PERIPHERAL NERVE LESIONS OF THE FOOT AND ANKLE

The term neuroma is actually
a misnomer. Most recent literature supports the theory that the
condition we call interdigital neuroma is an entrapment neuropathy of
the common digital nerve beneath the transverse metatarsal ligament (26,38,39,44).
These studies demonstrate that almost all the histologic changes in the
nerve occur distal to the transverse metatarsal ligament, and that the
nerve proximal to the ligament appears normal. The histologic changes
are characterized by perineural fibrosis, degeneration of the nerve
fibers, deposition of an amorphous eosinophilic material, and a
decrease in both the number and

the diameter of thick myelinated fibers (Fig. 114.1).
Although these studies seem to support the theory that the main cause
of an interdigital neuroma is an entrapment neuropathy, there are
anatomic factors that need to be considered.

Early reports regarding this painful entity, often referred to as Morton’s syndrome, focused on the third interspace (9,46,48).
Subsequent studies of the anatomy of the plantar nerves and their
branches have demonstrated a communicating branch between the medial
and lateral plantar nerves (9,32) (Fig. 114.2).
This branch was noted to course from the common digital nerve in the
fourth interspace to the third digital branch of the medial plantar
nerve in the third interspace. Jones and Klenerman (32)
found this communicating branch to be present in all 20 of the cadaver
specimens dissected. In two of the female specimens, they found the
communicating branch was enlarged, and they hypothesized that this
enlargement may be a factor for the frequent involvement of the nerve
to the third interspace. Mann and Reynolds (44)
reported an equal distribution of interdigital neuromas in the second
and third interspaces. They believed their data supported the theory
that neuromas are caused by repetitive local trauma related to footwear
(e.g., tight shoes, high heels, and thin soles) and shed doubt on the
role of the communicating branch as the main cause of interdigital
neuroma formation. Levitsky et al. (39) found
the communicating branch was present in only 19 (26.8%) of 71 specimens
dissected, and the incidence of third-interspace neuromas was no
greater in those feet with the communicating branch as those without
it. The information also questions the role of the communicating branch
in the etiology of interdigital neuromas. Both Mann and Levitsky failed
to identify a neuroma in the first and fourth interspaces.

Aside from finding a low incidence of the communicating

branch in their study, Levitsky et al. (39)
also measured the distance between the metatarsal heads and the
diameter of the common digital nerve to each interspace. They found the
intermetatarsal head distances in the second and third interspaces were
significantly smaller than in the first and fourth. They then
calculated a mean ratio of the intermetatarsal head distance to the
diameter of the common digital nerve and found that ratio was
significantly lower in the second and third interspaces compared to the
first and fourth interspaces. They believed their data lent support to
the theories that explain the formation of a neuroma in both the second
and third interspaces on a mechanical basis.

The incidence of interdigital neuromas is 8–10 times
more common in women than men. It is well known that with
hyperextension of the metatarsophalangeal joints, along with the action
of the plantar aponeurosis, the metatarsal heads are depressed. This
exposes the interdigital nerve to increased pressure. In a woman’s
fashionable high heel shoe, the metatarsophalangeal joints are
constantly hyperextended. This can cause the interdigital nerve to be
tethered across the transverse metatarsal ligament, leading to an
entrapment neuropathy. It is therefore realistic to consider a
“neuroma” as an entrapment neuropathy caused by a combination of
anatomic factors, such as a decreased ratio of the diameter of the
intermetatarsal head to that of the digital nerve, combined with
extrinsic factors, such as fashionable shoes and activity level.

The principles of treatment for interdigital neuroma are threefold:

A review of the literature about interdigital neuromas over a span of 120 years follows (13).

The key to a successful outcome from treatment of an
interdigital neuroma is first making the correct diagnosis. The
examiner needs to determine not only if the patient’s symptoms are
consistent with the diagnosis of a neuroma, but also at which
interspace the neuroma is located. This can be very challenging. The
diagnosis is made on the basis of a patient’s symptoms and the physical
examination. Certainly there are patients that present with classic
symptoms and physical findings. Although magnetic resonance imaging
(MRI) and ultrasound have been reported to be sensitive in diagnosing
interdigital neuromas, they have not gained wide acceptance and should
not take the place of a directed history and physical examination.

Once the diagnosis is made, treat nonoperatively initially in all patients. Bennett et al. (7)
developed a three-stage treatment protocol, the first two stages of
which were nonoperative. The first stage included patient education
about the condition. Footwear modifications were made to include a
wider shoe, and a metatarsal pad was applied proximal to the involved
interspace. A letter was sent to the patient to reinforce the program.
If little or no improvement was seen within 3 months, the patient
returned, and 2 ml of 1% Xylocaine and 1 ml of Aristocort
(triamcinolone, 40 mg/ml) was injected into the interspace (stage 2).
Immediate short-term pain relief was seen in all patients. They were
encouraged to continue with the shoewear modifications. If satisfactory
relief of the patient’s symptoms was not seen 3 months later, surgical
excision was carried out (stage 3). The authors’ results are summarized
in Table 114.3. They conclude that although
the nonsurgical treatment was not successful in all patients, the
protocol helped select those patients who might benefit most from
surgery. They also felt that the injection was diagnostically helpful
and that a positive response to the injection is a prerequisite to
recommending surgical treatment.

The treatment used by Mann and Reynolds (44)
was similar to stage 1 of the preceding protocol. These authors found
that although the patients responded well to nonoperative management,
70% to 80% were sufficiently symptomatic and dissatisfied with the
change in shoewear that they opted for surgery. Anti-inflammatory
medications or injections, with or without a steroid, did not provide
long-term relief and was not part of their routine management.
Rasmussen et al. (55) reported on 51 feet that
received a single corticosteriod injection for treatment of third
interspace neuromas. They concluded that injections generally did not
provide a cure for interdigital neuromas, but they did provide
temporary relief and did not preclude a good

surgical outcome. After 4 years, only 11% of the feet had lasting improvement. The authors felt, as did Bennett et al. (7), that injection can be useful in confirming the diagnosis and as a predictor of operative success.

Local steroid injection into superficial areas with
little subcutaneous tissue, such as the interspace in the foot, can
cause subcutaneous atrophy, altered cutaneous pigmentation, alopecia,
and telangectasia (56). The effects are more
pronounced with the use of relatively insoluble preparations, such as
triamcinolone. The more soluble preparations should be used in low
volume if a corticosteroid is to be injected into the foot for
treatment of an interdigital neuroma.

If the surgeon feels confident that patient’s symptoms
are from an interdigital neuroma, and the patient has failed
nonsurgical management, surgery is indicated. There are essentially
three options for surgical treatment: (a) dorsal approach, (b) plantar
approach, or (c) dividing the transverse metatarsal ligament and
leaving the nerve intact.

The postoperative management for all surgical techniques
is similar. Send the patient home the same day in a postoperative shoe.
Instruct the patient to elevate the foot as much as possible to
decrease swelling. Allow weight bearing, but the dressing should be
reapplied and kept in place for up to 3 weeks after surgery. The
patient may ambulate in the postoperative shoe during this time. After
3–4 weeks, the swelling and tenderness should subside enough for him to
begin ambulating in a wide, sensible shoe. Start passive and active
range-of-motion exercises of the foot and ankle at that time. The
patient can then slowly increase activities as tolerated, but he may
experience swelling and soreness for some months with vigorous
activities.

There are many pitfalls awaiting the physician in the
diagnosis and treatment of an interdigital neuroma. Making the correct
diagnosis of a neuroma and its location can be challenging. Suggestions
to avoid pitfalls in diagnosis have been given.

Be aware of the possibility of the presence of the
second neuroma in the same foot. This condition is rare, but it could
be the reason for unsatisfactory surgical outcomes. In addition, an
incorrect diagnosis about the interspace in which the neuroma is
located will lead to a poor surgical outcome. These two pitfalls have
some overlap, which is difficult to sort through at times.

Too many injections of corticosteroids into one
interspace can lead to atrophy of the fat pad and pigment changes of
the skin. I recommend only one injection, if any, at this time, based
on the previously presented data.

There have been few reported wound problems with the
dorsal approach. If done incorrectly, or if the patient forms a keloid,
it can lead to a painful incision that can be very difficult to cure.
Dissection outside the line of the incision or overvigorous activities
can lead to injury to the small dorsal cutaneous nerves, resulting in
uncomfortable paresthesias or dysesthesias in the toes.

If surgery is carried out for excision of simultaneous
neuromas in adjacent web spaces, the patient will experience dense
sensory loss under the third toe that can be

uncomfortable. Devascularization of the third toe due to injury to the digital arteries has been reported as well (Fig. 114.8).

Certainly not every patient with persistent pain following neuroma excision has a “recurrent” neuroma. Beskin and Baxter (8)
noted that two thirds of the 39 patients they treated for recurrent
neuroma had symptoms within 12 months of the original procedure. The
other one third noted symptoms 1–4 years later. Mann and Baxter (42)
hypothesized that the group with recurrent symptoms within 12 months
probably had surgery for the wrong diagnosis, and that the other third
had the interdigital nerve transected too far distal, and the neuroma
stump from the excision ended up between the metatarsal heads and took
1–4 years to become painful. In their own experience of 11 recurrent
neuromas, Mann and Reynolds (44) noted the
neuroma stump to be adherent to the plantar aspect of the metatarsal
head in all cases. They reported that 81% of these patients were
asymptomatic after surgery through a dorsal approach. The diagnosis,
nonoperative management, and surgical approach are almost identical to
those for the primary neuroma. At the time of surgery, you may need to
extend the incision a little more proximally to get down to virgin
tissue and nerve, then follow it distally into the neuroma stump. Also,
postoperatively, patients should be allowed a little longer healing
time before returning to vigorous activities.

The anatomy of the tarsal tunnel must be understood to
understand tarsal tunnel syndrome. The tarsal tunnel is a fibro-osseous
canal bounded by the tibia and medial malleolus anteriorly, the talus
laterally, and the flexor retinaculum medially. The medial surface of
the talus with the sustenaculum tali and the medial surface of the os
calcis form the osseous floor. The tunnel is completed by the laciniate
ligament (flexor retinaculum). The contents of the canal are, from
medial to lateral, the tibialis posterior tendon and its sheath, the
flexor digitorum longus tendon and its sheath, the posterior tibial
neurovascular bundle, and the flexor hallucis longus muscle–tendon unit
(Fig. 114.9).

The flexor retinaculum is triangular, with a proximal
malleolar apex and an inferior base along the superior border of the
abductor hallucis muscle. The anterior and posterior borders are
difficult to define because they blend with the dorsal and superficial
aponeuroses of the foot and leg, respectively. The tibial nerve divides
into the medial and lateral plantar nerves and gives off its calcaneal
branch within the tarsal tunnel in most cases. There is, however, great
variation in this branching pattern (Fig. 114.10).

Tarsal tunnel syndrome is the result of compression of
the posterior tibial nerve within the tarsal canal, or of one of its
terminal branches distal to the canal. Along its course, the nerve is
susceptible to compression from numerous sources, both intrinsic and
extrinsic. In about 60% of the patients with a tarsal tunnel syndrome,
a specific cause can be identified (41). Table 114.4 lists the differential diagnosis of tarsal tunnel syndrome (16).

The most common presenting complaint for tarsal tunnel
syndrome is “burning” dysesthesias or paresthesias on the plantar
aspect of the foot. The symptoms are aggravated by prolonged standing
or activity and partially relieved at rest. Many patients describe
worsening of their symptoms while in bed at night, making it difficult
to fall asleep. Some patients describe the Valleix phenomenon, which is
proximal radiation of the pain along the medial aspect of the leg to
the midcalf (16). Often the symptoms are
diffuse and vague and not very well localized. Take a carefully
directed history to identify any of the alternative diagnoses listed in
Table 114.4. Look for a history of previous
trauma such as an ankle sprain or fractures about the ankle or
hindfoot. It is very important to elicit a history of diabetes or
peripheral vascular disease, which can cause a peripheral neuropathy
and mimic some of the symptoms of a tarsal tunnel syndrome.

First, examine the foot in the weight-bearing position,
looking for any deformity such as varus or valgus of the hindfoot.
Perform gross examination for swelling, color,

and
temperature. Carry out a detailed neurovascular exam. Check pulses,
warmth, and capillary refill. Gross sensory examination is usually not
very localizing or helpful. Patients may note some subjective decrease
in sensation on the plantar aspect of the foot, but it is difficult to
quantify. Bailie and Kelikian (2)
reported a significant increase in two-point discrimination (2-PD) of 7
mm in affected feet compared to normal controls. Postoperatively, they
noted an improvement of 4 mm in 2-PD. They suggest using the patient’s
uninvolved foot as the control in unilateral disease because of the
wide range of normal values (8–15 mm). Check the range of motion of the
ankle, subtalar, and transverse tarsal joints for possible
arthrofibrosis from an old injury, or the presence of a tarsal
coalition.

Then palpate the entire course of the posterior tibial
nerve, starting proximal to the tarsal tunnel and proceeding distally
along the medial and lateral plantar nerves. In a patient with a tarsal
tunnel syndrome, one can often demonstrate radiation of neuritic
symptoms into the plantar aspect of the foot in the distribution of the
medial or lateral plantar nerves or both (Tinel’s sign). Carefully
palpate the tarsal tunnel to identify the presence of any
space-occupying lesion such as a ganglion cyst or tumor. Motor function
of the intrinsic and extrinsic muscles of the foot rarely reveals
weakness. Look for any subtle atrophy of the abductor hallucis or
abductor digiti quinti muscles as compared to the opposite foot.

Nonsurgical treatment depends heavily on the diagnosis
and identification of a cause. Nonsteroidal anti-inflammatory medicines
or an injection of a corticosteroid preparation can be tried if
tenosynovitis is suspected. If a flexible foot deformity is found, an
orthotic device can be helpful. If a lesion is found either on
examination or on MRI, surgical decompression is indicated. If a
patient’s symptoms persist after nonsurgical treatment, and you
strongly suspect compression or constriction of the posterior tibial
nerve within the tarsal tunnel, surgery is also indicated.

There is no controversy about the surgical technique for
decompression of the posterior tibial nerve within the tarsal tunnel.
Identify and decompress the distal branches (i.e., the medial and
lateral plantar nerves) at the same time.

Do not allow weight bearing for 3 weeks, then apply a
removable walking cast for an additional 3 weeks. During that time, the
patient may remove the cast and start early range-of-motion exercises.
Physical therapy is rarely indicated. Patients may increase activities
as tolerated after 6 weeks.

Overall, superior results are seen when an obvious
lesion is identified and treated. If no specific etiology can be
identified, approximately 75% of patients obtain relief but 25% obtain
little or no relief (42). It is rare for a patient to be more symptomatic following uncomplicated tarsal tunnel release. In 1990, Cimino (11) reviewed 24 articles and compiled the overall treatment results from these reports. Those data are summarized in Table 114.5.

Since Cimino’s review, Bailie and Kelikian (2)
reported 72% patient satisfaction following surgery. They also noted an
overall less-satisfied patient group in the presence of a worker’s
compensation claim. Pfeiffer and Cracchiolo (51) reported only 44% patient satisfaction after surgery and cautioned against surgery unless an obvious lesion is identified.

Most of the pitfalls associated with tarsal tunnel
syndrome are related to misdiagnosis. Tarsal tunnel syndrome is a rare
entity. It implies compression of the posterior tibial nerve or its
branches within the tarsal tunnel. Pain or neuritis along the course of
the posterior tibial nerve is not a tarsal tunnel syndrome. Peripheral
neuropathy, often in conjunction with diabetes, can mimic tarsal tunnel
syndrome, but surgical decompression will rarely be of benefit.
Additional nerve lesions in the same lower extremity can affect the
treatment outcome of tarsal tunnel syndrome. These additional lesions,
which can occur anywhere along the course of the sciatic, common
peroneal, posterior tibial, or plantar nerves, can be detected with
electrodiagnostic tests as well as with a thorough history and physical
examination (58). As noted, the best results
occur when a specific mass or lesion is identified, either clinically
or on an MRI scan. When a lesion is not identified,

surgical
decompression can still be of benefit, but the patient needs to
understand that satisfactory outcomes occur only 75% of the time on
average, or even less.

Electrodiagnostic studies and the criteria for
diagnosing tarsal tunnel syndrome are ever changing. Patients are often
referred with an electromyogram and/or nerve conduction velocity study
with an interpretation by the examiner of a tarsal tunnel syndrome. The
diagnosis is not made on electrodiagnostic studies alone. These studies
serve only to support the clinical impression.

Surgical complications have been infrequently reported
in the literature. A single case report of posterior tibial tendon
dislocation following decompression has been published (37).
One series reported an overall 13% complication rate, consisting of a
hematoma, suture abscesses, superficial wound infections, and
hypertrophic sensitive scars (2).

Recurrent symptoms can occur after initial relief. They
are believed to be secondary to adhesions or fibrosis around the nerve,
rather than the formation of another lesion. An MRI may be quite useful
to identify a possible surgical lesion. Revision surgery for tarsal
tunnel syndrome is rarely beneficial and should be avoided if possible.
This is especially true for the patient who did not obtain any relief
from the first surgical decompression.

The sural nerve is most often formed by the medial sural
nerve, a branch of the tibial nerve. It may receive branches from the
lateral sural nerve or the common peroneal nerve (Fig. 114.11).
The sural nerve is accompanied by the short saphenous vein as they
course lateral to the Achilles tendon. It passes 1.0–1.5 cm distal to
the tip of the lateral malleolus. Readers interested in a detailed
description of the anatomy and the many variations of the sural nerve
are referred to Sarrafian’s textbook (59).

The sural nerve is well protected throughout its course,
being surrounded by subcutaneous tissue, and is not subjected to sharp
fascial edges or tight constricting bands. Coert and Dellon (12)
identified a potential site of entrapment of the lateral sural nerve as
it pierces through the deep vein fascia near the knee. As the knee is
extended, the fascia can exert a compressive force on the nerve. Most
sural neuropathies, however, are either related to trauma (e.g.,
lacerations, fractures, ankle sprains) or external pressure (e.g.,
ganglia, Baker’s cyst). There are few reports in the literature
regarding this entity. In 1974, Pringle et al. (53)
reported four cases of sural nerve entrapment. Their report found a
fracture at the base of the fifth metatarsal, a recurrent ankle sprain,
and ganglion cysts to be underlying causes. Also, external compression
of the nerve at different levels has been reported (57).

The most reliable feature in making the diagnosis of
sural nerve entrapment is a history of neurogenic pain in the
distribution of the sural nerve. Often the symptoms occur only with
athletic activities. Physical findings are often absent, so the history
becomes paramount in making the diagnosis. On occasion one can palpate
a mass or cyst, or identify an associated fracture, but more often the
history is all there is to go on. Electrodiagnostic testing can be
performed to help localize an area of compression if the physical
examination is not helpful. Sensory nerve action potentials are reduced
in the affected extremity and normal in the contralateral limb. If a
mass is suspected, an MRI scan is useful to identify the extent and
location of the mass.

Treatment is directed based on the underlying cause. If
a history of external compression is identified, the symptoms resolve
1–2 months after removal of the offending

cause (57).
If the symptoms are secondary to trauma, a combination of casting or
rest, nonsteroidal anti-inflammatory medicines, and observation is
indicated. If nonsurgical methods fail to resolve the symptoms,
consider surgery. A trial injection of a local anesthetic agent around
the involved area with temporary resolution of symptoms preoperatively
will increase the chance that surgery may help. If a mass or ganglion
cyst is noted, surgical excision is indicated.

Postoperatively, the patient may increase activity as tolerated after the incision has healed.

In the distal third of the leg, the deep peroneal nerve
courses beneath the extensor hallucis longus muscle. As it approaches
the ankle, it is located between the extensor hallucis longus tendon
and the tendon of the extensor digitorum longus. It passes beneath the
superior and inferior extensor retinacula, then divides into a medial
and lateral branch. The medial branch accompanies the dorsalis pedis
artery, and it divides into two dorsal branches that supply the first
web space (Fig. 114.12). Just distal to the
inferior retinaculum, the lateral branch penetrates and innervates the
extensor digitorum brevis (EDB) muscle. These terminal branches of the
peroneal nerve may become compressed beneath the inferior extensor
retinaculum. Marinacci (45) called this entrapment the anterior tarsal tunnel

syndrome. Since that time, there have been scattered case reports in the literature (1,10,23,35,54), with the largest series being reported by Dellon (14).

Most patients reported in the literature have been
women. A history of trauma can often be elicited. Shoe straps or
tight-fitting boots, such as ski boots, that cross the dorsum of the
foot may irritate the nerve and lead to compression of the deep
peroneal nerve (Fig. 114.13). Classically,
patients complain of a deep ache over the dorsal and medial aspects of
the foot, with paresthesias into the first web space. Symptoms can
range from exacerbation with activities and relief with rest, to night
pain that awakens the patient. Physical findings include decreased
sensation in the first web space, a positive nerve percussion sign
(Tinel’s) over the course of the deep peroneal nerve, and atrophy of
the EDB muscle. Often, however, only a few—if any—of these signs are
present. There are a couple of reasons that atrophy of the EDB may be
lacking despite the presence of a true anterior tarsal tunnel syndrome.
If the entrapment occurs distal to the take-off of the motor branch, a
pure sensory neuropathy occurs. If the motor branch is involved,
atrophy and weakness of the EDB may be seen. Another reason is that in
22% of patients the accessory deep peroneal nerve, a branch of the
superficial peroneal nerve, innervates the EDB (27,36,43). In these cases, entrapment of the deep peroneal nerve would not manifest as denervation of the EDB muscle.

Electrodiagnostic abnormalities include prolonged distal

latencies of the peroneal nerve (Table 114.6) and needle findings described as representing “denervation” changes confined to the EDB muscle. Gessini et al. (23)
have suggested that a distal latency of greater than 5 msec confined to
the deep peroneal nerve is important in making the diagnosis. Because
abnormal needle findings in the EDB muscle have been reported in a high
number of normal subjects (1), one must be cautious about using this as the sole criterion for making a diagnosis.

A helpful diagnostic maneuver is to inject 3 ml of 1%
Xylocaine without epinephrine into the dorsal aspect of the foot
proximal to the cuneiform bones. This should provide complete, but
temporary, relief of symptoms. This nerve block is recommended prior to
surgery in any patient for whom the diagnosis is not clear based on
history and physical examination.

Nonoperative management is directed toward the
underlying cause. Whatever the treatment, it should be tried for at
least 3 months before considering surgery. If shoewear is identified as
the problem, alterations can help. Adjusting tight ski boots is
possible and would be optimal compared to surgery. Providing relief
from straps (e.g., over a bone prominence) should also be tried before
surgery. Alteration in athletic or daily activities as well as
nonsteroidal anti-inflammatory medications can provide relief of
symptoms. If these treatment modalities fail, operative intervention is
indicated.

The superficial peroneal nerve is a branch of the common
peroneal nerve. It innervates the peroneus longus and brevis muscles in
the lateral compartment of the leg. The nerve is most predictably found
about 10.5 cm proximal to the tip of the lateral malleolus as it
pierces the fascia in the distal anterolateral leg. Because of its
subcutaneous position as it courses between the peroneal muscles and
the extensor digitorum longus, it is especially prone to injury at this
site. The superficial peroneal nerve then divides into two terminal
sensory branches to form the medial dorsal cutaneous and intermediate
dorsal cutaneous nerves (Fig. 114.15).

Patients usually report paresthesias over the dorsum of
the foot, sparing the first web space. The symptoms have typically been
present for years and are worse with activities such as walking,
jogging, or running. Patients also complain of pain over the lateral
distal leg and lateral ankle. About 25% of the patients report a prior
history of trauma, mostly ankle sprain. Injury to the nerve has also
been reported following fibular shaft fractures, or compression by a
lipoma (3,40,47,62).

As with all compression syndromes of the foot and ankle,
start the physical examination with examination of the back, and look
for any sciatic tension signs. Examine the common peroneal nerve around
the fibula head for any swelling or a positive Tinel’s sign that
reproduces the location and quality of the patient’s complaints. The
most common area of entrapment is where the superficial peroneal nerve
pierces the deep fascia approximately 10.5 cm proximal to the tip of
the fibula. Point tenderness and a positive Tinel’s sign is often
elicited at this site. Styf and Morberg (63)
described three provocative tests for detection of nerve compression,
which are undertaken at rest and then again after exercise. In the
first, pressure is applied over the anterior intermuscular septum while
the patient actively dorsiflexes the ankle. In the second, the foot is
passively plantar flexed and inverted at the ankle. The third test is
performed by applying passive stretch with inversion, and percussing
over the course of the nerve. Pain or paresthesia caused by any of
these tests suggests entrapment of the superficial peroneal nerve.
According to the authors’ diagnostic criteria, entrapment of the
superficial peroneal nerve is diagnosed when sensation over the dorsum
of the foot is decreased and there is pain at rest or during exercise,
and when at least two of the three provocative tests are positive.

As with the other entrapment or compressive
neuropathies, a trial of activity modification, anti-inflammatories,
and an ankle strap or orthotic device may prove useful. If this fails,
operative management is indicated.

Preoperatively, identify the etiology and site of compression or entrapment. If a mass is present, an MRI

scan can help localize it. By examination, identify the area(s) of compression by the provocative tests and map this area out.

Allow the patient to bear weight in a walking boot the following day.

Painful conditions about the heel are common, and the
differential diagnosis is extensive. One cause of a painful heel
syndrome is an entrapment neuropathy of one of the branches of the
tibial nerve (4,5,28).
The first branch of the lateral plantar nerve has been implicated as a
source of heel pain. It supplies the abductor digiti quinti muscle on
the lateral side of the foot. Distal to the laciniate ligament (flexor
retinaculum), the tibial nerve divides into four or five branches.
There are one or two superficial branches, called the medial calcaneal
nerves. The medial and lateral plantar nerves, as well as the nerve to
the abductor digiti quinti, then course deep to the abductor hallucis
muscle. The nerve to the abductor digiti quinti may be a separate
branch of the tibial nerve or arise as a branch of the lateral plantar
nerve (Fig. 114.17). It passes beneath

the thick, inelastic, deep fascial edge of the abductor hallucis
muscle, where it can become compressed. The nerve continues laterally,
deep to the origin of the plantar fascia and flexor digitum brevis
muscle, and terminates in the proximal portion of the abductor digiti
quinti.

Patients with painful heel syndrome typically complain
of heel pain exacerbated by weight bearing. Pain is worse with the
first step in the morning or on arising after a period of rest. The
onset is often gradual, and a history of competitive sports is present
in 50% of the cases. In contrast to other patients with heel pain who
are generally older, heavier, and less active, those with nerve
compression as the etiology are younger and more athletic. This patient
often has had symptoms for many months or years before seeking medical
attention. The pain normally starts medially but can radiate laterally.
Rarely does the patient complain of numbness or paresthesias into the
foot.

Physical examination reveals tenderness over the origin
of the abductor hallucis muscle. Tenderness over the medial tubercle of
the calcaneus is a common finding as well. A Tinel’s sign is often
lacking, but on occasion one can elicit radiation of pain to the
lateral side of the foot. Electrodiagnostic studies can be useful as an
adjunct to the history and physical examination for entrapment of the
nerve to the abductor digiti quinti (60). However, the exact criteria and best method are yet to be determined.

Even if entrapment of the nerve to the abductor digiti
quinti is suspected as a cause of a patient’s symptoms, treat
nonoperatively for 6 to 12 months. The treatment is much the same as
for heel pain syndrome caused by plantar fasciitis. This includes
education, stretching, heel cups, over-the-counter or custom-molded
orthoses, nonsteroidal anti-inflammatory medications, and alteration in
athletic shoes and/or activity.

Baxter and coworkers reviewed their experience with the
operative results of 69 heels in 53 patients with recalcitrant heel
pain who had failed a minimum of 6 months of conservative therapy.
Their surgical technique is outlined below (4,5,42).

Postoperatively, place patients on crutches, and do not
allow weight bearing for 3–4 days. Then begin gradual weight bearing.
Dress the wound daily with antibiotic ointment and apply gauze. One
week postoperatively, the patient can try to put on an athletic shoe
with a soft heel pad. The patient can resume light jogging by 4 weeks,
but some symptoms persist for 3 months.