Peroneal Nerve Injury

Etiology

Peroneal nerve injury has been attributed to numerous causes, both traumatic and atraumatic.[4][5][6] Common causes of damage to the peroneal nerve include the following:

• Anatomic risk factors
• A fibrous band at the origin of the peroneus longus muscle near the fibrillar head predisposes to compressive neuropathy of the CPN [7][8]
• The extensor retinaculum atop the ankle can entrap the DPN between it and the underlying navicular and talus bones, causing the relatively rare condition known as anterior tarsal tunnel syndrome [9]
• Fabella syndrome occurs when the fabella, a sesamoid bone present in the gastrocnemius muscle in 1% to 30% of the general population, compresses the CPN through direct articular contact with the lateral femoral condyle [10][11]
• Trauma or injury to the knee joint
• Knee dislocation causes CPN injury in up to 40% of patients experiencing acute dislocations[12][13]
• Direct impact, penetrating trauma, or laceration predisposes to CPN injury as the nerve courses around the fibular head/neck
• Fracture of the fibula, especially at the proximal fibula
• Fracture of the tibia, including the tibial plateau
• External compression sources
• Tight splints or casts
• Compression wrappings or bandages
• Habitual leg crossing
• Prolonged bed rest, including in comatose patients or those intubated for long periods.
• Positioning during anesthesia and surgery can lead to compression injury, especially in the setting of inadequately padded bony prominences like the fibular head.
• Intraneural ganglion cysts [14]
• Peripheral nerve tumors [15]
• Iatrogenic injury following surgery on the hip, knee (including total knee arthroplasty and arthroscopic lateral meniscus repair), or ankle [16]

The common peroneal nerve is most vulnerable to injury as it passes around the fibular neck. Therefore, it is most susceptible to injury at the lateral aspect of the knee.[17][18]

Significant trauma around the knee can also result in peroneal nerve injury due to the nerve’s proximity to the knee joint and its superficial location; this can include a direct impact on the fibular neck, lacerations, and knee dislocations. CPN injuries are often encountered in athletes, especially football or soccer players, where they are most commonly associated with knee dislocation and ligamentous injury or occur in isolation.[18]

Several systemic illnesses can cause compressive peroneal neuropathy and injury to the common peroneal nerve, including:

• Diabetes mellitus [19]
• Inflammatory conditions, such as chronic inflammatory demyelinating polyneuropathy [20]
• Exceptionally thin body habitus, eg, arising from anorexia nervosa, wherein loss of subcutaneous fat creates vulnerability to compressive injury of the nerve [18]

Epidemiology

Peroneal nerve injury is recognized as the most common neuropathy of the lower extremity and the third most common neuropathy overall, with only neuropathy of the median and ulnar nerves occurring more often.[3] Traumatic injuries to the CPN usually occur in young athletic patients (eg, football and soccer players) and in adult patients following high-energy trauma (eg, motor vehicle collisions), with CPN injury reportedly occurring in 16% to 40% of patients following knee dislocations.[13] Low-energy knee dislocations can occur in morbidly obese patients during basic activities of daily living.[21]

Given the lack of prospectively acquired data, the overall incidence of peroneal nerve injury secondary to closed fractures is challenging to elucidate. Fractures of the tibia (including tibial plateau) and fibula are reportedly associated with approximately a 1% to 2% rate of peroneal nerve injury.[22] There are reports of even rarer incidences following total knee arthroplasty or arthroscopic lateral meniscal repair.[18] For foot drop, the most recognizable consequence of peroneal nerve injury, data regarding overall incidence has not been reported to date.[23]

History and Physical

A thorough history and physical exam to assess the status and functional integrity of the CPN is always required when injury is possible. Presentation varies according to the underlying locus of compression or other injury to the nerve.[7]

The examining clinician should always seek information about prior history of total knee arthroplasty, exposure to epidural anesthesia, prior knee conditions such as valgus deformity, periods of higher body weight, and the presence of diabetes.

The most common presentation of CPN injury is a weakness of ankle dorsiflexion leading to the classic foot drop, which often causes patients to catch their toes on the ground while ambulating or ambulate with a high steppage gait to prevent dragging their toes on the ground. Foot drop may develop acutely or over days to weeks, depending on the etiology. It can also be complete or partial in severity. Accompanying numbness or paresthesia may occur along the lateral leg, dorsal foot, and first toe webspace. Pain may be present in traumatic cases, but this is not universal.[18]

In the setting of traumatic injuries to the knee, including knee dislocations, the initial examination must rule out an acute neurovascular injury that could potentially compromise the lower extremity. Knee dislocations can notoriously compromise the neurovascular structures passing from the thigh and knee to the lower limb. If not addressed urgently, neurovascular compromise can lead to acute compartment syndrome, which can result in long-term compromise to the lower limb, even requiring amputation.[24][25]

To test for the motor involvement of the SPN and DPN, one must assess foot eversion (SPN) and dorsiflexion of the ankle and toe joints (DPN). A finding of weak foot eversion in the company of weak ankle and toe dorsiflexion suggests a lesion involving the CPN.[18] More proximal lesions, often secondary to traumatic knee dislocations, may present with varying degrees of numbness in both SPN and DPN distributions.

The Tinel sign is also a reliable clinical sign for localization of the area of nerve irritation or entrapment. The examiner performs the Tinel test by tapping along the course of the nerve, particularly around the fibular neck. Tingling or paresthesia elicited distally to the point of compression by tapping denotes a positive Tinel sign.[26]

The following tests can quickly evaluate the motor and sensory integrity of the CPN and its branches:

Motor

• Common peroneal nerve: none
• Superficial peroneal nerve: eversion of the foot
• Deep peroneal nerve: dorsiflexion of the foot and great toe extension

 Sensory

• Common peroneal nerve: lateral aspect of the leg just distal to the knee
• Superficial peroneal nerve: the anterolateral distal third of the leg and the majority of the dorsum of the foot (except the first webspace)
• Deep peroneal nerve: first dorsal webspace

Evaluation

The CPN’s superficial location and proximity to the fibular neck make the nerve particularly susceptible to injury, both from direct trauma and from entrapment by soft and bony tissue. When the history and physical examination indicate injury to the CPN, plain radiography should be part of the initial workup. In addition to plain radiography, CT scans can be used to evaluate for additional osseous abnormalities. MRI or ultrasound can be used to assess soft-tissue sources or masses.[5][27] 

Electrodiagnostic studies, including electromyography and nerve conduction velocity, can be helpful in assessing CPN palsy. These tests interrogate the motor and sensory axons of the CPN and its branches. They are also helpful in the localization of nerve injury. These tests are useful in patients presenting with a new onset of peroneal nerve symptoms, such as foot drop without a traumatic mechanism, in addition to evaluating patients in the postoperative setting of a known traumatic peroneal nerve injury to plan long-term management. 

Treatment / Management

There are operative and nonoperative options for the treatment of CPN injuries. Nonoperative treatments include ankle-foot orthoses and physical therapy. An ankle-foot orthotic device provides toe dorsiflexion during the gait’s swing phase, medial or lateral stability at the ankle during stance, and, if necessary, some push-off stimulation during the late stance phase.[28] Recent advances in ankle-foot orthotics include using carbon fiber to increase the energy available for push-off during the stance phase; the lighter weight improves patient comfort. Physical therapy for CPN injury consists of a program of stretching, strengthening, mobilization, manipulation, and proprioceptive and balancing exercises. Physical therapy may also include icing, ankle bracing, and taping. A recent case report described the use of ultrasound-guided pulsed radiofrequency treatment to alleviate symptoms of SPN entrapment neuropathy in a handball player.[29](B3)

Indications for surgical approaches to CPN injuries include a rapidly deteriorating lesion, refractoriness without improvement for 3 months, and open injuries with suspected nerve laceration.[5] Open lacerations should undergo exploration and surgical repair within 72 hours.[5] More than that, though, any patient with a subjectively disturbing foot drop and a clinically suspected compressive neuropathy of the CPN should be informed that surgical decompression of the nerve at the fibular head can be performed with little risk. Some patients have benefitted from muscle-transfer surgery in cases of a permanent foot drop. For spastic foot drop, the option of botulinum toxin injections should be evaluated.[23] During surgical procedures, prevention of CPN injuries entails the padding of relevant bony prominences, including the fibular head and neck at the lateral aspect of the knee.

Differential Diagnosis

Foot drop can be caused by (lower) lumbar radiculopathy and lesions of the sciatic notch, in addition to the more classic cause of CPN neuropathy.[30] Cases of peroneal injury have been reported after total hip arthroplasty.

Peroneal neuropathy is found in patients with multiple system atrophy. In one study, decreased compound muscle action potentials in the peroneal nerve were found in 8.6% of patients with the Parkinsonian variant and 4.3% of patients with the cerebellar variant.[31]

Prognosis

The prognosis depends on etiology. While some transient CPN neuropathies improve or resolve over time with nonsurgical measures, CPN palsy following traumatic knee dislocations has a poor prognosis for the long-term recovery of nerve function.[32] Surgical intervention and tendon transfers are often necessary for refractory CPN palsy, dictated by results of follow-up physical examination and serial electromyographic testing with nerve conduction velocities.

The prognosis has been described extensively in patients who experience CPN injury following total knee arthroplasty. In one study, 62% of patients experienced maximal neurologic recovery, and 38% had complete recovery at 12 months.[33] In another large case series study of 318 operatively-managed peroneal nerve lesions associated with various mechanisms, 84% of patients who underwent end-to-end suture repair received good recovery by 24 months.[5] In patients who required grafts, graft lengths less than 6 cm recovered 75% function. Longer grafts were associated with poorer outcomes.[5]

Complications

In patients with foot drop, the clinician must ensure that the physical therapy and rehabilitation care teams engage in passive stretching exercises to mitigate the risks of a fixed equinovarus contracture. Orthotic devices are used to ensure the ankle can achieve at least passive dorsiflexion to a neutral position.[18]