Electrophysiologic Studies in Tarsal Tunnel Syndrome

Abstract

Galardi G, Amadio S, Maderna L, Meraviglia MV, Brunati L, Dal Conte G, Comi G: Electrophysiologic studies in Tarsal Tunnel Syndrome (TTS): diagnostic reliability of motor distal latency, mixed nerve, and sensory nerve conduction studies. Am J Phys Med Rehabil 1994;73:193-198.

The tarsal tunnel syndrome (TTS) is an entrapment of the posterior tibial nerve at the ankle. Like carpal tunnel syndrome, TTS improves with surgery but requires an instrumental diagnosis to exclude other conditions. This study evaluates the diagnostic value of nerve conduction tests proposed for TTS diagnosis. Among 13 patients investigated, 12 had secondary unilateral and 1 had idiopathic bilateral TTS. Abnormal neurophysiologic parameters were found in all cases. The diagnostic value of each neurophysiologic parameter was calculated by comparing conduction on the affected side with conduction on the healthy side. The accuracies of sensory nerve action potential (SNAP) and mixed nerve action potential (MNAP) were similar, with SNAP being more sensitive and less specific, and MNAP less sensitive but more specific. Due to the clinical importance of avoiding false positives, the mixed nerve action potential is recommended for presurgical diagnosis of TTS. The coexistence of SNAP and MNAP abnormalities, especially if asymmetric, is highly indicative of TTS.

Key Words

Tarsal Tunnel Syndrome, Plantar Nerves, Motor Nerve Conduction, Sensory Nerve Conduction, Mixed Nerve Conduction

Introduction

The tarsal tunnel syndrome (TTS) is an entrapment of the posterior tibial nerve or its terminal branches where it passes behind and below the tibial malleolus under the flexor retinaculum.¹ Clinically, this syndrome is characterized by pain at the ankle and/or heel, sometimes extending to the sole, with associated paresthesia, dysesthesia, or hyperesthesia in the distribution area of the tibial nerve.²

Diagnosing TTS can be challenging due to symptom overlap with various peripheral neuropathies, such as interdigital neuropathy of the foot, dying back neuropathies, and certain radiculopathies. Foot pain may also be seen in orthopedic conditions like rheumatoid arthritis, talocalcaneal coalition, and ankle distortion.³

Similar to carpal tunnel syndrome, neurophysiologic studies are employed to support the clinical diagnosis of TTS. Motor conduction abnormalities in the posterior tibial nerve have been observed in approximately half of TTS patients. Sensory nerve conduction studies of the plantar nerves are highly sensitive for diagnosing TTS, though not sufficiently specific. Mixed nerve conduction studies have been suggested as reliable diagnostic tools for TTS, but they have been primarily reported in case studies.

Materials and Methods

Thirteen patients (9 women and 4 men) with a clinical diagnosis of Tarsal Tunnel Syndrome (TTS), admitted for surgical treatment at the Orthopedic Department of the San Raffaele Hospital between November 1991 and September 1992, were included in this study. Their mean age was 44.1 ± 15.5 years (range 17 to 74 years). The clinical diagnosis was based on symptoms, signs, and surgical confirmation. TTS was unilateral in 12 patients and bilateral in 1. Patients experienced ankle pain radiating to the foot, paresthesia, and dysesthesia on the sole, worsening at night. Tinel's sign, elicited by percussion posterior to the tibial malleolus, was present in all patients (Table 1).

Exclusion criteria included diseases causing neuropathy, such as infections, renal insufficiency, endocrine disorders, toxic medications, or exposure to toxic substances. Tendon reflexes, muscular segmental strength, malleolar vibratory perception, sensory conduction velocity of the sural nerve, motor conduction velocity of the deep peroneal nerve, and electromyographic needle examination of the tibialis anterior and triceps surae muscles were normal in all patients. Surgical decompression of the tibial nerve at the ankle resolved the symptoms in all patients. The control group consisted of 25 normal subjects (mean age 47.6 ± 14.0 years, range 19 to 71 years), including 17 women and 8 men; 5 women and 3 men were older than 60 years.

Results

Motor Conduction Study of the Posterior Tibial Nerve

The motor action potential (MAP) distal latency of the posterior tibial nerve was abnormal in three patients with unilateral Tarsal Tunnel Syndrome (TTS) (Table 3), and was always associated with NAP and SNAP abnormalities. MAP amplitude and motor conduction velocity of the posterior tibial nerve were normal.

Sensory Conduction Studies

Sensory conduction parameters were abnormal on the affected side in all patients (Table 3). Medial plantar nerve (MPN) sensory conduction parameters were abnormal in 13 limbs of 12 patients (bilaterally in the patient with bilateral TTS). Only 1 patient with unilateral TTS had normal MPN sensory parameters. Lateral plantar nerve (LPN) sensory conduction abnormalities were observed in all limbs. Absence of the sensory action potential (SAP) was the most frequent abnormality, accounting for 92.8% of LPN abnormalities and 76.9% of MPN abnormalities. SAPs were also absent in two unaffected limbs: in both nerves of a 74-year-old woman and in the LPN alone of a 51-year-old man.

Mixed Nerve Conduction Studies

Mixed nerve conduction parameters were abnormal in 12 of 14 limbs with clinical Tarsal Tunnel Syndrome (TTS) (Table 3). Nerve action potential (NAP) abnormalities were observed in both nerves of 7 limbs, MPN alone in 2, and LPN alone in 3. NAP alterations in the LPN were predominantly characterized by the absence of the NAP (60%), while in MPN they were mainly reduced amplitude or slowed nerve conduction velocity (NCV) (88.8%).

Mixed nerve conduction abnormalities were consistently associated with sensory conduction abnormalities: NAP and SAP abnormalities in both nerves were observed in 6 limbs; SAP and NAP abnormalities of the LPN and SAP of the MPN in 3 limbs; SAP and NAP abnormalities of the MPN and SAP of the LPN in 2 limbs; and in the last limb, there were NAP abnormalities in both nerves associated with SAP abnormalities of the LPN only.

False-positives, false-negatives, sensitivity, specificity, and diagnostic accuracy of each neurophysiologic test are reported in Table 4.

Discussion

The Tarsal Tunnel Syndrome (TTS) involves entrapment of the posterior tibial nerve at the ankle and typically improves with surgical treatment. Symptoms such as pain, paresthesias, and numbness in the toes and sole, particularly worsening at night, should raise suspicion for TTS. However, other clinical conditions must be excluded before surgical nerve decompression is considered.

Over the past 20 years, neurophysiologists have developed various techniques for the objective diagnosis of TTS. Initial studies focused on motor conduction in the tibial nerve and measurement of its terminal motor latency. A significantly prolonged latency in the medial or lateral plantar branches of the tibial nerve, or both, suggests compression within the tarsal tunnel. Goodgold et al. regarded this as an objective diagnostic criterion for TTS. Johnson and Ortiz observed prolonged terminal latency in the medial and lateral plantar nerves in five of eight TTS patients. However, more recent studies have found the diagnostic sensitivity of this parameter to be less useful. In this study, the MAP distal latency recorded from the abductor hallucis was prolonged in only 21.5% of TTS patients. Despite the low diagnostic sensitivity of posterior tibial motor conduction in TTS, Felsenthal et al. proposed a modified motor nerve conduction technique to identify nerve compression within or distal to the tarsal tunnel. This new method shows promise but requires further validation.

The differences between our findings and previous reports regarding MAP distal latency sensitivity may be due to the earlier clinical diagnosis of TTS in recent years, often when sensory symptoms predominate, as sensory fibers are thought to be more susceptible to compression. This is why sensory conduction studies of the plantar nerves are considered crucial for diagnosing TTS.

Sensory conduction studies are indeed highly sensitive in TTS diagnosis. Consistent with prior reports, we found SAP abnormalities in all affected limbs. However, SAP studies have limitations: (1) SAP recording is time-consuming and uncomfortable for patients; (2) SAPs may be absent in a small percentage of normal individuals. Guiloff and Sherratt reported absent MPN SAP in approximately 4% of normal patients, attributed to subclinical neuropathy. We observed absent plantar nerve SAPs in 8% of normal subjects, not limited to the elderly and always with normal sural and deep peroneal nerve conduction. Thus, while SAP abnormalities are highly sensitive, they lack specificity and must be interpreted with caution.

To address the limitations of MAP and SAP studies (low sensitivity and poor specificity, respectively), Saeed and Gatens developed a technique for evaluating a more proximal segment of the plantar nerves across the tarsal tunnel by measuring orthodromic mixed nerve action potentials, similar to midpalm stimulation of the median nerve in carpal tunnel syndrome diagnosis. NAPs resemble pure sensory potentials and likely reflect predominantly sensory fibers, but they are significantly larger than SAPs and do not require signal averaging. In this study, NAPs were easily recorded in all normal subjects, with mean amplitudes approximately five times greater than SAPs (10.9 μV vs. 2.0 μV). We did not encounter the technical challenges reported by others, such as difficulty obtaining mixed nerve potentials due to edema, adipose tissue, calluses, or discomfort from stimulation.

We found abnormal plantar nerve NAPs in 85.7% of limbs with Tarsal Tunnel Syndrome (TTS) but in no asymptomatic limbs, neither in patients nor controls. Absence or low amplitude mixed nerve potentials, likely indicating significant axonal loss due to focal damage of the plantar nerves at the tarsal tunnel, were the most common abnormalities. The lateral plantar nerve was more frequently abnormal than the medial one, indicating it may be more sensitive to early pathologic changes. However, evaluating both nerves is recommended for better diagnostic sensitivity.

Previous studies have also reported absent mixed nerve potentials in TTS, but these were mainly case reports. This study is the first to evaluate mixed nerve conduction of the plantar nerves in a TTS patient population and to confirm its good diagnostic validity as both a sensitive and specific test.

Our findings demonstrate the utility of sensory and mixed nerve potential studies in TTS diagnosis. Sensory nerve studies were the most sensitive, with abnormal results in all limbs with clinical TTS. However, the relatively high percentage of false positives limits the specificity of this method. It is important to remember that a plantar SAP abnormality may be the earliest sign of distal peripheral neuropathy. In cases of unilateral clinical TTS with bilateral absence of plantar nerve SAPs, a symmetrical neuropathy should be ruled out first. TTS is almost always unilateral or predominantly unilateral, so significant amplitude asymmetry of mixed nerve potentials strongly suggests TTS over symmetric neuropathy.

Due to their relatively large amplitude, NAPs, unlike SAPs, can be used to assess bilateral differences, playing a crucial role in TTS diagnosis. Additionally, in our experience, plantar NAP abnormalities in distal symmetric polyneuropathy usually coexist with sural SAP abnormalities, although none of our TTS patients showed sural nerve abnormalities.

In conclusion, our data suggest that assessing plantar nerve conduction via SAP and NAP studies is helpful for diagnosing TTS in nearly every case. NAP studies yielded abnormal results in approximately 85% of TTS patients. For patients with suspected TTS who have normal plantar NAP and abnormal plantar SAP, caution is advised before recommending surgery. Coexistence of NAP and SAP abnormalities, especially if asymmetric, are highly sensitive and specific electrophysiologic indicators of TTS.

Acknowledgments

We are grateful to Dr. Francesco Riti and Professor Gigino Di Lascio for their contributions to the revision of this manuscript.