Chronic heel pain is a common affliction, often hastily attributed to the ubiquitous plantar fasciitis. For many, this diagnosis leads to a familiar path of stretching, orthotics, and anti-inflammatories. However, for a significant subset of patients, these treatments fail, and the relentless, burning pain persists, a silent testament to a different, often overlooked culprit: Baxter’s neuropathy. This entrapment of the inferior calcaneal nerve is a master of misdiagnosis, a specific nerve compression syndrome that demands a distinct clinical approach to alleviate its unique and debilitating agony.
Baxter’s neuropathy, first described in 1984 by Dr. Donald Baxter, is a compressive neuropathy of the first branch of the lateral plantar nerve (LPN), also known specifically as the inferior calcaneal nerve. To understand this condition, one must first navigate the intricate anatomy of the foot’s medial heel. The tibial nerve passes behind the medial malleolus (the inner ankle bone) and divides into the medial and lateral plantar nerves within the tarsal tunnel. The lateral plantar nerve courses obliquely toward the little toe side of the foot. Its first branch is of critical importance: the inferior calcaneal nerve. This small but vital nerve makes a sharp, angled turn, piercing through a tight fibro-osseous tunnel between a taut, fibrous band of the abductor hallucis muscle (which moves the big toe) and the medial calcaneal bone itself. It is this precise anatomical location—a nerve navigating a narrow, unyielding passage—that sets the stage for entrapment.
The pathophysiology of Baxter’s neuropathy involves chronic compression and irritation of the nerve within this rigid canal. Repetitive microtrauma, excessive tension, or direct pressure leads to localized nerve ischemia (lack of blood flow), demyelination (damage to the nerve’s insulating sheath), and ultimately, neuropathic pain. The nerve’s function is to provide motor innervation to the abductor digiti minimi muscle (which moves the little toe) and sensory innervation to the periosteum (outer layer) of the anterior medial calcaneus. Consequently, its compression produces a very specific and often misunderstood pain profile.
Clinically, Baxter’s neuropathy presents a challenge because its symptoms can masquerade as those of plantar fasciitis. The pain is typically located in the medial heel and may radiate distally toward the arch. However, key differentiating features exist. Unlike the classic sharp, stabbing morning pain of plantar fasciitis, the pain of Baxter’s neuropathy is often described as a constant, deep, burning, or aching sensation. It may be more pervasive, worsening with prolonged standing or athletic activity, particularly those involving running and jumping. Patients might also experience paresthesia—a tingling or numbness—though this is not always present due to the nerve’s primarily motor function. Palpation reveals maximum tenderness not at the central plantar heel where the plantar fascia attaches, but rather over the medial heel, specifically anterior and inferior to the medial calcaneal tuberosity, along the course of the abductor hallucis muscle. A critical diagnostic sign is weakness in abduction of the fifth toe, a function of the compromised abductor digiti minimi muscle, though this can be subtle and difficult to assess.
The risk factors for developing this condition are often linked to activities and foot structures that increase strain on the nerve’s pathway. Runners and athletes are particularly susceptible due to repetitive impact and overuse. Biomechanical abnormalities are a primary driver; individuals with heel valgus (a heel that rolls outward), pes planus (flat feet), or excessive pronation (rolling in of the ankle) experience increased tension and compression on the nerve as the abductor hallucis muscle tightens to stabilize the arch. Other contributing factors include obesity, which increases mechanical load, direct trauma, and space-occupying lesions like ganglia or varicosities within the tarsal tunnel that can push on the nerve.
Diagnosing Baxter’s neuropathy requires a high index of suspicion. While plain radiographs can rule out other causes like stress fractures, and ultrasound can assess the plantar fascia and abductor muscle, the gold standard for confirmation is electrodiagnostic testing—specifically, nerve conduction studies (NCS) and electromyography (EMG). An EMG can detect denervation changes, such as fibrillations and positive sharp waves, in the abductor digiti minimi muscle, providing objective evidence of nerve entrapment. However, these tests can sometimes yield false negatives, making a thorough clinical examination paramount.
The management of Baxter’s neuropathy is a graduated process. Initial conservative treatment focuses on reducing nerve compression and irritation. This includes activity modification to avoid aggravating pursuits, anti-inflammatory medications, and immobilization in a walking boot to rest the area. Addressing biomechanical faults is crucial; custom orthotics with specific medial heel posting and arch support can reduce tension on the abductor hallucis muscle, thereby decompressing the nerve. Physical therapy aimed at stretching the calf muscles and intrinsic foot muscles, along with gait retraining, can be beneficial. For cases resistant to conservative care, local corticosteroid injections into the entrapment site can provide significant diagnostic and therapeutic relief by reducing inflammation around the nerve.
When conservative measures fail after six to twelve months, surgical intervention may be considered. The procedure involves a carefully planned incision over the medial heel to release the deep fascia of the abductor hallucis muscle, thereby decompressing the inferior calcaneal nerve. Surgical success rates are generally high, with most patients experiencing substantial pain relief and a return to normal function, though a prolonged recovery period is common.
Baxter’s neuropathy is a distinct and frequently underdiagnosed cause of chronic heel pain. Its ability to mimic the more common plantar fasciitis necessitates a discerning clinical eye. A detailed history focusing on the quality of pain and a meticulous physical examination to pinpoint its location are the first steps toward an accurate diagnosis. For the patient suffering in silence, enduring treatments that bring no respite, the recognition of Baxter’s neuropathy can be transformative. It shifts the narrative from a frustrating mystery to a definable, treatable condition, offering a pathway to finally quieting the unseen agony within the heel.