Tarsal tunnel syndrome

Principal authors: Gillian Jackson, Jim Barrie

Last evidence check March 2011


Tarsal tunnel syndrome (TTS) is a condition characterised by symptoms of pain, altered sensation or motor weakness affecting the branches of the posterior tibial nerve at the ankle. The cause of the syndrome is thought to be compression of the posterior tibial nerve  and its branches in the “tarsal tunnel” formed by the flexor retinaculum and the medial malleolus.

There may be alterations in objective findings on neurological examination or in electrophysiological tests of nerve function. It is important to be aware when using the literature on TTS that some papers define the syndrome clinically and others on the basis of electrophysiology.

There can be both systemic and local contributions to nerve dysfunction, such as diabetes or a space-occupying lesion. Compression may also or alternatively occur at the fibrous arch in abductor hallucis (distal tarsal tunnel syndrome).

Anterior tarsal tunnel syndrome is a condition of the deep peroneal nerve anterior to the ankle or on the dorsum of the foot.


The incidence of TTS has not been determined. None of the series in the literature include data from which incidence or prevalence can be estimated. However, in the Blackburn series of about 15000 new foot and ankle patients in 13 years, we have seen about 10 unequivocal new cases of TTS, several of whom were tertiary referrals. Our catchment area is such that few local patients go elsewhere, implying an incidence in East Lancashire of perhaps two new cases per million per year.

Age ranges in published series are generally 15-70 years, with more female than male patients.


The tarsal tunnel is a fibro-osseous tunnel, posterior and distal to the medial malleolus. It usually contains the posterior tibial artery, vena comitans, and nerve as well as the tendons of FDL, TP, FHL.

The tibial nerve branches in a variable manner, and not all of its branches run through the tarsal tunnel in all patients. Havel (1988) described various patterns.

Dellon et al(1984) report bifurcation of the posterior tibial nerve into the medial and lateral plantar nerves within the tunnel in 95% of cases. Other studies quote similar findings. Both branches enter the foot deep to abductor hallucis within 2 distal  fascial tunnels.

Davis and Schon’s study of anatomical variance in the branches of the tibial nerve the calcaneal nerve often arises proximal to the tunnel. They found multiple (2-3) branches in 12/20 ankles.


This is an entrapment neuropathy. Nerves in entrapment syndromes show narrowing and perineural fibrosis. However, as at other sites, perineural fibrosis can be found in asymptomatic individuals. De Stoop (1989) biopsied tibial nerve in 20 cadavers and found increased perineural fibrosis in 12%, which also had ipsilateral muscle atrophy. It is not stated whether these persons had had foot symptoms or systemic disease.

Precipitating factors

The local causes of tarsal tunnel syndrome can be broadly classified in 3 groups

Cimino (1990) in a review of 25 studies and case reports found trauma to be the cause in 17% including calcaneum and ankle fractures. Potential mechanisms include:

Takakura et al (1991) in their operative series of 50 feet found SOL in 2/3rds of cases; of that ganglia were the most common cause (36%) with bony prominence associated with talocalcaneal coalition in 15 feet (30%). Only 18% lacked a clear aetiology ( less than most other reported series). Other studies found lesions such as lipoma and varicosities.

Cimino’s review of the literature found foot deformities accounting for 19% (varus 11%, valgus 9%). Persons with planovalgus feet demonstrate abnormal electrophysiological indices; the clinical syndrome may be commoner in such persons. Bracilovic et al 2006 used MRI to measure mean tarsal tunnel volume and found that it is reduced in inversion and eversion compared with neutral positioning.

Tarsal tunnel syndrome is commoner in diabetics. Peripheral nerves in patients with diabetes have an increased susceptibility to compression. Increased water content in the nerve due to glucose metabolism to sorbitol increases the cross sectional volume. In areas of anatomical narrowing this increases external pressure on the nerve.

The syndrome is twicce as common in patients with carpal tunnel syndrome.

Presentation with plantar fascitis and posterior tibial tendonopathy is the “heel pain triad”. Inflammatory arthritis, tenosynovitis and myxedema are documented causative factors.

Guyton et al (2000) examined the relationship of TTS to cumulative industrial trauma and found no evidence of causation.

Clinical features

Clinical tests for tarsal tunnel syndrome:

Most series describe patients with pain, burning, paraesthesiae or numbness in the sole of the foot, sometimes confined to the territory of the medial or lateral plantar nerve only. In severe compression patients may have pain radiating proximally along the medial aspect of the leg.

Lindsheid et al (1970) found that symptoms were often worse on standing. Nocturnal pain is documented but symptoms are generally proportional to activity level. A positive Tinel test was present over the tarsal tunnel or the abductor hallucis in many patients; in some series this was a required diagnostic criterion. The prevalence of objective neurological deficit varies between series and in several is not reported. It is difficult to say how commonly the various features are present because of the different criteria used to include patients in each series.

Kinoshita et al (2001) described a clinical test in which the foot is positioned in dorsiflexion-eversion and the MTP joints are dorsiflexed. This induced or intensified pain, numbness and the Tinel test in the majority of patients with putative TTS but in none of 50 asymptomatic volunteers, and the signs disappeared after decompressive surgery in 41/44 feet. However, Alshami et al 2007 compared the windlass test for plantar fascitis with the dorsiflexion-eversion test using displacement tranducers in cadavers. Both tests mechanically challenge  the plantar fascia, the tibial nerve and  plantar nerves questioning the usefulness of the tests in differentiating causes of plantar heel pain.

Labib et al (2002) described the “heel pain triad” of TTS, plantar fascitis and posterior tibial tendonopathy. We have seen such patients, but in our experience neuritic heel symptoms in association with plantar fascitis are usually related to the medial calcaneal nerve rather than the main tibial nerve branches.

Differential diagnosis includes:

All of these are probably much commoner than TTS.

Electrophysiological testing

Overall accuracy around 90%. No single test can be used. Sensory studies appear more accurate than motor studies.

Measures which have been studied include:

Again, it is difficult to interpret the findings because of wide variations in inclusion criteria between studies. Some studies performed electrophysiology intermittently or by varying methods.

In diabetic peripheral neuropathy the conduction velocity and amplitude may be reduced such that an additional diagnosis of nerve compression must be clinical.

Mondelli et al (2004) published a series in which sensory conduction velocity and distal motor latency in the great and little toes were compared with ipsilateral sural nerve results and correlated with a clinical severity scale. This showed good correlation between clinical and electrophysiological findings, although this has not been shown to guide prognosis or treatment.


Both ultrasound and MR have been used to image nerve compression syndromes at various sites. Both can show  changes in entrapment, fibrosis or tenosynovitis and can also show space-occupying lesions such as ganglia and varicosities In one study of 33 feet with TTS, 27 (82%) had causative lesions identified on MRI. 17 of the 19 patients that went to theatre had the MRI findings confirmed (89%).

Frey and Kerr 1993 found that in a group of 20 feet with symptoms and positive electrodiagnostic tests, 17 (85%) had positive findings on MRI. In the 20 contralateral asymptomic feet, however, 5 (25%) had significant findings on MRI.  There is no mention of electrodiagnostic results in this contralateral foot group.

Patients with the “heel pain triad” may need imaging of the tibialis posterior tendon if surgery is planned.

Other diagnostic methods

A computer-aided pressure sensation device has been described and said to be highly accurate, although the authors had a financial interest in the device, Tassler and Dellon 1996.

Non-surgical treatment

A variety of non-surgical treatments have been described as first line treatments including NSAIDS, steroid injections, AFOs, in-shoe orthotic devices. These may be effective in the presence of specific etiological causes such as inflammatory arthritis, tenosynovitis, flexible foot deformities. In general, however, these seem to have been unhelpful in the majority of patients.

Published evidence for non-operative treatment is limited. The studies in question were largely reporting surgical treatment, and proper studies of non-surgical treatment may show different results. Only small numbers (16%) were treated non-operatively in Cimino’s review (1990).

Drugs such as amitryptiline, carbamazepine and gabapentin are commonly used to treat neuropathic pain, but there do not seem to have been any studies of these drugs in TTS or other entrapment syndromes.


Surgery for TTS includes:

Lamm et al (2007) describe a detailed surgical approach for a full tarsal tunnel decompression, proposing inadequate release as one reason for failure and lack of consistent results in the literature. They also discuss its prophylactic role in leg lengthening and deformity correction of the foot and ankle, although this was a review article without original data.

In a cadaveric study of pressure in the medial and lateral plantar  and tarsal tunnels, Barker et al (2007) demonstrated that release of the tarsal tunnel does not reduce the pressure distally. Resection of the septum between the medial and lateral plantar tunnels was necessary to ensure a full decompression including the distal branches.

Reported clinical results of surgical release for TTS vary widely. Kaplan and Kernohan (1981), in one of the earlier reports, had complete clinical success in 18 patients, but Ward and Porter reported less than 50% success. Many series report varying degrees of partial success, and Gondring et al (2003) noted a considerable discrepancy between surgeon’s and patient’s view of outcome.

Dellon (2004) studied surgical decompression of peripheral nerves in diabetics with peripheral neuropathy. Their review of 6 reported studies of tarsal tunnel decompression in these patients showed pain relief in over 80%. The recovery of some useful sensation in the feet of these patients can aid prevention of ulcers and amputation.

Some of the variation in results may reflect variation in inclusion criteria, follow-up and outcome measures, but also the fact that this is a rather rare and heterogenous condition. Pfeiffer et al (1994) had good or excellent results in only 44% of 32 feet, themselves acknowledging that 40% (12) had had previous foot surgery- 6 for tarsal tunnel. The only constant inclusion criteria was a positive Tinel test.

It is not clear how well neurophysiological studies predict surgical (or indeed non-surgical or natural) outcome. They are not used consistently in most of the reported series ie not on all patients or different techniques/ criteria used.

Several series have attempted to identify factors which predict a better result from surgery, but the results are inconsistent and sometimes conflicting:

We use fairly stringent diagnostic criteria:

We would generally offer surgery only if the diagnosis was supported by all 3 criteria. We advise patients that the results of decompression are not very predictable and that they may get only partial relief.