Common, Superficial & Deep Peroneal (Fibular) Nerve Anatomy
Overview
The common peroneal nerve is examined more than any other lower-limb nerve because it is the cause of foot drop and because it is so easily injured: it sits subcutaneously on the fibular neck with no protection. The clean way to hold the topic is a two-branch split. The deep peroneal nerve lifts the foot and toes and owns the first web space; the superficial peroneal nerve turns the foot out and owns the dorsum of the foot. Everything clinical flows from that: the pattern of foot drop, the sensory map, the distinction from an L5 root lesion, and the entrapment and surgical danger points down the leg.
Origin & Course
Origin. The common peroneal (fibular) nerve is the smaller terminal branch of the sciatic nerve, carrying fibres from the posterior divisions of L4-S2. It separates from the tibial nerve at (or above) the apex of the popliteal fossa and runs along the medial border of biceps femoris toward the fibular head.
The fibular neck. The nerve passes behind the fibular head, then winds laterally and subcutaneously around the neck of the fibula, where it lies directly on bone with little soft-tissue cover. This superficial, tethered position on bone makes it the most commonly injured nerve in the lower limb, and the site both of compression and of surgical release.
The division. Having rounded the neck, the nerve pierces peroneus longus and divides into the deep and superficial peroneal nerves. The deep peroneal nerve enters the anterior compartment and runs with the anterior tibial vessels; the superficial peroneal nerve descends in the lateral compartment and becomes cutaneous by piercing the deep fascia of the distal leg.
Innervation: Motor & Sensory Supply
Deep peroneal nerve. It supplies the anterior compartment: tibialis anterior, extensor hallucis longus, extensor digitorum longus and peroneus tertius, with extensor digitorum brevis in the foot. Its action is therefore ankle dorsiflexion and toe extension, and its terminal sensory branch covers a small but clinically vital zone, the first dorsal web space.
Superficial peroneal nerve. It supplies the lateral compartment, peroneus longus and brevis, so its action is foot eversion. It then supplies most of the dorsum of the foot, sparing the first web space and the lateral border, which is sural territory.
Lateral sural cutaneous nerve. A branch from the common peroneal nerve to the upper lateral leg, contributing to the sural nerve.
Prognosis: how long to wait, and why the mechanism decides it
When does a foot drop become irrecoverable? Not after any single interval, because the two common lesions behave completely differently, and that difference is also the answer to the knee-dislocation viva below.
- Compressive / neurapraxic
- Cast or brace, crossed legs, squatting, rapid weight loss, positioning, retraction at TKA
- Traction (knee dislocation, PLC)
- Knee dislocation, posterolateral corner disruption
- Compressive / neurapraxic
- Focal, at one point - the fibular neck
- Traction (knee dislocation, PLC)
- A long segment stretched beyond its elastic limit
- Compressive / neurapraxic
- The large majority; most spontaneous recovery happens by 3-6 months, though full recovery can take 12-24 months
- Traction (knee dislocation, PLC)
- For a complete palsy, only about 30-50% regain useful motor function
- Compressive / neurapraxic
- Reassure, splint, wait
- Traction (knee dislocation, PLC)
- Counsel honestly from the start - over-promising recovery here is a named trap
The mechanism explains the difference. A compression injury damages the nerve at a point, so the axons have a short distance of disrupted architecture to cross. A traction injury tears the internal architecture over a long segment, which is why the lesion is often not decompressible and why grafting a long defect gives modest results.
A workable timeline. In order:
- Immediately - document dorsiflexion, eversion and first-web-space sensation, before and after any reduction or manipulation. Fit an AFO early to prevent a fixed equinus contracture while you wait.
- 3-4 weeks - the earliest useful EMG. Fibrillations and positive sharp waves only appear once Wallerian degeneration has occurred, so a study done in the first fortnight can mislead by looking normal.
- 3-6 months - the decision point. No clinical or electrical recovery by then is the usual trigger to explore or decompress a compressive lesion.
- Beyond 6 months - reconstruction rather than repair: a tibialis posterior tendon transfer, rerouted through the interosseous membrane to the dorsum and often done as a Bridle procedure incorporating tibialis anterior and peroneus longus, to restore active dorsiflexion; or a nerve transfer where expertise exists.
The first sign of recovery to look for is sensory, not motor. Returning sensation in the first web space usually precedes any dorsiflexion.
Where this sits. The traction lesions belong to knee dislocation, multiligament knee injury and the posterolateral corner, where the nerve is injured in a substantial minority; the iatrogenic version is on TKA neurovascular injury; a recurrent palsy with no obvious cause should raise the proximal tibiofibular joint and its intraneural ganglion; the biology of what is actually happening while you wait is nerve injury and regeneration; and the compartment the nerve supplies is leg compartments.
Clinical Correlations
Common peroneal palsy. The picture is foot drop, loss of dorsiflexion, with a compensatory high-steppage gait and weak eversion, and sensory loss over the dorsum of the foot and first web space. Plantarflexion and inversion are preserved, because they belong to the tibial nerve.
An L5 radiculopathy also produces foot drop and dorsal-foot sensory change, so the discriminator is what else is weak. In a common peroneal palsy inversion (tibialis posterior, tibial nerve) and hip abduction are preserved, and a positive Tinel sign at the fibular neck supports a peripheral lesion. In L5 radiculopathy inversion is also weak, because tibialis posterior is L5 via the tibial nerve, as is hip abduction (gluteus medius), and back or radicular pain with a wider myotomal pattern points to the root rather than the nerve. So test inversion and hip abduction: weak means L5, spared means peroneal.
Causes at the fibular neck. The nerve is hurt where it is exposed:
- Trauma - fibular neck or head fracture, knee dislocation (often with the tibial nerve and popliteal vessels), direct blow
- Compression - tight plaster or brace, prolonged leg-crossing or squatting, bed-bound positioning, and rapid weight loss ("slimmer's palsy")
- Iatrogenic - positioning in surgery; proximal fibular surgery
- Intraneural ganglion - from the superior tibiofibular joint
Management. Identify and remove the cause, protect the foot with an ankle-foot orthosis (AFO) and maintain ankle range. Electrodiagnostics confirm the lesion level and monitor reinnervation. Compressive cases are released at the fibular neck; an irrecoverable foot drop is reconstructed by nerve repair or grafting or by tendon transfer, and when to stop waiting and do which is the subject of the prognosis section below.
Distal Entrapments and Surgical Risk
Beyond the classic fibular-neck palsy, two distal entrapments and a set of operative danger points complete the picture.
Superficial peroneal nerve entrapment. The nerve becomes subcutaneous by piercing the deep fascia of the anterolateral leg about 10-12 cm above the lateral malleolus. It can be entrapped at this fascial exit, or by a fascial defect or muscle herniation, or after inversion ankle sprains, causing lateral leg or dorsal foot pain and altered sensation that is worse on activity. That makes it a cause of chronic exertional leg pain and a pitfall at lateral ankle arthroscopy portals.
Deep peroneal nerve entrapment (anterior tarsal tunnel syndrome). The nerve can be compressed beneath the inferior extensor retinaculum at the ankle by tight footwear, osteophytes or ganglia, producing first-web-space numbness and, if the motor branch is involved, weakness and wasting of extensor digitorum brevis.
Surgical danger at the fibular neck and proximal fibula. The subcutaneous course makes the nerve vulnerable in lateral approaches to the knee, proximal fibula resection or biopsy, high tibial osteotomy, multiligament knee reconstruction (posterolateral corner) and knee dislocation. The same site is a graft and donor consideration, and it is where an intraneural ganglion arising from the superior tibiofibular joint presents, a recognised and recurrent cause of palsy.
The peroneal nerves in the ankle block. Both terminal branches are anaesthetised as part of the five-nerve ankle block for foot surgery, alongside the posterior tibial, sural and saphenous nerves. The deep peroneal nerve is blocked at the front of the ankle between the tendons of tibialis anterior and extensor hallucis longus, just lateral to the dorsalis pedis (anterior tibial) artery, for the first web space; the superficial peroneal nerve is blocked by a subcutaneous ring across the dorsum of the ankle, for the dorsum of the foot. Knowing which branch covers which territory tells you which to supplement when a block is patchy.
In roughly a fifth to a quarter of limbs an accessory deep peroneal nerve arises from the superficial peroneal nerve, runs down the lateral compartment and behind the lateral malleolus to supply part (or all) of extensor digitorum brevis (EDB). The consequences examiners probe:
- On nerve conduction studies the EDB response evoked by stimulating the deep peroneal nerve at the ankle is smaller than the response from stimulating below the fibular head (a paradoxical larger proximal CMAP) — the giveaway of an accessory deep peroneal nerve, not a technical error or conduction block.
- EDB may be partly preserved despite a deep peroneal lesion, so EDB wasting/function is an unreliable sole indicator of a deep peroneal palsy.
- It is the lower-limb counterpart of the hand's Martin-Gruber anastomosis as a classic innervation variant that confounds electrodiagnostic localisation — know it before you over-call or under-call a peroneal lesion.
Guidelines, Registries & Global Practice
Global Practice Picture
Common peroneal neuropathy is a universal clinical problem - the leading lower-limb compressive neuropathy and the prototypical cause of foot drop. Internationally consistent teaching: protect the fibular neck (positioning, casts), localise the lesion clinically (deep vs superficial branch; peroneal vs L5), confirm with electrodiagnostics, and manage with cause removal, an AFO, and decompression or tendon transfer when indicated.
Side-by-Side Synthesis
- Compartment / muscles
- Anterior (TA, EHL, EDL, per. tertius)
- Action
- Dorsiflexion, toe extension
- Sensory
- First web space
- Compartment / muscles
- Lateral (peroneus longus/brevis)
- Action
- Eversion
- Sensory
- Dorsum of foot (spares 1st web)
- Compartment / muscles
- (parent at fibular neck)
- Action
- Both of the above
- Sensory
- Lateral leg (sural contribution)
Viva Scenarios
Practise clinical reasoning and management decisions out loud
“A patient develops foot drop after a below-knee cast. They cannot dorsiflex or evert the foot and have numbness over the dorsum of the foot. How do you assess and manage this, and how do you exclude an L5 radiculopathy?”
“A patient sustains a knee dislocation. After reduction they have a foot drop. What is your concern, what structures are at risk, and how do you manage the nerve injury?”
Anatomy
- Smaller terminal branch of sciatic (L4-S2)
- Winds around the fibular neck (subcutaneous)
- Divides into deep + superficial peroneal
- Most commonly injured lower-limb nerve
Supply
- Deep: dorsiflexion + first web space
- Superficial: eversion + dorsum of foot
- Plantarflexion/inversion preserved (tibial)
- Lateral sural cutaneous → sural nerve
Clinical
- Palsy → foot drop, high-steppage gait
- Causes: cast, leg-crossing, fibular neck fracture, knee dislocation, weight loss, intraneural ganglion
- L5 differs: inversion + hip abduction also weak
- Distal entrapments: SPN fascial exit (~10-12 cm above lateral malleolus); deep peroneal = anterior tarsal tunnel
- Surgical risk: lateral knee approaches, HTO, proximal fibula, PLC; Mx remove cause, AFO, decompression, tib-post transfer (Bridle)
Evidence Base
Both references (checked against PubMed) are anatomical/clinical rather than outcome trials. McCool's cadaveric study confirms the entrapment mechanism — the deep fascia of peroneus longus compressing the nerve at the fibular neck, with release extended to the deep/superficial bifurcation — which is exactly the surgical anatomy you decompress. Bowley & Doughty situates common peroneal neuropathy within the foot-drop differential, reinforcing clinical localisation plus electrodiagnosis. For a viva the reproducible fibular-neck anatomy and the peroneal-versus-L5 discrimination matter more than either single paper.
Thread common peroneal nerve release-a cadaveric validation study
- Cadaveric validation (15 specimens) of an ultrasound-guided percutaneous 'thread' common peroneal nerve release at the fibular neck
- Confirms the nerve is compressed by the deep fascia of peroneus longus overlying it at the fibular neck
- Release extended to the bifurcation into the superficial and deep peroneal nerves
- No iatrogenic neurovascular or tendon injury; demonstrates the surgically relevant anatomy
Entrapment Neuropathies of the Lower Extremity
- Reviews lower-limb entrapment neuropathies including common peroneal neuropathy causing foot drop
- Emphasises accurate localisation to prevent pain, sensory loss and weakness affecting mobility
- Diagnosis combines clinical examination with electrodiagnosis and imaging
- Distinguishes peripheral peroneal palsy from other causes of foot drop