The Science of Tarsal Tunnel Syndrome

Tarsal tunnel syndrome results from compression of the posterior tibial nerve as it passes through the tarsal tunnel, a fibro-osseous space located behind the medial malleolus at the ankle. The tunnel is bounded by the flexor retinaculum (laciniate ligament) superficially and the tibia, talus, and calcaneus deep to the nerve. The posterior tibial nerve carries sensory fibers to the plantar surface of the foot and motor fibers to most of the intrinsic foot muscles. Within or just distal to the tarsal tunnel, the nerve divides into medial and lateral plantar branches, and sometimes a medial calcaneal branch. Compression can affect the main trunk proximally or individual branches distally, creating variable symptom patterns. Several mechanisms can cause nerve compression within this confined space. Space-occupying lesions such as ganglion cysts, lipomas, or varicose veins can directly compress neural structures. Inflammatory conditions like rheumatoid arthritis, tenosynovitis, or chronic ankle instability can cause swelling that reduces the available space for the nerve. Biomechanical factors contribute significantly to tarsal tunnel syndrome development. Excessive foot pronation increases tension on the flexor retinaculum and can cause the nerve to bow around the medial malleolus, creating a functional compression. This explains why the condition often occurs in association with posterior tibial tendon dysfunction or flexible flatfoot deformity. Chronic compression leads to intraneural edema, demyelination, and eventual axonal damage if left untreated. The progression from reversible conduction block to permanent nerve damage explains why early recognition and treatment are crucial for optimal outcomes.