While heel pain is the most common condition podiatrists see in practice, heel pain can often be complex and occasionally difficult to treat.1 In recent years, we have seen the introduction of new treatments as logical conservative preludes to fasciotomy, including extracorporeal shockwave therapy, injection of the plantar fascia with autologous growth factors and coblation therapy.2 Clinicians are able to employ some of these modalities, such as autologous growth factors, due to a better understanding of the true histological and physiological etiologic mechanism that occurs at the cellular level.3-5 The basic medical science research at the cellular level of tendonopathy has been a critical catalyst in changing our understanding of heel pain etiology. Lemont, et. al., reinforced this point when they observed no histological presence of inflammatory mediators in 50 specimens (100 percent) of plantar fascia that had been resected for the treatment of heel pain.6 These findings must propel us toward a change in our treatment paradigms. Equally important, if not more so, are similar findings and clinical experience in treating other analogous musculoskeletal conditions such as lateral epicondylitis or “tennis elbow.”7,8 While neurogenic etiologies of heel pain comprise the focus of this article, the prevalence of multiple etiology heel pain in clinical practice clearly indicates that our basic understanding of plantar fasciitis is changing and may in fact have been significantly erroneous all this time. Furthermore, the presence of multiple etiology refutes the mistaken tendency to categorize all heel pain as plantar fasciitis when the more correct terminology is plantar fasciosis. The previous catch-all categorization has led to misdiagnosis and less than desirable outcomes in some patients.
Understanding The Array Of Potential Etiologies In Heel Pain
Clinicians often fail to recognize that heel pain can commonly have an isolated neurogenic etiology or it can present concomitantly with other etiological mechanisms.9-11 There is frequently an interplay between the presence of plantar fasciosis and nerve entrapment. Fredericson, et. al., documented via MRI imaging that chronic inflammation of the proximal portion of the plantar fascia can predispose the lateral plantar nerve to entrapment.12 Heel pain etiologies can range from infracalcaneal fat pad atrophy to Reiter’s syndrome (see “A Guide To Potential Heel Pain Etiologies” below).1 More than 2 million patients will be diagnosed with heel pain in a given year, according to estimates from extrapolated data from the American Podiatric Medical Association.13 While the effectiveness of conservative management of plantar fasciitis (fasciosis) is well established, there are no specific studies that document the efficacy of conservative care for managing heel pain when it has a sole neurogenic etiology.1 Given the aforementioned numbers, even for a condition that is successfully diagnosed and treated conservatively more than 90 percent of the time, this still presents approximately 200,000 cases that are of neurogenic or mixed etiology, which may require more definitive and aggressive treatment. Sadly, many cases that fit this description are erroneously attributed to a “recalcitrant” plantar fasciitis status.
Emphasizing The Evolution Of Diagnostic Testing
Differential diagnosis of neurogenic etiologies of heel pain must include tarsal tunnel syndrome, lateral plantar nerve entrapment, medial calcaneal nerve entrapment and what has been described as an entrapment of the first branch of the lateral plantar nerve, which is commonly referred to as Baxter’s nerve. Diabetic peripheral neuropathy can predispose a patient to any of these nerve entrapments with the subsequent presentation of isolated heel pain. Frequently, the diagnosis of an isolated neurogenic cause of heel pain can be problematic and difficult. Technology such as diagnostic ultrasound and MRI can eliminate or substantiate the clinical diagnosis of plantar fasciitis (fasciosis).14 When it comes to determining neurogenic etiologies for the painful heel, one of the biggest problems for clinicians in the past was the lack of anything but electrodiagnostic studies to confirm or substantiate the clinical diagnosis of lower extremity peripheral nerve entrapment. Any experienced clinician knows the frustration of being confronted with overwhelming clinical evidence supporting a diagnosis of a nerve entrapment of the tarsal tunnel only to be informed that the electrodiagnostic studies are “normal.” It is well known that nerve conduction velocity studies are unreliable in the diagnosis of peripheral nerve entrapments in the lower extremity. In my experience, one may have approximately a 50 percent chance of getting a false negative finding in the face of an overwhelming clinical presentation. With the advent of neurosensory testing with the Pressure Specified Sensory Device (PSSD®, Sensory Management Services, LLC), the clinician can now expect a higher level of reliability in confirming the original clinical diagnosis. In a prospective blinded study, Weber demonstrated the sensitivity and specificity of the PSSD compared to standard neurological testing in patients with carpal tunnel syndrome.15 Keep in mind that the median nerve is the single best nerve in terms of reliability for sensitivity and specificity of electrodiagnostic study. Some have advocated making therapeutic decisions for carpal tunnel syndrome in patients with diabetic peripheral neuropathy without the use of electrodiagnostic studies as these diagnostic modalities cannot distinguish those with the syndrome.16 No nerve in the lower extremity even comes close to the median nerve when it comes to the reliability of electrodiagnostic testing. Not only does neurosensory testing with the PSSD modality give the clinician a higher degree of sensitivity, it also allows testing of nerves such as the medial calcaneal nerve which one cannot test with standard electrodiagnostic studies. While the algorithm (see “A Diagnostic Algorithm For Complex, Recalcitrant Heel Pain” below) and heel pain scoring questionnaire (see “How To Use The Heel Pain Scoring System” below) have not been prospectively validated on a large population of patients, these diagnostic tools can give the clinician a good frame of reference for an orderly and stepwise workup of the patient with heel pain. It is critical to take a careful and detailed history in order to determine the true etiology of heel pain. When using the questionnaire during the initial presentation, one can quickly assess the patient. Then assign a score to the patient and institute an appropriate algorithm based upon that score. The scoring is clinical and historical, and the questionnaire includes six patient history questions and five points of clinical evaluation. Diagnostic red flags should include patients who experience pain even at night when they are not on the foot, patients who have increased pain with an orthotic device, and those who say the pain becomes worse the longer they stay on their feet or the more they walk. A family history of diabetes should increase the clinician’s awareness of the possibility of nerve entrapment, even if patients themselves claim not to have diabetes. In many cases, one can further confirm the diagnosis of a neurogenic etiology via the process of elimination with highly reliable modalities such as musculoskeletal sonography. While a normal sonogram of the plantar fascia can eliminate plantar fasciosis as a potential cause, positive sonographic findings of plantar fasciosis cannot rule out a concomitant neural etiology. However, it is very helpful in managing the longstanding patient who has been misdiagnosed and unsuccessfully treated. It can also eliminate fasciosis as a component or contributing factor to the patient’s heel pain. Also be aware when patients present with previously treatedplantar fasciosis which has improved but their heel is still painful after conservative treatment. If they continue to have heel pain, it may be due to a coexistent nerve entrapment where the fasciosis component has been successfully treated. Often, when clinicians question these patients closely, they relate that the nature or type of heel pain changed during the course of treatment. Busy clinicians often miss this subtle difference.
What The Literature Reveals About Nerve Entrapment
Perhaps the most common neurogenic etiology of heel pain is erroneously attributed to Baxter’s nerve. Baxter reported decompression of an entrapment of the first branch of the lateral plantar nerve (which is sometimes referred to as the motor nerve) to the abductor digiti quinti.17 In 1981, Przylucki described this nerve as a potential cause of heel pain years before Baxter’s article.18 Many anatomical texts have also illustrated this nerve. Some of these texts date back to the early part of the 20th century to the point when Sobotta documented its existence.19 However, Roegholt was the first author to suggest that entrapment of this nerve branch could be a cause of heel pain.20 Given the high degree of variability of the neuroanatomy of the medial aspect of the heel, the first branch of the lateral plantar nerve can be a superficial medial calcaneal nerve or a deeper nerve which would be more infracalcaneal as Przylucki described.18 In their true anatomical dissection studies, Louisia and Masquelet identified this nerve in all cadavers.21 They also suggested that proper nomenclature would be the “inferior calcaneal nerve” (ICN). Other names in the literature for this branch include the first branch of the lateral plantar nerve, motor branch to the abductor hallucis muscle, calcaneal branch and Cruvelhier’s medial calcaneal nerve branch. In addition to the nomenclature being wrong for this potential nerve entrapment, there is skepticism if this nerve is really such a prominent neurogenic factor in heel pain. It may be that the medial calcaneal nerve(s) is more commonly a contributor to heel pain. In an important study of 97 heels, Rose, et. al., found a 72 percent incidence of a documented sensory impairment of either the medial calcaneal nerve or the medial calcaneal nerve in combination with the medial plantar nerve.11 This study indicates the prevalence of the medial calcaneal nerve as a neurogenic etiology in heel pain. They also argued that diagnosing medial calcaneal entrapment is difficult. However, with local anesthetic infiltration and a careful injection technique, it is fairly simple to determine whether the medial calcaneal nerve is the sole etiology of heel pain. The medial calcaneal nerve(s) is very superficial and one can easily block them with lidocaine. If the practitioner is careful not to infiltrate the anesthetic deeper than the superficial subdermal layer on the medial aspect of the heel and the patient’s heel pain completely resolves, then this would confirm that the cause of the heel pain is entrapment of the medial calcaneal nerve and not entrapment of the first branch of the inferior calcaneal nerve. Further clinical support for this diagnostic injection would include the lack of impaired sensation along the course of the lateral plantar nerve on the plantar aspect of the foot. This would indicate that the local anesthetic agent did not cause a nerve block of the lateral plantar nerve. It would also mean that its branch, referred to erroneously as Baxter’s nerve or, more properly, the inferior calcaneal nerve, was also not blocked. Additionally, if there is a documented loss of two-point discrimination on the medial skin of the heel, which is innervated by the medial calcaneal nerve(s), then one may confirm entrapment of the medial calcaneal nerve via neurosensory testing. Remember that the first branch of the inferior calcaneal nerve does not have a sensory component to the skin.
Other Key Considerations
Tarsal tunnel syndrome can be subtle and difficult to diagnose, and can have heel pain as its sole component. In a recent study of a series of 25 heels, Oztuna, et. al., found that electrodiagnostic studies documented abnormal sensory nerve conduction of either the lateral plantar nerve or medial plantar nerve in 88 percent of patients with heel pain.22 In 64 percent (14 heels) of the heels, there was an isolated sensory conduction of the lateral plantar nerve.22 The researchers did identify tarsal tunnel in four patients. Interestingly, they used any form of neuropathy, including diabetic peripheral neuropathy, as an exclusion criterion for their controlled study. Clinically, the presence of a provocation sign and a Tinel’s sign are strong indications of entrapment at the level of the tarsal tunnel. While it is very rare, the lateral calcaneal branch coming off the sural nerve is another nerve entrapment that can cause heel pain. There can be a variation in the neuroanatomy where the lateral calcaneal nerve comes all the way under the heel within the infracalcaneal fat pad and provides innervation to the medial aspect of the heel. One can verify this with an anesthetic blockade of only the sural nerve at the lateral aspect of the ankle with subsequent resolution of the patient’s pain. Finally, iatrogenic entrapment from previous heel surgery is common with any medial heel incision. It is nearly impossible with a medial DuVries type incision to retract and protect the branches of the medial calcaneal nerve during open heel surgery. Dellon’s study of the variation of patterns of the medial calcaneal nerve(s) illustrates perfectly why so many medial heel incisions can become problematic for the patient.10,23
When ordinary heel pain attributed to plantar fasciosis does not respond to conservative care or changes in nature during the conservative or surgical treatment phase, clinicians should start to think about nerve entrapment as being the culprit. By using a stepwise approach in the diagnosis of chronic, complex heel pain, the practitioner should be able to identify and subsequently treat the patient’s heel pain etiology appropriately. It cannot be stressed enough that high quality ultrasonography is a technology that should see more use in the treatment of heel pain as there are many “cases” of plantar fasciitis (fasciosis) that can be attributed to nerve entrapments. The clinical experience of pain exacerbation from wearing custom orthoses should also arouse suspicion of nerve entrapment for the practitioner as opposed to writing a new orthotic prescription. Dr. Barrett is an Associate Professor within the Arizona Podiatric Medicine Program at the Midwestern University College of Health Sciences. He is a Fellow of the American College of Foot and Ankle Surgeons. Dr. Barrett is a shareholder in the Baltimore-based Sensory Management Services, LLC, which manufactures and sells the Pressure Specified Sensory Device (PSSD).
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