J R Coll Surg. Edinb., 43, February 1998, 35-36

Orthopaedic section

Tarsal tunnel syndrome: a study of the clinical and neurophysiological results of decompression

P. J. WARD AND M. L. PORTER
Department of Orthopaedics, Preston Acute Hospitals Trust, Sharoe Green Lane, Preston, UK

The neurophysiological and clinical outcomes of surgical decompression of 22 cases of tarsal tunnel syndrome are analysed. Recent work by Pfeiffer & Cracchiolo1 has suggested a successful outcome in only 44% of cases. We have reviewed the outcome of surgery both clinically and with the use of nerve conduction studies. Pre- and post-operative motor conduction delays in the plantar nerves are compared with clinical results found both in the clinic and later by a postal questionnaire. Despite careful clinical and neurophysiological assessment prior to a full surgical release, only 42% of patients had a satisfactory outcome. A larger reduction in plantar nerve conduction delay post-operatively corresponded well to an improvement in symptoms. However, we were unable to predict which cases would respond to decompression using clinical or electrophysiological methods. We question the use of nerve conduction studies in the diagnosis of tarsal tunnel syndrome, and also the role of surgery in the management of this condition.

Keywords: nerve conduction study, tarsal tunnel syndrome.

Tarsal tunnel syndrome describes the entrapment of the posterior tibial nerve at the level of the medial malleolus, resulting in pain and/or sensory disturbance in the foot.

Tarsal tunnel syndrome was first described by Ward in 1948.2 Decompression of the posterior tibial nerve was first reported in 1962 by Keck.3 The syndrome was reported by Lam4 in the same year, when the first decompression was performed in the United Kingdom.

Kaplan & Kernaham5 reported the result of 21 unilateral decompressions, nine cases being reported to have had complete relief of symptoms. Pfieffer1 reported the result of 32 cases followed up for an average of 3 years, only 44% having good or excellent results.

The diagnosis of tarsal tunnel syndrome is on clinical grounds, the history being the most important factor. Nerve conduction studies are widely used to support a clinical diagnosis further.

The success of decompression is difficult to record or quantify objectively. We have attempted to overcome any clinical bias by using a postal questionnaire.

The role of the nerve conduction study, and more importantly the mode of the study and the interpretation of any results, remains controversial. Motor- and sensory-evoked potential amplitudes and the motor nerve latencies may all be recorded. Sensory conduction changes may be the most sensitive,6 but are not widely available.

Post-operative nerve conduction studies have been reported in only three patients by Oh7 in 1989. No changes in motor latencies were found despite a symptomatic improvement.

In this study we attempt to compare directly the clinical results of decompression with the neurophysiological results. We attempt to define the role of the nerve conduction study and the place of surgical decompression in the management of tarsal tunnel syndrome.

METHODS

Seventeen patients were identified over a 4-year period as having had a diagnosis of tarsal tunnel syndrome. Fifteen of these patients had nerve conduction studies. One patient died prior to surgery, of heart failure, and a second patient refused surgery. Fifteen patients had surgery, seven having bilateral decompression. A total of 22 tarsal tunnels were decompressed.

All but three patients were operated upon by the senior author or under his direct supervision. A full decompression was achieved. The posterior tibial nerve was identified as it entered beneath the flexor retinaculum, and was released and followed as it divided into medial and lateral plantar nerves. These were in turn followed above or into abductor hallucis brevis and were further decompressed as required.

All patients were asked to return for post-operative conduction studies at an average of 23 months. Each study was repeated by the original examining neurophysician in order to reduce inter-operator error.

All patients were reviewed at 6 weeks following surgery and a note of their clinical outcome was made. All patients were sent a simple questionnaire 20 months later and were asked to report their level of symptoms as worse, no change, slight improvement, much improved, or asymptomatic.

Patients were examined pre-operatively to exclude other foot pathologies, and a note of any deformities was made.

RESULTS

Twenty-two tarsal tunnels were decompressed, the average age of the patient being 55 years. Seven patients had bilateral problems.

Pre-operative nerve conduction studies were carried out on all of the patients. Post-operative conduction studies were repeated on 15 patients, the remainder being unwilling to return.

All patients had been seen in clinic following surgery, but only 12 patients (18 decompressions) replied to the questionnaire.

Pre-operative findings

Eight patients were noted to have markedly flattened medial arches. One patient had a history of previous ankle trauma. One patient had noted an occasional swelling over the medial aspect of her ankle.

Nine patients had received local steroid injections in the past, and three had been supplied with medial arch supports. No benefit had been gained from any conservative treatment.

Pre-operative motor latency times for both medial and lateral plantar nerves were recorded. The average medial plantar latency was 5.1 ms and the lateral latency was 5.5 ins.

Post-operative findings

Post-operative nerve conduction results were available in 15 cases. The average time between decompression and repeat testing was23 months.

In this smaller group of patients the pre-operative motor latencies were 5.4 and 5.8 ms for the medial and lateral plantar nerves respectively.

Following decompression the motor latencies were reduced on average to 4.6 and 4.7 ms for medial and lateral nerves respectively. Thus reductions of 0.91 ms for the medial plantar nerve and 1.1 ms for the lateral had been achieved.

When patients were reviewed in clinic, 11 of 15 patients reported an improvement in their symptoms, but when questioned at a later date (an average of 20 months) only five of 12 reported an improvement.

The results of clinical outcome were compared with the results of the pre- and post-operative nerve conduction studies. (One patient who had repeat nerve conduction studies did not reply to the questionnaire, but at review reported a marked improvement in her symptoms.)

Those six patients reporting marked improvement in their symptoms had an average reduction in conduction latency times of 1.4 ms in medial and lateral plantar nerves.

Those three patients reporting no clinical improvement or a worsening of their symptoms had on average no change in their conduction latencies.

The group of patients reporting improvement in symptoms had average pre-operative motor latencies of 5.0 and 6.4 ms in their medial and lateral plantar nerves, compared with 4.7 and 4.6 ms in those with no improvement. These values are difficult to interpret, as two patients reporting an improvement in their symptoms actually had an increase in their conduction delays post-operatively.

DISCUSSION

On initial review of the 15 patients who had a total of 22 tarsal tunnel decompressions, it appeared that 11 patients were helped by surgery. The postal questionnaire results gave a much less promising response, only five of 12 noting improvement in their condition. This later and less observer-biased assessment of outcome may be more realistic. The time delay will have recorded any recurrence of symptoms, and patients are perhaps more likely to express the failure of surgery when not facing the operating surgeon in clinic.

The majority of patients were noted to have no pre-existing foot pathology. Those with pes planus had a similar mixed outcome to the other patients: one no better, two improved and two slightly worse. Non-operative treatment was seen to have been of no success where used, but this may merely reflect the fact that we were studying a group of patients who had gone on to surgery.

The accepted values for the medial and lateral plantar nerve conduction latencies that our department has used are 3.4 and 3.6 ms respectively over 8 cm.8 These normal values are influenced by temperature and by the individual recording the latencies. The repeat studies were carried out by the same operator. Two patients' pre-operative delay times were below the accepted limits (one at 3.3 ms for a medial plantar and one at 3.3 ms for a lateral plantar), and neither had a satisfactory outcome when reviewed by questionnaire.

Those patients who had a larger reduction in conduction delay were those who had an improvement in their symptoms.

Our post-operative nerve conduction results disagree with the findings of Oh et al.7 who repeated studies in three patients and found no motor improvement. Our disappointing final outcome is very similar to that reported by Pfeiffer & Cracchiolo.1

CONCLUSION

We conclude that 11 of 15 (73%) patients undergoing surgical decompression for tarsal tunnel syndrome initially reported some improvement in the clinic, but that this fell to only five of 12 (42%) when later indirectly assessed by questionnaire. We were able to demonstrate a reduction in motor conduction delay in those patients who reported an improvement following surgery. We were not able, however, to predict which patients were likely to be helped by surgery by measuring the magnitude of their conduction delay. The value of such an investigation is therefore in question.

Furthermore, despite careful clinical assessment pre-operatively and a full surgical decompression, the results of our surgery have been very disappointing and the place of such surgery must also be open to debate. We recommend that any patient who is to undergo such surgery be fully informed of the likelihood of a successful outcome.

ACKNOWLEDGEMENTS

We wish to thank the Department of Neurophysiology, Preston and Professor Mitchel for their help and co-operation with this study.

REFERENCES

  1. Pfeiffer WH, Cracchiolo A. Clinical results after Tarsal Tunnel Decompression. J Bone Joint Surg 1994; 76-A: 1222-30.
  2. Ward W. Sth Surg 1948; 14:124.
  3. Keck C. The Tarsal Tunnel Syndrome. J Bone Joins Surg 1962; 44-A: 180-2.
  4. Lam SJS. A Tarsal Tunnel Syndrome. Lancet 1962; ii: 1354.
  5. Kaplan PE, Kernaham WT, Jr. Tarsal Tunnel Syndrome. An electrodiagnostic and surgical correlation.J Bone Joint Surg 1981; 63-A: 96-9.
  6. Ponsford SN. Sensory conduction in medial and lateral plantar nerves. J Neurol Neurosurg Pschiat 1988; 51: 188-91.
  7. Oh SI, Arnold TW, Park KH, Kim DE. Electrophysiological improvement following decompression surgery in Tarsal Tunnel Syndrome. Muscle Nerve 1991; 14: 407-10.
  8. Fu R, Delisa JA, Kraft GH. Motor nerve latencies through the tarsal tunnel in normal adult subjects: standard determinates corrected for temperature and distance. Arch Phys Med Rehab 1980; 61: 243-8.

Correspondence: Peter Ward, Gorse Cottage, Forest Road, Burley, Hampshire BH24 4DQ UK

© 1998 The Royal College of Surgeons of Edinburgh, J. R. Coll. Surg. Edinb., 43, February, 35-36

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