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Neurogenic Heel Pain And The Use Of Diagnostic Ultrasound

While heel pain is a very common condition, there are a variety of possible etiologies. With this in mind, this author discusses current anatomical and biomechanical insights, key considerations with degeneration in the plantar fascia and how ultrasound may help facilitate an improved diagnosis of plantar fasciopathy.

Heel pain in the world is endemic and the numbers of patients suffering from this malady are increasing every year. Heel pain can severely affect a patient’s overall quality of life.1

Unfortunately, we often and arbitrarily dismiss heel pain as nothing more than plantar fasciitis, simple to treat with a “cookie cutter” approach, and some authors have claimed that it is a self-limiting condition.2 Any physician who has spent significant time in the clinical management of this extremely perplexing disorder will acknowledge this is an erroneous statement. It was well documented in the early 2000s that this condition is not inflammatory but rather degenerative in nature.3

A 2003 survey by the American Podiatric Medical Association attributed up to 44 percent of patient visits to a podiatrist to a chief complaint of heel pain.4 With a population in the United States greater than 300 million and the estimation that up to 10 percent of the population will suffer from heel pain, there is a rapid realization that the number of complex heel pain cases is staggering.5 While researchers have estimated that up to 93 percent of the cases of heel pain are due to plantar fasciopathy, the average clinician is not well versed in the advanced diagnostic modalities that would help grade and quantify the severity of the fasciopathy, and further help determine all possible pain generators contributing to the presenting symptoms.4

Even with the assumption that 93 percent of cases of heel pain are due to an isolated plantar fasciopathy, it would still leave a number greater than 21 million patients with multiple etiology heel pain syndrome (MEHPS). This means that there are many people who have been misdiagnosed or only partially diagnosed, which results in suboptimal treatment. With the advent of diagnostic ultrasound and to a lesser extent magnetic resonance imaging (MRI), we can more effectively treat plantar fasciopathy because the practitioner can quickly and objectively appreciate the severity of the condition. There is no more guessing about the status of the patient’s fascia. A true working diagnosis can happen in seconds.

Current Insights On The Relationship Between The Plantar Fascia And The Achilles Tendon
There is often debate about whether the plantar fascia is a continuation of the Achilles tendon insertion on the inferior aspect of the calcaneus but in reality, it makes little difference from a mechanical standpoint.6 The mechanical action of the Achilles tendon will still have an unmitigated effect on the tension of the plantar fascia because of the closed chain kinetics.   

Authors have clearly demonstrated that an increase in Achilles tendon strain has a correlative increase in tension of the plantar fascia.7 Stecco and colleagues determined that the plantar fascia is more closely related to the paratenon of the Achilles tendon than the Achilles tendon itself.8 These authors also determined that there was an increase in the thickness of the plantar fascia when Achilles tendinopathy is present. They stated: “There was a statistically significant correlation between the thicknesses of the plantar fascia and the paratenon. These findings suggest that the plantar fascia has a role not only in supporting the longitudinal arch of the foot but also in its proprioception and peripheral motor coordination.”

While the human plantar fascia is very similar to the Achilles tendon, it has a distinct histology of its own. There has been much dogma relating tensile force to histologic breakdown of the fascia, but recent findings have redefined how we should look at what occurs during the degenerative process of the fasciopathy. These histologic findings include the following:

• Disruption of collagen fibrils both lengthwise and crosswise
• Vascular hyperplasia
• Increased tenocyte concentration

Although Lemont and colleagues found no inflammatory histologic mediators in their series of specimens, they did document a clear deposition of mucoid products between the collagen fibrils.3

Debating The Cause Of Degeneration In The Plantar Fascia
In the absence of inflammatory mediators, the question then becomes what causes degeneration in the plantar fascia to be painful? Obviously, there have to be some nociceptors within the plantar fascia and there has been identification of Pacini and Ruffini corpuscles in the fascia as well as free nerve endings.8 However, not all degeneration, as evidenced on MRIs or high-resolution diagnostic ultrasound, is painful.

Authors have proffered for decades that tensile force is the biomechanical force that causes the breakdown or degeneration of the fascia.9 However, there is abundant research contradicting this closely held belief and it is more likely that the degeneration of the plantar fascia results from shearing type forces rather than tensile ones.10

In their study of the relationship of heel spurs to surrounding tissue, Li and Muehleman demonstrated that the trabecular pattern of the inferior calcaneal exostosis does not support the concept of the etiology of fascia degeneration being excessive tensile forces acting on the plantar fascia.10 In their study, they found just the opposite: the trabeculae were perpendicular to the axis of the plantar fascia and the spur developed more likely in response to shielding forces from shear type stresses rather than axial tension. This fact leads to the conclusion that the long-held belief that a hypermobile flatfoot or pronation as a direct cause of plantar fasciopathy is erroneous.

This concept has further support from Menz and coworkers.11 They examined 216 patients and found inferior calcaneal exostoses in 119 patients (55 percent) and Achilles tendon spurs in 103 patients (48 percent). It is interesting that those with inferior calcaneal exostosis were two times more likely to develop an Achilles enthesopathy.

Menz and coworkers also found no relationship of spurring to foot type and no prevalent difference between sexes.11 Most importantly, in support of Li and Muehleman’s work, they stated: “These findings support the theory that plantar calcaneal spurs may be an adaptive response to vertical compression of the heel rather than longitudinal traction at the calcaneal enthesis.” An eccentric force of only 4 to 6 percent of the tendon or aponeurosis length results in pathologic breakdown in short time periods of two to three weeks without the histologic mediators of inflammation present.12

The presence of an inferior calcaneal exostosis indicates that a process has occurred at the inferior calcaneus in response to stress (shearing, not axial tension), which is likely a mechanism to increase surface area of the inferior calcaneus and research has alluded to it in the mechanical sense as a cantilever beam.13

The plantar fascia is distinctly different from tendon histologically although there is very little published data about these differences. The most detailed publication is from Wearing and colleagues, who sum up the possible causes of plantar fasciopathy and the histologic differences of the plantar fascia in comparison to tendon.9 These authors point out that there is a special cellular makeup of the plantar fascia that may allow for it to compensate mechanically because of the increased cellular matrix that it possesses. Factors that may play a role in the degenerative process include the following:

• Stress shielding
• Metabolic disorders
• Hyperthermia
• Microvascular impairment
• Formation of free radicals
• Genetic factors

Making A Diagnosis Of Plantar Fasciopathy
Prior to the nearly universal adoption of high-resolution diagnostic ultrasound by foot specialists, the diagnosis of plantar fasciitis was frequently based solely on the history of present illness (HPI) and whether the patient had pain at the medial calcaneal tubercle with palpation. This failure to appreciate the individual nature and condition of the plantar fascia from patient to patient led to the dogma that one must treat this condition with conservative measures for some arbitrary amount of time (usually six to 12 months). Then if there was no improvement, intervention with a more definitive treatment was warranted.

In addition to being clinically assessable, high-resolution diagnostic ultrasound allows for the quantitative grading of the extent of the degradation of the plantar fascia and provides an objective means of measuring further changes over time. A couple of other factors have led to the faster adoption of more aggressive intervention. The development of lesser invasive and endoscopic surgery and other modalities, such as Coblation techniques and extracorporeal shockwave treatment (ESWT), allow the practitioner a more efficacious intervention with decreased post-intervention morbidity. I have found more practitioners now advocate for an earlier implementation of intervention based on the level of pathology for the patient suffering from debilitating pain while obviating mostly suboptimal conservative modalities such as nonsteroidal anti-inflammatory drugs (NSAIDs) and orthotic devices.

The standard or traditional history of present illness can provide the treating physician with some very valuable information. However, it can sometimes lead to confusion and obfuscation of a proper and accurate diagnosis. I have found the “SOCRATES” mnemonic helpful in clarifying the history taking and diagnosis in patients with heel pain (see “Applying The ‘SOCRATES’ Mnemonic To History Taking In Patients With Plantar Fasciopathy” at left). Not only does this more specific HPI allow practitioners to know if they are dealing with an isolated plantar fasciopathy versus a multiple etiology heel pain syndrome, it also allows for a staging of the condition based on how long the heel pain has been present. Cases that have a longer period of duration can be more difficult to treat.

While the multiple etiology heel pain syndrome (MEHPS) questionnaire is not a scientifically validated instrument, it has proven to be very reliable in clinical practice and can provide some early insight as to whether a patient has more than one pain generator. (See “A Guide To The Multiple Etiology Heel Pain Syndrome (MEHPS) Questionnaire” at right.) Additional clinical and diagnostic workup are always needed, but the practitioner should be aware that multiple pain generators in heel pain cases are not unusual. A study by Rose and colleagues showed that 72 percent of patients who first presented to their clinic for plantar fasciitis had some type of coexisting nerve entrapment.14

Risk factors for an increased chance of developing plantar fasciopathy are equinus (decreased ankle joint dorsiflexion), high body mass index, prolonged periods of standing or walking, increased age, the presence of an inferior calcaneal exostosis, and decreased first metatarsophalangeal joint (MPJ) dorsiflexion.15,16

A Closer Look At The Potential Of Diagnostic Ultrasound
The use of high-resolution diagnostic ultrasound has changed the entire paradigm of treatment for heel pain. Within seconds, the skilled practitioner can quickly assess the degree of degeneration within the plantar fascia or completely rule out the diagnosis of plantar fasciopathy. There is scientific validity in the thickness of the plantar fascia as measured by high-resolution diagnostic ultrasound.17

A thorough diagnostic ultrasound examination of the heel must include evaluation of more than just the status of the plantar fascia at the insertional level. One must evaluate the different zones of the plantar fascia independently because there is a difference in the normative thickness values for each zone and an understanding of the severity for each zone, in my clinical experience, seems to correlate with treatment outcome.

The plantar fascia is divided into three zones: “A” for anterior to the insertion, “B” for the insertional level (this is the most traditional area evaluated) and “C” for the area inferior to the calcaneus itself. In my experience, those patients with a very thick zone C are the most problematic and difficult to treat.

In addition to the evaluation of each of the zones of the plantar fascia, individually and together, one should use diagnostic ultrasound to evaluate the infracalcaneal fat pad for the presence of fluid and elasticity. Studies with plain film radiography of unloaded feet have shown that the thickness of the fat pad ranges from 14 to 26 mm and that compressibility should be approximately 60 percent.18 This correlates to diagnostic ultrasound within a 1- to 2 mm range. We know that we can attribute some patients’ heel pain to an atrophy of the heel pad. Understand that this is a separate pathology and diagnosis from plantar fasciopathy. Several studies have determined there is no significant difference in the fat pad between patients with plantar fasciopathy and controls.19 However, if present, atrophy of the fat pad increases pressure on the periosteum of the inferior calcaneus, which results in another pain generator that one must address for optimal treatment outcomes.

I would recommend using diagnostic ultrasound in the first visit after the completion of the history of present illness and the MEHPS questionnaire. This will allow for immediate confirmation of the presence of degeneration of the plantar fascia as well as an assessment of the severity of the plantar fasciopathy if one exists.

Another interesting thing about the power of high-resolution diagnostic ultrasound is that if the patient has type 1 diabetes, assessing the thickness of the plantar fascia (typically at the insertional level) can have a prognostic benefit because this tissue has a high affinity of glycosylation and it can be a very accurate predictor of which of these patients may develop retinopathy.20 In addition to showing an increased odds ratio for the development of retinopathy in the adolescent patient with type 1 diabetes, Craig and colleagues showed an increased odds ratio for the development of diabetic peripheral neuropathy of 2.3 and autonomic neuropathy of 4.94.21

Staging gives the practitioner some insight to how recalcitrant the plantar fasciopathy is and the extent of treatment that may be required. Authors have shown clinically that the longer the duration of plantar fasciopathy, the greater the resistance to treatment. Staging is secondary to grading as grading is an objective status of the current condition of the plantar fascia. A stage of II or greater and a MEHPS score of >12 points must alert the practitioner to be highly suspicious of neural etiology, whether it is isolated or a coexisting pain generator.

Clinicians can employ diagnostic ultrasound to make the definitive diagnosis of plantar fasciopathy. Given the widespread availability of the technology and its relatively low cost, diagnostic ultrasound should be part of the standard of care for heel pain. Without diagnostic ultrasound, an accurate assessment of heel pain cannot occur. Diagnostic ultrasound has superseded MRI as the ultimate in imaging study for plantar fasciitis. However, researchers have documented that there is no statistical difference in the accuracy of measurement of the plantar fascia with MRI and diagnostic ultrasound.22 Magnetic resonance imaging supports the specificity of diagnostic ultrasound measurements of the thickness of the plantar fascia.

Case Study: How The Use Of Diagnostic Ultrasound Cleared Up A Heel Pain Diagnosis In A Patient With Diabetes
A 51-year-old, African-American, moderately obese female patient presents to the clinic with a chief complaint of right heel pain with a duration of three months. Previous treatments included stretching exercises, night splints and has off-the-shelf orthotic devices. Two different practitioners had diagnosed her with plantar fasciitis. She describes the pain as worse after periods of rest but says the pain sometimes burns, even when she is not on the foot. The patient has had two cortisone injections, which did not help her other than when the foot was numb from the local anesthetic. She had no history of trauma and no significant medical history. She does not have diabetes but has a family history of diabetes. Neither of the previous treating physicians examined her with diagnostic ultrasound.

The clinical examination revealed some tenderness with palpation of the right medial calcaneal tubercle but she had more pain with palpation of the medial calcaneal nerve on the medial aspect of the heel. A high-resolution diagnostic ultrasound examination showed a plantar fascia with a thickness of 3.95 mm at the insertion with a normal echogenic pattern. She had no Tinel’s sign of the tibial nerve at the medial aspect of the right ankle and no provocation sign. A neurosensory test with the Pressure Specified Sensory Device (PSSD, Sensory Management Services) showed that she had elevated thresholds and a loss of innervation density for all nerves tested as well as a complete loss of two-point discrimination for the right medial calcaneal nerve.

The patient went for two-hour postprandial lab testing the next day and the results showed elevated cholesterol and triglycerides, and a blood glucose of 160 g/dL. Her HgA1c was 7.5. The diagnosis was heel pain secondary to metabolic nerve entrapment of the medial calcaneal nerve caused by diabetes mellitus. This case illustrates that heel pain is often misdiagnosed and that clearly all heel pain is not plantar fasciopathy.

In Summary
Heel pain is endemic and often extremely complex. We can reduce the complexity of heel pain by accurate diagnosis and a highly developed appreciation of potential neural involvement. Decision making in the treatment of these complex cases is highly individualized and must factor in multiple variables ranging from the type of activity the patient desires or is required to do to the level of nerve entrapment present. Also consider any metabolic diseases that are present as well as biomechanical forces that contribute to create or increase pain generation.

Dr. Barrett is an Adjunct 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.


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This article has been adapted with permission from Practical Pain Management for the Lower Extremity Surgeon by S. L. Barrett (Ed.). Copyright 2015 by Data Trace Publishing Company, Brooklandville, MD.

Stephen Barrett, DPM, FACFAS
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