The Treatment of Baxter's Neuropathy in the Foot

Baxter's neuropathy, also known as Baxter's nerve entrapment or inferior calcaneal nerve entrapment, is a peripheral neuropathy involving the compression of the first branch of the lateral plantar nerve in the foot. This condition is a significant yet often underdiagnosed cause of chronic heel pain, accounting for up to 20% of such cases. Named after orthopedic surgeon Donald Baxter who first described it in 1992, the neuropathy typically manifests as persistent pain in the medial heel, which can radiate laterally and mimic other common foot disorders like plantar fasciitis. Unlike plantar fasciitis, which primarily affects the fascial band, Baxter's neuropathy targets the nerve supplying the abductor digiti minimi muscle, leading to potential muscle atrophy and neurological symptoms such as numbness or tingling. The foot's complex anatomy, with its high mechanical stress from weight-bearing activities, makes this nerve particularly vulnerable to entrapment. As awareness grows, effective treatment strategies have evolved, ranging from conservative measures to advanced interventions. This essay explores the multifaceted treatment approaches for Baxter's neuropathy, emphasizing evidence-based options to alleviate pain, restore function, and prevent recurrence. Understanding these treatments is crucial for clinicians and patients, as early intervention can significantly improve outcomes and quality of life.

Anatomy and Pathophysiology

To appreciate the treatments, it's essential to grasp the underlying anatomy and pathophysiology. The lateral plantar nerve, a branch of the posterior tibial nerve, divides in the tarsal tunnel, with its first branch—the inferior calcaneal nerve—innervating the abductor digiti minimi muscle, periosteum of the medial calcaneal tuberosity, and surrounding tissues. Entrapment often occurs at two primary sites: the deep fascia of the abductor hallucis muscle or anterior to the medial calcaneal tuberosity, where a heel spur or hypertrophied muscle can compress the nerve. Contributing factors include foot pronation, which alters biomechanics and increases pressure on the nerve; muscle hypertrophy from overuse; calcaneal spurs associated with plantar fasciitis; or even trauma. In chronic cases, denervation leads to fatty infiltration and atrophy of the abductor digiti minimi, visible on MRI as hyperintensity and muscle wasting. This pathophysiology explains why treatments focus on decompression, inflammation reduction, and biomechanical correction.

Symptoms and Diagnosis

Patients with Baxter's neuropathy typically present with sharp, burning heel pain that worsens with weight-bearing activities like walking or running, and may persist at rest or nocturnally—distinguishing it from pure plantar fasciitis, where pain often subsides quickly upon unloading. Symptoms include tenderness over the medial heel, radiating discomfort, paraesthesia, and in advanced stages, weakness or atrophy of the little toe abductor. Diagnosis relies on clinical examination, including Tinel's sign (tapping elicits tingling), neurodynamic testing (dorsiflexion and eversion reproduce pain), and muscle strength assessment. Imaging plays a key role: MRI reveals muscle edema in acute phases or atrophy in chronic ones, while ultrasound can guide differential diagnosis from fasciitis. Ruling out comorbidities like tarsal tunnel syndrome or systemic issues via serology is vital. Accurate diagnosis ensures targeted treatment, as misdiagnosis can lead to prolonged suffering.

Treatment Options

Treatment for Baxter's neuropathy follows a stepwise approach, starting with conservative methods and escalating to invasive options if symptoms persist beyond 3-6 months. The goal is to relieve nerve compression, reduce inflammation, and address biomechanical faults.

Conservative Treatments

Conservative management Baxter's neuropathy is the cornerstone, effective in 70-80% of cases, and focuses on non-invasive strategies to offload the nerve and promote healing. Rest and activity modification are foundational: patients are advised to avoid aggravating activities like prolonged standing or high-impact sports, allowing the nerve time to recover—nerves heal slower than other tissues, often requiring weeks to months. Ice therapy, applied 15-20 minutes several times daily, helps reduce local inflammation and numb pain.

Physical therapy is pivotal, incorporating stretching exercises for the gastrocnemius, soleus, and plantar fascia to improve flexibility and reduce tension on the nerve. Strengthening routines target foot intrinsics and the abductor digiti minimi to restore muscle balance. Soft tissue mobilization, such as massage or myofascial release, addresses tightness in the quadratus plantae and abductor hallucis. Kinesio taping provides support, reducing pronation and offloading the entrapment site.

Orthotic devices are highly recommended, with custom insoles or heel cups redistributing pressure away from the medial heel, correcting pronation, and stabilizing the foot. Footwear modifications, such as shoes with ample cushioning and arch support, complement this. In one case study, initial conservative efforts like stretching and physiotherapy failed, but they remain first-line due to low risk. Manipulation techniques, including joint mobilization of the ankle and foot, can release adhesions around the posterior tibial nerve, performed in sessions to avoid symptom exacerbation.

Pharmacological and Injection Therapies

For pain not responsive to basics, pharmacological interventions include non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen to manage inflammation and discomfort. Anticonvulsants such as gabapentin may be prescribed for neuropathic pain, addressing the burning or tingling sensations.

Injection therapies mark a bridge to more advanced care. Ultrasound-guided corticosteroid injections deliver anti-inflammatory agents directly to the entrapment site, providing rapid relief in many patients. In a reported case, a methylprednisolone injection resolved chronic pain after conservative failure, with the patient pain-free at one-year follow-up. Hydrodissection, using 5% dextrose or saline to separate the nerve from surrounding tissues, is an emerging technique, offering decompression without steroids' side effects. These procedures are minimally invasive, with high success rates when guided by imaging.

If Baxter's neuropathy symptoms persist, advanced non-surgical methods include cryoablation or radiofrequency ablation, which use cold or heat to disrupt pain signals from the nerve, providing long-term relief. Ultrasound-guided radiofrequency is particularly effective for refractory cases, targeting the nerve precisely to avoid muscle damage.

Surgical intervention is reserved for failures of conservative and interventional therapies, occurring in about 10-20% of patients. Procedures involve nerve decompression through release of the abductor hallucis fascia or removal of compressive structures like spurs. Endoscopic or open techniques minimize recovery time, with success rates over 80%, though risks include infection or incomplete relief. Post-surgery, rehabilitation mirrors conservative care to prevent recurrence.

Craig Payne is a University lecturer, runner, cynic, researcher, skeptic, forum admin, woo basher, clinician, rabble-rouser, blogger and a dad.