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AJR:200, April 2013 845

MRI of Heel Pain

David A. Lawrence1

Michael F. Rolen1

Khaled Abi Morshed2

Hicham Moukaddam1

Lawrence DA, Rolen MF, Morshed KA, Moukad-

dam H

1Department o Diagnostic Radiology, Yale University

School o Medicine, 333 Cedar St, PO Box 208 057,

New Haven, CT 065 20. Address correspondence to

H. Moukaddam ([email protected]).

2Department o Radiology, Beirut Arab University, Beirut,

Lebanon.

Musculoskeleta l Imaging • Review

CME/SAM

This article is available or CME/SAM credit.

AJR 2013; 200:845–855

0361–803X/13/2004–845

© American Roentgen Ray Society

Keywords: calcaneodynia, heel pain

DOI:10.2214/AJR.12.8824

Received February 28, 20 12; accepted ater revision

April 18, 2012.

Radiographs are oten obtained to exclude

acute causes o heel pain, such as calcaneal

racture; this has been well discussed in oth-

er articles and will not be urther addressed

here [2]. Some other causes o heel pain have

characteristic radiographic ndings, where-

as other causes have nonspecic ndings.

These will be discussed in this article.

MRI allows superior sot-tissue contrast

resolution, is noninvasive, and is widely avail-

able. It can be very helpul in equivocal cas-

es o heel pain. Additionally, some causes o

heel pain require surgical intervention (such

as an Achilles tendon tear), and the inorma-

tion gleaned rom MRI can infuence presur-

gical planning. In this article, we rst review

the normal anatomy o the posterior ankle and

hindoot and then review the causes o heel

pain, with attention to the clinical, radiograph-

ic, and MRI ndings.

Anatomy

Three ligamentous groups support the ankle:

the syndesmotic ligament complex, the lateral

collateral ligament, and the deltoid ligament.The syndesmotic ligament complex is com-

posed o the anterior and posterior tibiobular

(also known as the anterior inerior and posteri-

or inerior tibiobular) and interosseous liga-

ments. The lateral collateral ligament can be

subdivided into the anterior talobular, poste-

rior talobular, and calcaneobular ligaments.

The deltoid ligament contains the anterior and

posterior tibiotalar, tibiospring, tibiocalcaneal,

and tibionavicular ligaments.

Heel pain is a common problem that

may be due to a variety o sot-

tissue and osseous abnormalities.

Knowledge o the anatomy o the

posterior ankle and hindoot oers a useul way

to approach diagnosing the cause o the heel

pain: osseous, ligamentous, tendinous, and oth-

er sot-tissue structures. Some o the more com-

mon causes include Achilles tendinosis, Achilles

tendon tear, Achilles peritendinitis, Achilles

paratendinitis, insertional tendinitis o the Achil-

les tendon, retrocalcaneal bursitis, Haglund phe-

nomenon, plantar asciitis, plantar ascial tear,

calcaneal stress racture, calcaneal insuciency

racture, and Sever disease (in the pediatric

population). Radiographs are oten obtained

to exclude acute osseous abnormalities, such

as calcaneal ractures. MRI oers superior sot-

tissue contrast resolution and can be helpul

in diagnosis as well as in presurgical planning.

Heel pain, or calcaneodynia, is a common

problem, which may be present in up to 15%

o patients presenting to their primary care cli-

nician. Clinical examination is generally help-

ul in localizing the region o pain, which con-sequently can narrow the otherwise broad

dierential diagnosis (Table 1). Anatomical-

ly, heel pain may arise rom six structures: the

plantar ascia, tendons (e.g., Achilles, fex-

or digitorum longus), calcaneus, various bur-

sae, the tarsal tunnel, and the heel plantar at

pad [1]. Additionally, accessory muscles may

cause heel pain. The most common accessory

muscle is the accessory soleus muscle, which

may cause posteromedial ankle pain.

OBJECTIVE. The purpose o this article is to review the normal anatomy o the posterior

ankle and hindoot and review the causes o heel pain, with attention to the clinical, radio-

graphic, and MRI ndings.

CONCLUSION. Heel pain is a common problem that may be due to a variety o sot-

tissue and osseous abnormalities. Knowledge o the anatomy o the posterior ankle and hind-

oot oers a useul way in approaching heel pain. Some o the more common causes include

Achilles tendinosis, Haglund phenomenon, and plantar asciitis. MRI oers superior sot-tissue contrast resolution and can be helpul in diagnosis as well as in presurgical planning.

Lawrence et al.MRI o Heel Pain

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These ligaments, as is true o ligaments

throughout the body, appear as thin linear hypo-

intense structures on both T1- and T2-weighted

images. Interposition o at between the liga-

ments can be seen in normal individuals [3].

The ligaments can routinely be evaluated on

three-plane MRI with a slice thickness o 3

mm or less.

Several ankle tendons are present in the

posterior ankle and hindoot. These include

the Achilles, posterior tibial, fexor digitorum

longus, fexor hallucis longus, and peroneal

tendons. Pathology o these tendons has been

well described in the radiology literature [3].

We will discuss the most common tendon to

be diseased: the Achilles tendon. The Achilles

tendon is ormed by the junction o the medial

and lateral heads o the gastrocnemius tendons

joining with the soleus tendon. The Achilles

tendon lacks a tendon sheath but is instead sur-

rounded by a peritenon (connective tissue also

called the paratenon), which is composed o

visceral and parietal layers. The vascular sys-

tem o the peritenon extends within and out-

side o the Achilles tendon. Importantly, 2–6

cm proximal to the calcaneal insertion there is

an area o diminished blood supply to the ten-

don, known as the “critical zone.” The poor

vascular supply to this area results in slow-

er tendon repair. Subsequently, this is where

most Achilles tendon disease occurs [4]. The

insertion site o the Achilles is an enthesis and

is intimately related to the retrocalcaneal bur-

sa [5]. Posterior to the tendon, there may be

an acquired or adventitial bursa, known as the

“retro-Achilles bursa.”

The ankle tendons appear as hypointense

linear structures on T1- and T2-weighted im-

ages. T2-weighted images are helpul or show-

ing intratendinous or peritendinous edema, the

hallmark o tendinitis. It is important to note

the magic angle eect, which occurs at ap-

proximately 55° with the main magnetic vector

(B0) in sequences with TEs less than approx-imately 35 milliseconds and may produce in-

creased signal within normal structures [6].

Careul analysis o the tendon in question in

multiple planes and evaluation with prolonged

TE sequences (T2-weighted) will help avoid

this pitall. The Achilles tendon has a normal

thickness o 6 mm [4]. On axial images, the

anterior margin o the Achilles tendon should

be concave or most o its course.

The retrocalcaneal bursa should measure less

than 1–2 mm in anteroposterior dimension [7].

I enlarged, it may represent disease, especially

i surrounding edematous changes are present.

The subcutaneous at should be seen between

the Achilles tendon and the skin. I this at can-

not be seen on MRI, a blister or retro-Achil-

les bursitis may be present. In particular, retro-

Achilles bursitis is distinguished by edematous

changes without mass eect on the skin [4].

The plantar aponeurosis consists o medial,

central, and lateral bands. The plantar ascia

represents the thickest central band. The plan-

tar ascia is adherent to the underlying fexor

digitorum brevis muscle. The plantar ascia

originates rom the medial calcaneal tuberosity

and splits into ve bands that insert onto each

TABLE 1: Differential Diagnosis [62]

Category Dierential Diagnosis Considerations

Arthritic Gout, rheumatoid arthritis, seronegative arthropathy; primary or secondaryosteoarthritis

Inectious Diabetic ulcer, osteomyelitis, plantar warts

Mechanical Plantar—plantar asciitis, heel spur, calcaneal stress racture, medial or lateral

plantar nerve entrapment, heel pad syndrome, oreign body granulomatosisPosterior—Achilles tendinopathy, Haglund deormity, ret rocalcaneal bursitis, tarsal

coalition, accessory muscles, Sever disease (pediatrics)

Neuropathic Lumbar radiculopathy, nerve entrapment, neuroma, tarsal tunnel syndrome

Trauma

Tumor (rare) Ewing sarcoma, neuroma

Vascular (rare)

Fig. 1—60-year-old man with several months o posterior heel pain.A and B, Sagittal STIR image (A) and axial proton-density image (B) show thickening o distal Achilles tendon(arrows , A) with no evidence o tear, consistent with Achilles tendinosis. Note loss o normal concave shape oanterior aspect o Achilles tendon (arrowhead , B).

Fig. 2—45-year-old man with posterior heel andlower leg pain. Axial STIR image shows diuse

thickening o distal Achilles tendon (arrows ) withintratendinous small ocus o increased near-uidsignal intensity. Note that normal concavity alonganterior aspect o tendon has been los t (arrowhead ).Findings are consistent with distal Achilles tendinosisand small intrasubstance tendon tear.

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MRI of Heel Pain

o the proximal phalanges. On MRI, the nor-

mal ascia appears 2- to 4-mm thick and hypo-

intense on T1- and T2-weighted sequences [8].

Osseous anatomy is primarily dened by the

calcaneus. The calcaneus is the largest tarsal

bone and is designed to bear the weight o the

body. Traction trabeculae radiate rom the in-

erior cortex, and compression trabeculae ra-

diate to the anterior and posterior articular ac-

ets. The lateral surace o the calcaneus is fat

with a central peroneal tubercle where the cal-

caneobular ligament attaches. The lateral talo-

calcaneal ligament attaches anterosuperior to

the peroneal tubercle. Medially, the interos-

seous and medial talocalcaneal ligaments hold

the talus and calcaneus in close apposition.

The plantar aponeurosis inserts on the calca-

neus along the anterior and plantar aspect. The

Achilles tendon inserts along the middle por-

tion o the posterior aspect o the calcaneus.

The calcaneus usually ossies by the third

month o gestation. There is a normal vari-

ant in which the calcaneus develops rom two

ossication centers with an apophysis devel-

oping along the posteroinerior aspect o the

calcaneus. This apophysis begins ossication

at 4–7 years in girls and 7–10 years in boys. It

uses with the calcaneus by 12–15 years [9].

This can be important to remember in pediat-

ric patients presenting with heel pain.

Causes of Heel Pain

Achilles Tendinosis

Achilles tendinosis is oten the common

precursor by which most Achilles tendon dis-

ease stems and reers to intratendinous de-

generation by one o our main mechanisms:

hypoxic-bromatosis, myxoid, lipoid, and os-

seous-calcic [10].

Hypoxic degeneration is the most requent

type seen in ruptured Achilles tendons and is

thought likely secondary to the relative hypo-

A

A

Fig. 3—60-year-old man with acute onset oposterior heel pain while playing tennis.A, Sagittal T2-weighted image with at-saturationshows complete discontinuity o distal Achilles

tendon (arrowheads ), consistent with completeAchilles tendon tear with tendon retraction. Noteassociated increased T2 signal intensity, which likelyrepresents combination o edema and hemorrhage.B, Axial proton-density image shows residual

plantaris tendon (arrow ).

Fig. 4—30-year-old man with acute onset oposterior heel pain while playing basketball.A and B, Sagittal T1-weighted image (A) andT2-weighted image with at-saturation (B) showdiscontinuity o Achilles tendon (arrows , A)approximately 2 cm rom distal insertion, consistentwith complete Achilles tendon rupture. Note thathemorrhage in distal gast rocnemius muscle is seenas areas o increased T1 and T2 signal (circles ).

B

B





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vascularity o the 2–6 cm area o the tendon

that lies proximal to the calcaneal insertion,

known as the “watershed area” or “critical

zone” [11, 12]. This type o degeneration o-

ten ollows multiple symptomatic episodes

[12]. Axial MRI shows usiorm thickening

o the tendon with loss o the normal concave

anterior margin (Fig. 1) but oten lacks theinternal increased signal intensity seen with

other types o tendinosis [4].

The most common asymptomatic type o de-

generation is myxoid, whereby mucoid patches

and vacuoles intersperse between thinned ten-

don bers [13]. These vacuoles then coalesce,

resulting in the ormation o interstitial tears

along the long axis o the tendon. Because o

the asymptomatic nature o myxoid degenera-

tion, it is not rare or patients to show an Achil-

les tendon tear at initial presentation. On MRI,

mucoid deposits will show linear areas o in-

creased signal on T1-weighted and proton den-

sity sequences. T2-weighted and STIR imaging

will show interrupted and irregular areas o in-

creased signal within the tendon [4].

Lipoid degeneration results in atty de-

posits within the tendon and is the most age

dependent o the our types o degeneration

[14]. Interestingly, lipoid degeneration does

not alter the structural properties o the ten-

don and thus, does not predispose the tendon

to tear [15, 16]. However, lipoid degeneration

is related to xanthobromatosis, which o-

ten shows nodular thickening o the Achil-

les tendon with low to intermediate signal on

all MRI sequences but enhances ater the ad-

ministration o gadolinium [17].

The ourth type o degeneration resulting

in Achilles tendinosis is calcic tendinopathy.

Although rare, dystrophic calcication o the

tendon can progress to the ormation o cor-tical bone and trabeculae within the aected

area o the tendon, which distinguishes this

type o degeneration on radiography, CT, and

MRI [18].

Achilles Tendon Tear

Tears o the Achilles tendon oten occur in

middle-aged men between 30 and 50 years old

who engage in leisure athletic activities that in-

volve concentric loading, such as basketball

and tennis, resulting in indirect trauma to the

tendon [19]. Although most o these types o

tears occur in the watershed region o the ten-

don, more proximal tears at the myotendinous

junction can also occur, which are more com-

mon in younger men and can result rom direct

trauma [20]. Systemic diseases, such as rheu-

matoid arthritis, gout, lupus, and diabetes mel-

litus as well as fuoroquinolone use have also

been implicated in tears o the Achilles [21–23].

In terms o tear severity, the spectrum in-

cludes microtears, interstitial tears, partial tears,

and complete tears or ruptures [24]. Microtears

are not visible on imaging but are oten the incit-

ing event that leads to tendinosis [25]. Increased

signal on T2-weighted sequences is the MRI

nding common to interstitial, partial, and

complete tears [26].

Interstitial tears are oten the sequelae o

myxoid degeneration o the tendon as previ-

ously described and are longitudinally ori-

ented [4]. On MRI, linear areas o increasedsignal are seen on T1-weighted, proton den-

sity, and fuid-sensitive sequences, but the

surrounding bers are intact. Treatment in-

volves surgical débridement o the mucoid

degenerative center with oversewing o the

peripheral bers o the tendon [27].

Partial tears show heterogeneous high sig-

nal intensity on fuid-sensitive MRI sequenc-

es, and there is incomplete interruption o

the tendon bers (Fig. 2). Involved bers can

partially retract and display a rayed or cork-

screw appearance. Complete tears are identi-

ed by their high signal intensity fuid-lled

tendinous gap, with either distracted or over-

lapping bers (Figs. 3 and 4). Intratendinous

or peritendinous edema and hemorrhage are

oten present in the acute setting [23].

Surgical repair o partial and complete tears

is determined using the our-stage Kuwada

classication system, which is based primar-

ily on the size o the gap between the retract-

ed ends o the torn tendon: type I, partial tear

involving 50% or less o the tendon; type II,

complete tear with a gap o less than 3 cm;

A

Fig. 5—20-year-old man with posterior heel pain.A and B, Two sequential axial T2-weighted images with at-saturation show thin rim o increased signalaround Achilles tendon (arrows ), denoting inammation o peritenon. Findings are consistent with Achillesperitendinitis.

Fig. 6—35-year-old man with heel pain. AxialT2-weighted image with at saturation showsinammation o peritenon (around Achilles tendon),best appreciated as thin rim o increased signalintensity around tendon (arrows ). Findings areconsistent with Achilles peritendinitis.

B




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type III, complete tear with a gap o 3–6 cm;

and type IV, complete tear with a gap o great-

er than 6 cm. Type I and II tears are typically

repaired with end-to-end anastomosis, where-

as an autogenous tendon grat fap is used or

type III tears. Type IV tears usually require a

ree tendon grat or synthetic grat [28].

Chronic tears can result in varying degreeso muscle atrophy, which can be reversible

or irreversible [29]. Reversible atrophy is o-

ten seen in the acute setting and is character-

ized by diuse edema noted throughout the

muscle [30]. Over time, the muscle takes on

a more atty inltrated appearance, which o-

ten signals irreversible atrophy [31]. O note,

the soleus is more susceptible to atrophy than

the gastrocnemius secondary to its greater

proportion o slow twitch type I bers [32].

Thereore, imaging protocols should include

sagittal views o the distal soleus when evalu-

ating or Achilles tendon injury.

Achilles Peri tendiniti s and Paratendinitis

Achilles peritendinitis reers to infamma-

tion o the connective tissue peritenon that

surrounds the tendon. Clinically, this entity

is similar to synovitis or tenosynovitis that

is seen in sheathed tendons. MRI shows high

T2 signal intensity around the tendon, which

is partially circumerential and is most evi-

dent along the posterior surace o the ten-

don (Figs. 5 and 6). However, given that the

Achilles tendon lacks a true synovial mem-

brane, the high T2 signal intensity is not as

bright as that seen with synovial fuid [4].A related entity is Achilles paratendinitis,

which, although the term is oten used inter-

changeably with peritendinitis, more accurate-

ly describes infammation o the pre-Achilles

(Kager) at pad. Fat-suppressed fuid-sensitive

sequences show increased signal and edema

with irregularity o the at pad anterior to the

tendon. T1-weighted images show replace-

ment o the normal high-signal-intensity at

(Fig. 7). Both peritendinitis and paratendini-

tis can be ound in conjunction with tendinosis

but may also be isolated ndings.

Retrocalcaneal BursitisAnother common cause o posterior heel

pain is retrocalcaneal bursitis, which can be a

maniestation o Achilles tendinosis but can

also be a separate entity. Repetitive trauma is

the most common cause and is requently ound

in runners. Other causes include rheumatoid

arthritis and seronegative spondyloarthropa-

thies [33]. Treatment is usually conservative,

although corticosteroid injection is sometimes

A

C

B

B

A

Fig. 7—70-year-oldwoman with heel pain.A, Lateral radiograph oankle shows increasedsot-tissue density inregion o pre-Achilles atpad (arrow ).B and C, Sagittal T2-weighted image with

at-saturation (B) andT1-weighted image (C)show inammatorychanges (arrowhead,B)in pre-Achilles (Kager) atpad. Note replacemento normal at seen on T1-weighted image (curved arrow, C), consistent withAchilles paratendinitis.

Fig. 8—40-year-old man with right heel pain.A, Lateral radiograph shows increased sot-tissue density in region o pre-Achilles at pad (arrow ).B, Sagittal T2-weighted image with at saturation shows uid distended bursa (arrowhead ) and surroundingsot-tissue inammation, consistent with retrocalcaneal bursitis.





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used [34]. However, caution should be exer-

cised i there is coexisting Achilles tendino-

sis because steroids can urther weaken an al-

ready at-risk tendon, making the tendon more

susceptible to tear or rupture [35, 36].

Radiography can show obliteration o the

normal retrocalcaneal at by the enlarged fu-

id-lled bursa (Fig. 8A). On MRI, a fuid col-

lection between the posterior calcaneus and

the insertion o the Achilles tendon can be

seen, which shows low signal intensity on T1-

weighted sequences and high signal intensity

on T2-weighted and STIR sequences (Figs.

8B and 9). Enlargement o the normal bursal

sac is the hallmark MRI nding, with values

greater than 7 mm craniocaudal, 11 mm trans-

verse, and 1 mm anteroposterior considered

abnormal [7]. Additionally, adjacent sot-tis-

sue infammatory changes are common.

Insertional Tendinosis of the Achilles Tendon

Insertional Achilles tendinosis is one o the

main causes o posterior heel pain [37]. Gen-

erally, this condition is secondary to chronic

A

A

Fig. 9—43-year-old woman with chronic heel pain.A, Axial oblique T2-weighted image with at saturation shows abnormally increased signal in region oretrocalcaneal bursa (asterisk ) and in subcutaneous tissues between posterior aspect o Achilles tendon and

skin (arrow ), consistent with retrocalcaneal and adventitial bursitis, respectively.B, Sagittal T2-weighted image with at saturation shows abnormal increased intratendinous signal intensity indistal Achilles tendon at its insertion (arrow ), consistent with insertional Achilles tendinitis. Additionally, notereactive bone marrow edema along posterior superior calcaneal tuberosity (arrowhead ).

Fig. 11—60-year-old old woman with heel pain.A, Sagittal T1-weighted image shows osseous excrescence along posterosuperior aspect o calcaneal tuberosity (arrow ), consistent with Haglund deormity.B and C, Sagittal (B) and axial (C) T2-weighted images with at saturation show bone marrow edema in region o Haglund deormity (arrowhead , B). Additionally, there isabnormally increased T2 signal intensity in region o retrocalcaneal bursa (asterisk , C) as well as between tendon and sk in (arrow , C), consistent with retrocalcaneal andadventitial bursitis, respectively. Furthermore, region o insertion o Achilles tendon shows evidence o edema (arrow , B), consistent with insertional Achilles tendinosis.

These fndings o inammation taken together with Haglund deormity are consistent with Haglund syndrome.

Fig. 10—40-year-old man with heel pain. Normalcalcaneal tuberosity is present. Calcaneal pitchlines are created by frst drawing lower pitch line

tangent to anterior tubercle. Upper pitch line is then

drawn parallel to lower pitch line at level o subtalararticular acet. Calcaneal tuberosity is enlarged i itextends superior to upper pitch line.

B

B C







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repetitive trauma with associated microtears

due to excessive use o the cal muscles. This

condition is most oten seen in ballet danc-

ers, runners, and athletes who participate in

jumping sports. Additionally, systemic con-

ditions, such as rheumatoid arthritis and se-ronegative spondyloarthropathies, are also

associated with the condition [37]. Infam-

mation o the peritenon may precede or be

associated with insertional Achilles tendino-

sis. Insertional Achilles tendinosis is also re-

quently associated with Haglund deormity

o the calcaneus.

MRI shows thickening o the tendon at its in-

sertion, with loss o the normal concavity o the

anterior margin o the tendon [37, 38]. Intraten-

dinous areas o increased signal may be seen

with some edema o the adjacent sot tissue

and possibly the adjacent calcaneal tuberosi-

ty at the level o the tendon insertion (Fig. 9).

Haglund Deformity and Syndrome

Haglund syndrome, rst described by Pat-

rick Haglund in 1927, is not an uncommon

cause o posterior heel pain and consists o a

constellation o sot-tissue and osseous abnor-

malities. The Haglund deormity is dened by

the presence o a prominent bursal bony pro-

jection o the calcaneus, which is generally as-

sociated with wearing low-back shoes. The

bony deormity, along with the shoes in ques-

tion, may lead to a mechanically induced in-

fammation o the supercial bursa, Achilles

tendinosis, and retrocalcaneal bursitis. These

infammatory changes in the presence o the

bony deormity are together known as Haglund

syndrome [9, 39]. Hindoot varus and pes ca-

vus are predisposing actors [40]. Most impor-tant is the presence o chronic stress.

On radiographs, the Haglund deormity is

maniested by a bony projection along the supe-

rior posterior aspect o the calcaneal tuberosity

on the lateral view (the radiographic equivalent

o the “pump bump”). Diagnosing an enlarged

calcaneal tuberosity is accomplished by draw-

ing parallel pitch lines along the superior and

inerior aspects o the calcaneus. The lower

pitch line is tangent to the anterior tubercle. The

upper pitch line is drawn parallel to the lower

pitch line and at the level o the subtalar articu-

lar acet (Fig. 10). The calcaneal tuberosity is

enlarged i it extends superior to the upper pitch

line [41]. Although radiography cannot be reli-

ably used to diagnose Haglund syndrome, loss

o the normal radiolucent retrocalcaneal recess

is important to note because it indicates retro-

calcaneal bursitis [1].

MRI may be required or ambiguous or

clinically equivocal cases. I present, a bony

bump along the superior posterior corner o

the calcaneal tuberosity is well visualized on

sagittal T1-weighted images (Fig. 11). T2-

weighted images will show excessive fuid

in the retrocalcaneal bursa and fuid in the

retro-Achilles bursa [4]. The presence o bone marrow edema in the calcaneal tuber-

osity supports the theory o the condition be-

ing caused by chronic repetitive mechanical

compression and infammation [42].

Plantar Fasciitis

Plantar asciitis is the most common cause

o inerior heel pain [43]. Plantar asciitis is

most commonly due to repetitive mechani-

cal stress, specically, prolonged pronation

stresses. This produces microtears and in-

fammation o the ascia and periascial sot

tissues. The condition is commonly seen in

runners and obese patients [44]. Additional-ly, it may be a result o an enthesopathy in

association with seronegative spondyloar-

thropathies, such as ankylosing spondylitis,

Reiter syndrome, or psoriatic arthritis [1].

Lateral radiographs oten show a calcaneal

spur, a very nonspecic nding [3].

MRI ndings include plantar ascial thick-

ening, intraascial edema on T2-weighted

images, edema surrounding the ascia on T2-

B

B

A

A

Fig. 13—52-year-old woman with plantar heel pain.A and B, Sagittal (A) and axial (B) T2-weighted images with at saturation show complete discontinuity oplantar ascia (arrow , A and B), consistent with ull-thickness tear o plantar ascia. Also note some uidsurrounding exor hallucis tendon sheath on axial image (arrowhead , B).

Fig. 12—42-year-old man with heel pain.A and B, Sagittal T2-weighted image with at-saturation (A) and T1-weighted image (B) show plantar ascia

thickening (arrows , B) and edema (arrowheads , A) along calcaneal insertion o plantar ascia, with reactivebone marrow edema. Findings are consistent with plantar asciitis. Also noted is small calcaneal bone spur,nonspecifc fnding.





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weighted images (primarily that the proxi-

mal aspect o the ascia is edematous), and in-

creased intraascial T1 signal [44] (Fig. 12).

Fascial thickening is dened as greater than 3

mm, with some cases thickening to 7–8 mm

[3]. The thickening is usually usiorm as op-

posed to the ocal nodular thickening o the as-

cia seen in plantar bromatosis. In addition, the

nodular thickening o plantar bromatosis oc-

curs distal to the calcaneal insertion at the lev-

el o the midoot. Furthermore, marrow edema

in the calcaneal tuberosity may be present [45].

Tear of the Plantar FasciaRupture o the plantar ascia is typically a

sports-related injury that is generally seen in

athletes engaged in running and jumping [46].

Additionally, it can be seen in patients with

chronic plantar asciitis receiving local corti-

costeroid injections [47]. Most cases o plan-

tar ascia rupture involve the proximal ascia

near its calcaneal insertion—similar to the lo-

cal edema seen in plantar asciitis. Distal (an-

terior) tears also may occur [37, 45].

Radiography has little role in diagnosing

plantar ascia rupture aside rom excluding

other causes o plantar heel pain. MRI nd-

ings are the same as would be seen in other

ascial or aponeurosis tears. Acute tears show

partial or complete disruption o the normallylow-signal-intensity ascia, with areas o ede-

ma and hemorrhage best seen on T2-weight-

ed or STIR sequences [1] (Fig. 13). Periascial

fuid accumulation is oten also seen. Further-

more, it is important to inspect the fexor digi-

torum brevis muscle because plantar ascia

rupture is commonly associated with tears o

the fexor digitorum brevis muscle [45]. Acute

and subacute muscle tears show intramuscu-

lar areas o increased signal on T1- and T2-

weighted images, representing bleeding and

edema within the muscle [1]. Less commonly,

strains o other plantar muscles may be pres-ent, such as the abductor halluces or quadratus

plantae muscles [45].

B

B

A

A

Fig. 16—12-year-old boy who presented with posterior heel pain and ocal tenderness.A, Sagittal T2-weighted image with at saturation shows bone marrow edema in calcaneal apophysis (arrow ). Findings are consistent with calcaneal apophysitis (Severdisease).B, Follow-up sagittal T2-weighted MR image with at saturation obtained ater 5 months shows resolution o bone marrow edema in calcaneal apophysis with clinicalresolution o symptoms. Additionally, ollow-up examination shows aint bone marrow edema in talus (arrowheads ), nonspecifc fnding (normal signal on T1-weightedimage not shown).

Fig. 14—82-year-old woman with chronic poorly defned heel pain.A and B, Sagittal T2-weighted image with at saturation (A) and T1-weighted image (B) show ill-defned bonemarrow edema inerior to posterior subtalar articular acet (arrow ) and low-signal-intensity (nondisplacedracture) line just deep in relation to posterior articular acet (arrowhead ), consistent with calcaneal stress(insufciency) racture.

Fig. 15—38-year-old woman with posterior heelpain. Sagittal T2-weighted image with at saturationshows abnormal curvilinear area o decreased T2signal intensity (arrow ), consistent with racture oposterior calcaneal tuberosity. Increased T2 signalin region o retrocalcaneal bursa (arrowhead ) isindicative o associated retrocalcaneal bursitis

and inammatory changes in pre-Achilles at pad.Findings are consistent with calcaneus stress(atigue) racture.




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Calcaneal Stress Fracture

The calcaneus is the second most common

site o atigue stress ractures, ater the meta-

tarsal bones. Insuciency stress ractures may

be seen in patients with rheumatoid arthritis or

neurologic disorders. Stress ractures general-

ly involve the posterosuperior or posterior as-

pects o the calcaneus and are usually orientedvertically or perpendicular to the long axis o

the calcaneus [1]. Patients with diabetes mel-

litus are at increased risk o calcaneal insu-

ciency ractures, particularly those involving

avulsion o the posterior process o the calca-

neus [48]. Stress ractures o the anterior two

thirds o the calcaneus may be more requent

than previously thought [49].

Radiographs are insensitive or acute stress

ractures, appearing normal in more than 70%

o the cases in one series [2, 50]. Follow-up ra-

diographs are diagnostic in only 50% o cases

[51]. When abnormalities are present, a stress

racture will show incomplete linear sclerosis

running orthogonal to the major trabeculae,

best seen on lateral radiographs.

CT is occasionally used to diagnose cal-

caneal stress ractures because it will show

disruption o the bony cortex with surround-

ing periostitis. The sensitivity o CT is high-

er than radiography but poorer than MRI and

bone scanning.

MRI shows characteristic ndings, includ-

ing bandlike areas o low signal intensity in the

medullary space, surrounding marrow space

signal abnormalities with ill-dened areas o

T1 hypointensity and T2 hyperintensity that

represent medullary edema, and hemorrhage

[1, 51, 52] (Figs 14 and 15). Periosteal callus

ormation starts shortly ater the racture and

appears as a hypointense line running parallel

to the cortex, which represents the elevated

periosteum [48].

Sever Disease (Calcaneal Apophysitis)

Apophyseal injuries are unique to the im-

mature skeleton; traction apophyseal injuries

may occur acutely at the site o tendinous in-

sertion. Chronic apophysitis is caused by in-

fammatory changes at the site o tendinous

insertion into a bony prominence. When this

occurs at the calcaneal apophysis, the associ-

ated eponym is Sever disease, rst described

by J. W. Sever in 1912.

Several authors have argued that calcane-

al apophysitis is primarily a clinical diagno-

sis [53, 54]. However, oot radiographs are

oten obtained to exclude other causes. Unor-

tunately, there are no pathognomonic radio-

graphic ndings o calcaneal apophysitis [55,

56]. Nonspecic radiographic eatures include

increased density and greater ragmentation

o the apophysis, which may also be seen in

healthy children [55].

As might be expected, MRI will show edem-

atous changes within the calcaneal apophysis,

possibly extending into the adjacent calcane-

al tuberosity (Fig. 16). Furthermore, in equiv-

ocal cases, MRI can be helpul in excluding

other causes o heel pain.

Os Trigonum Syndrome

The posterolateral talus has a variety o ana-

tomic variants, including a normal tubercle; en-

largement o the lateral tubercle o the posterior

process o the talus, known as the “Stieda pro-

cess”; and a separate ossicle, known as an “os

trigonum,” which may or may not be used to

the posterior process o the talus. The os trigo-num is considered by some to represent a de-

velopmental anomaly analogous to a secondary

ossication center because it is ormed by en-

dochondral ossication within a cartilaginous

extension rom the talus [57]. The mineralized

os trigonum appears between the ages o 7 and

13 years and usually uses with the talus within

1 year. In approximately 10% o patients, it re-

mains as a separate ossicle [58].

Clinically, the os trigonum is asymptomatic

unless impingement occurs; hence, os trigonum

syndrome is also known as “posterior ankle

impingement syndrome.” Other osseous abnor-

malities o the posterior talus may also result in

posterior ankle impingement syndrome, such as

the Steida process [59]. Strenuous activities that

result in extreme plantar fexion can cause com-

pression o the adjacent synovial and capsular

tissue against the tibia [60]. Thus, the syndrome

is oten seen in athletes participating in ballet,

ootball, and soccer.

On radiography, the normal os trigonum

generally shows smooth margins. Repetitive

trauma to the os trigonum may result in a

racture o the ossicle.

On MRI, os trigonum syndrome shows ab-

normal signal intensity in the lateral talar tu-bercle, the os trigonum, or both because o

the bone impaction (Fig. 17). Furthermore, in-

fammatory changes will generally be present

in the sot tissues o the posterior ankle, es-

pecially in the posterior synovial recess o the

subtalar and tibiotalar joints [59]. Infamma-

tory changes aecting the fexor hallucis lon-

gus tendon sheath may variably be present.

However, it is important to remember that the

fexor hallucis longus tendon sheath normally

communicates with the tibiotalar joint in ap-

proximately 20% o normal individuals; there-

ore, fuid in the tendon sheath may be normal.

Septations, contour irregularities, and abruptcuto o the fuid at the level o the posterior

talus are helpul distinguishers in diagnosing

tenosynovitis o the tendon sheath [61].

Conclusion

There are a variety o causes o heel pain, and

we have reviewed the most common causes. We

have primarily reviewed mechanical causes, by

ar the most common; however, it is important

BA

Fig. 17—18-year-old man with posterior ankle and heel pain.A and B, Sagittal T1-weighted image (A) and T2-weighted image with at saturation (B) show os trigonum(arrow , A) with bone marrow edema (arrowhead , B), consistent with os trigonum syndrome.



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854 AJR:200, April 2013

Lawrence et al.

to remember that there may be other causes

o heel pain, such as osteomyelitis, which

will present with a much dierent clinical

picture. Although clinical examination is o-

ten useul, imaging the hindoot is helpul or

solving equivocal cases as well as or preop-

erative planning by showing the exact loca-

tion and extent o the pathology. MRI has su-perior sot-tissue contrast resolution to other

modalities; thereore, it can usually provide a

specic diagnosis.

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