Deep Peroneal Nerve Entrapment


The deep peroneal nerve is 1 of the terminal branches of the common peroneal nerve, originating just distal to the fibular head.49 The deep peroneal nerve enters the anterior compartment in front of the interosseous membrane. It courses lateral to the TA muscle. It travels along with and usually lateral to the anterior tibial artery and vein.

It courses between the TA and the EDL in the proximal third, and between the TA and EHL in the middle third of the leg and anterior to the anterior tibial vessels. At approximately 3-5 cm proximal to the mortise, the EHL crosses over the nerve, and the nerve is then seen between the EHL and EDL in the distal part of the leg, at an average of 1.25 cm above the ankle joint. Occasionally, the nerve does not enter this interval until just distal to the ankle mortise. At this level, the nerve is about 3 mm in size and may be under the extensor retinaculum, because the inferior extensor retinaculum can be centered, above, or below the ankle mortise level.

At approximately 1 cm distal to the ankle mortise, the nerve divides into lateral and medial branches. The terminal lateral branch curves laterally and supplies the EDB, the extensor hallucis brevis (EHB), the adjacent tarsal and tarsometatarsal joints (including 2-4 branches innervating the anterolateral part of the subtalar joint), and, occasionally, the second and third dorsal interosseous muscles.

The terminal medial branch is just medial to the dorsalis pedis artery and just lateral to the first tarsometatarsal joint. It travels between EHL tendon and EHB muscle on the dorsum of the foot. At approximately the metatarsophalangeal (MTP) joint level, the EHB crosses over the nerve, and the nerve is then between the EHB and the EDL to the second toe. It then divides into the dorsolateral cutaneous nerve of the great toe and the dorsomedial cutaneous nerve of the second toe. It supplies sensation to the web between the first and second toes, the dorsalis pedis artery, the adjacent MTP and interphalangeal joints, and usually the first dorsal interosseous muscle. It occasionally supplies the second and third interosseous muscles.


This entrapment is most commonly due to compression of the deep peroneal nerve and repetitive mechanical irritation of the nerve at the ankle beneath the extensor retinaculum. Entrapment of the deep peroneal nerve in this location has also been called the anterior tarsal tunnel syndrome. Within the anterior tarsal tunnel, there are 4 tendons, 1 artery, 1 vein, and the deep peroneal nerve. Typically, the nerve is trapped beneath the superior edge of the retinaculum. In this location, it is compressed by the crossing EHL tendon and under the EHB muscle, as well as directly over osteophytes, exostosis, or bony prominences of the talotibial, talonavicular, naviculocuneiform, or cuneiform metatarsal joints. Presence of an os intermetatarseum between the first and second metatarsal base has also been associated with entrapment symptoms.

Space-occupying lesions, such as ganglia, also contribute to symptoms in this tight canal. Repeated dorsiflexion and plantarflexion of the ankle contributes to this mechanical condition by pinching the nerve in this tight space, and inversion trauma has been shown to lower the motor conduction velocity of the deep peroneal nerve.

Postural causes, such as wearing high-heeled shoes, in which the nerve is stretched over the midfoot joint, and prolonged or repetitive sitting on the plantarflexed feet, such as is necessary for performing the namaz in Islam, are other commonly seen etiologies. Other etiologies include anomalies of the EHB distal to the retinaculum.

Entrapment of the deep peroneal nerve, however, can occur anywhere along the course of the nerve, including just distal to the neck of the fibula, anterior to the ankle joint, and distal to the inferior extensor retinaculum, but such entrapment would not be considered anterior tarsal tunnel syndrome. Common etiologies for proximal entrapment of the deep peroneal nerve include space-occupying lesions about the proximal fibula, surgical procedures about the lateral knee (including proximal tibial osteotomy), and chronic anterior exertional compartment syndrome seen in athletes.


The usual complaint of patients with deep peroneal nerve entrapment includes vague pain, a burning sensation, or a cramp over the dorsum of the foot, which may or may not involve the first webspace. Patients may have associated sensory changes in the first dorsal webspace. Some patients may present with neuritic symptoms along the course of the nerve, such as unrelenting pain at rest and during sleep. There may be pain in the ankle region even if only the motor nerve is involved. Symptoms may occur or worsen only with a certain shoe or boot or with certain activities. Although less common, patients with more proximal entrapment may present with frequent tripping due to foot drop or weakness of the EHL.

With proximal entrapment, motor dysfunction may be demonstrated on regular gait examination, with presentations such as a dramatic foot drop. However, symptoms are usually more subtle and are noted only on heel walk or a hop test. With long-standing dysfunction, plantarflexion of the ankle with extension of the toes can compress the nerve as it passes beneath the extensor retinaculum, which can worsen the symptoms. Muscular atrophy may also be noted in the anterior compartment of the EDB with distal entrapment of the nerve.

With distal entrapment, tenderness may be elicited along the entrapped segment of the nerve over the anterior ankle or just distal to it, and an underlying bony prominence is usually present. Provocative dorsiflexion and plantarflexion of the ankle may bring on or increase symptoms. A sensory deficit in the first webspace may also be detectable. Most patients have a positive Tinel test result over the entrapment site, commonly around the fibular neck or over the anterior ankle.

Incomplete involvement can also occur, affecting isolated sensory or motor branches. Temporary resolution of neuritic symptoms following an injection of the nerve with plain lidocaine at the site of entrapment is a good indicator verifying the diagnosis.

Bony impingement can usually be seen on conventional lateral ankle or foot radiographs. Oblique radiographs taken from different angles are necessary to better define smaller osteophytes, exostosis, or other bony masses about the anterior ankle or the dorsomedial midfoot. Knee radiographs are needed for suspected proximal involvement. If necessary, a CT scan will provide more detailed information on the bony anatomy of the area.

Ultrasonography has been useful for diagnosis and localization of cystic masses impinging on the nerve. Occasionally, MRI is necessary to obtain additional information about soft-tissue masses, synovial reaction, adjacent bone, and chondral and soft-tissue involvement.

Electrodiagnostic studies are helpful in further defining the zone of compression and in evaluating for concomitant radiculopathy or peripheral neuropathy. In deep peroneal nerve injury or entrapment, the results may show a decrease in the amplitude of the response if axonal involvement is present or conduction block occurs from demyelination. The distal latency may be prolonged if entrapment is present in the anterior tarsal tunnel region, and the NCV is decreased across the leg region if the entrapment or injury is more proximal. An accessory nerve may also be present. The accessory peroneal nerve originates from the superficial peroneal nerve and traverses posterior to the lateral malleolus to provide variable innervation to the EDB. This anomaly is identified when the response is recorded from the EDB that is larger with proximal stimulation (at the fibular head) than with distal stimulation (at the ankle).

Needle examination may reveal the presence of fibrillations and positive sharp waves in the EDB only if present at the anterior tarsal tunnel. If entrapment is present more proximally, the denervation is present in the TA as well as in the EDB.

Denervation may be present, however, with other neurologic conditions. The short head of the biceps femoris, as well as the medial gastrocnemius, tensor fascia lata, and lumbar paraspinal muscles, should be tested if findings in the deep peroneal muscles rule out a more proximal problem, such as a radiculopathy. The absence of findings in these muscles, as well as in the peroneus longus and brevis, confirms the presence of a deep peroneal motor-nerve injury.

Some reports have stated that there may be a high percentage of denervation in the foot intrinsic muscles in healthy subjects, but subsequent reports have found that the actual percentage of abnormal findings in healthy subjects is low for a well-trained electromyographer. Many times, electrodiagnostic test findings are normal because these dynamic syndromes frequently improve or resolve at rest.


Nonsurgical care most importantly involves patient education to eliminate predisposing factors. For example, padding of the tongue of the shoe, the elimination of shoes with laces, or the use of alternative lacing methods, as well as the avoidance of high heels, may be sufficient to resolve symptoms.

Physical therapy is useful for strengthening the peroneal muscles in cases associated with weakness and in individuals with chronic ankle instability; physical therapy may also improve symptoms.

In-shoe orthotic devices are helpful in certain instances, such as for correction of a biomechanical malalignment in gait (eg, in patients with severe flatfoot or cavus foot).

NSAIDs and antineuritic medication may be helpful as an adjunct to other treatment modalities. Injection of steroids plus lidocaine near the site of involvement can reduce symptoms in some individuals.

In addition, consideration should be given to a metabolic workup to rule out thyroid dysfunction and diabetes in select individuals. Further workup may be necessary to rule out lumbar radiculopathy.

Surgical options can be considered once symptoms are deemed refractory to nonoperative measures. Options include surgical release of the deep peroneal nerve in primary and idiopathic cases; and excision of the nerve in cases of direct nerve injury due to previous surgery, in cases of direct trauma, or in revision cases. Surgical decompression of the nerve can provide immediate improvement of symptoms.

Dellon reported on surgical release of the deep peroneal nerve in 20 patients.50 With a mean follow-up time of more than 2 years, he reported excellent results in 60% of patients, good results in 20% of patients, and no improvement in 20% of patients.

The surgical procedure can include part or all of a longitudinal straight or S -shaped incision on the dorsum of the foot, starting between the bases of the first and second metatarsals and extending proximally to the anterior ankle, depending on the predicted location of entrapment. The deep fascia overlying the deep peroneal nerve and the dorsalis pedis artery is released, as is the inferior part of the extensor retinaculum; the superior part can be preserved to maintain the function of the extensor tendons. The deep peroneal nerve is followed proximally and distally to verify a full release. Nerves that appear to be normal in consistency and size can be released.51

It is important to treat other underlying etiologies for entrapment or stretch, such as complete excision of underlying osteophytes during surgery. The decision to perform a neurolysis versus an excision, transposition, or both is dependent on the severity of injury to the nerve. Excision of the nerve in cases in which the nerve is abnormal, such as those directly manipulated during surgery or entrapped in scar tissue, is indicated. Neuroma in continuity is best excised and allowed to retract into deep tissues, and transposition of the stump into muscle belly may be possible, depending on the level of excision. Dellon and Aszmann reported on excision of the superficial and deep peroneal nerves in the lateral leg, with translocation of the nerves into a muscle (with excellent results obtained in 9 of 11 patients).48

When entrapment of the nerve is caused by the EHB muscle, the muscle is hypertrophied and has thick fibrous bands that compress the deep peroneal nerve. Decompression of the nerve and excision of the muscle and fibrous band can lead to complete resolution of pain, but numbness in the first webspace may be persistent.

Entrapment of the deep peroneal nerve can occur anywhere throughout its course, from the region just distal to the fibular head to the dorsal first webspace. The most common location of entrapment is just anterior to the ankle, under the extensor retinaculum. Entrapment at this site is also called anterior tarsal tunnel syndrome. The most common etiologies for entrapment include prominent bony or soft-tissue masses, such as exostoses, osteophytes, and ganglion cysts, as well as acute direct trauma and chronic compression or stretch, as with lace-up shoes or high heels.

The most common presenting symptom is a vague pain on the dorsum of the foot, with occasional, associated numbness or weakness. Treatment options are aimed at eliminating underlying etiologies of entrapment. Surgical release or excision is reserved for refractory cases.