Clinical history: A 26 year-old female presents with lateral foot pain and no prior trauma. Axial T2-weighted (1a) and coronal STIR (1b) images are provided. What are the findings? What is your diagnosis?
Baxter’s nerve (first branch of the lateral plantar nerve) impingement.
Heel pain is a common presenting complaint to the foot and ankle specialist, with a wide differential diagnosis including plantar fasciitis, fat pad atrophy, calcaneal stress fracture or apophysitis, inflammatory arthropathy, neoplasia, and infection1. One of the more elusive diagnostic considerations in heel pain is entrapment of first branch of the lateral plantar nerve (Baxter’s nerve impingement)2,3. Baxter’s nerve is a mixed sensory and motor nerve, providing motor innervation to the abductor digiti minimi (ADM) muscle2,4,5. Baxter’s nerve impingement can produce symptoms indistinguishable from plantar fasciitis6,7,8,9. While this diagnosis has been said to account for up to 20% of heel pain, it is often overlooked relative to other causes of heel pain8,10,11. Weakness of the ADM may be present but is difficult to detect clinically9. Electrodiagnostic studies are invasive and the results in heel pain can be inconclusive9,13,14. MR can be used to detect denervation-related muscle changes in the ADM, confirming the diagnosis of Baxter’s nerve impingement3,6,8,9,12.
Within the ankle tarsal tunnel, the posterior tibial nerve (PTN) bifurcates into medial (MPN) and lateral (LPN) plantar nerves. These nerves exit the tarsal tunnel and continue along the plantar aspect of the foot.
The MPN travels anterior to the LPN, carrying sensory information from the medial two thirds of the plantar foot, and motor innervation to the flexor digitorum brevis, abductor hallucis, flexor hallucis brevis, and first lumbrical9.
The LPN carries sensory information from the lateral plantar aspect of the foot, 5th toe, and lateral half of the 4th toe. Motor innervation involves all the remaining foot muscles, not innervated by the MPN9.
The first branch of the LPN, Baxter’s nerve (also known as the inferior calcaneal nerve), originates from the LPN at various levels beneath the deep fascia of the abductor hallucis muscle. The nerve courses vertically between the abductor hallucis and quadratus plantae muscles, then makes a sharp 90 degree horizontal turn, coursing laterally beneath the calcaneus to innervate the ADM muscle3,5,9,15. Motor innervation supplies the ADM, occasionally to the flexor digitorum brevis and lateral half of the quadratus plantae. Sensory information is carried from the calcaneal periosteum, long plantar ligament, and adjacent vessels3,4,6. While Baxter’s nerve is usually the first branch of the LPN, variation does exist and the nerve can originate directly from the PTN5,14,16.
Two sites of entrapment have been described with Baxter’s nerve impingement. The first site is located as the nerve passes between the deep fascia of the abductor hallucis muscle and the medial plantar margin of the quadratus plantae muscle. The second site is more distally as the nerve passes along the anterior aspect of the medial calcaneal tuberosity2,3,14. A calcaneal plantar enthesophyte3,8 and/or soft tissue changes of plantar fasciitis9 may also contribute to entrapment at this second location.
Similar to entrapment neuropathies elsewhere, resultant effects from nerve compression depend on the severity and chronicity of entrapment. Early diagnosis of a nerve compression syndrome may result in reversible damage, whereas late diagnosis nerve compression damage is not typically reversible17. With motor nerve injuries, skeletal muscle will become edematous in the acute to subacute phases. Left untreated, denervated muscle will eventually undergo volumetric atrophy, ultimately with irreversible fatty infiltration. If dual or redundant innervation exists, these changes may not occur18,19.
Reported risk factors for Baxter’s nerve impingement include advancing age, the presence of a calcaneal spur, plantar fasciitis, underlying mass, vascular enlargement, muscular enlargement (such as in athletes), obesity, and foot hyperpronation3,8,9,20.
MRI has been shown to be extremely valuable in demonstrating muscular changes associated with denervation. MRI is more sensitive to tissue changes within muscle compared to ultrasound or computed tomography and has advantages compared to electrodiagnostic studies due to its non-invasive nature, superior anatomic detail, ability to demonstrate pathology in muscles with dual innervation18, and ability to exclude alternative diagnoses (fracture, neoplasia, fasciitis). Normal muscle demonstrates intermediate signal on T1 and fluid sensitive sequences.
Acute and subacutely muscle denervation is best evaluated with fluid sensitive sequences, such as T2-weighted imaging with fat suppression (T2FS) or short tau inversion recovery (STIR) images, exhibiting increased signal within the muscle belly compared to normal muscle, related to neurogenic muscular edema18,19. Gadolinium enhancement within muscle will also occur in the acute to subacute phases of denervation18. In the setting of Baxter’s nerve impingement, muscular edema will occur selectively within the ADM, and potentially within the flexor digitorum brevis and quadratus plantae, depending on the innervation anatomy of the patient.
Chronically denervated muscle will eventually undergo volumetric atrophy, and subsequent irreversible fatty infiltration. These findings are best depicted on non-fat-suppressed T1-weighted images18,19. Typically, the atrophy and fatty infiltration occurs homogeneously within the muscle belly. If dual or redundant innervation exists, these changes may not occur or may occur heterogeneously18. In the case of Baxter’s nerve impingement, the ADM is typically involved homogeneously, unless dual innervation exists.
Initial treatment strategy of Baxter’s nerve entrapment is conservative, typically involving a combination of rest, non-steroidal anti-inflammatory medicines, corticosteroid injections, and orthotics1,21,22. If recalcitrant pain exists despite conservative treatment, operative intervention has proven successful1,21,23,24. Neurolysis of Baxter’s nerve is performed with deep fascia release of the abductor hallucis muscle. An impinging heel spur or tight plantar fascia is also partially removed or released, if it is associated with the entrapment2. Endoscopic approaches to the surgery11 and radiofrequency ablation techniques22 have also been described. The first patient above (Figures 1a,1b), underwent decompression of the tarsal tunnel in conjunction with Baxter’s nerve release, completely resolving her lateral foot pain.
Baxter’s nerve impingement is a difficult clinical diagnosis and often overlooked in the presentation of heel pain. MRI can be used to evaluate for denervation effects of Baxter’s nerve impingement by identifying abnormalities of the ADM muscle belly. In addition, potential causes of impingement (e.g. calcaneal spur, soft tissue mass, enlarged vessels) and associated pathology (e.g. plantar fasciitis, tendon pathology) may be seen, and alternative differential diagnoses (e.g. stress fracture) can be excluded.
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