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Review Article
Plantar and Medial Heel Pain:
Diagnosis and Management
Abstract
Heel pain is commonly encountered in orthopaedic practice.
Establishing an accurate diagnosis is critical, but it can be challenging
due to the complex regional anatomy. Subacute and chronic plantar
and medial heel pain are most frequently the result of repetitive
microtrauma or compression of neurologic structures, such as plantar
fasciitis, heel pad atrophy, Baxter nerve entrapment, calcaneal stress
fracture, and tarsal tunnel syndrome. Most causes of inferior heel pain
can be successfully managed nonsurgically. Surgical intervention is
reserved for patients who do not respond to nonsurgical measures.
Although corticosteroid injections have a role in the management of
select diagnoses, they should be used with caution.
Heel pain is a common complaint
among orthopaedic patients.
Establishing an accurate diagnosis can
be challenging due to the complex
regional anatomy and the close prox-
imity of potential pain generators. The
differential diagnosis should include
vascular, infectious, oncologic, and
systemic causes. Subacute and chronic
heel pain are most commonly due to
repetitive microtrauma or compres-
sion of neurologic structures.
Typically, diagnosis can be made
based on a detailed history and physical
examination that allow the clinician to
pinpoint the location of maximal ten-
derness (Figure 1). Weight-bearing
plain radiographs should be obtained
to assess alignment and degenerative
changes and to exclude fracture and
other skeletal abnormalities. Advanced
imaging studies and electromyography
(EMG) can be used to confirm or
rule out certain diagnoses and to
provide additional information when
the diagnosis is uncertain.
In general, initial management should
consist of one or more nonsurgical
modalities, including rest, shoe wear
modification, NSAIDs, home stretch-
ing exercises, physical therapy, pre-
fabricated shoe inserts, and custom
orthoses. Such measures are effective in
most patients, especially when both the
patient and physician allow adequate
time for them to work. Corticosteroid
injections should be used sparingly.
Although these are considered by many
to be capable of accelerating recovery,
the current literature demonstrates only
short-term benefit and indicates a con-
stellation of notable potential side
effects.
1-6
Surgical intervention is indi-
cated for carefully selected patients
with recalcitrant pain whose symptoms
have persisted despite an appropriate
course of nonsurgical measures. Further
study is needed to determine the efficacy
of the relatively new treatment modal-
ities, including platelet-rich plasma
(PRP) injection and extracorporeal
shock wave therapy (ESWT).
Plantar Fasciitis
Epidemiology, Anatomy, and
Pathophysiology
Plantar fasciitis (PF) represents the
most common cause of heel pain in
372 Journal of the American Academy of Orthopaedic Surgeons
Craig R. Lareau, MD
Gregory A. Sawyer, MD
Joanne H. Wang, BA
Christopher W. DiGiovanni, MD
From the Alpert Medical School, Brown
University, Providence, RI (Dr. Lareau,
Dr. Sawyer, and Ms. Wang), the Rhode
Island Hospital, Providence (Dr. Lareau
and Dr. Sawyer), and Harvard Medical
School and the Massachusetts General
Hospital, Boston, MA (Dr. DiGiovanni).
Dr. Sawyer or an immediate family
member serves as a paid consultant to
Mitek. Dr. DiGiovanni or an immediate
family member has received royalties
from Extremity Medical; is a member of
a speakers’bureau or has made paid
presentations on behalf of BioMimetic
Therapeutics, Extremity Medical, and
Wright Medical Technology; serves as
a paid consultant to BESPA, BioMimetic
Therapeutics, Extremity Medical, and
Wright Medical Technology; has stock
or stock options held in Extremity
Medical and Wright Medical
Technology; has received research or
institutional support from BioMimetic
Therapeutics and Wright Medical
Technology; and has received
nonincome support (such as equipment
or services), commercially derived
honoraria, or other non–research-
related funding (such as paid travel)
from CuraMedix and Performance
Orthotics. Neither of the following
authors nor any immediate family
member has received anything of value
from or has stock or stock options held
in a commercial company or institution
related directly or indirectly to the subject
of this article: Dr. Lareau and Ms. Wang.
J Am Acad Orthop
Surg 2014;22:372-380
http://dx.doi.org/10.5435/
JAAOS-22-06-372
Copyright 2014 by the American
Academy of Orthopaedic Surgeons.
Copyright
Ó
the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
adults, affecting 2 million persons
annually in the United States.
7
The
peak incidence occurs between ages 40
and60years,althoughithas
been known to occur in runners who
are younger.
8
Bilateral involvement,
which occurs in approximately one
third of patients, should prompt con-
sideration of inflammatory disease.
8
The plantar fascia is a fibrous
aponeurosis that originates from
the plantar medial aspect of the
calcaneal tuberosity and divides
into five slips that insert distally on each
of the proximal phalanges. These fibers
also merge with the surrounding der-
mis, transverse metatarsal ligaments,
and flexor tendon sheaths. Especially at
the first metatarsophalangeal joint,
dorsiflexion activates the windlass
mechanism, which increases plantar
fascial tension and elevates the medial
longitudinal arch.
9
The plantar fascia
lacks elasticity, exhibiting a maximal
elongation of only 4% of its length in
cadaver specimens.
10
PF is believed to result primarily from
repetitive microtrauma and excessive
strain.
11
Although it is considered to be
an inflammatory condition based on
historic descriptions, recent studies
suggest that it is a noninflammatory,
degenerative process that may be more
appropriately termed plantar fas-
ciosis.
11,12
Histologically, PF involves
myxoid degeneration with disorienta-
tion of collagen fibers, angiofibro-
blastic hyperplasia, and calcification.
11
Reduced ankle dorsiflexion due to
tightness of either the Achilles tendon
or the gastrocnemius muscle may be
associated with the development of PF;
obesity and weight-bearing professions
are other independent risk factors.
13-15
Other risk factors include advanced
age, poor footwear, overtraining, and
reduced subtalar joint mobility.
8
Presentation and Physical
Examination
Patients usually experience start-up
pain, that is, plantar medial heel pain
that culminates either with their first
steps in the morning or subsequent to
prolonged periods of rest. This pain is
typically sharp and does not radiate.
Physical examination reveals tender-
ness at the site of the plantar fascial
insertion on the medial calcaneal
tuberosity. Tenderness may extend
along the plantar fascia, and it in-
creases with maneuvers that stretch
the plantar fascia, including passive
toe dorsiflexion. Restricted ankle
dorsiflexion may be identified due to
contracture of the Achilles tendon or
the gastrocnemius muscle itself. The
Silfverskiöld test can be performed
to differentiate between primary con-
tracture of the gastrocnemius muscle
itself and of the gastrocnemius-soleus
complex.
16
This specific maneuver
involves comparative manual stress
assessment of resultant maximal ankle
dorsiflexion during neutral foot align-
ment when the knee is in full extension
and again when the knee is flexed
90°. When a significant improvement
(approximately 10°or more) in ankle
dorsiflexion can be obtained during
knee flexion compared with knee
extension, this test indicates the
presence of a primary gastrocnemius
muscle contracture. In the event that
no such substantive difference exists
between these two testing conditions
but there is still significant dorsi-
flexion restriction, the patient is likely
to have an Achilles contracture (spe-
cifically, combined gastrocnemius
and soleus muscle tightness).
Diagnosis
Typically, advanced imaging is not
necessary to confirm the diagnosis of
PF. However, weight-bearing plain
radiographs usually are obtained to
rule out other skeletal causes of heel
pain. The radiographic finding of
a heel spur, or plantar calcaneal
calcification, should be considered
nonspecific because these are often
present in asymptomatic patients.
17
Cadaver dissection has shown that
these spurs are localized to the flexor
Figure 1
Clinical photographs of the medial (A) and plantar (B) aspects of a left foot
demonstrating locations of tenderness for five diagnoses of heel pain: heel pad
atrophy (1), plantar fasciitis (2), Baxter nerve entrapment (3), calcaneal stress
fracture (4), and tarsal tunnel syndrome (5).
Craig R. Lareau, MD, et al
June 2014, Vol 22, No 6 373
Copyright
Ó
the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
digitorum brevis (FDB) origin and
do not lie in the true substance of the
plantar fascia itself.
18
MRI is rarely required for the diag-
nosis of PF. It is perhaps better used to
rule out alternative pathologies, such as
calcaneal stress fracture. In the patient
with PF, MRI usually demonstrates
thickening of the plantar fascia—one
study showed it to be twice the
thickness of healthy controls—and
edema within the soft tissues.
19
Edema
in the medial calcaneal tuberosity,
however, is only variably present on
MRI.
Management
In all cases, initial management should
be nonsurgical. Rest, structured phys-
ical therapy, home stretching exercises,
heel cushions, orthoses, ice, NSAIDs,
and weight loss all have been linked to
the successful nonsurgical manage-
ment of PF.
20-26
Barefoot activities and
wearing shoes with inadequate cush-
ioning and support should be avoid-
ed.
12
Shoe wear modifications, such
as use of a rocker sole, have been
shown to reduce dorsiflexion of the
first metatarsophalangeal joint and
thereby decrease the peak tensile strain
of the plantar fascia.
27
Stretching
specific to the plantar fascia has
recently been shown to provide supe-
rior pain relief when compared with
Achilles tendon stretching at 8 weeks;
however, no significant difference was
seen at 2-year follow-up.
21
In a level I
study, celecoxib was shown to provide
short-term pain reduction compared
with placebo.
22
Other management options include
night splinting, prescription orthoses,
and a period of immobilization.
12
Night splints are designed to prevent
and correct passive contracture of
the plantar fascia and gastrocnemius-
soleus complex. In one study, foot
orthoses were found to improve pain
and function at 3 months but not
at 12 months.
23
Prefabricated shoe
inserts have been shown to be as
effective as more costly custom
orthoses.
23
Following a dedicated
trial of such treatment measures, 90%
to 95% of patients experience reso-
lution of symptoms within 1 year.
12
For the small number of refractory
patients, more invasive techniques,
such as injection and ESWT, may be
considered.
In level I trials, corticosteroid in-
jections have resulted in significantly
improved pain relief in patients with
PF at 4 weeks compared with pla-
cebo.
2,6
These same studies, however,
also suggest that corticosteroid in-
jections may only provide short-term
pain relief; injection did not provide
significant pain relief compared with
placebo at 3-month follow-up.
Corticosteroid injections are associ-
ated with a risk of plantar fascia rup-
ture.
28
This finding was observed in
2.4% of patients whoreceivedcorti-
costeroid injections.
29
Inasurveyof
members of the American Orthopae-
dic Foot and Ankle Society, this
complication was found to occur an
average of 1.5 times per provider over
thecourseoftheircareers.
4
Plantar
fascia rupture itself is not believed to be
a common sequela of injection. Long-
term consequences of rupture include
longitudinal arch strain, lateral and
dorsal midfoot strain, lateral plantar
nerve dysfunction, stress fracture, and
hammer toe deformity.
28,30
Other
potential side effects of corticosteroid
injection include skin and fat atrophy
at the injection site, postinjection
flare, inadvertent intraneural/intra-
vascular injection, hyperglycemia in
patients with diabetes, tendon rup-
ture, infection, and facial flushing.
31
Of these, postinjection flare, facial
flushing, and skin and fat atrophy are
the most common. Systemic compli-
cations are rare.
31
ESWT uses acoustic waves that elicit
an inflammatory response; in theory,
this leads to neovascularization and
healing.
32
Level I and II evidence,
however, have not convincingly dem-
onstrated it to be superior to placebo
in the management of PF. Of eight
double-blind placebo-controlled ran-
domized clinical studies, four con-
cluded that ESWT significantly
improved some short-term outcome
measures.
33-36
The remainder dem-
onstrated no significant differences in
any outcome measure.
32,37-39
One
study demonstrated that plantar fas-
cial stretching exercises were superior
to ESWT.
24
Level I studies investigating pulsed
radiofrequency electromagnetic field
therapy
40
and botulinum toxin A
injection
41
for the management of PF
have failed to demonstrate a significant
difference compared with placebo.
Neither has PRP injection demon-
strated comparative superiority over
corticosteroid injection in the man-
agement of PF.
42
Surgery for recalcitrant disease most
often entails partial plantar fas ciotomy
without heel spur resection. In the past
two decades, endoscopic techniques
have gained in popularity due to
the purported advantage of a more
rapid postoperative recovery.
43
Open
plantar fasciotomy, the traditional
mainstay of surgical management,
has been shown to provide pain relief
in 76% of patients.
18
In a recent level
IV study, endoscopic plantar fas-
ciotomy completely relieved symp-
toms in 76% of patients and was
associated with a low complication
rate.
44
Gastrocnemius recession may be
considered for the patient with PF
and a concomitant gastrocnemius
contracture. In a retrospective series,
25 patients with PF and isolated
gastrocnemius contracture experi-
enced significant pain relief after
gastrocnemius recession, with the
average visual analog scale score
decreasing from 8.1 to 1.9.
14
In
2012, Abbassian et al
45
reported
that proximal gastrocnemius release
resulted in complete or significant
pain relief for 81% of patients; 58%
of patients experienced relief within
2 weeks of surgery.
Plantar and Medial Heel Pain: Diagnosis and Management
374 Journal of the American Academy of Orthopaedic Surgeons
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Heel Pad Atrophy
Anatomy and
Pathophysiology
The heel pad, which is located beneath
the calcaneus, consists of adipose tis-
sue within a highly organized and
specialized confluence of fibrous sep-
tae that extend from the skin to the
calcaneal periosteum. These septae are
arranged into a stiff superficial micro-
chamber and a deep macrochamber
that undergoes substantial deforma-
tion with loading.
46
The heel pad
serves as a shock absorber, allowing
the heel to tolerate high loads and
repetitive load bearing. Heel pad
atrophy typically begins in the fifth
decade of life and likely is the result of
loss of water, collagen, and elastic
tissue.
47
The heel pad becomes less
elastic in both the elderly and in per-
sons with diabetes, and these patients
are particularly prone to heel pad
atrophy. Prichasuk
17
defined the heel
pad compressibility index as the ratio
of the heel pad thickness in loaded
and unloaded positions. An increase
in the heel pad compressibility index
indicates loss of elasticity.
Presentation and Physical
Examination
Heel pad atrophy results in deep, non-
radiating pain that typically involves
the central weight-bearing portion of
the calcaneal tuberosity. It is com-
monly misdiagnosed as PF. Symptoms
of heel pad atrophy are usually exac-
erbated by walking barefoot or on
hard surfaces and are relieved by
the absence of heel pressure. Physical
examination typically elicits centrally
located tenderness over the plantar
aspect of the calcaneal tuberosity;
this tenderness can be associated with
varying degrees of swelling. Usually,
pain is not reproducible with passive
motion of the ankle or toes or
with side-to-side compression of the
tuberosity.
Diagnosis
Although radiographic studies are not
required to either make or confirm the
diagnosis of heel pad atrophy, imaging
should be considered to rule out alter-
native pathology. Heel pad thickness
is typically greater in men than in
women.
17
This thickness is measured
on the weight-bearing lateral view as
the distance between the ground and
the plantar aspect of the calcaneal
tuberosity. The relationship between
this measurement and the presence of
symptoms remains unclear because
not all patients with heel pad atrophy
are symptomatic. MRI is usually
unnecessary, but it may demonstrate
edema and atrophy of the heel pad.
Management
Resolution of symptomatic heel pad
atrophy can be challenging. Manage-
ment may include NSAIDs, properly
padded shoes, and customized ortho-
ses or over-the-counter silicone heel
cups. Given that the inherent nature of
this pathology is mechanical, lower-
impact and offloading activities can be
very helpful. Corticosteroid injection
should be avoided because it can result
in further atrophy of the plantar fat.
1
Surgical management is not rec-
ommended. There are no proven
techniques capable of adequately
recreating or replacing the normal
heel pad architecture. Furthermore,
the plantar skin is prone to problems
with wound healing, and infection in
this region can be difficult to manage.
Baxter Nerve Entrapment
Anatomy and
Pathophysiology
The first branch of the lateral plantar
nerve, that is, the Baxter nerve, is the
only nerve branch that lies deep to the
abductor hallucis and FDB muscles. It
travels superficial to the quadratus
plantae (QP) muscle along the medial
aspect of the calcaneus, providing
motor function to the QP, FDB, and
abductor digiti quinti (ADQ) muscles,
as well as sensation to the lateral
plantar skin, calcaneal periosteum,
and long plantar ligament.
48
The two
potential points of compression are
the deep margin of the abductor
hallucis muscle and the point at
which the nerve passes anterior to
the medial calcaneal tuberosity
49
(Figure 2). Pain is felt approximately
4to5cmanteriortotheposterior
aspect of the heel or just distal to the
medial calcaneal tuberosity at the
junction of the glabrous and non-
glabrous skin.
50
Nerve compression
causes burning pain that may radiate
distally toward the plantar lateral foot.
The diagnosis commonly coexists
with PF. In one study, PF occurred in
52.5% of patients with an MRI finding
of ADQ atrophy, a manifestation of
chronic compression of the first branch
of the lateral plantar nerve.
51
In con-
trast, ADQ atrophy on MRI is seen in
only 6.3% of the general population.
49
Although Baxter and Pfeffer
52
reported
that in some cases a small portion of
the medial plantar fascia was removed
to facilitate exposure, to our knowl-
edge there are no studies that specify
the percentage of patients with Baxter
nerve entrapment who required plan-
tar fascia release.
Presentation and Physical
Examination
Physical examination should include
an evaluation of gastrocnemius-soleus
contracture and hindfoot alignment.
Both hindfoot valgus due to posterior
tibial tendon insufficiency and ankle
plantar flexion resulting from equinus
contracture can accentuate symp-
toms. Pressure has been shown to be
highest in the lateral plantar tunnel
during plantar flexion and pro-
nation.
53
Percussion over the nerve
should be performed to assess for
reproduction of symptoms. Dimin-
ished sensation in the plantar lateral
foot may be seen in chronic cases.
50
Craig R. Lareau, MD, et al
June 2014, Vol 22, No 6 375
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the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
Diagnosis
Similar to other etiologies of chronic
heel pain, entrapment of the first branch
of the lateral plantar nerve is primarily
a clinical diagnosis. Imaging modalities
are of limited usefulness because ADQ
atrophy is seen in 6.3% of all patients
who undergo MRI of the foot.
49
Elec-
trodiagnostic studies in conjunction
with clinical evaluation can help
delineate whether compression exists
in the lateral plantar tunnel or more
proximally in the tarsal tunnel.
50
Management
Initial management may include rest,
ice, NSAIDs, orthoses for hindfoot
malalignment, and physical therapy
with local modalities. There is no evi-
dence to support one nonsurgical
method over another. If nonsurgical
measures have been exhausted and
symptoms persist for .3 months, sur-
gical decompression consisting pri-
marily of release of the superficial and
deep fascia of the abductor hallucis
overlying the nerve is warranted and
usually effective.
52
Although Baxter
and Pfeffer
52
also mentioned resection
of small spurs that might be encoun-
tered in some patients, the experience
of the senior author (C.W.D.) indicates
that this is rarely necessary. In our
practice, however, we have on occa-
sion felt the need to provide additional
decompression via release of the FDB
and even the QP depending on their
relative size, proximity, and perceived
direct effect on the course of the lateral
plantar nerve branch as assessed
visually.
54
However, although our
experience in finding and treating this
latter presentation is positive, it is quite
limited and lacks formal study. Baxter
and Pfeffer
52
described excellent or
good results in 89% of heels managed
with open surgical release.
Calcaneal Stress Fracture
Anatomy and
Pathophysiology
The calcaneus is the largest tarsal bone
and is subject to considerable weight-
bearing stresses on a routine basis.
Despite these chronic loads, however,
the bone remains predominantly can-
cellous in nature. As a result, stress
fractures of the calcaneus are not
uncommon; typically, they occur
immediately posterior and inferior to
the posterior facet
12
(Figure 3). The
calcaneus is one of the most common
locations of stress fracture in the foot,
second only to the metatarsals.
19
Calcaneal stress fractures occur
most frequently in athletes, military
trainees, and elderly patients with
osteopenia. These injuries are caused
by repetitive overload and the
inability of bone formation to match
resorption. A thorough history often
elicits changes in exercise or activity,
typically involving recent adoption of
a more rigorous exercise regimen.
Presentation and Physical
Examination
Patients with calcaneal stress fracture
typically report intense, diffuse heel
pain along the medial and lateral
aspects of the posterior tuberosity. Pain
is exacerbated by activity and weight
bearing, and it may progress to become
persistent even at rest.
55
Patients often
experience tenderness along the lateral
wall of the calcaneal tuberosity. A
positive calcaneal squeeze test, or pain
on direct compression of both the
medial and lateral walls of the calca-
neus, is pathognomonic. This maneu-
ver helps to differentiate a calcaneal
stress fracture from other causes of
heel pain.
56
The amount of ecchymosis
and swelling depends on the acuity of
the injury.
Diagnosis
Radiographs, specifically the lateral
foot view, may reveal disruption of
Figure 2
Illustration of a left heel showing the potential sites of compression of the Baxter
nerve: the deep margin of the abductor hallucis muscle (1) and the point at which
the nerve passes anterior to the medial calcaneal tuberosity (2).
Plantar and Medial Heel Pain: Diagnosis and Management
376 Journal of the American Academy of Orthopaedic Surgeons
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the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
the trabecular pattern of the calcaneus
2to8weeksaftersymptomonset,
56
although these images are frequently
interpreted as normal during the early
course of this disease process (Figure 3).
The rare finding of a linear sclerotic
line in the tuberosity perpendicular to
the natural trabecular pattern indicates
thepresenceofahealingstressfrac-
ture.
19,57
During the early stages of
fracture, radiographic sensitivity can
be as low as 10%, but follow-up
radiography reveals diagnostic fea-
tures in 50% of patients.
19,56
When
pain persists but radiographs appear
normal, MRI or bone scanning may be
helpful to establish the diagnosis.
Technetium bone scans typically detect
a stress fracture 1 to 2 weeks before
changes become apparent radio-
graphically.
57
MRI demonstrates high
signal intensity due to marrow edema
and hemorrhage on T2-weighted im-
ages.
19
MRIissuperiortobonescan-
ning because it enables concomitant
evaluation of soft-tissue structures.
57
Management
Treatment consists of activity modi-
fication and protected weight bearing
in a fracture boot or short leg cast for
4 to 8 weeks. The treating clinician
also should consider a metabolic
workup, including vitamin D levels and
bone density testing, especially for the
patient with a previous history of frac-
ture. Normal activities can be resumed
after this period of immobilization,
once tenderness resolves. The prog-
nosis is excellent, and surgery is rarely
required. Significant displacement
and malalignment are uncommon,
and nonunion is rare.
Tarsal Tunnel Syndrome
Anatomy and
Pathophysiology
Tarsal tunnel syndrome (TTS) is an
entrapment neuropathy of the tibial
nerve as it courses through the tarsal
tunnel. The tarsal tunnel is a fibro-
osseous space located posterior and
distal to the medial malleolus. Its roof
is formed by the flexor retinaculum,
and the medial wall of the calcaneus
serves as its floor. The posterior tibial
neurovascular bundle passes through
this tunnel, along with the tendons of
the tibialis posterior, flexor digitorum
longus, and flexor hallucis longus
muscles. The tibial nerve divides into
the medial and lateral plantar nerves
as well as the medial calcaneal branch.
TTS is a relatively uncommon clinical
entity that may be overdiagnosed.
Pesplanusisoneofthemorecom-
monly purported causes of TTS because
hindfoot valgus and forefoot abduction
place the nerve under tension.
58
Other
reported causes include fracture, space-
occupying lesions, tenosynovitis, and
an accessory abductor hallucis mus-
cle.
19,58,59
Systemic inflammatory
arthropathy, diabetes, and rheumatoid
arthritis may also play a role in the
development of TTS.
60
This syndrome
is not typically bilateral, so systemic
and spinal pathology should be
excluded first in patients who present
with neurologic findings in both feet.
Presentation and Physical
Examination
Identification of TTS can be chal-
lenging. Patient complaints may be
vague and difficult to localize. Never-
theless, pain and paresthesia are clas-
sically localized to the posteromedial
ankle and heel, often radiating distally
into the plantar foot. Symptoms are
often exacerbated by stance and
exercise. Dysesthesia can disrupt the
patient’ssleep.Severecompression
may cause weakness; this finding is
among the latest, presenting first
in the toe abductors and subsequently
in the short toe flexors.
60
Impaired
sensation along the tibial nerve dis-
tribution associated with a Tinel sign
along the tarsal canal is considered
to be the most pathognomonic find-
ing.
59
Other provocative maneuvers,
such as the dorsiflexion-eversion test,
which stretches the tibial nerve, may
also elicit reproducible discomfort in
this anatomic region.
Diagnosis
MRI is the modality of choice for eval-
uating the anatomy of the tarsal tunnel
and detecting space-occupying lesions
responsible for tibial nerve compression
(Figure 4). Nerve conduction velocity
(NCV) studies and EMG can be per-
formed to confirm the diagnosis;
however, an overview of four pro-
spective level III studies indicates that
false-negative rates are high with these
modalities.
61
Negative NCV findings
do not exclude the diagnosis. Sensi-
tivity of sensory NCV abnormalities
ranged from 90.5% to 96% (false-
negative rate [range], 4% to 9.5%),
and sensitivity of prolonged distal
motor latency ranged from 21.5% to
52.4% (false-negative rate [range],
47.6% to 78.5%).
The usefulness of NCV and EMG in
diagnosis and prediction of outcomes
in TTS remains questionable. These
techniques also vary greatly between
studies, and few high-quality reports
either correlate NCV and EMG with
Figure 3
Lateral foot radiograph
demonstrating a calcaneal stress
fracture (arrow). (Reproduced with
permission from Spitz DJ, Newberg
AH: Imaging of stress fractures in the
athlete. Radiol Clin North Am
2002;40[2]:313-331.)
Craig R. Lareau, MD, et al
June 2014, Vol 22, No 6 377
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the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
outcome or provide supportive evi-
dence for significant diagnostic util-
ity. In an evidence-based review of the
use of NCV and EMG in the diag-
nosis of TTS, sensory NCV was
determined more likely to be abnor-
mal than motor NCV; however, the
actual sensitivity and specificity of
these tests could not be determined.
61
Management
Nonsurgical options for TTS include
NSAIDs and immobilization. Pa-
tients with pes planus deformity may
benefit from custom orthoses.
58,59
Local corticosteroid injection into
the tarsal tunnel has been advocated
by some authors, but its use should
be carefully considered because of
the potential for tendon rupture and
intravascular injection.
59
Surgery is reserved for patients who
do not respond to nonsurgical treat-
ment and who have no other reason-
able explanation for their symptoms as
well as for those with identifiable space-
occupying lesions. Traditional tarsal
tunnel release involves careful division
of the flexor retinaculum overlying the
posterior tibial nerve as it courses
behind the medial malleolus as well as
release of the fascia over the abductor
hallucis. Complete release minimizes
the chance of persistent or recurrent
symptoms. To this end, anatomic and
clinical studies also suggest release of
the medial septum deep to the abductor
hallucis, under which the lateral and,
sometimes, the medial plantar nerves
pass.
54,62
In a recent series, all patients demon-
strated improvement in mean sensory
threshold as defined by monofilament
examination 12 months after surgical
decompression.
63
Surgical interven-
tion should be carefully considered,
however, because results can be
unpredictable. For example, surgical
decompression successfully relieves
symptoms in only approximately
50% of patients for whom a definite
etiology cannot be identified.
64
In one study, 56% of patients had
fair or poor results at long-term
follow-up.
65
In patients with diabe-
tes, decompression has been reported
to significantly improve one-point
pressure threshold as measured by
monofilament examination but not
two-point discrimination 8 to 9 months
postoperatively.
66
Another report sug-
gests that in patients with diabetes,
a positive Tinel sign has a 90% positive
predictive value of symptom relief
following extended decompression.
67
In patients with TTS resulting from
a space-occupying ganglion in the
tarsal tunnel, excision of the ganglion
results in satisfactory outcomes.
68
Summary
Pain of the plantar and medial heel is
a common complaint. A thorough
history and physical examination is
paramount to establish an accurate
diagnosis. In most patients, the diag-
nosis can be made clinically, taking
care to characterize the quality, loca-
tion, timing, and duration of pain. On
occasion, advanced imaging or neuro-
diagnostic studies may be necessary
Figure 4
Axial proton density-weighted magnetic resonance images without (A) and with (B) fat saturation, and sagittal short tau
inversion recovery (C) sequence image, demonstrating a tarsal tunnel ganglion (*) compressing the medial (red arrow) and
lateral (blue arrow) plantar nerves. (Courtesy of Peter T. Evangelista, MD, Providence, RI.)
Plantar and Medial Heel Pain: Diagnosis and Management
378 Journal of the American Academy of Orthopaedic Surgeons
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the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
when radiographs and clinical exami-
nation are inconclusive. Initial man-
agement is typically nonsurgical. For
the small percentage of patients whose
symptoms persist despite an adequate
course of nonsurgical management
surgical intervention can be considered.
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Plantar and Medial Heel Pain: Diagnosis and Management
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