Tarsal Tunnel Syndrome

Tarsal Tunnel Syndrome is compression of the posterior tibial nerve or its terminal branches beneath the flexor retinaculum on the medial aspect of the ankle.

The topic repeatedly names pes planus and hindfoot valgus as causes ("increased nerve tension") and tells you to assess hindfoot alignment, but the mechanism — and what it means for treatment — is never developed. It matters because it is a fundamentally different problem from a space-occupying lesion.

The mechanism is traction, not compression. A planovalgus hindfoot (collapsed medial arch with heel valgus) places the posterior tibial nerve and its branches under stretch. As the heel everts and the arch falls, the nerve is tensioned and angulated as it curves around the medial malleolus and sustentaculum tali. Tellingly, dorsiflexion-eversion — the position of the most sensitive provocative test — is essentially the resting posture of the valgus foot, so the nerve is chronically loaded. This is a traction (stretch) neuropathy, distinct from the pressure of a ganglion or lipoma.

What it changes:

• Assessment: always examine and document standing hindfoot alignment. A flexible planovalgus foot that corrects on tiptoe (double-heel-rise) flags a biomechanical, potentially correctable contributor; a rigid valgus (e.g. tarsal coalition) does not.
• Conservative care: for biomechanical TTS, orthotic correction of the valgus (medial arch support, medial heel posting) is genuinely therapeutic — it offloads the traction and can relieve symptoms without surgery, which is why orthotics feature so prominently in the conservative plan.
• Surgical nuance (the unresolved point): a tunnel release that leaves the deforming traction force uncorrected may fail. For a fixed symptomatic valgus, some surgeons advocate realigning the hindfoot (e.g. a medialising calcaneal osteotomy or flatfoot reconstruction) alongside, or instead of, a simple release — recognising that you must address the cause of the stretch, not just the tunnel. This is not standardised, but it is why the traction mechanism is worth understanding. (General flatfoot reconstruction is developed in the pes-planus / flatfoot topics.)

Provocative Tests:

The must-know list and a viva trap both warn you to "exclude proximal nerve compression (L4-S2 radiculopathy)" and "consider double crush", but the concept is never explained — and it is one of the commonest reasons a tarsal tunnel release fails.

The double-crush hypothesis (Upton and McComas). A nerve compressed at one point along its length is rendered more susceptible to symptomatic dysfunction from a second, often subclinical, compression elsewhere — the two lesions summate rather than acting independently. The proposed mechanism is that the proximal compression impairs axoplasmic flow, lowering the threshold at which a distal site becomes symptomatic.

Why it applies to TTS. The tibial nerve carries L4-S3 fibres, so a coexisting lumbosacral radiculopathy (disc or foraminal stenosis) — or a more proximal sciatic/tibial lesion — can "prime" the very axons that are then finished off at the tarsal tunnel. The same logic links TTS to a coexisting diabetic polyneuropathy, which is itself a diffuse "crush".

What it changes in practice:

• It explains some "idiopathic" and "failed-release" TTS — a distal decompression cannot fix a missed proximal contributor.
• It mandates a proximal screen before committing to surgery: examine the lumbar spine, straight-leg raise, reflexes and proximal myotomes, and ask the electrodiagnostician to sample proximal muscles and paraspinals, not just the foot.
• It supports treating both sites (and tempering surgical expectations) when two lesions coexist — and raises the threshold for releasing a tunnel when the dominant problem is proximal.

Prognostic Factors:

There are no dedicated national-society clinical practice guidelines specific to tarsal tunnel syndrome from the major bodies, reflecting its rarity and the limited high-level evidence. Practice is instead shaped by foot-and-ankle society consensus, electrodiagnostic practice parameters and surgical experience, and is broadly consistent worldwide.

Global epidemiology and practice variation:

• TTS is uncommon and consistently under-recognised; precise population incidence is unknown across all regions.
• No arthroplasty/implant-style registries track TTS, as treatment is soft-tissue decompression rather than implantation.
• High-resource settings: routine pre-operative MRI and electrodiagnostics, ultrasound-guided diagnostic injection, and access to microsurgical neurolysis.
• Limited-resource settings: diagnosis is predominantly clinical with provocative tests; MRI and nerve conduction studies may be unavailable, so identifiable causes (post-traumatic deformity, large masses) are prioritised for surgery.
• Across all settings the surgical principle is identical: complete release of the flexor retinaculum, decompression of all branches, distal release through the abductor hallucis fascia, and excision of any space-occupying lesion.