Common Peroneal Neuropathy

Common peroneal (fibular) neuropathy is the most frequent mononeuropathy of the lower limb. It is usually caused by compression or traction of the nerve as it winds around the fibular neck, where it is superficial, producing foot drop, a steppage gait and sensory loss over the lateral lower leg and dorsum of the foot.

• The common peroneal nerve (L4 to S2 fibres of the sciatic nerve) divides into the superficial peroneal nerve (foot eversion, sensation on the lower lateral leg and dorsum of the foot) and the deep peroneal nerve (ankle dorsiflexion, toe extension, sensation in the first web space).
• Causes: leg crossing, prolonged squatting or kneeling, tight casts, splints, stockings or bandages, weight loss with loss of protective fat, bed rest or coma (ICU, surgery), lithotomy position, knee surgery or dislocation, fibular fracture, ganglion or synovial cyst, Baker cyst, lipoma, nerve sheath tumour, diabetes, vasculitis, alcohol, hereditary neuropathy with pressure palsies, leprosy, and traction injury (inversion ankle sprain).
• Most compressive injuries are neurapraxia and recover within weeks to a few months.

• Foot drop: inability to dorsiflex the ankle or extend the toes, with a high stepping (steppage) gait and foot slapping; the toes catch on the ground and patients trip.
• Weak ankle dorsiflexion and eversion; ankle inversion and plantar flexion are preserved (inversion weakness suggests L5 radiculopathy or sciatic nerve injury).
• Sensory loss or paraesthesia on the lateral lower leg, dorsum of the foot and toes, or in the first web space (deep peroneal only).
• Tinel sign over the fibular head; local tenderness; sometimes a palpable mass or scar.
• Knee, ankle and hamstring reflexes are normal (ankle jerk preserved), unlike S1 or sciatic lesions; the tibialis posterior is preserved.
• Bilateral lesions suggest polyneuropathy, hereditary neuropathy, or central disease.
• Examine the back, hip abductors (L5), sciatic function, peripheral pulses, and skin for signs of leprosy, vasculitis or trauma.

• Clinical examination distinguishing common peroneal neuropathy from L5 radiculopathy, sciatic neuropathy, lumbosacral plexopathy and motor neurone disease: preservation of inversion and hip abduction, and sparing of the tibialis posterior and gluteus medius.
• Nerve conduction studies and EMG (3 weeks or later after onset for axonal loss): focal slowing or conduction block across the fibular head, reduced amplitude, and EMG of short head of biceps femoris (sparing it suggests a distal lesion).
• Ultrasound or MRI of the knee and fibular neck when trauma, mass or no recovery is suspected; MRI lumbar spine if L5 radiculopathy is likely.
• Blood tests: HbA1c, vitamin B12, ESR, CRP, antinuclear antibodies, ANCA, and others for vasculitis or other causes of mononeuropathy multiplex.
• Differentials: L5 radiculopathy, sciatic neuropathy, lumbosacral plexopathy, motor neurone disease, polyneuropathy, myopathy (distal), upper motor neurone lesion (stroke, cord), and anterior compartment syndrome.

Remove the cause

• Stop leg crossing and prolonged squatting; loosen or replace tight casts, bandages or compression stockings; pad the fibular head in bed bound patients and during anaesthesia and surgery; encourage regular position change.
• Optimise nutrition and manage weight loss; treat diabetes and alcohol use; investigate vasculitis if multiple nerves are involved.

Supportive care

• Ankle foot orthosis (a lightweight plastic one, or a spring leaf device) to hold the ankle in neutral and prevent tripping, until recovery.
• Physiotherapy: passive ankle range of motion and Achilles tendon stretching twice daily to avoid equinus contracture; strengthening of dorsiflexors and evertors; gait training; functional electrical stimulation when available.
• Falls prevention: footwear review, clear walkways, and walking aids when required.
• Neuropathic pain, if present: amitriptyline 10 to 50 mg at night, or gabapentin 300 mg at night increasing to 300 to 600 mg three times daily, or pregabalin 75 mg twice daily (renal dose adjustment); topical lidocaine 5 percent plaster.

Surgical

• Early exploration for open injury, laceration, or mass lesion (ganglion, cyst, tumour).
• Decompression (neurolysis) at the fibular neck for compression without recovery after 3 to 4 months, or entrapment with a confirmed lesion on imaging.
• Nerve repair, graft or transfer for transection or traction injury with no recovery by 3 to 6 months (best within 6 to 12 months).
• Tendon transfer (tibialis posterior to the dorsum of the foot) when no recovery after 12 to 18 months.

Prognosis and follow up

• Compression neurapraxia: recovery in weeks to 3 months; axonal injury: recovery of about 1 mm per day over 6 to 18 months, with poorer outcome after traction injury and complete deficit.
• Review at 4 to 6 weeks and 3 months with repeat nerve studies if no improvement; refer to a peripheral nerve surgeon when there is no recovery by 3 months or a mass.