Tarsal Tunnel Syndrome

Michael S. Downey

Daniel J. Yarmel

The first report of compression of the posterior tibial nerve under the flexor retinaculum was provided by Kopell and Thompson (1) in 1960. In 1962, Keck and Lam independently introduced the term tarsal tunnel syndrome to describe the condition created by compression of the tibial nerve within the fibroosseous tunnel posterior to the medial malleolus (2,3). Tarsal tunnel syndrome is an entrapment neuropathy of the posterior tibial nerve or one of its branches (4). Clinical manifestations typically include burning, aching, radiating, sharp, electric-type pain along the distribution of the involved nerves (2,4,5 and 6). Several causes are possible, and this may complicate the diagnosis (7). Although objective tests, such as electrodiagnostic studies, quantitative sensory testing (QST), musculoskeletal ultrasound, and magnetic resonance imaging (MRI) provide helpful information, they do not replace the history and clinical examination in making the diagnosis (8). Treatment options range from conservative to surgical and depend on the origin, severity, and duration of the nerve entrapment (9).

ETIOLOGY

The most common origin of tarsal tunnel syndrome is idiopathic, occurring in 21% to 36% of cases (10). In approximately 60% to 80% of cases, a specific cause of tarsal tunnel syndrome can be identified (11,12,13 and 14). When the etiology is known, trauma accounts for the majority of cases and ranges in incidence from 17% (14) to 87.5% (15). In their 87 cases, Grumbine and associates found a traumatic source in 34.5% of their patients, followed by systemic disease (33.3%), biomechanical origins (17.2%), and idiopathic causes (14.9%) (16). In another review of 186 cases, female patients were found to have a higher predilection (56%), and the average patient age was 47 years. The most common etiologies included trauma (17%), varicosities (13%), heel varus (11%), fibrosis (9%), and heel valgus (8%) (10).

The posterior tibial nerve is particularly vulnerable to compression after traumatic injuries of the hindfoot and ankle (17). Myerson and Berger (18) reported a case of a fractured sustentaculum tali fragment that migrated into the tarsal tunnel and created compression. Similarly, a fractured medial tubercle of the posterior process of the talus has been shown to compress the tibial nerve (19). In one larger series, distal tibia and ankle trauma accounted for 49 of 56 cases of tarsal tunnel syndrome (15). Traumatic soft tissue lacerations and injuries have also been reported as a source of tarsal tunnel syndrome, including an acute case of tarsal tunnel syndrome resulting from a partial avulsion of the flexor hallucis longus muscle (20). Sports-related injuries have also been a documented etiology (21,22 and 23). Kinoshita et al (23) reported over a 16-year period that 39.1% of tarsal tunnel-related surgeries resulted from repetitive strenuous sporting activities. Oh and Meyer (24) found that 13% of traumatic injuries were associated with jogging and aerobic exercise.

In addition to trauma, space-occupying lesions also cause compression on the tibial nerve (25). The most common spaceoccupying lesions contributing to tarsal tunnel syndrome are varicosities (26,27). Other lesions include ganglia (26,28,29,30,31,32 and 33), lipomas (34,35), neurilemomas (36,37,38,39,40,41,42,43 and 44), an amyloidoma (45), thickened flexor retinacula (10), a pulsating artery (46), and an angioleiomyoma (47). Accessory muscles are another common cause of tarsal tunnel syndrome and can often be difficult to discern on MRI (38,48,49,50,51,52 and 53). Although most lesions are benign, cases of synovial sarcomas causing tarsal tunnel syndrome have been documented (54,55). Proliferative synovitis secondary to inflammatory arthropathies, soft tissue or osseous infection, and metabolic disorders can cause compression in the tarsal tunnel and needs to be excluded (56,57). Finally, bony abnormalities such as tarsal coalition (30,31,33,58,59) a malunited calcaneal fracture (60), talar exostoses (61,62), and even a residual osteophyte after ankle implant arthroplasty (63) have been described as causative factors in tarsal tunnel syndrome.

Tarsal tunnel syndrome has been found to be associated with systemic disease (64). Park and Del Toro (65), in a study of 49 patients, found that 34.4% of the patients had systemic disease, most commonly diabetes and inflammatory arthritis. Oloff et al (64) reported similar results in an analysis of 73 cases. Systemic diseases were encountered in 34.7% of patients, with diabetes (20.4%) and inflammatory arthritis (12.2%) comprising the majority. Rheumatoid arthritis (66), hypothyroidism (67), seronegative arthropathies (68,69), and hyperlipidemia (70) have also been linked to tarsal tunnel syndrome (Table 67.1).

Foot deformities have also been correlated with tarsal tunnel syndrome. Radin (14) found that two-thirds of patients had varus deformity of the heel with a pronated forefoot. He believed that compensatory pronation contracted the abductor hallucis and compressed the distal tarsal tunnel. Pes planovalgus deformity can contribute to tarsal tunnel syndrome by increasing tension on the posterior tibial nerve. Daniels et al (71), in a cadaver study, demonstrated that surgically created pes valgus feet increased posterior tibial nerve tension through ankle joint dorsiflexion, hindfoot eversion, and combined ankle joint dorsiflexion and hindfoot eversion. In a follow-up laboratory study, surgical reconstruction of pes valgus deformity decreased tension on the posterior tibial nerve (72). Although these investigators did not advocate surgery, they did recommend the use of an ankle-foot orthosis to control the pes valgus deformity. The stress of prolonged stretch or tension on a nerve has been shown to have physical consequences. Lundborg and Rydevik (73) found that elongation of a nerve by 15% resulted in complete intraneural vascular occlusion. Other authors recommend prophylactic tarsal tunnel decompression for correction of large deformities, when limb lengthening and significant hindfoot osteotomies are planned (74).

TABLE 67.1 Etiologies of Tarsal Tunnel Syndrome

Endogenous				Exogenous			Iatrogenic
I.	Congenital			I.	Traumatic		A.	Tourniquet compression
	A.	Anomalous development			A.	Laceration	B.	Surgical positioning
		1.	Accessory muscle		B.	Blunt trauma	C.	Cast or bandage constriction
		2.	Tarsal coalition		C.	Fractures/dislocation	D.	Surgical technique planning
	B.	Overuse						1.	Improper incision
	C.	Overpronation (pes planus)						2.	Poor dissection
	D.	Traction						3.	Inadequate hemostasis
II.	Neoplastic/space-occupying lesions							4.	Nerve handling
	A.	Varicosities						5.	Suturing
	B.	Ganglion cyst					E.	Injection
	C.	Lipoma						1.	Puncture
	D.	Neurilemmoma (schwannoma)						2.	Chemical
	E.	Metastatic infiltration
	F.	Synovial sarcoma
III.	Metabolic
	A.	Diabetes mellitus
	B.	Rheumatoid arthritis/connective tissue disease
	C.	Peripheral vascular disease
	D.	Thyroid dysfunction
	E.	Hyperlipidemia
	F.	Drug toxicity
	G.	Seronegative arthropathy
Adapted from Chang TJ. Master techniques in podiatric surgery: the foot and ankle. Philadelphia, PA: Lippincott Williams & Wilkins, 2005.

In addition to tension, foot position can cause increased pressure within the tarsal tunnel. Trepman et al (75) measured tarsal tunnel pressures of cadaver specimens in neutral and maximum inversion and eversion. These investigators found a significant increase in pressure with maximum inversion and eversion compared with neutral. Also, Bracilovic et al (76), using MRIs to calculate tarsal tunnel volume, showed that volumes were significantly greater in the neutral position than inverted or everted positions and advocated neutral immobilization as a treatment modality. Hence, foot deformity may be a contributing factor in the pathogenesis of tarsal tunnel syndrome.

EVALUATION, DIAGNOSIS, AND FUNCTIONAL ANATOMY

CLINICAL PRESENTATION

The symptoms of tarsal tunnel syndrome can often be extensive with variable physical findings (11). The history and physical examination can be essential to making the diagnosis. Patients with tarsal tunnel syndrome may relate a history of previous trauma that precipitated the pain. Most frequently, symptoms are unilateral with an insidious onset, but they have been found to occur bilaterally (77). Common clinical features seen in the majority of patients include burning, tingling, and numbness over the distribution of the involved nerve or nerves (13,14 and 15,78,79). With plantar nerve involvement, symptoms are localized to the toes and distal sole of the foot. When the medial calcaneal branch is involved, symptoms are localized to the heel (24).

Classically, these symptoms are aggravated by multiple activities such as prolonged standing or walking and are relieved by rest, elevation, and removal of shoes (8,80). Nocturnal aggravation of symptoms is a common finding. Mosimann (15) found that 42% of patients had nocturnal paresthesias. When advanced, these paresthesias may radiate proximally to the calf and leg (i.e., Valleix phenomenon) (2,14,78).

Positive Tinel sign and sensory impairment of the involved plantar nerves are two of the most common findings in tarsal tunnel syndrome (24). Tinel sign is elicited by percussion of the tibial nerve over the tarsal tunnel. When the sign is positive, an electrical sensation or tingling sensation radiates distally into the sole of the foot or digits (81). A positive sign is present in 50% to 90% of cases (79,82). Sensory impairment has been reported in more than two of three patients and is most simply evaluated by pinprick and two-point discrimination (79). The “dorsiflexion-eversion test,” a diagnostic tool for tarsal tunnel syndrome, has been discussed in the literature since 1964 and has more recently evolved to include maximal dorsiflexion of the digits at the metatarsophalangeal joints in an effort to apply both tension and compression to the tibial nerve (83,84 and 85).

Tenderness with direct palpation over the tarsal tunnel is another common clinical finding (9). Motor symptoms, such as weakness or muscle atrophy, are relatively rare and present only in advanced cases. Oh and Meyer (24) found weakness of toe flexion the only reliable motor function test, a finding present in 19% of their cases.

DIAGNOSIS

Critical for making the diagnosis of tarsal tunnel syndrome is an accurate history and physical examination with neurologic evaluation. As already described, the two most helpful tests are positive Tinel sign and sensory loss in the distribution of the involved branches. Despite these tests, tarsal tunnel syndrome can be a challenging diagnosis (86).

Oh and Meyer (24) pointed out that two neurologic conditions that can be confused with tarsal tunnel syndrome are L5 or S1 radiculopathy and sensory polyneuropathy. Clinical and objective findings help to distinguish among these conditions. Objective findings favoring radiculopathy include a positive straight leg raise test, calf muscle atrophy, radiating pain to the lower back, sensory abnormalities on the dorsum of the foot, and absent or negative Tinel sign. Clinical signs suggestive of polyneuropathy consist of a bilateral presentation, a stocking-glove distribution of sensory loss, and absent or negative Tinel sign. Painful conditions in the heel, medial ankle, or low back regions should be included in the differential diagnosis of tarsal tunnel syndrome (Table 67.2) (86,87 and 88). It is important to rule out more proximal sites of nerve entrapment because tarsal tunnel syndrome has been reported to occur with additional nerve lesions in the same limb (89).

The history and physical examination serve as guides for other tests to narrow the differential diagnosis further. For example, radiographs may be used to determine foot deformity, fracture, or accessory ossicles. Injections of local anesthetic or corticosteroid can aid in the diagnosis and can provide temporary relief. Laboratory studies may be indicated to rule out metabolic disorders such as hypothyroidism, rheumatoid arthritis, or diabetes mellitus. Perthes tourniquet test may be of value if varicosities are the suspected cause (38). This test consists of inflating a cuff around the lower calf of the affected side to 30 to 50 mm Hg, which causes occlusion of the superficial venous system but not the deep venous system or arterial system. If the deep venous system of the tarsal tunnel is incompetent (e.g., valvular damage or insufficiency), the posterior tibial venae comitantes in the tarsal tunnel will engorge and will reproduce the symptoms.

MAGNETIC RESONANCE IMAGING

MRI has been a valuable tool in the diagnosis of tarsal tunnel syndrome primarily because of its ability to demonstrate space-occupying soft tissue lesions (Fig. 67.1) (56,90,91). Recht and Donley proposed using transaxial imaging since it provides excellent visualization of the tarsal tunnel and associated structures (92). Erickson et al (56), using MRI, were able to identify neurilemomas, tenosynovitis, ganglion cysts, posttraumatic fibrosis, and posttraumatic neuromas causing tarsal tunnel syndrome. Kerr and Frey (93) found lesions in 82% of their cases, with the most common causes being a focal mass lesion and varicose veins. Another study by the same authors used MRI to study 40 symptomatic feet (94). Electrodiagnostic studies confirmed the diagnosis in 20 feet. Seventeen of these 20 (85%) had positive MRI findings, with the most common being flexor hallucis tenosynovitis. Surgery was required in 21 feet and confirmed MRI findings in 19 of the 21. MRI may also be helpful in patients in whom revisional surgery is considered because it has been able to show incomplete release of the flexor retinaculum (91). Downey also described the combined use of the Perthes test and MRI to confirm venous insufficiency of the venae comitantes as a cause of tarsal tunnel syndrome (90) (Fig. 67.2).

TABLE 67.2 Differential Diagnosis of Tarsal Tunnel Syndrome

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