Review Article

Peroneal Nerve Palsy: Evaluation

and Management

Chad Poage, DO
Charles Roth, MD
Brandon Scott, MD
From the Andrews Research and
Education Foundation, Gulf Breeze,
FL (Dr. Poage and Dr. Roth), the
Abstract
Peroneal nerve palsy is the most common entrapment neuropathy of
the lower extremity. Numerous etiologies have been identified;
however, compression remains the most common cause. Although
injury to the nerve may occur anywhere along its course from the sciatic
origin to the terminal branches in the foot and ankle, the most common
site of compressive pathology is at the level of the fibular head. The
most common presentation is acute complete or partial foot drop.
Associated numbness in the foot or leg may be present, as well.
Neurodiagnostic studies may be helpful for identifying the site of a
lesion and determining the appropriate treatment and prognosis.
Management varies based on the etiology or site of compression.
Many patients benefit from nonsurgical measures, including activity
modification, bracing, physical therapy, and medication. 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.

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).
Dr. Roth or an immediate family
member has received research or
institutional support from Arthrex.
Neither of the following authors nor
any immediate family member has
received anything of value from or has
stock or stock options held in a
commercial company or institution
related directly or indirectly to the
subject of this article: Dr. Poage and
Dr. Scott.
J Am Acad Orthop Surg 2016;24:1-10
http://dx.doi.org/10.5435/
JAAOS-D-14-00420
Copyright 2015 by the American
Academy of Orthopaedic Surgeons.
C
ommon peroneal nerve (CPN)
palsy is associated with the onset
of acute and progressive foot drop and
is the most common compressive neu-
ropathy of the lower extremity.1,2
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.3,4 As
with all compressive neuropathies, the
key to a successful outcome is early
identification and treatment.4
Peripheral Nerve Structure
and Pathophysiology
When evaluating patients with dis-
orders 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 en-
cased 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.5 In 1942,
Seddon6 described a classification
system for peripheral nerve 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). Ax-
onotmesis is characterized by axon
discontinuity, with the development of
wallerian degeneration being the key

January 2016, Vol 24, No 1 1

Copyright ª the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
Peroneal Nerve Palsy: Evaluation and Management

Figure 1

Illustration of a normal nerve fiber and the three grades of nerve injury described by Seddon.6

Table 1
Classification of Nerve Injuries Described by Seddon6 and Sunderland8
Seddon Sunderland Injury Neurosensory Impairment Recovery Potential

Neurapraxia I Intrafascicular edema with Neuritis and paresthesia Full/good; 1 wk to 2 mo

conduction block and possible
segmental demyelination
Axonotmesis II Axon severed, endoneurial tube Paresthesia, episodic Full/fair; 2–4 mo
intact dysesthesia
Axonotmesis III Endoneurial tube torn Paresthesia, dysesthesia Incomplete/fair; 12 mo
Axonotmesis IV Only epineurium intact Hypoesthesia, dysesthesia, Incomplete/poor;
neuroma formation neuroma in continuity
Neurotmesis V Loss of continuity Anaesthetic, intractable pain, None
neuroma formation

Adapted with permission from Juodzbalys G, Wang HL, Sabalys G: Injury of the inferior alveolar nerve during implant placement: A literature review.
J Oral Maxillofac Res 2011;2(1):e1.

component. Neurotmesis, the most
severe nerve injury, is complete dis-
ruption of the nerve, including sep-
aration of the axons and the
epineurium. Although full or partial
spontaneous recovery is expected
with neurapraxia and axonotmesis,
minimal recovery is expected with
neurotmesis.7 In 1951, Sunderland8
modified this classification by cate-
gorizing nerve injury by five degrees
and incorporating clinical ramifica-
tions as well as potential nerve
healing (Table 1).
With acute nerve compression, dys-
function 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 conduc-
tion 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.9 Axonal
degeneration is seen with compression
lasting 4 weeks.

2 Journal of the American Academy of Orthopaedic Surgeons

Copyright ª the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.

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.10
The peroneal division of the sciatic
nerve travels through the posterior
compartment of the thigh and sup-
plies 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 inter-
muscular septum and becomes sub-
cutaneous while it curves around the
head of the fibula deep to the per-
oneus longus muscle (Figure 2). The
lateral cutaneous nerve of the calf
branches off here, and the nerve
subsequently divides into the super-
ficial 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.11
The SPN travels distally in the
lateral compartment of the leg,
providing motor innervation to the
peroneus longus and peroneus bre-
vis 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
January 2016, Vol 24, No 1
Copyright ª the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
Chad Poage, DO, et al
as the intermediate and medial dorsal Figure 2
cutaneous nerves.
The DPN travels for 3 to 4 cm
along the anterior cortex of the fib-
ula and then courses distally. It then
courses just anterior and medial to
the intermuscular septum between
the anterior and lateral compart-
ments 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 ti-
bialis anterior (TA), extensor dig-
itorum 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.
Etiology Illustration of the knee joint
demonstrating the course of the
The etiologies for peroneal nerve common peroneal nerve (CPN) as it
wraps around the fibular neck and
palsy are numerous. Although branches into its three terminal
compressive etiology remains the branches. PL = peroneus longus
most common cause, many other muscle, SN = sciatic nerve,
factors contribute to injury. Trau- TN = tibial nerve
matic causes include knee disloca-
tion, severe ankle inversion injuries,
lacerations, and direct blunt weight loss has been shown to be
trauma. These traumatic injuries related to nerve compression at the
are typically associated with poorer fibular head and may be associated
outcomes.12,13 The link between with the loss of subcutaneous fat at this
diabetes mellitus and lower ex- level.19 Habitual leg crossing and
tremity neuropathies (eg, poly- prolonged squatting are also associ-
neuropathy, mononeuropathy) has ated with an increased risk of pero-
been well established.14 Iatrogenic neal palsy and acute foot drop.1
injury is common as well, with Compressive masses, including both
acute foot drop often seen as a intraneural and extraneural lesions,
result of surgery about the hip, may manifest with acute or pro-
knee, and ankle; positioning during gressive onset of symptoms (Figure 3).
anesthesia; prolonged bed rest; cast- Finally, similar to other compressive
ing; bracing; compression wrapping; peripheral neuropathies, entrapment
and the use of pneumatic compression of the CPN within the fibular tunnel
devices.15-18 by a fibrous band at the origin of the
Several risk factors for compres- peroneus longus muscle is a common
sive peroneal neuropathy have been finding and must not be overlooked
described. A recent history of significant during nerve decompression.20
3
Peroneal Nerve Palsy: Evaluation and Management
Figure 3
Intraoperative photograph
demonstrating a tibiofibular cyst that
caused peroneal nerve compression
and foot drop in a 43-year-old man.
(Courtesy of Andrews Research and
Education Foundation, Gulf Breeze,
FL.)
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 com-
monly, 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
Physical Examination
The clinical examination is directed
by the symptoms reported by the
patient and requires a thorough
understanding of the relevant anat-
omy. Gait assessment may provide
important clues to the etiology
4 Journal of the American Academy of Orthopaedic Surgeons
Copyright ª the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
Figure 4
Clinical photograph of the feet in a
patient with right foot drop and
abnormal sensation in the superficial
peroneal nerve (dorsum of foot) and
the deep peroneal nerve (web space
between great toe and second toe).
The skin markings indicate the area of
altered sensation. (Reproduced with
permission from Stewart JD: Foot
drop: Where, why, and what to do?
Pract Neurol 2008;8[3]:158-169.)
of the symptoms. A patient with
weakened or paralyzed ankle dor-
siflexors 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.21 If
injury to the peroneal nerve is sus-
pected, a thorough examination
should be performed, focusing on
the elements of each component of
the nerve’s 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.22 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 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 pres-
ent, and abductor strength testing
may help the clinician to identify a
peroneal nerve injury resulting from
L5 radiculopathy.23
Decreased or abnormal sensation
in the lower lateral leg and the dor-
sum 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 dorsi-
flexion (DPN involvement) may be
present in isolation; however, appre-
ciation of both of these findings sug-
gests 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.
Diagnostic Studies
Imaging
When clinical examination indicates a
potential injury to the peroneal nerve,
plain radiography should be consid-
ered as part of the initial workup. The
close proximity of the CPN to the fib-
ular 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
masses1,5 (Figure 5).
Electrodiagnostic Studies
Nerve conduction velocity (NCV)
studies and electromyography (EMG)
are valuable tools for diagnosing sus-
pected peroneal nerve palsy. These
studies help the clinician evaluate the
motor and sensory axons of the pero-
neal 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.22 An electrophysi-
ology 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 dete-
rioration. In the setting of traumatic
injury or postoperative palsy, immedi-
ate neurodiagnostic tests are not war-
ranted and should not be performed
for 2 to 6 weeks.
Motor nerve conduction studies
should be performed to evaluate the
EDB and TA muscles, with stimula-
tion applied above and below the fib-
ular head. These results should be
compared with those of the contralat-
eral extremity. Because the EDB may
be innervated by an accessory pero-
neal nerve from the SPN in approxi-
mately one third of the population,
stimulation of the peroneal muscula-
ture may be performed, as well.24
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 set-
ting of a neuropathy of the CPN
secondary to the increased vulnera-
bility of the deep nerve fibers to
stretch and compression.22 These
studies can also be specifically
directed to further delineate find-
ings from previous studies and the
January 2016, Vol 24, No 1
Copyright ª the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
Figure 5
A, Longitudinal sonogram of the fibula demonstrating a normal peroneal nerve
(PN) and fibula (F). B, Longitudinal sonogram demonstrating an intraneural
ganglion. (Reproduced with permission from Visser LH: High-resolution
sonography of the common peroneal nerve: Detection of intraneural ganglia.
Neurology 2006;67[8]:1473-1475.)
clinical examination. For example,
conduction studies of the postero-
lateral 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.24
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.22
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
Chad Poage, DO, et al
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 sub-
stantial disruption of the CPN inner-
vation to the musculature, surgical
nerve decompression is indicated and
may increase the likelihood of a
favorable outcome.
Management
Nonsurgical
When left untreated, CPN palsy is
associated with foot drop, equi-
novarus deformity, and limb disability
ranging from 30% to 35%.25 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 contribute to peroneal
nerve palsy, activity modification,
such as cessation of leg crossing, is
crucial. Padding of the prominent
fibular head may be helpful, particu-
larly after a direct traumatic injury,
and may be worn at night to prevent
compression while sleeping. Night
5
Peroneal Nerve Palsy: Evaluation and Management
Figure 6
Axial proton density-weighted
magnetic resonance image of the leg
below the knee. The tibia lies
superiorly and to the left, and the
fibula lies inferiorly and to the right. A
large mass (arrow) is visible lateral to
the neck of the fibula, compressing
the common peroneal nerve and
resulting in a peroneal neuropathy.
The neuroma arose from a branch of
the nerve and was excised.
(Reproduced with permission from
Loredo R, Hodler J, Pedowitz R,
et al: MRI of the common peroneal
nerve: Normal anatomy and
evaluation of masses associated
with nerve entrapment. J Comput
Assist Tomogr 1998;22:925-931.)
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 manag-
ing the symptoms of foot drop
and eversion weakness related to
peroneal palsy. For significant dorsi-
flexion weakness, a custom ankle-
foot orthosis may be helpful for foot
clearance during ambulation. Physi-
cal therapy should initially focus on
stretching the contralateral muscle
groups, including the foot plantar
flexors and inverters. In the setting of
substantial muscle weakness, elec-
trical stimulation may be used to ini-
tiate muscle contractions. Progressive
strengthening of the dorsiflexors and
evertors should begin once autono-
mous muscle contraction is present.
6 Journal of the American Academy of Orthopaedic Surgeons
Copyright ª the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
Surgical
Acute Injuries
Acute nerve injuries, including con-
tusions, stretch injuries, lacerations,
and crush injuries, should be as-
sessed to determine the degree of
functional loss. Injuries with neu-
rapraxia should be monitored ini-
tially because excellent results have
been obtained with nonsurgical
management.26 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 decom-
pression 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 possi-
ble, and if minimal gapping is found
at the site of injury, primary repair
should be attempted with an epi-
neurial or fascicular technique. A
clinical study of surgical nerve
repair showed that there was no
single superior epineurial or fas-
cicular technique.27 In the setting of
wound contamination, débride-
ment 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 pro-
cedure. Autologous grafting is the
standard of care, with sural nerve
graft most commonly used. Alter-
natively, 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.28
Although the efficacy of nerve
transfer remains unproven, this
technique is an emerging option for
irreparable nerve injuries, such as
those with segmental nerve loss or a
long regeneration distance. The prin-
ciples 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 com-
monly a branch of the tibial nerve.29
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 initi-
ated. As with any tumor, the clini-
cian must assess the mass to
determine whether it is malignant.
Excision of a compressive mass is
similar to excision of a mass else-
where 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 pero-
neal nerve by such benign extra-
neural masses is rare but should
nonetheless be included in the dif-
ferential diagnosis.30
Intraneural lesions should be ap-
proached with caution because sur-
gical dissection of these lesions
is more meticulous and difficult
(Figure 6). Referral to an orthopae-
dic oncologist or a specialist skilled
in microsurgery should be consid-
ered. An experienced surgeon should
perform resection of schwannomas
and neurofibromas using an appro-
priate technique at the fascicular
level and intraoperative nerve mon-
itoring.31 Nerve monitoring can
assist the clinician in localizing the
lesion and confirming nerve function
after dissection. Intraneural ganglion
cysts originate from the superior
 Chad Poage, DO, et al

tibiofibular joint and should be dis- Figure 7

sected free, with the stalk traced and
disconnected from the joint to pre-
vent recurrence.32 Good outcomes
can be obtained with surgical man-
agement of intraneural lesions by
an experienced surgeon. Suspected
malignancy should be confirmed
with a frozen section unless a biopsy
has been performed.

Idiopathic/Postoperative
Compression
Surgical decompression should be
considered for management of com-
pressive lesions at the fibular head or
fibular tunnel and nerve palsies that
present after knee arthroplasty or
high tibial osteotomy if no improve-
ment is seen after a trial of non-
surgical management. Although the
time frame for nonsurgical manage-
ment 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.33 How- Intraoperative photographs demonstrating the authors’ preferred technique for
ever, if the patient fails to show surgical management of peroneal nerve palsy. A, The fibular head and incision
clinical signs of improvement or if are marked on the skin. B, The common fibular nerve is identified proximally and
tagged with a vessel loop. C, Incision of the fibular tunnel at the site of
motor loss is rapidly progressive, compression. D, The nerve is released, as distally as possible, down to the
decompression is warranted. Simi- bifurcation into superficial and deep peroneal nerve branches. (Reproduced with
larly, when EMG and/or NCV permission from Maalla R, Youssef M, Ben Lassoued N, Sebai MA, Essadam H:
studies show evidence of severe Peroneal nerve entrapment at the fibular head: Outcomes of neurolysis. Orthop
Traumatol Surg Res 2013;99[6]:719-722.)
conduction loss or disruption of
motor innervation, surgical inter-
vention should be more strongly
secure the pelvis. The fibular head is The nerve is cautiously dissected and
considered over nonsurgical treat-
marked, and the CPN can be pal- inspected in this region and then
ment. Favorable outcomes have
pated beneath the subcutaneous tis- tagged with a vessel loop. The fascia
been reported with the use of
sues just distal to this landmark overlying the peroneus longus muscle
neurolysis, with return of function
(Figure 7). An oblique or curvilinear is then incised in line with the inci-
reported in up to 97% of cases in
incision is made beginning posterior sion. After the nerve is exposed deep
one study.34
to the fibular head near the anterior to the peroneus longus, three inter-
popliteal fossa and courses anteri- muscular septal planes are encoun-
Authors’ Preferred Technique orly and distally for approximately 6 tered and released. The posterior
Our preferred technique for CPN cm. Dissection is carried through the crural intermuscular septum is the
release at the proximal fibula pro- subcutaneous tissues, with care first intermuscular plane encoun-
vides comprehensive decompression taken to avoid the lateral cutaneous tered, and it is the most important to
and adequate exposure for concomi- nerve in the calf in the proximal release because it is the most common
tant procedures, such as excision of a aspect of the incision. site of nerve compression. When the
mass. The patient is placed in the The CPN is palpated just distal to nerve is free distal to the bifurcation
lateral recumbent position with the the fibular head, and the fascia over- into the SPN and DPN, neurolysis is
affected leg up, using a bean bag to lying the nerve is incised and opened. adequate.

January 2016, Vol 24, No 1 7

Copyright ª the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
Peroneal Nerve Palsy: Evaluation and Management

Figure 8

Intraoperative photographs of the ankle demonstrating the transfer of the posterior tibialis tendon (PTT) to the lateral
cuneiform to restore ankle dorsiflexion. A, An incision is made just distal to the medial malleolus, extending
approximately 5 cm to expose the PTT, and the tendon is harvested subperiosteally from distal to proximal at the
naviculocuneiform joint to ensure adequate tendon length. B, A second incision is made approximately 15 cm proximal
to the tip of the medial malleolus. C, The PTT is delivered through the proximal incision and tagged with suture to
facilitate transfer. D, The skin is marked for a 5-cm incision along the anterior border of the fibula. E, The PTT is
transferred from the medial proximal incision to the lateral incision. (Reproduced with permission from Ho B, Khan Z,
Switaj PJ, et al: Treatment of peroneal nerve injuries with simultaneous tendon transfer and nerve exploration. J Orthop
Res Surg 2014;9:67-77.)

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.35 Goh
et al36 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 ankle
dorsiflexion with minimum pro-
nation. Although many variations
exist, techniques for transferring the
PTT through the interosseous mem-
brane typically involve harvesting the
tendon at its insertion, delivering it
through a proximal incision, passing
it through the interosseous mem-
brane, and anchoring it into the
dorsal midfoot35 (Figure 8).
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 poste-
rior compartment. The soleus and
flexor digitorum longus muscles are
retracted posteriorly, exposing the
PTT adjacent to the tibia and inter-
osseous membrane. The PTT is
pulled through the proximal inci-
sion 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 plac-
ing the PTT over the anterolateral
aspect of the leg. After careful dis-
section 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 proxi-
mal incision to the lateral incision.

8 Journal of the American Academy of Orthopaedic Surgeons

Copyright ª the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
 Chad Poage, DO, et al

Care must be taken to pass directly Figure 9

posterior to the tibia to prevent
damage to the neurovascular bun-
dle. The tendon is then passed sub-
cutaneously 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 dorsi-
flexion 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.37 Vigasio Illustrations demonstrating the anterior tibialis tendon transfer technique
described by Vigasio et al.37 A, The anterior tibialis tendon (dashed lines) is
et al38 described a technique in
identified. B, The tendon is extracted distally from beneath the retinaculum, as
which the PTT is transferred to the indicated by the arrow, and a drill hole is created from the medial to the lateral
anterior tibial tendon (rerouted cuneiform. C, The tendon is passed to its new origin and is pulled proximally
through a new insertion on the lat- under the retinaculum, as indicated by the arrow, and reattached to the posterior
tibialis tendon transferred through the interosseous membrane.
eral cuneiform) and the flexor dig-
itorum longus is transferred to the
EDL and extensor hallucis longus of significant equinus contracture or the prognosis for nerve recovery is
tendons (Figure 9). The technique and atrophy of the ankle dorsiflexors poor, nerve or tendon transfers may
was performed in 16 patients with and to improve regeneration of nerve restore some function.
complete CPN palsy, and at fibers when tendon transfer is com-
a minimum follow-up of 24 months, bined with nerve repair and/or graft-
the authors noted good to excellent ing procedures.39,40 References
results in .80% of their patients.
The authors concluded that this Evidence-based Medicine: Levels of
method is a reliable means for ob- evidence are described in the table of
Summary
taining balanced dorsiflexion of the contents. In this article, reference 10
foot and toes, eliminating the need CPN palsy is the most common com- is a level II study. References 4, 7, 12,
for orthoses during ambulation. pressive neuropathy of the lower 14, 16, 29, 34, 35, and 40 are level
The timing of the procedure is extremity. The most common pre- III studies. References 13, 17, 19, 31-
somewhat controversial. Tradition- sentation is acute foot drop, although 33, and 36-38 are level IV studies.
ally, this procedure has been per- symptoms may be progressive and may References 6, 15, 18, and 30 are level
formed in a delayed fashion to await include sensory loss or pain. Most V expert opinion.
possible return of nerve function. instances of CPN palsy improve or References printed in bold type are
This often resulted in the patient resolve over time with nonsurgical those published within the past 5 years.
waiting approximately 1 year after measures. Surgery is typically reserved
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January 2016, Vol 24, No 1 9

Copyright ª the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
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