Rethinking Tarsal Tunnel Syndrome

By Paul R. Scherer, DPM

   Podiatrists have been treating tarsal tunnel syndrome (TTS) conservatively for decades although there is no clinical outcome study to document the effectiveness of orthotics for this syndrome. Most podiatrists rely on the anecdotal evidence and their own experience to prescribe orthoses, which are intended to change the position of the foot and reduce the trauma and traction of the posterior tibial nerve at the flexor retinaculum.

   First defined by Keck in 1962, tarsal tunnel syndrome is a relatively common problem that podiatrists see in their practice and is frequently associated with extremely pronated feet and patients with standing occupations.1 The hallmark of the syndrome is pain in the proximal medial arch with paresthesias extending along the course of the medial and lateral plantar nerve. The thinking is the pathology is the result of traction on the tibial nerve and compression by the flexor retinaculum or occurs due to compression of the medial plantar nerve as it perforates the fascia and intrinsics at the porta pedis.

   Conservative treatment is always the first step. This includes strapping and orthotics to hold the foot in a less pronated position. One may use antiinflammatory or anesthetic injections in some areas to reduce concomitant symptoms. In cases of resistant pathology, podiatrists would proceed with surgical treatment by releasing the retinaculum at the medial malleolus or decompressing the nerve at the porta pedis.

Reviewing The Anatomy Of Tarsal Tunnel Syndrome

   However, before discussing the etiology, pathology and differential diagnosis of tarsal tunnel syndrome, one must have a strong grasp of the involved anatomy. After all, it is highly likely that abnormal anatomy or dysfunction due to abnormal anatomy that produces the trauma on the nerve leads to the symptoms we call tarsal tunnel syndrome.

   The tarsal tunnel is actually a channel produced by the septa of the flexor retinaculum, which has a constantly changing volume dependent on the position of the foot. The flexor retinaculum blends with the plantar fascia and is affected to some degree by the tension on this structure since the flexor retinaculum and the plantar fascia are both anchored at the calcaneus and connected to each other. Tension on the plantar fascia (think pronation) may affect the tension on the retinaculum and alter the volume of the tunnel.

   Four fibrous septa emerge from the interior surface of the flexor retinaculum. They each create an independent channel that allows leg structures to transition to foot structures. The third channel, counting from medial to lateral, contains the nerve with the vascular structures. The walls of the tunnel are the septa, the roof is the retinaculum and the floor is the sheath of the three flexor tendons. Swelling of the tendon sheaths from overuse, trauma or inflammation has the capability to also decrease the volume of the tunnel. It is all about the size.

   Not only is the size of the tunnel vulnerable to the swelling and movement of the structures creating it, but one author believes the bifurcation of the nerve — before it enters the tunnel — increases the size of the nerve tissue going through the tunnel. Havel dissected 68 feet and discovered the bifurcation occurred within or after the tunnel in 93 percent of the feet.2 The bifurcation occurred before the tunnel in 7 percent of the feet, producing two nerves instead of one traversing the tunnel. Could this increase in nerve tissue make the nerve more susceptible to injury from inflammation of the tendon sheaths and motion of the plantar fascia? Does tarsal tunnel syndrome occur at a 7 percent frequency in the general population to match this anatomical variant?

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