AJR 2000; 175:613-625
© American Roentgen Ray Society
MR Imaging of Disorders of the Achilles Tendon
Mark E. Schweitzer1 and
David Karasick
1
Both authors: Department of Radiology, Thomas Jefferson University Hospital,
111 S. 11th St., 3390 Gibbon, Philadelphia, PA 19107.
Received May 3, 1999;
accepted after revision February 24, 2000.
Address correspondence to M. E. Schweitzer.
Introduction
The Achilles tendon is among the most frequently injured tendons of the
body with a variety of types of traumatic and overuse conditions affecting it.
These conditions are common, often come to clinical attention, and are
frequently imaged. The pathophysiology of Achilles disorders is complex, and
the nomenclature is irregularly applied; this leads to miscommunication
between clinicians and radiologists and inconsistencies in the literature.
Therefore, we review the anatomy, MR imaging findings, and pathologic findings
in an attempt to develop a systematic nomenclature.
Gross Anatomy
The Achilles tendon originates in the mid leg and is formed by the junction
of the two heads of the gastrocnemius muscles and the soleus muscle
[1,
2]. The bulk of the Achilles is
formed from the gastrocnemius muscle. The larger medial head originates almost
entirely from just proximal to the medial femoral condyle, and the smaller
lateral head arises from both the posterior and lateral surfaces of the
lateral femoral condyle. At the junction of the proximal and mid calf, the two
heads of the gastrocnemius muscles and their tendons approximate midline. The
gastrocnemius tendon origin is gradual, occurring over approximately 3-4 cm.
The fibers of the medial head originate slightly lower than those of the
lateral head. The Achilles tendon is not formed until the soleus muscle
inserts onto the gastrocnemius tendon, approximately 3-4 cm more distally
[2].
The plantaris muscle originates from the lateral meniscus and the lateral
femoral epicondyle in close association with the lateral head of the
gastrocnemius muscle. The plantaris tendon then crosses obliquely between the
soleus and gastrocnemius muscles and continues just medial to the Achilles.
Various plantaris insertions are seen, but most fibers insert on the medial
aspect of the superior calcaneal tuberosity or 1 cm anterior and medial to the
Achilles on the calcaneus, a distinct insertion point separate from that of
the Achilles. The Achilles-plantaris complex is termed the
"triceps-surae complex"
[3].
The Achilles tendon is enclosed almost completely within a paratendon. This
paratendon has both visceral and parietal layers
[4]. The paratendon is
analogous to synovium in that it provides nutrition for the tendon, but
because the Achilles tendon does not change its axis of motion, there is no
need for the lubrication function of synovium.
Two layers of filmy fibrous tissue with fine internal mesotendal blood
vessels make up the paratendon
[5]. The interwoven fibers of
the paratendon allow it to stretch up to several centimeters in length with
tendon movement and provide some degree of tendon gliding
[4].
Mesotendal vascular anastomoses provide tendon nourishment. However, 2-6 cm
proximal to the calcaneal insertion, this blood supply is diminished
[6]. This region of decreased
vascularity is the usual region of Achilles rupture
[7]. Proximal tears are
uncommon because of the nutrition provided by the muscular branches from the
gastronemius [8]. Distal tears
are uncommon because the blood supply from the periosteal vessels is near the
calcaneal insertion.
As the Achilles tendon descends, the fibers rotate laterally approximately
90°. Therefore, the gastrocnemius fibers insert laterally onto the
posterior calcaneus, whereas the soleus fibers insert medially
[9].
The insertion site of the Achilles onto the calcaneus is an enthesis and is
intimately related to the only true anatomic bursa in the ankle, the
retrocalcaneal bursa [10].
The retrocalcaneal bursa is horseshoe-shaped, filled with synovial fluid,
and surrounded anteriorly by Kager's fat pad. The function of the
retrocalcaneal bursa is to protect the distal Achilles tendon from frictional
wear against the posterior calcaneus
[11]. Posterior to the tendon
lies an acquired bursa, termed the "retro-Achilles." The enthesis
itself is fibrocartilage directly intermeshing into the marrow of the
calcaneus [10]. This direct
meshing of tendon fibrils into marrow provides significant strength at the
enthesis and makes it a rare site of tendon failure.
Tendon Ultrastructure
Approximately 15 cm in length, the Achilles is the strongest, largest, and
thickest tendon in the human body. The Achilles is made of fascicles, with an
interfascicular membrane separating the fascicles into bundles. Each bundle of
fascicles is roughly shaped like a quarter of a pie. On a microstructural
level, the fascicles are made of fibroblasts, which have a sinusoidal
structure. This sinusoidal structure allows the Achilles to stretch
considerably before tendon rupture. The fibroblasts are made of fibrils, the
fibrils are made of microfibrils, and the microfibrils are made of
tropocollagen [12]. The
fibrils normally have an undulating pattern. This undulation decreases with
aging, which leads to a decrease in the Achilles' elasticity
[13]. In addition, the average
diameter, density, and cellularity of the collagen fibrils also decrease with
aging. The combination of cellular changes, ultrastructural changes, and a
tenuous blood supply predisposes the aged Achilles to degeneration and
injury.
Functional Anatomy
The gastrocnemius, soleus, and plantaris muscles act to flex the foot
[14]. The gastrocnemius is
also a knee flexor. The gastrocnemius muscle is active in walking, jumping,
and running, and therefore it is composed predominantly of type II fibers
[15]. Because the soleus
muscle has more of a stabilization effect on the foot for standing, it
consists primarily of type I fibers
[16]. Consequently, muscle
fiber atrophy of the soleus occurs more rapidly than does that of the
gastrocnemius [17], making the
soleus muscle a more sensitive indicator of atrophy as a result of complete
tears or denervation.
Normal MR Appearance
The normal average thickness of the Achilles tendon is 6 mm. The Achilles
tendon is thicker in tall patients, in men, and in the elderly
[18]. Achilles size is also
directly related to lean body mass and is somewhat related to total body
mass.
On sagittal images, the anterior and posterior margins of the Achilles
tendon should be parallel below the soleus insertion (Fig.
1A,1B).
On axial images, the anterior margin of the Achilles is concave for most of
its course. Somewhat proximally, just above the soleus insertion, the margin
may be straight or convex; at the soleus insertion, the margin is typically
convex and may be focally bulbous. On coronal images, both sides of the
Achilles are fairly straight and the tendon widens as it extends distally at
the lesion.

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Fig. 1A. 41-year-old man with normal tendon. Sagittal T2-weighted MR image
(TR/TE, 6000/70) shows normal parallel anterior and posterior margins of
tendon (open arrows). Note normal volume of fat in Kager's fat pad
anterior to tendon (solid arrows) and insertion of soleus muscle onto
tendon.
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The normal retrocalcaneal bursa is visible on MR imaging but should measure
less than 6 mm superior to inferior, 3 mm medial to lateral, and 2 mm anterior
to posterior [19].
Subcutaneous fat should be seen between the Achilles and the skin. Focal
absence of fat may represent a skin callus, a blister (if it has high signal
on T2-weighted images and bows the skin out), or retro-Achilles bursitis (if
it has high signal and is without mass effect on the skin). Fat should also be
normally seen anterior to the tendon in Kager's fat pad. Occasionally, vessels
within Kager's fat pad can mimic edema, although their tubular morphology
should allow differentiation.
The Achilles tendon is usually dark on all imaging sequences. However, the
normal fascicular anatomy of the Achilles tendon may be visible as a single
line and can mimic an interstitial tear
[20]. This fascicular signal
is usually not present or fades on T2-weighted images. Small punctate areas of
high signal, seen distally in the Achilles tendon on axial images, are
interfascicular membranes (Figs.
2 and
3). Lastly, some fraction of
distal internal signal may represent the "magic angle" artifact.
This phenomenon occurs in the Achilles tendon even though it does not grossly
change its axis, because the fibers twist internally. This artifact is not
present on T2-weighted images
[21].

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Fig. 2. 37-year-old woman with normal fascicles of Achilles tendon. Axial
proton densityweighted MR image (TR/TE, 4000/40) shows normal
fascicular anatomy. Fascicles appear as intratendon signal (arrows)
in Achilles tendon.
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Fig. 3. 45-year-old man with normal fascicles and peritendonitis. Axial
T2-weighted MR image (TR/TE, 6000/78) with fat suppression shows barbed-wire
appearance of fascicles (curved arrow). Also note partially
circumferential high signal (straight arrow) consistent with small
degree of peritendonitis.
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Epidemiology
True rupture of the Achilles tendon was first described by Ambroise Pare in
1575 and first reported in the medical literature in 1633. Achilles tendon
rupture was a rarely reported injury until the 1950s
[22]. Before 1929, fewer than
70 cases were reported in the world literature. During the 1970s, the reported
incidence increased by up to 50% a year in developed countries
[23].
Achilles tendon tears are most common in developed countries, but the
prevalence varies among developed countries. The highest rates are seen in
Germany, Austria, Sweden, Denmark, and Switzerland. Lower rates occur in
France, Spain, the United Kingdom, and the United States
[23]. However, some
industrialized nations, such as The Netherlands, Japan, and Korea, have an
extremely low incidence of Achilles tears, and in the third world, the
incidence of Achilles tears is even lower
[24]. Currently, the incidence
in industrialized nations is approximately seven cases per 100,000 inhabitants
per year [24].
Achilles tendon rupture occurs in younger patients, with a mean age of 36
years, as compared with ruptures of other tendons, but Achilles rupture almost
never occurs in patients before the onset of adolescence
[25]. Of all the tendons in
the foot and ankle, the Achilles tendon is the only one for which disorders
have a male predominance [26].
Achilles tendon disorders are also more common on the left than on the right
side for unknown reasons [27].
Because Achilles tendon disorders are activity-related disorders, incidence
peaks during the summer
[28].
A significant relationship between leisure athletic activities and tendon
injuries exists [27]. The
sedentary lifestyle of modern whitecollar workers results in decreased blood
flow and nutrition to the Achilles tendon
[29]. This situation is
compounded by the effects of aging on the vascular supply. Recreational
physical activities that intermittently stress the ischemic Achilles tendon,
without giving it time to adapt, may lead to "spontaneous"
Achilles tendon rupture
[29].
The specific causative activity varies among countries according to the
popularity of sporting events in the country involved. In the United States,
running sports, particularly those that involve pivot motion, are the most
common causative sport, with jogging as the leading cause of Achilles
disorders [28]. However, in
Germany, soccer is the leading cause
[27].
MR Imaging and Pathologic Anatomy
"Achilles tendonosis" is a preferable term to "Achilles
tendonitis" because this disorder is manifested as intratendinous
degeneration without a significant inflammatory response
[18]. The Achilles tendon is
protected against inflammatory processes because no true synovial sheath is
present. However, because of the intimate association between the distal
Achilles tendon and the retrocalcaneal bursa, the Achilles tendon is
secondarily affected by inflammatory processes involving the retrocalcaneal
bursa [10]. In addition,
involvement of the Achilles paratendon has been noted to be reasonably
frequent in systemic inflammatory diseases, such as rheumatoid arthritis
[30]. This manifestation of
rheumatoid arthritis has not been widely recognized previously because this
inflammation, similar to that of many wrist tendons, is often clinically
occult [31].
Most imaging findings represent the pathologic processes of tendon
degeneration and repair [32].
Grossly, the degenerated tendon appears nodular and yellow and loses its usual
glistening luster, often appearing edematous or fibrillated
[33].
On a microscopic level, four predominant types of tendon degeneration are
seen including fibromatosis or hypoxic, lipoid, osseous or calcific, and
myxoid [34]. Although only the
former two frequently lead to macroscopic tears, all pathologic changes may be
the result of microscopic tears
[35]. These microscopic tears
evolve and coalesce to form the spectrum of Achilles disorders that is seen on
imaging. It is the coalescence of these microtears that leads to the
development of focal mycoid regions and interstitial tears along the long axis
of the tendon. Therefore, tears on a microscopic level begin the cascade of
tendon disorders, and tears on a macroscopic level end it
[35].
Fibromatous degeneration is also termed "hypoxic degenerative
tendonopathy" and is the most frequently seen degenerative finding in
ruptured Achilles tendons
[36]. These hypoxic changes
are likely caused by ischemia because of the relative hypovascularity of the
critical zone of the Achilles tendon
[37]. This hypovascularity
results in anoxic injury to tenocytes and collagen fibers
[34]. Hypoxic degenerative
tendonopathy leads to a thickened dysmorphic Achilles tendon
[36] (Figs.
4A,4B
and 5). This type of
degeneration usually occurs after multiple symptomatic episodes
[37] and usually lacks
internal signal on MR imaging. A similar MR appearance can be seen in
rheumatoid arthritis (Fig. 6)
and gout (Fig. 7) and after
tendon repair.

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Fig. 4A. 60-year-old man with hypoxic degeneration. Sagittal T1-weighted
(A) (TR/TE, 500/10) and sagittal short tau inversion recovery
(B) (6000/40; inversion time, 150 msec) MR images show bulbous
thickening (solid straight arrows) of Achilles tendon and that
anterior and posterior margins of Achilles tendon are no longer parallel. No
internal signal can be seen. Note normal volume of retrocalcaneal bursa fluid
(solid curved arrow). Incidentally noted is cartilaginous calcaneal
navicular coalition (open arrow).
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Fig. 4B. 60-year-old man with hypoxic degeneration. Sagittal T1-weighted
(A) (TR/TE, 500/10) and sagittal short tau inversion recovery
(B) (6000/40; inversion time, 150 msec) MR images show bulbous
thickening (solid straight arrows) of Achilles tendon and that
anterior and posterior margins of Achilles tendon are no longer parallel. No
internal signal can be seen. Note normal volume of retrocalcaneal bursa fluid
(solid curved arrow). Incidentally noted is cartilaginous calcaneal
navicular coalition (open arrow).
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Fig. 5. 48-year-old man with hypoxic degeneration, Axial T2-weighted
fat-suppressed MR image (TR/TE, 6000/80) shows extensive thickening of
Achilles tendon with loss of normal concave anterior margin
(arrows).
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Fig. 6. 55-year-old woman with rheumatoid arthritis. Sagittal T1-weighted MR
image (TR/TE, 500/20) shows markedly thickened Achilles tendon (white
arrows) caused by rheumatoid arthritis. Also, note findings consistent
with retrocalcaneal bursitis (straight black arrow) and with subtalar
joint disease (curved black arrow). Erosion of calcaneus can be seen
as well.
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Fig. 7. 50-year-old man with gout. Sagittal T1-weighted MR image (TR/TE,
500/12) shows thickening of Achilles tendon (straight arrows)
representing gouty infiltration. Gouty infiltration of anterior tibialis
tendon (curved arrow) can also be seen.
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The second most common type of degeneration is mucoid. Most patients with
mucoid degeneration also have some degree of hypoxic degeneration
[33]. This is the most common
degeneration to occur asymptomatically. In mucoid degeneration, large mucoid
patches and vacuoles are seen between the thinned degenerated tendon fibers
[35]. Interrupted signal on
T2-weighted images is the best marker for mucoid deposits (Figs.
8A,8B,9,10).
Grossly, these tendons appear enlarged, and enlargement may also be seen on MR
imaging. It is the coalescence of vacuoles and lacunae that is the beginning
of an interstitial tear. Patients with mucoid degeneration may have a tear at
first clinical presentation because earlier episodes were asymptomatic.

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Fig. 8A. 55-year-old woman with mucoid degeneration. Sagittal T1-weighted
(TR/TE, 500/20) and sagittal short tau inversion recovery (6000/70) MR images
show thickened Achilles tendon with internal signal (arrows). This
signal was nonlinear and interrupted on T2-weighted image (not shown).
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Fig. 8B. 55-year-old woman with mucoid degeneration. Sagittal T1-weighted
(TR/TE, 500/20) and sagittal short tau inversion recovery (6000/70) MR images
show thickened Achilles tendon with internal signal (arrows). This
signal was nonlinear and interrupted on T2-weighted image (not shown).
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Fig. 9. 58-year-old woman with mucoid degeneration. Sagittal F-short tau
inversion recovery image (TR/TE, 4000/48; inversion time, 150 msec) shows
irregular longitudinal mucoid deposit in Achilles tendon
(arrows).
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Fig. 10. 48-year-old man with mucoid degeneration. Axial T2-weighted
fat-suppressed MR image (TR/TE, 6000/80) shows thickened Achilles tendon
(arrows) with multifocal speckled appearance consistent with mucoid
degeneration.
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Tenolipomatosis is the most age-dependent type of tendon degeneration.
Tenolipomatosis occurs with fatty deposits between normal tenocytes
[38]. Because the tenocytes
are normal, lipoid degeneration does not seem to affect the structural
properties of the Achilles
[39] and does not predispose
the tendon to tear [40]. This
disorder, like hypoxic degeneration, is often clinically silent and is related
to, but distinct from, tendinous xanthoma. Xanthomas are the result of
lipomatosis seen in inherited metabolic diseases such as type 2 and type 3
hyperpoproteinemias and cerebrotendinous xanthomatosis
[41]. Although severe forms of
these metabolic disorders are rare, one diagnostic criterion for familial
hyperlipoproteinemia is focal thickening of the Achilles tendon on imaging
[42]. Xanthomas can mimic
hypoxic Achilles tendonitis or various rheumatologic conditions, with diffuse
tendon thickening and, often, quite subtle internal signal.
Calcifying tendonopathy is rare in the Achilles tendon, seen in only 3% of
ruptured tendons [43]. This
dystrophic calcification may progress to Achilles ossification
[41]
(Fig. 11). On a macroscopic
level in the Achilles, tendon ossification occurs more frequently than tendon
calcification and is relatively more common than in other tendons in the body
[42]. Therefore, not only is
ossification distinct from calcification because of the presence of cortical
bone and trabeculae, but it may represent a different degenerative pathway
than calcification.
The first symptomatic stage of Achilles disorders is paratendonitis, which
is often mistakenly termed "tendonitis"
[44] (Figs.
3 and
12). This stage is analogous
to synovitis in sheathed tendons. On T2-weighted MR sequences, paratendonitis
appears as partially circumferential high signal around the Achilles tendon.
Fat suppression is usually necessary to visualize this high signal. The high
signal is not as bright as synovial fluid because the paratendon is not made
of a synovial membrane. The external margins of the signal are typically
slightly ill defined, and the high signal predominates posteriorly and extends
medially up to three quarters around the tendon. In isolated paratendonitis,
the tendon itself is normal. True acute tendonitis is an infrequent entity and
is an even less frequent entity to be imaged. Most clinical cases of
tendonitis are either paratendonitis or an exacerbation of hypoxic tendonosis.
True tendonitis, if imaged, occasionally appears as edema not only in the
paratendon but also in Kager's fat pad anterior to the Achilles tendon
[45]
(Fig. 13).

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Fig. 12. 47-year-old male runner with peritendonitis. Axial T2-weighted
fat-suppressed MR image (TR/TE, 4000/78) shows thin rim of partially
circumferential high signal (arrows), which represents mild
peritendonitis. Background mucoid degeneration within tendon and intratendon
signal can be seen.
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The spectrum of tears ranges from microtears to interstitial tears
(parallel to the long axis of the Achilles), to partial tears, and eventually
to complete tears [46]. This
abrupt demarcation between tears and "nontears" is misleading
because there is a junctional entity, mucoid degeneration
[35]. In mucoid degeneration,
the vacuoles may coalesce into an interstitial tear
[36]; also, in tendonosis
perhaps the inciting event is a microtear
[47]. Lastly, many cases of
tendonosis are treated identically to cases of interstitial tears with
débridement of the degenerative center of the
tendon and oversewing of the preserved peripheral aspects of the tendon
[48].
Almost all tears, interstitial (Figs.
14 and
15), partial (Figs.
16 and
17), or complete (Figs.
18 and
19) show high signal on
T2-weighted imaging [49].
Tendon-end retraction can also be seen occasionally in acute tears
[50]. Because one of the
treatments for an Achilles tendon tear is casting in plantar flexion, sagittal
images can be obtained after casting. If the tendon edges are not opposed in
this position, the treatment will be unsuccessful
[48].

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Fig. 14. 45-year-old man with interstitial tear. Sagittal short tau inversion
recovery image (TR/TE, 4000/48; inversion time, 150 msec) shows multiple
longitudinal lines (arrows) inside thickened Achilles tendon
consistent with interstitial tear.
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Fig. 15. 58-year-old male runner with interstitial tear. Sagittal short tau
inversion recovery image (TR/TE, 4000/48; inversion time, 150 msec) shows
longitudinal area (arrowheads) inside distal Achilles tendon
consistent with insertional interstitial tear. Small amount of reactive marrow
edema (straight arrow) is seen in calcaneus as well as excessive
retrocalcaneal bursitis (curved arrow).
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Fig. 16. 58-year-old woman with partial Achilles tendon tear. Sagittal
T2-weighted MR image (TR/TE, 6000/80) shows partial posterior Achilles tendon
tear (black arrow). Longitudinal interstitial tear (white
arrows) and evidence of underlying hypoxic degeneration with thickened
tendon can also be seen.
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Fig. 17. 25-year-old male runner with partial Achilles tendon tear. Axial
T1-weighted fat-suppressed MR image (TR/TE, 500/10) obtained after IV
administration of gadolinium shows focal enhancement in medial partial
Achilles tendon tear (arrow).
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Fig. 18. 58-year-old woman with spontaneous Achilles tendon tear. Sagittal
T2-weighted MR image (TR/TE, 7000/90) shows complete Achilles tendon tear
(arrows) in typical location: 5 cm from its insertion. Gap is
approximately 1 cm.
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Fig. 19. 50-year-old man with spontaneous Achilles tendon tear. Sagittal
short tau inversion recovery image (TR/TE, 4000/48; inversion time, 150 msec)
shows completely avulsed Achilles tendon (arrow) with significant gap
because proximal fibers have been retracted. Fluid can be seen within gap.
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Achilles tendon tears can also occur abruptly without a definite history of
overuse [45]. In some
patients, MR images show evidence of mucoid (silent) degeneration but not of
interstitial tear, and in a smaller number of these patients, MR images show
chronic tendonosis related to hypoxic degeneration
[51] or no evidence of
degeneration at all.
With chronic Achilles tendon tears not only are the tendon edges retracted
from each other, but there is ongoing atrophy of the Achilles tendon fibers
and, to a greater and more mechanically important degree, of muscle
[52]. Muscle atrophy can be
classified either as acute or subacute and potentially reversible or as remote
and irreversible [53]. Acute
atrophy manifests as diffuse edema throughout the muscle belly
[54]
(Fig. 20). A patient with
acute atrophy has the best prognosis after surgery. Irreversible atrophy
appears as a fatty infiltrated or fatty marbled muscle
[55]. A small muscle may have
undergone either reversible or irreversible atrophy
[56].

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Fig. 20. 45-year-old man with acute Achilles tendon tear and atrophy. Axial
short tau inversion recovery image (TR/TE, 6000/58; inversion time, 150 msec)
shows evidence of edema within soleus muscle (arrows), which is
consistent with acute atrophy.
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In disorders of the Achilles, atrophy occurs first in the soleus because of
the predominance of slow-twitch fibers. Because the soleus muscle is part of
the Achilles tendon, soleus atrophy can be thought of as a predictor of a
dysfunctional myotendinous unit. Therefore, when imaging the Achilles tendon,
sagittal images should include at least 3 cm of the distal soleus belly to
reveal whether soleus fatty infiltration is present. Occasionally,
gastrocnemius muscle atrophy can be seen, but atropy of this muscle is rare
even in remote Achilles tendon tears.
Nomenclature
One difficulty in interpreting images of Achilles tendon disorders is the
inconsistent use of nomenclature in imaging and clinical articles. Clinically,
there is an abrupt demarcation between tendon disorders in which the tendon is
overtly torn versus those in which it is not
[57]. This demarcation,
although useful in triaging patients for surgery, is arbitrary and inaccurate.
Mucoid degeneration can mimic a tear clinically, and silent Achilles disorders
frequently have microscopic tears. We describe some commonly used clinical
terms and their meanings in an attempt to develop a systematic nomenclature
(Table 1).
Associated Osseous Injuries and Abnormalities
The most common associated osseous abnormality in Achilles disorders is an
enthesophyte at the insertion of the Achilles into the calcaneus. This
enthesophyte usually maintains normal marrow signal on MR images.
Occasionally, these enthesophytes show evidence of marrow edema on MR imaging
(Fig.
21A,21B).
In this situation, the enthesophyte may be acutely symptomatic. These
edematous spurs are the types of enthesophytes that respond best to focal
surgical resection. Rarely, an enthesophyte can also cause pain as the spur
grows past the protective margin of the retrocalcaneal bursa.

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Fig. 21A. 48-year-old man with symptomatic spur. Sagittal T1-weighted (TR/TE,
600/12) (A) and short tau inversion recovery (TR/TE, 6000/40; inversion
time, 150 msec) (B) MR images show subtle edema in posterior calcaneal
spur (arrows).
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Fig. 21B. 48-year-old man with symptomatic spur. Sagittal T1-weighted (TR/TE,
600/12) (A) and short tau inversion recovery (TR/TE, 6000/40; inversion
time, 150 msec) (B) MR images show subtle edema in posterior calcaneal
spur (arrows).
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Tendon ossification predominates distally in the tendon, appearing as focal
fatty marrow. This calcification is related to insertional enthesopathy
[58]. However, true Achilles
enthesopathy occurs at the edge of rather than within the tendon. This
dystrophic ossification may have the appearance of a broken enthesophyte,
although enthesophytes are not related to the Achilles disorders. Distal
ossification appearing as a broken enthesophyte is thought to be the result of
partial insertion tears [59].
Whether ossification also increases the risk of Achilles tears or is merely
the result of prior partial tears is unclear. Although proximal ossification
may present as a mass, most patients provide a history of repetitive
running-related tendonitis
[60].
Somewhat more common than proximal ossification is marrow edema around the
enthesophyte in response to inflammatory retrocalcaneal bursitis or as a
degenerative cystic phenomenon
[61] (Fig.
22A,22B).
The marrow edema caused by retrocalcaneal bursitis is seen at the calcaneal
margin of an enlarged bursa. The degenerative edema is often cystic or has a
cyst within it, is located at the inferiormost aspect of the Achilles
insertion, and is well defined.

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Fig. 22A. 49-year-old man with degenerative cyst. Sagittal T1-weighted (TR/TE,
600/12) (A) and short tau inversion recovery (6000/40; inversion time,
150 msec) (B) MR images show degenerative cyst at posterior calcaneus
(arrows) adjacent to thickened Achilles tendon insertion. Small
amount of reactive edema can be seen around cyst.
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Fig. 22B. 49-year-old man with degenerative cyst. Sagittal T1-weighted (TR/TE,
600/12) (A) and short tau inversion recovery (6000/40; inversion time,
150 msec) (B) MR images show degenerative cyst at posterior calcaneus
(arrows) adjacent to thickened Achilles tendon insertion. Small
amount of reactive edema can be seen around cyst.
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In addition, calcaneal edema can also be a response to altered mechanics
[62]. This reactive marrow
edema, although seen in several ankle tendon disorders, is less commonly
related to Achilles disorders (Fig.
23). If present, this calcaneal response to altered mechanics is
seen anterior to the Achilles insertion.

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Fig. 23. 60-year-old man with acute Achilles tendonitis clinically. Sagittal
short tau inversion recovery image (TR/TE, 4500/48; inversion time, 150 msec)
shows edema (curved arrows) in Kager's fat pad anterior to Achilles
tendon, which is consistent with acute Achilles tendonitis. Extensive reactive
marrow edema (straight arrows) can also be seen.
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An associated osseous injury to the calcaneus occurs in Achilles disorders
as well [63]. This
microavulsion injury is similar to changes seen in the elbow with
epicondylitis or in the knee with medial collateral ligament tears
[58,
64], but this injury may occur
in Achilles disorders other than tears. It is often difficult to differentiate
the types of calcaneal marrow edema (Fig.
23).
Another consideration in the differential diagnosis of calcaneal marrow
edema is stress fracture [65].
Typically, stress fractures occur several millimeters anterior to the
posterior aspect of the calcaneus, do not occur posterior at the Achilles
insertion, and are vertically oriented.
One final differential diagnosis to consider is residual red marrow.
Residual red marrow may be bright, closely mimicking marrow edema, on
fat-suppressed T2-weighted or short tau inversion recovery images
[66]. Residual red marrow in
the calcaneus occurs in children and adolescents but rarely persists in
adults. Residual red marrow has a typical location superiorlyjust
posterior to the posterior facet of the calcaneusand does not closely
approach the Achilles insertion. Most important, this entity is usually
multifocal in the foot. If necessary, in-phase and out-of-phase imaging can
confirm the diagnosis of red marrow.
Insertional Tendonitis
Insertional Achilles tendonitis is an important subtype of injury that is
common in runners and frequently leads to the development of an enthesophyte.
Insertional Achilles tendonitis may be the only true form of acute Achilles
tendonitis. On MR imaging, the Achilles is thickened distally with vaguely
seen ill-defined longitudinal high signal (Figs.
24A,24B,25,26).
This signal may be fairly intense and can mimic a partial tear, albeit fairly
distally.

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Fig. 24A. 50-year-old male runner with insertional tendonitis. Sagittal short
tau inversion recovery (TR/TE, 6000/48; inversion time, 150 msec) (A)
and axial T2-weighted fat-suppressed (TR/TE, 7000/80) (B) MR images
show slightly thickened distal Achilles tendon with distal insertional signal
(open arrow, A; short arrow, B) that is
relatively high signal on fat suppressed image. Excessive retrocalcaneal
bursitis (solid arrow, A) and peritendonitis (long
arrows, B) can also be seen.
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Fig. 24B. 50-year-old male runner with insertional tendonitis. Sagittal short
tau inversion recovery (TR/TE, 6000/48; inversion time, 150 msec) (A)
and axial T2-weighted fat-suppressed (TR/TE, 7000/80) (B) MR images
show slightly thickened distal Achilles tendon with distal insertional signal
(open arrow, A; short arrow, B) that is
relatively high signal on fat suppressed image. Excessive retrocalcaneal
bursitis (solid arrow, A) and peritendonitis (long
arrows, B) can also be seen.
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Fig. 25. 60-year-old woman with insertional tendonitis. Sagittal short tau
inversion recovery image (TR/TE, 4000/52; inversion time, 150 msec) shows
internal signal linearly oriented in Achilles tendon (arrow). If this
finding were in more proximal location, it would be consistent with tear, but
at insertion tendonitis often mimics partial tears on MR imaging.
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Fig. 26. 48-year-old male runner with distal tendonitis. Axial fast spin-echo
MR image (TR/TE, 6000/80) shows extensive retrocalcaneal bursitis (solid
arrow) with linear thick signal within Achilles tendon (open
arrow) representing insertional tendonitis.
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Atypical Achilles Tears
Although most Achilles tears occurs 2-6 cm from the insertion, Achilles
tears can be seen in two other locations: distally and proximally. Distal
tears occur as a result either of severe end-stage "pump-bump,"
with attritional tendon tearing caused by shoe friction, or of inappropriately
treated or severe insertional tendonitis.
More common than an insertional tear, a proximal Achilles tear is, in
reality, a musculotendinous junction injury. This strain injury is listed in
the differential diagnosis for "tennis leg"
[67]. Proximal Achilles tears
typically involve the medial head of the gastrocnemius, are twice as common in
males as in females, usually involve the dominant leg, and occur in patients
ranging in age from 23 to 57 years
[68] (Figs.
27,28,29).
The most common risk factor is participation in sports such as football,
tennis, and squash [69]. Like
all muscle strain injuries, the muscles at highest risk are those that cross
two joints, function eccentrically, and have a high percentage of fast-twitch
fibers [56], which is the
reason the gastrocnemius is affected but the soleus is not.

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Fig. 27. 38-year-old woman with medial gastrocnemius tear. Axial fast
spin-echo MR image (TR/TE, 6000/85) shows complete tear of medial
gastrocnemius myotendinous junction filled with fluid (arrows).
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Fig. 28. 47-year-old man with partial proximal Achilles tear. Sagittal short
tau inversion recovery image (TR/TE, 6000/40; inversion time, 150 msec) shows
edema (arrows) at myotendinous junction of medial head of
gastrocnemius with U-shaped dissecting fluid.
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Fig. 29. 53-year-old woman with proximal Achilles tear. Axial fast spinecho
MR image (TR/TE, 6000/70) shows partial tear (curved arrow) of medial
head of gastrocnemius with associated hematoma (straight arrows).
Clinically, this finding is often termed "proximal Achilles
tear."
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On axial images, myotendinous junction tears are manifested as focal fluid
at the musculotendinous junction of the Achilles tendon. Fluid follows the
distal margins of the muscle belly. On coronal images, tears have a U
appearance because the fluid dissects down along the fascial plane of a distal
muscle belly of the gastrocnemius. The tear may be complete with focal absence
of the tendon at a specific level or, more commonly, the tear is partial.
Incomplete tear or edema from muscle strain occurs focally in the center of
the muscle.
Adjacent edema can be seen in the muscle as a component of the strain
injury or as a manifestation of acute atrophy. Although the medial head of the
gastrocnemius is usually involved, the resulting atrophy can affect both heads
because they act in concert
[69].
In these circumstances, whether an adjacent hematoma
(Fig. 29) is present should be
noted. A hematoma is a frequent sequela of muscle injury. Clinically,
hematomas are evacuated [70].
Complete myotendinous junction tears are also treated surgically, but partial
proximal myelotendinous junction tears are treated conservatively
[68].
Plantar Muscle Injury
The symptoms of a ruptured plantaris tendon have been described with
specific sports (e.g., "tennis leg"). The tendon can tear when
forcefully contracted, resulting in the patient feeling a "pop" in
the calf [71]. Sudden
dorsiflexion of the ankle with the knee in extension has been implicated as
the mechanism for this injury. The symptoms consist of calf pain followed by
medial swelling. Clinically, this condition needs to be differentiated from
Achilles tendon injuries and medial gastrocnemius muscle injuries. Clinically,
the torn plantaris is considered a less severe injury than gastrocnemius
muscle tears and is conservatively treated with ice, rest, and
antiinflammatory medications
[72].
On T2-weighted MR imaging, plantaris injury shows high signal cephalad to
the location of typical gastrocnemius injury. The fluid tends to dissect
medially and proximally to the bulk of the soleus muscle (Figs.
30,31,32).

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Fig. 30. 49-year-old woman with plantaris tendon tear. Sagittal short tau
inversion recovery image (TR/TE, 6000/78; inversion time, 150 msec) shows
edema anterior to gastrocnemius caused by plantaris tear
(arrows).
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Fig. 31. 58-year-old man with plantaris tendon tear. Axial fast spin-echo MR
image (TR/TE, 7000/85) shows retracted plantaris filled with fluid
(arrows) between gastrocnemius (G) and soleus (S) muscles.
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Fig. 32. 55-year-old man with plantaris tendon tear. Sagittal short tau
inversion recovery image (TR/TE, 7000/55; inversion time, 150 msec) shows line
of fluid (arrows) just between gastrocnemius and soleus muscles.
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Haglund's Disease
Haglund's disease is frequently associated with "pump"-style
shoes. More important than the shoe style is the presence of a stiff-heel
counter, which compresses the retro-Achilles bursa against the posterior
lateral calcaneal prominence
[73]. The calcaneal tuberosity
may focally enlarge in response to chronic irritation
[74]. This enlargement further
irritates the retro-Achilles bursa and the Achilles tendon, which increases
the irritation that causes further enlargement of the tuberosity. This results
in a cycle of injury, response to injury, and reinjury
[75].
In patients with Haglund's disease, MR images reveal excessive fluid in the
retrocalcaneal bursa, fluid in the retro-Achilles bursa, and an enlarged
calcaneal tuberosity (Figs.
33A,33B
and 34).

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Fig. 33A. 53-year-old woman with Haglund's disease. Sagittal T1-weighted
(A) and sagittal T2-weighted fat-suppressed short tau inversion
recovery (B) MR images (TR/TE, 600/12) show soft-tissue signal
displacing fat posterior to thickened Achilles tendon consistent with
retro-Achilles bursitis (open arrow, B), Ill-defined fluid can
be seen in retrocalcaneal bursa, which is consistent with retrocalcaneal
bursitis (curved arrows). Edema in enlarged tuberosity (straight
arrows) is seen as well. All these findings are suggestive of Haglund's
disease.
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Fig. 33B. 53-year-old woman with Haglund's disease. Sagittal T1-weighted
(A) and sagittal T2-weighted fat-suppressed short tau inversion
recovery (B) MR images (TR/TE, 600/12) show soft-tissue signal
displacing fat posterior to thickened Achilles tendon consistent with
retro-Achilles bursitis (open arrow, B). Ill-defined fluid can
be seen in retrocalcaneal bursa, which is consistent with retrocalcaneal
bursitis (curved arrows). Edema in enlarged tuberosity (straight
arrows) is seen as well. All these findings are suggestive of Haglund's
disease.
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Fig. 34. 48-year-old woman with Haglund's disease. Sagittal short tau
inversion recovery image (TR/TE, 6000/48; inversion time, 150 msec) shows
edema in calcaneal tuberosity (arrow) and enlarged tuberosity. In
addition, Achilles tendon is chronically thickened without evidence of
internal signal. Hypertrophy of calcaneal tubercle is shown its projection
above parallel pitch lines (dashed lines).
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The diagnosis of an enlarged calcaneal tuberosity (or of a bursal
projection) is made by drawing parallel pitch lines on the upper and lower
aspects on the calcaneus on sagittal images. The lower parallel pitch line is
tangent to the anterior tubercle and the medial tuberosity of the calcaneus.
The upper line is drawn parallel to the lower pitch line at the level of the
posterior lip of the subtalar articular facet. In Haglund's disease, a portion
of the tuberosity is seen above the upper pitch line
[76]
(Fig. 34).
Conclusion
MR imaging can provide important information about the pathologic state of
the Achilles tendon, and these imaging findings can provide information that
is useful in patient treatment.
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