Peroneal nerve palsy

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peroneal nerve palsy anatomy foot drop

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common peroneal nerve anatomy fibular head branches diagram

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Here is a comprehensive overview of Peroneal Nerve Palsy based on authoritative textbook sources:

Peroneal Nerve Palsy (Common Fibular Neuropathy)

Anatomy

The common peroneal (fibular) nerve is the lateral terminal branch of the sciatic nerve, arising in the popliteal fossa. It winds around the fibular head — where it is superficial and poorly protected — before dividing into two main branches:

Sciatic nerve bifurcation in popliteal fossa showing CPN (common peroneal nerve) and TN (tibial nerve) with their branches including LSCN, MSCN, RCF, and SUN

Deep peroneal nerve → innervates toe and foot dorsiflexors (tibialis anterior, extensor hallucis longus, extensor digitorum longus); sensory to the 1st web space
Superficial peroneal nerve → innervates peronei (foot evertors); sensory to the lateral lower leg and dorsum of the foot (sparing the 1st web space)

The fibular head is the most common site of injury because the nerve is superficial, poorly cushioned, and tethered as it wraps anteriorly around the bone.

Causes

In a series of 318 knee-level peroneal nerve lesions, the distribution was:

Stretch/contusion without fracture (44%)
Tumors (13%)
Laceration (12%)
Entrapment (9%)
Stretch/contusion with fracture (7%)
Compression (7%)
Iatrogenic (4%)
Gunshot wounds (4%)

Common specific scenarios:

Leg crossing — habitual pressure at the fibular head
Prolonged bed rest / weight loss — loss of subcutaneous padding
Lithotomy position — stretch with hip/knee flexion
Lateral decubitus positioning (operative) — limb resting against a leg strap
Total knee arthroplasty (TKA) — valgus-flexion deformity is the highest-risk configuration; aberrant retractor placement compressing the nerve against the proximal fibula
Knee dislocation — traction or blunt injury to the lateral knee
Sports injury — "punter's palsy" from forced inversion/plantarflexion
Intraneural ganglia — from the superior tibiofibular joint capsule (underappreciated but treatable); associated with higher BMI, knee/peroneal distribution pain, and fluctuating weakness with weight bearing
Casts, Baker cysts, tumors, hematomas, leprosy

— Localization in Clinical Neurology, 8e, p. 153–157; Miller's Review of Orthopaedics 9th Edition, p. 484

Clinical Features

Motor deficits:

Deficit	Muscle	Branch
Foot drop (impaired dorsiflexion)	Tibialis anterior	Deep peroneal
Toe extension weakness	EHL, EDL	Deep peroneal
Foot eversion weakness	Peroneus longus/brevis	Superficial peroneal

The deep branch is more commonly affected than the superficial, so foot drop tends to dominate over eversion weakness
In some patients, only the extensor hallucis longus is affected, producing big toe drop rather than full foot drop
Gait: high-stepping (steppage gait) to avoid tripping

Sensory deficits:

Dorsum of the foot and toes
Lateral distal lower leg
1st web space (deep branch only)

Reflexes: Ankle (Achilles) reflex is preserved (tibial nerve function)

Tinel sign may be elicited by percussion at the fibular head.

Clinical foot drop — preoperative (A) showing plantarflexion deformity and inability to dorsiflex, versus postoperative (B) showing restored dorsiflexion after peroneal nerve decompression

Differential Diagnosis

The key differentials for foot drop include:

Condition	Distinguishing feature
L5 radiculopathy	Back/leg pain; hip abduction and foot inversion also weak; normal EMG at fibular head
Lumbosacral plexopathy	Widespread L4–S1 weakness
Sciatic nerve palsy	Hamstring weakness + tibial distribution deficit
Paramedian cerebrocortical lesion	Foot inversion also weak (tibial nerve territory); UMN signs (brisk Achilles, upgoing plantar)
Tibialis anterior tendon rupture	No toe extensor or eversion weakness; palpable tendon defect; normal EMG

Key distinguishing feature: In peroneal nerve palsy, foot inversion is preserved (tibialis posterior is tibial nerve). Weakness of foot inversion suggests a central or proximal (sciatic/plexus) lesion.

— Bradley and Daroff's Neurology in Clinical Practice, p. 480

Investigations

EMG/Nerve Conduction Studies (NCS): Localise the lesion to the fibular head; distinguish axonotmesis from neuropraxia; assess prognosis
MRI: Can identify intraneural ganglia, tumors, cysts, or structural compression
If intraneural ganglion suspected: MRI of the knee with dedicated nerve imaging (SPGR FS sequences show fascicular architecture at the fibular head)

Management

Conservative (most cases):

Remove compressive factors — change position, remove casts/wraps, avoid leg crossing
Ankle-foot orthosis (AFO) — maintains ankle at 90° to prevent equinus contracture while awaiting nerve recovery
Physiotherapy — maintain joint range of motion and muscle conditioning

Postoperative peroneal palsy (e.g., after TKA):

First step: flex the knee and remove compressive wraps to decompress the nerve

Surgical:

If no recovery after 3 months and nerve is intact on EMG/NCV → surgical exploration and decompression
If intraneural ganglion: resection of the articular branch and ganglion with joint capsule repair
For complete laceration or failed decompression: nerve repair or transfer

— Miller's Review of Orthopaedics 9th Edition, p. 484; ROSEN's Emergency Medicine, p. 3225–3228; Localization in Clinical Neurology, 8e, p. 155–157

Prognosis

Neuropraxia (compression only, axons intact): Most recover within days to weeks; if not cut, most palsies show return within 3 months
Axonotmesis: Slower recovery (axonal regeneration ~1–3 mm/day); outcome depends on length of nerve to reinnervate
Neurotmesis (complete severance): Poor spontaneous recovery; requires surgical reconstruction
Intraneural ganglia treated surgically have good outcomes if decompressed early

Summary: Peroneal nerve palsy most commonly results from compression at the fibular head, producing foot drop, toe extension weakness, and variable eversion deficit with sensory loss over the dorsum of the foot. EMG/NCS confirm localisation and guide prognosis. Management is initially conservative with an AFO; surgical decompression is indicated if no recovery by 3 months.

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