NB This page is from the 2005 Hyperbook.
Last evidence check November 2004.
Tarsal tunnel syndrome (TTS) is a condition characterised by symptoms of pain, altered sensation or neurological deficit affecting the branches of the posterior tibial nerve at the ankle. There may or may not be alterations in objective findings on neurological examination or in electrophysiological tests of nerve function. It is important to be aware in using the literature on TTS that some papers define the syndrome clinically and others on the basis of electrophysiology.
The cause of the syndrome is thought to be compression of the posterior tibial nerve branches in the “tarsal tunnel” formed by the flexor retinaculum and the medial malleolus. There are often one or more additional factors in nerve malfunction, such as diabetes or a space-occupying lesion. Compression may occur at the fibrous arch in abductor hallucis (distal tarsal tunnel syndrome) instead of, or in addition to, the flexor retinaculum.
The term “anterior tarsal tunnel syndrome” is sometimes applied to irritation 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 could be estimated. However, in the Blackburn series of nearly 10000 new foot and ankle patients in nearly 10 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 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.
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.
The commonest finding in tarsal tunnel syndrome is an additional space-occupying lesion such as a lipoma, varices of the venae comitantes of the posterior tibial artery or an osteochondroma.
Many series have a number of patients with previous trauma to the ankle or calcaneum. Persons with planovalgus feet demonstrate abnormal electrophysiological indices; the clinical syndrome may be commoner in such persons.
Tarsal tunnel syndrome is commoner in diabetics. There is an association with carpal tunnel syndrome, and with plantar fascitis and posterior tibial tendonopathy (the “heel pain triad”).
Guyton et al (2000) examined the relationship of TTS to cumulative industrial trauma and found no evidence of causation.
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. Lindsheid et al (1970) found that symptoms were often worse on standing. 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.
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.
Measures which have been studied include:
Again, it is difficult to interpret the findings because of wide variations in inclusion criteria between studies.
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 show typical changes in entrapment, and can also show space-occupying lesions such as ganglia. As yet there have been no studies comparing diagnostic accuracy with clinical assessment or neurophysiology in TTS.
Patients with the “heel pain triad” may need imaging of the tibialis posterior tendon if surgery is planned.
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.
A variety of non-surgical treatments have been described, including steroid injections, AFOs, in-shoe orthotic devices. In general, these seem to have been unhelpful in the majority of patients. A few may have been helped by injections. However, the studies in question were largely reporting surgical treatment, and proper studies of non-surgical treatment may show different results.
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:
Reported 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. 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.
Several series have attempted to identify factors which predict a better result from surgery, but the results are inconsistent and sometimes conflicting:
It is not clear how well neurophysiological studies predict surgical (or indeed non-surgical or natural) outcome.
We therefore advise patients that the results of decompression are not very predictable and that they may get only partial relief. We would generally offer surgery only if the diagnosis is strongly supported by clinical findings of neuropathic pain, sensory abnormalities and a positive Tinel test, preferably intensified on the dorsiflexion-eversion test. We would normally expect abnormalities of neurophysiological testing.