Tarsal Tunnel Syndrome

Tarsal tunnel syndrome, first described by Keck and Lam in 1962, is a condition that is caused by compression of the tibial nerve or its associated branches as the nerve passes underneath the flexor retinaculum at the level of the ankle or distally. ^{[1, 2, 3, 4, 5, 6, 7, 8]}  It is analogous to carpal tunnel syndrome of the wrist.

Tarsal tunnel syndrome is a multifaceted compression neuropathy that typically manifests with pain and paresthesias that radiate from the medial ankle distally and, occasionally, proximally. These findings may have a variety of causes, which can be categorized as extrinsic, intrinsic, or tensioning factors in the development of signs and symptoms of tarsal tunnel syndrome.

Extrinsic causes may contribute to the development of tarsal tunnel syndrome. Examples include external trauma due to crush injury, stretch injury, fractures, dislocations of the ankle and hindfoot, and severe ankle sprains.

Local causes may be intrinsic causes of the neuropathy. Examples include space-occupying masses, localized tumors, bony prominences, and a venous plexus within the tarsal canal.

Nerve tension caused by a valgus foot can cause symptoms that are identical to those of a circumferential nerve compression.

Symptoms of tarsal tunnel syndrome vary from individual to individual, but clinical findings generally include the following:

• Sensory disturbance that varies from sharp pain to loss of sensation
• Motor disturbance with resultant atrophy of intrinsic musculature
• Gait abnormality (eg, overpronation and a limp due to pain with weightbearing)

A hindfoot valgus deformity may potentiate the symptoms of tarsal tunnel syndrome because the deformity may increase tension due to an increase in eversion and dorsiflexion.

The tarsal tunnel is a structure in the foot that is formed between the underlying bones of the foot and the overlying fibrous tissue. The flexor retinaculum (laciniate ligament) constitutes the roof of the tarsal tunnel and is formed by the deep fascia of the leg and the deep transverse fascia of the ankle. The proximal and inferior borders of the tunnel are formed by the inferior and superior margins of the flexor retinaculum. The floor of the tunnel is formed by the superior aspect of the calcaneus, the medial wall of the talus, and the distal-medial aspect of the tibia.

The remaining fibro-osseous canal forms the tibiocalcaneal tunnel. The tendons of the flexor hallucis longus muscle, flexor digitorum longus muscle, tibialis posterior muscle, posterior tibial nerve, and posterior tibial artery pass through the tarsal tunnel.

The posterior tibial nerve lies between the posterior tibial muscle and the flexor digitorum longus muscle in the proximal region of the leg and then passes between the flexor digitorum longus and the flexor hallucis longus in the distal region of the leg. The tibial nerve passes behind the medial malleolus and through the tarsal tunnel and then bifurcates into cutaneous, articular, and vascular branches.

The main divisions of the posterior tibial nerve include the calcaneal, medial plantar, and lateral plantar nerve branches. The medial plantar nerve passes superior to the abductor hallucis and flexor hallucis longus muscles and later divides into the three medial common digital nerves of the foot and the medial plantar cutaneous nerve of the hallux. The lateral plantar nerve travels directly through the belly of the abductor hallucis muscle, where it later subdivides into branches.

The innervation of the branches of the posterior tibial nerve is as follows:

• Calcaneal branch – Medial and posterior aspects of the heel
• Medial plantar branch – Cutaneous branches to the plantar medial aspect of the foot; motor branches to the abductor hallucis and flexor digitorum brevis muscles; and branches to the talonavicular and calcaneonavicular joints
• Lateral plantar branch – Motor branches to the abductor digiti quinti and quadratus plantae muscles; cutaneous nerve to the fifth digit; communicating branch to the fourth common digital nerve; motor branches to the lumbricals; second, third, and fourth interossei branches to the transverse head of the adductor hallucis and the muscles of the first interosseous space

Tarsal tunnel syndrome is a compression neuropathy of the tibial nerve that is situated in the tarsal canal. The tarsal canal is formed by the flexor retinaculum, which extends posteriorly and distally to the medial malleolus.

The symptoms of compression and tension neuropathies are similar; therefore, differences in these conditions cannot be simply identified by the symptoms alone. In certain instances, compression and tension neuropathies may coexist.

The double-crush phenomenon originates from work published by Upton and McComas in 1973. The hypothesis behind this phenomenon may be stated as follows: Local damage to a nerve at one site along its course may sufficiently impair the overall functioning of the nerve cells (axonal flow), such that the nerve cells become more susceptible to compression trauma at distal sites than would normally be the case.

The nerves are responsible for transmitting afferent and efferent signals along their length, and they are also responsible for moving their own nutrients, which are essential for optimal functioning. The movement of these intracellular nutrients is accomplished through a type of cytoplasm within the nerve cell called axoplasm (referring to cytoplasm of the axon). The axoplasm moves freely along the entire length of the nerve. If the flow of the axoplasm (ie, axoplasmic flow) is blocked, the nerve tissue that is distal to that site of compression is nutritionally deprived and more susceptible to injury. ^[9]

Upton and McComas further suggested that a high proportion (75%) of patients with one peripheral nerve lesion did, in fact, have a second lesion elsewhere. The authors implied that both lesions contribute to the patients' symptoms. These lesions were originally studied in cases of brachial plexus injury with an increased incidence of carpal tunnel neuropathy. An analogous example of the double-crush phenomenon in the feet would be a compression of the S1 nerve root, resulting in an increased likelihood of compression neuropathy in the tarsal canal.

Several factors may contribute to the development of tarsal tunnel neuropathy. Soft-tissue masses may all contribute to compression neuropathy of the posterior tibial nerve. Examples of such masses include the following:

• Lipomas
• Tendon sheath ganglia
• Neoplasms within the tarsal canal
• Nerve sheath and nerve tumors
• Varicose veins

Parkhurst et al reported three cases in which an accessory flexor digitorum longus presented as tarsal tunnel syndrome. ^[10]

Tibial nerve entrapment is common in diabetics

Bony prominences and exostoses may also contribute to the disorder. A study by Daniels et al demonstrated that a valgus deformity of the rearfoot may contribute to the neuropathy by increasing the tensile load on the tibial nerve. ^[11]

To the authors' knowledge, no studies have demonstrated a statistical association for tarsal tunnel syndrome with work conditions or activities of daily living (ADLs). The prevalence and incidence of tarsal tunnel syndrome have not been reported.

Properly performed decompression may yield satisfactory results. An initial marked decrease in pain and paresthesias may occur, followed by a reduction of symptoms to the extent that the patient may be able to tolerate the symptoms. Complete resolution of symptoms may not be possible because the disorder has numerous etiologies and because the likelihood of irreversible nerve damage exists. An increase in pain after decompression, however, is extremely rare.

Studies by Mann demonstrated that approximately 75% of patients who undergo surgical decompression have appreciable pain relief, and 25% obtain little or no relief. ^[12]  Mann also stated that a repeat surgical exploration of a previous tarsal canal release rarely causes appreciable benefit to the patient.

Gondring et al did a prospective evaluation of 46 consecutive patients (56 feet) who underwent nonoperative and surgical treatment for tarsal tunnel syndrome and documented pain intensity before and after treatment with the Wong-Baker FACES Pain Rating Scale applied to the anatomic nerve regions of the plantar aspect of the foot. ^[13]

In this study, patients who had successful nonoperative treatment experienced significantly reduced overall pain intensity in the medial calcaneal, medial plantar, and lateral plantar nerve regions. ^[13] In patients who had ongoing symptoms despite nonoperative treatment, surgical treatment significantly reduced pain in the medial calcaneal and medial plantar nerve regions but not in the lateral plantar nerve area. Pretreatment motor nerve conduction latency was significantly greater in surgically treated patients than in those who had only nonoperative treatment. The authors concluded that anatomic pain intensity rating models may be useful in  pretreatment and follow-up evaluation of tarsal tunnel syndrome.

Antoniadas et al performed a literature review of posterior tarsal tunnel syndrome and found that accurate diagnosis required proper clinical, neurologic, and neurophysiologic examinations. Success rates of 44-91% were attained with operative treatment. The results were found to be better in idiopathic cases than in posttraumatic cases, and if surgery failed, reoperation was indicated only in patients with inadequate release. ^[14]

McSweeney et al conducted a rigorous review of this condition that included the Cochrane Neuromuscular Group's Specialized Register (Cochrane Library 2013), as well as EMBASE, AMED, MEDLINE, CINAHL, Physiotherapy Evidence Database (PEDro), Biomed Central, Science Direct, and Trip Database (1972-2015). ^[15]  They found that there was limited high-level robust evidence to guide and refine the clinical management of tarsal tunnel syndrome. Requirements for small-scaled randomized controlled trials in groups with homogenous etiology are needed to analyze the effectiveness of specific treatment modalities. 

A study by Yu et al (N = 107) found that the efficacy of surgical treatment of tarsal tunnel syndrome was correlated with the cause of the syndrome, the nerve bundles involved, the operative method employed, and whether neurolysis of the epineurium was performed. ^[16]

A study (N = 45; mean follow-up, 3.6 ± 1.8 y) aimed at evaluating surgical results in relation to the etiology of tarsal tunnel syndrome divided subjects into the following three groups ^[17] :

• Group 1 - Permanent intra- or extratunnel space-occupying compressive structure
• Group 2 - Intermittent intratunnel venous dilatations
• Group 3 - Idiopathic tarsal tunnel syndrome

The main endpoint was subjective postoperative improvement on the Likert scale. Group 1 reported greater improvement than groups 2 and 3, suggesting that surgical treatment of this syndrome yields better results when the etiology invovles involving structural compression.