While there are many different causes of primary heel pain, it is often misdiagnosed as simple plantar fasciitis without the proper diagnostic tools. This is especially true for patients who have recurring symptoms and/or have failed multiple conservative and or surgical treatments. It takes a conscientious clinician to know when to begin thinking of a different diagnosis and a new course of treatment. This is especially true when it comes to heel pain. Many of the patients who walk into our offices complaining of heel pain have either been told by another doctor they have plantar fasciitis or have diagnosed themselves. Armed with that knowledge, it would be easy to assume this is the correct diagnosis and to perform only the minimum of diagnostic examinations. However, this approach would be ineffective in treating the patient and his or her symptoms fairly. A more effective approach would be one that we have employed in our offices. Key Pointers On Making An Accurate Diagnosis After obtaining a thorough history of the symptoms and complaints, one should perform a physical examination. Begin by palpating the medial tuberosity of the calcaneus and the surrounding areas to determine the point of maximum tenderness. If the patient relates a specific area of pinpoint tenderness at this site, one cannot assume a diagnosis of plantar fasciitis even if there is a correlation of subjective signs. A further examination of the heel should include side to side compression of the calcaneus to rule out any fractures. Proceed to gently tap on the posterior tibial nerve with a finger or reflex hammer as it passes posterior to the medial malleolus to determine any nerve involvement. Use the same approach at the level of the medial calcaneal branch as well. If the patient relates any positive reaction from the nerve palpation, one may suspect nerve pathology. To complete the physical exam, clinicians should determine the presence of ankle equinus. Proceed to perform an ultrasound examination of the plantar fascia of the symptomatic and non-symptomatic foot. If the plantar fascia is less than 4 mm, one cannot make a diagnosis of plantar fasciitis. If there is hypertrophy of the fascia, you will be able to see an increase in its thickness from 5 mm and higher. You can also determine if there is any attenuation or complete tear in the fascia. Using ultrasound also allows one to visualize the plantar calcaneal bursae. Keep in mind that pathology of the bursae can mimic symptoms of plantar fasciitis without any pathology to the fascia itself. At this point, if you are satisfied that a diagnosis of plantar fasciitis is accurate, proceed with conservative treatment. If there is any suspicion of nerve involvement at this time or any time during the treatment course, then a neurosensory examination is indicated. How PSSD Neurosensory Testing Can Enhance Your Diagnosis In our offices, we use the PSSD sensory unit from Sensory Services Management. This is a very sensitive test that can identify early changes in sensation, document the extent of sensory loss and monitor conservative or surgical management of the patient. This test can be very useful when attempting to determine if a patient truly has a plantar fasciitis versus a tarsal tunnel or other nerve pathology around the heel. The PSSD neurosensory examination will determine if there is any sensory loss and which nerve is affected. In order to use this test effectively, one should have a strong understanding of nerve injury, specifically nerve compression. (See “What You Should Know About Nerve Compression” below.) The PSSD also tests the patient’s ability to determine between one point and two points of pressure. Distinguishing two points of pressure is important in evaluating the extent of axonal damage. As the patient’s ability to distinguish two points of pressure decreases — as the two points are brought closer together — there is more severity of axonal damage and death to the nerve. Accordingly, more aggressive treatment would be indicated. With one point sensory testing, one is testing for the level of sensory function. Pressure thresholds above normal indicate abnormal functioning of touch receptors and the nerve fibers innervating those receptors. The loss of two point sensation is to the sensory nerve what weakness is to muscle. The PSSD measurements are pressure measurements in gm/mm2. With two-point sensory testing, we are testing the level of innervation density. Two-point discrimination wider than normal indicates loss of receptors and degeneration of nerve fibers. Loss of innervation density is to sensory nerve what atrophy is to muscle. The PSSD measurements are distance (mm) and pressure measurements. What You Should Know About Nerve Compression The effects of compression on nerve fibers are extensive. Nerve compression can result from edema around the nerve externally, edema within the nerve or external compression from other anatomical structures in the area. There is variability in the severity of injury, depending on acute or chronic compression of the nerve. The A-beta fibers (large diameter) are the most susceptible to compression and ischemia. One will see a loss of circumferential A-beta fibers. Mechanical and ischemic factors can also impair the function of the nerve. Clinicians will also see inhibited microcirculation and axoplasmic transport, intraneural scar formation and edema, and eventually fiber degeneration and death. Static touch on the skin is translated by Merkle cells with slow-adapting A-beta nerve fibers. Moving touch is translated by Meissner corpuscles, which have quickly-adapting A-Beta nerve fibers. Diminished oxygen slows axonal transport, leading to disruption to the A-beta fibers and loss of light touch. With compression, there is a decreased perception circumferentially of the large diameter A-beta fibers. For the Merkle cell, there are three to eight receptors to an A-beta fiber. For the Meissner cell, there are two to eight A-beta fibers to one receptor. This means when there is damage to the nerve, the first sensation to be lost is the static two-point discrimination and the first to return with nerve regeneration is moving touch. Given this knowledge, one can understand the importance of performing static measurement to determine the extent of damage, and interpreting moving touch tests in order to evaluate the rate of healing. Comparing The PSSD With Other Testing Methods The use of the PSSD test is much more reliable than the traditional 5.07 Semmes Weinstein monofilament. The filament test provides only an estimate range of the force applied. It’s not a true measurement. The filament bends at a pressure of 95 gm/mm2. It has been shown that diabetics are susceptible to skin breakdown at a level of 30 gm/mm2. With the PSSD, we can measure pressures as low as 1 gm/mm2. This will help in earlier detection of nerve damage. With nerve conduction studies (NCV), it is not possible to clearly identify the specific branches that are affected from the posterior tibial nerve. The rate of false negatives with NCV testing is approximately 45 percent for tarsal tunnel syndrome. Environmental factors and examiner technique affect NCV recorded measurements. NCV testing favors the faster conducting impulses rather than the slower ones. There is a poor correlation with its results and symptoms. Most importantly, it is less sensitive to early damage as compared to pressure threshold studies. How To Interpret Test Results With The PSSD When testing for tarsal tunnel syndrome, one will examine three areas with the PSSD. To test the sensitivity of the medial plantar branch of the posterior tibial nerve, use the pulp of the great toe. For the medial calcaneal branch, use the medial aspect of the heel. Test a third site at the first dorsal web space to rule out any global neuropathy. (It is beyond the scope of this article to relate the entire testing procedure and the nuances of the measurements.) When testing the medial plantar nerve (great toe pulp), if the test results show an increase in the pressure threshold of one point discrimination above the normal, you may conclude there is some compression or injury of the nerve at some level. After testing the medial calcaneal nerve (medial heel), if the results are within normal limits, you may conclude this nerve is not involved and there is only a compression of the medial plantar nerve after its division from the posterior tibial nerve. When testing the medial calcaneal branch, there can be an elevation above normal with no elevation of the medial plantar nerve test. If this is the case, one can diagnose a compression of the medial calcaneal branch alone. When there is an elevation at both test sites, you can assume there is pathology at a higher level than the posterior tibial nerve branches. Therefore, one can make a diagnosis of tarsal tunnel syndrome that may also be due to compression from a more proximal location. When testing two-point discrimination at these sites, one will be able to determine the severity of the damage to the nerve. If the distance between the points needs to be increased above normal for any one test site, then one can determine there is axonal damage to the nerve and the pathology is more severe. Therefore, one should opt for more aggressive treatment. When the results of the PSSD testing show there is a tarsal tunnel syndrome and the ultrasound shows no evidence of increased thickness of the plantar fascia, then one can make an informed and thorough diagnosis of tarsal tunnel syndrome, its specific level of involvement, and the absence of a plantar fascial component. While there is no argument that there can be a combination of plantar fasciitis and tarsal tunnel syndrome, it is crucial to identify the presence of one or both pathologies and their severity in order to treat the patient effectively. Weighing Appropriate Treatment Options The treatment for a mild to moderate tarsal tunnel syndrome would begin with a combination of functional foot orthotics and physical therapy. Physical therapy would include ultrasound therapy, strength training and iontophoresis. One may want to emphasize a walking boot in order to facilitate support of motion at the ankle joint as the area heals and aid in decreasing the inflammation. Oral antiinflammatory medications may also be indicated. If conservative measures fail or if there is a moderate to severe tarsal tunnel, one should consider surgery to release the compression on the nerve or nerves involved. If there is axonal damage and loss, it is more likely that the patient would benefit from surgical decompression to slow or stop the progression of death to the involved nerve(s). Finally, it is important to take the time with every patient who has complicated heel pain that has not resolved. When conservative treatments fail, using other diagnostic modalities may be indicated to further explore and determine the cause of the patient’s symptoms. As technology advances, as with ultrasound and PSSD neurosensory testing, we may find that our percentage of misdiagnosed heel pain will decrease and our patients will be more satisfied with their treatment outcomes. Dr. Soomekh is in private practice at the Foot And Ankle Institute of Santa Monica in Santa Monica, Ca. His e-mail address is firstname.lastname@example.org. Dr. Baravarian (pictured here) is an Assistant Clinical Professor at the UCLA School of Medicine. He is also the Co-Director of the Foot and Ankle Institute of Santa Monica in Santa Monica, Ca. His e-mail address is email@example.com.