OBJECTIVE: To describe the examination and intervention strategy utilized in the differential diagnosis and treatment of a patient with subcalcaneal heel pain. BACKGROUND: The patient was a 44-year-old man with an 8-month history of left subcalcaneal heel pain. He presented with a chief complaint of limited standing and walking tolerance secondary to pain in the left heel. He had not responded to previous treatments of rest, anti-inflammatory medication, cortisone injections, and exercise prescription. MATERIALS AND METHODS: The patient's subcalcaneal heel pain was reproduced utilizing the straight leg raise (SLR) in combination with ankle dorsiflexion and eversion to sensitize the tibial nerve. These findings suggested a neurogenic component to the dysfunction. Because restricted ankle dorsiflexion, excessive pronation, and posterior tibialis weakness were also found, mechanical dysfunctions also likely contributed to the etiology of heel pain. The patient was treated for 10 visits over a period of 1 month. Treatment consisted of active and passive motions aimed at restoring pain-free soft-tissue motion along the course of the tibial nerve. In addition, low-dye taping and therapeutic exercises were utilized to control excessive pronation and reduce stress on the plantar structures of the foot. RESULTS: The patient's SLR increased from 42 degrees to 54 degrees and became pain-free. Dorsiflexion range of motion increased from 3 degrees to 8 degrees in the left ankle, and left posterior tibialis strength was normalized. Over a period of 1 month the patient's symptoms were resolved, and his standing and walking tolerance was fully restored. CONCLUSION: Assessment and potential contribution of neural dysfunction should be considered in patients with subcalcaneal heel pain.
OBJECTIVE: To describe the examination and intervention strategy utilized in the differential diagnosis and treatment of a patient with subcalcaneal heel pain. BACKGROUND: The patient was a 44-year-old man with an 8-month history of left subcalcaneal heel pain. He presented with a chief complaint of limited standing and walking tolerance secondary to pain in the left heel. He had not responded to previous treatments of rest, anti-inflammatory medication, cortisone injections, and exercise prescription. MATERIALS AND METHODS: The patient's subcalcaneal heel pain was reproduced utilizing the straight leg raise (SLR) in combination with ankle dorsiflexion and eversion to sensitize the tibial nerve. These findings suggested a neurogenic component to the dysfunction. Because restricted ankle dorsiflexion, excessive pronation, and posterior tibialis weakness were also found, mechanical dysfunctions also likely contributed to the etiology of heel pain. The patient was treated for 10 visits over a period of 1 month. Treatment consisted of active and passive motions aimed at restoring pain-free soft-tissue motion along the course of the tibial nerve. In addition, low-dye taping and therapeutic exercises were utilized to control excessive pronation and reduce stress on the plantar structures of the foot. RESULTS: The patient's SLR increased from 42 degrees to 54 degrees and became pain-free. Dorsiflexion range of motion increased from 3 degrees to 8 degrees in the left ankle, and left posterior tibialis strength was normalized. Over a period of 1 month the patient's symptoms were resolved, and his standing and walking tolerance was fully restored. CONCLUSION: Assessment and potential contribution of neural dysfunction should be considered in patients with subcalcaneal heel pain.
Authors: Shane M McClinton; Timothy W Flynn; Bryan C Heiderscheit; Thomas G McPoil; Daniel Pinto; Pamela A Duffy; John D Bennett Journal: Trials Date: 2013-12-03 Impact factor: 2.279