The fibular nerve has been historically referred to as the peroneal nerve because the fibula can also be referred to as the perone. It has recently become more commonplace to refer to the peroneal nerve as the fibular nerve to distinguish it from the similar-sounding perineal nerve. The fibular nerve terminology will be used in all parts of this article. Fibular neuropathy is considered the most common neuropathy in the lower extremities and tends to occur secondary to compression, entrapment, direct trauma, or ischemia.[1][2] In fibular neuropathy, both the deep and superficial nerves tend to be affected. If a single branch is being affected, the deep fibular nerve tends to be more frequently affected than the superficial fibular nerve.[2] This occurs as the deep fibular nerve fascicles are more superficial at the fibular head; thus, they are more exposed to trauma and compression. The fibular nerve's most common compression site is found at the fibular head/neck, where the nerve is most superficial.[2]
Patients tend to present with either an acute or a gradual foot drop. Patients may give a history of falls and possibly tripping due to the foot drop. They may also complain of paresthesias or numbness in the lower leg's lateral portion and the foot's dorsum. Pain can be absent in many cases presenting with a foot drop.[3] However, pain can be an initial presenting symptom in patients without a foot drop but can show a slight weakness in ankle dorsiflexion only when carefully examined.[4] One-third of these patients can have normal electrodiagnostic tests.[4]
Injuries to the common fibular nerve can be due to compression from the prolonged crossing of legs, poor positioning during surgery (most common in acute settings), weight loss (most common in a subacute or chronic setting), poor application of a cast, prolonged squatting position (carpet layers, carpentry workers, farmworkers), or diabetes mellitus.[2][5] An isolated weakness of the ankle dorsiflexors and evertors can help clinicians differentiate a fibular neuropathy from L5 radiculopathy, which would also involve the ankle invertors.[5] Studies of the tibialis posterior or gluteus medius muscles, which are not supplied by the fibular nerve but have an L5 innervation, can differentiate L5 radiculopathy.[5] Fibular neuropathies can also be mistaken for lumbosacral plexopathy and sciatic neuropathy.[1] Sciatic neuropathy frequently shows a foot drop and can be confused with common fibular neuropathy.[2][6][7] Sciatic neuropathy is the second most common neuropathy in the lower extremity.
Deep fibular neuropathy can occur by patients whose nerves are compressed by trauma (ankle sprains or fractures), footwear (high heeled shoes, tight shoes, or high boots), or intrinsic causes as the nerve passes under the extensor retinaculum (osteophytes, ganglion cysts, or lipomas). Pressure from an anterior compartment syndrome can cause an isolated injury to the deep branch.[5] The superficial fibular nerve can be injured by compression related to trauma, sprained ankles, or lipomas.
The common fibular nerve receives innervation from the L4-S1 nerve roots with a minor contribution from the L2 nerve root. The nerve is formed at the lumbosacral plexus and initially travels within the sciatic nerve.[2][5] The sciatic nerve contains fiber bundles that are anatomically separated. Just above the popliteal fossa, these separated fiber bundles form the common fibular nerve and the tibial nerve.
The sciatic nerve’s fibular branch innervates the short head of the biceps femoris muscle. This finding is significant from an electrodiagnostic standpoint because it is the only muscle proximal to the knee that the fibular nerve innervates. If a patient experiences fibular neuropathy at the fibular neck, the short head of the biceps femoris muscle will not be affected. The knee's lateral surface is innervated by the lateral cutaneous nerve, a sensory branch of the common fibular nerve. Following this branch, the common fibular nerve curves around the fibular neck and passes between the fibula and the peroneus longus muscle through the fibular tunnel.
The tibialis longus and brevis muscles are innervated by the superficial fibular nerve, terminating in sensory branches that supply the lateral portion of the two-thirds of the lateral lower leg and the dorsum of the foot and toes except for the first dorsal web space.[2][5]
The deep fibular nerve, also called the anterior tibial nerve, supplies the tibialis anterior muscle, the extensor digitorum longus muscle, extensor hallucis longus muscle, peroneus tertius muscle, and the extensor digitorum brevis (EDB) muscle. Terminal sensory branches provide innervation of the skin of the first dorsal webspace.[2] Approximately 15 to 25% of people have an accessory fibular nerve that arises from the superficial fibular nerve.[8][9][10] This accessory nerve provides an atypical innervation to the EDB muscle.[8]
For common fibular nerve neuropathy, the patient may complain of weakness in the dorsiflexors (extensor hallucis longus, extensor digitorum longus, tibialis anterior), which could result in a foot drop or a foot slap with a steppage gait.[5] A sensory loss could also be observed over the deep and superficial fibular nerve distributions. Tinel’s sign could also be positive at the fibular head.[5] Deficits in strength could also be appreciated when the ankle is dorsiflexed and with the great toe extension.
For deep fibular neuropathy, patients may complain of pain, weakness, or atrophy of the foot, especially the EDB muscle. Patients may also experience numbness/paresthesias of the first and second webspace. They may experience pain over the dorsum of the foot, which is relieved with motion.
For superficial fibular neuropathies, patients may complain of pain, numbness, paresthesias, or loss of sensation in the distal anterolateral calf and the foot's dorsum, except for the first webspace. Patients can present with weakness in foot eversion if the injury is proximal to the innervation of the tibialis longus and brevis muscles.[11]
Performing electrodiagnostic studies in patients with fibular neuropathy have few absolute contraindications. Needle electromyography (EMG) should not be performed on patients with severe bleeding disorders. Needles should not be inserted into areas with active soft tissue infections.
Nerve conduction studies are contraindicated in patients with external cardiac defibrillators or implanted cardiac defibrillators. Before conducting electrodiagnostic studies, patients should be screened for pacemakers. It is essential that electrical stimulation not be performed directly or near the device itself.[11]
Before performing an electrodiagnostic study, a clinician must conduct a comprehensive review of the patient’s history, including any applicable clinical course and a physical exam. A systematic and empathetic physician will inform the patient, and any relative involved in decision-making, of the indications for the studies and provide an overview of the procedure to be performed.
A comprehensive electrodiagnostic test includes motor conduction to the EDB muscle above and below the knee to assess a conduction block at the fibular head.[5] Should the EDB muscle response be small or unobtainable, it is acceptable to measure the motor response at the anterior tibialis muscle. Superficial fibular sensory nerve action potential (SNAP) is tested, indicating axonal loss distal to the dorsal root ganglion if there is amplitude loss.[5]
EMG should also sample muscles from the sciatic nerve's branches, including the short head of the biceps femoris, to distinguish it from more proximal fibular nerve lesions.[1][12] It is essential to compare with the opposite side. To evaluate for an accessory fibular nerve, the stimulation is done posterior to the lateral malleolus while recording at the EDB muscle.
Electrodiagnostic studies have a low risk of complications.
Fibular neuropathy is primarily an axonal sensorimotor peripheral neuropathy, which will be made apparent on electrodiagnostic studies.
Sensory Nerve Conduction Studies
In axonal or mixed axonal/demyelinating lesions, the superficial fibular SNAP amplitude is usually low or absent.[1] Purely demyelinating fibular neck lesions, however, have a normal distal superficial fibular sensory response.[13] A lesion distal to the dorsal root ganglia will show a decrease in the response with the sensory stimulation of the superficial fibular nerve.[5]
Motor Nerve Conduction Studies
Demyelinating lesions show a conduction block with a focal slowing in fibular motor studies performed across the fibular neck. Focal slowing is observed when there are a greater than 10 meters/sec difference from the distal conduction velocities. Conduction block is observed when there is a greater than 20% drop in amplitude of the proximal compound muscle action potential (CMAP).
Needle Electromyography
This test tends to be abnormal in fibular axonal lesions if axonotmesis is present. Clinicians will find abnormalities in lesions distal to the fibular nerve innervated muscles. Axonal lesions will show fibrillation potentials, positive sharp waves, and spontaneous activity, with decreased motor unit action potential recruitment depending on the timing of an injury. The results can be used to determine the chronicity of an injury.[1]
Fibular neuropathy is the most common lower extremity neuropathy. Physiatrists, neurologists, neurosurgeons, and orthopedists must recognize that further evaluation with electrodiagnostic testing is warranted when patients present with foot drop/slaps, steppage gait, weakness, or sensory deficits in areas of the lower extremity innervated by the fibular nerve. Doing so will help expedite a patient’s recovery process and improve their quality of life in the long term.
Electrodiagnostic studies can prove to be an integral component for determining etiology and guiding management.[1] Once a fibular neuropathy diagnosis is made, an interprofessional team involved in the management should include physiatrists and therapists for physical/occupational rehabilitation. Nutritionists, social workers, and case managers from the inpatient standpoint must coordinate and ensure early mobilization with bedside therapy and aggressive multifaceted rehabilitation. Only through a well-coordinated effort between these multidisciplinary components will a patient achieve their best outcome.
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