Clinical manifestations

Presentation and course

Common fibular neuropathy usually presents with foot drop (weakness of ankle dorsiflexion). Although foot drop usually occurs acutely, it sometimes develops subacutely over days or weeks. Foot drop may be complete, with failure to dorsiflex the ankle and toes, or partial. The foot drop may cause the patient to fall. Numbness of the leg usually involves the dorsum of the foot and lower lateral leg. Pain is rare and, when present, is deep and ill-defined, usually located around the knee. On examination, the weakness is restricted to ankle eversion and ankle and toe dorsiflexion. Ankle inversion, toe flexion, and plantar flexion strength are preserved. An apparent weakness of ankle inversion is commonly incorrectly assessed with complete foot drop because inversion is best obtained with the foot slightly dorsiflexed. To avoid this misleading sign in a patient with foot drop, the ankle should be dorsiflexed passively to 90 degrees while testing ankle inversion strength. Strength of the hamstrings, glutei, and quadriceps is normal in a fibular neuropathy at the knee. Hypesthesia to touch is limited to the lower two-thirds of the lateral leg and dorsum of foot. Tinel sign may be elicited by percussion of the fibular nerve around the fibular head. Patellar and ankle jerk deep tendon reflexes are normal. Overall, patients with common fibular neuropathy complain of motor deficit in more than 99% of cases, sensory symptoms in 88% of cases, and pain in 20% of cases (02).

Partial sciatic neuropathies can present similarly to fibular neuropathy at the fibular neck, causing weakness of foot dorsiflexion and foot eversion. Sensory disturbances involve the lateral lower leg and dorsum of the foot. Most partial sciatic nerve injuries primarily affect fibular nerve fascicles, leading to this outcome (39).

Compression of the superficial fibular nerve is rare but is reported in athletes, especially those who wear tight-fitting legwear or boots, such as skiers or dancers (18; 39). Weakness with foot eversion will be present, and ankle dorsiflexion and great toe extension will be spared. Sensory disturbances involve the lateral lower leg and dorsum of the foot. Sensation in the first webbed space is spared (18).

Compression of the deep fibular nerve at the ankle is another rare entrapment neuropathy that occurs due to compression of the deep fibular nerve under the extensor retinaculum at the ankle. This type of entrapment is commonly referred to as “anterior tarsal tunnel syndrome.” The sensory loss will be restricted to the first webbed space of the foot, and ankle eversion strength is normal. Weakness and atrophy involve the extensor digitorum brevis muscle. Plantar flexion tends to worsen symptoms, and patients may present with a positive Tinel sign at the anterior ankle (39).

Prognosis and complications

It is difficult to make a prognosis for recovery from fibular neuropathy based on clinical evaluation only. Because most cases have prominent axonal loss, the prognosis is generally guarded, and recovery may be prolonged.

Electrodiagnostic evaluation is essential in identifying these lesions because it separates lesions with primarily demyelinating injury from those with significant axonal loss. Segmental demyelination has a good prognosis, with recovery occurring in 6 to 8 weeks. The prognosis of axonal loss lesions is variable because it is dependent on the degree of structural nerve injury as defined by the Sunderland (46) and Seddon (42) classification.

Table 1. The Degree of Structural Injury as Defined by Sunderland and Seddon

With common fibular nerve injury secondary to knee dislocation, if the nerve is in continuity with less than 7 cm of the nerve involved, complete recovery may occur over 6 to 18 months (34). Partial recovery occurs in patients with more extensive common fibular nerve lesions.

As with other peripheral nerve injuries, partial axonal lesions fare better than complete lesions because local sprouting effectively reinnervates muscle fibers. Also, children with fibular nerve lesions typically do well (25).

The etiology of the traumatic injury in common fibular neuropathy has an impact on the outcome. Sharp injuries and severe dislocations of the knee tend to have an excellent recovery, whereas crush injuries and gunshot wounds lead to a good recovery much less often (19). Common fibular neuropathy due to prolonged squatting or posture tends to be a benign lesion and recovers with conservative therapy over 9 weeks in more than 90% of patients with avoidance of precipitating factors (41). Complete or near complete recovery of fibular neuropathy following hip arthroplasty ranges from 60% to 80% (44). The mean time to recovery was approximately 1 year for partial fibular palsy and 1.5 years for complete palsy. Weight of the patient has been observed as an important prognostic factor (36).

In nontraumatic, acute-onset compressive fibular mononeuropathy, patients with denervation on needle electromyography, older age, and severe initial weakness carry a poorer prognosis (10).

Clinical vignette

A 57-year-old man with a medical history of morbid obesity, type 2 diabetes mellitus, and gastric bypass surgery (3 months prior) presented for evaluation of painless, progressive right lower-leg weakness, numbness, and tingling sensation primarily localized to the right lower leg and foot. He reported a 45 lb weight loss over a 3-month period.

On examination, muscle bulk was normal and symmetric. There was weakness of right ankle dorsiflexion (Medical Research Council [MRC] score 2/5) and ankle eversion (MRC 3/5) with preserved strength in ankle inversion, ankle plantarflexion, and knee flexion. He had hypoesthesia along the right lateral leg and dorsum of the foot. Sensation was normal over the sole of the foot and medial calf. Deep tendon reflexes were intact and symmetric at the patellae and ankles. Tinel sign was negative at the fibular neck.

Electrodiagnostic testing revealed absent superficial fibular sensory nerve action potential (SNAP) on the right. There were normal SNAP responses of the right sural and left superficial fibular sensory nerves. The distal fibular compound muscle action potential (CMAP) amplitude, recorded from the right extensor digitorum brevis, was normal and symmetric compared to the left, but proximal sites of stimulation revealed conduction block with slowing of conduction velocity across the fibular head, and minimal F-wave latency of the right common fibular nerve was prolonged. Needle EMG revealed signs of active denervation and reduced recruitment in the tibialis anterior and fibularis longus muscles. Needle EMG testing was normal in the gastrocnemius, short head of the biceps femoris, gluteus medius, and L5 paraspinal muscles.

The patient was treated with physical therapy. At the 3-month follow-up, he had significant improvement in his foot drop, with only mild residual dorsiflexion weakness and improved mild, persistent sensory loss over the dorsum of the foot.

Biological basis

Etiology and pathogenesis

A review of the anatomy of the fibular nerve is essential to understanding the causes and clinical manifestations of its injury. The fibular nerve primarily originates from the nerve roots of L4-S1. These roots traverse the lower lumbosacral plexus and eventually become part of the sciatic nerve. The sciatic nerve is composed of two separate nerves: the common fibular nerve (also called lateral popliteal nerve) and the tibial nerve (also called medial popliteal nerve). Both share a common sheath within the sciatic nerve but do not exchange any fascicles. In the upper thigh, the common fibular nerve innervates the short head of biceps femoris only, whereas all other hamstring muscles (long head of biceps femoris, semitendinosus, and semimembranosus) are innervated by the tibial nerve. The common fibular and tibial nerves separate completely in the upper popliteal fossa. Soon after this split, the common fibular nerve gives off the lateral cutaneous nerve of the calf, which innervates the skin over the upper third of the lateral aspect of the leg. It winds around the fibular neck and passes through a tendinous tunnel between the edge of the peroneus longus muscle and the fibula (the fibular tunnel). Near that point, the common fibular nerve divides into its terminal branches, the superficial and deep fibular nerves. The superficial fibular nerve innervates the peroneus longus and brevis and the skin of the lower two thirds of the lateral aspect of the leg and the dorsum of the foot. It is important to note that, in 15% to 20% of patients, an accessory fibular nerve branches off from the superficial fibular nerve and courses posteriorly behind the lateral malleolus to supply the lateral extensor digitorum brevis muscle. The deep fibular nerve serves primarily motor function; it innervates all ankle and toe extensors (tibialis anterior, extensor hallucis, extensor digitorum longus and brevis) and peroneus tertius, in addition to sensory function in the skin of the web space between the first and second toes.

Fibular neuropathy is usually caused by external compression around the fibular neck or by trauma (fibular neck fracture, tibiofibular fractures, or knee trauma). Less commonly, it may be due to intraoperative injury, benign nerve tumors, fibular intraneural ganglia (30), extraneural ganglion cysts (35), herpes zoster infection (48), and vasculitis.

Fibular nerve entrapments at the ankle can occur with ankle fracture or with prolonged wearing of tight-fitting boots (“ski boot neuropathy”).

The fibular component of the sciatic nerve can also be injured in the thigh. This can occur as the result of trauma or, in a comatose or sedated patient, lying with the posterior thigh across a compressing object for a prolonged period. Sciatic nerve injury can additionally be a complication of surgery, most often related to tourniquets applied to the thigh for knee surgery or as a complication of hip replacement surgery.

Common fibular mononeuropathies in children are similar to those of adults with compression and trauma as the leading causes (25). Weight loss is often associated with anorexia nervosa. Iatrogenic lesions include casts or tibial osteotomies. Bone tumors, such as osteochondromas, causing fibular neuropathies are more common than in adults. Neonatal fibular nerve injuries are uncommon, usually associated with breech presentations and malpositioning, and often result in intrauterine stretching of the infant’s fibular nerve (21).

Common causes of fibular neuropathy include the following.

Knee dislocation and injury. In a study by Niall and colleagues, injury to the common fibular nerve occured in 25% of patients with dislocation of the knee. All underwent ligament reconstruction. In patients presenting with anterior or anteromedial dislocation with associated disruption of both cruciate ligaments and the posterolateral structures of the knee, common fibular nerve palsy occured in 41% of patients (34).

Multiple ligament knee injury that includes posterolateral corner disruption requiring surgery can be associated with displaced common fibular nerves in cases with biceps femoris tendon rupture or avulsion-fracture of the fibular head (16). Nerve injury is believed to occur due to the nerve being pulled anteriorly by the biceps tendon (08).

Knee surgery. In an Italian study, 22% of common fibular neuropathies were due to surgery (02). Knee surgery is the most common surgical procedure associated with the development of common fibular neuropathy, which appears to occur with 0.3% to 1.3% of all knee arthroplasties. Possible risk factors for postoperative fibular neuropathy include valgus deformity, postoperative epidural anesthesia, or postoperative hematoma formation (44). Additionally, the presence of preexisting peripheral neuropathy appears to be a significant risk factor for fibular nerve palsy after knee or hip arthroplasty (14). A thigh tourniquet may also cause injury to the fibular portion of the sciatic nerve during knee surgery.

Other surgery. Common fibular nerve injury, though rare, has been reported following total hip arthroplasty. This is typically associated with a poor functional outcome (20). Risk factors for common nerve palsy post-hip arthroplasty include high body max index, developmental dysplasia of the hip, posttraumatic arthritis, lengthening of the extremity, cement-less femoral fixation, and a posterior surgical approach (17; 20).

Uncommonly, fibular nerve lesions may occur with thoracoabdominal surgery, perhaps related to surgical positioning (02a). Improper positioning of patients during gynecologic surgeries can also lead to compression neuropathies (09).

Weight loss. In a prospective series, 15% of common fibular neuropathies were associated with and possibly attributed to weight loss (02a). Some of these patients have a concurrent polyneuropathy (13). An underlying hereditary neuropathy with liability to pressure palsies should be considered (13). The exact cause of common fibular neuropathy in weight loss is unknown but may relate to a loss of cushioning adipose tissue around the nerve at the knee.

Prolonged maintenance of posture. Bedridden patients represent 7% to 23% of all cases of common fibular neuropathy (02a; 02b); in one series (02b), this was the most common cause of common fibular nerve palsy.

External compression and nerve tumors. External compression comprises 5.8% of cases of common fibular neuropathy in one prospective series (02a). Intraneural ganglion cysts of the fibular nerve can be associated with the “wishbone” sign on MRI, with the ascending limb of the fibular intraneural ganglion intersecting with the longitudinal limb of the vascular adventitial cyst in the axial plane (45). Extraneural ganglion cyst causing fibular neuropathy is another reported cause of external compression (35). Arthrogenic cysts at the fibular head compress the common fibular nerve in 1.4% of cases (02a). Rare causes include extrinsic masses (osteomas, lipomas, ganglia, Baker cysts) or intrinsic nerve sheath tumors. Iatrogenic lesions include casts or tibial osteotomies. Bone tumors, such as osteochondromas, that cause fibular neuropathies are more common in children than in adults. Cast placement for broken bones may lead to as many as 6% of all common fibular neuropathies (02b).

Trauma. Trauma was responsible for 10% of cases of common fibular neuropathy in one series (02a) and was likely the second most common cause overall, next to perioperative compression. Traumatic causes include fibular or tibiofibular fractures (31), knee surgery and arthroscopy, lacerations, and blunt injuries. Stretch injuries of the fibular nerve may occur following severe ankle inversion sprains.

Common causes of fibular neuropathy are listed in Table 2.

Table 2. Causes of Common Peroneal Neuropathy

Epidemiology

Peroneal neuropathy at the fibular head is the most common compressive neuropathy in the lower extremity; however, its exact incidence and prevalence are unknown. Men are more frequently affected than women (male:female = 4.1:1) (03).

Prevention

Proper positioning of patients and protective padding during anesthesia and surgical procedures and in hospital beds and intensive care are essential in the prevention of fibular neuropathy (01). It is unknown whether avoiding leg crossing in persons with weight loss will prevent fibular neuropathy at the fibular neck.

Differential diagnosis

Confusing conditions

Foot drop is a common presentation in neurologic practice. Although fibular neuropathy is one of the most common causes of foot drop, other sites of peripheral nerve injury and central nervous system disorders can also cause foot drop and should be considered in the differential diagnosis.

The most common conditions to consider in the differential diagnosis of fibular neuropathy are as follows:

Sciatic nerve injury may mimic a fibular neuropathy, particularly when the fibular component of the nerve is predominantly affected. Although both a sciatic nerve lesion and common fibular neuropathy can present with foot dorsiflexion weakness and sensory abnormalities in the lower lateral leg and dorsum of the foot, a sciatic nerve injury will also present with weakness in knee flexion and foot inversion. Sensory loss is widespread and includes the lateral knee and calf, dorsum of the foot, including the first webbed space, posterior calf, lateral foot, and sole of the foot. The ankle jerk reflex will be depressed or absent. Sciatic nerve injuries are frequently associated with surgery, trauma, compression, or other localized pathology affecting the sciatic nerve (39).

Partial sciatic nerve lesions usually affect the lateral division (fibular nerve) more than the adjacent medial division (tibial nerve). These proximal fibular nerve lesions often present a diagnostic challenge because they imitate a distal selective fibular nerve injury due to compression at the fibular head. The greater vulnerability of the fibular division of the sciatic nerve to physical injury is related to differences in fascicular pattern, cushioning effects of the perineurium, and a more taut anatomic course of the fibular nerve (46).

Lumbosacral plexus lesions affecting the lumbosacral trunk can also present with a clinical presentation similar to fibular neuropathy or sciatic neuropathy. In addition to the weakness and sensory loss seen in sciatic neuropathy, a lower lumbosacral plexus lesion will also present with weakness in the glutei muscles and sensory loss in the posterior thigh. Patients typically have pelvic pain. Patellar and ankle jerk reflexes will be depressed or absent. Etiologies may include trauma, radiation therapy, neoplastic infiltration, or other systemic diseases affecting the plexus, such as diabetes (39).

Lumbar radiculopathy affecting the L5 nerve root is perhaps the most common condition to mimic a fibular neuropathy. In L5 radiculopathy, there is weakness in foot dorsiflexion, big toe extension (extensor hallucis longus), and ankle inversion and eversion. Severe L5 radiculopathy can cause weakness in leg abduction due to weakness in the glutei muscles. Sensory loss typically affects the lower lateral leg, although sensory loss in radicular lesions is typically not as well defined as in peripheral nerve injury. Ankle jerk reflexes are preserved. Patients usually complain of radiating pain from the low back into the lower leg and foot.

Motor neuron disease may also present as a mimic of fibular neuropathy. Foot drop is a prominent feature of lower limb onset motor neuron disease during the initial stages. Limb-onset occurs in about 70% of individuals diagnosed with motor neuron disease (29). In any patient presenting with painless foot drop without sensory involvement, motor neuron disease must be strongly considered.

Occasionally, a stroke affecting the anterior cerebral artery may cause leg weakness, mimicking a fibular neuropathy. An anterior cerebral artery stroke is typically characterized by both proximal and distal leg weakness (12). Sensory symptoms are typically absent. In any patient presenting with leg weakness without pain or sensory symptoms, stroke should be considered.

Table 3. Clinical Differential Diagnosis of Common Causes of Foot Drop

Associated or underlying disorders

Fibular neuropathy can be associated with various underlying conditions, including diabetes mellitus, hereditary neuropathy with liability to pressure palsies, and generalized polyneuropathy.

Neuropathy is a common complication of diabetes that can present with a broad clinical spectrum from generalized neuropathy to focal or multifocal nerve involvement. Chronic compression, leading to entrapment of the nerve is the major cause of mononeuropathies seen in diabetes. As such, patients with diabetes are more likely to develop fibular neuropathy compared to the general population (40).

Hereditary neuropathy with liability to pressure palsies is a genetic disorder that most commonly arises from a deletion of the PMP22 gene. Individuals with HNPP are susceptible to nerve compression injuries. Patients with HNPP can present with multiple entrapment neuropathies, often with minimal injury or no obvious cause. The most frequently affected nerves include the axillary, median, radial, ulnar, or fibular nerves or the brachial plexus (04). HNPP should be considered in young patients presenting with fibular neuropathy without apparent underlying cause.

The presence of a generalized polyneuropathy of nearly any cause increases the risk for entrapment neuropathies, including fibular neuropathy. Causes can include metabolic, autoimmune, inherited, infectious, and toxic exposures.

Diagnostic workup

Electrodiagnostic testing with nerve conduction studies and electromyography is essential in the diagnosis, assessment, and prognosis of fibular neuropathy. Electrodiagnostic studies can confirm the site of the lesion (fibular head, thigh, deep branch), estimate the extent of injury and its type (demyelinating versus axonal), and, hence, predict the expected course of recovery (weeks or months) (27; 43).

The fibular motor and sensory nerve conduction studies should be obtained by recording from the extensor digitorum brevis and tibialis anterior muscles because the extensor digitorum brevis muscle is commonly atrophic in normal subjects (15; 37).

The superficial fibular sensory nerve action potential is commonly absent or low in amplitude except when the lesion is purely demyelinating or is restricted to the deep fibular branch. In common fibular neuropathy defined by electrophysiology, 88% of patients have clinical or electrophysiological evidence of superficial fibular nerve involvement. However, only 50% of these patients have a reduced superficial fibular nerve sensory nerve action potential amplitude (26). The superficial fibular sensory nerve action potential amplitude is normal in radiculopathy but usually low or absent in lumbosacral plexopathy, sciatic neuropathy, or peripheral polyneuropathy. Therefore, the tibial motor and sural sensory studies and H-reflexes should be done to evaluate these possibilities.

Motor nerve conduction studies should assess for slowing of conduction velocity across the fibular head or conduction block at that site. In more severe injuries, there will be absent motor-evoked responses or reduced motor amplitudes, indicating axonal loss.

Needle EMG testing should assess for signs of active denervation and chronic reinnervation changes in fibular innervated muscles. Testing nonfibular muscles with shared plexus and nerve root innervation, such as the tibialis posterior, flexor digitorum longus, or gluteus medius, is essential. These are normal in fibular lesions but abnormal in L5 radiculopathy and lumbosacral plexopathy. Testing the short head of the biceps femoris is necessary to evaluate for a high fibular lesion (sciatic neuropathy affecting the fibular component predominantly or exclusively) (28). In sciatic lesions, the other hamstring muscles, gastrocnemius, and abductor hallucis are also affected, but the glutei are spared. Table 4 summarizes the electrodiagnosis of common causes of foot drop.

Table 4. Electrodiagnosis of Common Causes of Foot Drop

Nerve ultrasonography can be useful in evaluating fibular neuropathy. Ultrasound can be used to confirm the site of entrapment at the fibular head when nerve conduction studies are unable to localize the site of nerve injury. Additionally, ultrasound can be used to identify potential structural processes that may compress the nerve, including ganglion cysts and bony lesions (24; 22; 49; 07; 05). Ultrasound is more sensitive than MRI in detecting peripheral nerve pathologies. In one study comparing the diagnostic accuracy of MRI and ultrasonography in patients with common fibular neuropathy, the authors found a higher sensitivity and specificity in diagnosing common fibular neuropathy with ultrasound over MRI (06). Ultrasound may also be useful in the assessment of axonal loss in fibular neuropathy and can correlate with electrodiagnostic findings of conduction block (32; 47).

Management

When left untreated, common fibular nerve palsy is associated with foot drop, equinovarus deformity, and limb disability in 30% to 35% of patients. Initial management is typically nonsurgical. In managing acute compressive lesions, patients should be observed to allow for improvement by remyelination or reinnervation. Patients with the electrodiagnostic finding of conduction block (due to segmental demyelination) recover spontaneously in 2 to 3 months if further compression is prevented. Ankle bracing or night splints are important when the foot drop is severe to prevent ankle contractures (38). In general, nonsurgical management of common fibular neuropathy involves bracing and physical therapy.

Surgical intervention is appropriate in certain situations:

Surgical management includes neurolysis, primary repair, nerve grafting, nerve transfer, or tendon transfer. Among these procedures, neurolysis is frequently conducted to relieve compression of the common fibular nerve at the fibular head or fibular tunnel.

Neurolysis of common fibular neuropathy is a safe procedure and can significantly improve ankle dorsiflexion strength (11). After categorizing the injuries based on their mechanism of injury, the systematic review and meta-analysis performed by Chow and colleagues demonstrated statistically significant improvements in ankle dorsiflexion strength in cases caused by traction, trauma, iatrogenic factors, and idiopathic reasons but not in instances of compression.

Nerve grafting is indicated if primary repair is not possible due to significant nerve damage or gapping of the nerve. Autologous grafting, with the use of the sural nerve, is most commonly used (38). A motor grade of greater than or equal to MRC 3 was achieved in 49% of patients who underwent nerve grafting (33).

Tendon transfer may also be used to restore function in the foot and ankle in refractory cases with persistent foot drop (23; 38). Garozzo and colleagues performed a one-stage procedure of nerve repair and tibialis tendon transfer. At a 2-year follow-up, evidence of nerve regeneration was present in 90% of patients undergoing this procedure (19).