Ankle and foot neuropathies & entrapments

Author(s): Brionn K. Tonkin, MD, Alexander Senk, MD

Originally published:09/16/2015

Last updated:09/16/2015

1. DISEASE/DISORDER

Definition

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.

Etiology

While each entrapment neuropathy has its own set of characteristic 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:

  1. Dynamic – i.e., internal foot derangement or aberrant gait pattern leading to nerve injury related to limb positioning1,2
  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 one’s foot
  3. Space-occupying lesions (SOLs) – i.e., edema, ganglia, lipomas, osteophytes, scars, supernumerary muscles, tumors and varicosities1,3
  4. Systemic – i.e. peripheral vascular disease and diabetes mellitus1

Epidemiology including risk factors and primary prevention

As a whole, 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 examination and distraction by more apparent injuries.1,5 In general, middle-aged women have a subtle predisposition for developing an entrapment neuropathy.6,7 Sports related repetitive microtrauma is a contributing causative factor in approximately 50% of inferior calcaneal neuropathies (ICN).1,8

Patho-anatomy/physiology

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

  1. 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) muscle.
  2. Saphenous nerve (SaN)3
    After entering the anteromedial aspect of the ankle, the SaN delivers sensation to the dorsomedial ankle and midfoot.
  3. 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. Then 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.
  4. 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.9
  5. Tibial nerve (TN)1,3,7
    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) 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.7,10 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)

  1. 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 predominately sensory neuropathy. Weakness and atrophy of the EDB may occur if compression occurs at the superior edge.
  2. 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
  3. SuN
    Sural Nerve Entrapment1
    Commonly mistaken for Achilles tendinopathy, this entity typically occurs due to trauma.9 It presents as pain and paresthesias of the lateral ankle, heel and foot.
  4. TN
    There are many distinct FAEN of the TN. These have been listed in a proximal to distal fashion.
  5. 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.2,7
  6. Medial calcaneal neuropathy
    The MCN is the first branch from the PTN past the TT.1,10 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
  7. Entrapment of the first branch of the lateral plantar nerve
    The first branch of the LPN is a sensorimotor nerve that is 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 a 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.
  8. Entrapment of the Medial Plantar nerve1,2,3,7
    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.
  9. Digital neuromas
    Interdigital1,6,7,11
    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.Digitial1,9
    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 medioplantar 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 (ie. 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.7

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 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.12

2. ESSENTIALS OF ASSESSMENT

History

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, history of prior local trauma, athletic endeavors and occupational duties may aid in determining an etiology.9 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 eliciting symptom reproduction consistent with a particular FAEN. Allow history and exam findings to guide closer examination of focal areas on concern.

In addition to routine neuromuscular evaluation with gait analysis, inspect the feet for alignment, atrophy and deformity like a clawtoe, which would indicate 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.7

Evaluate for peripheral nerve irritability with Tinel’s along the course of the nerve(s) in question and for radiculitis with a straight leg raise test. Perform provocative maneuvers like the plantarflexion-inversion test, also known as Phalen’s, which will reproduce patient’s symptoms if positive as the PTN and its branches become compressed within the TT.12 The cuff test may also reproduce symptoms in TTS.7

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

N/A

Laboratory studies

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

Imaging

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

  1. X-ray1,3,7
    Radiography is useful in identifying exostoses as well as osseous malalignment when performed weight-bearing.
  2. Computed tomography (CT)3
    CT may better depict osseous projections than x-ray.
  3. 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.
  4. 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 and hypoechoic appearance due to swelling. Dynamic testing may be utilized to evaluate for position-dependent compression.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.6US provides additional clinical value as a Morton neuroma with >5 mm2 cross-sectional in the transverse plane is likely to be symptomatic.6,11 In comparison with the contralateral side, a >1.8 mm2 cross-sectional area difference of the TN at the TT is deemed significant.11

Supplemental assessment tools

Electromyography 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.3,4,7 In the setting of a peripheral neuropathy, electrodiagnostic studies (EDx) are of low clinical utility for FAEN diagnosis.14

If EDx is negative, evaluation with a pressure-specified sensory device, which measures cutaneous pressure thresholds, may be considered, as it is more sensitive but less specific than EDx.7 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.1,2,3,10

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.7 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

Environmental

N/A

Social role and social support system

N/A

Professional issues

In general, there is an inverse relationship to the size of the nerve in question and the quality of the US equipment required to adequately visualize it.15 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.

3. 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.3,7

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 and limiting range of motion. Metatarsal padding may provide relief for interdigital neuromas.

For runners who over pronate, 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.3,7

Associated pain may respond positively to trials of anti-neuropathic agents including gabapentin and tricyclic antidepressants.10 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.1,2,3,10 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 shoe are encouraged for about 7-10 days during which 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 and 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.10,12

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.10,16

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

4. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

N/A

REFERENCES

  1. Donovan A, Rosenberg ZS, Conrado F. MR Imaging of Entrapment Neuropathies of the Lower Extremity – Part 2. The Knee, Leg, Ankle and Foot. RadioGraphics. 2010;30(4):1001–1019.
  2. Delfaut E, Demondion X, Bieganski A, Thiron M-Ca, Mestdagh H, Cotten A. Imaging of Foot and Ankle Nerve Entrap- ment Syndromes : From Well-demonstrated to Unfamiliar Sites. RadioGraphics. 2003;23(3):613–623.
  3. Beskin JL. Nerve Entrapment Syndromes of the Foot and Ankle. J Am Acad Orthop Surg. 1997;5(5):261–269.
  4. Park T. Tarsal Tunnel Syndromes. In: Foot and Ankle Nerve Disorders. Rochester: American Association of Neuromuscular & Electrodiagnostic Medicine; 2011:7–16.
  5. Kopell H, Thompson W. Peripheral Entrapment Neuropathies of the Lower Extremity. N Engl J Med. 1960;262(2):56–60.
  6. Bianchi S, Martinoli C. Foot. In: Ultrasound of the Musculoskeletal System. Springer; 2007:835–888.
  7. Lau JT, Daniels TR. Tarsal Tunnel Syndrome: A Review of the Literature. Foot Ankle Int. 1999;20(3):201–209.
  8. Del Toro DR. First Branch Lateral Plantar Neuropathy“ ”Baxter’s Neuropathy”. In: Foot and Ankle Nerve Disorders. Rochester: American Association of Neuromuscular & Electrodiagnostic Medicine; 2011:17–24.
  9. McCrory P, Bell S, Bradshaw C. Nerve Entrapments of the Lower Leg, Ankle and Foot in Sport. Sport Med. 2002;32(6):371–391.
  10. Mann J. Surgical Management of Entrapment Neuropathies in the Foot, Including Indications and Outcomes. In: Foot and Ankle Nerve Disorders. Rochester: American Association of Neuromuscular & Electrodiagnostic Medicine; 2011:33–50.
  11. Peck E, Strakowski J. Ultrasound evaluation of focal neuropathies in athletes: a clinically-focused review. Br J Sports Med. 2015;49(3):166–175.
  12. Hendrix CL, Jolly GP, Garbalosa JC, Blume P, DosRemedios E. Entrapment Neuropathy: The Etiology of Intractable Chronic Heel Pain Syndrome. J Foot Ankle Surg. 1998;37(4):273–279.
  13. Martinoli C, Bianchi S. Ankle. In: Ultrasound of the Musculoskeletal System. Springer; 2007:773–834.
  14. Preston DC, Shapiro BE. Tarsal Tunnel Syndrome. In: Electromyography and Neuromuscular Disorders. 3rd ed. Elsevier; 2013:365–371.
  15. Valle M, Zamorani MP. Nerve and Blood Vessels. In: Ultrasound of the Musculoskeletal System. Springer; 2007:97–136.
  16. Patel AT. Foot Pain Related to Peroneal (Fibular) Nerve Entrapments (Deep and Superficial) and Digital Neuromas. In: Foot and Ankle Nerve Disorders. Rochester: American Association of Neuromuscular & Electrodiagnostic Medicine; 2011:25–32.

Bibliography

Jacobson JA. Ankle, Foot and Lower Leg Ultrasound. In: Fundamentals of Musculoskeletal Ultrasound. 2nd ed. Elsevier Saunders; 2013:257–337.

Author Disclosure

Brionn K. Tonkin, MD
Nothing to Disclose

Alexander Senk, MD
Nothing to Disclose

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