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.[1] 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. The peroneal nerve is also known as the superficial peroneal nerve and more recently the superficial fibular nerve.[2]
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.[3]
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.
The superficial branch supplies the foot everters and sensation to the skin of the lateral calf and dorsum of the foot.
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.
Common peroneal nerve decompression is a useful procedure to improve sensation and strength as well as to decrease pain.[5]
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.[6]
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.
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Peroneal sensory distribution: The striped area is the superficial peroneal sensory distribution. The green solid area represents the deep peroneal se....
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.[7]
Isolated acute repetitive strain injury such as repetitive kicking[8] and dancing[4] .
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[9] , blunt or open trauma, and intrinsic masses (e.g. ganglionic cysts, schwannoma, lipoma)[10] .
Knee dislocation or bicruciate injury can cause peroneal nerve injury in 10-40% of cases.[11] The superficial peroneal nerve is at risk for traction injury during an ankle inversion sprain.[12] Varus deformity in osteoarthritis of the knee can result in peroneal nerve injury with conduction block at the fibular neck.[13]
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[14] or anorexia nervosa[15] 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.[16] It has been observed in weight lifters[6] and football players[17] and can be associated with anabolic steroid use.[18]
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.[19] Lyme disease has been reported to cause peroneal nerve palsy.[20] 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.[21]
Peroneal neuropathy can occur following liver transplantation. Risk factors include intraoperative positioning, poor nutritional status, tall and slender body shape, and alcoholic liver disease.[22]
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.[23]
The following imaging studies are useful in peroneal mononeuropathy.[24]
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.[25]
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.[26]
Color duplex ultrasonography and angiography can reveal a popliteal artery pseudoaneurysm in the popliteal fossa.[27]
High resolution sonography of the common peroneal nerve may identify structural lesions of the peroneal nerve such as intraneural ganglion[28] and inflammatory changes in vasculitic neuropathy[29] .
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 primarily—the 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.
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.[30]
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.[31] Additionally, ankle foot orthosis (AFO) helps to stabilize the gait and prevent tripping due to the foot drop.
Evaluation for surgical intervention[32] 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.[33]
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.[34]
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.[35]
What is peroneal mononeuropathy?What is the pathophysiology of peroneal mononeuropathy?What is the pathophysiology of ischemic injuries and nerve transection in peroneal mononeuropathy?What is the anatomy relevant to peroneal mononeuropathy?What is the racial predilection of peroneal mononeuropathy?What is the sexual predilection of peroneal mononeuropathy?Which age groups are at highest risk for peroneal mononeuropathy?Which profession increases the risk for peroneal mononeuropathy?What is the prognosis of peroneal mononeuropathy?What are the signs and symptoms of peroneal mononeuropathy?Which physical findings are characteristic of peroneal mononeuropathy?What causes peroneal mononeuropathy?What are the nerve, sensory, and weakness findings indicative of peroneal mononeuropathy?What are the differential diagnoses for Peroneal Mononeuropathy?What is the role of imaging studies in the diagnosis of peroneal mononeuropathy?What is the role of nerve conduction studies in the diagnosis of peroneal mononeuropathy?What is the role of electromyography (EMG) in the diagnosis of peroneal mononeuropathy?Which histologic findings are characteristic of peroneal mononeuropathy?What is the initial treatment for peroneal mononeuropathy?When is evaluation for surgical intervention for peroneal nerve repair indicated?What is the efficacy of surgery for peroneal mononeuropathy?
Shaheen E Lakhan, MD, PhD, MS, MEd, Adjunct Professor of Neuroscience, Virginia Tech Carilion School of Medicine
Disclosure: Nothing to disclose.
Specialty Editors
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 in St Louis School of Medicine; Consulting Staff, Department of Neurology, Barnes-Jewish Hospital
Disclosure: Nothing to disclose.
Chief Editor
Nicholas Lorenzo, MD, MHA, CPE, Co-Founder and Former Chief Publishing Officer, eMedicine and eMedicine Health, Founding Editor-in-Chief, eMedicine Neurology; Founder and Former Chairman and CEO, Pearlsreview; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc; Chief Strategy Officer, Discourse LLC
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
Disclosure: Received research grant from: Lundebck pharma.
Alida Griffith, MD, Movement Disorders Neurologist, Booth Gardner Parkinson’s Care Center
Disclosure: Nothing to disclose.
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
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.
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.
Nerve
Sensory
Weakness
Common peroneal nerve
Lateral calf and dorsum of foot
Ankle dorsiflexion and eversion
Toe extension
Deep peroneal nerve
Area between first and second toes
Ankle dorsiflexion and partial eversion > inversion
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