Document 145919

Journal of Orthopaedic & Sports Physical Therapy
2OOO;3O (2) :68-77
Posterior Tibial Tendon Dysfunction
William M. Geideman, MD
)effrey E. )ohnson, MD
Posterior tibial tendon dysfunction is the most common cause of acquired flatfoot
deformity in adults. Although this term suggests pathology involving only the posterior tibial
tendon, the disorder includes a spectrum of pathologic changes involving associated tendon,
ligament, and joint structures of the ankle, hindfoot, and midfoot. Early recognition and
treatment is the key to prevention of the debilitating, long-term consequences of this
disorder. Conservative care is possible in the earliest stages, whereas surgical reconstruction
and eventually arthrodeses become necessary in the latter stages. The purpose of this article
is to review the symptoms, physical examination, radiological examination, classification,
and treatment of posterior tibial tendon dysfunction. / Orthop Sports Phys Ther 2000;30:6877.
Key Words: flatfoot, pes planovalgus, posterior tibial tendon dysfunction,
Holmes and MannI7 found that
60% of patients with rupture of
the posterior tibial tendon had 1
or more of the following associated conditions: hypertension, obesity, diabetes mellitus, previous surgery or trauma about the medial
aspect of the foot, or exposure to
steroids. Local injections of steroids near the posterior tibial tendon have also been reported as a
cause of
osterior tibial tendon dysfunction is the major cause of acquired flatfoot deformity in adults. The later stages of the
disorder are characterized by increased heel valgus, plantarflexion of the talus, flattening of the medial longitudinal
arch, and abduction of the forefoot at Chopart's joint. Posterior tibial tendon dysfunction includes a broad range of progressive disorders, ranging from tenosynovitis to tendon rupture with or without
hindfoot collapse to a fixed, rigid, flatfoot deformity.
The causes of posterior tibial tendon dysfunction are varied. They include age-related degeneration or overuse with attenuation, chronic recurrent tenosynovitis, inflammatory arthritides,';"' and, infrequently,
An association with seronegative spondyacute traumatic rupture.1J.21.34
loarthropathy (ie, Reiter's syndrome, ankylosing spondylitis, and psoriatic arthritis) was found in one series in 47 of 76 patientsJ2 Most r u p
tures are the result of an intrinsic abnormality of the tendon. There is a
zone of hypovascularity in the region of the medial malleolus that is the
most common site of rupture,'" but this does not explain the reason for
rupture proximal to the malleolus or at the navicular insertion.
The prevalence of rupture is increased in middle-aged, obese women.ll.lY27.33
It is uncommon to see ruptures in young patients, except for
acute tra~maticrupture^.".".^'.^!'^^^
Most patients present with a history of insidious onset of unilateral acquired flatfoot deformity, as
only 50% can recall a history of
some form of ua~ma.~"ymptoms
may be present for months or
years. Bilateral posterior tibial tendon dysfunction is rare.
Early symptoms include pain
and swelling along the medial foot
and ankle, pain in the plantar medial arch, and occasionally pain radiating into the medial proximal
calf. Patients find standing on
their toes painful and difficult.
Over time, patients note a gradual
worsening of their condition, with
progressive collapse of the medial
longitudinal arch. With the development of severe hindfoot valgus,
they may perceive that they are
walking on their medial ankle.
Chief resident, Department of Orthopaedic Surgery, Washington University School of Medicine, St They frequently report abnormal
Louis, Mo.
wear of the sole of their shoe.
Chief, Foot and Ankle Service, and Associate professor, Department of Orthopaedic Surgery,
- . WashWalking
increases the pain, and
ington University School of Medicine, St, louis, Mo.
Send correspondence to William M. Geideman, 10651 Steppington Drive, Apt 5052, Dallas, TX they note earlier fatigue and a decrease in their e n d ~ r a n c e . ' ~
75230. E-mail: [email protected]
FIGURE 1. (A) Stage I posterior tibial tendon dysfunction. Note swelling posterior to the medial malleolus. (B)Single limb heel rise. Patient with stage
1 disease is able to perform this with normal inversion of the heel on the right.
In the final stages, the planovalgus deformity progresses. Pain will shift laterally because of calcaneofib
ular or lateral subtalar impingement, and medial
pain frequently will d i ~ a p p e a r . ~ ~
Early in the development of posterior tibial tendon
dysfunction, swelling and fullness in the posteromedial ankle is common. With an established flatfoot
deformity, the involved foot will be abducted and will
have lost the longitudinal arch. When viewing the
standing patient from behind, the examiner will note
the increased hindfoot valgus and the appearance of
the "too many toes sign." This sign, originally described by Johnson,"' indicates that with advanced
forefoot abduction, more toes will be visible on the
affected side laterally.
The single limb heel rise tesf"' is a sensitive indicator of posterior tibial tendon dysfunction. This is performed by asking patients to stand near a wall, gently
balancing themselves with their arms forward and
their hands resting on the wall. Patients then flex
the knee of one leg, lifting the opposite foot off the
ground, and then attempt to rise up onto the ball of
the affected foot. With posterior tibial tendon dysfunction, inversion of the heel is weak or absent, and
either the heel remains in valgus or the patient is
unable to rise onto the forefoot. If able to perform
this test, the patient may note medial ankle pain. Repetitive heel rises may reveal a subtle weakness of the
With the patient seated, the posterior tibial tendon
J Orthop Sports Phys Ther-Volume 30. N~unber2. Febnvaly 2000
should be palpated from above the medial malleolus
to its insertion onto the navicular to assess its integrity and to assess any pain or swelling from tenosynovitis. Lateral tenderness in the subfibular or sinus tarsi
region indicates calcaneofibular abutment or subtalar
Another useful test for recognizing early posterior
tibial tendon dysfunction is the first metatarsal rise
sign. This test is performed by externally rotating the
shank of the affected foot with 1 hand or passively
aligning the heel of the affected foot into a varus position with the patient standing, full weight bearing on
both feet. The head of the first metatarsal will rise in
the presence of posterior tibial tendon dysfunction
and will remain on the floor if posterior tibial tendon
function is normal.'"his
is caused by the loss of posterior tibial tendon function, resulting in flattening of
the medial longitudinal arch and the consequent
elongation of the supporting plantar medial ligamentous structures, in particular the caspsuloligamentous
complex of the first metatarsalcuneiform joint. This
allows the gastrocnemius-soleus complex to act at the
level of the first metatarsal head and cause dorsiflexion with weight bearing and external rotation of the
shank of the foot or passive heel varus.
The strength of the tendon is evaluated by asking
the patient to attempt to invert the foot from a plantarflexed and everted position. This position isolates
the posterior tibial tendon, neutralizing the synergistic
inversion from the anterior tibialis m~scle.'"~The
contralateral foot also should be tested in a similar
fashion to determine the strength of the patient's
nonimpaired ankle and to help identify a partial tear
J Orthop Sports Phys Ther .Voh~me30 -Number 2 - February 2000
FIGURE 2. Continued.
based on comparative ~eakness.~'
It is important to
palpate the posterior tibial tendon behind the medial
malleolus to feel it actively contract during inversion.
An active, palpable contraction in a patient with an
acquired flatfoot deformity puts the diagnosis of posterior tibial tendon rupture in doubt; tendonitis or
partial rupture of the posterior tibial tendon or r u p
ture of the spring or deltoid ligament then may be
the cause of flatfoot deformityJJ
Motion of the ankle and subtalar joints should also
be evaluated. Ankle motion is usually normal, whereas subtalar motion becomes more limited as the dysfunction progresses. The subtalar joint may become
fixed in valgus in cases of long-standing deformityaJ4
The amount of passive hindfoot inversion is an important variable in the selection of treatment and
therefore should be assessed a c ~ u r a t e l y . ~ ~
Long-standing hindfoot valgus is often associated
with an Achilles tendon c o n t r a ~ t u r eThis
. ~ is assessed by dorsiflexing the ankle while holding the
hindfoot in subtalar neutral position and the knee in
The relationship of the forefoot to the hindfoot
should be assessed because as the hindfoot valgus
worsens, the forefoot and midfoot assume a compensatory supinated position that may become fixed.
This forefoot supination is evident as a forefoot varus
posture. This, too, will affect selection of treatment,
as well as the design of any foot o r t h o s i ~ . ~ ~ . ~ ~
With attenuation or rupture of the posterior tibial
tendon, the medial longitudinal arch of the foot coll a p s e ~and
, ~ there is a relative internal rotation of
the tibia and talus. The subtalar joint everts, causing
the heel to assume a valgus position and the foot to
abduct at the talonavicular joint. A compensatory
forefoot varus deformity ensues. As the heel assumes
an increased valgus alignment, the Achilles tendon
becomes positioned lateral to the axis of rotation of
the subtalar joint. Over time, the shortened position
of the hindfoot results in an Achilles tendon contracture. As the deformity progresses, the fibula abuts
against the lateral wall of the calcaneus, causing pain
in the lateral hindfoot.
Johnson and Strom"' described the clinical stages
of posterior tibial tendon dysfunction. In stage I (Figure I ) , the length of the tendon is normal, although
mild degeneration is present. There is medial foot
and ankle pain, swelling, and mild weakness, but no
deformity. The single limb heel rise is painful, but
normal. A flexible planovalgus foot characterizes
stage I1 (Figures 2 and 3). The tendon is ruptured
o r functionally incompetent and shows more advanced degeneration. The "too many toes sign" is
FIGURE 2. (A) Stage I1 posterior tibial tendon dysfunction. Note the "too many toes sign" on the left foot with more toes seen laterally when viewing
the patient from behind. Also, note the hindfoot valgus, which is more pronounced on the left side than the right. (B)Lateral radiograph of the same
patient. Note the plantarflexedposition of the talar head. (C)Postoperative photograph of the same patient after a calcaneal osteotomy with medialization.
Note the correction of the hindfoot valgus. (D) Postoperative radiograph showing 2-screw fixation of the calcaneal osteotomy and the improved pitch
of the talus.
J Orthop Sports Phys TheroVohme SO Number 29 Febn~aly2000
FIGURE 3. (A) Stage II posterior tibia1 tendon dysfunction. Again, note the hindfoot valgus and the "too many toes sign." (B) and (CI Patient treated
with a short articulated AFO with correction of the hindfoot valgus.
1 Orthop Sport5 Phys Ther .Volume 30. Number 2. Febnran 2000
FIGURE 4. (A) Stage Ill posterior tibia1 tendon dysfunction. Note the medial hindfoot fullness and iixed valgus position. (BIPreoperative lateral radiograph
showing severe transverse tarsal joint collapse and osteoarthritis of the subtalar and talonavicular joints. (C) Postoperative lateral radiograph aiter triple
arthrodesis showing much improved midfoot and hindioot alignment.
present, indicating secondary deformity of the midf~ot.~"he patient will be unable to perform a single
limb heel rise, but the hindfoot remains flexible. In
stage 111 (Figure 4), all the signs of stage I1 are present except that some component of the hindfoot deformity is fixed. In advanced disease, there may be
lateral abutment pain at the calcaneal-fibular articulation. Stage IV (Figure 5 ) . alluded to by Johnson and
Strom's article and later added to their classification
by Myerson,J4 involves valgus tilt of the talus in the
ankle mortise leading to lateral tibiotalar degeneration.Zl.J4
Anteroposterior and lateral weight bearing radiographs of both feet, as well as radiographs of the ankle with the patient weight bearing should be o b
tained. Early in the disease, radiographs may reveal
normal findings or show minimal changes of angular
deformity. As the clinical deformity progresses, charJ Orthop Sports Phys Ther*Voliime 30 Number 2. February 2000
acteristic radiographic changes occur. With increasing deformity, the anteroposterior view of the foot
will show lateral subluxation of the talonavicular joint
as the navicular rotates laterally on the talus, uncovering the talar head."','".:'!' There is an increase in the
talo-first metatarsal angle, as well as an increase in
the divergence of the talus and calcaneus.'!' The lateral view reveals a plantarflexion deformity of the talus, a decrease in the lateral talocalcaneal angle, the
collapse of the longitudinal arch, a variable increase
in the talo-first metatarsal angle, and sag at the talonavicular, naviculocuneiform, or metatarsalcuneiform
joints.2" decrease in the distance from the medial
cuneiform to the floor compared with the contralatera1 foot also has been de~cribed.~:'
With advanced deformity, narrowing of the talonavicular and subtalar joints may be seen."' Anteriorposterior radiographs of the ankles with the patient
standing may reveal tibiotalar arthritis, talar tilt, and
calcaneofibular impingement in severe deformities.
Magnetic resonance (MR) imaging is the method
cally demonstrated on short-tau inversion recovery
(STIR) images.%
Ultrasound evaluation of the posterior tibial tendon is currently under investigation. Diagnostic ultrasound can detect changes in tendon size, the presence of fluid, and any intratendinous echogenic
changes, thereby differentiating intratendinous and
peritendinous structural changes. In addition, it is
cheaper and faster than MR imaging, although significant skill and experience by the ultrasonographer is
required to obtain the maximum amount of information from this t e ~ h n i q u e . ~ . ~
FIGURE 5. Anteroposterior ankle radiograph of stage IV disease dernonstrating severe hindfoot valgus with osteoarthrosis and valgus tilt of the
tibio-talar joint.
of choice to evaluate pathologic conditions of the
posterior tibial
however, some controversy exists over the exact role of MR imaging in the
treatment plan of patients with posterior tibial tendon dysfunction. '7344.JJ
Conti et alqeveloped a classification scheme of
tears of the posterior tibial tendon based on MR imaging. The classification takes into account structural
features and abnormal signals within the substance
of the tendon. In a type I tear, the MR image shows
1 or 2 fine, longitudinal splits in the tendon, often
on the undersurface, without patterns of degeneration. T1 weighted images reveal a homogeneous
black signal throughout the tendon. Type I1 tears are
characterized by wider longitudinal tendon splits and
intramural degeneration. These are seen as gray areas within the normally uniform black tendon. The
tendon also may show variable diameter on selected
cuts where a bulbous section may be distal to an attenuated portion. Type I11 tears are notable for more
diffuse swelling and uniform degeneration of the
tendon. A few tendon strands may remain, or the
tendon may be replaced entirely with scar tissue.
Complete ruptures with tendon gap are most graphi-
The majority of adult acquired flatfoot deformities
are the result of posterior tibial tendon dysfunction,
but several conditions have a similar clinical presentati~n.'~:'~
Attenuation or rupture of the calcaneonavicular (spring) ligament complex including the talonavicular capsule will have a similar clinical presentation as posterior tibial tendon dysfunction. A
strong voluntary contraction of the posterior tibial
tendon on manual testing supports the diagnosis of
spring ligament pathology.
Degenerative arthritis of the ankle joint with valgus
talar tilt places the hindfoot in marked valgus with
midfoot pronation and leads to a flatfoot def~rmity.'~
Standing anterior-posterior radiographs of the ankle
will rule out degenerative arthritis as a cause of adult
acquired flat foot deformity.
Arthritis of the talonavicular joint, spontaneous or
after trauma, causes forefoot abduction deformity,
collapse of the midfoot, and prominent callus formation on the plantar-medial aspect of the foot.'J
Posttraumatic tarsometatarsal (Lisfranc) joint arthritis can present as an acquired flatfoot deformity.
Usually the first, second, and third tarsometatarsal articulations are involved, and patients have painful osteophyte formation on the dorsal midfoot and progressive abduction and dorsiflexion of the forefoot
on presentati~n.'~
Inflammatory arthritis of the hindfoot, usually secondary to rheumatoid disease, can cause valgus tilt at
the ankle or subtalar joint instability. Lacerations of
the posterior tibial tendon, although uncommon,
have caused an acquired
Neuroarthropathy, such as diabetes, as well as other peripheral neuropathies, may cause an acquired
flatfoot deformity.'"
Treatment is based on an accurate staging of the
disease with both nonsurgical and surgical treatments
designed to correct the abnormalities particular to
that stage of disease and to prevent progression to
the next stage.
J Orthop Sports P h y Ther-Volume SOeNumber 29Febnlary 2000
FIGURE 6. A University of California, Berkeley Laboratories (UCBL) orthosis with medial posting.
The goals of nonoperative treatment include the
elimination of clinical symptoms, improvement of
hindfoot alignment, and the prevention of progressive foot deformity. For stage I disease, nonsurgical
treatment should be tried for at least 3 to 4 months.
A short walking cast or removable cast boot immobilization is indicated for patients with acute tenosynov i t i ~ . ~ ~ If
. Jsymptoms
are improved after immobilization, then a custom orthotic or ankle foot orthosis
(AFO) may be fitted to the patient. The orthotic
should be a full-length, semirigid, totalcontact insert
with medial posting. The primary function of the orthotic is to provide arch support and correct the
flexible component of the deformity. Physical therapy for Achilles tendon stretching and posterior tibia1
tendon strengthening is also b e n e f i ~ i a l . " Nonste~~~
roidal antiinflammatory medicine may decrease pain
and associated swelling.
Surgical treatment should be undertaken only after failure of nonsurgical measures. Surgically, a synovectomy will remove any hypertrophic tenosynovium. If a necrotic portion of the tendon is encountered, as evidenced by discoloration, attenuation, and
longitudinal rents, this area may be excised and the
remaining tendon repaired in an end-toend fashi ~ n . ~ " na study by Teasdall and Johnson4%th an
J Orthop Sports Phys Ther-Volume SOeNumber 2.Febnla1-y 2000
average 30-month follow-up, 16 of 19 patients reported feeling "much better" after this procedure and
74% had complete relief of pain. This repair may be
reenforced by means of a side-tu-side tenodesis to
the adjacent flexor digitorum longus tendon.'JR+'
In stage I1 disease, nonsurgical treatment involves
an initial period of cast or removable cast boot immobilization or, in subacute cases, an AFO. Longterm nonsurgical treatment requires more rigid s u p
port of the foot and ankle. This may be accomplished with an AFO, corrective total contact insert,
o r a University of California, Berkeley Laboratories
orthosis (UCBL) (Figure 6) .3 The UCBL functions to
place the hindfoot in neutral and limit the motion
of the subtalar joint. Many designs of AFO have been
described for treatment of the flexible flatfoot deformity including a 1-piece molded polypropylene AFO,
a short articulated AFO (Figure 3), a short lace-up
leather (Figure 7), and a plastic AFO, as well as the
traditional double upright AFO with T-strap. These
all function to limit subtalar motion. In addition,
shoe modifications such a medial flare, wedge, or stabilizer may be
Surgical treatment of patients with stage I1 disease
is controversial. There are many described procedures, each with only short-term follow-up and all
. ~ ~ options for
placement may be a p p r ~ p r i a t eOther
treatment include a lateral column lengthening to
recreate the medial longitudinal arch performed
through the calcaneal neck, as described by Evans,
or through the calcaneocuboid joint with subsequent
f u s i ~ n . ~ Lengthening
through the calcaneal neck
in adults has led to calcaneocuboid joint overload
and early arthro~is.~'
Lateral column lengthening
may be performed alone or with a medial displace
ment calcaneal osteotomy, thereby addressing both
the pes planus deformity and the valgus deforming
force of the Achilles t e n d ~ n . ~ '
Stage I11 disease (fixed deformity) is not passively
correctable, and therefore, any nonoperative treatment will need to accommodate the deformity. Custom foot orthotics, shoes, and AFOs, may help alleviate pain and slow progression. Because the deformity
is not passively correctable, tendon reconstruction
alone is not helpful, and to correct the deformity, a
subtalar or triple arthrodesis usually is performed. In
stage IV, the tibiotalar joint is involved. Treatment
thus involves a tibiotalocalcaneal, pantalar fusion, or
hindfoot arthrodesis combined with bracing.
FIGURE 7. Short leather lace up ankle-ioot orthosis (AFO)with copolymer
reinforcement medial and lateral for added support.
Accurate diagnosis requires a high index of suspicion and an understanding of the physical signs,
symptoms, and natural history of the acquired flatfoot deformity. Physicians must accurately stage the
extent of the disease, as treatment depends on the
stage and the response to nonsurgical therapy.
with nearly equivalent outcomes. It is not within the
scope of this article to discuss each of these treatREFERENCES
ments thoroughly; instead, each will be presented
1. Alexander IJ,Johnson KA, Berquist TH. Magnetic resowith relevant articles referenced for further review. If
nance imaging in the diagnosis of disruption of the posa large gap is present in the posterior tibial tendon,
terior tibial tendon. Foot Ankle. 1987;8:144-147.
the nonviable ends are resected, and a side-to-side
2. Anzel SH, Covey KW, Weiner AD, Lipscomb PR. Disruptenodesis to the flexor digitorum longus tendon is
tion of muscles and tendons: an analysis of 1,104 cases.
If the tendon is torn off its inSurgery. 1959;45:406-414.
3. Chao W, Wapner KL, Lee TH, Adams J, Hecht PJ. Nonopsertion into the navicular tuberosity, then nonviable
erative management of posterior tibial tendon dysfunctissue is resected, and the tendon is advanced and
tion. Foot Ankle Int. 1996;17:736-741.
reinserted into the navicular by means of an anchor4. Clain MR, Baxter DE. Simultaneous calcaneocuboid and
ing suture or by passing the tendon through a drill
talonavicular fusion: long-term follow-up study. ) Bone
hole and suturing it to itself. Transfer of the flexor
joint Surg BE 1994;76B:133-136.
5. Conti S, Michelson J, Jahss M. Clinical significance of
digitorum longus tendon through a drill hole in the
magnetic resonance imaging in preoperative planning for
navicular may also be required if the tendon is torn
reconstruction of posterior tibial tendon ruptures. Foot
off its insertion.'42i-:':' Some studies recommend that
Ankle. 1992;13:208-214.
at the time of tendon reconstruction, an evaluation
6. Conti SF. Posterior tibial tendon problems in athletes. Orof the spring ligament be performed and repair perthop Clin North Am. 1994;25:109-1 2 1.
formed if there are signs of i n j ~ r y . ~Severe
defor7. Cracchiolo A. Evaluation of spring ligament pathology in
patients with posterior tibial tendon rupture, tendon transmity with hindfoot subluxation or arthritis may refer, and ligament repair. Foot Ankle Clin. 1997;2:297quire isolated arthrodesis of the subtalar j~int,".~".:'~
talonavicular joint,'.' or a double4 or triple arthrode
8. Deland JT, Otis JC, Lee KT, Kenneally SM. Lateral column
~ i s , :either
alone or in combination with tendon relengthening with calcaneocuboid fusion: range of motion
pair. For severe hindfoot valgus with lateral impingein the triple joint complex. Foot Ankle Int. 1995;16:729733.
ment, osteotomy of the calcaneus with medial disJ Orthop Sports Phys Ther.Volrme 30 Number 2 Febnraly 2000
9. Evans D. Calcaneovalgus deformity. J Bone Joint Surg Br.
10. Frey C, Shereff M, Greenridge N. Vascularity of the posterior tibial tendon. J Bone Joint Surg. 1990;72A:884888.
11. Funk DA, Cass JR, Johnson KA. Acquired adult flat foot
secondary to posterior tibial tendon pathology. J Bone
Joint Surg. 1986;68A:95-102.
12. Gazdag A, Cracchiolo A. Posterior tibial tendon rupture:
evaluation of spring ligament pathology and clinical assessment of tendon transfer and ligament repair. J Bone
Joint Surg. 1997;79:675-681.
13. Goldner JL, Keats PK, Bassett FH Ill, Clippinger FW. Progressive talipes equinovalgus due to trauma or degeneration of the posterior tibial tendon and medial plantar
ligaments. Orthop Clin North Am. 1974;5:39-51.
14. Harper MC, Tisdel CL. Talonavicular arthrodesis for the
painful adult acquired flatfoot. Foot Ankle Int. 1996;17:
15. Henceroth W D 11, Deyerle WM. The acquired unilateral
flatfoot in the adult: some causative factors. Foot Ankle.
16. Hintermann B, Gachter A. The first metatarsal rise sign: a
simple sensitive sign of tibialis posterior tendon dysfunction. Foot Ankle Int. 1996;17:236-241.
17. Holmes GB Jr, Mann RA. Possible epidemiological factors
associated with rupture of the posterior tibial tendon. Foot
Ankle. 1992;13:70-79.
18. Jahss MH. Spontaneous rupture of the tibialis posterior
tendon: clinical findings, tenographic studies, and a new
technique of repair. Foot Ankle. 1982;3:158-166.
19. Johnson KA. Tibialis posterior tendon rupture. Clin Orthop. 1983; 177: 140-147.
20. Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. Clin Orthop. 1989;239:196-206.
21. Kettelkamp DB, Alexander HH. Spontaneous rupture of
the posterior tibial tendon. J Bone Joint Surg. 1969;SlA:
22. Kitaoka HB, Patzer GL. Subtalar arthrodesis for posterior
tibial tendon dysfunction and pes planus. Clin Orthop.
23. Mann RA. Acquired flatfoot in adults. Clin Orthop. 1983;
24. Mann RA. Rupture of the tibialis posterior tendon. Instructional Course Lectures. 1984;33:302-309.
25. Mann RA. Flatfoot in adults. In: Mann RA, Coughlin MJ,
eds. Surgery of the Foot and Ankle. Vol 1. 6th ed. St Louis,
Mo: The CV Mosby Co; 1993:757-784.
26. Mann RA, Beaman DN, Horton GA. Isolated subtalar arthrodesis. Foot Ankle Int. l998;l9:5ll-5l9.
27. Mann RA, Thompson FM. Rupture of the posterior tibial
tendon causing flat foot. Surgical treatment. J Bone Joint
Surg. 1985;67A:556-56.
28. Michelson J, Easley M, Wigley FM, Hellman D. Posterior
tibial tendon dysfunction in rheumatoid arthritis. FootAnkle Int. 1995;16:156-161.
J Orthop Sports Phys Ther.\'olr~me 30. Nr~nlber2 February 2000
29. Miller SD, Van Holsbeeck M, Boruta PM, Wu KK, Katcherian DA. Ultrasound in the diagnosis of posterior tibial
tendon pathology. Foot Ankle Int. 1996;17:555-558.
30. Mink JH. Tendons. In: Deutsch AL, Mink JH, Kerr R, eds.
MRI of the Foot and Ankle. New York: Raven Press; 1992:
135-1 72.
31. Monto RR, Moorman CT Ill, Mallon WJ, Nunley JA Ill.
Rupture of the posterior tibial tendon associated with
closed ankle fracture. Foot Ankle. 1991;11:400-403.
32. Myerson M, Solomon G, Shereff M. Posterior tibial tendon dysfunction: its association with seronegative inflammatory disease. Foot Ankle. 1989;9:219-225.
33. Myerson MS. Posterior tibial tendon insufficiency. In:
Myerson MS, ed. Current Therapy in Foot and Ankle Surgery. St Louis, Mo: The CV Mosby Co; l993:123-135.
34. Myenon MS. Adult acquired flatfoot deformity. J Bone
Joint Surg. 1996;78A:780-792.
35. Myenon MS, Corrigan J, Thompson F, Schon LC. Tendon
transfer combined with calcaneal osteotomy for treatment
of posterior tibial tendon insufficiency: a radiological investigation. Foot Ankle Int. 1995;16:712-718.
36. Nazarian LN, Rawool NM, Martin CE, Schweitzer ME.
Synovial fluid in the hindfoot and ankle: detection of
amount and distribution with US. Radiology. 1995;197:
37. Noto AM, Cheung Y, Rosenberg ZS, Norman A, Leeds NE.
MR imaging of the ankle: normal variants. Radiology.
38. O'Malley MJ, Deland JT, Lee KT. Selective hindfoot arthrodesis for the treatment of adult acquired flatfoot deformity: an in vitro study. Foot Ankle Int. 1995;16:41141 7.
39. Pedowitz WJ, Kovatis P. Flatfoot in the adult. 1 Am Acad
Orthop Surg. 1995;3:293-302.
40. Phillips GE. A review of elongation of the os calcis for
flat feet. J Bone Joint Surg Br. 1983;65B:15-18.
41. Pomeroy GP, Manoli A 11. A new operative approach for
flatfoot secondary to tibialis posterior tendon insufficiency: a preliminary report. Foot Ankle Int. 1997;18:206212.
42. Rosenberg ZS, Cheung Y, Jahss MH, Noto AM, Norman
A, Leeds NE. Rupture of the posterior tibial tendon: CT
and MR imaging with surgical correlation. Radiology.
43. Sangeorzan BJ, Mosca V, Hansen ST Jr. Effect of calcaneal
lengthening on relationships among the hindfoot, midfoot, and forefoot. Foot Ankle. 1993;14:136-141.
44. Shereff MJ. Treatment of ruptured posterior tibial tendon
with direct repair and FDL tenodesis. Foot Ankle Clin.
45. Teasdall RD, Johnson KA. Surgical treatment of stage I
posterior tibial tendon dysfunction. Foot Ankle Int. 1994;
46. Williams R. Chronic non-specific tenovaginitis of tibialis
posterior. J Bone Joint Surg Br. 1963;45B:542-545.
47. Woods L, Leach RE. Posterior tibial tendon rupture in athletic people. Am J Sports Med. 1991;19:495-498.