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Home > January 2016 - Volume 24 - Issue 1 > Peroneal Nerve Palsy: Article Tools
Evaluation and Management
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Journal of the American Academy of Orthopaedic Surgeons:

January 2016 - Volume 24 - Issue 1 - p 110
doi: 10.5435/JAAOS-D-14-00420

Review Article

Peroneal Nerve Palsy: Evaluation and

Management
Poage, Chad DO; Roth, Charles MD; Scott, Brandon MD
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Article Outline

Author Information

From the Andrews Research and Education Foundation, Gulf

Breeze, FL (Dr. Poage and Dr. Roth), the Department of
Orthopedic Surgery, Florida State University College of
Medicine, Tallahassee, FL, and the Department of Physician
Assistant Studies, University of South Alabama Medical Center,
Mobile, AL (Dr. Roth), and the Department of Orthopaedic
Surgery, University of South Alabama (Dr. Scott).

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Dr. Roth or an immediate family member has received research

or institutional support from Arthrex. Neither of the following Article Level Metrics
authors nor any immediate family member has received anything

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Articles in PubMed by Chad

of this article: Dr. Poage and Dr. Scott.
Poage, DO
Received November 19, 2014

Accepted April 15, 2015

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by Chad Poage, DO
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Abstract

Keyword Highlighting
Peroneal nerve palsy is the most common entrapment neuropathyHighlight selected keywords in
the article text.
of the lower extremity. Numerous etiologies have been
identified; however, compression remains the most common
Peroneal nerve palsy
cause. Although injury to the nerve may occur anywhere along
foot drop
its course from the sciatic origin to the terminal branches in the
foot and ankle, the most common site of compressive pathology
nerve decompression
is at the level of the fibular head. The most common presentation
nerve injury
is acute complete or partial foot drop. Associated numbness in
the foot or leg may be present, as well. Neurodiagnostic studies
nerve repair
may be helpful for identifying the site of a lesion and
grafting
determining the appropriate treatment and prognosis.
Management varies based on the etiology or site of compression. Search for Similar Articles
You may search for similar articles
Many patients benefit from nonsurgical measures, including
that contain these same keywords
activity modification, bracing, physical therapy, and medication. or you may modify the keyword list
to augment your search.
Surgical decompression should be considered for refractory
cases and those with compressive masses, acute lacerations, or
severe conduction changes. Results of surgical decompression
are typically favorable. Tendon and nerve transfers can be used
in the setting of failed decompression or for patients with a poor
prognosis for nerve recovery.
Common peroneal nerve (CPN) palsy is associated with the
onset of acute and progressive foot drop and is the most common
compressive neuropathy of the lower extremity. When onset is
atraumatic, compressive pathology may be identified anywhere
along the course of the nerve, from the peroneal division of the
sciatic nerve to the terminal branches in the foot and ankle. The
most common site of compression is located at the bony
prominence of the fibular neck. As with all compressive
neuropathies, the key to a successful outcome is early
identification and treatment.
1,2

3,4

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Peripheral Nerve Structure and Pathophysiology

When evaluating patients with disorders of the peripheral nerves,

the clinician must take into account the structural composition of
the nerve and the pathophysiology of nerve injury. Individual
myelinated fibers and groups of unmyelinated fibers are encased
in a layer of endoneurium. These fibers are grouped into
fascicles covered by perineurium and combine to form peripheral
nerves that are covered with two layers of epineurium. In 1942,
Seddon described a classification system for peripheral nerve
5

Search

injuries that was based on the degree of structural disruption and

the sequelae that follow (Figure 1). In the Seddon classification,
the least severe injury is neurapraxia, which involves myelin
damage with delayed conduction and intact components (Table
1). Axonotmesis is characterized by axon discontinuity, with the
development of wallerian degeneration being the key
component. Neurotmesis, the most severe nerve injury, is
complete disruption of the nerve, including separation of the
axons and the epineurium. Although full or partial spontaneous
recovery is expected with neurapraxia and axonotmesis, minimal
recovery is expected with neurotmesis. In 1951,
Sunderland modified this classification by categorizing nerve
injury by five degrees and incorporating clinical ramifications as
well as potential nerve healing (Table 1).
7

Table 1

Figure 1

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With acute nerve compression, dysfunction results from ischemic

changes that may cause a conduction block. Varying degrees of
intraneural edema are seen in acute cases, but this typically
resolves over time, after the causative factor is addressed. With
chronic compression or compression that lasts >28 days, slowing
of nerve conduction is seen along with an endoneurial
inflammatory response. This response results in the formation of
fibroblast-moderated scar tissue that may further exacerbate the
compression. Axonal degeneration is seen with compression
lasting 4 weeks.
9

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Anatomy

The CPN is derived from the nerve roots of L4, L5, S1, and S2
as a part of the sciatic nerve. In the thigh, the peroneal division
of the sciatic nerve is located in the lateral and posterior portion
of the nerve. This anatomic position leaves the peroneal division
more vulnerable than its tibial counterpart to stretch or direct
injury during the exposure for hip arthroplasty.
The peroneal division of the sciatic nerve travels through the
posterior compartment of the thigh and supplies the short head of
the biceps femoris muscle before separating from the tibial nerve
in the upper popliteal fossa. Here, it becomes the CPN and
crosses posterior to the lateral head of the gastrocnemius muscle
through the posterior intermuscular septum and becomes
subcutaneous while it curves around the head of the fibula deep
to the peroneus longus muscle (Figure 2). The lateral cutaneous
nerve of the calf branches off here, and the nerve subsequently
divides into the superficial peroneal nerve (SPN), deep peroneal
nerve (DPN), and an articular branch. The DPN lies directly on
the bony surface of the fibula and wraps around it, thus
predisposing it to compression in this area.
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Figure 2

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The SPN travels distally in the lateral compartment of the leg,

providing motor innervation to the peroneus longus and peroneus
brevis muscles and sensory innervation to the lateral lower leg
and the dorsum of the foot. The nerve lies on the cortex of the
fibular shaft in the mid leg and then pierces the fascia anterior to
the bone 10 to 12 cm above the tip of the fibula. On the anterior
aspect of the distal fibula, the nerve is vulnerable to injury during
fixation of an ankle fracture. Finally, the SPN terminates distally
as the intermediate and medial dorsal cutaneous nerves.
The DPN travels for 3 to 4 cm along the anterior cortex of the
fibula and then courses distally. It then courses just anterior and
medial to the intermuscular septum between the anterior and
lateral compartments as it travels with the anterior tibial artery.
This is a potential source of DPN entrapment when the nerve is
stretched. The DPN supplies motor innervation to the foot and
toe dorsiflexors, including the tibialis anterior (TA), extensor
digitorum longus (EDL), extensor hallucis longus, peroneus
tertius, and extensor digitorum brevis (EDB) muscles. The nerve
passes under the extensor retinaculum at the ankle and then
terminates as a sensory branch in the dorsal first web space.
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Etiology

The etiologies for peroneal nerve palsy are numerous. Although

compressive etiology remains the most common cause, many
other factors contribute to injury. Traumatic causes include knee
dislocation, severe ankle inversion injuries, lacerations, and
direct blunt trauma. These traumatic injuries are typically
associated with poorer outcomes. The link between diabetes
mellitus and lower extremity neuropathies (eg, polyneuropathy,
mononeuropathy) has been well established. Iatrogenic injury is
common as well, with acute foot drop often seen as a result of
surgery about the hip, knee, and ankle; positioning during
anesthesia; prolonged bed rest; casting; bracing; compression
wrapping; and the use of pneumatic compression devices.
Several risk factors for compressive peroneal neuropathy have
been described. A recent history of significant weight loss has
been shown to be related to nerve compression at the fibular
head and may be associated with the loss of subcutaneous fat at
this level. Habitual leg crossing and prolonged squatting are
also associated with an increased risk of peroneal palsy and acute
foot drop. Compressive masses, including both intraneural and
extraneural lesions, may manifest with acute or progressive onset
of symptoms (Figure 3). Finally, similar to other compressive
peripheral neuropathies, entrapment of the CPN within the
fibular tunnel by a fibrous band at the origin of the peroneus
longus muscle is a common finding and must not be overlooked
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during nerve decompression.

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Figure 3

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Presentation

In patients with an injury to the peroneal nerve, clinical

presentation varies based on the location and severity of the
injury and the presence of anatomic variations. Most commonly,
patients report the classic symptoms of foot drop or catching the
toes while ambulating. Foot drop can develop acutely or over a
period of days to weeks, depending on the etiology, and can be
complete or partial in severity. Numbness or dysesthesia may
also be present along the lateral leg, dorsal foot, and/or the first
toe web space (Figure 4). Pain may be present in some cases (eg,
traumatic wounds, compressive lesions), but it is not a common
complaint.
2

Figure 4

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Physical Examination

The clinical examination is directed by the symptoms reported

by the patient and requires a thorough understanding of the
relevant anatomy. Gait assessment may provide important clues
to the etiology of the symptoms. A patient with weakened or
paralyzed ankle dorsiflexors may ambulate with a steppage gait
in which the ipsilateral knee is lifted higher than normal during
the swing phase to avoid dragging the toes on the ground,
followed by slapping the forefoot on the ground after heel
strike. If injury to the peroneal nerve is suspected, a thorough
examination should be performed, focusing on the elements of
each component of the nerves innervation.
Numbness or dysesthesia in the upper lateral leg indicates a
lesion proximal to the fibular head, which may represent
involvement of the sciatic nerve or lumbosacral nerve
root. Tibial nerve involvement should be ruled out in this
scenario by testing foot inversion with the foot passively
dorsiflexed because inversion is normally weak in a
plantarflexed foot. If examination reveals no compromise to the
long head of the biceps femoris muscle, knee flexion strength
will likely test normal despite possible weakness of the short
head. Palpation may reveal decreased muscle contraction over
the short head, although this may be difficult to appreciate by
physical examination alone. Involvement of both the peroneal
and tibial nerve divisions of the sciatic nerve may result in
21

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decreased knee flexion, ankle plantar flexion, and toe flexion in

addition to weakness of the anterior and lateral compartments of
the leg. Muscle stretch reflex will typically be normal unless
severe damage to the sciatic nerve is present, and abductor
strength testing may help the clinician to identify a peroneal
nerve injury resulting from L5 radiculopathy.
Decreased or abnormal sensation in the lower lateral leg and the
dorsum of the foot indicates involvement of the SPN or the
portion of the sciatic nerve in those areas. Similarly, altered
sensation in the dorsal aspect of the first web space of the foot
suggests involvement of the DPN fibers. Weakness of foot
eversion (SPN involvement) or foot/toe dorsiflexion (DPN
involvement) may be present in isolation; however, appreciation
of both of these findings suggests a lesion involving the CPN
fibers. When injury about the fibular head occurs, the DPN may
be severely affected. Tenderness or a Tinel sign near the fibular
head may be present, but reflexes are typically preserved.
23

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Diagnostic Studies
Imaging

When clinical examination indicates a potential injury to the

peroneal nerve, plain radiography should be considered as part of
the initial workup. The close proximity of the CPN to the fibular
neck as well as its superficial location makes it susceptible to
injury secondary to direct trauma and impingement from both
soft-tissue and bony sources. CT may be used to further evaluate
bony abnormalities. MRI and ultrasonography should be
considered to evaluate for potential soft-tissue sources of
impingement or masses (Figure 5).
1,5

Figure 5
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Electrodiagnostic Studies

Nerve conduction velocity (NCV) studies and electromyography

(EMG) are valuable tools for diagnosing suspected peroneal
nerve palsy. These studies help the clinician evaluate the motor
and sensory axons of the peroneal nerve and its branches. They
also are useful for localizing the site of injury, determining the
severity of a lesion, and monitoring recovery after a nerve injury
has been identified. An electrophysiology study should be
performed to obtain a baseline in all patients who present with
new-onset foot drop; the study may be repeated every 3 months
to monitor for improvement or deterioration. In the setting of
traumatic injury or postoperative palsy, immediate
neurodiagnostic tests are not warranted and should not be
performed for 2 to 6 weeks.
22

Motor nerve conduction studies should be performed to evaluate

the EDB and TA muscles, with stimulation applied above and
below the fibular head. These results should be compared with
those of the contralateral extremity. Because the EDB may be
innervated by an accessory peroneal nerve from the SPN in
approximately one third of the population, stimulation of the
peroneal musculature may be performed, as well.
Sensory nerve conduction studies should be used to evaluate
both sensory branches of the SPN at the level of the ankle and
the DPN. However, SPN conduction study findings may be
normal in the setting of a neuropathy of the CPN secondary to
the increased vulnerability of the deep nerve fibers to stretch and
compression. These studies can also be specifically directed to
further delineate findings from previous studies and the clinical
examination. For example, conduction studies of the
posterolateral cutaneous nerve of the calf may be performed in
the setting of numbness in that area. Studies involving the tibial
and sural nerve distributions may be performed to help rule out
other causes of clinical findings, including plexopathy or injury
to the sciatic nerve.
Needle EMG provides further detail to help the clinician identify
the location and severity of peroneal nerve lesions. Muscles
innervated by both the DPN and SPN should be tested, including
the TA muscle, which is most commonly affected in patients with
peroneal palsy. Studies may also be performed on the short head
of the biceps and a tibial-innervated muscle distal to the knee to
identify more proximal lesions and/or injury to the sciatic nerve.
If the findings are abnormal, investigation should be extended to
include more proximal sciatic-innervated muscles, gluteal
muscles, and lumbosacral paraspinal muscles.
The results of NCV and EMG studies can help to dictate the
course of treatment. When these findings suggest a more
advanced disease state, surgical intervention may be indicated.
At our institution, when EMG/NCV studies show severe
changes, including severe conduction delay across the CPN
(>50%) on NCV and evidence on EMG of substantial disruption
of the CPN innervation to the musculature, surgical nerve
decompression is indicated and may increase the likelihood of a
favorable outcome.
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Management
Nonsurgical

When left untreated, CPN palsy is associated with foot drop,

equinovarus deformity, and limb disability ranging from 30% to
35%. Initial management of peroneal nerve palsy involves a
nonsurgical approach because partial or full function often
returns over time. In addition to knowledge of the causative
positions or activities (eg, squatting, strenuous exercise) that
25

contribute to peroneal nerve palsy, activity modification, such as

cessation of leg crossing, is crucial. Padding of the prominent
fibular head may be helpful, particularly after a direct traumatic
injury, and may be worn at night to prevent compression while
sleeping. Night splints may also be used to prevent contractures
in cases of complete foot drop.
Rehabilitation, including physical therapy and the use of orthotic
devices, may be effective for managing the symptoms of foot
drop and eversion weakness related to peroneal palsy. For
significant dorsiflexion weakness, a custom ankle-foot orthosis
may be helpful for foot clearance during ambulation. Physical
therapy should initially focus on stretching the contralateral
muscle groups, including the foot plantar flexors and inverters.
In the setting of substantial muscle weakness, electrical
stimulation may be used to initiate muscle contractions.
Progressive strengthening of the dorsiflexors and evertors should
begin once autonomous muscle contraction is present.
Back to Top | Article Outline

Surgical
Acute Injuries

Acute nerve injuries, including contusions, stretch injuries,

lacerations, and crush injuries, should be assessed to determine
the degree of functional loss. Injuries with neurapraxia should be
monitored initially because excellent results have been obtained
with nonsurgical management. A more aggressive approach
should be used for nerve injuries of any severity (including
neurapraxia) that present with complete motor or sensory loss.
Surgical exploration and decompression should be considered
when a rapidly deteriorating lesion is present or there are no of
signs of improvement within 3 months. For open injuries with a
suspected nerve laceration, the nerve should be explored within
72 hours, if possible, and if minimal gapping is found at the site
of injury, primary repair should be attempted with an epineurial
or fascicular technique. A clinical study of surgical nerve repair
showed that there was no single superior epineurial or fascicular
technique. In the setting of wound contamination, dbridement
of the wound and nerve edges, suturing of the local soft tissues,
and a repair performed within 2 to 7 days is acceptable.
If primary repair is not possible secondary to significant gapping
or nerve damage, nerve grafting is indicated. This can be done as
a primary procedure but is more commonly done as a delayed
procedure. Autologous grafting is the standard of care, with sural
nerve graft most commonly used. Alternatively, nerve conduits,
including veins, bioabsorbable tubes, and pseudosheaths, may be
used. These conduits have been shown to regenerate nerves
across short gaps (<3 cm), with reported results comparable to
those of autograft.
Although the efficacy of nerve transfer remains unproven, this
technique is an emerging option for irreparable nerve injuries,
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such as those with segmental nerve loss or a long regeneration

distance. The principles of nerve transfer are similar to those of
tendon transfer; an attempt is made to select the most synergistic
nerve, and in the case of irreparable CPN nerve injury, this is
most commonly a branch of the tibial nerve.
29

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Compressive Masses

When a mass is found to be the cause of compression, a

thorough workup and evaluation should be performed before
invasive treatment is initiated. As with any tumor, the clinician
must assess the mass to determine whether it is malignant.
Excision of a compressive mass is similar to excision of a mass
elsewhere in the body, and lesions causing significant or
progressive motor loss should be removed, as well. Extraneural
lesions, such as fibular osteochondromas, vascular
malformations, or extraneural cysts, should be resected in the
standard fashion. Compression of the peroneal nerve by such
benign extraneural masses is rare but should nonetheless be
included in the differential diagnosis.
Intraneural lesions should be approached with caution because
surgical dissection of these lesions is more meticulous and
difficult (Figure 6). Referral to an orthopaedic oncologist or a
specialist skilled in microsurgery should be considered. An
experienced surgeon should perform resection of schwannomas
and neurofibromas using an appropriate technique at the
fascicular level and intraoperative nerve monitoring. Nerve
monitoring can assist the clinician in localizing the lesion and
confirming nerve function after dissection. Intraneural ganglion
cysts originate from the superior tibiofibular joint and should be
dissected free, with the stalk traced and disconnected from the
joint to prevent recurrence. Good outcomes can be obtained
with surgical management of intraneural lesions by an
experienced surgeon. Suspected malignancy should be confirmed
with a frozen section unless a biopsy has been performed.
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Figure 6
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Idiopathic/Postoperative Compression

Surgical decompression should be considered for management of

compressive lesions at the fibular head or fibular tunnel and
nerve palsies that present after knee arthroplasty or high tibial
osteotomy if no improvement is seen after a trial of nonsurgical
management. Although the time frame for nonsurgical
management is controversial, most authors agree that a minimum
trial of 3 months should be attempted because improvement in
nerve function may be seen for up to 6 months. However, if the
patient fails to show clinical signs of improvement or if motor
33

loss is rapidly progressive, decompression is warranted.

Similarly, when EMG and/or NCV studies show evidence of
severe conduction loss or disruption of motor innervation,
surgical intervention should be more strongly considered over
nonsurgical treatment. Favorable outcomes have been reported
with the use of neurolysis, with return of function reported in up
to 97% of cases in one study.
34

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Authors Preferred Technique

Our preferred technique for CPN release at the proximal fibula

provides comprehensive decompression and adequate exposure
for concomitant procedures, such as excision of a mass. The
patient is placed in the lateral recumbent position with the
affected leg up, using a bean bag to secure the pelvis. The fibular
head is marked, and the CPN can be palpated beneath the
subcutaneous tissues just distal to this landmark (Figure 7). An
oblique or curvilinear incision is made beginning posterior to the
fibular head near the anterior popliteal fossa and courses
anteriorly and distally for approximately 6 cm. Dissection is
carried through the subcutaneous tissues, with care taken to
avoid the lateral cutaneous nerve in the calf in the proximal
aspect of the incision.
Figure 7

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The CPN is palpated just distal to the fibular head, and the fascia
overlying the nerve is incised and opened. The nerve is
cautiously dissected and inspected in this region and then tagged
with a vessel loop. The fascia overlying the peroneus longus
muscle is then incised in line with the incision. After the nerve is
exposed deep to the peroneus longus, three intermuscular septal
planes are encountered and released. The posterior crural
intermuscular septum is the first intermuscular plane
encountered, and it is the most important to release because it is
the most common site of nerve compression. When the nerve is
free distal to the bifurcation into the SPN and DPN, neurolysis is
adequate.
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Tendon Transfer

Tendon transfer also may be used to restore function to the foot

and ankle in refractory cases. This procedure typically involves
transfer of the posterior tibial tendon (PTT) to the lateral
cuneiform or cuboid, which removes the primary deforming
force to restore ankle dorsiflexion. Goh et al compared two
methods of PTT transfer: (1) subcutaneous transfer around the
medial aspect of the tibia and (2) transfer of the tendon through
the interosseous membrane to the dorsal foot. Biomechanically,
the transinterosseous membrane technique provided superior
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ankle dorsiflexion with minimum pronation. Although many

variations exist, techniques for transferring the PTT through the
interosseous membrane typically involve harvesting the tendon
at its insertion, delivering it through a proximal incision, passing
it through the interosseous membrane, and anchoring it into the
dorsal midfoot (Figure 8).
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Figure 8

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An incision is made just distal to the medial malleolus, extending

approximately 5 cm to expose the PTT. The tendon is then
harvested subperiosteally from distal to proximal at the
naviculocuneiform joint to ensure adequate tendon length. A
second incision is made approximately 15 cm proximal to the tip
of the medial malleolus. Dissection is carefully performed and
the saphenous vein and nerve are retracted anteriorly to expose
the fascia overlying the deep posterior compartment. The soleus
and flexor digitorum longus muscles are retracted posteriorly,
exposing the PTT adjacent to the tibia and interosseous
membrane. The PTT is pulled through the proximal incision and
tagged with suture. A 5-cm incision is made along the anterior
border of the fibula. The distal end of the incision is identified by
placing the PTT over the anterolateral aspect of the leg. After
careful dissection and retraction of the EDL medially,
approximately 4 cm of the interosseous membrane is dissected
off the fibula and excised to allow passage of the PTT. The PTT
is transferred from the medial proximal incision to the lateral
incision. Care must be taken to pass directly posterior to the tibia
to prevent damage to the neurovascular bundle. The tendon is
then passed subcutaneously to a dorsal incision made over the
lateral cuneiform. The PTT is then anchored into the lateral
cuneiform using interference screw fixation.
One potential downfall of this method is inadequate tendon
length, which may require maximal dorsiflexion of the ankle or
changing the location of the tendon insertion to achieve a stable
transfer. Tendon-to-tendon suturing is an alternative to this
technique. Direct tendon-to-tendon suturing, however, often
decreases dorsiflexion strength because of dispersion of the force
supplied by the PTT, and it may lead to an unbalanced
foot. Vigasio et al described a technique in which the PTT is
transferred to the anterior tibial tendon (rerouted through a new
insertion on the lateral cuneiform) and the flexor digitorum
longus is transferred to the EDL and extensor hallucis longus
tendons (Figure 9). The technique was performed in 16 patients
with complete CPN palsy, and at a minimum follow-up of 24
months, the authors noted good to excellent results in >80% of
their patients. The authors concluded that this method is a
reliable means for obtaining balanced dorsiflexion of the foot
and toes, eliminating the need for orthoses during ambulation.
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Figure 9
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The timing of the procedure is somewhat controversial.

Traditionally, this procedure has been performed in a delayed
fashion to await possible return of nerve function. This often
resulted in the patient waiting approximately 1 year after the
initial injury or attempted nerve repair to monitor neurologic
activity. Some studies, however, suggest that tendon transfers
should be considered as early as 3 to 4 months after the initial
injury to prevent development of significant equinus contracture
and atrophy of the ankle dorsiflexors and to improve
regeneration of nerve fibers when tendon transfer is combined
with nerve repair and/or grafting procedures.
39,40

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Summary

CPN palsy is the most common compressive neuropathy of the

lower extremity. The most common presentation is acute foot
drop, although symptoms may be progressive and may include
sensory loss or pain. Most instances of CPN palsy improve or
resolve over time with nonsurgical measures. Surgery is typically
reserved for refractory cases, although some circumstances (eg,
EMG and/or NCV findings, the presence of a compressive mass,
an acute open injury) warrant earlier intervention. When nerve
decompression or repair is unsuccessful or the prognosis for
nerve recovery is poor, nerve or tendon transfers may restore
some function.
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References

Evidence-based Medicine: Levels of evidence are described in

the table of contents. In this article, reference 10 is a level II
study. References 4, 7, 12, 14, 16, 29, 34, 35, and 40 are level III
studies. References 13, 17, 19, 31-33, and 36-38 are level IV
studies. References 6, 15, 18, and 30 are level V expert opinion.
References printed in bold type are those published within the
past 5 years.
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8. Sunderland S: A classification of peripheral nerve injuries
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10. Park JH, Hozack B, Kim P, et al.: Common peroneal nerve
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Keywords:
Peroneal nerve palsy; foot drop; nerve decompression; nerve
injury; nerve repair; grafting
2016 by American Academy of Orthopaedic Surgeons

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