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Foot and ankle entrapment neuropathies (FAEN) are a collection of syndromes affecting the motor and sensory branches of peripheral nerves innervating the distal lower extremity.


While each entrapment neuropathy has its own set of causes, the etiologies of FAENs produce narrowing of the fibrous and fibro-osseous tunnels leading to focal impingement of the respective nerve(s) with resulting neurologic impairment. This manifests as pain, paresthesia, sensory deficits and weakness. These causes span a variety of issues including the following:

  • Dynamic – i.e., internal foot derangement or aberrant gait pattern leading to nerve injury related to limb positioning1,2
  • Mechanical – i.e., acute trauma such as contusions or fractures; repetitive microtrauma like ill-fitting footwear or sports-related activities such as dancing in pointe or kicking a ball with the dorsum of the foot
  • Space-occupying lesions (SOLs) – i.e., edema, ganglia, lipomas, osteophytes, scars, supernumerary muscles, tumors and varicosities1,3
  • Systemic – i.e. peripheral vascular disease, thyroid disorders, and diabetes mellitus1

Epidemiology including risk factors and primary prevention

FAENs are relatively uncommon though clinically important entities.

  • Tarsal tunnel syndrome, a more recognized entrapment neuropathy, has a reported incidence rate up to 0.6%.4 However, its true incidence and that of other FAENs are unclear secondary in part to under-diagnosis related to occasional unreliability of the clinical and electrodiagnostic (EDX) examination & distraction by more apparent injuries.1,5
  • A recent meta-analysis suggests that strenuous activity and a prior history of trauma could serve as potential risk factors in patients with TTS.6 In general, middle-aged women have a subtle predisposition for developing an entrapment neuropathy.7,8
  • Sports-related repetitive microtrauma is a contributing causative factor in approximately 50% of inferior calcaneal neuropathies (ICN).1,9


Five major peripheral nerves traverse the ankle and innervate the foot:

  • Deep peroneal nerve (DPN)3,5
    The DPN enters the foot anteriorly. It divides into a lateral and medial branch about 1 cm proximal to the ankle. The medial branch runs through the anterior tarsal tunnel (TT) alongside the anterior tibial artery to provide sensation to the first dorsal web space. It courses deep to and between the extensor hallucis longus (EHL) and extensor digitorum longus (EDL) tendons beneath the extensor retinaculum. The lateral branch exits about the anterior TT and innervates the extensor digitorum brevis (EDB) and extensor hallucis brevis (EHB) muscles.
  • Saphenous nerve (SaN)3
    After entering the anteromedial aspect of the ankle, the SaN delivers sensation to the dorsomedial ankle and midfoot.
  • Superficial peroneal nerve (SPN)1,3
    Approximately 8-15 cm proximal to the ankle, the SPN pierces the lateral compartment’s deep fascia to become subcutaneous. About 6 cm above the lateral malleolus, it bifurcates into the medial and intermediate dorsal cutaneous nerves, which supply sensation to the dorsum of the foot.
  • Sural nerve (SuN)1,3
    The SuN, a pure sensory nerve, accesses the foot via a posterior approach to innervate the lateral aspect of the ankle through the base of the 5th ray. This may be absent in up to 20% of individuals per cadaveric studies.10
  • Tibial nerve (TN)1,3,8
    The TN is a direct continuation of the medial trunk of the sciatic nerve. It courses to the medial aspect of the ankle where it becomes the posterior tibial nerve (PTN) and travels beneath a flexor retinaculum along with the flexor digitorum longus (FDL), flexor hallucis longus (FHL), and posterior tibialis (PT) tendons and the posterior tibial vasculature. Distally, it sequentially branches into the medial calcaneal nerve (MCN) and then bifurcates into the lateral plantar (LPN) and medial plantar (MPN) nerves. The level where each branch takes off is variable. Approximately 70% of MCN originate proximal to the TT and 4-7% of PTN bifurcations occur superior to the TT.8,11 Collectively, the plantar nerves innervate the intrinsic foot musculature. In addition, the MPN supplies sensation to the medial two-thirds of the plantar surface while the LPN gives sensation to the lateral one-third of the foot.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

  • DPN
    Anterior Tarsal Tunnel Syndrome
    The DPN is most commonly entrapped at the inferior edge of the extensor retinaculum where the extensor hallucis brevis crosses over top.2,3 It results in a predominantly sensory neuropathy. Weakness and atrophy of the EDB may occur if compression occurs at the superior edge. With compression at the dorsum of the foot, the sensory branch is compressed by the EHB tendon, osteophytes of the navicular-cuneiform or tarsometatarsal joints, or extrinsic factors.
  • SPN
    Superficial Peroneal Nerve Entrapment Syndrome 1,3
    Dysesthesias along the lateral aspect of the lower leg and dorsum of the foot with sparing of the first dorsal web space may develop secondary to entrapment of the SPN as it pierces the deep fascia of the lateral compartment or due to ankle sprain. If the SPN exits more distally, a tension neuropathy may occur because of a tethering-like action.2
  • SuN
    Sural Nerve Entrapment1
    Commonly mistaken for Achilles tendinopathy, this entity typically occurs due to trauma.10 It presents as pain and paresthesias of the lateral ankle, heel and foot.
  • TN
    There are a multitude of distinct FAEN of the TN. These have been listed in a proximal to distal fashion.
    • Tarsal Tunnel Syndrome (TTS)
      TTS results from entrapment of the PTN as it traverses beneath the flexor retinaculum producing sensory impairment and noxious paresthesias along the plantar aspect of the foot and rays. Typically, the symptom severity is proportional to an individual’s amount of activity. Studies reveal the presence of varus heel deformity with pronated forefoot in two-thirds of TTS cases suggesting there is a tension neuropathy component to its pathophysiology.2,8 Beyond these extrinsic causes, there is growing evidence of the role of intrinsic causes such as tendinopathy, tenosynovitis and osteophytes.12 Another rare intrinsic cause could be associated with accessory or variant muscles, most commonly of the flexor digitorum longus.6
    • Medial Calcaneal Neuropathy
      The MCN is the first branch from the PTN past the TT.1,11 When compromised, its symptoms may closely resemble that of Baxter’s neuropathy. (see below) However, it may be distinguished by the presence of sensory loss over the medial heel.3
    • Entrapment of the First Branch of the Lateral Plantar Nerve
      The first branch of the LPN is a sensorimotor nerve, also known as the inferior calcaneal nerve (ICN) or more commonly as Baxter’s nerve. As it courses inferiorly into the foot, it abruptly changes to a lateral direction under the abductor hallucis muscle (ABH). It is vulnerable to compression at this site, which coincides with the medial edge of the quadratus plantae muscle (QP). Other entrapment sites include the medial calcaneal tuberosity and the fascial edge of hypertrophied ABH.1 Its injury results in denervation of the flexor digitorum brevis, QP, and abductor digiti minimi muscles and pain within the medial heel that can be indistinguishable from plantar fasciitis.
    • Entrapment of the Medial Plantar Nerve1,2,3,8
      Referred to as Jogger’s Foot, entrapment of the MPN by the abductor canal is characterized by neuritic discomfort along the medial arch with extension into the medial 3½ rays. It is appropriately named for its prevalence in runners especially those with a high medial arch, valgus hindfoot dynamic deformity and excessive pronation. The resultant repetitive trauma over the anatomic crossover between the FHL and FDL, also known as the knot of Henry, leads to symptom onset.
  • Digital Neuromas
    • Interdigital1,7,8,13
      Morton’s or intermetatarsal neuromas are mechanically induced perineural fibrotic nodules most commonly found in the third intermetatarsal space. They typically form at this location as the third common digital nerve has a larger cross-sectional area than others and there is a greater degree of mobility of the metatarsal heads at this point. Forceful toe dorsiflexion as occurs in running, dancing, and walking can elicit the respective web space pain and paresthesias.
    • Digitial1,10
      Joplin’s or medial plantar proper digital neuropathies are a rare pathology. The MPN’s terminal sensory branch is susceptible to microtrauma and compression where it crosses the first metatarsophalangeal joint and along the hallux’s plantar aspect. It manifests as a palpable mass medial plantar to the distal first metatarsal with associated numbness and pain distributed in that region.

Specific secondary or associated conditions and complications

When evaluating FAEN, it is important to consider all confounding factors that can affect the integrity of peripheral nerves including metabolic disorders (i.e. thyroid dysfunction, diabetes mellitus), alcoholism, vitamin deficiencies, and drug side effects.3 If the symptoms radiate proximally, known as Valleix phenomenon, other contributing etiologies such as double crush syndrome should be entertained.8

While challenging, it is essential to determine if a patient’s symptoms and exam findings are primary or secondary issues. For instance, individuals with heel pain may develop an aberrant gait pattern to reduce the amount of pressure distributed on their heels during the stance phase. However, the foot positioning maintained during an equinovarus gait, where heel strike may be absent, causes reduction of the width of the TT making the ICN, LPN and MPN more susceptible to entrapment.14

Essentials of Assessment


As FAENs may cause impaired motor, sensory and autonomic functions, care should be taken to investigate each of these domains.1 The symptoms accompanying FAEN typically have an insidious onset; however, a history of prior local trauma, athletic endeavors and occupational duties may aid in determining an etiology.10 Associated pain complaints are often difficult to define and are characterized as diffuse, radiating, burning, tingling, numb, and cramping. Activity usually precipitates or exacerbates symptoms, while rest alleviates them.

Physical examination

A thorough proximal-to-distal evaluation of the foot and ankle with contralateral comparison aids in identifying focal deficits and predisposing anatomy as well as reproducing symptoms consistent with a particular FAEN. Allow history and exam findings to guide closer examination of focal areas of concern.

In addition to routine neuromuscular evaluation with gait analysis, inspect the feet for alignment, atrophy and deformity like a claw toe, indicating intrinsic muscle denervation. Stress the ankle ligaments to assess for laxity and joint stability. Palpate along the common sites of entrapment observing for tenosynovitis, SOLs, and tenderness. A monofilament may be used for sensory testing to light touch; however, loss of 2-point discrimination is reported to be the earliest sign of sensory impairment in TTS.8 Later findings of TTS might also include deficits in strength.12 Evaluate for radiculitis with a straight leg raise and/or slump test and for peripheral nerve irritability with Tinel’s (percussion) along the course of the nerve(s) (sensitivity of 0.58 and specificity of 0.70).12

Specific provocative maneuvers include the following:

  • TTS
    • Cuff test8
    • Plantarflexion-inversion test, also known as Trepman’s test, which may cause the PTN and its branches to become compressed within the TT14 
    • Dorsiflexion-eversion test results in pain or numbness at the ankle or sole secondary to PTN tension and compression within the TT (sensitivity 0.98 and specificity of 1.00)15
    • Triple compression test combines Trepman’s and Tinel’s test (sensitivity of 0.86 and specificity of 1.00)15

Clinical functional assessment: mobility, self-care cognition/behavior/affective state

Assessment of gait mechanics is important to reduce falls and ensure safety. An assistive device may be required.

Laboratory studies

Diagnostic studies may help identify metabolic etiologies as well as guide the patient’s response to their medical management. Rheumatologic screening may also be performed if there is associated tenosynovitis and joint swelling.3


There are 4 main diagnostic imaging modalities for the examination of FAEN.

  • X-ray1,3,8
    • Radiography is useful in identifying exostoses as well as osseous malalignment when performed weight-bearing.
  • Computed tomography (CT)3
    • CT may better depict osseous projections than x-ray.
  • Magnetic resonance imaging (MRI)1
    • MRI and high-resolution MR neurography enable direct visualization and tracking of the nerves. This is most easily accomplished in the axial view.
    • MRI is useful in the evaluation of soft tissues and osseous structures. Muscular atrophy is an indirect indication of denervation, while increased T2-weighted signal intensity and changes in the size of a nerve are direct signs of injury.
    • There are limitations and challenges associated with diagnosing TTS; however, MRI has been demonstrated to have utility in identifying the etiologies or causative factors that result in TTS, which is often attributed to idiopathic causes. As a result, MRI is the preferred diagnostic modality when evaluating patients for possible TTS.16
  • Ultrasound (US)
    • US enables point-of-care evaluation of nerves, muscles, tendons, ligaments and other soft tissues that may contribute to an entrapment neuropathy. Nerve entrapment may be signified by a focal flattening of the nerve with proximal increase in cross-sectional area (CSA) and hypoechoic appearance due to swelling. Dynamic testing may be utilized to evaluate for position-dependent compression.17
    • Absolute CSA within the tunnel of 15 mm2 (74% sensitivity and 100% specificity) or change in CSA of 5 mm2 (81% sensitivity and 100% specificity) 18. In comparison with the contralateral side, a >1.8 mm2 CSA difference of the TN at the TT is deemed significant.13
    • Studies indicate that US has 100% sensitivity and 83.3% specificity for the detection of Morton neuromas, which may appear hypoechoic, anechoic or mixed echotexture.6 US provides additional clinical value as a Morton neuroma with >5 mm2 CSA in the transverse plane is likely to be symptomatic.7,13 Recent literature has demonstrated improved accuracy of ultrasound (compared with MRI) in identifying Morton neuromas.19
    • Ultrasound guidance can be used in conjunction with electrodiagnostic studies for diagnosis.20,21
    • Although ultrasound provides a cost-effective means of assessment, results are operator dependent.

Supplemental assessment tools

Electrodiagnostics (EDX) may be used to confirm clinical suspicions of a FAEN. Although it is 90% accurate in identifying well-established TTS, its performance is fraught with technical challenges due to the small size of the distal nerve branches, which is why a normal study does not rule out a FAEN.3,4,8 Ultrasound guidance has been combined with EDX to more efficiently localize affected nerves/branches, leading to a more accurate test and less pain. Guided near-needle sensory tests have been used to make a positive diagnosis in 90% of patients. In the setting of a peripheral neuropathy, EDX studies are of low clinical utility for FAEN diagnosis.22

If EDX is negative, evaluation with a pressure-specified sensory device, which measures cutaneous pressure thresholds, may be considered. It is more sensitive but less specific than EDX.8 Results should be clinically correlated due to a higher incidence of false positives.

Performance of an ultrasound guided injection of local anesthetic and corticosteroid to the point of maximum tenderness or within the respective fibro-osseous tunnel may be diagnostic and therapeutic.1,2,3,11

Early prediction of outcomes

Symptom duration and severity may indicate the extent of injury and potential for functional recovery.1 Positive prognostic indicators for surgery include young age, short duration of symptoms, absence of prior ankle sprains, identifiable focal lesion, and diagnosis before onset of motor dysfunction.8 Individuals with idiopathic or post-traumatic cases typically fare worse.

Of note, there is not a consistent correlation between EDX and operative findings or post-surgical recovery.3



Social role and social support system


Professional issues

In general, there is an inverse relationship between the size of the nerve in question and the quality of the US equipment required to adequately visualize it.23 Therefore, absence or suboptimal appearance of a small nerve under US may be multifactorial and may not indicate pathology. For this reason, quantitative measurements of the DPN, SuN, and plantar nerves are usually not utilized for US diagnosis. Instead, evaluation of the surrounding musculature for indirect signs of denervation is performed.

Rehabilitation Management and Treatments

Available or current treatment guidelines

Treatment is dependent on the site and etiology of the pathology. If the FAEN is a secondary issue, the primary etiology must be addressed. For instance, optimizing blood glucose levels for diabetes mellitus, weight loss for obesity, sobriety from alcoholism, compression garment or decongestion therapy for edema, and vitamin supplementation for deficiencies.3,8

Accommodative footwear may decrease focal compression, while use of wedges and foot & ankle orthoses may improve symptoms by reducing neural tension via maintenance of proper foot and ankle alignment & limiting range of motion. Metatarsal padding may provide relief for interdigital neuromas.

For runners who overpronate, modifying their technique to incorporate a subtle toe-in to promote striking of the lateral aspect of the foot may decrease their amount of dynamic nerve impingement. Functional rehabilitation with physical therapy to address ankle instability and medial longitudinal arch compromise due to extrinsic and intrinsic muscle weakness is also recommended.3,8

Associated pain may respond positively to trials of anti-neuropathic agents including gabapentin and tricyclic antidepressants.11 Nonsteroidal anti-inflammatory agents may also provide relief, especially in the acute phase.

As mentioned previously, ultrasound guided injection of local anesthetic and corticosteroid to the point of maximum tenderness or within the respective fibro-osseous tunnel may be diagnostic and therapeutic.1,2,3,11 This may be an effective option to facilitate participation and progress with physical therapy.

In the context of clinical FAEN, surgery should be considered when SOLs are present or an individual has symptoms persisting for at least 2-3 months despite non-operative management.1

At different disease stages

Following surgery, a compression dressing is typically placed to manage post-operative swelling in collaboration with elevation. Rest, ankle immobilization and partial weight bearing with crutches and post-operative shoes are encouraged for about 7-10 days. During this period, light range of motion exercises may be performed. This is followed by a graduated return to activity as tolerated.

Coordination of care

Diagnosis and treatment of FAEN requires a thorough knowledge of the foot and ankle’s neuroanatomy & an interdisciplinary approach that should be led by a physiatrist and include physical therapy, orthoses, and orthopedic and podiatric surgery as needed.

Patient & family education

After surgery, patients may appreciate signs of nerve recovery within 6 weeks. Maximum functional return may occur in 6 – 12 months.3

Measurement of Treatment Outcomes including those that are impairment-based, activity participation-based and environmentally-based

Approximately 90% of individuals with chronic heel pain and 20% of patients within interdigital neuromas achieve satisfactory pain levels to resolution of symptoms with non-operative management.11,14

Surgical outcomes vary according to lesion addressed. Satisfactory results are obtained in 60-91% of TT releases, approximately 85% of ICN decompressions, and 75% of SPN decompressions.11,24

Translation into Practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

FAEN should be considered when pain, paresthesias and associated functional impairment extend beyond a sensible healing time.5

Despite technological advancements with diagnostic imaging, the etiology of TTS remains unknown in up to 40% of cases.1

Cutting Edge/ Emerging and Unique Concepts and Practice


  • Triple Compression Stress Test15
    • Ankle is plantarflexed and inverted position while the TN is compressed by the examiner’s 2nd through 4th fingers. 
  • Proposed Sonographic Criteria for TTS
    • Measure the CSA of the PTN within the TT and at the proximal tunnel. Proposed optimum cutoffs:
      • 1 for within tunnel-to-proximal tunnel CSA ratio25
      • Absolute CSA within the tunnel of 15 mm2 (sensitivity 0.74 and specificity 1.00)
      • Change CSA of 5 mm2 (sensitivity 0.81 and specificity 1.00).18
  • One emerging therapy involves utilization of intraoperative neuromonitoring during tarsal tunnel decompression procedures, which may improve surgical outcomes. 26
  • Ultrasound-guided decompression of the distal and proximal TT has been demonstrated to be technically feasible in cadaveric studies and subsequent clinical application has validated its utility as effective means of decompression of the TN. 27,28,29

Gaps in the Evidence-Based Knowledge

There continues to be controversy regarding the diagnosis of TTS. Given the absence of gold standard testing, it remains primarily a clinical diagnosis.


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  8. Lau JT, Daniels TR. Tarsal Tunnel Syndrome: A Review of the Literature. Foot Ankle Int. 1999;20(3):201–209.
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  15. Bowley, MP, & Doughty, CT. (2019). Entrapment Neuropathies of the Lower Extremity.  In: Medical Clinics, 103(2), 371-382.
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  19. Xu Z, Duan X, Yu X, Wang H, Dong X, Xiang Z. The accuracy of ultrasonography and magnetic resonance imaging for the diagnosis of Morton’s neuroma: A systematic review. Clinical Radiology.  2015; 70(4), 351-358.
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  28. Fernández-Gibello, A, Moroni, S, Camuñas, G, Montes, R, Zwierzina, M, Tasch, C, Konschake, M. (2019). Ultrasound-guided decompression surgery of the tarsal tunnel: A novel technique for the proximal tarsal tunnel syndrome—Part II. Surgical and Radiologic Anatomy (English Ed.), 41(1), 43-51.
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Original Version of the Topic

Brionn K. Tonkin, MD, Alexander Senk, MD. Ankle and foot neuropathies & entrapments. Original Publication Date 9/16/2015

Previous Revision(s) of the Topic

Alexander Senk, MD, Michael V. Nguyen, MD, MPH, Sima C. Patel, MD, Philip T. Kuball, Brionn K. Tonkin, MD. Ankle and foot neuropathies & entrapments. Original Publication Date 1/14/2020

Author Disclosure

Alexander M. Senk, MD
Nothing to Disclose

Kersten L. Schwanz, MD
Nothing to Disclose

Dean Wundrach
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Katherine Weir
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Sima C. Patel, MD
Nothing to Disclose

Michael V. Nguyen, MD, MPH
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