0198-021 1/93/14030129$03.
00/0
FOOT B ANKLE
Copyright Q 1993 by the American Orthopaedic Foot and Ankle Society. Inc.
Heel Pain Syndrome: Electrodiagnostic Support for Nerve Entrapment
Lew C. Schon, M.D.,’ Terrence P. Glennon, M.D.,t and Donald E. Baxter, M.D.S
ABSTRACT
A local entrapment neuropathy has been proposed as one
of the etiologies of heel pain, but it has never been
documented by electrodiagnostic studies. Primary symp-
toms in patients suspected of having a neurologic basis
for their heel pain include neuritic medial heel pain and
radiation either proximally or distally. On physical exami-
nation, all patients in our series had reproduction of their
symptomatology with palpation over the proximal aspect
of the abductor hallucis and/or the origin of the plantar
fascia from the medial tubercle of the calcaneus. Twenty-
seven patients (20 women and seven men; average age
49) with these clinical characteristics were examined by
electromyography and motor/sensory/mixed nerve con-
duction studies. Bilateral heel signs and symptoms were
present in 11 patients. Ten of the patients had a significant
history of back pain with referral to the legs. In 23 of the
38 symptomatic heels, abnormalities were identified in the
lateral and/or the medial plantar nerves. The number of
abnormal values per heel ranged from one to four, with a
mean of 2.1. The most common finding was involvement
of the medial nerve (57%). Thirty percent of the heels had
isolated findings in the lateral plantar nerve and 13% had
abnormalities in both plantar nerves. Two patients had
electrophysiologic evidence of active S1 radiculopathy,
with ipsilateral evidence of plantar nerve entrapment sug-
gesting a “double crush” syndrome. The results of this
study support the presence of abnormalities of plantar
nerve function in a selected group of patients with neuritic
heel pain.
The heel pain syndrome is a well-known clinical entity
with numerous proposed etiologies, including heel spur
fracture, calcaneal stress fracture, plantar fasciitis, bur-
sitis, plantar fascia1 rupture, seronegative arthritis,
Clinical Instructor of Orthopaedics, University of Texas Medical
School in Houston, and Attending Orthopedic Surgeon, Foot and
Ankle Center, The Union Memorial Hospital, 201 E. University Park-
way, Baltimore, Maryland 21218. To whom requests for reprints
should be addressed.
t Department of Physical Medicine and Rehabilitation, Baylor Col-
lege of Medicine, Houston, Texas.
$Director of Foot and Ankle Fellowship, Clinical Professor of
Orthopaedic Surgery, Baylor College of Medicine.
129
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Baltimore, Maryland and Houston, Texas
thrombophlebitis, and intrinsic heel pad pathology.
Although first suggested by R ~ e g h o l in t ~ 1940,
~ the
possibility of a neurologic cause for heel pain
has recently been championed by several au-
thors,2-6.20.24.26.29.32.34.35.38.39
While some have implicated
the medial calcaneal nerve,’*8*’0-’2 most speculate that
the first branch of the lateral plantar nerve is responsi-
ble. Other neurologic causes of heel pain have been
recognized, including sacral radiculopathy and tarsal
tunnel syndrome, but in these entities, the heel pain is
referred from the more proximal site and local heel
tenderness is typically l a ~ k i n g . ~ . ~Neuritic . ’ ~ ~ ’ ~ ~ ~ ~
heel pain may also occur when a primary condition (i.e.,
plantar fasciitis) leads to local swelling and inflammation
with secondary neuronal involvement. Thus, two local
processes (i.e., plantar fasciitis and nerve entrapment)
may be responsible for the symptomatology. In addi-
tion, we have noted a concurrence of two neuronal
processes, such as a radiculopathy and a distal nerve
compression, as a cause for the heel pain syndrome.
This situation, called the “double crush” phenomenon,
has been well described in the upper extremity, but in
the lower extremity it has received little atten-
tion 9.21.25,28.30.31.40-42 In order to substantiate both a
local neurologic process and, in some cases, the pres-
ence of a double crush syndrome, we have studied a
group of patients with painful heels using electrodi-
agnostic procedures.
MATERIALS AND METHODS
In a foot and ankle subspecialty practice that has an
established reputation for the evaluation of heel pain,
over 200 patients per year are referred with this chief
complaint. During a 1-year period, 33 patients (25 fe-
males and eight males) from 29 to 74 years old (mean
age 48 years) were suspected of having a neurologic
etiology to their heel pain. Fourteen patients had bilat-
eral heel pain (28 heels) and 19 were affected unilater-
ally (total 47 heels). These patients had complaints of
burning, shooting, radiating, and shock-like or electric-
type pain in their affected heel of 1 month to 15 years
duration (average 3 years). In two thirds of the patients,
130 SCHON ET AL.
the pain radiated up the leg or across the heel from the
medial to the lateral side. Typically, the pain was worse
with activity and better with rest. One fourth of the
patients experienced severe pain in the morning after
rising from their beds. Pain during the night was rare.
Two patients had a history consistent with a com-
plete or partial rupture of the plantar fascia. None of
the patients had a previous fracture or dislocation in
the ankle or hindfoot. Three patients had previous
surgery to release the plantar fascia and resect a heel
spur. One had a previous tarsal tunnel release. Six of
the patients were runners and one was a clogger (a
form of tap dancing). Three patients were on supple-
mentation for hypothyroidism but were well controlled.
One patient had a history of seronegative arthritis. Two
patients had a past history of borderline diabetes but
did not require any medications. In the other patients,
there was no history of systemic disease, thrombophle-
bitis, nutritional deficiencies, moderate or heavy alcohol
consumption, or exposure to neurotoxic medications.
Seventeen of the patients had a history of back pain.
Ten of these patients recounted past episodes of re-
ferred pain down their legs. Most of these patients had
previous documentation of nerve root compromise by
either magnetic resonance imaging, CT scan, myelo-
gram, or electrodiagnostic studies. Four of the 17 pa-
tients with back pain had undergone laminectomies
several years prior to the study.
Every patient had exquisite palpable tenderness at
the posterior medial aspect of the heel at the junction
of the medial and plantar skin 4 to 5 cm anterior to the
posterior aspect of the heel. Palpation at this point,
which is just distal to the medial tubercle of the calca-
neus, reproduced the neuritic symptomatology. A third
of the patients had tenderness extending in a proximal
direction from the point of maximal heel tenderness
toward the junction of the medial and lateral plantar
nerves. Tenderness was noted proximal to the axis
established from the tip of the medial malleolus to the
posterior inferior aspect of the heel along the tibial
nerve in four of the patients. Two of these four patients
and one other patient had decreased sensation. All but
three of the patients had intact sensation along the
medial and lateral aspects of the sole of the foot. Seven
had tenderness along the medial plantar nerve as it
passed underneath the abductor hallucis.
All electrodiagnostic studies were performed by the
same electromyographer (T.P.G.) and equipment (No-
mad, Tracor Northern, Middleton, WI). Distal motor
latencies represent the time required for the impulse to
travel along the nerve from the depolarizing electrode
to the recording electrode, which is placed over the
motor point of an appropriate muscle. Prolonged distal
latencies due to delays in nerve conduction may result
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Foot & Ankle/Vol. 14, No. 3/MarchlAprill993
from nerve entrapment which is present between the
stimulating and recording electrodes. Distal motor la-
tencies were obtained according to established proto-
cols for the medial plantar nerve,15 and represent de-
polarization of the tibial nerve at the medial malleolus
with the recording electrode over the abductor hallucis.
Study of the lateral plantar nerve was performed by
recording over the abductor digiti quinti pedis."
Sensory nerve conduction studies have been shown
to be more sensitive for the diagnosis of certain entrap-
ment syndromes, such as carpal tunnel syndrome.
While study of purely sensory branches of the plantar
nerves is difficult, a technique for eliciting compound or
mixed nerve responses (segments of the nerve contain-
ing both sensory and motor fibers) was used in this
study.37 These responses are believed to represent
predominantly the function of the sensory fibers, and
are attained by stimulation of the medial and lateral
plantar nerves at the sole of the foot while recording
over the tibial nerve near the medial malleolus.
In the presence of axonal damage, abnormal findings
upon insertion of an electromyography (EMG) needle
into the denervated muscle may be present. An EMG
using a monopolar needle was performed on all sub-
jects bilaterally, with a minimal examination that in-
cluded a screen of all root levels in the back and limbs,
plus the abductor hallucis and abductor digiti quinti
pedis.
Any patients with abnormal sural sensory or peroneal
motor responses were excluded from the study in order
to eliminate patients with possible peripheral neuropa-
thy. "Abnormal" values in this study were those that
did not fall within two standard deviations of the mean
according to the respective references, which also cor-
related with our laboratory normals. Temperatures
were carefully monitored and recorded on all limbs and
were within the limits stated in the protocols.
Of the 33 patients referred for electrodiagnosticeval-
uation, peripheral neuropathy could not be ruled out in
six, and these were excluded from statistical analysis,
leaving a study population of 27 patients with 38 symp-
tomatic heels.
RESULTS
In 23 of the 38 heels, at least one abnormal value
pertaining to the medial and/or lateral plantar nerves
was found in the affected foot. The number of abnormal
values in these 23 affected heels ranged from one to
four with a mean of 2.1. Six patients each had one
borderline abnormal value in an unaffected foot and
three patients had one or two abnormal values on the
uninvolved side. In unaffected heels, the abnormality
was usually a borderline low motor amplitude. The most
Foot & Ankle/Vol. 14, No. 3lMarchlApril 1993
common abnormal findings in painful heels were pro-
longed motor latencies and decreased motor nerve
amplitudes. Twelve heels (26%) had EMG findings in
the abductor digiti quinti and/or abductor hallucis (fi-
brillations, positive sharp waves, or complex repetitive
discharges). The next most common findings were low
mixed nerve response amplitudes and prolonged mixed
response latencies, in those feet with obtainable re-
sponses.
In the 23 heels with abnormal findings, both the lateral
plantar nerve and medial plantar nerve were involved in
three heels (13%). In seven heels, findings were isolated
to the lateral plantar nerve (30°/o), and in 13 heels,
findings were isolated to the medial plantar nerve (57%)
(Table 1). In 16 patients with unilateral symptoms,
motor conduction abnormalities were located ipsilat-
erally in eight, bilaterally in two, and contralaterally only
in one. Thus, the electrophysiologic studies correlated
well with side of involvement.
Since this was a pilot study and no control group
was used, a subgroup of 16 patients with strictly uni-
lateral symptoms and comparable electrodiagnostic re-
sults was evaluated using the asymptomatic extremity
as a control. Paired sample t-tests were performed,
revealing significantly prolonged medial plantar distal
motor latencies (P < .06), when comparing the affected
feet (mean = 5.2 msec) to the unaffected feet (4.7
msec). In addition, the lateral plantar motor latencies of
the affected feet (mean = 6.5 msec) were significantly
prolonged compared with the unaffected feet (6.1
msec, P < .05). The amplitudes of the lateral plantar
motor responses were also significantly reduced in the
affected feet (mean = 5.1 mV) in comparison to the
unaffected feet (5.8 mV, P < .06).
In a separate group of subjects in whom mixed nerve
responses were obtainable, comparison of the latencies
and amplitudes of more versus less symptomatic feet
revealed no significant differences.
DISCUSSION
The findings of the study support the hypothesis of
a neurologic basis for local heel pain syndrome. No
known published studies have demonstrated abnormal
TABLE 1
Summary of Test Results: Local Entrapment Neuropathy'
Patients 27
Affected heels 38
MPN and LPN findings 3
MPN findings 13
LPN findings 7 croscopy and reported findings consistent with a
Total with abnormal EDS (61%) 23
"MPN, medial plantar nerve; LPN, lateral plantar nerve; EDS,
electrodiagnostic studies.
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HEEL PAIN SYNDROME 131
electrodiagnostic tests in patients with this condition.
The concept that heel pain may be a presenting mani-
festation of a tarsal tunnel syndrome has been pre-
Sented,7,14,18.19 In these reports, patients had associ-
ated tenderness along the tibial nerve and often a
positive Tinel's sign, but no localized tenderness at the
proximal medial aspect of the heel. Studies have also
documented the presence of heel pain in association
with a L5, S1, or S2 r a d i ~ u l o p a t h y .Again,
~ ~ , ~ ~in these
cases, none of the patients had localized tenderness
over the tibial nerve or over the proximal medial aspect
of the heel.
Authors have speculated that the medial calcaneal
nerve is responsible for heel pain syndrome. Byank and
co-workers7 noted that the calcaneal nerve may be
symptomatic although medial and lateral plantar nerve
electrodiagnostic tests are normal. Unfortunately, there
is no way to substantiate electrodiagnostically an iso-
lated calcaneal nerve lesion. Clinically, in these cases,
the calcaneal nerve should be tender at the suspected
entrapment sites and along its course from the medial
malleolus to the tip of the heel. In the literature describ-
ing the anatomy of the tarsal tunnel change, a calcaneal
nerve branch has not been found to penetrate any
fascia1 structures as distal to the superior edge of the
abductor hallucis, the point of maximal tenderness in
the typical heel pain patient. Studies suggested that
calcaneal neuromas are responsible for the painful heel
syndrome.' ,8,10-12.17 Davidson and Copoloffl1reviewed
200 cases of patients who underwent surgical excision
of a "neuroma" in this vicinity. These findings have not
been confirmed by any other reports in the orthopaedic
literature. In D.E.B.'s 16-year experience of over 200
heels treated surgically for plantar fasciitis with or with-
out first branch entrapment, only in the cases where
previous surgery had been performed was a calcaneal
neuroma identified. Thus, in only five of the 200 cases
could the painful heel be attributed to calcaneal neu-
roma.
It is the author's contention that, in most cases, the
nerve responsible for heel pain is the first branch of the
lateral plantar nerve (i.e., nerve to the abductor digiti
minimi pedis). The anatomy of this nerve, its location in
relation to the point of maximal tenderness, and its
response to surgical decompression have been re-
corded in the l i t e r a t ~ r e .Despite ~ - ~ this ~ ~recent
~ ~ ~ ~ ~ ~ ~
attention to this nerve, no previous study has demon-
strated electrodiagnostic abnormalities. One paper by
Baxter and Pfeffe? evaluated two resected first
branches of the lateral plantar nerve by electron mi-
compression neuropathy. The results of the current
study support this hypothesis by demonstrating that
44% of the heels with electrophysiologic abnormalities
132 SCHON ET AL.
have involvement of the lateral plantar nerve with or
without the medial plantar nerve.
Common clinical features in patients with positive
electrodiagnostic studies can be identified. Most pa-
tients are middle-aged women with bilateral heel pain,
although unilateral symptoms may exist. These patients
complain of neuritic symptoms emanating proximally
and/or distally from their heel. A history of a long
duration of symptoms (average 3 years) is common.
Typically, there is a slow and incomplete response to
conservative modalities during these years. One third
of the patients will have a history of back pain referred
to the lower limbs. Local tenderness over the proximal
medial edge of the plantar fascia is characteristic. How-
ever, a true Tinel’s sign in this location is usually not
demonstrated. Tibia1 nerve tenderness proximal to the
medial malleolus calcaneal axis is often absent.
Regarding the role of electrodiagnostic tests in di-
agnosing a neurologic lesion, it must be emphasized
that they are an adjunct and not a substitute for clinical
evaluation. It is generally accepted that low grade le-
sions may not manifest with abnormal data. Also, some
nerves are more readily tested than others. Thus, le-
sions may be missed if one relies on electrodiagnosis.
These tests are not specific as to location. The lesion
may occur anywhere between stimulation point and the
recording electrode.
Motor conduction studies were the most helpful di-
agnostic tests in our series, in part because the mixed
nerve responses were completely unobtainable in so
many patients. This is probably related to the patient’s
age and to technical limitations of the study, and not to
a particular nerve pathology. Unlike carpal tunnel syn-
drome, in which sensory conduction studies are quite
helpful, the utility of mixed nerve studies in plantar
neuropathy may be restricted to younger patients.
The explanation of electrodiagnostic findings involv-
ing the medial plantar nerve can be theorized in several
ways. First, in understanding the method of testing for
abnormalities of the medial plantar nerve by motor
conduction studies, recall that the tibial nerve is stimu-
lated proximal to the tip of the medial malleolus and the
signal is picked up over the belly of the abductor hallucis
muscle. Thus, the assumption is made that the medial
plantar nerve always innervates this muscle. Although
this is certainly true according to all anatomy texts, one
of the authors (L.C.S.) has identified a branch of the
tibial nerve which begins just proximal to the branching
of the lateral and medial plantar nerve (Figs. 1 and 2).
This nerve runs posterior to these nerves and travels
lateral to the deep fascia of the abductor hallucis mus-
cle. One centimeter from the superior edge of the
abductor hallucis and 1 cm distal to its origin on the
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Foot & AnkleIVol. 14, No. 3/MarchlAprill993
calcaneus, the nerve pierces the deep fascia and
ramifies within the abductor hallucis muscle. This vari-
ation was only demonstrated in one of five cadavers
and may represent a unique abnormality. If one were
to speculate that in some patients with prolonged distal
latency, when recording from the abductor hallucis that
a variation as described has occurred, the presence of
proximal medial heel pain in association with absent
tenderness over the course of the medial plantar nerve
could be understood. This would also explain why a
clinical improvement is reported in our patients with
“medial plantar nerve lesion’’ who undergo release in
the area of maximal tenderness on the posteromedial
aspect of the heel. Typically, the deep fascia of the
abductor is transected and partial resection of the
plantar fascia (along the course of either the first branch
of the lateral plantar nerve or the lateral plantar nerve)
without releasing the medial plantar nerve is performed.
One such patient, who had a positive nerve study for
medial plantar nerve, had virtually immediate relief of
her heel pain with release of the first branch of the
lateral plantar nerve but without the medial plantar
nerve release.
Other theories to explain medial plantar nerve find-
ings include trauma to the abductor hallucis by chronic
repetitive microinjury from impact with the ground, local
injection, shoe wear, and agir~g.’~.’~ It is also possible
that the findings in this nerve reflect a compression by
the tight deep fascia of the abductor hallucis, with
symptoms present only in the first branch of the lateral
plantar nerve. Since the first branch of the lateral plantar
nerve is a mixed nerve, it is possible that the sensory
fibers are compressed but the motor fibers are suffi-
ciently spared, so that electrodiagnostic tests are un-
remarkable. It is also possible that the medial plantar
nerve findings reflect a more proximal and possibly
subclinical compression in the tarsal tunnel that predis-
poses the nerve to a more distal symptomatic compres-
sion in the first branch of the lateral plantar nerve (a
local double crush syndrome). A final explanation for
the abnormal medial plantar nerve findings may be that
the nerve compression is clinically present but that the
heel pain is referred. This, however, does not explain
why a release over the first branch of the lateral plantar
nerve would alleviate the symptoms.
The existence of a double crush phenomenon has
been described in the upper extremities where carpal
tunnel syndrome has been associated with cervical
radiculopathy, cervical spondylosis, or thoracic outlet
syndrome. Although the existence of this lesion in the
lower extremity has been suggested by other au-
t h o r ~ electrodiagnostic
, ~ ~ ~ ~ ~ studies documenting its
presence have not been published. The patients with
Foot & Ankle/Vol. 14, No. 3/March/April 1993
Fig. 1. Normal landmarks of medial heel. MM, medial malleolus; TT, tarsal tunnel; AH. abductor hallucis; PF, plantar fascia; CT, calcaneal
tuberosity.
double crush in this report will have further evaluation
after heel fascia1 decompression to establish whether
isolated decompression of the distal lesion without
addressing the proximal lesion is sufficient to decrease
the patient's symptomatology. Additional studies to
elucidate the nature of neurologic heel pain are currently
under way.
Electrodiagnostic studies of patients with neuritic
heel pain should include medial and lateral plantar motor
studies, with comparison to the unaffected limb. A
mixed nerve study of these branches may also be
attempted, with prolonged latencies or unilaterally
unobtainable responses arousing suspicion. Bilaterally
absent responses, particularly of the lateral' plantar
branch, are not diagnostic. Peripheral neuropathy
should be ruled out before reaching a conclusion re-
garding plantar nerve entrapment. Maintaining appro-
priate temperature of the limb is vital to obtaining
accurate data. Also, an EMG of the intrinsic foot mus-
cles should be performed. Abnormalities of these mus-
cles should prompt a study of S1 innervated muscles
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HEEL PAIN SYNDROME 133
proximal to the ankle to rule out a concurrent radiculop-
athy.
CONCLUSION
The presence of a large number of electrodiagnostic
abnormalities in this study population helps to substan-
tiate the presence of compression neuropathy of the
medial or lateral plantar nerve in patients with neuritic
heel pain. The significant differences between sympto-
matic and asymptomatic feet detected by medial and
lateral plantar motor studies also support the presence
of focal neurologic abnormality corresponding to the
site of symptoms in this population. While the sensitivity
of electrodiagnostic evaluation of individual patients
with suspected plantar nerve entrapment remains un-
certain, complete electrodiagnostic evaluation may im-
prove the clinical assessment and provide objective
evidence of neurologic abnormalities. Once identified,
treatment directed at relieving the cause of entrapment
may improve the prognosis of this disorder.
134 SCHON ET AL.
Fig. 2. The branches of the tibial nerve with a variant branch of the tibial nerve innervating the abductor hallucis (same orientation as Fig. 1).
MPN, medial plantar nerve; LPN, lateral plantar nerve; FB, first branch of LPN; VB. variant branch innervating abductor hallucis; CN, calcaneal
nerve.
ACKNOWLEDGMENTS
The authors would like to recognize the assistance
of David Shotte, Ph.D., Erika Pardes Schon, Chris
Robinson, and Jo Ann Verzier in the preparation Of the
manuscript.
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