Peroneal Mononeuropathy Treatment &

Management
Author
Shaheen E Lakhan, MD, PhD, MS, MEd Associate Professor of Neurology and Medical
Education, Assistant Dean of Curriculum (Years 3-4), California University of Science and
Medicine School of Medicine
Shaheen E Lakhan, MD, PhD, MS, MEd is a member of the following medical societies:
American Academy of Neurology
Disclosure: Nothing to disclose.
Specialty Editor Board
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska
Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Glenn Lopate, MD Associate Professor, Department of Neurology, Division of
Neuromuscular Diseases, Washington University School of Medicine; Consulting Staff,
Department of Neurology, Barnes-Jewish Hospital
Glenn Lopate, MD is a member of the following medical societies: American Academy of
Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, Phi
Beta Kappa
Disclosure: Nothing to disclose.
Chief Editor
Nicholas Lorenzo, MD, MHA, CPE Founding Editor-in-Chief, eMedicine Neurology;
Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc
Nicholas Lorenzo, MD, MHA, CPE is a member of the following medical societies: Alpha
Omega Alpha, American Association for Physician Leadership, American Academy of
Neurology
Disclosure: Nothing to disclose.
Additional Contributors
Aashit K Shah, MD, FAAN, FANA Professor and Associate Chair of Neurology, Director,
Comprehensive Epilepsy Program, Program Director, Clinical Neurophysiology Fellowship,
Detroit Medical Center, Wayne State University School of Medicine

Aashit K Shah, MD, FAAN, FANA is a member of the following medical societies: American
Academy of Neurology, American Neurological Association, American Clinical
Neurophysiology Society, American Epilepsy Society
Disclosure: Received consulting fee from UCB pharma for speaking and teaching; Received
grant/research funds from UCB Pharma for other; Received consulting fee from Sunovion for
speaking and teaching; Received consulting fee from Lundbeck for speaking and teaching.
Pinky Agarwal, MD Clinical Associate Professor, Department of Neurology, University of
Washington School of Medicine; Attending Neurologist, Medical Director, Booth Gardner
Parkinson's Care Center
Pinky Agarwal, MD is a member of the following medical societies: American Academy of
Neurology, International Parkinson and Movement Disorder Society
Disclosure: Nothing to disclose.
Alida Griffith, MD Movement Disorders Neurologist, Booth Gardner Parkinsons Care
Center
Disclosure: Nothing to disclose.

Background
Mononeuropathies are a form of peripheral neuropathy characterized by sensory disturbances
and/or motor deficits in the distribution of the affected nerve. They can occur secondary to
direct trauma, compression, stretch injury, ischemia, infection, or inflammatory disease. In
the lower extremity, peroneal neuropathy is the most common isolated mononeuropathy and
the third most common mononeuropathy overall. Peroneal mononeuropathy may result in the
clinical complaint of pain and sensory disturbances in the lateral lower limb and dorsal
foot, and weakness of the ankle dorsiflexors and evertors.

Pathophysiology
Compression and entrapment neuropathies are predominantly demyelinating.

Myelin loss results in slowing of the nerve conduction through the area involved.

When acute compression occurs, this may result in a conduction block. When the
compression is more chronic, only slowing across the involved segment may be seen.

When compression is severe, ischemic changes occur that cause secondary axonal
damage.

Pure demyelinating lesions typically have a better capacity to recover.

The pathophysiology of ischemic injuries and nerve transection is axonal damage. When
axonal damage occurs, recovery is slower and longer and may not be complete.

This results in wallerian degeneration distally, and recovery requires the nerve to
regenerate and reinnervate.

This process is slower than healing from other types of injuries and may not be
complete.

Nerve conduction studies and electromyography (EMG) can aid in defining the lesion
location and type.

Knowledge of peroneal nerve anatomy is essential to understanding the mechanism of its

injury and to localizing the site of the lesion.[1]

The peroneal nerve is a division of the sciatic nerve, which splits at or slightly above
the popliteal fossa to form the tibial and common peroneal nerves.

The common peroneal nerve extends anterolaterally to wind around the neck of the
fibula.

At this level, the nerve is superficial, covered only by skin and subcutaneous tissue.
Here, it is predisposed to direct compression.

The nerve then dives into the peroneus longus muscle, where tethering can occur,
making it susceptible to stretch injury at this level.

The nerve then divides into the superficial and deep peroneal branches.
o The superficial branch supplies the foot everters and sensation to the skin of
the lateral calf and dorsum of the foot.
o The deep peroneal branch supplies the foot and toe dorsiflexors and has a
small sensory component, which innervates only the skin of the web space
between the first and second toes.

Epidemiology
Race
No racial predilection is known.

Sex
No gender proclivity is known.

Age

Peroneal mononeuropathy is uncommon in children but has been reported in all age groups.

Profession
Dancers are also prone to superficial and deep peroneal nerve entrapments.[2]

Prognosis
Common peroneal nerve decompression is a useful procedure to improve sensation and
strength as well as to decrease pain.[3]
A retrospective study evaluated electrodiagnostic prognostic factors after peroneal nerve
injury in 39 subjects. Outcome was associated with compound muscle action potential
responses from extensor digitorum brevis and tibialis anterior: 81% of subjects with any
tibialis anterior response and 94% with any extensor digitorum brevis response had a good
outcome (at least 4 of 5 ankle dorsiflexion strength) compared with those with absent
responses (46% and 52%, respectively). In addition, all patients with nontraumatic
compression had a good outcome.[4]

History
See the list below:

Patients with peroneal mononeuropathy present with frequent tripping due to a foot
drop.

Night cramps may occur in the anterior lower leg early in the course (if the
compression is chronic).

If the compression is acute, the symptoms are likely to be maximal at onset.

Pain may occur at the site of compression and early in the lateral lower leg and foot.

Sensory disturbances (e.g. tingling, numbness) in the lateral lower leg and foot may
be noted.

Physical
See the list below:

If the lesion is severe, a complete foot drop that spares plantar flexion and foot
inversion is noted (compared with L5 radiculopathy, lumbosacral plexopathy, or
sciatic neuropathy).

The gait will be high-stepping with "foot slapping."

In milder cases, weakness of foot eversion and dorsiflexion may be noted only by
asking the patient to walk on his or her heels.

Tapping of the nerve at the fibular head may produce pain and tingling in the peroneal
sensory nerve distribution.

Distribution of peroneal sensory disturbance assists in localizing the lesion.

Numbness in the lower part of the lateral distal leg suggests superficial peroneal
sensory involvement, while numbness of the upper part of the lateral distal leg
suggests deep peroneal sensory distribution (see following image). With common
peroneal lesions, sensory loss is noted over the lateral calf and dorsum of the foot but
spares the fifth toe.

Peroneal sensory distribution: The striped area

is the superficial peroneal sensory distribution. The green solid area represents the
deep peroneal sensory distribution. All 3 areas shaded would be numb in a patient
with a common peroneal nerve lesion.

Causes
Peroneal neuropathies are classically associated with external compression at the level of the
fibular head.

The most common etiology is habitual leg crossing (which compresses this area).

Prolonged positioning with pressure at this area (e.g. sitting on an airplane or

positioning during surgery) are other causes. Peroneal nerve entrapment has been
reported at the fibular head on the hemiparetic side in stroke patients.[5]

Isolated acute repetitive strain injury such as repetitive kicking[6] and dancing[2] .

Short casts or braces around this area can be factors in external compression.

Other causes include operative trauma (knee surgery), fibular fracture, fibular head
osteochondroma[7] , blunt or open trauma, and intrinsic masses (e.g. ganglionic cysts,
schwannoma, lipoma)[8] .

Knee dislocation or bicruciate injury can cause peroneal nerve injury in 10-40% of
cases.[9] The superficial peroneal nerve is at risk for traction injury during an ankle
inversion sprain.[10] Varus deformity in osteoarthritis of the knee can result in peroneal
nerve injury with conduction block at the fibular neck.[11]

Lack or loss of the fat pad over the fibular head due to a thin body habitus or sudden
weight loss such as after bariatric surgery[12] or anorexia nervosa[13] predisposes the
nerve to external compression at this site.

The peroneal nerve, if tethered where it dives into the peroneus longus muscle, also
may be damaged by stretch injury. Causes include prolonged squatting or a sudden
stretch.

Foot drop can be a presentation of exertional compartment syndrome.[14] It has been

observed in weight lifters[4] and football players[15] and can be associated with anabolic
steroid use.[16]

Other conditions that mimic peroneal mononeuropathy include sciatic nerve lesions.
Sciatic nerve lesions involving predominantly the peroneal division are difficult to
distinguish clinically. If the foot drop is associated temporally with hip surgery or
trauma, then it is more likely to be due to sciatic nerve involvement.

L5 radiculopathy can also present with a foot drop but can be distinguished clinically
from a peroneal mononeuropathy by involvement of the foot inverters.

Generalized neuropathy can present with slowly progressive, bilateral foot drop but
also is associated with plantar flexion weakness and stocking-distribution sensory
loss.

Clinically, the peroneal nerve may appear to be involved selectively in vasculitis,

chronic inflammatory demyelinating neuropathy, hereditary neuropathy with liability
to pressure palsy, or sarcoidosis.[17] Lyme disease has been reported to cause peroneal
nerve palsy.[18] However, nerve conduction studies showing a more generalized or
multifocal neuropathy may aid in the diagnosis.

Intermittent pneumatic compression to prevent deep vein thrombosis causing

compression of the peroneal nerve at the fibula head may cause bilateral peroneal
nerve palsy.[19]

Peroneal neuropathy can occur following liver transplantation. Risk factors include
intraoperative positioning, poor nutritional status, tall and slender body shape, and
alcoholic liver disease.[20]

Deep peroneal neuropathy resulting in foot drop with preserved toe extension has
been rarely reported in patients with anatomical variation of an accessory deep
peroneal nerve.[21]

Physical Examination
Table 1. Physical Examination in Peroneal Mononeuropathy (Open Table in a new window)
Nerve

Sensory

Weakness
Ankle dorsiflexion and eversion

Common peroneal
nerve

Lateral calf and dorsum of

foot
Toe extension

Ankle dorsiflexion and partial

eversion > inversion
Deep peroneal nerve

Superficial peroneal
nerve

Area between first and

second toes

Toe extension

Lateral calf and dorsum of

Ankle eversion
foot

Differential Diagnoses

Diabetic Neuropathy

HIV-Associated Multiple Mononeuropathies

Leptomeningeal Carcinomatosis Imaging

Neurosarcoidosis

Nutritional Neuropathy

Polyarteritis Nodosa

Systemic Lupus Erythematosus (SLE)

Toxic Neuropathy

Traumatic Peripheral Nerve Lesions

Uremic Neuropathy

Vasculitic Neuropathy

Imaging Studies
The following imaging studies are useful in peroneal mononeuropathy.

MRI of the lower thigh or popliteal fossa may be indicated if a mass lesion is
suspected. Peripheral nerve nodular mass lesions and inflammatory pseudotumors of
the peripheral nerves may be detected and confirmed by pathological excision.[22]

MRI can also detect variations in the posterior and distal extents of the biceps femoris
muscle, which can produce a tunnel in which the common peroneal nerve travels
causing peroneal nerve compression.[23]

Color duplex ultrasonography and angiography can reveal a popliteal artery

pseudoaneurysm in the popliteal fossa.[24]

High resolution sonography of the common peroneal nerve may identify structural
lesions of the peroneal nerve such as intraneural ganglion[25] and inflammatory
changes in vasculitic neuropathy[26] .

Other Tests
Nerve conduction studies and needle EMG aid in defining the location and type of lesion.

Nerve conductions should show isolated peroneal nerve abnormalities. If the lesion is
at the knee, then conduction block or, less commonly, conduction velocity slowing
over that segment of the nerve should be documented. When axonal loss occurs in
direct nerve trauma or with long-standing compression, a small compound muscle
action potential may be noted. If other mononeuropathies with conduction blocks are
found, then consideration should be made for an underlying vasculitis causing
mononeuritis multiplex or possibly for hereditary neuropathy with liability to pressure
palsy. If more diffuse nerve abnormalities are noted, then a generalized neuropathy
should be considered, especially chronic inflammatory demyelinating
polyneuropathy.

EMG is useful to localize the lesion. It can be helpful in determining which nerve is
involved primarilythe common peroneal nerve at the knee or one of its two
branches, the superficial or deep peroneal nerve. The tibialis anterior or extensor
hallucis longus muscles (ie, innervated by the deep peroneal) and the peroneus longus
or brevis muscles (ie, innervated by the superficial peroneal) are useful to study for
this purpose.

EMG also is helpful in determining if the foot drop is due to an L5 radiculopathy or a

sciatic lesion. In an L5 radiculopathy, the tibialis posterior, which is a foot inverter,
and the lumbosacral paraspinous muscles are involved.

Involvement of the peroneal division of the sciatic nerve in the thigh or hip area is
more difficult to determine clinically. In the thigh, the peroneal division of the sciatic
nerve innervates the short head of the biceps femoris muscle, a knee flexor. As
isolating this muscle clinically is difficult, EMG may be necessary to determine
involvement.

If lesions in the thigh are suspected on EMG, then MRI of the thigh (evaluating for
cysts or tumors) is indicated.

Histologic Findings
Peroneal neuropathy from intraneural ganglia of the peroneal nerve may have various
patterns: outer (epifascicular) epineurial, inner (interfascicular) epineurial, and combined
outer and inner epineurial.[27]

Medical Care
Most peroneal nerve lesions respond to conservative management with rest and elimination
of triggering factors such as leg crossing. Physical therapy is helpful in recovery of function.
A large Italian study showed good spontaneous improvement in patients with peroneal
mononeuropathy and rehabilitation helped with recovery of deambulation.[28] Additionally,
ankle foot orthosis (AFO) helps to stabilize the gait and prevent tripping due to the foot drop.

Surgical Care
Evaluation for surgical intervention for peroneal nerve repair is rarely necessary except in the
following situations:

The lesion is due to a mass compressing the nerve.

Release of nerve tethering is indicated.

Severe or complete transection is suspected as with blunt or open trauma.

A group from Turkey has reported good results after tibialis posterior tendon transfer for
persistent foot drop after peroneal nerve repair.[29]
Another group has reported good results from patients with deep peroneal nerve injuries
resulting in foot drop undergoing nerve transfer of functional fascicles of either the
superficial peroneal nerve or of the tibial nerve as donor for deep peroneal-innervated muscle
groups.[30]
A group from Italy has reported good motor improvement with a double tendon transfer
method from the tibialis posterior to tibialis anterior, and flexor digitorum longus transfer to
the extensor digitorum longus and extensor hallucis longus tendons.[31]

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