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.
Contributing Factors
Normal posterior tibial nerve function requires unimpeded passage through the tarsal tunnel during all phases of gait. The tunnel dimensions change dynamically with foot and ankle position, with maximum space available in plantarflexion and inversion, and minimum space in dorsiflexion and eversion.
During normal gait, the foot progresses through pronation during loading response, followed by supination during push-off. This biomechanical sequence requires the tarsal tunnel structures to accommodate changing positions and loads. When excessive pronation occurs, several problems develop that can compromise nerve function.
Excessive pronation increases tension on the flexor retinaculum as it attempts to maintain the tunnel's integrity against abnormal forces. This can create a bowstring effect where the nerve becomes compressed against the rigid medial malleolus. The prolonged pronated position also maintains the tunnel in its most confined configuration for longer periods during the gait cycle.
The posterior tibial tendon plays a crucial role in controlling pronation and maintaining the medial longitudinal arch. When this tendon becomes dysfunctional, excessive pronation results, directly affecting tarsal tunnel dimensions. This explains the frequent association between posterior tibial tendon dysfunction and tarsal tunnel syndrome.
Footwear and activity patterns influence biomechanics significantly. Shoes with inadequate arch support allow excessive pronation, while high-heeled shoes can alter ankle positioning and tunnel dimensions. Prolonged standing or walking activities may exceed the nerve's tolerance for sustained compression, particularly in the presence of underlying biomechanical abnormalities.
Recovery requires not only addressing the acute nerve compression but also correcting the underlying biomechanical factors that contributed to the problem. This often involves orthotic management to control pronation and posterior tibial tendon rehabilitation to restore normal foot mechanics.