized to a compartment. This is a diffuse

Fig. 8. T1-weighted fat-suppressed indirect arthrographic image through the anterior ankle (A) shows enlargement and

interstitial tearing of the tibialis anterior tendon with extensive synovial enhancement (arrow) in this soccer player.

Correlative sonographic image (B) of the same patient in the axial plane demonstrates the same pathology with tibialis

anterior tendon enlargement and interstitial hypoechogenicity indicative of tear.


pattern of edema, in contrast to the linear edematypical of intrinsic muscle tears. More frequently,these disorders manifest as fatty replacement of

a muscle compartment, indicating chronicity. Thisfrequently subtle finding may be imperceptiblewithout conscious comparison of directly adjacent

compartments (Fig. 13) [20,21].Another entity encountered with some fre-

quency in the setting of sports medicine MR is de-layed onset muscle soreness (DOMS). With a new

activity, or a dramatic increase in an activity, entiremuscle groups respond in a typical pattern ofdiffuse edema and hypertrophy. This syndrome

may mimic focal musculotendinous injuries onphysical examination, but the MR pattern ofdiffuse edema in one or multiple muscle groups

without more focal fluid signal is seen in DOMS.

Other sports-related nerve impingement disor-ders of the foot and ankle include tarsal tunnelsyndrome, deep peroneal nerve entrapment, andsinus tarsi syndrome. These three entities overlap

clinically as a result of posterior tibial nerveanatomy and its variable branching pattern. Thetarsal tunnel (tibiotalocalcaneal tunnel or Richet’s

tunnel) is formed medially by the concave medialcalcaneus, posteroinferiorly by the medial calca-neal tuberosity and anterosuperiorly by the

posteromedial segment of the talus and thesustentaculum tali. The posterior tibial tendon isparticularly likely to cause posterior tibial nerve

impingement as it passes through the tarsaltunnel. In most cases of tarsal tunnel syndrome,MR imaging is normal. But if a lesion with thepotential to cause mass effect is seen within the

Fig. 9. On this coronal T1-weighted fat-suppressed

image from the delayed phase of a biphasic indirect

arthrogram, a traumatic ankle effusion allows for

excellent joint opacification by the intravenous gadoli-

nium contrast aiding in visualization of the completely

disrupted calcaneofubular ligament (arrows).

Fig. 10. T2-weighted axial fat-suppressed image in

a basketball player with an acutely disrupted anterior

syndesmotic ligament (large arrow). As is often the case

in syndesmotic injuries, the posterior syndesmotic liga-

ment remains intact (small arrow).


tarsal tunnel, commonly a ganglion or a nervesheath tumor, then the diagnosis can be suggestedand clinical correlation is warranted. Less com-monly, MR imaging of patients with tarsal tunnel

syndrome demonstrates subtle edema between themedial tendons distal to the tunnel or adjacent to

the flexor retinaculum. Focal enlargement of the

posterior tibial nerve at the level of the tarsaltunnel may indicate edema within the nervesheath, also associated with tarsal tunnel syn-

drome (Fig. 14) [17,21,22].The sinus tarsi is at the lateral aspect of the

talocalcaneal articulation, its floor being the

superior surface of the anterolateral calcaneus.Fat within the sinus tarsi is a reassuring MRfinding, but normal variant anatomy includesa posterior subtalar joint extending into the sinus

tarsi and a small but normal quantity of fat withinthe sinus tarsi, limiting its perceptability. If edemais seen within the sinus tarsi, impingement of

the interosseous nerve should be suspected, but,again, MR imaging is often normal in these pa-tients. Fluid or edema within the sinus tarsi may

also represent sequelae of cervical ligament in-jury (Fig. 15). This structure, which can also betermed the external talocalcaneal ligament,

courses from the cervical tubercle on the medialtalus to the inferior aspect of the talar neck and isthe chief stabilizer of the talocalcaneal joint [21].

The subtalar articulation is predominantly

ligamentous and allows for stability during footinversion and eversion. Normal inversion at thisjoint is typically 30 degrees, with 15 degrees

characterized as normal for eversion. The plantarcalcaneonavicular ligament, or spring ligament,originates at the coronoid process of the calcaneus

and inserts on the plantar aspect of the navicular.Most spring ligament injuries are chronic andrelated to posterior tibial tendon dysfunction, and

Fig. 11. Peroneus brevis splits syndrome: note the

boomerang-like configuration of the peroneus brevis

(arrow) at the level of the distal fibula on this proton

density axial image.

Fig. 12. A sagittal T1-weighted fat-suppressed image

from an indirect arthrogram in plantar fasciitis. Note the

proximal fascial enlargement and enhancement (large

arrows) and the insertional bone marrow edema at the

calcaneus (small arrow).

Fig. 13. Short axis T1-weighted image through the

forefoot demonstrating near complete fatty replacement

of a medial flexor muscle group, including the flexor

hallicus brevis. This pattern of fatty atrophy is typical of

long-standing impingement of the medial plantar nerve.


abnormal eversion forces. On MR, the springligament can often be identified on coronal orlong axis images of the foot, but injury may be

difficult to perceive without noting abnormalhyperintensity on fluid-sensitive sequences alongits course [21,23].

Injury at the tarsometatarsal articulation orLisfranc’s joint can be a diagnostic and therapeu-tic dilemma. Lisfranc ligament injury may bea prototype for sports medicine, as it rarely occurs

outside the realm of athletic activity and it cancause a prolonged course of recovery and re-habilitation. Stabilization of Lisfranc’s joint in-

tricately involves the base of the secondmetatarsal and its articulations with the first andsecond cuneiforms as well as the third metatarsal

base. The second cuneiform is normally posi-tioned in recess of the first cuneiform byapproximately 8 mm, allowing for a mortiseconfiguration of the elongated second metatarsal

base. The Lisfranc ligament courses from thelateral aspect of the first cuneiform obliquely tothe plantar-medial aspect of the second metatarsal

base. Of note, there is no plantar ligament joiningthe second cuneiform to the second metatarsalbase, leaving the integrity of the Lisfranc ligament

vital to alignment of the tarsometatasal joint. OnMR, there are two mechanisms for evaluating the

Lisfranc ligament. One should try to visualize theligament directly and verify its integrity on longaxis images. As with other intrinsic ligament

injuries, edema within the expected course of theligament or at its insertions is indicative ofdisruption (Fig. 16). Additionally, one can and

should use bony alignment of the tarsometatarsaljoint as a secondary indicator of Lisfranc ligament

Fig. 14. Axial T1-weighted (A) and T2-TSE (B) images through the tarsal tunnel showing an enlarged, edematous

posterior tibial nerve (arrows) in this patient with clinical tarsal tunnel syndrome.

Fig. 15. This sagittal STIR image at the level of the

midfoot demonstrates extensive edema in the sinus tarsi

(arrows) in a patient with posttraumatic sinus tarsi

syndrome.


integrity in a manner similar to that used withradiographic evaluation. It has been suggestedthat a congenitally shallow Lisfranc mortise canpredispose athletes to Lisfranc ligament injury

[21,24,25].Springing forward off a plantar flexed foot, as

in a runner accelerating from the starting blocks,

generates tremendous dorsiflexion forces at themetatarsophalangeal joints, predominantly thefirst. This joint is stabilized from dorsiflexion

failure by the plantar plate or plantar accessoryligament, which is formed by the deep transverseligament combining with fibers from the flexor

hallicus longus, abductor hallicus, and adductorhallicus tendons. The plantar plate is a thickfibrocartilaginous structure contiguous with thefirst metatarsophalangeal joint capsule at its

anterior or plantar aspect. This mechanism hasbeen shown to be more prone to failure in athletesperforming on firm surfaces such as artificial turf,

giving rise to the popular term ‘‘turf toe.’’ Thoughturf toe is analogous to a volar plate injury in the

hand, the integral role of the plantar plate inrunning and jumping create for a uniquely dis-abling, and consequently frustrating, group ofinjuries. In the acute plantar plate injury, fluid-

sensitive MR sequences demonstrate intenseedema in the soft tissues of the first metatarso-phalangeal articulation and often flexor hallicus

longus tenosynovitis. Occasionally, a plantar cap-sular rupture can be identified on T1-weightedsagittal or short axis sequences. In the setting of

a lingering or chronic turf toe, a striking synovitisoften accompanies these findings. This is a di-agnosis that can be more readily made using an

indirect MR arthrographic protocol when there isdoubt (Fig. 17) [6,20,21].

Embedded in the plantar plate are the tibialand fibular sesamoids, which are also subject to

acute and chronic injury in athletic activities. Themedial sesamoid or tibial sesamoid is usuallythe larger of the two, but more insertions reside

on the lateral or fibular sesamoid. As a complex,sesamoid and plantar plate insertions include the

Fig. 16. Axial T2-TSE fat-suppressed image (A) at the level of the Lisfranc joint demonstrates marked edema in the

expected location of the ligament (small arrow). Note the bone marrow edema at the base of the second metatarsal (large

arrow). A coronal fat-suppressed image (B) shows an enlarged, abnormal Lisfranc ligament with surrounding edema

(arrows). Using radiographic criteria, an abnormal alignment of the proximal second metatarsal with the middle

cuneiform image confirmed a Lisfranc ligament rupture.


two heads of the flexor hallicus brevis, the abductorhallicus, the flexor hallicus longus fibrous tunnel,the oblique and transverse portions of the adductorhallicus, the metatarsosesamoid ligaments, the

deep transverse metatarsal ligaments, an intersesa-moid transverse ligament, and portions of theplantar aponeurosis. The medial metatarsosesa-

moid ligament is larger and stronger than its lateralcounterpart, sending oblique fibers to both thecloser tibial sesamoid and the more distant fibular

sesamoid. Depending on the vector of stress, eithermetatarsosesamoid ligament can rupture and thusallow for a rotational malalignment of the hallux-

sesamoid complex away from the injured ligament.Additionally, the thick, fibrous transverse interse-samoid ligament within the plantar plate canrupture, allowing for a divergent configuration of

the sesamoids. Once the hallux-sesamoid complexis displaced, abnormal weightbearing vectors ofstress can cause sesamoid contusion, fracture, and

even avascular necrosis. These entities are some-

times grouped together as different stages ofsesamoiditis. On MR, therefore, it is importantnot only to confirm a normal sesamoid configura-

tion, suggesting ligamentous integrity, but also toevaluate bone marrow signal within the sesamoidson a non–fat-suppressed sequence (Fig. 18) [2,21].

Evaluation of bony pathology and bone

marrow patterns in traumatic foot and ankleinjuries is a complex and challenging task, butcorrelating the injury with its vector of traumatic

force can serve as a guidance mechanism in thisundertaking. In the foot, fractures can result fromrepetitive forces that would not be great enough to

cause a fracture had they occurred only once, orfrom normal forces along abnormal axes, as ina result of abnormal weightbearing related toanother injury. Some typical stress fracture

locations are invariably linked with specificathletic activities. In basketball players or otherjumping athletes, the tarsal navicular is particu-

larly susceptible to fracture (Fig. 19). Calcanealfractures can also occur in basketball players,though they are more commonly encountered as

insufficiency fractures in an older population. Amultitude of stress fractures are seen in distancerunners, with locations likely related to running

form and individual anatomy. The third, fourth,and fifth metatarsals as well as the cuboid andcuneiforms are all commonly involved, whethera primary injury or secondary to altered weight-

bearing after a soft tissue injury (Fig. 20). Andsecond metatarsal stress fractures occur with suchfrequency in young military recruits that the term

‘‘march fractures’’ has become popular. MRconcepts for diagnosing stress fractures hold trueregardless of location. STIR and fat suppressed

T2-weighted sequences are most sensitive to cir-cumferential, intense bone marrow edema typicalof stress fractures. But loss of fat and ultimatelya hypointense fracture line as well as periosteal

reaction on non–fat-suppressed T2-weighted orsometimes T1-weighted sequences are more spe-cific indicators. It is important to remember that

radiographs have a sensitivity reported as lowas 15% in early stress fractures, so MR imagingis often the cornerstone in making an imaging

diagnosis [18,26,27].MR evaluation of bone marrow in the foot and

ankle also is useful outside the realm of fractures.

Stress reaction can manifest as bone marrowedema across articulations and can be an earlyimaging indicator of eventual bony or soft tissuefailure. It also has been noted that distance run-

ners can demonstrate a pattern of bone marrow

Fig. 17. Sagittal STIR image at the first metatarsopha-

langeal joint after an acute dorsiflexion stress on a hard

surface. The extensive edema in the thick fibrous plantar

plate is typical of a ‘‘turf toe’’ injury.


edema in multiple tarsal bones, though the sig-nificance of this finding is not entirely clear. Sub-tendinous bone marrow edema, notably with

regard to posterior tibial and Achilles tendoninsertions, has been described as associated withevolving tendinopathy. Finally, a pattern of dif-

fuse bone marrow edema is well described afterperiods of immobilization [1,28,29].

MR imaging evaluation of bone marrow

edema also plays an integral role in guidingtherapy in the setting of bony contusion. Themost common traumatic contusion pattern is seenin conjunction with inversion stresses and lateral

ankle sprain. This pattern includes a large impac-tion contusion with bone marrow edema in themedial malleolus, the medial talus, and the medial

calcaneus with a smaller microavulsive contusionat the lateral talus and fibula. Often, the pattern ofbone marrow edema can lend insight into axes

of abnormal weightbearing or atypical stresses.

Bone marrow edema patterns related to alteredbiomechanics are characteristically only seen onfluid-sensitive sequences without periosteal re-

action. When this marrow pattern is present,attention should be paid to regional ligamentousand tendinous insertions as the cause of the

altered biomechanics or abnormal stresses canoften be identified on the same study. Serial MRimaging examinations frequently play a role in

evaluation of high-level athletes to evaluate re-sponse to therapy and interval resolution of bonycontusion and soft tissue injury [4,16,18].

Although more often a secondary injury,

a discussion of sports injuries of the ankle wouldnot be complete without touching on the topic ofosteochondral defects. Articular cartilage injury

at the talar dome is particularly common with re-newed weightbearing at some point after anklefracture or ligamentous injury. Non–fat-suppres-

sed T1-weighted sequences and gradient echo (or

Fig. 18. This short axis T2-TSE fat-suppressed image (A) demonstrates edema in the location of the transverse

intersesamoid ligament (arrow) and an abnormally large distance between the two sesamoids. A long axis T1-weighted

image (B) confirms the diagnosis of an intersesamoid ligament rupture.


spoiled gradient echo) sequences are most sensitivefor osteochondral injuries, and the ankle mortise

should be evaluated in coronal and sagittal pro-jections.When evaluating an osteochondral defect,fluid signal surrounding the fragment indicates

an unstable, loose fragment; peripheral edema

suggests a partially loose fragment. It is impor-tant to differentiate fluid signal from the slightlymore hypointense signal typical of granulation

tissue in a healing defect. If an articular cartilagedefect alone is present, it is important to measurethe defect so as to monitor potential progression.

Additionally, localized collapse of the articular

Fig. 19. A T2-TSE axial image in this basketball player

with chronic midfoot pain is significant for hypointensity

in a navicular stress fracture indicative of sclerosis and

suggesting chronicity.

Fig. 20. A short axis fat-suppressed T2-TSE image (A) in this recreational runner draws attention to a metatarsal stress

fracture by virtue of the striking bone marrow edema (small arrows). But a non–fat-suppressed T1-weighted image (B) is

helpful in visualizing a discrete fracture line (large arrows).

Fig. 21. This indirect arthrographic T1-weighted fat-

suppressed image in a patient with a talar dome

osteochondral defect shows enhancing fluid surrounding

the osteochondral fragment (arrows), suggesting its

instability.


surface is an important finding and portendsa poor prognosis. Indirect or direct arthrographycan be helpful in evaluation of osteochondraldefects as contrast can imbibe into a defect and

surround a free osseous or chondral fragment(Fig. 21) [5,6,30,31].

Summary

The complexity of foot and ankle anatomy andfunction is unique in the musculoskeletal system.Understanding the complex anatomy alone is

a daunting task, not to mention transferring thatunderstanding to the two-dimensional planesencountered on imaging studies. When evaluating

sports injuries in the foot and ankle, the interpret-ing radiologist must take into account the type ofactivity, vector of stress, and inherent character-istics of the involved structures. A strong working

relationship with the health care providers man-aging patient care, ideally orthopedists, is essen-tial. But in this age of decreasing specialization

and increasing availability of imaging resources,the interpreting radiologist must use all availabletools for clinical investigation. When interpreting

an ankle or foot MR imaging, one finding shouldtrigger a search for the next finding along a logicalpathway of injury evolution. Bone marrow edema

patterns are guides to tendon and ligament failure.And a clinical syndrome without correlativeimaging diagnosis should call attention to poten-tial alternative diagnoses. As the number of MR

imaging studies performed continues to increaseand MR technology continues to improve, weexpect further advancements in MR evaluation of

foot and ankle injury. We hope to continue towork closely with our referring orthopedists inthis arena to improve our diagnostic skills and our

understanding of foot and ankle injury.

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tibial tendon dysfunction: secondary MR signs.

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Winter sports injuriesThe 2002 Winter Olympics experience

and a review of the literatureJulia R. Crim, MD

Department of Radiology, University Hospital and Clinics, University of Utah Health Sciences Center,

50 North Medical Drive, Salt Lake City, UT 84132, USA

The 2002 Winter Olympics in Salt Lake City,Utah, brought together 2345 athletes from 80countries. A wide variety of competitions took

place, which can be divided into broad categoriesof alpine (downhill) and nordic (cross-country)skiing, snowboarding, ice skating (figure skating,speed skating, and ice hockey), and bobsledding

(bobsleigh, luge, and skeleton).Medical care for the Olympians was provided

at several levels. Care was directed and coordi-

nated by the Medical Commission of the Inter-national Olympic Committee. On-site clinics atthe Olympic venues provided triage and acute

care. Intermountain Health Care provided in-hospital services. Provisions were made to airliftmajor trauma cases, but fortunately these did not

occur. Instead, the hospitals treated ailments suchas heart problems, frostbite, and altitude sickness.

Musculoskeletal injuries and ambulatory med-ical problems were evaluated and treated at a

multispecialty clinic in the Olympic village, builtand staffed by the University of Utah. Musculo-skeletal radiologists from around the country vol-

unteered their services. At the clinic, all serviceswere provided free of charge to the Olympians,their coaches, and other members of the Olympic

teams. Kodak, as a major sponsor of the Olympics,contributed the Picture Archiving and Communi-cation System (PACs) and digital radiography tothe Olympic clinic. They provided organizational

support during the building of the clinic and tech-nical support throughout the time the clinic was

open. MR imaging was provided by GeneralElectric, and ultrasound was provided by Siemens.

One of the difficulties in obtaining data about

injuries in recreational sports is that the injuriesoccur in a mobile population; vacationers oftenwait until they return home before having injuriesevaluated. One study found that 38% of Seattle

students suffering ski injuries returned homewithout reporting their injuries to the ski patrolor local physicians [1]. In contrast, at the 2002

Olympics, the availability of rapid, free, high-levelservices led patients to be evaluated at theOlympic clinic. Therefore, the Olympic clinic pro-

vided an excellent window into the types of in-juries suffered by high-level athletes in wintersports.

Study population

The 2002 Olympic records were reviewed for

sports-related injuries. Only competing athleteswere included in the analysis of injuries. Onlyinjuries for which positive imaging studies were

obtained are included. Injuries for skiing, snow-boarding, bobsled, and luge are given per raceper person, because an accurate measurement of

number of practice hours could not be obtained.The injury patterns of the Olympians were com-pared with injuries in recreational athletes.

Alpine (downhill) skiing

A variety of events are grouped under alpine,or downhill, skiing: downhill, super-G, slalom andgiant slalom, moguls, and aerials. Moguls andE-mail address: [email protected] (J. Crim).


doi:10.1016/S1064-9689(03)00027-8


11 (2003) 311–321

aerials are classified as freestyle skiing, wherejumps feature prominently. Aerial skiing takesoff from a ramp to a 12-foot-high takeoff point,

from which flips, twists, and somersaults areaccomplished.

The overall risk of injury from skiing isestimated at 0.25/1000 skier days [2]. The rate of

injuries found on MR imagine at the Olympics, incontrast, was 20/1000 person-races. (This figureincludes any on-site practice for the races.)

The knee is the joint most commonly injured inalpine skiers, and the most common skiing-relatedknee injury is anterior cruciate ligament (ACL)

tear. At the 2002 Olympics, four alpine skiers(three women, one man) suffered an acute ACLtear (Fig. 1). In the general population, ACL tearsare more common in women, but that does not

appear to be true in high-level skiers. A retrospec-tive study of professional skiers found an injuryrate of 0.004/1000 skier days in men, and 0.0044/

1000 in women [3].A number of different mechanisms of injury can

lead to ACL tear. In skiers, tears usually occur in

one of three ways: first, the skier catches an insideedge of the ski and falls forward between the skis(valgus-external rotation.) Second, the skier falls

backward between the skies and catches the insideedge of the downhill ski (flexion-internal rotation).Third, the skier lands at the back of the ski, whilethe boot goes forward (transient anterior disloca-

tion) [2]. In high-level athletes, strong contractionof the quadriceps muscle in landing from a jumpor in falling backward appears to be an impor-

tant contribution to transient anterior dislocationof the knee [4]. Although there are numerousmechanisms causing ACL tear, the ACL is more

vulnerable to injury in certain positions: onecadaveric study found that internal rotation ofthe tibia was most likely to cause ACL tear whenthe knee was either fully extended or fully flexed,

and that internal rotation was more likely to causea tear than external rotation [5].

An ACL tear does not preclude a return to

competitive skiing. One report of four competitivealpine skiers found that after surgical repair, allreturned to racing [6]. One skier was disabled by

Fig. 1. Tears of the medial collateral ligament (MCL), anterior cruciate ligament (ACL), and lateral meniscus in an

alpine skier. (A) Coronal STIR through the midknee shows abnormal signal at the femoral attachment of the ACL

(arrow). There is a horizontal cleavage plane tear of the lateral meniscus and a sprain of the MCL (arrowhead ).

(B) Sagittal PD image through the intercondylar notch shows the discontinuity of the ACL.

312 J.R. Crim / Magn Reson Imaging Clin N Am 11 (2003) 311–321

arthrofibrosis, but the other racers returned to com-peting at the World Cup. Moreover, their meanWorld Cup rankings improved from 24 beforethe injury to 14.6 after the injury.

After an athlete has suffered an ACL tear, thereis an increased risk of recurrent injury to the knee.Oates et al [7] found that compared with skiers

with intact ACLs, skiers who were ACL-deficienthad a 6.2 times higher rate of injuries, and skierswho had undergone ACL repair had a 3.1 times

higher rate.Five alpine skiers who suffered knee injuries in

the 2002 Olympics had preexisting, unrepaired

ACL tears. The new injuries in this group in-cluded medial and lateral meniscal tears, medialand lateral collateral ligament injury, cartilage in-jury, bone bruises, and popliteus injury (Fig. 2).

Eight downhill skiers suffered recurrent inju-ries while competing with a repaired ACL. Fora graft ACL to replicate the function of a native

ACL, the tibial tunnel should enter the joint in itsmiddle third, and the femoral tunnel should be atthe posterior margin of the intercondylar notch. If

the graft is placed in a more vertical orientation

than this, it will not prevent anterior translation ofthe tibia. If the graft is farther anterior than therecommended position, it also can cause impinge-ment of the graft on the roof of the intercondylar

notch. Of the eight downhill skiers with recurrentinjuries following ACL repair, four had sub-optimal position of the graft (Fig. 3). Five had

a lax ACL graft, with secondary buckling of theposterior cruciate ligament (PCL).

Foot and ankle injuries due to skiing have de-

clined in incidence since the 1970s because of im-provements in ski bindings. At the 2002 Olympics,six foot or ankle injuries were seen in five alpine

skiers. Three aerialists suffered foot fracturesranging from microtrauma to midfoot fracturedislocation. One of these had bilateral calcanealmicrofractures. Two downhill skiers suffered syn-

desmosis sprains; one of them also had a partialtear of the peroneus brevis tendon (Fig. 4).

Shoulder injuries constitute approximately

11% of alpine skiing injuries [8]. They are usuallycaused by falls, and much less commonly the re-sult of collisions with other skiers or trees, or to

pole planting. The most common shoulder injuries

Fig. 2. New injury in an alpine skier competing with a previously torn ACL. (A) Coronal STIR image through the

posterior aspect of the knee demonstrates an osteochondral injury with a free fragment in the medial femoral condyle

(arrow) and an impaction fracture of the lateral femoral condyle. The fibular collateral ligament is torn (arrowhead ).

There is extensive bone marrow edema in the proximal tibia. (B) Sagittal FSE T2-weighted image with fat saturation

through the medial femoral condyle. There is a condylar osteochondral injury (arrow) and a slightly displaced tear of the

posterior horn of the medial meniscus (arrowhead). Additional injuries in this patient included a lateral meniscal tear,

a posterior capsular tear, and a popliteus muscle strain.

313J.R. Crim / Magn Reson Imaging Clin N Am 11 (2003) 311–321

are rotator cuff injury, anterior glenohumeral dis-location or subluxation, acromioclavicular sepa-rations, and clavicle fractures. Only one alpine

skier suffered a shoulder injury at the 2002Olympics, a supraspinatus tendon tear.

Ulnar collateral ligament tears are a common

injury in skiing, occurring when the skier falls andthe thumb is forcibly abducted and deviated ra-dially by the ski pole when the thumb is held in

the pole strap [2]. A single skier in our series suf-fered a tear of the ulnar collateral ligament, whichwas evaluated with ultrasound.

Spine injuries are uncommon in alpine skiing,

although they can occur during collisions withother skiers or with trees, or from crashes duringjumps. One retrospective review of 10 years ex-

perience at a ski resort found 0.001 significantspinal injury for every 1000 skier days, of whichonly 9% required surgery [9]. One alpine skier in

our series had an acute back injury caused bya collision. MR imaging showed an L5 pedicle

fracture (Fig. 5). Three athletes with acute backpain had disc protrusions, one cervical and twolumbar.

Nordic (cross-country) skiing

Nordic skiing has a lower rate of injuries than

Alpine skiing. Incidence of injury has been esti-mated to be between 0.2 and 0.5 per 1000 skierdays [10]. Telemark (ski jumping) and nordic

combined (ski jumping plus cross-country sprint-ing) have a higher rate of injury, close to that ofalpine skiers [11]. Only one nordic skier sufferedan injury at the 2002 Olympics, a semimembrano-

sus strain.

Snowboarding

Snowboarding has a higher reported injuryrate than skiing. A large study at Lillehammer

attempted to estimate the number or injuries per

Fig. 3. Recurrent injury in an alpine skier with a poorly placed ACL graft. (A) Sagittal T1-weighted image with fat

saturation, intravenous gadolinium, at the intercondylar notch of the femur. The tibial tunnel is appropriately positioned

(arrowhead), but the femoral tunnel is too far anterior. No intact fibers are seen entering the femoral tunnel; only a mass

of amorphous, enhancing scar tissue (arrow) is present in this region. The graft was from autologous patellar tendon. (B)

Coronal T1-weighted image through the midzone of the medial meniscus. The patient complained of ‘‘locking’’ of the

knee, due to a bucket handle tear of the medial meniscus. Arrowhead points to the torn meniscal remnant; arrow points

to the fragment that is displaced into the intercondylar notch.


kilometer of skiing or snowboarding and de-termined a risk of 13.5 per 1000 km for snow-boarders, compared with 3.9 for alpine skiers and

3.0 for telemark skiers [11]. The injury rate at the2002 Olympics was 28/1000/person per race.

Half of all snowboarding injuries in the generalpopulation are to the upper extremity [12]. Almost

half of the upper extremity injuries are to thewrist. Wrist injuries are common in inexperiencedsnowboarders, who tend to fall on an outstretched

hand. As might be expected in our elite group, noathletes suffered wrist fractures. Shoulder injuriesinclude dislocations, fractures, and tendon tears.

One 2002 Olympic snowboarder suffered a shoul-der injury, a posterior dislocation (Fig. 6).

Snowboarders are less likely than skiers to in-jure the knee [13,14]. Three 2002 Olympic snow-

boarders injured the knee, all suffering ACL andmeniscal tears.

Foot injuries are common in snowboarders.One Olympic snowboarder underwent bilateralfoot MR imaging for ongoing foot pain and was

shown to have bilateral plantar fasciitis. The‘‘snowboarder’s fracture’’ is a fracture of the lateralprocess of the talus, which is reported to represent15% of ankle snowboarding injuries [15]. No such

fractures occurred in the 2002 Olympic snow-boarding population. Although common in snow-boarders, this underreported fracture occurs with

a wide variety of other sports, and even from trip-ping going down stairs. At the 2002 Olympics,a potential luge athlete was sidelined because of

foot pain. MR imaging showed a nonunited lateralprocess fracture and the severe secondary subtalarosteoarthritis that develops when this fracture isuntreated.

Snowboarders have a higher rate of spinalinjuries (0.004/1000 snowboarding days) than do

Fig. 4. Syndesmosis sprain and peroneal tendon partial tear in an alpine skier. (A) Axial FSE T2-weighted image with

fat saturation at the level of the tibiofibular ligaments. Anterior (arrow) and posterior (arrowhead) tibiofibular ligaments

are torn. (B) Coronal FSE T2-weighted image with fat saturation through the hindfoot. Splitting of the peroneus brevis

tendon is present (arrow). Bone marrow edema related to the syndesmosis sprain is seen, centered on the syndesmosis

and also in the medial malleolus. Other images also showed a partial tear of the deltoid ligament.


skiers (0.001/1000 skiing days) [16]. Most injuriesare related to jumping, and the higher rate in

snowboarders most likely is due to the greaternumber of jumps in recreational snowboarding.One snowboarder in our series, who had a preexist-

ing L5 spondylolysis, developed a stress responseof an L4 pedicle.

Bobsled

Bobsled competition is performed by eithera two-person or four-person team. The team

members push the sled from a stationary positionand then jump aboard into a seated position. Thepilot steers while the remaining members keep

their heads down. Injuries occur during the push-ing phase and as a result of crashes. Athletescommonly complain of back problems.

Bobsledding injuries at the 2002 Olympics oc-

curred primarily in the initial sled-pushing phase.There were three patients with strains or tears ofthigh musculature, and one acute injury of the

plantar fascia (Fig. 7). Two patients presented for

evaluation of back pain; one had a stress responsein the L5 pedicle, and one an annular tear and

premature osteoarthritis of the facet joints. Oneathlete suffered a shoulder injury (Fig. 8), a tear ofthe superior labrum involving the biceps anchor

(SLAP tear, so-called because it is a tear of thesuperior labrum from anterior to posterior). In-juries, calculated as positive imaging findings per

person per race, were 8/1000.

Luge

Luge is a sledding sport where the athletes(either solo or as part of a doubles team) lie supineand feet first in a narrow, curved sled. Rather than

having a running start, as in bobsled, the athleterocks back and forth to start downward motion atspeeds of up to 90 miles per hour.

There has been only one published epidemio-

logic study of luge injuries [17]. The study found407 injuries in 57,244 track runs (1043 athletes).This translates to 0.7 injuries per 1000 runs/person.

Most injuries were contusions (51%) or muscle

Fig. 5. Left L5 pedicle fracture in an alpine skier, due to a collision. The study was read blinded to clinical history, and

subsequent review with the patient and his physicians confirmed that the subtle fracture identified on MR imaging

corresponded to his site of pain. (A) Sagittal FSE T2-weighted image with fat saturation through the left pedicles. Arrow

points to focal bone marrow edema, and a thin vertically oriented low signal-intensity black line represents the actual

fracture. (B) Axial FSE T2-weighted image through the L5 pedicles. Edema is seen in the left pedicle (arrow). It is less

prominent on this non–fat-saturated sequence than on the sagittal image, which was obtained with a fat saturation pulse.


strains (27%). Only 3% of injuries were concus-

sions and 3% were fractures. Sixty-four percentof injuries were the result of crashes.

At the 2002 Olympics, nine athletes had

imaging studies showing injuries related to luge.This is a rate of 20 injuries per 1000 runs/person.Four were knee injuries: one ACL and PCL tear;

one chronic ACL tear with a new MCL injury;

one patellar fracture; and one ruptured Baker’scyst. There was one acute foot injury, a first distalphalanx fracture from dropping the sled on a toe.

This patient and one other presented with chronicperoneal tenosynovitis. Three patients presentedwith acute back pain and disc protrusions or an-

nular tears, including one patient who also hadbilateral spondylolysis. In considering spondylol-ysis as a risk of luge, comparison must be made toa background risk of 6% in normal college-aged

controls [18].

Skeleton

Skeleton is a variant of luge, but the solo ath-lete rides on the sled head first, reaching speeds of

up to 80 mph. Steering is done by shifting bodyweight, primarily using the shoulders.

Because of the body position and high speed,there is a high risk of injury. An Olympic hopeful

was killed in training when he ran headfirst intothe blade of another sled. Fortunately, there wereno serious injuries at the Olympics. No imaging

studies showed acute injuries, although negativeplain radiographs were obtained in several pa-tients who had suffered contusions.

Fig. 6. Posterior shoulder dislocation in a snowboarder. (A) Axial FSE T2-weighted image with fat saturation through

the midglenohumeral joint shows avulsion of the posterior labrum (arrow) and edema at the attachment of the posterior

capsule to the humeral head. Edema anteriorly in the humeral head is related to impaction of the humeral head against

the posterior glenoid. (B) Axial FSE T2-weighted image with fat saturation through the inferior portion of the joint

demonstrates a humeral avulsion of the posterior band of the inferior glenohumeral ligament (reverse HAGL). The free

edge of the torn ligament is shown by the arrow.

Fig. 7. Plantar fascia tear occurring during initial phase

of a bobsled race. Sagittal STIR through the hindfoot.

Arrow points to the focal tear in the plantar fascia.


Fig. 8. Shoulder injury in a bobsledder, resulting in SLAP tear. (A) Coronal FSE T2-weighted image with fat saturation

through anterior edge of tendon anchor shows fluid between the biceps tendon and the superior labrum (arrow).

(B) Coronal FSE T2-weighted image with fat saturation posterior to the biceps anchor shows continuation of the

superior labral tear (arrow).

Fig. 9. Anterior dislocation of the shoulder in a speed skater. (A) Axial FSE T2-weighted image with fat saturation

above level of coracoid. Bone marrow edema is seen at the posterosuperior aspect of the humeral head (arrow), and there

is a displaced tear of the anterior glenoid labrum (arrowhead). (B) Axial FSE T2-weighted image with fat saturation

below level of coracoid. Arrow points to the complex tear of the anterior glenoid labrum.

Ice hockey

Ice hockey, as a high-speed contact sport,causes a wide range of injuries, most commonlycontusions, strains, and sprains. Injuries are much

more common during games than during practice.One study of junior league athletes found aninjury rate of 96.1/1000 player-game hours, of

which 51% were due to collisions [19]. Pro-fessional ice hockey teams in Finland had an in-game injury rate of 66/1000 player-game hours

[20].Four ice hockey players presented with acute

knee injuries at the 2002 Olympics. Two of them

had preexisting ACL tears and now suffered acutemeniscal tears. Two had direct blows to the lateralaspect of the knee. In one of these, MR imagingshowed a lateral collateral ligament tear and lat-

eral bone bruise. The second had only a bonebruise of the lateral femoral condyle.

Imaging studies found shoulder injuries in threeice hockey players at the 2002 Olympics: oneanterior glenohumeral dislocation, one acromio-clavicular separation, and one fracture of the

greater tuberosity of the humerus. Two musclehematomas were seen, and there was a single injuryto the ankle, a syndesmosis sprain.

One patient presenting with back pain hadadvanced premature degenerative disc disease.

Speed skaters and figure skaters

Two speed skaters suffered shoulder injuries,one a rotator cuff contusion, and one an anteriordislocation (Fig. 9). MR imaging of the contra-

lateral shoulder in the second patient showedresidua of a prior anterior dislocation on that side.There was only one knee injury, an ACL tear ina speed skater. One speed skater had MR imaging

evidence of tenosynovitis of the tibialis anterior

Fig. 10. Tibialis anterior tenosynovitis in a speed skater. (A) Axial FSE T2-weighted image with fat saturation above

level of tibiotalar joint. Arrow points to intact tibialis anterior tendon, surrounded by abnormal signal material. The

abnormalities extended from above the ankle to the insertion of the tibialis anterior tendon. (B) Axial FSE T2-weighted

image with fat saturation showing distal tibialis anterior tendon surrounded by fluid (long arrow). Patient also had

a thickened, lax anterior talofibular ligament (arrowhead), consistent with old injury. Fluid surrounding the FHL tendon

(short arrow) was believed to represent normal extension of intraarticular fluid into the FHL tendon sheath.


tendon (Fig. 10), and one figure skater had teno-synovitis of the extensor hallucis longus tendon.Tenosynovitis of the anterior tendons of the ankle

is uncommon, and in these cases may be related toimpingement from the athlete’s ice skates.

MR imaging in a figure skater with a history ofrecurrent ankle sprains showed a calcaneonavicu-

lar coaltion with bone marrow edema. Recurrentankle sprains are a frequent presenting complaintin patients with tarsal coalition [21].

Curling

No injuries were seen in Olympic curlers.Reported curling injuries include blisters, ligamentand muscle strains, and contusions [22].

Summary

Injury patterns at the 2002 Winter Olympics

were similar to those in recreational winterathletes, although injury rates were higher. Thehigh rates of injury compared with reported rates

in recreational athletes reflect the intensity of thecompetition and the high speeds of the athletes. Inaddition, rates are artificially elevated because we

were not able to count the number of practice runsby each athlete, only the number of races. Thehighest rates of injuries resulting in positive MR

imaging or plain radiographs were in snow-boarders (28/1000 races), followed by alpine skiers(20/1000).

In all of the winter sports, the most commonly

injured joint was the knee (37 injuries), and themost common knee injury was the ACL tear. In-juries to the foot and ankle were second in

frequency (15 injuries). It is interesting that threeof the ankle injuries were syndesmosis sprains; thismay be an underreported injury in winter sports.

There were 12 injuries to the upper extremity, allbut two to the shoulder. Back complaints werefrequent, but only seven patients had significantimaging abnormalities found in the lumbar spine:

two stress fractures of the pedicles, one acutepedicle fracture, one spondylolysis, and four discprotrusions.

Acknowledgments

My sincere thanks to Dr. Patrick Schamasch,director of the Medical Commission of the In-

ternational Olympic Committee, for his supportand permission to use data from the 2002 WinterOlympics for this article.

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Imaging of stress fractures in the athleteDamon J. Spitz, MD*, Arthur H. Newberg, MD

Department of Radiology, New England Baptist Hospital, 125 Parker Hill Avenue, Boston, MA 02120, USA

Stress reactions and stress fractures represent

a spectrum of soft tissue and osseous injuries thatoccur in response to a changing mechanicalenvironment. Stress fractures occur when ab-normal repetitive stress is applied to normal bone.

They are caused by prolonged periods of unac-customed or strenuous activities, such as runningor marching [2,10,11,17]. Stress-related bone

injuries are common among members of activesociety and account for up to 10% of patients ina typical sports medicine practice. In 17% of

cases, injuries are bilateral, and the incidence ofsustaining a stress fracture approaches 16% inrunners [5]. Stress fractures were originally de-scribed in 1855 before the advent of radiographs.

Since then, numerous publications, especiallyfrom the military ranks, have described theseinjuries [17]. Although stress fractures can occur

throughout the body, they are common in thelower extremities, especially the femoral neck,tibia, and metatarsals [8,9].

Mechanism of injury

Stress fractures occur when normal bone is

subjected to repetitive stress. Although no in-dividual stress is capable of producing a fracture,over time bone fatigue and failure result. Stress is

the force or absolute load applied to a bone thatmay arise from weight-bearing or muscular ac-tion. The force may be applied as an axial, bend-

ing, or torsional load [2,10,11].The precise pathogenesis of stress fracture is

poorly understood; however, there are several

theories to explain the mechanism of these

fractures. According to Radin et al [28], one ofthe major roles of muscle is to minimize the tensilestress on bone. Their experience demonstratesthat soft tissue stabilizing structures, such as

muscles and tendons, decrease bending or tensileforces in bone and increase compressive forces.Because bone is more resistant to force in

compression than tension, the supporting muscleshelp prevent fatigue fractures. When the support-ing structures fatigue, the tensile forces increase,

rendering bone failure more likely. Accordingly,fatigue of muscles in the poorly conditionedathlete creates increased tensile stress on bone,resulting in stress fracture (Fig. 1).

The physiologic response of bone to stress isalso important in the pathophysiology of stressinjury. Bone is a dynamic tissue that requires

stress for normal development, and it undergoesconstant remodeling in response to changingenvironmental forces [2]. Initially, osseous remod-

eling manifests as osteoclastic activity and re-sorption of lamellar bone. This is subsequentlyreplaced by denser, stronger osteonal bone. In

repetitive stress overload, however, the acceler-ated remodeling results in an imbalance betweenbone resorption and bone replacement, leading toweakening of the bone. Continued stress results in

further imbalance, leading to bone fatigue, injury,and fracture. Osseous stress injury is not an all-or-nonephenomenon, but aphysiologic continuum

ranging from normal osseous remodeling, toaccelerated remodeling with fatigue and earlyinjury, to frank stress fracture.

Another explanation of the pathogenesis ofstress fractures relates to increased musclestrength. Under normal conditions when a newstress is applied, muscle tone is achieved more

quickly than bone strengthening. This results in


of North America 2002;40(2):313–31.


E-mail address: [email protected]


doi:10.1016=S1064-9689(03)00021-7


11 (2003) 323–339

a mechanical imbalance, with muscle exertingexcess force on bone, resulting in bone fatigue.

According to Wolff’s law, as the amount ofstress on a bone is increased, progressive de-formity occurs throughout the bone’s elasticrange. As long as the deformity remains within

the elastic range, when the deforming force stops,the bone returns to normal. Beyond the elasticrange, further stress results in plastic deformity

and microfractures. Continued stress results inprogression of microfractures leading to furtherstructural failure [11].

Clinical features

In most circumstances the athlete sustaining

a stress injury is engaged in a vigorous activity towhich he or she is not accustomed. Alternatively,a conditioned athlete may sustain a stress injury

when he or she changes a training regimen,performs a new repetitive activity, returns toactivity too soon after an injury, changes foot-

wear, uses worn-out footwear, changes trainingsurfaces, or in general uses poor training tech-niques. Women athletes with amenorrhea areespecially susceptible to stress injuries of bone [2].

Patients with stress fracture usually have painrelated to their activity. The diagnosis of a stressfracture should be considered in patients present-

ing with pain after a change in activity, especiallyif the activity is strenuous and the pain is in thelower extremities. Classically, the pain is relieved

by rest and then reoccurs when activity isrestarted. As the injury becomes more severe,

the patient may have rest pain and this can bea source of clinical confusion for the treatingphysician. A careful history is important inestablishing the clinical diagnosis. Findings on

physical examination include localized pain,redness, swelling, and warmth. In areas of theskeleton where there is not a thick soft tissue

covering, like the anterior tibia, periosteal newbone may be palpable and tender.

Imaging evaluation

Radiography

In early osseous stress injury and fracture,radiographs may initially be normal and more

sensitive and specific tests, such as MR imagingand bone scintigraphy, may be necessary. Thesensitivity of early fracture detection by radiog-

raphy can be as low as 15%, and follow-upradiographs may demonstrate diagnostic findingsin only 50% of cases [3].

In bones that are predominantly cancellous,such as the calcaneus or femoral neck, radio-graphs demonstrate a line of sclerosis perpendic-ular to the trabeculae representing the fracture

(Fig. 2). In cortical bone, there is typicallyperiosteal reaction, a cortical fracture line, orboth. The radiographic findings depend on when

the images are obtained relative to the spectrum ofosseous remodeling (Fig. 3).

Fig. 1. Mechanism of injury. Muscles play a significant role in reducing the tensile stress across bone. On the left the

telephone pole represents an unsupported bone showing equal tensile and compressive forces. On the right a guy wire

represents the supporting soft tissue structures such as the iliotibial band’s effect on the femur. The tensile or bending

forces are reduced and the compressive forces are increased. Bone is known to be stronger in compression than in

tension. (Adapted from Radin E, Blaha J, Rose R, Litsky A. Practical biomechanics for the orthopedic surgeon. 2nd

edition. New York: Churchill Livingstone; 1992; with permission.)

324 D.J. Spitz, A.H. Newberg / Magn Reson Imaging Clin N Am 11 (2003) 323–339

The differential diagnosis of stress fractures onradiographs includes osteoid osteoma; osteosar-

coma; round cell lesions, such as Ewing’s sar-coma; and Langerhans’ cell histiocytosis. Usuallya careful clinical history and sequential radio-

graphs help differentiate a stress fracture from

a more aggressive lesion (Fig. 4). Patients withosteoid osteoma usually present with a distinct

pain pattern with symptoms often present at nightrelieved by analgesics. In osteosarcoma, the lesionhas a more aggressive appearance with bone

destruction, aggressive periosteal reaction, and

Fig. 3. Second metatarsal stress fracture. Sequential radiographs from left to right in a patient with a stress fracture. The

initial radiograph is negative but radiographs at two weeks show faint periosteal reaction along the medial diaphysis of

the second metatarsal (arrow). At one month there is callous around the fracture (arrows). By three months the stress

fracture has healed.

Fig. 2. Calcaneus stress fracture. (A) Image from a radionuclide bone scan demonstrates marked increase tracer uptake

in the posterior right calcaneus. (B) Several weeks later the lateral radiograph demonstrates a sclerotic line perpendicular

to the trabeculae of the posterior calcaneus. (arrow) This sclerotic line is the characteristic appearance of a stress fracture

occurring in cancellous bone.

325D.J. Spitz, A.H. Newberg / Magn Reson Imaging Clin N Am 11 (2003) 323–339

the presence of tumor osteoid. Cross-sectionalimaging may show a soft tissue mass.

Sequential radiographs are important in eval-uating the evolution of a stress fracture and oftenhelp or eliminate the need for a biopsy. It shouldbe noted that biopsy of a stress fracture is

problematic because the pathologist can mistakethe new bone formation of fracture for a moreaggressive osseous lesion.

MR imaging

MR imaging is an effective diagnostic tech-nique for the evaluation of patients in whom there

is clinical suspicion for stress fracture. Numerousrecent studies have demonstrated the efficacy ofMR imaging in the evaluation of stress injuries tobone [4,14,41]. MR imaging allows depiction of

abnormalities weeks before the development ofradiographic abnormalities and has comparablesensitivity and superior specificity compared with

radionuclide techniques for the detection of

osseous abnormalities [12,29]. MR imaging hasthe additional advantage of demonstrating con-comitant soft tissue injury. MR imaging is non-

invasive, has no ionizing radiation, and is morerapidly performed than bone scintigraphy.

Both resorption and replacement of bonecharacterize the early changes of stress injury to

bone. This is manifest by local hyperemia andedema [12,42]. Because of its high sensitivity forthe detection of edema, MR imaging is an ex-

cellent modality for the detection of early osseousstress injury [2,3,14]. Subsequently, MR imagingclearly depicts the more advanced findings of

cortical bone breakdown and frank stress frac-ture. It is this differentiation between the changesof early stress injury to bone, and later stressfracture, that has predictive value in estimating

the duration of disability, helping to guide therapy[4,14]. In the symptomatic athlete, an early stressinjury may be treated with a short period of rest,

in contrast to the several months required forhealing of an overt stress fracture.

When evaluating for stress injury, MR imaging

parameters should include both a T1-weightedsequence and an edema-sensitive sequence, such asshort tau inversion recovery (STIR) or T2 with

frequency-selective fat suppression. The STIR orfat-suppressed T2 sequences are important fordetection of the earliest changes of stress reaction,such as periosteal, muscle, or bone marrow edema

[36]. The edema, or increased water content,results in high signal intensity against the darkbackground of the suppressed fat [2]. T1-weighted

sequences depict anatomy and more advancedstress-related findings. Imaging should be per-formed in multiple orthogonal planes, with specific

planes designated for particular locations (eg,coronal plane for femoral neck stress fracture).Dedicated surface coils and use of a relativelysmall field of view improve image quality.

Early MR imaging findings in osseous stressinjury begin with periosteal, muscle, or bonemarrow edema that is only appreciated on the

STIR or fat-suppressed T2-weighted sequence. Asinjury becomes more severe, findings includemarrow edema identified on both T2- and T1-

weighted images and signal abnormalities in thecortical bone. Frank stress fractures are diagnosedwhen identifying band-like areas of low signal in

the intramedullary space that may be continuouswith the cortex [23]. The most common patternof a fatigue-type fracture is a fracture line that islow signal on all pulse sequences, surrounded by

a larger, ill-defined zone of edema (Fig. 5). ‘‘The

Fig. 4. Proximal tibial stress fracture. Anteroposterior

radiograph of the left tibia in a 17-year-old female.

There is sclerosis across the medullary cavity represent-

ing the fracture line. There is exuberant periosteal new

bone formation and this appearance could be mistaken

for an aggressive bone lesion. The history and sequential

radiographs are helpful in making a diagnosis of stress

fracture.


fracture line is continuous with the cortex andextends into the intramedullary space oriented

perpendicular to the cortex and the major weight-bearing trabeculae’’ [12].

Fredericson et al [14] have described a contin-uum of MR imaging findings and a MR imaging

classification of osseous stress injury [4]. Grade 1injuries (mild) demonstrate periosteal edema,without focal bone marrow abnormality. Grade

2 injuries demonstrate more severe periostealedema with bone marrow edema detected on T2-weighted images only. Grade 3 injuries demon-

strate moderate to severe edema of both theperiosteum and marrow on both T1- and T2-weighted images. Grade 4 injuries demonstratea low signal fracture line on all sequences, with

changes of severe marrow edema on both T1- andT2-weighted sequences. Using this classification,Fredericson et al [14] studied 14 runners with 18

symptomatic legs (tibia) with radiographs, bonescintigraphy, and MR imaging. In 14 of 18symptomatic legs, MR imaging findings corre-

lated with the technetium bone scan and moreprecisely defined the anatomic location and extentof injury. In their study, patients with grade 1

stress injuries were able to return to running ongrass within 2 to 3 weeks. Patients with grade 2

injuries were able to reach that level in 4 to 6weeks, and patients with grade 3 changes were

notably more symptomatic and were withheldfrom impact running for 6 to 9 weeks. Grade 4injuries (stress fractures) were treated with a castfor 6 weeks followed by 6 weeks of nonimpact

activity. Notably, by the time the pain was presentin the runners during training and persisting withdaily ambulation, there was an 81% incidence of

grade 3 or 4 stress injury. They concluded thatMR imaging is more accurate than bone scan incorrelating the degree of bone involvement with

clinical symptoms, allowing for more accuraterecommendations for rehabilitation and return toactivity [14].

In a more heterogeneous group of patients,

Yao et al [41] examined the prognostic value ofMR imaging in stress injury to bone. Thirty-fivepatients with clinically suspected stress fractures

underwent MR imaging. The MR imaging find-ings were classified according to the MR imagingclassification system proposed by Fredericson et al

[14], and correlated with total duration of symp-toms and time to return to sports activity.Although they were unable to demonstrate the

prognostic value of the MR imaging classificationsystem, they did find that the MR imaging finding

Fig. 5. Distal fibular stress fracture. This long distance runner reported pain over the distal fibula, increasing over

several weeks. (A) Sagittal STIR image of the distal fibula demonstrates extensive bone marrow edema (curved arrow).

There is adjacent periosteal and soft tissue edema and a horizontal low signal fracture line. (B) T1-weighted sagittal

image demonstrates diffuse low signal representing edema within the marrow of the fibula with a low signal horizontal

fracture line (arrow). The findings are in keeping with a grade 4 stress fracture.


of a fracture or fatigue line or a cortical signalabnormality was predictive of a longer symptom-atic period. They also found that muscle edema, by

itself, was predictive of a shorter clinical course.They concluded that the MR imaging finding ofeither a medullary line or a cortical abnormalityseems to indicate a more severe stress injury to

bone, and has prognostic value (Fig. 6) [40].

The term shin splints has been used to describethe clinical entity of activity related lower leg pain,typically associated with diffuse tenderness along

the posteromedial tibia. Bone scintigraphic studieshave concluded that shin splints represent a dis-tinct clinical entity from early osseous stressinjuries [42]. Recent MR imaging studies have,

however, suggested that shin splints are a part of

Fig. 6. Tibial stress fracture. Thirty-four-year-old ultra-marathoner presented with chronic bilateral lower leg pain. (A)

Lateral radiograph of the lower leg demonstrates a horizontal lucent anterior cortical stress fracture (curved arrow) with

adjacent sclerosis. (B) Bone scan demonstrates foci of increased tracer activity uptake in both mid tibiae. (C ) Axial STIR

images of the lower legs in the same patient demonstrates bilateral anterior tibial cortical linear high signal (arrows)

compatible with bilateral stress fractures.


the continuum of fatigue damage in bone[3,14,15]. Gibbon [15] reported MR imaging

findings in 10 professional athletes with clinicalfeatures of shin splints. Medial tibial periostealedema was present in all 10 patients and bone

marrow edema was present in eight patients(Fig. 7). Increased cortical signal reflecting overt

stress fracture was identified in two of the athletes.Fredericson et al [14] have also shown that in allgrades of tibial stress injuries in runners, there is

a consistent distribution of contiguous periostealedema at the origins of the tibialis posterior, flexordigitorum longus, and soleus muscles.

Fig. 8. Multiple stress fractures. Twenty-three-year-old

female runner with amenorrhea presented with a right

proximal femoral stress fracture (curved arrow). Bone

scintigraphy demonstrates multiple foci of increased

uptake in the lower legs and feet (arrows). The patient

had pain only in the right hip, and the other areas of

abnormal uptake represent previous stress fractures.

Fig. 9. Advanced tibial stress fracture (grade 4). Runner

with right tibia pain. Delayed, skeletal phase image of

the lower legs demonstrates an extensive focus of in-

creased tracer uptake in the right mid tibia (arrow).

Fig. 7. Mild osseous stress injury (shin splints). Long distance runner training for the Boston marathon with pain in the

medial right tibia. Axial STIR image of both tibia demonstrates the findings of early osseous stress injury on the right.

There is both periosteal edema (curved arrow) and bone marrow edema (straight arrow). No fracture line or cortical

signal abnormality was identified and the patient was diagnosed with a mild osseous stress injury.


The clinical significance of bone marrowedema depends on the severity of the findings

and the clinical context. The finding of bonemarrow edema on STIR is a relatively sensitivefinding and may be seen very early in the stress

response. Lazzarini et al [22] imaged ankles andfeet of 20 runners and 12 nonrunners with a STIRsequence at 1.5 Tesla (T). Sixteen of 20 of therunners had bone marrow edema compared with 3

of 12 in the nonrunner group (P \ 0.002). Theaverage number of bones with edema was 3.6 inthe runner group and 0.3 in the nonrunner group

(P\ 0.001). All subjects with positive MR imageswere asymptomatic. They concluded that inrunners, bone marrow edema seen on STIR

imaging may be caused by exercise alone.Schweitzer and White [32] studied 12 volun-

teers with STIR images at 1.5 T before and 2

weeks after altered weight bearing achieved withoverpronation of one foot. Changes were seen onthe STIR images in 11 of the 12 volunteers. Mostchanges were a diffuse increase in marrow edema,

usually in the foot on the overpronated side. Intwo of the volunteers the changes resembleda stress fracture.

Fig. 11. Sacral stress fracture. Coronal oblique CT scan

in a 21-year-old college football wide receiver with low

back pain. There is an oblique line of sclerosis in the

upper left sacrum (arrow) representing a stress fracture.

Corresponding bone scan (not shown) demonstrated

increased tracer uptake.

Fig. 10. Shin splints. Twenty-three-year-old soccer player with bilateral shin pain. Skeletal phase of a bone scan of the

lower legs demonstrates long, linear foci of increased tracer uptake along the tibial cortices bilaterally (arrows). The flow

and soft tissue phase images were normal.


The finding of bone marrow edema by itself is

not a finding specific to stress injury. Manypathologic conditions may cause bone marrowedema and reference should always be made to theclinical history. Differential considerations for the

bone marrow edema pattern, in addition to stressinjury, include acute bone bruise, fracture, oste-omyelitis, avascular necrosis, transient osteopo-

rosis, and tumor. Just as radiographs may

demonstrate findings suggesting the diagnosis of

an aggressive lesion in patients with stressfracture, so too can the MR imaging findings ofextensive edema appear aggressive and misleadingand correlation to the clinical setting helps to

avoid this pitfall. Additionally, the detection ofmore advanced stress-related changes, such as thepresence of a fracture line, ensures the diagnosis

of fracture.

Fig. 12. Tibial stress fracture. (A) Anteroposterior radiograph of the right tibia demonstrates cortical thickening of the

tibia medially. There is an oblique fracture line identified in the cortex (arrow). (B) Axial CT scan through both lower legs

demonstrates benign periosteal new bone formation along the medial aspect of the right tibia. (curved arrow) In this

patient with an atypical pain pattern for stress fracture, the CT scan was obtained to rule out an osteoid osteoma. There

is no radiolucent nidus identified.


Bone scintigraphy

Bone scintigraphy is an effective modality inthe evaluation of athletes with clinically suspectedosseous stress injuries. Before the advent of MR

imaging it had been the gold standard forevaluating stress fractures [2] and studies havedescribed its high sensitivity in detecting stress

fractures [37]. Bone scintigraphy demonstratesabnormal findings early in the continuum of thestress response in bone, by detecting the increased

bone metabolism and osteoblastic activity associ-ated with osseous remodeling (Fig. 8). Scintigra-phy is typically abnormal 1 to 2 weeks or more

before the radiographic changes of stress fracture.Bone scintigraphy should optimally be per-

formed using a three-phase technique, because thistechnique can help differentiate between soft tissue

injury and osseous injury. In the first phase, the

blood flow phase, imaging is performed byacquiring dynamic 2- to 5-second images over thearea of clinical concern for 60 seconds after the

bolus intravenous injection. In the second phase,the blood pool or soft tissue phase, imaging isacquired immediately after for time (5 minutes) orcounts (300 k) [37]. Imaging at multiple angles in

relation to the symptomatic region helps tolocalize abnormalities on these soft tissue–phaseimages. The final phase of imaging is the delayed

skeletal phase. These images should be acquiredapproximately 2 to 4 hours after injection tomaximize clearance of the radiopharmaceutical

from the overlying soft tissues. Medial andposterior views are required for optimal assess-ment of the tibia, whereas plantar views are

Fig. 13. Ulnar stress fracture. Nineteen-year-old college weightlifter with forearm pain. (A) Radiograph of the forearm

demonstrates lamellated periosteal reaction in the mid ulna (curved arrow). (B) Bone scan demonstrates extensive tracer

uptake in the mid ulnar diaphysis (arrow). Follow-up radiographs demonstrated healing of the fracture.


mandatory to evaluate fully the tarsal and meta-tarsal bones. Medial and lateral views of the feetare important for evaluation of the tarsal bonesand differentiating between the first metatarsal

head and sesamoid bones [12]. Single photonemission CT may be helpful in the pelvis and isespecially helpful in the lumbar spine for the

diagnosis of spondylolysis.In the early stages of osseous stress injury,

scintigrams demonstrate ill-defined areas of

slightly increased tracer uptake. As injury becomesmore severe, scans exhibit more intense and focaltracer localization [30]. Based on their experience

of the bone scintigraphic findings in 310 militaryrecruits suspected of having stress fracture, Zwaset al [42] described a scintigraphic classificationof stress fractures ranging from grade 1 (mild) to

grade 4 (severe). Grade 1 lesions are small ill-defined foci of increased tracer with mildly in-creased activity in the cortical region. Grade 2

lesions are larger lesions with well-defined elongat-ed areas of activity with moderately increasedactivity. Grade 3 lesions are wide fusiform lesions

with highly increased activity in the corticomedul-lary bone. Grade 4 injuries are wide extensivelesions with increased activity in the transcortico-medullary region (Fig. 9). Eighty-five percent of the

lesions in their patients were classified as mild andshowed early and more complete resolution on

follow-up studies after treatment as compared withthe severe grades. Long-term observations of thescintigraphs in their patients revealed progression

of lesions from mild to severe in those cases leftuntreated, and regression and healing from severeto mild in cases diagnosed and treated. They

concluded that early recognition of mild scinti-graphic patterns representing the beginning ofpathologic bone response to stress enabled promptand effective treatment to prevent progression of

lesions, protracted disability, and complications.Acute stress fractures typically demonstrate

abnormal tracer activity on all three phases of the

bone scan. Soft tissue injuries are characterized byincreased uptake in the first two phases only. Shinsplints are typically positive on only the delayed

images, demonstrating long, linear foci of in-creased tracer uptake along the posterior cortex ofthe tibia (Fig. 10) [12].

Although false-negative bone scans have been

reported in patients with tibial stress fracture [25],bone scintigraphy has very high sensitivity. De-spite this high sensitivity, bone scintigraphy lacks

specificity and such conditions as tumors, in-fection, and infarction may mimic stress injury.

Fig. 14. Bilateral medial malleolar stress fractures. Twenty-three-year-old professional basketball player with bilateral

ankle pain (A) Radionuclide bone scan demonstrates increased tracer uptake in the left medial distal tibia. There also is

uptake in the right medial malleolus representing a known previously diagnosed stress fracture. (B) Coronal CT through

both ankles demonstrates a fracture line in the left medial malleolus (arrow). The sclerotic right medial malleolus

represents a healing fracture (curved arrow).


Additionally, although scintigraphy may be usefulin the initial staging of bone injury, it is less usefulfor follow-up because abnormal uptake may

persist for several months [2].

Computed tomography

CT is limited in its ability to detect early

osseous stress injuries, and is less sensitive thanbone scintigraphy and MR imaging. It does,however, have a role in more advanced injuriesand injuries in specific locations where radiogra-

phy is limited. CT is particularly well suited forstress fractures of the tarsal navicular; longitudinalstress fracture of the tibia; pars interarticularis

stress fractures (spondylolysis); and stress frac-tures in the sacrum (Fig. 11).

CT also may help problem solve when thereare equivocal findings on radiographs, MRimaging, or scintigraphy. The value of CT in this

regard lies in the detection of a discrete lucent orsclerotic fracture line or periosteal reaction (Fig.12). CT is also extremely helpful in differentiat-ing between stress fracture and osteoid osteoma,

because both entities may be hot on bone scan,show edema at MR imaging, and demonstratesclerosis on radiographs. CT, however, detects the

radiolucent nidus of osteoid osteoma.CT has also proved valuable in the diagnosis of

pediatric stress fractures. Initial radiographs may

demonstrate marked periosteal proliferation,which may mimic tumor. The CT demonstrationof endosteal bone formation in these cases oftenleads to the correct diagnosis [2,18].

Fig. 15. Tarsal navicular stress fracture. (A) Coronal CT scan through the right and left midfoot demonstrates a right

tarsal navicular stress fracture in this high school senior basketball player recruited to play division I basketball. The CT

demonstrates the sagittal orientation of this fracture. (B) Repeat coronal CT 10 months later shows almost complete

fracture healing (arrow). The patient was asymptomatic at this time.


Sites of injury

Although most common in the lower extrem-ity, stress injury to bone and stress fractures have

been reported in nearly every bone in the body[10,34]. Stress fracture sites in the upper extremityinclude the ulna (Fig. 13), humerus, carpal bones,

and ribs. Lower-extremity stress fractures can alsooccur anywhere and include the pubic symphysis;lumbar spine (spondylolysis); femur; tibia; distal

fibula; medial malleolus (Fig. 14) [31]; calcaneus;tarsal navicular; metatarsals; and sesamoids.Sacral fatigue fractures have also been recognizedin runners [7,24].

Tarsal navicular stress fractures

Navicular stress fractures usually occur inelite athletes including runners; gymnasts; basket-

ball players; and football players, typically line-backers. In addition, this injury has been seen inathletes that practice and play extensively on anartificial turf surface, including football and

women’s field hockey. The correct diagnosis ofa navicular stress fracture is often delayed forseveral months, partly because the clinical onset is

insidious with nonspecific signs and symptomsand also because these stress injuries are notevident on radiographs in most cases [16,21]. The

interval between the onset of symptoms and thediagnosis may be from 7 weeks [39] to 4 months[20], but may be much longer in some patients.

Clinically, patients report pain along the dorsalmedial aspect of the midfoot associated with run-ning [6,38]. Patients complain of ill-defined footsoreness or cramping that increases during ath-

letic activity, and there is often pain to palpationalong the medial longitudinal arch or on thedorsum of the foot [27]. Many patients with an

incomplete fracture can continue to jog or evenrun especially if the forefoot is not used in footstrike [13]. Sprinting and jumping, however, are

typically followed by pain and limp.Navicular stress fractures are treated with cast

immobilization [20]. This treatment results in

a successful outcome in 80% of patients and mostathletes have a return to sports in 5 to 6 months[20].

Most navicular stress fractures occur in the

middle third of the navicular. Microvascularstudies show that there is relative avascularity ofthe middle third of this bone. These findings

suggest that repetitive cyclic loading may result infatigue fracture through the relatively avascularcentral portion of the navicular [39]. The consis-

tent site of the fracture seems to correspond withthe plane of maximum shear stress especiallyduring plantar flexion combined with pronation.

Navicular stress fractures may be incomplete

or complete. Incomplete fractures usually involvethe dorsal 5 mm of the navicular adjacent to thetalonavicular joint, an area that is difficult to

evaluate on radiographs [27].There may be associated foot anomalies in

patients with navicular stress fractures. These

include a short first metatarsal, a relatively longsecond ray, metatarsal hyperostosis, or an asso-ciated stress fracture of the second through fourth

digits [27]. A short first metatarsal or long secondmetatarsal may tend to accentuate shear stressbecause of the greater force being transmittedthrough the second metatarsal and intermediate

cuneiform [13].

Fig. 16. Tarsal navicular stress fracture. (A) Coronal CT

image at the level of the midfoot demonstrates an un-

united stress fracture of the navicular (arrow). The

fracture extends the full length of the navicular. (B)

Corresponding coronal STIR image demonstrates high

signal at the fracture site and surrounding bone marrow

edema.


The imaging of suspected stress fracture of thetarsal navicular should begin with radiographs ofthe foot. Historically, bone scans and tomography

were recommended as the diagnostic imaging testsof choice [27]. Currently, however, the authorsbelieve that if suspicion is high, CT or MR

imaging are better initial imaging modalities.Because all of these fractures are linear, in thesagittal plane, and are located in the central thirdof the navicular, CT imaging performed parallel

and perpendicular to the midfoot clearly demon-strates the fracture line (Fig. 15). New multisliceCT scanners allow image acquisition in one plane

with subsequent multiplanar reformatting of thedata set.

MR imaging detects the bone marrow edema

associated with osseous stress reaction that maybe present before a fracture line is visualized andMR imaging is a good imaging choice if there is

suspicion of early injury. Coronal, sagittal, andaxial imaging sequences are recommended, and atleast one fat-suppressed sequence should beperformed. In the authors’ experience with MR

imaging of this fracture, the fracture line is bestseen on the coronal images (Fig. 16).

Because radiographs are often not sensitive

enough to detect the original fracture, it is clearthat this imaging modality does not providea reliable indicator of fracture healing. Once

a fracture is identified, CT should be used toassess fracture healing. Imaging both feet with CT

allows an internal comparison and may alsodetect an asymptomatic or unsuspected contralat-eral fracture. Again, both axial and coronal

images are valuable for the assessment of fracturehealing [21].

The CT appearance of healing fractures does

not necessarily mirror clinical union. In general,the imaging evidence of navicular fracture healinglags behind the clinical picture [20].

Stress fracture of the femoral neck

Stress fracture of the femoral neck in the

athlete is an injury with potentially severe con-sequences and prompt diagnosis is necessary toprevent complications. An inadequately treated

stress fracture can progress to a complete fractureand result in prolonged disability with furthercomplications including nonunion and osteone-crosis of the femoral head. The clinical diagnosis

of a hip stress fracture may be difficult. Often thepain pattern is atypical and pain may be referredto the knee [5]. The team physician or coach must

have a high clinical index of suspicion for thisfracture and should pursue additional imagingtests even if radiographs are normal [26].

Femoral neck stress fracture may occur on themedial (compression) side of the femoral neck orthe lateral (tensile) side of the neck. Most athletic-

induced stress fractures occur medially where,fortunately, there is less danger of the fracturedisplacing. Usually, these patients are managed

Fig. 17. Stress fracture of the right femoral neck. Twenty-one-year-old female athlete with right hip pain and normal

radiographs. (A) Coronal T1 weighted image demonstrates low signal intensity area along the medial aspect of the right

femoral neck. (B) Coronal STIR image demonstrates bright signal intensity in the femoral neck, and a fracture line in the

medial aspect of the femoral neck (arrow).


conservatively and do not need cannulated screwfixation. In a noncompliant patient, however,operative intervention may be necessary.

Whereas radiographs are usually normal at the

time of presentation, radionuclide bone scanningis usually positive. After several weeks, the radio-graphs may show a linear area of ill-defined

sclerosis perpendicular to the primary trabeculaeof the medial aspect of the femoral neck of thesymptomatic hip. This faint linear sclerosis can be

difficult to visualize, and careful inspection of theradiographs and comparison with the contralat-eral hip are helpful.

MR imaging is the diagnostic test of choice indetecting and following stress fractures of thefemoral neck. Stress fractures are diagnosed onMR imaging as a rounded area of decreased signal

intensity on the T1-weighted sequence withcorresponding bright signal intensity on T2 orSTIR sequences, extending a variable distanceacross the femoral neck from its medial margin

[35]. If a fracture line is present on MR imaging itappears as a line of decreased signal intensityperpendicular to the cortical margin and is seen

on all the coronal imaging sequences (Fig. 17).In one study, 7 of 10 patients with non-

displaced medial (compressive side) femoral neck

stress fractures showed return of the normal bonemarrow signal intensity on STIR images at 3months following the fracture diagnosis. In

another two patients, the MR image returned tonormal by 6 months [35]. Full clinical healing maynot be synonymous with MR imaging edemasignal resolution. Slocum et al [35] hypothesize

that in patients imaged 6 months following a hipstress fracture, persistent diffuse increase in signalis abnormal and may represent new or ongoing

injury.

Longitudinal tibial stress fracture

Tibial stress fractures may account for up to73% of all stress fractures [40]. Most tibial stressfractures are identified by the development of

a fracture line in the cortex of the proximal ordistal tibia. Often, a variable amount of corticalthickening or periosteal reaction is present.

Alternatively, jumping athletes, such as basketballplayers and ballet dancers, may develop single ormultiple horizontal anterior tibial striations best

visualized on lateral radiographs.An unusual type of stress fracture is the

longitudinal tibial stress fracture [33]. This fractureis oriented in the vertical plane and may involve

the anterior or posterior tibial cortex. Patientsusually have normal radiographs, and axial CT orMR imaging demonstrate the fracture line (Fig.

18). Periosteal new bone formation can be detectedand there may be some focal endosteal sclerosisadjacent to the fracture [19]. MR imaging has the

advantage of demonstrating the presence of bonemarrow or soft tissue edema if present. In mostcases, the fracture defect extends through a single

cortex, with abnormal signal in the marrow cavityand in the adjacent soft tissues [40].

Radionuclide imaging demonstrates a longarea of increased uptake in the distal tibia [33].

This reflects the length of this longitudinal type ofstress fracture. The bone scan can be misleadingespecially in an older patient where a more

aggressive lesion is often suggested by the bonescan appearance [1]. It should be noted that

Fig. 18. Longitudinal stress fracture of the distal tibia.

(A) Bone scan demonstrates increased uptake of the

tracer diffusely in the distal tibia. (B) Axial T1 weighted

fat suppressed MR images after the administration of

Gadolinium demonstrate periosseous and bone marrow

enhancement and an anterior longitudinal tibial cortex

fracture (arrows).


although this stress fracture is seen in athletes,a small number of these patients may be older andnonathletic.

Summary

Osseous stress fractures and stress reactionsrepresent the effect of abnormal repetitive stress onnormal bone. An accurate and thorough clinicalhistory and sequential radiographs often suffice to

make the diagnosis especially when the fractureoccurs in one of the common locations, such as thetibia, metatarsals, or calcaneus. In cases that are

atypical in location or clinical presentation theauthors rely more on MR imaging, radionuclidebone scanning, and occasionally CT. MR imaging

detects early changes of osseous stress injury andallows precise definition of anatomy and extent ofinjury, and is the preferred modality for evaluating

the continuum of osseous manifestations of stressinjury. MR imaging is useful in evaluating shinsplints, early osseous stress injuries, and overtstress fracture. In the elite athlete prompt diag-

nosis and early rehabilitation are the goals.

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Imaging of sports-related muscle injuriesRobert D. Boutin, MDa,*, Russell C. Fritz, MDb,

Lynne S. Steinbach, MDc

aMed-Tel International, 3713 Lillard Drive, Davis, CA 95616, USAbNational Orthopedic Imaging Associates, 1260 South Elisio Drive, Greenbrae, CA 94904, USA

cDepartment of Radiology and Orthopedics, University of California at San Francisco,

505 Parnassus, San Francisco, CA 94143, USA

Physical activity is associated with good healthand long life. In particular, exercise is correlated

with a substantially reduced risk of fatality fromsuch major killers as heart disease [222] and stroke[72,114]. Investigators also have proposed thatexercise has salutary effects in preventing diseases

as diverse as cholelithiasis and cancers of thecolon, breast, uterus, and prostate [208]—all whiletending to improve one’s sense of well-being [32].

Although exercise does have proved healthbenefits, overzealous activity is a common causeof injuries to muscle that may result in pain and

disability.This article focuses primarily on MR imaging

as the imaging test of choice for evaluating sports-

related muscle injuries. Although the authorsrecognize the usefulness of other imaging techni-ques (eg, sonography), it is their experience thatMR imaging is the most versatile and robust of all

radiographic methods for examining injured ath-letes. After discussing practical MR imagingtechniques used for imaging muscle, the most com-

mon sports-related muscle injuries are reviewed.

Practical MR imaging techniques

Routine MR imaging protocol

Although recognizing that each patient isunique, certain generalizations may be helpful in

designing an appropriate MR imaging protocol.As an absolute minimum, eachMR imaging exam-

ination generally includes at least two orthogonalplanes and pulse sequences. In addition to therequisite axial plane, the second long-axis plane isgenerally sagittal (when evaluating abnormalities

at the anterior or posterior aspect of an extremity)or coronal (when evaluating abnormalities at themedial or lateral aspect of an extremity). At least

one of these pulse sequences should use a fat-sup-pression technique (Fig. 1).

For example, when evaluating a suspected

rectus femoris strain in the anterior thigh on a 1.5-TMR imaging unit, an abbreviated protocol usingfour pulse sequences might begin with sagittal T1-

weighted and inversion recovery (IR) fast spin echo(FSE) images to show the big picture, the longitu-dinal extent of the abnormality. In addition, twoaxial series are obtained: one with and one without

fat suppression. The images acquired with fat-suppression can use a long TR (3000 to 4000milliseconds) and intermediate TE (40 to 60 milli-

seconds). These fat-suppressed proton densityimages are adequatelyT2-weighted todetect patho-logic changes in muscles and other structures in a

reasonable amount of time without compromisingthe signal-to-noise ratio. These images, sensitivefor most pathologic changes, can be compareddirectly with corresponding axial images that are

intended for high-resolution display of anatomicstructures. These ‘‘anatomic’’ axial images maybe either T1-weighted or FSE proton density im-

ages (with a relatively long TR of 2000 to 3000milliseconds and a short TE of 25 to 40 milli-seconds) [85].


of North America 2002;40(2):333–62.



doi:10.1016=S1064-9689(03)00022-9


11 (2003) 341–371

Supplemental scans

Gradient echo imagingGradient echo sequences accentuate certain

paramagnetic effects. This ‘‘blooming’’ effect may

indicate the presence of hemosiderin, metallic for-eign bodies, or gas, and help in honing a differen-tial diagnosis. Indeed, these paramagnetic effects

may be so conspicuous that low-resolution local-izer images may be sufficient to demonstrate thesedistinctive findings.

Fast gradient echo images have been used forhigh temporal resolution to study anatomic andpathologic changes in muscle. For example, musclecontraction during the MR imaging examination

may demonstrate retraction of a torn muscle orherniationof amuscle througha fascial defect. Cine

MR imaging has been described as a method of

diagnosing particular entrapment neuropathies,such as tarsal tunnel syndrome that may be causedby a hypertrophied accessory soleus muscle [195].

Gadolinium enhancementThe administration of gadolinium-based con-

trast material generally is not necessary. Muscle

disorders caused by recent trauma, inflammation,and neoplasm generally are displayed conspicu-ously with fat-suppressed T2-weighted or IR-FSE

images. Occasionally, intravenous gadolinium ad-ministration may be helpful in assessing injuries tothe muscles of athletes [73,150,159]. In particular,contrast-enhanced T1-weighted images have been

advocated when a clinically suspected muscle in-jury is not visualized on T2-weighted and IR-FSE

Fig. 1. Calf hematoma. These MR sequences are routinely used in the axial and longitudinal planes. Coronal T1-

weighted (A), axial T1-weighted (B), and axial FSE fat-suppressed T2-weighted (C) MR images demonstrate a hematoma

in the region of the gastrocnemius. Note the elevated signal intensity within the hematoma on T1-weighting (A) and (B).

There is low signal intensity hemosiderin within the hematoma (arrows) and in the capsule on T1- and T2-weighted

studies.

342 R.D. Boutin et al =Magn Reson Imaging Clin N Am 11 (2003) 341–371

sequences. Detection of torn muscle fibers may bemore conspicuous after gadolinium administra-tion, particularly when there is extensive hemor-rhage and edema [159]. Several cases have been

reported in which professional athletes had musclestrains thatwere not diagnosedonT2-weighted andIR-FSE images, but were visualized on contrast-

enhanced T1-weighted images [73].

Exercise enhancementAfter amuscle is exercised, acute elevation in T2

signal intensity occurs [79], a phenomenon that hasbeen termed exercise enhancement. This hyper-intensity onT2-weighted images seems to be caused

by increased water content in muscle after exercisethat is mostly extracellular in location [197,231].Extracellular water in muscle has a long T2,

whereas intracellular water in muscle has a shortT2 [54,141]. Signal intensity changes are onlyslightly the result of increased osmolarity causedby lactate and may be independent of blood flow

[19,81,198].MR imaging with exercise enhancement has

been used experimentally in assessing muscle re-

cruitment during exercise to optimize sports train-ing and physical therapy programs. For example,when comparing trained and untrained athletes,

MR imaging can document differences in musclerecruitment by showing obvious disparities in thelocation, extent, and degree of T2 signal intensity

changes induced by exercise [101]. Furthermore,after completion of a training program, MR im-aging demonstrates that individuals performinga given exercise use less muscle volume [196], and

that the exercise-induced T2 hyperintensity in mus-cle is reduced [51]. Of greatest practical importanceto practicing radiologists, however, is awareness

that spurious increased signal intensity on T2-weighted and IR-FSE MR images may occur ifimaging is performed within 30 minutes after exer-

cise [238].

Sports-related injuries

The myotendinous unit in athletes may beavulsed, strained, fatigued, contused, lacerated,

herniated, devitalized, or denervated [57,71,235,236]. When an excessive stretching force is applied,the weak link in the chain formed by muscle,tendon, and bone tends to vary depending on the

age of the individual. In children, injury caused byexcessive tension on the muscle-tendon-bone chaintends to result in apophyseal avulsion fractures

because the weak link is located at the physeal

(growth) plate. In young adults, biomechanicalfailure tends to target the interfacebetweenamuscleand its tendon. In older adults with tendonosis,overload of the myotendinous unit commonly

results in fibers tearing at sites that are structurallyweakened by tendon degeneration. Interestingly,conservative treatment of a purely tendinous injury

generally has aworse prognosis than an incompletetear located at the myotendinous junction [200].Although exceptions to these generalizations do

occur, imagers should be aware that the patient’sage tends to influence where a strain-type injuryoccurs in the chain of bone, tendon, and muscle.

Apophyseal avulsion injury

In skeletally immature individuals, the weakestbiomechanical link tends to be the apophysealgrowth plate. A displaced avulsion fracturefragment generally can be recognized with ease

on radiographs. Radiographs may be interpretedas negative in children, however, when an apoph-yseal avulsion is essentially nondisplaced or when

the apophysis is unossified. In such cases, anadvanced imaging technique, such as MR imag-ing, may prove helpful (Fig. 2). In the subacute or

chronic setting, an avulsion injury potentially mayresemble a neoplastic or infectious process, es-pecially when no history of trauma is provided

[236].Knowledge of the major tendinous attach-

ments to bone is imperative in achieving thecorrect diagnosis, and avoiding misdiagnosis of an

osteosarcoma or osteochondroma. The pelvis, forexample, has many apophyses, and is a commonlocation of avulsion fractures. The single most

common site of avulsion is at the ischial apophysis(Fig. 3). In a small minority of cases, avulsioninjuries are multiple at the time of presentation.

TreatmentNondisplaced apophyseal avulsive injuries usu-

ally heal with conservative therapy. Surgerymay be

considered with a recent apophyseal avulsiondisplaced more than 2 cm. With old avulsions,surgical excision of a malunited or hypertrophic

fragment may provide relief of pain in somepatients [134].

Myotendinous strain injury

Myotendinous strain or tear results from

excessive stretch, especially while the muscle isbeing activated. Such strain injuries typicallyoccur when a powerful muscle contraction is

343R.D. Boutin et al =Magn Reson Imaging Clin N Am 11 (2003) 341–371

combined simultaneously with forced lengthening

of the myotendinous unit. Strains tend to occur inmuscles that cross two joints; have a high pro-portion of fast twitch fibers; and undergo eccen-

tric contraction (ie, stretch during contraction).As such, the most commonly strained muscles inthe extremities include the rectus femoris, ham-

strings, and gastrocnemius muscles (Fig. 4).Eccentric contraction of certain muscles that do

not cross two joints also may result in strain injury

(eg, the hip adductors, especially the adductorlongus muscle) (Fig. 5) [113,121,204,234,254].

The degree of strain may be graded along

a spectrum of injury, from mild (first-degree),to moderate (second-degree), to severe (third-degree). This grading system is used to facilitate

communication and research. Low-grade injuriesare more common than high-grade injuries. For

Fig. 2. Minimally displaced avulsion of the medial elbow apophysis not seen on conventional radiographs. Coronal T1-

weighted (A) and fat-suppressed FSE T2-weighted (B) MR images reveal abnormal signal intensity within the

synchondrosis between the humerus and the medial epicondyle, most evident as high signal intensity on the T2-weighted

image (arrow).

Fig. 3. Displaced ischial apophyseal avulsion injury. Axial gradient-echo MR image shows the fragment separated from

the rest of the ischium with high signal intensity edema/hemorrhage between the two osseous structures (arrow).


example, in a retrospective study of 431 pro-fessional football players with hamstring injuries

[142], 324 (75%) of the injuries were first-degreestrains. Second- or third-degree injuries wereobserved in 107 players (25%), with 58 players(13%) sustaining severe injuries with a discrete,

palpable defect in the hamstring muscle.

First-degree strainMild strains are characterized by microscopic

injury to the muscle or tendon, typically with lessthan 5% fiber disruption. No significant loss in

strength or range of motion is observed clinically.With MR imaging in the acute setting, edema

and hemorrhage located at the myotendinous

junction creates high signal intensity focally ordiffusely on T2-weighted or IR-FSE images (Fig.6). This edema and hemorrhage may track alongmuscle fascicles, creating a feathery margin. In

addition, a rim of hyperintense perifascial fluidmay track around a muscle belly or group of

muscles. Perifascial fluid or edema is common,occurring in up to 87% of athletes with acutepartial tears [58]. No architectural distortion ofthe muscle or tendon is present with first-degree

strains. Pain and imaging abnormalities resolvewith appropriate rest from aggravating activities.

Second-degree strainModerate strains may be defined as a partial-

thickness (macroscopic) tear, with continuity of

some fibers at the site of injury. Partial tears maybe subclassified as low-grade injuries if less thanone-third of fibers are torn; moderate if one-third

to two-thirds are torn; and high-grade if morethan two-thirds are torn [52]. Partial fiber dis-ruption may be associated with some loss ofstrength.

Fig. 4. Second-degree strain of the rectus femoris muscle in a soccer player. Axial T1-weighted MR image (A) does not

reveal the strain. The axial FSE T2-weighted MR image (B) shows a high signal intensity lesion within the rectus femoris

muscle (arrow). This lesion rim enhances on the postintravenous gadolinium fat-suppressed T1-weighted MR images (C)

(arrow), consistent with internal seroma/hemorrhage.


The MR imaging appearance varies with theacuity and severity of the partial tear. In the acutesetting, high signal intensity on T2-weighted or

IR-FSE images reflects the extent of edema andhemorrhage (see Fig. 4). Hematoma at the myo-tendinous junction is highly characteristic of

second-degree strain injuries [183]. Perifascial fluidalso is common in this situation. In the setting ofan old second-degree strain, the presence of hemo-

siderin or fibrosis may cause low signal intensityon T2-weighted images. Diminished caliber of themyotendinous unit at the site of injury also may beobserved if healing has been incomplete.

Treatment of second-degree strains is gener-ally conservative. Management includes activity

modification, physical therapy, ice, massage,therapeutic ultrasound, electrical stimulation, andnonsteroidal anti-inflammatory medications. In-

tramuscular injection of corticosteroid solution(eg, 1 mL [4 mg] dexamethasone with 3 mL of 1%lidocaine) may be effective, but it is highly

controversial [142].Most of these strains resolve clinically within

approximately 2 weeks, although some of these

injuries are associated with persistent pain andincreased susceptibility to recurrent strain. Giventhat a myotendinous unit is significantly more sus-ceptible to injury after an initial strain injury

[87,242], imaging may provide objective informa-tion regarding the status of recovery. In particular,

Fig. 5. Adductor muscle strain. Axial fat-suppressed FSE T2-weighted (A) and coronal fat-suppressed FSE T2-weighted

(B) MR images show a retracted, grade-three tear of the adductor longus muscle (arrows).


the presence of persistently altered signal intensityin strained muscles may define a period ofvulnerability to reinjury, despite clinical resolu-

tion of symptoms [82,100,242].

Third-degree strainSevere strains are characterized by complete

musculotendinous disruption, with or without re-traction. Retraction of fibers may result in a pal-pable defect or a focal soft tissue mass. Physical

examination usually reveals loss of strength in theaffected muscle group.

Accurate clinical diagnosis of injury severity can

be hampered in at least three ways. First, clinicalattempts to palpate an acutemyotendinous rupturemay be frustrated by patient guarding, swelling,hematoma, or the presence of a deeply situated in-

jury. Second, muscle weakness, which is most char-acteristic of a complete rupture, may be masked byrecruitment of synergistic muscles during clinical

strength testing. Third, pain and spasm in a patientwith a low-grade strainmay result in themisleadingimpression of a high-grade tear owing to weakness

in the acute clinical setting.MR imaging demonstrates complete disconti-

nuity of fibers, commonly with fiber laxity. A

hematoma often is seen in the gap created by anacute tear (Fig. 7). Surgery may be indicatedoccasionally for loss of function after a completerupture in the acute setting, or for persistent pain

and functional limitations that may be causedby scarring and adhesions in the chronic setting[31,135,213]. Muscular atrophy begins to develop

within 10 days after immobilization and may beirreversible by 4 months [34].

Hematoma and pseudotumor appearanceHematomas are common after a myotendinous

injury, and may be predominantly intramuscularor intermuscular in location. Intramuscular he-matomas often resorb spontaneously over a period

of 6 to 8 weeks [71]. Most of the intramuscularhematomas that have been evaluated with MRimaging between 2 days [65] and 5 months [59]

after injury display characteristics of methemo-globin, with increased signal intensity on bothT1- and T2-weighted images (Figs. 1, 8) [57].

Occasionally, serous-appearing fluid from a hema-toma may linger within a connective tissue sheath,creating an intramuscular pseudocyst (Fig. 9)

[107].With an equivocal or remote history of

trauma, imaging may be indicated to assess asoft tissue mass that is suspected of being neoplas-

tic clinically [115,183,212,244,259]. Pseudotumorsoccurring after a muscle strain have been reportedmost commonly to involve the rectus femoris, but

may be observed at other sites, such as the semi-membranosus or semitendinosus (Fig. 10). MRimaging may show a ruptured tendon with

retraction or an ill-defined signal intensity abnor-mality at the myotendinous junction that may beinterpreted as a soft tissue neoplasm, such as a fib-rous tumor or sarcoma [212,244]. Histologically,

such abnormal signal intensity often correspondsto the presence of fibrosis, muscle fiber degen-eration, and chronic inflammatory cells [244].

Differentiation between a simple hematomaand a hemorrhagic neoplasm may be difficult insome patients both clinically and with imaging.

Fig. 6. First-degree strain of the flexor carpi radialis muscle in the forearm. Axial FSE T2-weighted image shows the

feathery edema pattern without architectural distortion (arrow).


Administration of contrast material aids in ex-

cluding a neoplasm when the lesion in questionshows no enhancement. Conversely, the presenceof an enhancing nodule in a muscle lesion may

suggest the diagnosis of a neoplasm rather thana hematoma [147]. Three potential diagnostic pit-falls must be recognized, however, when inter-

preting the enhancement of a focal lesion afterintravenous administration of gadolinium con-trast material. First, contrast enhancement ispossible in the fibrovascular tissue of an evolv-

ing hematoma, potentially making differentiationfrom neoplasm difficult [132]. Second, gadoliniummay diffuse slowly into a fluid-filled space, such as

a hematoma or abscess. Consequently, imagingshould be performed promptly after contrast ad-ministration to avoid spurious enhancement

within a mass that falsely might suggest it to besolid. Third, minimal or mild enhancement maybe observed in a myxoid lesion (eg, intramuscular

myxoma or myxoid liposarcoma), which thenmay be confused with a cyst or a lesion with acystic component [131]. When the diagnosis of a

probably benign hematoma is in doubt, clinical

correlation and a follow-up MR imaging exami-nation may be indicated to establish appropriateevolution of the abnormality.

Strain injury of specific muscles: pectoralis major,hamstring, and gastrocnemius muscles

Pectoralis major muscleThe pectoralis major is the largest, most

superficial muscle in the anterior chest wall[15,45,52,139,175]. This fan-shaped muscle origi-nates primarily from the medial half of the clavicle,the sternum, and the first six costal cartilages. The

clavicular and sternal heads converge as they passlaterally, generally producing a bilaminar tendonthat inserts into the lateral lip of the humeral

bicipital groove. The pectoralis major musclefunctions to adduct, flex, and internally rotate thehumerus. Pectoralis major tears most commonly

occur while the arm is abducted during eccentriccontraction (eg, in weight lifters) or during a directblow (eg, in a motor vehicle accident).

Fig. 7. Third-degree strain (complete tear) of the biceps tendon at the elbow with significant retraction and fluid-filled

gap consisent with a hematoma. Sagittal fat-suppressed FSE T2-weighted (A) and fat-suppressed T1-weighted image (B)

following intravenous gadolinium reveal the fluid-filled rim enhancing region distal to the biceps muscle (arrows).


Partial tears of the pectoralis major are gener-ally more common than complete tears [52,185].Partial tears tend to occur at the myotendinous

junction, and are usually managed nonoperatively.Complete tears usually occur more distally at theenthesis (Fig. 11). With avulsion of the tendon

from its insertion site, high T2 signal intensity maybe seen superficial to the adjacent cortex becauseof periosteal stripping [52]. Complete tears, par-

ticularly avulsion injuries from the humerus,are treated optimally in active individuals withprompt surgical repair to hasten rehabilitationand improve functional outcome [26,133,185,

267,271].

Hamstring musclesThe hamstring muscles (biceps femoris, semite-

ndinosus, and semimembranosus) principally

originate proximally from the posterolateral ischialtuberosity and insert distally into the tibia. Theshort head of the biceps femoris muscle originates

from themidshaft of the femur posteriorly [58]. Thehamstrings function primarily to flex the knee andextend the hip. While running or jumping, the

hamstrings play a pivotal role in decelerating theknee before foot strike and assisting with hipextension after foot strike.

The hamstrings are the most commonly injured

muscles in sprinting and jumping athletes [4,135].

Fig. 8. Adductor muscle hematoma. Axial T1-weighted (A) and FSE T2-weighted (B) images show a hematoma with

classic features (arrows). There is subtle high signal intensity methemoglobin within the hematoma on the T1-weighted

image. This region remains with high signal intensity on the T2-weighted image along with higher signal intensity serous

fluid.


For example, 10% of 180 soccer players sufferedhamstring injuries during a single season in one

prospective study [135]. In young adults, mosthamstring injuries are partial tears [4,135]; com-plete hamstring tears or avulsions are relatively

uncommon (Figs. 12, 13) [137,177,213]. Of thethree hamstring components, the biceps femorisis the most commonly injured [58,135,200,234].

Injury to more than one component of the ham-strings is not uncommon, with a prevalence of25% [88] to 33% [58].

In the hamstrings, the zone of transitionbetween the muscles and tendons is particularly

long. Indeed, each hamstring tendon extendscompletely or almost completely down the lengthof each muscle [88]. Consequently, when strain

injuries occur at the myotendinous junction, theseinjuries can be located at the ends of the mus-cle belly or in the muscle belly itself. In one study

of MR imaging in 15 college athletes [58],acute hamstring injuries at the myotendinousjunction occurred in diverse locations: the

Fig. 9. Residual hematoma within the gastrocnemius muscle. Axial FSE fat-suppressed T2-weighted (A) and fat-

suppressed T1-weighted images following intravenous gadolium administration (B) show a classic hematoma that has

created a rim-enhancing pseudocyst in the muscle (arrows).

Fig. 10. Pseudotumor after a muscle strain. Sagittal FSE fat-suppressed T2-weighted MR image shows a nonacute

midsubstance rupture of the semitendinosus muscle that retracted distally and balled up posterior to the knee (arrow),

resulting in a soft tissue mass that was clinically thought to represent a popliteal cyst.


proximal myotendinous junction (33%); the in-

tramuscularmyotendinous junction (53%); and thedistal myotendinous junction (13%). Hamstringstrain injuries also may occur at other sites, such

as partial or complete avulsions at the tendinousorigin when underlying tendinosis is present[213].

After a hamstring strain, convalescence peri-

ods reportedly vary from less than 3 months to1.5 years before patients can return to vigorousactivities [213]. Recurrent injuries are common,

occurring in one fourth of athletes [110]. Evenminor hamstring injuries may double the risk ofa more severe injury within 2 months [70].

Fig. 11. Complete tear of the sternal portion of the pectoralis major tendon distally at the enthesis on the humerus. Axial

fat-suppressed FSE T2-weighted MR image shows a completely avulsed tendon with muscle retraction and a high signal

intensity fluid-filled gap (solid arrow). Note the nearby biceps tendon (open arrow).

Fig. 12. Complete hamstring avulsion. Axial T2-wieghted MR image shows a full-thickness avulsion of the right

hamstring tendons which are separated from the ischial tuberosity by high signal intensity fluid/hemorrhage (arrow).


Gastrocnemius muscleSeveral muscles and tendons at the posterior

aspect of the knee and calf may be subjected tostrain injuries, including the gastrocnemius [29,

83,89,232,234], soleus [47,183], plantaris [9,111],and popliteus [40,262,266] muscles (Fig. 14).

The most common isolated muscular strain inthe calf affects the medial head of the gastrocne-

mius muscle, and is referred to in commonparlance as tennis leg [29,89]. Sudden onset ofsharp pain classically occurs in middle-aged

athletes participating in racquet sports, skiing,and running. Clinical differential diagnosis occa-sionally includes chronic exertional compartment

syndrome, overuse tendinitis, ruptured popliteal

cyst, stress fracture, fascial herniation, venousthrombosis, nerve entrapment, and poplitealartery entrapment syndrome [144,232,251].

MR imaging may be used to help determine anaccurate diagnosis and determine its severity[29,89]. In one recent MR imaging study of 23injuries to the distal gastrocnemius [261], the

myotendinous junction was involved in 96% ofcases. The medial head was more frequentlyinvolved than the lateral head (86% and 14%,

respectively), and low-grade or partial tears weremore common than complete tears. In anotherrecent study of 65 patients with suspected tennis

Fig. 13. Complete tear of the hamstring associated with a large hematoma. Axial T2-weighted (A) and coronal fat-

suppressed FSE (B) MR images display a full thickness tear of the hamstring tendons (arrow) with a 2–3 cm gap between

the proximal and distal retracted musculotendinous unit (small arrow). There is a large hematoma associated with this

tear.


leg [29], 51 partial and 14 complete tears werediagnosed sonographically. Treatment is conser-

vative, typically with relief of pain within approx-imately 2 weeks and return to sports after at least3 weeks [89].

Delayed-onset muscle soreness

Delayed-onset muscle soreness (DOMS) refersto the muscular pain, soreness, and swelling that

follows unaccustomed exertion. Activities thatrequire eccentric muscle contractions are commonculprits, such as hiking downhill or certain types

of manual labor. DOMS is thought to occur fromreversible structural damage at the cellular level;no permanent damage to muscle function ensues.

Patients with DOMS do not recall any oneparticular moment of trauma or experience anacute onset of pain. Rather, symptoms tend tobegin within 1 to 2 days after exercise. Soreness

often crescendos until it peaks 2 to 3 days after theinciting exercise, and then generally subsideswithin 1 week. Interestingly, this soreness often

is associated with temporarily diminished musclestrength.

With MR imaging, high signal intensity in-

dicative of interstitial edema is observed on T2-weighted or IR-FSE images. Perifascial fluid-likecollections occasionally may be seen in the early

phase. The MR imaging appearance of DOMS isgenerally similar to a first-degree muscle strain.Clinical history allows for easy differentiationbetween these two entities in most instances.

The history of a provocative event may notbe forthcoming in all cases, however, because

abnormal signal intensity reportedly may remainfor up to 80 days in patients with DOMS [221].

Muscle contusion

Contusion of muscle is produced by directtrauma, usually by a blunt object. Interstitialedema and hemorrhage result in varying degrees

of pain, swelling, ecchymosis, and spasm. In ad-dition, a recognized complication of muscularcontusion is myositis ossificans. Uncommon or

rare complications of muscle contusions includecompartment syndrome [168] and even pyomyo-sitis [5,149,186]. Blunt trauma presumably results

in muscle damage, hematoma formation, andhyperemia that may create a fertile ground forsubsequent infection.

With MR imaging, the girth of the muscletypically is increased, but no fiber discontinuity orlaxity is observed. Fat-suppressed T2-weightedand IR-FSE images provide a conspicuous display

of high signal intensity that may have a diffuse orgeographic appearance, often with feathery mar-gins (Fig. 15). Although contusion injuries often

appear larger in size than strain injuries, therecovery time for contusions tends to be signifi-cantly shorter (mean time: 19 � 9 days versus

26 � 22 days) [247]. The duration of disability,ranging from 6 to 60 days, also may correlate withthe degree that range of motion is restrictedacutely after a contusion [118].

Myositis ossificans

The most common type of heterotopic ossifi-cation occurs in muscle and commonly is referred

Fig. 14. Rupture of the plantaris tendon with adjacent gastrocnemius strain. Axial T1-weighted (A) and fat-suppressed

FSE T2-weighted (B) MR images show a hematoma between the soleus and gastrocnemius muscles in the region of the

torn plantaris tendon (arrow).


to as myositis ossificans. The moniker ‘‘myositis’’generally is regarded as misleading because it is

not a primary inflammatory process pathologi-cally [3,20]. Clinically, myositis ossificans may beconfused with an inflammatory or neoplastic

process, with symptoms and signs that includepain, tenderness, swelling, and a palpable mass[93,106,129,225]. Myositis ossificans affects the

large muscles in the extremities in approximately80% of cases [130].

Well-recognized precursors are observed in37% to 75% of patients with myositis ossificans

[124,173,187,218]. Predisposing factors most com-monly include traumatic insults (eg, contusion[116], surgery [43,207], and burns [76]); neurologic

insults (eg, paraplegia [126], traumatic brain in-jury [109], and stroke [104]); or bleeding dyscra-

sias (eg, hemophilia [50]). Myositis ossificans isdiagnosed, on average, 4 months after a phys-ical or neurologic insult [125].

In the clinical and radiologic arenas, threetypical phases of evolution occur: (1) an acute orpseudoinflammatory phase; (2) a subacute or

pseudotumoral phase; and (3) a chronic, self-limited phase that often undergoes spontaneoushealing [36]. In the acute and subacute stages ofmyositis ossificans, imaging examinations have

a notoriously nonspecific appearance. In the finalstage, the essential imaging findings that permitconfident differentiation of myositis ossificans

Fig. 15. Muscle contusion after a car ran over this patient’s foot. Sagittal T1-weighted (A) and fat-suppressed FSE

T2-weighted (B) MR images of the foot show high signal intensity methemoglobin within the muscles of the

flexor compartment of the foot (curved arrows). There also is associated high signal intensity within the muscles on

T2 weighting (solid arrow).


from neoplasm-containing areas of mineralizationare threefold: (1) the ossific mass is well-defined,sharply marginated, and appears more matureperipherally than centrally; (2) the lesion generally

decreases in size with the passage of time, and (3)the lesion is not in continuity with the underlyingbone. In contradistinction to calcification that has

an amorphous appearance, the sine qua non ofmature myositis ossificans with all imagingtechniques is its recognizable architecture that

approximates native bone: an area of cancellousbone centrally surrounded by compact boneperipherally (Fig. 16).

Radiography and CTDuring the first week, radiographs are gener-

ally negative, whereas CT scans may demonstratevague muscle swelling. Within 2 to 6 weeks afterthe onset of symptoms, radiography and CT

characteristically demonstrate vague, faint, floc-culent mineralization [3,203]. The benign nature

of the lesion is suggested when the cortex of anadjacent bone is intact and not in continuity withthe area of soft tissue mineralization.

At this subacute stage, the imaging findings of

a soft tissue mass with ill-defined marginscontaining foci of mineralization are confusedmost commonly with a soft tissue sarcoma (eg,

osteosarcoma [257], chondrosarcoma, or synovialsarcoma [152]). Periostitis also may be seen,although osseous destruction is absent. Given

that this early, immature mineralization is notdiagnostic, short-term follow-up radiography orCT (repeated at an interval of 3 to 4 weeks) is

necessary to confirm suspected myositis ossificans.This allows postponement of a percutaneous bi-opsy or surgical procedure in the appropriateclinical setting until diagnostic imaging features

have declared themselves [106]. By 1 to 2 monthsafter the onset of symptoms, CT effectively showsa peripheral rind of mineralization. Decreased

radiodensity inside the lesion may correspond to

Fig. 16. Myositis ossificans in the medial thigh of an 18-year-old water polo player. Anteroposterior radiograph of the

thigh demonstrates a well-organized oval ossified mass with a rim of compact bone, consistent with myositis ossificans

(arrow).


developing cancellous bone, whereas decreasedattenuation around the lesion may be secondaryto edema. The ossific mass matures over a period

of 6 months to 1.5 years [125,143,248]. Resorptionof the osseous lesion may occur over a period of1 to 5.5 years [50,203].

Bone scintigraphyBone scintigraphy with technetium Tc-99m

medronate is more sensitive than radiographyfor the detection of myositis ossificans in the early

stages. The three-phase bone scan typicallydemonstrates an area of nonspecific increasedtracer uptake in all three phases [237]. As thelesion matures, the intensity of radiopharmaceu-

tical accumulation lessens, approaching the ap-pearance of normal adjacent bone [179].

MR imagingMR imaging findings also evolve over time. In

the acute and subacute stages, MR imaging

findings are nonspecific. The involved muscle isenlarged and exhibits ill-defined, poorly-margin-ated intermediate T1 and high T2 signal intensity

[225]. Enhancement occurs in the lesion aftercontrast administration. In the adjacent muscleand bone marrow [106], areas of high T2 signal

intensity and contrast enhancement also may beobserved. Although periostitis may be present inthe adjacent bone, myositis ossificans does not

arise from or destroy the adjacent bone. Intrale-sional fluid-fluid levels can be observed in myositisossificans, a feature that also may be seen withcertain soft tissue neoplasms (eg, synovial sar-

coma) (Fig. 17) [253]. As the intermediate stageprogresses, edematous changes in and around thelesion diminish. High T1 and low T2 signal

intensity areas begin to appear in the lesion,corresponding to (fat-containing) medullary boneand compact bone, respectively. In the mature

lesion, the margins become more well defined.The character of the signal intensity mayremain inhomogeneous, although areas of highT1 signal intensity may be seen that represent fat

interposed between bone trabeculae in the lesion[129,225].

TreatmentManagement of myositis ossificans may in-

clude nonsteroidal anti-inflammatory agents (eg,indomethacin); diphosphonates; low-dose irradi-

ation therapy; physical therapy; and in uncom-mon cases, surgical resection [143]. Surgicalresection of myositis ossificans traditionally has

been performed after the mass matures in thehopes of minimizing the risk of recurrence[84,167,190,248,250]. The surgical excision of

myositis ossificans occasionally may be indicatedfor purposes of a histopathologic diagnosis, un-remitting pain, a bulky area of ossification thatlimits range of motion, or nerve entrapment

[106,160,174]. Nerve impingement by heterotopicossification most commonly involves the ulnar[49,63,169], median [169], radial [78], and sciatic

nerves [120]. Given that the acute and subacutestages of myositis ossificans potentially may beconfused with a sarcoma [6,7,10,12,92,93,98,106],

myositis ossificans has been designated a ‘‘do nottouch’’ lesion that should not undergo biopsyinjudiciously.

Muscle laceration

Muscle lacerations are uncommon athletic

injuries produced by a penetrating insult. In theacute setting, these types of injuries rarely areevaluated with MR imaging. MR imaging soonafter a muscle laceration shows focal, sharply

marginated discontinuity of fibers and high T2signal intensity caused by hemorrhage and edema(Fig. 18). In the chronic setting, MR imaging of

the affected muscle characteristically demon-strates scarring as low T2 signal intensity andfatty infiltration associated with atrophy as high

T1 signal intensity. In addition, muscle occasion-ally may be seen herniating through a lacerationin the surrounding fascia.

Muscle herniation

Muscle herniation refers to protrusion of

muscle tissue through a focal fascial defect [28].These fascial defects most commonly occursecondary to muscle hypertrophy and increased

intracompartmental pressure, with subsequentherniation of muscle through relatively weakareas in the fascia, such as those traversed byblood vessels and nerves [158]. Less commonly,

a tear of the fascial sheath occurs with trauma,such as that associated with fractures or penetrat-ing trauma. Muscle herniation also has been re-

ported in a familial setting, suggesting congenitalweakness in the fascia in some individuals [37].

LocationMuscle hernias characteristically occur in the

middle to lower portions of the leg. The tibialisanterior is the most commonly involved muscle


[228], although virtually any muscle in the leg canbe affected, including the extensor digitorum lon-

gus [95], peroneus brevis [223], peroneus longus[24], and gastrocnemius [8]. Herniation of musclein the thigh [41,206,224] and in the forearm

[97,176,210] is uncommon. Muscle hernias maybe multiple [123,148] and bilateral [37,230].

Symptoms and signsClinically, patients typically present with a

small, superficial, soft tissue bulge that becomesmore prominent and firm with muscle contraction.

Although most muscle herniations are asymptom-atic, they can cause substantial pain, cramping, and

tenderness [28,41]. Fascial defects also may enlargeover time [41], resulting in cosmetic complaints.Rarely, herniated muscle may become incarcerated

[230] or result in nerve entrapment. For example,herniation of the gastrocnemius muscle can com-press the peroneal nerve and result in a clinicalpresentation that resembles sciatica [8]. Muscle

herniation also may be observed in patients withcompartment syndrome owing to intracompart-mental hypertension.

Fig. 18. Laceration anterior to the elbow. Axial T1-weighted (A) and fat-suppressed FSE T2-weighted (B) MR images

reveal a linear defect that demonstrates elevated signal intensity on T2-weighting in the anterior musculature (solid

arrows). This is consistent with a muscle laceration from a stab wound. Some methemoglobin is seen in the wound on

T1-weighting (open arrows)

Fig. 17. Myositis ossificans of the arm. Axial T1-weighted (A) and T2-weighted (B) MR images reveal an inhomogeneous

soft tissue mass that contains a fluid-fluid level (arrows). This nonspecific appearance might be confused with a hematoma

or a soft tissue neoplasm.


ImagingImaging examinations characteristically dem-

onstrate outward bulging of muscle, sometimes

with mild irregularity in contour peripherally(Fig. 19). MR imaging [37,158,270] may docu-ment herniation of muscle and discontinuity in theoverlying fascia. In uncomplicated cases, the

signal intensity of the herniated tissue matchesthat of the adjacent muscle belly. MR imagingmay be performed dynamically during muscle

contraction and relaxation, which may increasethe conspicuity of a fascial tear or herniatedmuscle tissue. For example, fast gradient echo

MR imaging of the leg during active dorsiflexionof the ankle may show an increased volume ofherniated muscle compared with images obtainedduring active plantar flexion. Conversely, in other

patients, active plantar flexion may depict a fascialtear to better advantage in some patients [158].

TreatmentTreatment of asymptomatic muscle hernias is

usually conservative [24]. For symptoms that arerecalcitrant or severe, management may include

local injection of botulinum toxin [41] or fasciot-omy [24,162]. Fascial repair with suture or

synthetic mesh also has been reported as a thera-peutic option [148,228], although this techniquemay be complicated by compartment syndrome in

some cases [13]. In patients with muscle herniasowing to compartment syndrome, fasciotomymay be indicated.

Compartment syndrome

Compartment syndrome refers to elevatedpressure in a relatively noncompliant anatomicspace that is associated with ischemia and may

result in neuromuscular injury [119,166]. The termVolkmann’s ischemic contracture applies to thesequelae of compartment syndrome, in which

fibrous tissue replaces necrotic muscle and nervetissue [119]. Potential complications of compart-ment syndrome not only include contractures, butalso myonecrosis, rhabdomyolysis, renal failure,

and even death [27,77,112,136,214,252].

PathogenesisThe fundamental derangement in patients with

compartment syndrome is elevated intracompart-mental pressure. A vicious cycle can occur inwhich muscle ischemia results in increased capil-

Fig. 19. Muscle herniation. Sagittal T1-weighted image of the distal thigh shows herniation of the semimembranosus

muscle and semitendinosus tendon posteriorly through a defect in the overlying fascia (arrow). A fascial release was

subsequently performed.


lary permeability, increased interstitial edema, andincreased intramuscular pressure that exceeds theintravascular pressure of small vessels. Thethin walls of these small vessels may collapse,

thereby impeding blood flow [67]. Regardlessof the type of insult in any particular patient, thefinal common pathway to compartment syndrome

involves a decreased arteriovenous gradient thatcan result in ischemia and, ultimately, tissue nec-rosis. Factors that may predispose a compartment

to this syndrome include a history of trauma;external compression; systemic hypotension; in-creased intracompartmental volume (eg, hemor-

rhage, edema, poor venous return, and musclehypertrophy); and loss of compartment elasticity(eg, fibrotic or constricted fascia) [35,219].

Compartment syndrome is classified most

commonly according to its duration, cause, andlocation. Knowledge of compartmental anatomyis fundamental to accurate diagnosis and treat-

ment of this potentially devastating condition [16].

Acute compartment syndromeNumerous common and uncommon causes

of acute compartment syndrome have beendescribed [17,18,22,23,33,42,55,56,69,86,103,122,138,145,146,156,165,171,182,192,194,201,205,209,

217,233,239,243,246,256,268].Althoughmostcasesof acute compartment syndrome are associatedwith fractures, the second most common cause is

injury to soft tissues (eg, contusion) withoutfracture [157]. Compartment syndrome caused byathletics occasionally may present acutely in the

absence of direct trauma. Muscle rupture, forexample, may cause compartment syndrome innumerous locations, including the biceps brachiicompartment of the arm, [156] the flexor compart-

ment of the forearm [103], the superficial posteriorcompartment of the leg [245], and the peronealcompartment of the leg [103]. Acute compartment

syndrome in the absence of muscle rupture alsomay occur (eg, in the triceps and deltoid muscles ofweight lifters [62] and in the anterior compartment

of the legs of soccer players [265]).

Chronic compartment syndromeChronic compartment syndrome may occur

because of exertional causes (eg, exercise or

occupational overuse) or nonexertional causes(eg, a mass lesion or infection). Exertional chroniccompartment syndrome occurs because muscle

activity can increase muscle volume by up to 20%,causing hypertension in noncompliant com-partments [68]. Consequently, particular activities

are associated with chronic exertional com-partment syndrome targeting specific sites [2,11,25,30,48,96,102,105,108,128,163,172,178,188,193,202,220,226,229,258,260]. In running athletes, for

example, the most common site of chronic com-partment syndrome is the leg. The thigh, forearm,and foot are the next most common sites in athletes

[117]. Compartment syndromes affecting the para-spinous musculature and other sites are considereduncommon [44,61,127,140,180,214].

Symptoms and signsPatients initially complain of painful throbbing,

aching, tightness, or pressure that worsens with

palpation and passive stretching of the affectedmuscles. With acute compartment syndrome, themost important early symptom is pain out ofproportion to that expected for the given injury

[264]. With chronic exertional compartment syn-drome, symptoms typically begin during or imme-diately after exercise, and tend to resolve at rest

after a variable period. With both acute andchronic compartment syndrome, the arterial pulsesusually remain palpable, although venous and

lymphatic drainage are impaired [255]. Relativelylate findings of acute and chronic compartmentsyndrome are deficits in motor and sensory nervefunction caused by muscle and nerve ischemia.

Diagnostic examinationsDiagnostic tests used to evaluate for com-

partment syndrome include compartment pres-sure measurements, near infrared spectroscopy

[39,91,164,181], and imaging examinations. Nor-mally, intracompartmental pressures should beless than 15 mm Hg to 20 mm Hg at rest and

within 5 minutes after finishing exercise [117,189].Chronic exertional compartment syndrome isdiagnosed when intracompartmental hypertension

is documented before exercise (15 mm Hg to 20mm Hg or more) or immediately after completingan exercise session (30 mm Hg or more). Although

direct pressure measurements are the gold stan-dard for objective diagnosis, potential problemsof blindly placed percutaneous catheters includecatheter insertion into an unintended compart-

ment, inadvertent damage to neurovascular struc-tures, and inaccurate or inconsistent pressuremeasurements [64,154].

MR imagingAlthough cross-sectional imaging is not the

primary technique for diagnosing compart-ment syndrome, imaging may complement direct


pressure measurements by providing noninvasivedata on the compartment or compartments thatare involved, particularly in the nonacute setting.

Imaging also assists in evaluation for an un-derlying lesion (eg, hematoma or neoplasm) thatmay contribute to compartment hypertension andneed to be addressed at surgery. Other potential

indications for MR imaging include the diagnosticevaluation of atypical cases (eg, uncommonlocation or cause for compartment syndrome

and borderline pressure measurements) and fol-low-up evaluations.

Familiarity with the imaging appearance of

compartment syndrome is important, given thatimaging may be performed for assessment of painthat initially is thought to be caused by othercauses (eg, stress fracture, myotendinous strain, or

soft tissue tumor). MR imaging can be used toclarify the location and extent of ischemic damageto muscle [227,263]. In the setting of acute and

chronic compartment syndrome, increased musclevolume commonly is caused by muscle hypertro-phy, edema, or both (Fig. 20). This increased

intracompartmental volume and pressure mayresult in herniation of muscle through a tear inthe surrounding fascia [178]. Once established,

compartment syndrome may demonstrate at leastfive other features:

1. Hyperintense signal on fat-suppressed T2-weighted images caused by increased inter-stitial water or edema (acute or chronic

compartment syndrome) [178].

2. Increased signal intensity on T1-weightedimages, caused by foci of hemorrhage (sub-acute compartment syndrome) or fatty

infiltration (sequelae of established compart-ment syndrome) [14,90,178].

3. Decreased signal intensity on T1-weightedimages, caused by fibrosis or dystrophic

calcification (sequelae of established compart-ment syndrome) [90,178].

4. Decreased muscle volume, relating to atro-

phy, fibrosis, or both (sequelae of establishedcompartment syndrome).

5. Fascial thickening (sequelae of established

compartment syndrome).

Although controversial, gadolinium-enhancedMR imaging may be helpful in evaluating patientswith impending compartment syndrome by show-ing avid contrast enhancement in the affected

muscles. This enhancement can be useful indistinguishing muscles that are still perfused fromthose with devitalized areas.

In patients with suspected chronic exertionalcompartment syndrome, MR imaging beforeand after exercise may be helpful [75]. The change

of signal intensity between pre-exercise andpostexercise images is significantly greater incompartments with postexercise hypertension.Furthermore, the magnitude of this change in

signal intensity correlates significantly with thechange in pre-exercise and postexercise pressuremeasurements, and with the absolute postexercise

pressure.

Fig. 20. Compartment syndrome of the vastus intermedius muscle. Axial T1-weighted (A) MR image shows enlargement

of the vastus intermedius muscle with splaying of the surrounding quadriceps musculature. The overlying fascia is

thickened (curved arrow). Fat-suppressed FSE T2-weighted (B) MR image shows abnormal high signal intensity within

the enlarged muscle (straight arrow). (Courtesy of Vincent McCormick, MD)


Other MR imaging techniques also haveshown promise in evaluating acute and chroniccompartment syndrome. Diffusion-weighted echo-planar MR imaging potentially can depict alter-

ations in the circulating blood volume in muscleinduced by exercise and changes in compartmentpressure [269]. MR spectroscopy with phosphorus-

31 has been used experimentally to determine thepressure threshold for metabolic deterioration ofskeletal muscle. This technique also has been used

clinically to document the extent of muscle da-mage after ischemia and healing after fasciotomy[263].

Although MR imaging may be sensitive in theevaluation of compartment syndrome, it is not

specific. Depending on the clinical context, theimaging differential diagnosis may include othercauses of painful, swollen extremities, such asDOMS, muscle strain, deep venous thrombosis,

cellulitis, and lymphedema. Like compartmentsyndrome, deep venous thrombosis may result inmuscle edema, particularly in the deep posterior

compartment of the calf. Unlike compartmentsyndrome, however, deep venous thrombosiscauses venous occlusion and commonly results

in subcutaneous edema and skin thickening,which are all findings that can be displayed bysonography and MR imaging. Cellulitis and

lymphedema show prominent subcutaneousedema and skin thickening on MR images, butswelling and abnormal signal intensity centeredin muscle often are absent.

TreatmentThe critical threshold at which myoneural

necrosis occurs may vary according to thelocation of the compartment syndrome; its acuity

and duration; and individual patient factors (eg,hypotension and soft tissue trauma). For example,in athletes with acute anterior compartment

syndrome in the thigh caused by a contusion,conservative treatment reportedly yields resultssuperior to fasciotomy, despite sustained pressure

elevations above 50 mm Hg [211]. In general,surgical decompression is performed when acutecompartment pressures reach 30 mm Hg to 80 mm

Hg [74,170,216,240]. Findings favoring fascialrelease include increasing compartment pressuresover time, paresthesia, and paresis. For chroniccompartment syndrome, fasciotomy generally is

recommended if symptoms persist more than6 months despite conservative therapy.

Muscle denervation

Athletes with hypertrophy of muscles, espe-cially anomalous muscles in anatomically vulner-

able sites, may result in entrapment neuropathy.Entrapment neuropathy and denervation can bea cause of pain and weakness that simulates

a primary abnormality in skeletal muscle. MRimaging may be a useful adjunct to electromyog-raphy (EMG) in detecting muscle denervation and

its causes (Fig. 21) [38,46,85,99,155]. For example,in a study of 90 patients with clinical evidence ofperipheral nerve injury or radiculopathy [155], the

Fig. 21. Varying stages of denervation of the anterior tibial muscle. Axial T1-weighted (A) MR image shows fatty

atrophy of the muscle consistent with chronic denervation (arrow). Fat-suppressed FSE T2-weighted (B) MR image

demonstrates high signal intensity in the muscle, consistent with extracellular water related to subacute denervation

(arrow). Note the lack of perifascial edema.


sensitivity and specificity of IR-FSE MR imagingrelative to EMG were 84% and 100%, respec-tively. Although less sensitive than EMG, MR

imaging may display the site and cause of nerveentrapment in many cases (eg, intervertebral diskherniation, ganglion cyst, or hematoma).

With denervation, the signal intensity and

morphology of muscle undergo characteristicchanges with MR imaging. Although these de-nervation changes have been reported as early as

4 days after a nerve insult, hyperintense signal onT2-weighted or IR-FSE MR images usually arenot detectable for 2 to 3 weeks in most cases

[80,85,199]. Three imaging features may helpdistinguish the hyperintense T2 signal in dener-vated muscles from that seen with strained mus-cles. First, unlike strain injury, the hyperintense

T2 signal in denervated muscles is not associ-ated with perifascial edema. Second, the patternof muscle involvement may suggest a specific

nerve territory responsible for the denervationchanges. Third, abnormally hyperintense T2signal in peripheral nerves is a hallmark of most

neuropathies. Normally, peripheral nerves areisointense to the normal muscle on T2-weightedimages and only mildly hyperintense to normal

muscle on fat-suppressed T2-weighted or IR-FSEMR images [1,85].

With chronic denervation, diminished bulk andfatty infiltration occur in muscle. These atrophic

changes are best displayed on T1-weighted MRimages (see Fig. 21). Whereas the signal intensity

changes of acute muscle denervation are revers-ible, profound atrophic changes seen late in thecourse of denervation may be irreversible [235].

The atrophic changes from denervation are notspecific, and may be seen with conditions asdiverse as motor neuron diseases (eg, poliomyelitis[249]) and demyelination (eg, hereditary motor

and sensory neuropathies [215]).Although chronic denervation usually results

in atrophy, pseudohypertrophy and true hyper-

trophy have been reported [53,60,66,151,161,184,191]. Both conditions may present clinicallyas a palpable soft tissue mass that serves as an

indication for MR imaging. Pseudohypertrophyrefers to prominent accumulation of fat andconnective tissue that causes paradoxical enlarge-ment of the affected muscle. On T1-weighted MR

images, the enlarged muscle contains hyperintensesignal from adipose tissue. True hypertrophy ofsynergistic muscle fibers that remain innervated

also may occur. In this situation, the affectedmuscle is enlarged, but is typically isointense withnormal muscle.

In addition to entrapment neuropathy, hyper-trophied muscles in athletic individuals occasion-ally may result in other abnormalities, including

intermittent claudication, arterial stasis, aneu-rysm, and venous stasis. For example, a hypertro-phied anomalous muscle in the popliteal fossa mayresult in popliteal artery entrapment syndrome.

Specific anomalous muscles that may be respon-sible for popliteal artery entrapment include

Fig. 22. Radiation therapy mimicking a muscle strain. Axial fat-suppressed FSE T2-weighted MR image shows high

signal intensity within the left obturator externus muscle (arrows) with some abnormal signal intensity in the medial

aspect of this muscle on the opposite side. This ‘‘feathery edema’’pattern was produced by radiation for prostate cancer.


a third head of the gastrocnemius muscle and ananomalous intercondylar origin of the medialhead of the gastrocnemius muscle [21,94,241].This syndrome is diagnosed characteristically in

young adults with gradually progressive intermit-tent claudication in the leg.

Differential diagnosis

MR imaging facilitates the diagnostic process

primarily by detecting alterations in muscle size orsignal intensity. Although these alterations maybe diagnostic in the appropriate clinical setting,a wide array of focal and systemic pathologic

conditions affecting muscle may have a similar ap-pearance. In addition to traumatic muscle injuriesthat may be related to sports, common categories

of disease affecting muscle include ischemia andnecrosis, inflammation and infection, congenitaland inherited conditions, neoplasms, and various

iatrogenic insults.Given that the potential causes for abnormal

signal intensity in muscle are diverse, the differ-

ential diagnosis approach may be simplified byrecognizing one of three basic patterns [153]. The‘‘muscle edema pattern’’ may be seen with acuteor subacute sports-related trauma (eg, strain

injury or early myositis ossificans); subacutedenervation; infectious or autoimmune myositis;rhabdomyolysis; or recent iatrogenic insults (eg,

surgery or radiation therapy) (Fig. 22). The ‘‘fattyinfiltration pattern’’ may be observed in thechronic setting after a high-grade myotendinous

injury, and with other causes of chronic muscledisuse, chronic denervation, and corticosteroiduse. The ‘‘mass lesion pattern’’ can be seen withtraumatic injuries (eg, myositis ossificans); neo-

plasm; infection (eg, pyomyositis and parasiticinfection); and muscular sarcoidosis.

Regardless of the disorder affectingmuscle,MR

imaging may help in honing the clinical differentialdiagnosis; defining the location, extent, and sever-ity of a disorder; predicting the prognosis or

possible complications associated with a disorder;directing the type and location of an intervention,such as surgery (when indicated); and assessing

treatment response or failure after medical orsurgical therapy.

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Index

Note: Page numbers of article titles are in boldface type.

A

Achilles tendon, injuries of, in athletic activities,

296

Achilles tendonitis, 296–297

Adductor insertion avulsion syndrome, 273

Adductor muscle, strain of, 344, 346

Ankle, accessory muscles of, 202–203

accessory ossicles and sesamoid bones of, 203

foot and, bony injury of, 295, 296

force on, during athletic activities, 295

sports injuries of, imaging of, 295–310

sports protocols, for direct

MR arthrography, 296

‘‘high sprain’’ of, 300, 302

imaging of, after physical activity, 202

injuries of, in alpine skiing, 313, 314

lateral, ligamentous injury of, 299

ligaments and tendons of, asymptomatic

findings about, 202

normal fluid collections in, 201

Anterior cruciate ligament, ganglion cyst of,

290, 292

in meniscal and cruciate ligament injuries,

283–293

normal fibrous bundles of, 287, 291

rupture of, 289, 291

sprains of, 289

tears of, 291–293

in alpine skiing, 312–313

MR imaging to diagnose, 291

Apophyseal avulsion injuries, 343, 344

clinical features of, 267

MR imaging of, 267

treatment of, 267

Arthritis, septic, of hip, 264

Athletes, stress fractures in, imaging of,

323–339

Athletic pubalgia, 271–272

MR imaging in, 272

B

Bankart lesions, 227, 229

Baseball pitch, basic positions of, 226–227

Bennett lesion, 230–231

Biceps tendon, 250

distal, rupture of, 250–251

Bobsledding, injuries associated with, 316, 317,

318

Bone scintigraphy, in myositis ossificans, 356

in stress fractures, 332–334

C

Calf, hematoma of, imaging of, 342

Capitellum, pseudodefect of, elbow and,

196, 197

Cervical ligament injury, 303, 304

Compartment syndrome, 358–361

acute, 359

chronic, 359

diagnostic examinations of, 359–360

MR imaging of, 360–361

pathogenesis of, 359

symptoms and signs of, 359

treatment of, 361

Computed tomography, in sports-related muscle

injuries, 355–356

in stress fractures, 330, 331, 334

Coracoid impingement syndrome, 230

Coxa saltans, 270–271

MR imaging in, 271

Cruciate ligament, anterior. See Anterior cruciate

ligament.

injuries of, and meniscal injuries, MR imaging

of, 283–293

posterior, injuries of, 291, 292, 293


doi:10.1016=S1064-9689(03)00039-4


11 (2003) 373–378

D

Delayed onset muscle soreness, 302

Deltoid ligament, tears of, 298

Dysplasia, of hip, osteoarthritis and, 257–258

E

Elbow, capsule anatomy and pathology of,

241–242

common extensor tendon, and lateral muscles,

248

dislocation of, posterolateral rotary instability

and, 245–247

epicondylitis and overuse syndromes of,

248–250

flexor tendon of, and medial muscles, 248

fracture dislocations of, 246–247, 248

imaging of, normal variants and pitfalls of,

196–197

instability at, 243–244

lateral muscles of, common extensor tendon

and, 248

ligamentous anatomy and pathology of,

242–247

medial muscles of, flexor tendon and, 248

osseous anatomy and pathology of, 239–241

osteochondral lesions of, 240–241

posterolateral rotary instability of, and

dislocation, 245–247

pseudodefect of capitellum and, 196, 197

sports injuries of, 239–253

subluxation or dislocation of, 246–247, 248

tendons of, anatomy and pathology of,

247–252

valgus stress at, 240, 242

varus stress at, 245, 246

Epicondylitis, and overuse syndromes of elbow,

248–250

Exercise, for enhancement of MR imaging, 343

F

Femoral neck, stress fractures of, 336–337

Femoroacetabular impingement, in osteoarthritis

of hip, 263

Fibrocartilage, asymtomatic triangular, 197–198

Foot, and ankle, bony injury of, 295, 296

force on, during athletic activities, 295

sports injuries of, imaging of, 295–310

sports protocols, for direct

MR arthrography, 296

injuries of, associated with snowboarding, 315

in alpine skiing, 313, 314

normal fluid collections in, 201

Foramen sublabrum, 224

Forefoot, asymptomatic findings in, 203

G

Gadolinium enhancement, of magnetic resonance

imaging, 342–343

Ganglion cyst, of anterior cruciate ligament, 290,

292

Gastrocnemius muscle, residual hematoma in,

347, 350

strain injury of, 352–353

Glenohumeral instability, atraumatic, 228

classification of, 227

traumatic, 227–228

Glenohumeral joint, microinstability of, 228

posterosuperior instability of, 234–235

Glenohumeral ligament(s), 222

humeral avulsion of, 227, 229

inferior, 224

middle, 223–224

superior, 223

Gradient echo imaging, in magnetic resonance

imaging, 342

Groin pain, acute, in athletes, 271–272

H

Haglund’s deformity, 297, 298

Hamstring muscles, strain injury of, 349–352

Hand, imaging of, normal variants and pitfalls of,

197–198

Hematoma, and pseudotumor appearance,

347–348, 349, 350

of calf, imaging of, 342

residual, in gastrocnemius muscle, 347, 350

Hip, arthroscopy of, indications for, and

contraindications to, 255–256

technique of, and complications of, 256

bursae of, and bursitis of, 267–270

disorders of, sports-related, MR imaging of,

255–281

dysplasia of, osteoarthritis and, 257–258

extra-articular derangement of, protocol for,

257

374 Index = Magn Reson Imaging Clin N Am 11 (2003) 373–378

extrinsic ligaments of, anatomy and function

of, 261

MR imaging of, 261

instability of, clinical manifestations of, 261

internal derangement of, imaging protocol for,

256–257

joint effusion of, 261–262

ligaments of, and ligament injuries, 260–261

MR imaging of, 198

technical considerations for, 256–257

musculotendinous injuries of, 270–273

osseous injuries of, 265–267

osteoarthritis of. See Osteoarthritis, of hip.

osteochondral injury of, 262

septic arthritis of, 264

stress fracture of, 265–266

I

Ice hockey, injuries associated with, 319

Iliopsoas bursa, and bursitis, 268

Iliotibial band friction syndrome, joint effusion in

knee versus, 201, 202

Interosseous ligament, lesions of, 197–198

Intersesamoid ligament, rupture of, 306, 307

J

Joints, injuries of, related to sports, MR imaging

in. See specific joints.

Jumper’s knee, high signal in patellar tendon

versus, 201

K

Knee, chondrocalcinosis of, versus meniscal tear

of, 199, 200

joint effusion in, versus iliotibial band friction

syndrome, 201, 202

meniscal tear of, versus chondrocalcinosis of,

199, 200

MR imaging of, normal variants and pitfalls

in, 199–201

transverse ligament of, 199, 200

L

Labrum, acetabular, variability of, 198, 199

anatomic variations in, 260

anatomy and function of, 257

glenoid, 222–223

MR imaging of, 260

posterior tear of, 227–228, 230

superior, lesions of, 231–234

rotator cuff tears in, 231

tear(s) of, classification of, 258–259


diagnostic criteria for, 258

secondary findings in, 259–260

treatment of, and prognosis in, 260

Ligamentum teres, anatomy and function of, 260

arthroscopy of, 261

derangements of, 260

MR imaging of, 261

Lisfranc ligament, anatomy of, 304

injury of, 304–305

Luge, injuries associated with, 316–317

M

Magnetic resonance arthrography, direct, foot

and ankle sports protocols for, 296

of rotator cuff tears, 212

Magnetic resonance imaging, exercise

enhancement of, 343

gadolinium enhancement of, 342–343

gradiant echo imaging in, 342

of instability injuries of shoulder, 221–238

of joint, artifacts in, 193–194

magic angle phenomenon in, 194

truncation artifacts in, 193–194

variants in, related to sports injury, 193–205

of meniscal and cruciate ligament injuries,

283–293

of sports injuries to rotator cuff, 207–219

of sports-related hip disorders, 255–281

of stress fractures, 326–331

practical techniques for, 341–343

routine protocol for, 341–342

supplemental scans, 342–343

to classify osseous stress injury, 327

Malleolus, medial, stress fractures of, 333

Meniscocapsular separation, 200

Meniscofemoral ligaments, 199, 200

Meniscus, injuries of, and cruciate ligament

injuries, MR imaging of, 283–293

ossifications of, 200–201

postoperative, 200

tear(s) of, 284–291

asymptomatic, 199

mimics of, 199

Metatarsal stress fracture, 306, 308

375Index = Magn Reson Imaging Clin N Am 11 (2003) 373–378

Muscle(s), and tendons, of elbow, 248

denervation of, 362–363

herniation of, 356–358

imaging in, 358

location of, 357

symptoms and signs of, 357–358

treatment of, 358

injuries of, sports-related, apophyseal avulsion,

343, 344

delayed-onset muscle soreness in, 353

differential diagnosis of, 362, 363

first-degree strain, 344–345, 346

hematoma and pseudotumor

appearance, 347–348, 349, 350

injuries of, 341–371

muscle contusion in, 353–354

myositis ossificans, 354–355

myotendinous strain injury, 344–345,

346

radiography and computed tomography

in, 355–356

second-degree strain, 345–347

specific, 348–353

third-degree strain, 347, 348

lacerations of, 356, 357

Musculotendinous injuries, of hip, 270–273

Myositis ossificans, 354–356

bone scintigraphy in, 356

MR imaging in, 356, 357

treatment of, 356

Myotendinous strain injury, 344–345, 346

N

Navicular stress fracture(s), 306, 308, 335

O

Osteitis pubis, 273

Osteoarthritis, of hip, clinical features of, 262–263

differential diagnosis of, 264

dysplasia and, 257–258

femoroacetabular impingement in, 263


treatment of, 264

Overuse syndromes, of elbow, epicondylitis and,

248–250

P

Patellar tendon, high signal in, versus jumper’s

knee, 201

Pectoralis major muscle, strain injury of, 348–349,

351

Peroneus brevis splits syndrome, 300, 303

Pigmented villonodular synovitis, 265

Plantar fasciitis, 300–301, 303

Plantar nerve, impingement of, 301–302, 303

Plantaris tendon, rupture of, with muscle strain,

352, 353

Posterior cruciate ligament, injuries of, 291, 292,

293

Posterosuperior impingement syndrome, 234

Pseudo dorsal intercalated segment instability,

197, 198

R

Radial collateral ligament complex, 244–245,

247

Radiography, in sports-related muscle injuries,

355–356

in stress fractures, 324–326

Radionuclide imaging, of tibial stress fracture,

337–338

Rotator cuff, contusion of, 214

injuries of, MR imaging of, 213–218

instability of, secondary impingement and,

208–209

macrotrauma of, from contact sports, 209, 211

normal interval, 225

normal MR imaging appearance of, 211,

212–213

posterior impingement of, 209

primary impingement of, 207–208

secondary impingement of, and instability,

208–209

sports injuries to, categories of, 207


strain of, 214

tear(s) of, 214

conventional MR imaging technique in,

210, 211–212

in older athlete, 211

in SLAP lesion, 231

MR arthrography of, 212

posterosuperior impingement, 215–218

rim-rent, 213, 214–215

standard, 214

tensile overload of, 211


S

Septic arthritis, of hip, 264

Shin splints, 328–329

Shoulder, acute traumatic instability of, 234

Buford complex versus labral tear of, 195

injuries of, in alpine skiing, 313–314

instability injuries of, MR imaging of, 221–238

labral variability in, MR imaging of, 194

MR imaging of, in normal anatomy and

biomechanics, 222–227

pathophysiology and, 227

strategies for, 221–222

muscles around, 225

os acromiale versus acromial fracture, 195–196

pain in, causes of, 207

postopertive, imaging of, 196

primary disease of, 230–231

sublabral hole versus labral tear of, 194–195

sublabral recess versus superior labrum

anteroposterior lesion, 195, 196

Sinus tarsi syndrome, posttraumatic, 303, 304

Skiing, alpine (downhill), events grouped as,

311–312

knee injuries associated with, 312–313

mechanisms of injury in, 312

risk of injury from, 312

nordic (cross-country), risk of injury in, 314

Snapping hip syndrome, 270–271

MR imaging in, 271

Snowboarding, foot injuries associated with, 315

risk of injury in, 314–315

spinal injuries associated with, 315–316

upper extremity injuries in, 315, 317

Speedskating, injuries associated with, 318,

319–320

Sports injuries, hip disorders related to, MR

imaging of, 255–281

in winter sports, 2002 Winter Olympics

experience, 311–321

of elbow, 239–253

of foot and ankle, imaging of, 295–310

of muscle, imaging of, 341–371

related to joint, MR imaging of, variants in,

193–205

to rotator cuff, MR imaging of, 207–219

Stress fracture(s), bone scintigraphy in, 332–334


computed tomography in, 330, 331, 334

in athlete, imaging of, 323–339

mechanism of injury in, 323–324


navicular, 306, 308, 335

of femoral neck, 336–337

of hip, 265–266

of medial malleolus, 333

pathogenesis of, 323–324

radiography in, 324–326

sites of, 335–338

tibial, 328, 329, 330, 331, 337–338

ulnar, 332

Stress injury, osseous, MR imaging classification

of, 327

Sublabral recess, 224

Synovial (osteo)chondromatosis, idiopathic,

264–265

Synovial plicae, 197

Synovitis, pigmented villonodular, 265

T

Talar dome, osteochondral defect of, 308, 309

pseudodefect of, 203

Tarsal tunnel syndrome, 302–303

Tendonitis, Achilles, 296–297

Tendonosis, 214

Tendons, of elbow, anatomy and pathology of,

247–252

Tennis leg, 352

Tibia, stress fractures of, 328, 329, 330, 331

longitudinal, 337–339

Tibiofibular syndesmotic injury, 300, 302

Transverse acetabular ligament, 261

Triceps tendon, rupture of, 251–252

Trochanteric bursae, and lateral hip pain,

268–270

Trochlear groove, variations of, 197

Turf toe injury, 305, 306

U

Ulna, stress fractures of, 332

Ulnar collateral ligament, tears of, in alpine

skiing, 314

Ulnar collateral ligament complex, 242

377Index = Magn Reson Imaging Clin N Am 11 (2003) 373–378

V

Volkmann’s ischemic contracture, 358–359

W

Winter sports, injuries associated with, alpine

skiing and, 311–314

bobsledding and, 316

ice hockey and, 319

luge and, 316–317

nordic (cross-country) skiing and, 314

skeletal, 317

snowboarding and, 311–314

speedskating and, 318, 319–320

study population for, 311

2002 Winter Olympics experience,

311–321

Wrist, imaging of, normal variants and pitfalls of,

197–198


mri clinics - imaging of sports injuries

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