A 305-pound, 35-year-old white man presented to our clinic with a diree-month history of severe pain below the right medial malleolus, radiating distally along die course of the medial plantar nerve, as well as proximally along the medial calf for several centimeters. The symptoms were insidious in onset and unrelated to any traumatic event. He has a history of Dercum's disease (adiposis dolorosa), and two mondis previously bad undergone a surgical exploration in another city with a preoperative diagnosis of a painful lipoma in the right foot. The postoperative diagnosis was normal abductor hallucis muscle; his symptoms remained unchanged. Physical examination of the right foot revealed no abnormal masses or deformity. He had generalized tenderness to palpation distal to the medial malleolus, a positive Tinel's sign at die laciniate ligament, and a decreased pinprick sensation and two point discrimination in the distribution of die medial plantar nerve. There was no evidence of vascular compromise and no change in symptomatology with ankle, subtalar or midfoot range of motion. Plain roentgenograms revealed no bony abnormality. Electromyographic findings were as follows:
Previous treatment consisted of four weeks of ambulation in a wide, cushion soled shoe, then four weeks of non-weightbearing on the right foot with crutches. The symptoms remained unchanged. Three montiis after die onset of symptoms we performed a surgical decompression of the tibial nerve within die tarsal tunnel. The inferior edge of die laciniate ligament was noted to create a stenotic area within die tarsal tunnel. The patient initially had complete relief of his symptoms postoperatively. He was allowed to ambulate on die second postoperative day and developed considerable edema at die medial ankle. At die same time he developed parestiiesias in die distribution of the lateral plantar nerve. With continued elevation these symptoms abated, but die patient required tiiree months to become free of his remaining local wound tenderness.
This patient demonstrates a typical presentation of tarsal tunnel syndrome: a symptomatic pressure neuropadiy of the posterior tibial nerve in die flexor retinaculum region of the ankle. The electromyographic findings are characteristic, as is die poor response to initial nonoperative treatment.
Tarsal tunnel syndrome was first described by Kopel and Thompson in I960.1 A review of the literature reveals 193 reported cases, but its prevalence is felt to be much more extensive titan this.
The posterior tibial nerve (L4-S3) divides into a calcaneal sensory branch, which penetrates die proximal portion of die laciniate ligament (flexor retinaculum) to supply die medial and plantar surfaces of die heel.2 The laciniate ligament arises from the inferior surface of the medial malleolus and inserts into the periosteum of the calcaneus. The remainder of the posterior tibial nerve courses beneath this ligament in a fibrous compartment between the flexor digitorum longus and the flexor hallucis longus tendon sheaths. The posterior tibial nerve divides into medial and lateral plantar nerves (mixed motor and sensory) roughly at the level of the laciniate ligament. The lateral plantar nerve enters the foot more proximally than the medial branch.3 Both branches enter deep to the fibrous origin of the abductor hallucis muscle.
MOTOR INNERVATION OF INTRINSIC FOOT MUSCULATURE
CHARACTERISTIC ELECTRODIAGNOSTIC FINDINGS
Any process that compromises the caliber of the tarsal tunnel, either intrinsic or extrinsic, can cause a pressure neuropathy of the tibial nerve. Factors that have been described include a hypertrophic laciniate ligament, hypertrophic abductor hallucis muscle or fascia, pronated forefoot with either a valgus2 or varus4 heel, bony deformity after fracture, edematous changes associated with flexor tenosynovitis, ganglion cysts, flexor tendori cysts, perineural fibrosis, neurilemmoma, varicies and thrombi of the posterior tibial vein, and unaccommodated fat within the tarsal tunnel.4 Damage to the nerve can occur via two mechanisms. Vascular embarrassment via pressure on the vasa nervosum gives initial symptoms of sensory loss without motor loss, which often respond immediately to decompression.5 Direct pressure neuropathy will often present with both sensory and motor loss. Denny-Brown and Brenner6 have classified the histologic changes seen in pressure neuropathy as follows:
Stage 1: local edema, cellular infiltration, myelin vacuoles
Stage 2: moderate axonal degeneration
Stage 3: Wallerian degeneration
The symptoms depend upon the level of stenosis (thereby affecting different branches of the nerve), the duration and extent of pressure, and which components of the individual branches are damaged. This latter factor accounts for the variations in degree of sensory, motor, and vasomotor symptoms seen in different cases.2 The most frequently found symptoms include tingling, burning, sharp pain, hyperesthesia or hypoesthesia, intrinsic muscle weakness, and vasomotor changes. These symptoms should parallel the distribution of the specific nerve branches rather than that of the lumbar and sacral dermatomes. The syndrome is rarely bilateral.7 A Valleix phenomenon is often seen. This is radiation of pain proximal to the site of stenosis via proximal excitation of autonomic fibers.2,8,9
A positive TinePs sign is often present initially at the level of stenosis, or it will appear within three to four weeks after decompression.6 A palpable mass is sometimes noted within the tarsal tunnel. Often there is tenderness to palpation along the tibial nerve and its branches. Vasomotor changes and motor weakness are often subtle and difficult to elicit.2 A tourniquet applied to the calf will increase the venous engorgement within the tarsal tunnel and sometimes reproduce the neurological symptoms by this transient increase in intrinsic tunnel stenosis.5
Electromyograms and nerve conduction studies may be used to confirm the clinical impression. In tarsal tunnel syndrome the most consistent finding is a decreased amplitude and an increased duration of evoked potentials in the abductor hallucis or the abductor digiti minimi when compared with the normal foot. One usually also sees an increased latency to these same muscles.7 Some authors feel that sensory nerve conduction velocities are more reliable than the motor tests.10,11
The more common conditions that must be included in the differential diagnosis include a flexor tenosynovitis, longitudinal arch strain, arthritic tarsal joints, lumbosacral root irritation with radicular symptoms, hypoperfusion vascular symptoms, reflex sympathetic dystrophy, interdigital neuroma, plantar fasciitis or fibromatosis, and systemic peripheral neuropathy.
There is a consensus among authors on the treatment of tarsal tunnel syndrome. This is a condition that is consistently relieved only by surgical decompression. Steroid injections and shoe modifications have been consistently ineffective.1'4,7 Cast immobilization for one to two months has been beneficial only in rare instances. The surgical approach has been well described.2,5,7 It is important to resect the laciniate ligament and decompress all three branches of the nerve along meir entire course within the tunnel.7 Most series show 80% to 90% excellent results with surgical decompression.4 Interestingly, most patients with successful surgical decompression had no intraoperative patiiology demonstrable.5
The tarsal tunnel syndrome is a relatively rare but often misdiagnosed syndrome. Symptoms of pain, paresthesias, motor and vasomotor changes may present in any or all of the branches of die posterior tibial nerve at the ankle. The pressure neuropathy may be caused by a wide variety of abnormalities. Clinical examination augmented with electrodiagnostic testing is the mainstay of diagnosis. Good results can be expected only with surgical decompression, which gives an 80% to 90% cure rate.
1. Koppelt HP, Thompson WAL: Peripheral entrapment neuropathies of the lower extremity. N Engl J Med I960; 262:56.
2. Edwards WG, Lincoln CR. Bassett FH. et al: The tarsal tunnel syndrome: Diagnosis and treatment. JAMA 1969; 207:716.
3. Goodgold J. Koppeil HP. Spielholz Nl: The tarsal tunnel syndrome: Objective diagnostic criteria. N Engl J Med 1965: 273:742.
4. Radin EL: Tarsal tunnel syndrome. Clin Orthop 1983; 181:167-170.
5. Lam SJS: Tarsal tunnel syndrome. J Bone Joint Surg 1967; 49B:87.
6. Denny-Brown. Brenner C: Paralysis of nerve induced by direct pressure and by tourniquet. Arch Neurol Psychiat 1944; 51:1-26.
7. Kaplan PE, Kernahan WT: Tarsal tunnel syndrome, an electrodiagnostic and surgical correlation. J Bone Joint Surg 1981: 63A:96-99.
8. Keck C: The tarsal-tunnel syndrome. J Bone Joint Surg 1962: 44 A: 180.
9. Wileman WK: Tarsal runnel syndrome. A fifty year survey of the world literature and a report of two new cases. Orthop Rev Nov 1979; 8:111-117.
10. GuilofT RJ. Sherratt RM: Sensory conduction in medial plantar nerves: Normal values, clinical applications and a comparison of the dural and upper limb sensory nerve action potentials in peripheral neuropathy. J Neurol Neurosurg Psychiat 1977: 40:1168-1181.
11. Oh SJ. Sarala PK. Kuba T, et al: Sensory nerve conduction velocity of the plantar nerves: A superior objective diagnostic test for tarsal tunnel syndroroe. Trans Am Neurol Assoc 1979; 103:256.
12. Gray H: Anatomv of the Human Body. Philadelphia. Lea and Febtger. 1975. pp 997-999.
13. Johnson EW, Oritz PR: Electrodiagnosis of tarsal tunnel syndrome. Arch Phys Med Rehab 1966; 47:776-780.
14. Mann RA: Tarsal tunnel syndrome. Orthop Clin North Am 1974; 5:109.
MOTOR INNERVATION OF INTRINSIC FOOT MUSCULATURE
CHARACTERISTIC ELECTRODIAGNOSTIC FINDINGS