Heel Neuroma

This is another neuroma but just of any or a mixture of any of the 4 nerve branches innervating in or near the bottom of the heel bone, and accounts for at least 90 percent of all heel pain. It is clearly visible on ultrasound.

Like the forefoot neuromas, they are caused by repetitive weight bearing activity on abnormal foot structure over years of activity. They never go away, once the pain starts, and it also starts suddenly, without guided and directed therapy. The pain also disappears here 99.9 percent of the time with the therapy.

The distinction from plantar fasciitis is that this pain is worst after standing up from a resting position, and actually eases up after taking multiple steps.

To prevent recurrence, once again, it is medically necessary to perform biomechanical measurements, determine the inherited abnormal structure, and prepare Root Functional Orthoses to neutralize the abnormal structural forces causing the heel neuroma.

In the case of heel neuroma, the pain must be resolved by directed therapy before the orthoses can be used and be comfortable. This is a major difference from fasciitis where the orthoses actually provide the relief.

Heel neuroma: the enigma of recalcitrant heel pain and an innovative approach highlighting six surgical cases and a review of two hundred and fifty-seven symptomatic but non-surgical cases


Ira D. Shandles, James Pruchniewski and Katy L. Reynolds

The authors report resolution of recalcitrant heel pain by describing new insights into innervation of the heel. They elucidate biomechanical mechanisms responsible for entrapment of this innervation and explain the diagnostic and therapeutic techniques necessary to manage this etiology, including an innovative therapeutic approach. A one-to-ten year follow-up of the course of 317 heel pain syndrome patients was conducted. The first 216 cases were treated by basic technology providing a cure, with 161 patients responding to a conservative approach and 55 requiring surgery. The final 101 cases received DiapulseĀ® combined with their conservative care and 96 responded while only five required surgery. A 95% success rate of cure was achieved using the new technology without surgery. The sixty surgical cases are proposed as confirmation of the diagnosis because all are accompanied by irrefutable pathological reports. All surgical cases preoperatively were in turn subjected to the same diagnostic and therapeutic protocols as the non-surgical. © 2002 Elsevier Science Ltd. All rights reserved.


Heel neuroma and its correction is offered as the solution to the heel pain problem frequently seen in podiatric medicine (Beito et al. 1991). The differential d diagnoses offered for this symptom have included calcaneal spur, bursitis, plantar fasciitis, calcaneal stress fracture, osteomyelitis, rheumatic and seronegative arthropathies, as well as cutaneous manifestations, fat pad atrophy, neoplasms, vascular insufficiency or vascular congestion, and L-5 to S-1 radiculopathy (Leis et al. 1986, Jennings et al. 1988, Kulund 1988). A biomechanical fault is found to exist in almost all heel pain patients and its control is an important element in their management (Root et al. 1977). When conservative therapy fails, patients may undergo heel spur resection with plantar fasciotomy (Murphy & Baxter 1985, Baxter et al. 1989) as authors recognized the need for a better understanding of the etiology for recalcitrant heel pain in order to explain the unacceptable rate of disappointment.

Heel neuroma and its correction is offered as the solution.

Researchers and surgeons worldwide have successfully, over the past fourteen years, dissected and elucidated the exact branch of the tibial nerve responsible for the onset of a heel neuroma (Przylucki & Jones 1981, Murphy & Baxter 1985, Savastano 1985, Baxter et al. 1989, Weil1994). The questions became:

a. From what etiology can this neuroma's appearance be attributed? b. By what easily reproducible means can its presence be demonstrated? c. How should it be systematically treated?

Understanding the anatomy

The consensus of independent researcher surgeons has been that the unique branch of the tibial nerve involved in the process of heel neuroma development is some part of the first branch (FB) of the lateral plantar nerve (Przylucki @ 2002 Elsevier Science Ltd. All rights reserved Heel neuroma & Jones 1981, Murphy & Baxter 1985, Baxter et al. 1989, Weil1994).

The reluctance to accept nerve entrapment as a source of heel pain may stem from a misconception regarding the course of the FB of the lateral plantar nerve, placing it well distal to the usual area of heel pain near the medial portion of the calcaneal tuberosity (Baxter et al. 1989). Recent studies show that the FB bifurcates from the lateral plantar nerve more proximally than was formerly believed, and as it passes across the heel it innervates the periosteum overlying the medial tuberosity of the calcaneus (Weil1994).

The FB is comprised of three separate divisions:

a. The first, to the medial portion of the calcaneal tuberosity - medial and lateral perichondrium included
b. The second, supplying the flexor digitorum brevis
c. The third, supplying the abductor digiti quinti brevis (Baxter et al. 1989, Weil1994)

Fortunately, the neuroma's body appears to be principally isolated to the division innervating the medial portion of the tuberosity and associated perichondrium, which is the first branch of the first branch of the lateral plantar nerve, a purely sensory branch, superior to, but contiguous with the region above the developing inferior calcaneal spur. It is important to envision that when this calcaneal branch leaves the first branch anatomically, it runs due plantarward to a branch of the laciniate ligament on the medioplantar aspect of the heel before sharply turning due lateralward into the medial portion of the tuberosity of the calcaneus, a superficial position, before reaching its final deep destination. Therefore, understanding the anatomy of the entire FB explains why the pain tends to occur about the heel plantarly, medially and laterally, and is sometimes associated with radiations both dorsally and proximally, and even along the lateral margins of the foot. The FB, by its very anatomy, solves the riddle of the source of these varied but associated focal complaints.


Biomechanics explains the etiology of the tumour once the existence of the precise branch of the peripheral nerve tissue is accepted. Pronation secondary to compensated forefoot or rearfoot varus, flexible forefoot valgus or rearfoot valgus, and compensated equinus can all contribute to heel pain (Root et al. 1997, Davis et al.). It has been suggested that the plantar fascia is caused to rub against nerves resulting in 'pronation neuritis' (Kulund 1988). Hyperpronation will also create compression where the FB passes the medial portion of the calcaneal tuberosity.

A heel spur or inflammation at the origin of the plantar fascia could produce enough swelling to compress the FB against the long plantar ligament and calcaneus during the stance phase of gait (Baxter eta!. 1989). Recurrent irritation can lead to chronic neuritis and ultimately hypertrophy of the nerve sheath fibres (Beito et al. 1991).

The challenge for the clinician is to reproduce the neuroma-type pain near the medial junction of the heel in order to make the differential diagnosis from true fasciitis or 'bursitis'.

The phenomenon of simple plantar fasciitis should be reproducible easily upon forced passive dorsiflexion of the foot at the level of the, The Foot (2002) 12, 10-20, metatarsal heads upon the leg, without palpation of the fascial band (Kulund 1988). If this manouvre fails to reproduce the plantar heel pain of which the patient is so aware, fasciitis is unlikely.

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