How To Address Baxter's Nerve Entrapment
Heel pain is arguably the most common complaint that foot and ankle specialists hear. The majority of these complaints are linked to plantar fasciitis and we all have developed our own unique treatment algorithms for this condition. What happens when we are months into our treatment algorithm and the patient has not had much improvement or a fasciotomy has been performed and the heel pain returns? Is it still plantar fasciitis? No. In both of these scenarios, we must revert back to our differential diagnoses. While heel pain is commonly caused by plantar fasciitis, it is also attributed to heel pad atrophy, seronegative arthritis-induced inflammation, tarsal tunnel syndrome, medial calcaneal neuritis, heel spurs, calcaneal stress fractures, periosteal inflammation and entrapment of the first branch of the lateral plantar nerve (Baxter’s nerve). Baxter says as much as 20 percent of heel pain is caused by entrapment of the first branch of the lateral plantar nerve.1 While this is not new information for many, too many patients continue to slip under the radar with a diagnosis of plantar fasciitis that is refractory to exhaustive conservative and sometimes surgical care.
Understanding The Anatomy And Etiology
The first branch of the lateral plantar nerve has sensory components to the calcaneal periosteum, the long plantar ligament and the lateral plantar skin, and motor fibers to the abductor digiti minimi, flexor digitorum brevis and quadratus plantae. The first branch of the lateral plantar nerve originates from the lateral plantar nerve near the bifurcation of the tibial nerve or it may arise from the tibial nerve prior to its bifurication. It then dives through the superficial fascia at the superior border of the abductor. At this level, the investing fascia of the abductor is thicker laterally because of the reinforcement from the interfasicular ligament in continuity with the medial intermuscular septum.2 It travels distally between the lateral abductor fascia and the medial edge of the quadratus. When it reaches the lower border of the abductor hallucis, it turns and courses laterally, passing 5.5 mm anterior to the medial calcaneal tuberosity (or spur) and between the quadratus and the underlying flexor brevis until it reaches its distal target of the abductor digiti minimi.3 This is a true entrapment neuropathy. Sammarco reported histological evidence of perineural fibrosis and hypertrophy of affected nerves.4 Researchers have cited two primary points of potential entrapment.5,6 The first is the point where the nerve turns laterally between the medial edge of the quadratus plantae and the thick lateral fascia of the abductor hallucis. The second is the point where the nerve courses anterior to the tuberosity and/or spur. An increase in cubic contact of this passage (via a spur or muscle hypertrophy) and/or pronation of the rearfoot/midfoot complex, causing impingement at the nerve’s sharp turn are both possible predisposing conditions. When one sees entrapment neuropathy of the Baxter’s nerve after a plantar fasciotomy, it is typically caused by distal migration of the fascia which can entrap the nerve or is the result of scar tissue which has bound the nerve down. Be aware that overzealous spur resection can also cause iatrogenic nerve damage.