Peripheral nerve entrapments

Christopher B. Hirose, MD, William C. McGarvey, MD

*
Department of Orthopaedic Surgery, University of Texas School Health Science Center at Houston
Medical School, 6411 Fannin, Suite 1100, Houston, TX 77030, USA
Peripheral nerve entrapment is a rare, but important, cause of foot and ankle
pain that often is underdiagnosed and mistreated. Although a nerve may be
compressed anywhere along its course, a few anatomic locations are typical of
nerve entrapment.
Entrapment points are anatomic locations that constrict a peripheral nerve as a
result of the unyielding constraints of an osseofibrous tunnel or fascial opening. A
compressed nerve may, within minutes, show decreased intraneural blood flow,
inhibition of axonal transport, and an increase in endoneurial edema. Twenty mm
Hg of pressure compromises epineurial blood flow, 30 mm Hg can limit axonal
transport, and 50 mm Hg can change the structure of the myelin sheath. When a
nerve becomes entrapped, an inflammatory reaction occurs within hours of com-
pression. Fibrous tissue proliferation occurs within days; fibrosis with generation
of sheets of fibrous tissue forms within one month [1].
Nerves may become entrapped by external or internal forces that work
alone or in concert. External compression may occur from direct trauma or other
external forces, such as constrictive shoe wear, whereas internal compression
may arise from space-occupying lesions, increased compartment pressures, or
from traction due to ligamentous instability. The two forces may occur concomi-
tantly to break the symptom threshold; an osteophyte that tents a nerve may be
asymptomatic until the constraints of a shoe compress the nerve and leads to
neuritic symptoms.
Clinically, nerve entrapment is divided into three stages that have been cor-
related with histologic changes. In stage I, patients feel rest pain and intermittent
paresthesias that are worse at night. The increase in nighttime symptoms is
believed to be due to changes in intraneural microvascular perfusion that dis-
appear during the day along with increased activity. In stage II, continued nerve
compression leads to paresthesias, numbness, and, occasionally, muscle weak-
ness that does not disappear during the day. Microscopically, there is segmental
demyelination of the nerve. Finally, in stage III, patients report constant pain,
1083-7515/04/$ see front matter D 2004 Elsevier Inc. All rights reserved.
doi:10.1016/j.fcl.2004.02.001
* Corresponding author.
E-mail address: wmcgarvey@ucplus.org (W.C. McGarvey).
Foot Ankle Clin N Am
9 (2004) 255269
muscle atrophy, and permanent sensory loss. Nerve fibers show pronounced
degeneration [2].
Although the natural history of an entrapped peripheral nerve is unpredictable
on a case by case basis, it is believed that most of these become asymptomatic
over the course of months [3]. Whether this occurs as a result of a decline of the
inflammatory response or from atrophy of the nerve is unknown. Patients who
have stage I compression may be managed with splints or steroid injections. This
form of treatment may be adequate to reverse the intraneural edema. With more
severe stage II or stage III nerve entrapment, conservative management may fail;
these cases may benefit from operative intervention if a definite point of
entrapment is found.
In general, nerves may be compressed by space-occupying lesions, conditions
that are associated with an accumulation of total body fluid (pregnancy, chronic
heart failure), an accumulation of extracellular matrix (myxedema, mucopoly-
saccharidosis), generalized inflammatory conditions (rheumatoid arthritis), or
metabolic conditions (alcoholic or diabetic peripheral neuropathy). In many of
these situations, medical, rather than surgical, management is optimal.
Because of the multiple etiologies of peripheral nerve entrapments and their
complex physical and temporal relation, confusion often results. A thorough
understanding of the causes of peripheral nerve entrapments, the anatomic course
and variation of the peripheral nerves, the diagnostic modalities, and the treatment
options can simplify this complex problem greatly. When a direct anatomic point
of entrapment can be discovered, surgical intervention may be curative.
Anterior tarsal tunnel syndrome
Introduction
Compression of the deep peroneal nerve was recognized by Kopell and
Thompson in 1960 [3]. The term anterior tarsal tunnel syndrome is used to
describe the specific compression of the deep peroneal nerve under the inferior
extensor retinaculum [4]. With nerve compression, patients complain of a burning
sensation across the dorsum of the foot with paresthesias in the first web space.
There also may be wasting and weakness of the extensor digitorum brevis. The
syndrome is rare. There have been a dozen case reports in the literature; however,
anecdotal references much higher in number [5]. In a study of 320 patients who
had chief complaint of pain and numbness of the feet, only 14 (4%) met the criteria
for the diagnosis of anterior tarsal tunnel syndrome [6].
Anatomy of the deep peroneal nerve
In the proximal one third of the leg, the deep peroneal nerve, a mixed motor and
sensory nerve, is located between the tibialis anterior and the extensor digitorum
longus. It travels in conjunction with the anterior tibial artery. As the nerve
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descends the leg, it is found in the interval between the extensor digitorum longus
and the extensor hallucis longus, 5 cm proximal to the ankle joint. At 1 cm above
the ankle joint, the nerve branches to form a lateral mixed branch which innervates
the musculature of the extensor digitorum brevis and provides sensation to the
lateral tarsal joints. The main medial branch, which is now a sensory branch,
continues distally with the artery of the dorsalis pedis in the interval between the
extensor hallucis longus and the extensor hallucis brevis tendons to innervate the
skin of the first web space.
Overlying this nerve is the extensor retinaculum which consists of several
bands: the superior extensor retinaculum and the inferior extensor retinaculum.
The superior extensor retinaculum is located 5 cm above the ankle joint. The
inferior extensor retinaculum is split into two bands: the superomedial and in-
feromedial band.
The anterior tarsal tunnel is located just distal to the inferior medial band of the
extensor retinaculum and is formed by the anatomic confines of the inferior
extensor retinaculum which makes up the roof and the capsule of the talona-
vicular joint makes up the floor. The superior extent of the anterior tarsal tunnel is
defined by the inferior edge of the inferomedial band of the extensor retinaculum;
the distal extent is defined by the talonavicular joint. The lateral boundary is the
lateral malleolus and the medial boundary is defined by the medial malleolus. The
dorsalis pedis artery and vein and the deep peroneal nerve lie within the canal
together with four tendons that include the extensor hallucis longus, tibialis
anterior, extensor hallucis longus, and the extensor digitorum longus [7].
Variations in anatomy
The branching pattern of the deep peroneal nerve varies. In some, the nerve
does not provide sensory innervation to the first web space; in others, it may
supply sensation to the inner side of the great toe and the second and third web
space or to the lateral border of the foot [8,9].
An accessory deep peroneal nerve is present in 28% of subjects [10]. A
branch of the superficial peroneal nervethis accessory branch courses poste-
rior to the lateral malleolus and is motor to the lateral portion of the extensor
digitorum brevis.
Etiology
The nerve may become entrapped at several points along its course either by
intrinsic or extrinsic mechanisms. Intrinsic compression may occur from any
space-occupying lesion, including osteophytes, traumatic bony fragments, hy-
pertrophied muscle bellies of the extensor hallucis brevis, ganglia, or tumors. An
increase in compartmental pressure from peripheral edema also may compress the
nerve. Finally, traumatic injury that results from ligamentous laxity may stretch
the nerve [5]. Baxter [11] noted that most patients have a history of recurrent
ankle sprain.
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Extrinsic compression may occur from a single, direct traumatic contusion or
repetitive trauma that is secondary to increased shoe contract pressure [4,12].
Lindenbaum [13] reported a case that was due to ski boot compression; Mu-
menthaler and Schliack [14] described a sensory deficit that was due to narrow
shoe wear. Baxter [11] noted several cases of external compression in runners who
wore keys under the tongues of their running shoes, as well as in athletes who
performed sit-ups with their feet hooked under a metal bar.
Complete versus partial syndrome
This syndrome may be further classified by involvement of sensory or motor
nerve modality. A complete lesion involves motor and sensory components of the
nerve, whereas a partial lesion involves either the motor or the sensory branch of
the nerve. Complete lesions are located proximal to the bifurcation of the motor
and sensory branches, whereas partial lesions are located distal to this bifurcation
of the motor and sensory branches [12].
Sites of compression
Known classically as the anterior tarsal tunnel syndrome, the most common
site of compression of the deep peroneal nerve occurs at the inferior edge of the
inferomedial extensor retinaculum. This results in a pure sensory deficit because
the motor branch has left the trunk superior to the lesion (Fig. 1) [4].
The deep peroneal nerve also may be compressed by an injured or hypertro-
phied extensor hallucis brevis muscle that results in a pure sensory deficit in the
first web space [15]. A complete lesion results with compression by the superior
edge of the inferior extensor retinaculum under the tendon of the extensor hallucis
longus [16].
Evaluation
History
Patients commonly describe a burning sensation with numbness over the
dorsum of the foot and first web space. Others report a deep aching in the dorsal
midfoot or sinus tarsi. Pain usually increases with physical activity and subsides
with rest [11]. This may reflect transient muscle edema or coincide with an
undiagnosed exertional compartment syndrome. Nighttime pain is common as the
foot is held in a plantarflexed posture. Borges et al [16] noted that the plantarflexed
posture places a maximum stretch on the nerve as it is draped over the talo-
navicular joint. Inquiries about the type of shoe wear should be sought. High-
heeled shoes mimic the plantarflexed posture; tight fitting narrow shoes may
compress the nerve directly.
Clinical
Inspection of the foot for masses or other space-occupying lesions may reveal
the site of internal compression of the deep peroneal nerve. The extensor digitorum
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brevis may be atrophied. A sensory examination may reveal numbness and par-
esthesias in the first dorsal web space. Percussion of the deep peroneal nerve and a
resultant Tinels sign may locate the area of compression. The motor examination
may or may not demonstrate subtle weakness in the toe extensors because as motor
redundancy and the strong pull of the extensor digitorum longus and the extensor
hallucis longus make this examination difficult. The most reliable way to detect
involvement of the extensor digitorum brevis is to observe and palpate the muscle
belly of the brevis during resisted extension of the toes. Forced plantarflexion and
inversion of the foot may exacerbate symptoms by stretching the nerve [8].
The path of the nerve should be traced proximally to rule out pathology at the
fibular neck. A lesion here results in weakness of the anterior tibialis, the extensor
hallucis longus, and the extensor digitorum longus, in addition to sensory losses
across the dorsum of the foot. A thorough lumbar spine examination, including
provocative tension signs, differentiates this from lumbar nerve root pathology,
which L5S1 radiculopathy may mimic
Differential diagnosis
The differential diagnosis of anterior foot pain includes lumbosacral nerve root
impingement, peripheral neuropathy, tarsal tunnel syndrome, Mortons neuroma,
Fig. 1. Deep peroneal nerve points of compression. The inferior edge of the inferomedial extensor
retinaculumthe classic anterior tarsal tunnel syndrome; under the hypertrophied extensor hallucis
brevis; and under the tendon of the extensor hallucis longus at the superior edge of the inferior
extensor retinaculum.
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superficial peroneal nerve entrapment, gout, peripheral vascular disease, bony
ankle impingement, and ankle sprain or fracture [7,12,15,17,18].
Imaging/tests
Radiographs may reveal osteophytes, traumatic bony fragments, or soft tissue
shadows in the area of the deep peroneal nerveparticularly in the area of the
dorsal talonavicular joint. Electrodiagnostic testing may be helpful in determining
the location of a compressive lesion. The results should be correlated with clinical
findings, however, because abnormal fasciculations have been found in up to
76% of normal subjects and decreased motor recruitment has been found in up to
38% of normal adults [19]. A distal latency of more than 5 milliseconds is be-
lieved to correlate with deep peroneal nerve compression [8]. Electromyographic
studies may show denervation of the extensor digitorum brevis with spontaneous
fibrillation potentials and positive sharp waves [12,20]. Obtaining electrodiag-
nostic data is technically difficult at best. Ponsford [21] was able to obtain distal
latency data in only 50% of patients. Anatomic variation further complicates
electrodiagnostic interpretation. The accessory deep peroneal nerve originates
from the superficial peroneal nerve and supplies motor innervation to the lateral
portion of the extensor digitorum brevis. In these cases, electrodiagnostic results
may show a normal electromyographic examination of the extensor digitorum
brevis although the deep peroneal nerve is compressed [22].
Treatment
Conservative measures should be tried first. Decreasing the pressure over the
nerve with the use of orthotics or accommodative shoes often helps [8]. If chronic
edema is present, then treatment of the primary condition may be effective.
Injection of local anesthetic with corticosteroid is useful in evaluation of the
location of the neuropathy and in treatment. Local anesthetic provides immediate
relief; corticosteroids provide longer-lasting relief. Resolution of pain and par-
esthesias may be obtained with serial injections into the tarsal tunnel with local
anesthetic and corticosteroids [8].
Surgery
When the conservative options fail, surgical release of the anterior tarsal
tunnel can be effective if a definitive point of entrapment can be found. The
incision is straight vertical or S-shaped and extends from proximal to the ankle
joint down to the base of the first and second tarsometatarsal joints. Care is taken
to preserve nerve branches of the superficial peroneal nerve. Space-occupying
lesions or osteophytes of the talonavicular joint are removed. Murphy and Baxter
[23] described internal nerve compression by a talar osteophyte with complete
resolution after decompression and exostectomy. An hypertrophied extensor
hallucis brevis may be resected [5]. The extensor retinaculum is divided and
the superior portion intact is kept intact. The deep peroneal nerve, along with the
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lateral and medial branches, is neurolysed. Mosimann [24] reported that 16 of
31 (52%) cases had complete recovery and an additional 11 (35%) cases had
partial improvement with this method of operative decompression. Dellon [5]
reported that 12 of 20 (60%) patients had excellent results, 4 of 20 (20%) patients
had good results, and 4 of 20 patients (20% had ) no improvement.
Superficial peroneal nerve entrapment
Introduction
Named mononeuralgia of the peroneal nerve by Henry in 1945 [25], en-
trapment of the superficial peroneal nerve is a rare occurrence that has multiple
causes. Patients note pain in the anterior lateral lower leg and the dorsum of the
foot. A minority report sensory disturbances. In a study of 480 patients who had
chronic leg pain, Styf and Morberg [26] found that only 17 (3.5%) patients were
diagnosed with entrapment of the superficial peroneal nerve.
Anatomy
The superficial peroneal nerve branches off from the common peroneal nerve
at the neck of the fibula. It usually is located in the lateral compartment of the leg
and is found between the peroneus longus and peroneus brevis muscles which it
innervates. Distally, it comes to lie between the peroneus muscle bellies and the
extensor digitorum longus. It pierces the crural fascia through a short fibrous
and noncompliant tunnelthe peroneal tunnel. This tunnel is located between
the anterior intermuscular septum and the fascia of the lateral compartment. It
emerges as a purely sensory nerve between 3 cm and 18 cm above the lateral
malleolus to become subcutaneous. In one study, 75% of the specimens exhibited
nerve division into the medial and intermediate dorsal cutaneous branches at an
average of 10.5 cm proximal to the lateral malleolus [9]. The intermediate dorsal
cutaneous nerve passes medial to the lateral malleolus, where it is superficial and
often is visible over the sinus tarsi along the lateral foot with plantarflexion of the
ankle. It continues onto the dorsum of the foot to supply sensory branches to the
dorsum of the foot and the third, fourth, and fifth toes. The medial branch passes
lateral to the tendon of the extensor hallucis longus and supplies sensory branches
to the medial dorsum of the foot, including the medial great toe and the second
and third toes.
Variations in anatomy
In general, variability of the nerve is found in up to 30% of specimens. The
nerve may be found in the lateral compartment (73%), the anterior compartment
(14%), or superficial to the peroneus longus muscle (1%) [27]. The medial and
intermediate branches may arise independently from the superficial peroneal
nerve with individual exit sites in the crural fascia. More than 40 variations have
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been described for the terminal sensory branching patterns of the superficial
peroneal nerve, beginning with its presence in the anterior compartment [28].
Etiology
Cases of superficial peroneal nerve entrapment most commonly occur with
direct trauma to the nerve; this accounted for 25% of cases that were seen by
Banerjee and Koons [29]. Traction injury also may occur with ankle sprains and
often can be disguised as a bad ankle sprain that does not go away, [30],
muscle herniations [31], or chronic exertional compartment syndromes [32,33]. It
also is seen in the setting after compartment fasciectomy with resultant shifting of
the peroneal tunnel [32], fibular fractures [34], postsurgical approaches to the
fibula with fractures or ankle fusions, chronic edema, lipomas, or extrinsic
compression from high-riding boots and tight laces [29].
Evaluation
History
Most patients report pain in the middle to distal one third of the leg. The pain
is worse with physical activity and relief by conservative measures is infrequent,
contradictory to its deep counterpart. Nocturnal pain is rare.
Clinical
Pain and sensory abnormalities are the predominant findings. Motor and reflex
examinations are normal. The most common site of pain is at the fascial opening
where the nerve pierces the crural fascia (Fig. 2). The pain often involves the
Fig. 2. Superficial peroneal nerve entrapment.
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anterior lateral lower leg and continues onto the dorsum of the foot. Retrograde
pain has been reported, but pain in the L5 nerve distribution is characteristic.
Sensory disturbances are found in approximately one third of patients and most
patients report no sensory loss [11]. There should be no specific muscle weak-
ness. The pain and sensory abnormalities may be elicited with three provocative
maneuvers that were described by Styf [32]. In the first maneuver, the examiner
applies pressure over the entrapment site while the patient actively dorsiflexes
and everts the foot against resistance. With the second maneuver, the examiner
passively plantarflexes the foot and inverts the ankle. In the third maneuver,
percussion over the course of the nerve is performed while maintaining passive
stretch with ankle inversion. A test is considered positive with the finding of pain
and paresthesias over the distribution of the superficial peroneal nerve in two of
the three provocative maneuvers.
Differential diagnosis
First on the differential diagnosis list is chronic ankle sprains. Patients may give
a history of an ankle sprain that does not get any better with time. Other differential
diagnoses include lateral ankle ligament injuries, chronic lateral compartment
syndrome [33], fascial defects with muscle herniation, lipomas, proximal peroneal
nerve lesions at the fibular neck, and lumbar nerve root impingement at L5.
Banergee and Koons [29] described a case of missed superficial peroneal nerve
entrapment in a patient who underwent L45 discectomy without resolution of
lower extremity numbness. Low back pain, long tract signs, and motor weakness
should be tested thoroughly to rule out nerve root impingement.
Imaging/tests
The diagnosis of superficial peroneal nerve entrapment is made largely by
history and physical examinationnot by nerve conduction studies [32]. Nerve
conduction tests may aid in the diagnosis of nerve compression when history and
physical examinations are in doubt. Abnormal findings include nerve conduction
tests with velocity of less than 44 m/sec [35], prolonged distal latencies, or at-
tenuation of sensory nerve action potentials [36,37]; however, a normal test
does not exclude compression of the superficial peroneal nerve [32]. Methods
for measuring superficial peroneal nerve conduction velocities have been stan-
dardized and are obtainable. In one study, action potentials were obtained in 98%
of subjects [38].
MRI may be a useful diagnostic tool to demonstrate peroneal nerve sheath
thickening and constriction by the crural fascia [39].
Treatment
Conservative measures should be exhausted before any surgical intervention.
These include lateral wedges in the shoes and ankle rehabilitation physical
therapy exercises. Corticosteroid and local anesthetic injections aid in defining
the location of nerve entrapment and serve as therapeutic modalities.
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Surgery
If surgical intervention is warranted, a release of the superficial peroneal nerve
as it exits the deep fascia is performed. Preoperatively, the nerve is percussed to
find the point at which it exits the crural fascia; it is decompressed at the entrance
of the peroneal fibrous tunnel. The tunnel can vary in length from 3 cm to 11 cm.
Styf reported on 19 cases of superficial peroneal nerve entrapment with surgical
release of the peroneal tunnel; there was an 80% clinical improvement and 50%
to 82% satisfaction rate [26,32]
Lateral compartment fasciectomy may be performed if the patient satisfies the
criteria for exertional compartment syndrome; these patients represent a minority
(10%) of cases of superficial peroneal nerve entrapment [26]. Chronic compart-
ment syndrome is diagnosed when the intramuscular pressure is at least 15 mm
Hg pre-exercise, at least 30 mm Hg at 1 minute postexercise, and at least 15 mm
Hg at 5 to 10 minutes postexercise [33]. In a study of 30 legs that had chronic
anterior compartment syndrome of the leg, Styf [40] reported that 28 legs had
an unlimited or increased functional capacity after fasciectomy. In addition,
fasciectomy was shown to normalize intramuscular pressure and relieve the symp-
toms of chronic exertional compartment syndrome.
Sural nerve entrapment
Introduction
Entrapment of the sural nerve was described 1974 [41]; only a handful of
case reports have been published. Patients report a neuritic pain, burning, and
paresthesias along the course of the sural nerve sensory distribution on the lateral
side of the ankle and foot that extends to the fifth metatarsal head [42].
Anatomy
The sural nerve is a pure sensory nerve that is derived from the S1 and
S2 nerve roots. It is formed from contributions from the tibial and peroneal
nerves. Medially, the medial sural cutaneous nerve branches from the tibial nerve,
courses between the two heads of the gastrocnemius, and exits the crural fascia
through a nonextensible fibrous arcade at midcalf. Laterally, the lateral sural
cutaneous nerve arises from the common peroneal nerve at the level of the fibular
head. This branch subdivides to form a peroneal communicating branch that joins
the medial sural cutaneous nerve at the musculotendinous junction of the gas-
trocnemius. It continues distally on the lateral border of the tendo Achilles. The
nerve is closest to the Achilles tendon 7 cm above the tip of the lateral malleolus.
It comes to lie posterior and superficial to the peroneal tendon sheath and courses
14 mm posterior and 14 mm inferior to the lateral malleolus [43]. It forms two or
three lateral calcaneal branches. Distally, it bifurcates again to form a medial and
a lateral branch. The lateral branch forms the lateral dorsal cutaneous branch of
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the sural nerve which traverses the base of the fifth metatarsal and supplies
sensation to the lateral border of the foot and the interphalangeal joint of the fifth
toe. The larger, but often less recognized, medial branch continues onto the dor-
sum of the foot and communicates with the intermediate branch of the superficial
peroneal nerve to supply sensory innervation to the lateral aspect of the fourth
digit. In addition, the sural nerve sends articular branches to the inferior tibio-
fibular joint, ankle joint, and the talocalcaneal joint [44]
Variations in anatomy
The sural nerve contains differing contributions from the tibial and common
peroneal nerves. In one study, a minority of cadaveric specimens demonstrated
the origin of the nerve from 100% of the tibial nerve or 100% of the common
peroneal nerve. At the level of the lateral malleolus, the nerve gives off an
average of three branches (range, one to five). The anatomic location of the lateral
calcaneal branches also varies significantly [43].
Etiology
Entrapment of the nerve may occur with direct traumatic contusion or in
conjunction with fractures of the calcaneus; fractures of the base of the fifth
metatarsal [11,45]; fractures of the posterolateral process of the talus; anterior
process fractures of the calcaneus; or space-occupying lesions of the peroneal
tendons, sinus tarsi, or calcaneal cuboid joint. Os trigonum syndrome, osteochon-
droma of the talus [46], fracture of an os perineum [47], peroneal tendonitis,
Achilles tendonitis [41], and fibroaponeurotic bands from the Achilles tendon [48]
have also been described in conjunction with nerve entrapment. Traction injury
is seen with severe ankle sprains [49], Bakers cysts [50], gastrocnemius hema-
tomas [42], or myositis ossificans in the gastrocnemius. As with other peripheral
nerves, traction injury leads to fibrosis of the nerve [41,51], Fabre et al [52]
described 18 cases of sural nerve entrapment at the fibrous crural fascia arcade
in athletes. Percutaneous Achilles tendon repairs also place the sural nerve at
risk, as noted by Hockenbury and Johns (Fig. 3) [53].
History
Patients describe pain, paresthesias, and tenderness on the lateral aspect of the
foot, which may radiate proximally to the knee. Pain usually is worse at night. A
history of frequent ankle sprains is common [11].
Clinical
Percussion along the course of the nerve with elicitation of a Tinels sign and
resultant pain and paresthesias along the course of the sural nerve are typical.
Provocative maneuvers, such as plantarflexion of the foot and inversion, may
reproduce the patients symptoms. Pain may occur with palpation anywhere
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along the length of the nerve, from the popliteal fossa to the base of the meta-
tarsals [50]. Motor and reflex examinations are normal.
Differential diagnosis
More proximal lesions at the sacrum, with S1S2 nerve root impingement,
should be evaluated with a thorough lumbosacral examination. Exertional com-
partment syndrome, popliteal artery entrapment syndrome, ankle sprains [11],
and pathology of the tendo Achilles may mimic this neural entrapment [54],
Imaging/tests
Radiographs are obtained to rule out fractures, osteochondromas, or myositis
ossificans; MRI is the imaging modality of choice for soft tissue compressive
lesions. Sural nerve conduction studies may confirm clinical suspicions of sural
nerve entrapment. Obtaining electrodiagnostic data are not problematic. Lee [55]
obtained data in 40 of 40 volunteers in measuring distal sural conduction. With
entrapment, these tests usually show an increase in the distal latency or a decrease
in the amplitude of the nerve action potential.
Treatment
Conservative treatment modalities include accommodative shoe wear to
relieve extrinsic pressure on the sural nerve. Treatment of underlying conditions,
such as peripheral edema, may alleviate symptoms.
Fig. 3. Sural nerve entrapment over a fracture of the base of the fifth metatarsal.
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Surgery
When conservative measures fail, nerve decompression has been successful.
Gould and Trevino [45] described three cases of fractures of the base of the fifth
metatarsal with dorsal displacement of the fracture fragment and tenting of the
sural nerve. With reduction of the fracture fragment and neurolysis of the sural
nerve, all patients improved within several months. Decompression of the nerve
by ganglia with neurolysis also may be curative [41]. Fabre et al [52] described
18 cases of sural nerve entrapment at the fibrous crural fascial arcade. Surgical
release and neurolysis resulted in 9 excellent results, 8 good results, and 1 fair
result. Ten patients had cessation of calf pain.
Summary
Although infrequent, peripheral nerve entrapments are the cause of signifi-
cant morbidity. A history of burning, aching, neuritic pain should stimulate the
physician to evaluate the nervous pathology. Awareness, appropriate history,
thorough knowledge of peripheral nervous anatomy and their entrapment points,
physical examination, and appropriate use of neurologic and radiographic tests are
necessary to make the correct diagnosis. A physician should have all of these
components in his or her armamentarium to sort out simple solutions from the
initial confusing array of factors.
Treatment of the primary cause of nerve compression should be sought and
corrected, whether it is the control of peripheral edema or the discontinuation
of constrictive footwear. Not infrequently, conservative measures are curative.
When these fail and when a precise anatomic location of nerve constriction or
traction is located, surgical decompression can be successful and satisfying for
the patient and surgeon.
Acknowledgments
We would like to thank Dr. Matthew Morrey for help with the illustrations.
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