Applied Anatomy

After innervating the gastrocnemius, soleus, tibialis posterior, flexor digitorum profundus, and flexor hallucis longus in the calf, the tibial nerve passes through the tarsal tunnel at the medial aspect of the ankle. There, the tibial nerve is accompanied by the tibial artery and the tendons of the flexor digitorum longus, flexor hallucis longus, and tibialis posterior muscles. This tunnel’s roof is composed of a thin fascia, the laciniate ligament (flexor retinaculum), which connects the medial malleolus to the calcaneus.

The tibial nerve bifurcates into its two terminal branches within 1 cm of the malleolocalcaneal axis in 90+ of patients (Figure C6-1). Its terminal branches are: (1) the calcaneal branch, a purely sensory nerve, which has a variable takeoff in relation to the flexor retinaculum and explain its involvement or its lack of in nerve entrapments at that site (Figure C6-2); (2) the medial plantar nerve, which innervates the abductor hallucis, flexor digitorum brevis, and flexor hallucis brevis, in addition to the skin of the medial sole and, at least, the medial three toes; and (3) the lateral plantar nerve, which innervates the abductor digiti quinti pedis, flexor digiti quinti pedis, adductor hallucis, and the interossei, in addition to the skin of the lateral sole and two lateral toes. The innervation of the skin of the sole of the foot is provided primarily through the three terminal branches of the tibial nerves, with minimal contribution from the saphenous and sural nerves (Figure C6-3).

Figure C6-1 The distribution of location of the tibial nerve along the malleolocalcaneal axis and the flexor retinaculum.

(From Dellon AL, Mackinnon SE. Tibial nerve branching in the tarsal tunnel. Arch Neurol 1984;41:645–646, with permission from the American Medical Association.)

Figure C6-2 Patterns of origin of the medial calcaneal branch from the tibial nerve in 20 patients.

(From Dellon AL, Mackinnon SE. Tibial nerve branching in the tarsal tunnel. Arch Neurol 1984;41:645–646, with permission from the American Medical Association.)

Figure C6-3 The cutaneous innervation of the sole of the foot.

(From Dyck PJ, Thomas PK. Peripheral neuropathy, 3rd ed. Philadelphia, PA: WB Saunders, 1993, with permission from the American Medical Association.)

Clinical Features

Tarsal tunnel syndrome (TTS) is caused by compression of the tibial nerve or any of its three terminal branches under the flexor retinaculum. It was first described by Keck in 1962. Its true incidence is unknown, though it is an uncommon entrapment mononeuropathy. TTS is sometimes referred to as the medial tarsal tunnel syndrome, to distinguish it from the anterior tarsal tunnel syndrome which is an entrapment of the terminal segment of the deep peroneal nerve under the extensor retinaculum in the dorsum of the foot.

The disorder is insidious in onset, more common in women and is usually unilateral. Bilateral TTS is rare accounting for 10–20+ of cases. Most cases of TTS are idiopathic but remote ankle trauma, particularly sprains and fractures, is common. Runners, joggers, and dancers are particularly at high risk for developing TTS. Other causes include arthritis or tenosynovitis of the ankle with or without rheumatoid arthritis, hypertrophic or anomalous muscles, biomechanical factors (such as ill-fitting foot wear or heel varus and valgus deformity), or a mass lesion within the tunnel (ganglion, lipoma, schwannoma, or varicose vein).

The most common symptom of TTS is burning foot pain, which often worsens after prolonged standing or walking. Sometimes, the pain radiates proximally to the calf. Paresthesia in the sole is common, but weakness or imbalance is extremely rare. The neurologic examination shows sensory impairment in the sole in the distribution of one or more of the three terminal tibial branches (medial plantar, lateral plantar, or calcaneal). In 40+ of patients, the medial and lateral plantar nerves are involved while the heel is spared. In 25+ of patients, the sensory loss involves all three terminal branches territory, and in another 25+, the sensory loss is only in the medial plantar nerve distribution, while selective entrapment of the lateral plantar nerve is only present in 10+ of the cases. The sensory symptoms may be triggered or exaggeration by foot eversion. Tinel sign, induced by percussion of the tibial nerve at the flexor retinaculum, is a useful sign and is present in the majority of patients. Muscle atrophy in one sole is rarely encountered. Weakness is rare because the long toe flexors are intact. Ankle jerk and sensation of the dorsum of the foot are normal.

True TTS is likely a clinical rarity, despite that some podiatrists and orthopedists consider it to be a common disorder. A variety of more common orthopedic, rheumatologic, and neurologic conditions may result in foot pain and may be misdiagnosed as TTS (Table C6-1). The diagnosis of TTS is particularly difficult in patients with a history of foot or ankle trauma. Careful evaluation of the ankle and foot, including x-rays, bone scan, tomogram, magnetic resonance imaging, and EMG, is often necessary before a correct diagnosis is made. Of the neurologic disorders that mimic TTS, proximal tibial mononeuropathy, caused by nerve compression by the tendinous arch of the soleus muscle or due to a nerve sheath tumor, may present with indolent symptoms that are very similar to those of TTS. These rare lesions manifest with foot pain and numbness, but they are usually associated with calf weakness or atrophy and absent or depressed ankle jerk, findings not consistent with TTS. An S1 or S2 radiculopathy, in isolation or as a component of lumbar spinal canal stenosis, may result in foot numbness or pain which is often worse with walking or standing. However, there is usually low back and posterior thigh pain (“sciatica”), depressed or absent ankle jerk or weakness of gastrocnemius, hamstrings, or glutei muscles. A particularly troublesome task is distinguishing patients with TTS from those with early sensory peripheral polyneuropathy, particularly in the elderly. A useful feature is that TTS is rarely bilateral while peripheral polyneuropathy often affects both feet. Also, the sensory loss in polyneuropathy usually involves both the sole and dorsum of the foot and is rarely associated with a Tinel sign at the flexor retinaculum.

Table C6-1 Differential Diagnosis of Tarsal Tunnel Syndrome

* Due to trauma, bunion surgery, foot deformities, or ill-fitted shoes.

Conservative treatment of TTS should be provided first to all patients. Sources of pressure, such as ill-fitting shoes, should be identified and eliminated. Other helpful measures include minimization of ankle edema through elevation, the use of special stockings or a medial arch orthotic support, bracing of the foot with a light orthosis, administration of anti-inflammatory agents, or local injection with long-acting corticosteroids. Only a small proportion of patients require surgical decompression with variable results. Good outcome can be achieved by selecting either patients with documented entrapment who have failed conservative treatment or those with an identifiable mass. Although most patients improve without any sequelae, in some, especially those who experienced ankle trauma, chronic pain and features of complex regional pain syndrome (reflex sympathetic dystrophy) may develop.

Electrodiagnosis

Electrodiagnostic confirmation of TTS relies on techniques studying nerve fibers that traverse either the medial or the lateral plantar nerves. The following are the most commonly utilized EDX studies in patients with suspected TTS:

Figure C6-4 Medial and lateral mixed plantar responses in a 45-year-old woman with a right tarsal tunnel syndrome. Note that the medial and, to a lesser extent, the lateral plantar mixed responses (arrows) were significantly delayed on the right when compared to the left (right medial and lateral plantar latencies were 4.7 ms and 4.0 ms respectively, while both latencies on the left were 3.5 ms).

In practical terms, tibial motor NCS, recording AH and ADQP, and medial and lateral plantar mixed NCS should be performed bilaterally for comparison. These should be followed by needle EMG sampling of the AH and ADQP muscles bilaterally for comparison. In a classical case of unilateral TTS, the motor amplitudes are low with delayed distal latencies and the mixed plantar studies are delayed or absent on the affected side only. Needle EMG shows fibrillation potentials in the AH and ADQP muscles with chronic neurogenic MUAP changes on the symptomatic side only. Findings restricted to the medial or lateral plantar nerves do also occur. In these situations, all the NCS and needle EMG abnormalities point to the compressed terminal nerve only. Unfortunately, it has been the experience of many physicians that the lesion is far more likely to be manifested as axon loss only without focal demyelinating slowing. In these situations, none of the above NCS techniques used to diagnose TTS is effective. Instead, the EDX study is nonlocalizing, since the NCS will demonstrate low amplitude or unelicitable responses without slowing, and the needle EMG will confirm the axonal nature by showing neurogenic MUAP changes.

An important task of the EDX study is to differentiate TTS from a peripheral polyneuropathy and S1/S2 radiculopathy. All three disorders have foot numbness and result in abnormal tibial motor conduction studies and denervation of intrinsic muscles of foot. Table C6-2 lists an EDX guide to help in differentiating TTS from these two neurologic disorders. It should be pointed out that distinguishing these three illnesses from one another sometimes is very difficult, especially in elderly patients in whom the sural SNAPs and H reflexes may be absent.