Welcome to the Footsore nation! The American Podiatric Medical Association reports heel pain is the most common ailment reported for foot issues, impacting almost 50% of patients surveyed in a recent study. From women wearing tight fitting high heel shoes to people wearing shoes in the wrong size and standing for many hours on end, American feet are taking a pounding.
As physical therapists know, diagnosing heel pain is not always simple. The article below offers an in-depth study on the diagnoses and treatment of heel issues. Author Mark Brooks offers a study showing evidence-based proof and case studies that physical therapists utilizing diagnostic tools such as Nerve Conduction Studies and musculoskeletal ultrasound (MSKUS) results in much better outcomes for patients.
Read this article and study here.
Atypical Heel Pain: A Case Presentation
By Mark Brooks, HODS VP Of Clinical Education
Heel pain is a common complaint for which patients seek medical attention from physicians and physical therapists. There are a wide variety of differential diagnoses including heel spur, calcaneal stress fracture, plantar fasciitis, inflammation and fat pad atrophy.1
Among the most commonly diagnosed etiologies of heel pain is plantar fasciitis. Typically, plantar fasciitis causes symptoms that are often worse after sitting or getting up from bed and the symptoms are worse with the first few steps. This is known as “post static dyskinesia”. Symptoms of plantar fasciitis are often aggravated by activity and walking, but subside after sitting or non-weightbearing. The pathophysiology of plantar fasciitis is from repetitive stretching of the plantar fascia, a structure that maintains the normal arch in the foot. With excessive repetition, the fascia becomes irritated and inflamed and in chronic conditions may tear or rupture.
Diagnosis of plantar fasciitis starts with a medical history and physical exam. Imaging studies include x-rays, which may show heel spurring, musculoskeletal ultrasound (MSKUS), which may show inflammation, swelling and tearing, and magnetic resonance imaging, which can reveal small details of pathology not seen in x-ray or MSKUS.
Common treatment include rest, anti-inflammatory medications, physical therapy, splinting, orthotics, steroid injection extracorporeal wave therapy and surgery. Generally, these modalities are effective, but in up to 20% of cases of heel pain which are refractory to these treatments, involvement of the Baxter’s nerve should be considered.2 Baxter’s nerve impingement often produces symptoms that are indistinguishable from plantar fasciitis. However, in Baxter’s nerve impingement, symptoms of continue unabated after sitting or lying and patients often indicate the symptoms radiate from the heel to the medial or lateral heel edges.
Diagnosis of Baxter’s neuritis include MSKUS, which may show enlargement or swelling of the nerve and MRI may show muscle denervation and fatty degradation. The advantage of MRI is that it can exclude other etiologies of heel pain including fasciitis, fracture or neoplasm. The most sensitive technique for diagnosis of neural pathology, however, are electrodiagnostic studies (EDX). Although invasive, it is the only technique which can quantify the severity of pathology and degree of neural involvement.
As the posterior tibial nerve passes through the tarsal tunnel with branches into both medial and lateral plantar branches. The medial plantar nerve travels anteriorly, has motor innervation of the flexor digitorum brevis, abductor hallucis, flexor hallucis brevis and 1st lumbrical. The medial plantar sensory fibers provide cutaneous sensory innervation of the medial 2/3 of the foot.3 The lateral plantar nerve provides motor innervation of intrinsic foot muscles not innervated by the medial branch and sensory cutaneous innervation of the lateral plantar foot, 5th toe and lateral half of the 4th toe.3
Baxter’s nerve is the 1st branch of the lateral plantar nerve. It is also known as the inferior calcaneal nerve. It courses deep and through the fascia an under the calcaneus. It provides motor innervation of the abductor digiti minimi, occasionally the flexor digitorum brevis and lateral half of the quadratus plantae. Sensory innervation is to the periosteum of the calcaneus, long plantar ligament and adjacent vessels. There is typically no cutaneous sensory innervation. There is also a wide variety of variation of branching patterns of the Baxter’s nerve.4, 5
A 47 year old male presented in clinic with a 2-3 year history of left heel and plantar foot pain and burning. He denies any disturbance of skin sensation. There is no history of injury or specific trauma, but is a competitive runner and runs 20-25 miles per week. His symptoms are worsened by standing, walking and running and non-weightbearing often does not alleviate his symptoms. He has sought treatment from multiple podiatrists and a foot and ankle orthopedics. X rays showed calcaneal heel spurring, but no MSKUS, MRI or EDX has been performed. Treatment has been for plantar fasciitis including medications, splinting, taping, steroid injection and activity modification. None have been of help. After being seen by a 3rd podiatrist, the treating podiatrist ordered MSKUS and EDX studies.
MSKUS imaging indicated a partial tear of the proximal plantar fascia attachment with intrasubstance edema.
EDX studies showed no evidence of tarsal tunnel syndrome or radiculopathy, but did show involvement of the Baxter’s nerve. Nerve conduction studies (NCS) revealed both prolongation of the distal motor latency and a diminished CMAP amplitude response when compared to the unaffected side. Needle electromyography (EMG) revealed muscle membrane instability secondary to axonal pathology, increased numbers of polyphasic motor units and reduced numbers of functioning motor units in the left abductor digiti minimi.
Initial treatment of Baxter’s neuritis is conservative, including rest, activity modification, orthotics, anti-inflammatory medications and corticosteroid injection. In cases that are refractory to conservative treatment, operative management has been proven effective. Operative management includes neurolysis, deep fascia release and radiofrequency ablation techniques.8, 9
Two primary sites of Baxter’s nerve entrapment are typically described.6, 7 The first is in the interspace between the deep fascia of the abductor hallucis and quadratus plantae. The second is more distal as the nerve passes at the anterior aspect of the medial calcaneal tuberosity. Calcaneal plantar enthesophyte and inflamed tissues of the plantar fasciitis have also been described as a source of Baxter’s nerve pathology.
As with most entrapment neuropathies, the effects from nerve compression is dependent on both severity and chronicity of the entrapment. Consequently, early diagnosis is important and may result minimal or no permanent nerve damage. Late diagnosis with severe compression often is not reversible. Risk factors for Baxter’s nerve impingement include advancing age, calcaneal heel spur, plantar fasciitis, obesity, muscular enlargement (typically seen in athletes) and hyperpronation of the foot.1, 8
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1. Thomas JL, Christensen JC, Kravitz SR, Mendicino RW, Schuberth JM, Vanore JV, Weil LS Sr, Zlotoff HJ, Bouche R, Baker J, American College of Foot and Ankle Surgeons heel pain committee. The diagnosis and treatment of heel pain: a clinical practice guideline-revision 2010. J Foot Ankle Surg 2010; 49(3 Suppl):S1-19.
2. Baxter DE, Thigpen CM. Heel pain: operative results. Foot Ankle 1989; 5:16-25.
3. Donovan A, Rosenberg ZS, Cavalcanti CF. MR imaging of entrapment neuropathies of the lower extremity. Part 2. The knee, leg, ankle, and foot. Radiographics. 2010; 30:1001-1019.
4. Dvonovan A, Rosenberg ZS, Cavalcanti CF. MR imaging of entrapment neuropathies of the lower extremity. Part 2. The knee, leg, ankle, and foot. Radiographics. 2010; 30:1001-1019.
5. Louisia S, Masquelet AC. The medial and inferior calcaneal nerves: an anatomic study. Surg Radiol Anat 1999; 21:169-173.
6. Alshami AM, Souvlis T, Coppieters MW. A review of plantar heel pain of neural origin: differential diagnosis and management. Manual Therapy 2008; 13:103-111.
7. Govsa F, Bilge O, Ozer A. Variations in the origin of the medial and inferior calcaneal nerves. Arch Orthop Trauma Surg 2006; 126:6-14.
8. Mesmar M, Amarin Z, Shatnawi N, Bashaireh K. Chronic heel pain due to the entrapment of the first branch of the lateral plantar nerve: analysis of surgical treatment. Eur J Orthop Surg Traumatol 2010; 20:563-567.
9. Goecker RM, Banks AS. Analysis of release of the first branch of the lateral plantar nerve J Am Podiatr Med Assoc 2000; 90:281-286.
Figure 1. NCS studies of the Baxter’s nerve show a prolonged motor distal latency, 5.85ms, and a diminished CMAP amplitude, 2.8mV, when compared to the unaffected (right) side.
Figure 2. Comparison of Baxter’s nerve responses side to side, left (white), right (yellow). Note the significant side to side CMAP amplitude difference.
Figure 3. EMG findings showing muscle membrane instability and evidence of axon loss pathology in the left abductor digiti minimi.
Figure 4. Common sites of axter’s nerve impingement.