- Email: [email protected]
Posterior tibial nerve—primary
Foot Ankle Clin N Am 9 (2004) 271 – 285
Posterior tibial nerve—primary Johnny T.C. Lau, MD, MSc, FRCSCa,b,*, Peter Stavrou, MBBS, FRACSb,c a
Department of Surgery, University of Toronto, University Health Network, Toronto Western Division, Division of Orthopaedic Surgery, 339 Bathurst Street, ECW-1-038, Toronto, Ontario M5T 2S8, Canada b Toronto Western Hospital, University Health Network, University of Toronto, Toronto, Ontario, Canada c Wakefield Orthopaedic Clinic, 270 Wakefield Street, Adelaide, South Australia 5000, Australia
Tarsal tunnel is an uncommon disorder of the foot [1,2] that presents as a burning or tingling pain that is located diffusely on the plantar aspect of the foot. These symptoms were described in 1960 by Kopell and Thompson [3]. The use of the term ‘‘tarsal tunnel syndrome’’ to describe these symptoms first appeared in the literature in 1962 when it was used by Keck [4] and Lam [5] independently. Many investigators have considered tarsal tunnel syndrome to be analogous to carpal tunnel syndrome [3 –10]. As more becomes known about tarsal tunnel syndrome, it is evident that this is not purely an entrapment neuropathy. It differs from carpal tunnel syndrome in anatomy, etiology, clinical presentation, and response to nonoperative and operative treatment.
Anatomy The anatomy of the tarsal tunnel is the key to understanding its clinical presentation because herein the tibial nerve or its branches are affected. The tarsal tunnel consists of proximal and distal tarsal tunnels [11]. The proximal tarsal tunnel contains the tibial nerve and the distal tarsal tunnel contains the branches of the tibial nerve: the medial calcaneal nerve, medial plantar nerve, and lateral plantar nerve (Fig. 1) [11]. Although tarsal tunnel syndrome classically refers to
* Corresponding author. Department of Surgery, University of Toronto, University Health Network, Toronto Western Division, Division of Orthopaedic Surgery, 339 Bathurst Street, ECW-1-038, Toronto, Ontario, M5T 2S8, Canada. E-mail address: [email protected] (J.T.C. Lau). 1083-7515/04/$ – see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.fcl.2003.12.002
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Fig. 1. Anatomy of the tarsal tunnel.
the proximal tarsal tunnel, failure to take the existence of the distal tarsal tunnel into account has led to poor results with therapy [8,11 –13]. The tarsal tunnel is the continuation of the deep posterior compartment of the leg that leads to the plantar aspect of the foot [14]. The proximal tarsal tunnel is a fibro-osseous structure that is located behind the medial malleolus. The osseous floor is formed by the medial surface of the talus, sustentaculum tali, and medial wall of the calcaneus. The fibrous roof is the flexor retinaculum, also known as the laciniate ligament. The flexor retinaculum is the continuation of the superficial and deep aponeurosis of the leg on its posterior border; its anterior border is continuous with the dorsal aponeurosis of the foot. The base of the flexor retinaculum corresponds to the superior border of the abductor hallucis muscle and divides into superficial and deep fascia around this muscle [15]. The continuation of the flexor retinaculum proximally and distally with these aponeurotic structures makes it difficult to define its borders accurately [1]. The retinaculum may extend up to 10 cm proximal to the medial malleolus; failure to recognize this may lead to a failure of surgical decompression [16]. Dellon and Mackinnon [17] defined the flexor retinaculum as being 2 cm either side of the malleolar-calcaneal axis—a reference line drawn from the center of the me-
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dial malleolus to the center of the calcaneus. Hence, the flexor retinaculum extends from its origin at the medial malleolus in an inferior and posterior direction roughly to the calcaneal tuberosity. The contents of the proximal tarsal tunnel are, from anterior to posterior, tibialis posterior tendon, flexor digitorum longus tendon, posterior tibial artery, tibial nerve, and the flexor hallucis longus tendon. Each tendon has its own synovial sheath and lies in a separate fibro-osseous compartment that is formed from projections between the underside of the flexor retinaculum and the periosteum of the calcaneus [6,18,19]. The neurovascular bundle lies in its own fibroosseous compartment and is attached to the fibrous septae by a surrounding layer of dense areolar tissue [19]. Thus, the tibial nerve is in a fixed position in a fibroosseous tunnel and is susceptible to compression by a lesion within or outside this tunnel as well as tension forces. Branching of the nerves is variable; usually three nerves arise from the tibial nerve: the medial calcaneal nerve(s), the medial plantar nerve, and the lateral plantar nerve. The medial calcaneal nerve provides sensation for the medial and plantar aspects of the hindfoot after exiting the tarsal tunnel—either through or distal to—the flexor retinaculum. Usually, the medial calcaneal nerve arises from the tibial nerve itself (69% –90%); less frequently it arises from the lateral plantar nerve [1,8,17]. Nine different branching patterns were described for the medial calcaneal nerve [1]. A single branch was seen in 79% of feet; multiple branches were seen in 21%. The most common pattern is for the medial calcaneal nerve to arise from the tibial nerve as a single branch; failure to account for anatomical variants may result in paresthesia or painful neuromas after damage to nerve branches during surgery [20,21]. The tibial nerve ends by bifurcating into the medial and lateral plantar nerves. In a cadaver study, this bifurcation usually occurred within the confines of the tarsal tunnel (93% –96%). In the remaining 4% to 7% of feet, the bifurcation occurred proximal to the tarsal tunnel in the lower leg [1,17,22]. A high bifurcation of the tibial nerve is believed to be a predisposing factor in tarsal tunnel syndrome by ‘‘presenting a larger cross-sectional area at the narrowed entrance to the tarsal tunnel’’ [17]. Havel [1] considered that the low incidence of the tibial nerve bifurcation proximal to the tarsal tunnel accounted for the low incidence of tarsal tunnel syndrome. The distal tunnel contains the medial and lateral plantar nerves that pass through fibrous openings in the origin of the abductor hallucis [11]. These are separate fibrous tunnels that are divided by a partition that originates from the medial side of the calcaneus and attached to the deep fascia of abductor hallucis. The medial plantar nerve is the larger of the terminal branches of the tibial nerve and passes between the plantar calcaneonavicular ligament and the abductor hallucis muscle. The medial plantar nerve is analogous to the median nerve in the hand; it supplies sensation to the medial three and half toes and the sole of the foot. The lateral plantar nerve, after passing through the origin of the abductor hallucis, provides sensation to the lateral one and half toes of the foot and is analogous to the ulnar nerve in the hand.
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Etiology The true incidence of tarsal tunnel syndrome is unknown [23]. A specific etiology can be found in 60% to 80% of patients; thus, in a significant number of patients no specific cause can be found [2,6– 9,16,24 – 28]. Although many investigators consider tarsal tunnel syndrome as purely an entrapment neuropathy, other factors have been investigated [3,8,12,29]. In a review of the literature, Cimino [16] examined 25 studies and case reports of tarsal tunnel syndromes that involved 164 subjects and 186 tarsal tunnel syndromes. Patients ranged in age from 14 to 80 years old. Women were more likely to be involved (56%). Of the causes identified, the most frequent were; trauma (17%), varicosities (13%), heel varus (11%), fibrosis (9%) and heel valgus (8%). In broad terms, the causes can be classified into three groups: (1) trauma, (2) space-occupying lesion, and (3) foot deformity. Trauma Trauma was the most common cause in Cimino’s [16] review of the literature. Fractures in the bones that surround the tarsal tunnel—distal tibia, talus, calcaneus, and tarsal bones—especially if displaced, can precipitate tarsal tunnel syndrome. Soft tissue trauma in the same region (eg, sprains of the deltoid ligament) may produce the same effect [6,9,30 – 32]. Traumatic synovitis of the tendons in the tarsal tunnel also may compress the tibial nerve and produce tarsal tunnel syndrome [3,12,16,30,33,34]. Space-occupying lesions Space-occupying lesions can compress the tibial nerve from within or from outside its compartment in the tarsal tunnel. The most common space-occupying lesions are varicosities [6,35,36]. Other lesions that were reported in the literature include ganglia [9,37 – 40], perineural fibrosis [9], lipoma [41], neurilemoma [9,18,40,42,43], bony exostosis [16], hypertrophic sustentaculum tali [44], medial talocalcaneal bar [8,28,45], hypertrophic flexor retinaculum [16], hypertrophic or accessory abductor hallucis muscle [6,19], flexor digitorum accessorius longus muscle [46 – 48], accessory soleus muscle [48], partial rupture of the flexor hallucis longus tendon [49], rapid weight gain [6,16], fluid retention [16], and chronic phlebitis [16]. Inflammatory disorders, such as rheumatoid arthritis [24,26,50 – 53], ankylosing spondylitis [54 – 56], and synovial osteochondromatosis [57], can produce a proliferative synovitis that exerts a mass effect in the tarsal tunnel. Recently, a case was documented that had an inflatable ice hockey boot as the cause of tarsal tunnel syndrome [58]. Foot deformities Foot deformities accounted for 19% of tarsal tunnel syndromes in Cimino’s review of the literature [16]. Varus heels accounted for 11% of these and valgus
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heels accounted for 8%. In varus heel deformity, Radin [59] stated that two thirds of patients who had tarsal tunnel syndrome had concurrent varus heel and pronated forefoot. The forefoot pronation compensated for the varus hindfoot and allowed the forefoot to make contact with the ground. The varus heel deformity also shortens the abductor hallucis muscle which gives it the appearance of being hypertrophied and decreases the cross-sectional area of the tarsal tunnel. Forefoot pronation stretches the tibial nerve. Thus, the nerve is compressed within the tibial tunnel and under tension which precipitates tarsal tunnel syndrome. Conversely, hindfoot valgus and forefoot abduction also can cause tarsal tunnel syndrome by putting the tibial nerve under tension [3– 5,8,12,25,29,33,38, 52,60]. Francis et al [12] reported on 11 patients who had pes planus and tarsal tunnel syndrome; of these, 8 had mobile deformities. Six patients underwent surgical release; none had an identifiable lesion. Most patients described paresthesias ‘‘like an electric shock with each step taken.’’ The investigators believed that mobile pes planus with associated hindfoot valgus put the tibial nerve or its branches under tension on weight bearing which makes the nerve vulnerable to neurapraxia. Any trivial trauma could initiate tarsal tunnel syndrome and the symptoms could be aggravated with weight bearing. Dynamic foot deformities that led to tarsal tunnel syndrome also have been documented in the literature [16,30,33,61]. Rask [61] reported on ‘‘jogger’s foot,’’ a condition that is produced by hindfoot valgus in running that stretches the medial plantar nerve against the tarsal navicular bone. Running with excessive pronation is believed to stretch the tibial nerve and predispose it to injury. Occupations that are associated with repeated dorsiflexion, such as crouching, and squatting, were reported to be associated with tarsal tunnel syndrome [16,50,62]. More recently, a combination of pathologies was reported by Labib et al [63]. They reported on a group of patients who had tarsal tunnel syndrome, plantar fasciitis, and posterior tibial tendon dysfunction; they labeled this the ‘‘heel pain triad’’. The loss of static (plantar fascia) and dynamic (posterior tibial tendon) supports for the longitudinal arch was believed to lead to traction injury of the tibial nerve and tarsal tunnel syndrome. Of their 14 patients, 87% reported significant improvement after surgery.
Pathophysiology of neuropathy Tarsal tunnel syndrome is produced by damage to the tibial nerve as a result of compression [3,19,30,64] or tension [3,8,12,29,33]. Compression is recognized as the most common cause of tarsal tunnel syndrome. Nerve compression In their classic paper, Kopell and Thompson [3] defined an entrapment point as a location ‘‘where the anatomic configuration may cause constriction of the nerve, or, if trauma has occurred to the area, the particular anatomic disposition
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will maintain the nerve in a state of inflammation.’’ Entrapment occurs because the structure of the fibro-osseous tarsal tunnel is made of strong and unyielding tissues compared with the nerve and ‘‘there is little latitude for dimensional alteration in the cross-sectional area permitted for the passage of the nerve.’’ The nerve is injured directly by neural compression or indirectly by causing local vascular insufficiency [19]. In tarsal tunnel syndrome, the initial sensory dysfunction is believed to be due to nerve ischemia that is caused secondary to local compression, whereas the later motor dysfunction is due to direct neural compression and structural alteration [19,30]. Tibial nerve entrapment in the tarsal tunnel is most common at the anterior, inferior aspect of the canal [3,12,25,65]; the lateral plantar nerve is affected more often than the medial plantar nerve [7,12,18,23]. The lateral plantar nerve passes through a fibrous opening in the abductor hallucis muscle, separately and more proximal than, the medial plantar nerve [6], which makes it more vulnerable [7]. Nerve tension In a pes planus foot, the heel valgus and abducted forefoot place the tibial nerve under tension [3– 5,8,12,25,29,33,38,52,60]. The tibial nerve can be damaged by an acute or chronic stretch [34,66,67]; the severity of the injury is dependent on the magnitude of the force and the rate of deformation [67]. Over time, chronically injured nerves become stiffer because of fibrosis within the epineurium [68] and are unable to compensate for tension as easily as normal nerves; this makes them more susceptible to ischemia and injury.
Clinical presentation The diagnosis of tarsal tunnel syndrome is difficult and often is undiagnosed or misdiagnosed [1,4,8,16,18,19,23,25,30,38,65]. The symptoms can be diffuse and poorly localized [18,25].
History Tarsal tunnel usually presents with an insidious onset of pain or paresthesia that is located diffusely on the plantar aspect of the foot. Initially, symptoms are intermittent and then become constant [26]. The pain is characterized as a burning, tingling, or numb type of pain and its location will varies depending on which nerves are involved. The pain can radiate distally along the involved nerve branches. In one third of patients who have severe compression of the nerve, the pain migrates proximally along the medial aspect of the leg; this is called the Valleix phenomenon [4 –6,25,59]. Patients who have tarsal tunnel syndrome may have a history of significant or trivial trauma that precipitates the pain. Some patients complain of pain with each step [12,38]. Generally, the
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amount of burning and aching pain is proportional to the patient’s activity level [6,8,18,25,26,56,69]. The pain is relieved by rest, elevation, and loose shoes. Some patients have nocturnal pain that is severe enough to wake the patient and is relieved by walking [3,5,6,19,26,30,38,42]. This may be due to venostasis and engorgement of the tibial veins at night [19].
Physical examination The foot is examined for any significant hindfoot varus or valgus deformity [3– 5,8,12,16,25,33,38,52,59]. The course of the tibial nerve and its branches is palpated for any evidence of thickening or swelling, which may be indicative of a space-occupying lesion [5,8,18,30,34,70]. The range of motion of the ankle, subtalar, and transverse tarsal joints is documented. Although patients may complain of dysesthesia and numbness, it is difficult to define areas of numbness on the plantar aspect of the foot [8,25,30]. The earliest sign of this condition is decreased two-point discrimination on the plantar aspect of the foot [30]; with disease progression, hypoesthesia to pinprick occurs in the distribution of the involved nerve. Motor power is assessed by testing plantarflexion of the toes, especially the lateral toes to indicate weakness of the intrinsic muscles of the foot. Motor weakness is a common finding and is difficult to assess [18,25,38]. In the advanced stages, atrophy of the abductor hallucis or abductor digiti minimi may be observed. Paradoxically, the medial arch may appear full because of an accessory abductor hallucis muscle that compresses the nerve [16]. Objective physical findings of tarsal tunnel syndrome are found by exacerbating tibial nerve compression or tension to reproduce symptoms. Palpation of the tibial nerve and its branches can cause tenderness and reproduce symptoms. Tinel’s sign, the reproduction of pain by pressure on the tibial nerve behind the medial malleolus, is a specific finding [4,5,25,30– 32,38,70] and also may produce proximal migration of the pain into the leg. The cuff test involves inflating a pneumatic pressure cuff around the leg which acts as a venous tourniquet and causes venous engorgement; this increases local ischemia and reproduces symptoms [6,16,19,26,30,31,38,59]. Increasing the tension on the tibial nerve by forcing the ankle into maximal dorsiflexion [50,62] or the heel into eversion [4,6,16,25 –27,56,71] may aggravate symptoms. Some investigators believe that placing the heel into inversion relieves symptoms by reducing tibial nerve tension [4,6,26,27], whereas others believe that this maneuver reproduces symptoms by reducing the cross-sectional area of the tunnel, and hence, compressing the tibial nerve [16,18,19,30,56]. These apparently conflicting findings can be explained when one considers the cause of the tarsal tunnel syndrome. Because tibial neuropathy can result from nerve compression or tension, the physical maneuver that exacerbates the causative factor reproduces symptoms. Thus, in a tibial nerve that is under tension, heel eversion reproduces symptoms, whereas heel inversion reduces nerve tension and relieves symptoms. Although heel inversion reduces the cross-
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sectional area of the tunnel, the nerve is able to accommodate the reduction in volume without any deleterious effects. In the case of tarsal tunnel syndrome that results from a compression, the nerve cannot accommodate any further reduction in tarsal tunnel cross-sectional area and so inversion of the heel reproduces symptoms.
Diagnosis Because the history and physical examination for tarsal tunnel syndrome may not be conclusive, investigations, such as electrodiagnostic studies and radiologic imaging, may aid in clarifying the diagnosis of tarsal tunnel syndrome.
Electrodiagnostic studies Electrodiagnostic studies measure nerve function and can be classified into motor, sensory, or mixed compound nerve tests. There is controversy about which test is the most sensitive and specific for diagnosis of tarsal tunnel syndrome [2,7,23,25,35,65,69,72]. Mixed motor and sensory action potentials are much larger than sensory potentials alone and more sensitive for detecting early change [73]. Galardi et al [23] studied the sensitivity and specificity of distal motor latencies, sensory conduction velocities, and mixed motor and sensory conduction velocities. They concluded that distal motor latencies were insensitive (21.5%) but that sensory conduction velocities were too sensitive (92.8% –100%); sensory conduction velocity was abnormal in 8% of normal controls who were tested. Mixed motor and sensory conduction velocities were abnormal in 85.7% of patients who had tarsal tunnel syndrome, but there were no abnormalities in asymptomatic limbs or normal controls [25]. Abnormal conduction velocities in sensory and mixed motor and sensory action potentials increases the sensitivity and specificity for the diagnosis of tarsal tunnel syndrome. Studies must include the tibial nerve proximal to the tarsal tunnel and the opposite leg so as to exclude double crush phenomenon and peripheral neuropathy as causes. The relevance of electrodiagnostic studies is controversial. Pfeiffer and Cracchiolo [27] reported no correlation between results of electrodiagnostic studies and clinical results. Cimino [16] calculated the false negative rate of electrodiagnostic studies to be at least 9.5% and stated that a negative test did not preclude the diagnosis. Mann and Baxter [8] recommended that tarsal tunnel syndrome be diagnosed only when the following triad exists: pain and paresthesia in the foot, positive Tinel’s sign, and positive electrodiagnostic studies. A suggested algorithm is one that considers Mann and Baxter’s three findings. If all three are present, the patient has tarsal tunnel syndrome. If only two findings are present, the patient probably has tarsal tunnel syndrome and should be followed carefully. If only one finding is present, the patient does not have tarsal tunnel syndrome and other diagnoses should be entertained.
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Radiologic investigations Radiologic investigations are important in defining the anatomy within the tarsal tunnel. Plain radiograph Plain radiograph examination of the foot identifies displaced or malunited fractures, accessory ossicles, or bony exostoses within the vicinity of the tarsal tunnel. Weight-bearing radiographs of the foot and ankle also are useful for determining the presence of a foot deformity. Venography Venography may be indicated in patients who have a positive cuff test [74]. MRI In the absence of a abnormality on plain radiographs, MRI is the most effective method for assessing the contents of the tarsal tunnel, the flexor retinaculum, and the branches of the tibial nerve [51,75 –77]. It can image the foot and ankle in all three orthogonal planes and allows one to define any lesion in terms of size, site origin, and relation to the tibial nerve [51,75 – 77]. In failed tarsal tunnel syndrome surgery, MRI allows one to define the tarsal tunnel when considering inadequate decompression [76]. In a study of 29 feet that had electrodiagnostically-proven tarsal tunnel syndrome, 88% had a lesion identified by MRI. The lesions included tenosynovitis, varicosities, masses, and scar tissue. MRI is recommended in children who tend to have neoplastic mass lesions [75].
Treatment and results The treatment of tarsal tunnel syndrome is classified into nonoperative and operative methods. Except in acute cases, operative treatment should not be considered until after an adequate trial of nonoperative therapy. Nonoperative treatment The nonoperative treatments that are recommended in tarsal tunnel syndrome are rest, immobilization, orthotics, oral nonsteroidal anti-inflammatory drugs (NSAIDs), local corticosteroid injections, physiotherapy, stockings, and weight loss [6– 8,10,12,19,28,33,34,42,52,53,55,56,59,78]. Immobilization and orthotics The immobilization methods include ankle-foot orthosis [7], and, occasionally, a walking cast [8,42,74]. Orthotics to maintain a neutral foot position are effective if the foot deformity is flexible [12,16,19,59]. In flexible valgus heel, medial longitudinal arch supports and medial heel wedges have been used with success [12,19]. In more severe deformities, University of California Biome-
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chanics Laboratory –type inserts, which hold the calcaneus in neutral alignment and force the abducted forefoot into neutral, can be used [79]. More control can be gained by supplementing with a polypropylene ankle foot orthosis. Lateral heel wedges effectively treat flexible varus heels, whereas medial arch supports aggravate symptoms and should be avoided [59]. In patients who have symptoms that are reproduced by dorsiflexion, a 1-inch heel lift helped by decreasing tension on the tibial nerve [50,62]. Anti-inflammatory medication Oral NSAIDs and local corticosteroid injections into the region may have a transient effect in many cases [6,7,12,27]. In inflammatory conditions where tenosynovitis is a factor, however, such as rheumatoid arthritis or ankylosing spondylitis, NSAIDs have proven to be effective treatments [10,27,50,52, 53,55,56]. Physiotherapy Physiotherapy to strengthen the intrinsic muscles of the feet—the flexor digitorum longus, flexor hallucis longus, and tibialis posterior—was recommended to help restore the medial longitudinal arch and to stabilize the foot in a neutral position [12,34,55,61]. In runners who had ‘‘jogger’s foot,’’ where a hyperpronated foot stretches the tibial nerve, retraining to toe-in slightly and strike the lateral aspect of the foot helped to decrease the deformity [61]. Other treatment In patients who have varices, stockings are used to decrease the amount of swelling in the leg and the amount of venous stasis present [8,19,34,42]. In obese patients, some investigators recommend weight loss [6,61].
Summary of non-operative treatment Although nonoperative therapy is the first line of treatment, patients should be warned that it is effective in the presence of specific etiologic factors that are amenable to therapy, such as flexible foot deformities, tenosynovitis, and inflammatory arthritis. Nonoperative treatments have no significant effects on space-occupying lesions within the tarsal tunnel [16,27,28]. In Cimino’s review [16], only 16% of patients were treated nonoperatively. Orthotic management was successful in 34% of patients, all of whom had flexible deformity. Spontaneous resolution or corticosteroid injection was successful in 24%. Although nonoperative therapy is the recommended initial treatment, many investigators believe that it provides transient relief and that surgery is the only effective treatment [6,28,31,38].
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Operative treatment When tarsal tunnel syndrome results from a space-occupying lesion, surgical treatment provides predictably good results [6,8,18,19,27,28,42,70]. Surgical treatment was described by Lam [30]; it consists of release of the flexor retinaculum; neurolysis of the medial and lateral plantar nerves as far distally as possible; and surgical treatment of any etiologic factors, such as repairing fractures to restore normal spatial arrangement, excising a mass lesion, or resecting synovium. The tibial nerve is exposed proximal to the flexor retinaculum through a curved medial incision that starts 10 cm proximal to the medial malleolus and 2 cm posterior to the margin of the tibia and extends toward the talonavicular joint. The flexor retinaculum is divided completely and the tibial nerve is mobilized along its course as far distally as possible. The medial and lateral plantar nerves must be decompressed adequately—at least 2 cm distally into the sole of the foot. The medial plantar nerve is followed distally as it passes in its fibrous tunnel inferior to the talonavicular joint. The lateral plantar nerve travels behind the abductor hallucis muscle; part of the origin of the abductor hallucis may have to be released to expose the nerve adequately. Postoperatively, the patient remains nonweight bearing for 3 weeks; thereafter, weight bearing is permitted as tolerated and active and passive range of motion is encouraged. Failure to recognize the proximal extent of the flexor retinaculum and to decompress the distal tarsal tunnel can result in failure of therapy [13,76]. In a review of the literature, 65% of patients required surgical treatment; 91% had good or improved results [16]. This corresponds with surgical results from the literature, which have 79% to 95% good results [2,6,7,30,31,38,59]. Surgical results were better when: (1) patients were younger [28], (2) surgery was performed early in the disease process before motor involvement [28,30], and (3) a localized lesion was identified [6,8,18,19,27,28,42,70,80]. Takakura et al [28] reported that coalition and tumors gave the best surgical results, whereas idiopathic causes and trauma were associated with the poorest results; hemorrhage associated with trauma was believed to produce adhesions within the tarsal tunnel. More recently, Sammarco and Chang [81] stated that even without a discrete lesion or with symptoms that had been present for more than a year, a predictable improvement could be gained after surgery. Considering the excellent results in the literature from operative treatment and the poor results from nonoperative treatment methods, many investigators have advocated surgical therapy for lasting results in tarsal tunnel syndrome [6,8, 19,38]. A recent study, however, cast doubt on the long-term effectiveness of surgery [27]. Only 44% of 30 patients benefited markedly from surgical treatment. This discrepancy can be explained by the use of more precise and stringent subjective questionnaires and a minimum follow-up of 24 months (average 31 months), which is considerably longer than many earlier studies [2,6,7, 30,38,59]. Pfeiffer and Cracchiolo noted that early results of surgery were encouraging but results deteriorated. They concluded that ‘‘unless there is an associated lesion near or within the tarsal tunnel preoperatively, decompression of
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the posterior tibial nerve should be considered with caution,’’ and that patients who had undergone previous surgery for pain in the foot, plantar fasciitis, or symptoms of systemic inflammatory disease should be managed conservatively. A recent study examined 60 patients with 68 operations; subjective and objective outcomes were examined after return-to-normal function. Although objectively there was 85% symptom relief, subjectively, only 51% of patients had symptom relief [82]. Further investigation with similar studies is required.
Summary Tarsal tunnel syndrome is an uncommon condition whose signs and symptoms are ill-defined, this has lead to under- and misdiagnosis of the disorder. A high degree of suspicion, combined with a thorough history and physical examination, is required to make the diagnosis. Investigations, such as electrodiagnostic studies and MRI, improve diagnostic accuracy. Most patients warrant initial nonoperative therapy. Operative treatment is indicated in those who have acute onset or a definite space-occupying lesion. Results have been reported as excellent after surgery, but recent work suggests that long-term outcomes may not be so favorable. The worst results of operative treatment are found in patients who have posttraumatic or idiopathic etiology. Operative treatment after tarsal tunnel decompression is warranted only in those patients in whom an inadequate release can be identified.
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[13] Skalley TC, Schon LC, Hinton RY, Myerson MS. Clinical results following revision tibial nerve release. Foot Ankle Int 1994;15(7):360 – 7. [14] Deland JT, Arnoczky SP, Thompson FM. Adult acquired flatfoot deformity at the talonavicular joint: reconstruction of the spring ligament in an in vitro model. Foot Ankle 1992;13(6): 327 – 32. [15] Sarrafian SK. Nerves. In: Anatomy of the foot and ankle: descriptive, topographic, functional. Philadelphia: J.B. Lippincott; 1993. p. 365 – 83. [16] Cimino WR. Tarsal tunnel syndrome: review of the literature. Foot Ankle 1990;11(1):47 – 52. [17] Dellon AL, Mackinnon SE. Tibial nerve branching in the tarsal tunnel. Arch Neurol 1984;41(6): 645 – 6. [18] Janecki CJ, Dovberg JL. Tarsal-tunnel syndrome caused by neurilemmoma of the medial plantar nerve. A case report. J Bone Joint Surg Am 1977;59(1):127 – 8. [19] DiStefano V, Sack JT, Whittaker R, Nixon JE. Tarsal-tunnel syndrome. Review of the literature and two case reports. Clin Orthop 1972;88:76 – 9. [20] Kim J, Dellon AL. Neuromas of the calcaneal nerves. Foot Ankle Int 2001;22(11):890 – 4. [21] Kim J, Dellon AL. Pain at the site of tarsal tunnel incision due to neuroma of the posterior branch of the saphenous nerve. J Am Podiatr Med Assoc 2001;91(3):109 – 13. [22] Horwitz MT. Normal anatomy and variations of the peripheral nerves of the leg and foot. Arch Surg 1938;36:626. [23] Galardi G, Amadio S, Maderna L, Meraviglia MV, Brunati L, Dal Conte G, et al. Electrophysiologic studies in tarsal tunnel syndrome. Diagnostic reliability of motor distal latency, mixed nerve and sensory nerve conduction studies. Am J Phys Med Rehabil 1994;73(3):193 – 8. [24] Baylan SP, Paik SW, Barnert AL, Ko KH, Yu J, Persellin RH. Prevalence of the tarsal tunnel syndrome in rheumatoid arthritis. Rheumatol Rehabil 1981;20(3):148 – 50. [25] DeLisa JA, Saeed MA. The tarsal tunnel syndrome. Muscle Nerve 1983;6(9):664 – 70. [26] Grabois M, Puentes J, Lidsky M. Tarsal tunnel syndrome in rheumatoid arthritis. Arch Phys Med Rehabil 1981;62(8):401 – 3. [27] Pfeiffer WH, Cracchiolo III A. Clinical results after tarsal tunnel decompression. J Bone Joint Surg Am 1994;76(8):1222 – 30. [28] Takakura Y, Kitada C, Sugimoto K, Tanaka Y, Tamai S. Tarsal tunnel syndrome. Causes and results of operative treatment. J Bone Joint Surg Br 1991;73(1):125 – 8. [29] Daniels TR, Lau JT, Hearn TC. The effects of foot position and load on tibial nerve tension. Foot Ankle Int 1998;19(2):73 – 8. [30] Lam SJS. Tarsal tunnel syndrome. J Bone Joint Surg Br 1967;49(1):87 – 92. [31] Linscheid RL, Burton RC, Fredericks EJ. Tarsal-tunnel syndrome. South Med J 1970;63(11): 1313 – 23. [32] Stefko RM, Lauerman WC, Heckman JD. Tarsal tunnel syndrome caused by an unrecognized fracture of the posterior process of the talus (Cedell fracture). A case report. J Bone Joint Surg Am 1994;76(1):116 – 8. [33] Jackson DL, Haglund BL. Tarsal tunnel syndrome in runners. Sports Med 1992;13(2):146 – 9. [34] Schon LC. Nerve entrapment, neuropathy, and nerve dysfunction in athletes. Orthop Clin North Am 1994;25(1):47 – 59. [35] Goodgold J, Kopell HP, Spielholz NI. The tarsal-tunnel syndrome. Objective diagnostic criteria. N Engl J Med 1965;273(14):742 – 5. [36] Gould N, Alvarez R. Bilateral tarsal tunnel syndrome caused by varicosities. Foot Ankle 1983; 3(5):290 – 2. [37] Kenzora JE, Lenet MD, Sherman M. Synovial cyst of the ankle joint as a cause of tarsal tunnel syndrome. Foot Ankle 1982;3(3):181 – 3. [38] Mann RA. Tarsal tunnel syndrome. Orthop Clin North Am 1974;5(1):109 – 15. [39] Matricali B. Tarsal tunnel syndrome caused by ganglion compression. J Neurosurg Sci 1980; 24(3 – 4):183 – 5. [40] Taguchi Y, Nosaka K, Yasuda K, Teramoto K, Mano M, Yamamoto S. The tarsal tunnel syndrome. Report of two cases of unusual cause. Clin Orthop 1987;217:247 – 52.
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[41] O’Malley GM, Lambdin CS, McCleary GS. Tarsal tunnel syndrome. A case report and review of the literature. Orthopedics 1985;8(6):758 – 60. [42] Menon J, Dorfman HD, Renbaum J, Friendler S. Tarsal tunnel syndrome secondary to neurilemoma of the medial plantar nerve. J Bone Joint Surg Am 1980;62(2):301 – 3. [43] Still GP. Neurilemoma of the medial plantar nerve: a case report. J Foot Ankle Surg 2001; 40(4):236 – 9. [44] Garchar DJ, Lewis JE, DiDomenico LA. Hypertrophic sustentaculum tali causing a tarsal tunnel syndrome: a case report. J Foot Ankle Surg 2001;40(2):110 – 2. [45] Lee MF, Chan PT, Chau LF, Yu KS. Tarsal tunnel syndrome caused by talocalcaneal coalition. Clin Imaging 2002;26(2):140 – 3. [46] Sammarco GJ, Stephens MM. Tarsal tunnel syndrome caused by the flexor digitorum accessorius longus. A case report. J Bone Joint Surg Am 1990;72(3):453 – 4. [47] Burks JB, DeHeer PA. Tarsal tunnel syndrome secondary to an accessory muscle: a case report. J Foot Ankle Surg 2001;40(6):401 – 3. [48] Kinoshita M, Okuda R, Morikawa J, Abe M. Tarsal tunnel syndrome associated with an accessory muscle. Foot Ankle Int 2003;24(2):132 – 6. [49] Mezrow CK, Sanger JR, Matloub HS. Acute tarsal tunnel syndrome following partial avulsion of the flexor hallucis longus muscle: a case report. J Foot Ankle Surg 2002;41(4):243 – 6. [50] Chater EH. Tarsal-tunnel syndrome is rheumatoid arthritis. BMJ 1970;3(719):406. [51] Erickson SJ, Quinn SF, Kneeland JB, Smith JW, Johnson JE, Carrera GF, et al. MR imaging of the tarsal tunnel and related spaces: normal and abnormal findings with anatomic correlation. AJR Am J Roentgenol 1990;155(2):323 – 8. [52] Lloyd K, Agarwal A. Tarsal-tunnel syndrome, a presenting feature of rheumatoid arthritis. BMJ 1970;3(713):32. [53] Nakano KK. The entrapment neuropathies of rheumatoid arthritis. Orthop Clin North Am 1975; 6(3):837 – 60. [54] Enright T, Liang GC, Fox TA, Mueller RF. Tarsal tunnel syndrome with ankylosing spondylitis. Arthritis Rheum 1979;22(1):77 – 9. [55] Kucukdeveci AA, Kutlay S, Seckin B, Arasil T. Tarsal tunnel syndrome in ankylosing spondylitis. Br J Rheumatol 1995;34(5):488 – 9. [56] Olivieri I, Gemignani G, Sicilliano G, Pasero G. Tarsal tunnel syndrome in seronegative spondyloarthropathy. Br J Rheumatol 1989;28(6):537 – 9. [57] Sugimoto K, Iwai M, Kawate K, Yajima H, Takakura Y. Tenosynovial osteochondromatosis of the tarsal tunnel. Skeletal Radiol 2003;32(2):99 – 102. [58] Watson BV, Algahtani H, Broome RJ, Brown JD. An unusual presentation of tarsal tunnel syndrome caused by an inflatable ice hockey skate. Can J Neurol Sci 2002;29(4):386 – 9. [59] Radin EL. Tarsal tunnel syndrome. Clin Orthop 1983;181:167 – 70. [60] Lau J, Daniels TR. Effects of tarsal tunnel release and stabilization procedures on tibial nerve tension in a surgically created pes planus foot. Foot Ankle Int 1998;19:770 – 7. [61] Rask MR. Medial plantar neurapraxia (jogger’s foot): report of 3 cases. Clin Orthop 1978;134: 193 – 5. [62] Chater EH, Wilson AL. Tarsal tunnel syndrome. J Ir Med Assoc 1968;61(375):326 – 8. [63] Labib SA, Gould JS, Rodriguez-del-Rio FA, Lyman S. Heel pain triad (HPT): the combination of plantar fasciitis, posterior tibial tendon dysfunction and tarsal tunnel syndrome. Foot Ankle Int 2002;23(3):212 – 20. [64] Roaf R. Suture of the external and internal popliteal nerves. Br J Surg 1946;33:382 – 5. [65] Fu R, DeLisa JA, Kraft GH. Motor nerve latencies through the tarsal tunnel in normal adult subjects: standard determinations corrected for temperature and distance. Arch Phys Med Rehabil 1980;61(6):243 – 8. [66] Dawson DM, Hallett M, Millender LH. Pathophysiology of nerve entrapment. In: Entrapment neuropathies. Little, Brown and Company; 1990. p. 5 – 23. [67] Bodine SC, Lieber RL. Peripheral nerve physiology, anatomy and pathology. In: Simon SR,
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Posterior tibial nerve—primary Johnny T.C. Lau, MD, MSc, FRCSCa,b,*, Peter Stavrou, MBBS, FRACSb,c a
Department of Surgery, University of Toronto, University Health Network, Toronto Western Division, Division of Orthopaedic Surgery, 339 Bathurst Street, ECW-1-038, Toronto, Ontario M5T 2S8, Canada b Toronto Western Hospital, University Health Network, University of Toronto, Toronto, Ontario, Canada c Wakefield Orthopaedic Clinic, 270 Wakefield Street, Adelaide, South Australia 5000, Australia
Tarsal tunnel is an uncommon disorder of the foot [1,2] that presents as a burning or tingling pain that is located diffusely on the plantar aspect of the foot. These symptoms were described in 1960 by Kopell and Thompson [3]. The use of the term ‘‘tarsal tunnel syndrome’’ to describe these symptoms first appeared in the literature in 1962 when it was used by Keck [4] and Lam [5] independently. Many investigators have considered tarsal tunnel syndrome to be analogous to carpal tunnel syndrome [3 –10]. As more becomes known about tarsal tunnel syndrome, it is evident that this is not purely an entrapment neuropathy. It differs from carpal tunnel syndrome in anatomy, etiology, clinical presentation, and response to nonoperative and operative treatment.
Anatomy The anatomy of the tarsal tunnel is the key to understanding its clinical presentation because herein the tibial nerve or its branches are affected. The tarsal tunnel consists of proximal and distal tarsal tunnels [11]. The proximal tarsal tunnel contains the tibial nerve and the distal tarsal tunnel contains the branches of the tibial nerve: the medial calcaneal nerve, medial plantar nerve, and lateral plantar nerve (Fig. 1) [11]. Although tarsal tunnel syndrome classically refers to
* Corresponding author. Department of Surgery, University of Toronto, University Health Network, Toronto Western Division, Division of Orthopaedic Surgery, 339 Bathurst Street, ECW-1-038, Toronto, Ontario, M5T 2S8, Canada. E-mail address: [email protected] (J.T.C. Lau). 1083-7515/04/$ – see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.fcl.2003.12.002
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Fig. 1. Anatomy of the tarsal tunnel.
the proximal tarsal tunnel, failure to take the existence of the distal tarsal tunnel into account has led to poor results with therapy [8,11 –13]. The tarsal tunnel is the continuation of the deep posterior compartment of the leg that leads to the plantar aspect of the foot [14]. The proximal tarsal tunnel is a fibro-osseous structure that is located behind the medial malleolus. The osseous floor is formed by the medial surface of the talus, sustentaculum tali, and medial wall of the calcaneus. The fibrous roof is the flexor retinaculum, also known as the laciniate ligament. The flexor retinaculum is the continuation of the superficial and deep aponeurosis of the leg on its posterior border; its anterior border is continuous with the dorsal aponeurosis of the foot. The base of the flexor retinaculum corresponds to the superior border of the abductor hallucis muscle and divides into superficial and deep fascia around this muscle [15]. The continuation of the flexor retinaculum proximally and distally with these aponeurotic structures makes it difficult to define its borders accurately [1]. The retinaculum may extend up to 10 cm proximal to the medial malleolus; failure to recognize this may lead to a failure of surgical decompression [16]. Dellon and Mackinnon [17] defined the flexor retinaculum as being 2 cm either side of the malleolar-calcaneal axis—a reference line drawn from the center of the me-
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dial malleolus to the center of the calcaneus. Hence, the flexor retinaculum extends from its origin at the medial malleolus in an inferior and posterior direction roughly to the calcaneal tuberosity. The contents of the proximal tarsal tunnel are, from anterior to posterior, tibialis posterior tendon, flexor digitorum longus tendon, posterior tibial artery, tibial nerve, and the flexor hallucis longus tendon. Each tendon has its own synovial sheath and lies in a separate fibro-osseous compartment that is formed from projections between the underside of the flexor retinaculum and the periosteum of the calcaneus [6,18,19]. The neurovascular bundle lies in its own fibroosseous compartment and is attached to the fibrous septae by a surrounding layer of dense areolar tissue [19]. Thus, the tibial nerve is in a fixed position in a fibroosseous tunnel and is susceptible to compression by a lesion within or outside this tunnel as well as tension forces. Branching of the nerves is variable; usually three nerves arise from the tibial nerve: the medial calcaneal nerve(s), the medial plantar nerve, and the lateral plantar nerve. The medial calcaneal nerve provides sensation for the medial and plantar aspects of the hindfoot after exiting the tarsal tunnel—either through or distal to—the flexor retinaculum. Usually, the medial calcaneal nerve arises from the tibial nerve itself (69% –90%); less frequently it arises from the lateral plantar nerve [1,8,17]. Nine different branching patterns were described for the medial calcaneal nerve [1]. A single branch was seen in 79% of feet; multiple branches were seen in 21%. The most common pattern is for the medial calcaneal nerve to arise from the tibial nerve as a single branch; failure to account for anatomical variants may result in paresthesia or painful neuromas after damage to nerve branches during surgery [20,21]. The tibial nerve ends by bifurcating into the medial and lateral plantar nerves. In a cadaver study, this bifurcation usually occurred within the confines of the tarsal tunnel (93% –96%). In the remaining 4% to 7% of feet, the bifurcation occurred proximal to the tarsal tunnel in the lower leg [1,17,22]. A high bifurcation of the tibial nerve is believed to be a predisposing factor in tarsal tunnel syndrome by ‘‘presenting a larger cross-sectional area at the narrowed entrance to the tarsal tunnel’’ [17]. Havel [1] considered that the low incidence of the tibial nerve bifurcation proximal to the tarsal tunnel accounted for the low incidence of tarsal tunnel syndrome. The distal tunnel contains the medial and lateral plantar nerves that pass through fibrous openings in the origin of the abductor hallucis [11]. These are separate fibrous tunnels that are divided by a partition that originates from the medial side of the calcaneus and attached to the deep fascia of abductor hallucis. The medial plantar nerve is the larger of the terminal branches of the tibial nerve and passes between the plantar calcaneonavicular ligament and the abductor hallucis muscle. The medial plantar nerve is analogous to the median nerve in the hand; it supplies sensation to the medial three and half toes and the sole of the foot. The lateral plantar nerve, after passing through the origin of the abductor hallucis, provides sensation to the lateral one and half toes of the foot and is analogous to the ulnar nerve in the hand.
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Etiology The true incidence of tarsal tunnel syndrome is unknown [23]. A specific etiology can be found in 60% to 80% of patients; thus, in a significant number of patients no specific cause can be found [2,6– 9,16,24 – 28]. Although many investigators consider tarsal tunnel syndrome as purely an entrapment neuropathy, other factors have been investigated [3,8,12,29]. In a review of the literature, Cimino [16] examined 25 studies and case reports of tarsal tunnel syndromes that involved 164 subjects and 186 tarsal tunnel syndromes. Patients ranged in age from 14 to 80 years old. Women were more likely to be involved (56%). Of the causes identified, the most frequent were; trauma (17%), varicosities (13%), heel varus (11%), fibrosis (9%) and heel valgus (8%). In broad terms, the causes can be classified into three groups: (1) trauma, (2) space-occupying lesion, and (3) foot deformity. Trauma Trauma was the most common cause in Cimino’s [16] review of the literature. Fractures in the bones that surround the tarsal tunnel—distal tibia, talus, calcaneus, and tarsal bones—especially if displaced, can precipitate tarsal tunnel syndrome. Soft tissue trauma in the same region (eg, sprains of the deltoid ligament) may produce the same effect [6,9,30 – 32]. Traumatic synovitis of the tendons in the tarsal tunnel also may compress the tibial nerve and produce tarsal tunnel syndrome [3,12,16,30,33,34]. Space-occupying lesions Space-occupying lesions can compress the tibial nerve from within or from outside its compartment in the tarsal tunnel. The most common space-occupying lesions are varicosities [6,35,36]. Other lesions that were reported in the literature include ganglia [9,37 – 40], perineural fibrosis [9], lipoma [41], neurilemoma [9,18,40,42,43], bony exostosis [16], hypertrophic sustentaculum tali [44], medial talocalcaneal bar [8,28,45], hypertrophic flexor retinaculum [16], hypertrophic or accessory abductor hallucis muscle [6,19], flexor digitorum accessorius longus muscle [46 – 48], accessory soleus muscle [48], partial rupture of the flexor hallucis longus tendon [49], rapid weight gain [6,16], fluid retention [16], and chronic phlebitis [16]. Inflammatory disorders, such as rheumatoid arthritis [24,26,50 – 53], ankylosing spondylitis [54 – 56], and synovial osteochondromatosis [57], can produce a proliferative synovitis that exerts a mass effect in the tarsal tunnel. Recently, a case was documented that had an inflatable ice hockey boot as the cause of tarsal tunnel syndrome [58]. Foot deformities Foot deformities accounted for 19% of tarsal tunnel syndromes in Cimino’s review of the literature [16]. Varus heels accounted for 11% of these and valgus
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heels accounted for 8%. In varus heel deformity, Radin [59] stated that two thirds of patients who had tarsal tunnel syndrome had concurrent varus heel and pronated forefoot. The forefoot pronation compensated for the varus hindfoot and allowed the forefoot to make contact with the ground. The varus heel deformity also shortens the abductor hallucis muscle which gives it the appearance of being hypertrophied and decreases the cross-sectional area of the tarsal tunnel. Forefoot pronation stretches the tibial nerve. Thus, the nerve is compressed within the tibial tunnel and under tension which precipitates tarsal tunnel syndrome. Conversely, hindfoot valgus and forefoot abduction also can cause tarsal tunnel syndrome by putting the tibial nerve under tension [3– 5,8,12,25,29,33,38, 52,60]. Francis et al [12] reported on 11 patients who had pes planus and tarsal tunnel syndrome; of these, 8 had mobile deformities. Six patients underwent surgical release; none had an identifiable lesion. Most patients described paresthesias ‘‘like an electric shock with each step taken.’’ The investigators believed that mobile pes planus with associated hindfoot valgus put the tibial nerve or its branches under tension on weight bearing which makes the nerve vulnerable to neurapraxia. Any trivial trauma could initiate tarsal tunnel syndrome and the symptoms could be aggravated with weight bearing. Dynamic foot deformities that led to tarsal tunnel syndrome also have been documented in the literature [16,30,33,61]. Rask [61] reported on ‘‘jogger’s foot,’’ a condition that is produced by hindfoot valgus in running that stretches the medial plantar nerve against the tarsal navicular bone. Running with excessive pronation is believed to stretch the tibial nerve and predispose it to injury. Occupations that are associated with repeated dorsiflexion, such as crouching, and squatting, were reported to be associated with tarsal tunnel syndrome [16,50,62]. More recently, a combination of pathologies was reported by Labib et al [63]. They reported on a group of patients who had tarsal tunnel syndrome, plantar fasciitis, and posterior tibial tendon dysfunction; they labeled this the ‘‘heel pain triad’’. The loss of static (plantar fascia) and dynamic (posterior tibial tendon) supports for the longitudinal arch was believed to lead to traction injury of the tibial nerve and tarsal tunnel syndrome. Of their 14 patients, 87% reported significant improvement after surgery.
Pathophysiology of neuropathy Tarsal tunnel syndrome is produced by damage to the tibial nerve as a result of compression [3,19,30,64] or tension [3,8,12,29,33]. Compression is recognized as the most common cause of tarsal tunnel syndrome. Nerve compression In their classic paper, Kopell and Thompson [3] defined an entrapment point as a location ‘‘where the anatomic configuration may cause constriction of the nerve, or, if trauma has occurred to the area, the particular anatomic disposition
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will maintain the nerve in a state of inflammation.’’ Entrapment occurs because the structure of the fibro-osseous tarsal tunnel is made of strong and unyielding tissues compared with the nerve and ‘‘there is little latitude for dimensional alteration in the cross-sectional area permitted for the passage of the nerve.’’ The nerve is injured directly by neural compression or indirectly by causing local vascular insufficiency [19]. In tarsal tunnel syndrome, the initial sensory dysfunction is believed to be due to nerve ischemia that is caused secondary to local compression, whereas the later motor dysfunction is due to direct neural compression and structural alteration [19,30]. Tibial nerve entrapment in the tarsal tunnel is most common at the anterior, inferior aspect of the canal [3,12,25,65]; the lateral plantar nerve is affected more often than the medial plantar nerve [7,12,18,23]. The lateral plantar nerve passes through a fibrous opening in the abductor hallucis muscle, separately and more proximal than, the medial plantar nerve [6], which makes it more vulnerable [7]. Nerve tension In a pes planus foot, the heel valgus and abducted forefoot place the tibial nerve under tension [3– 5,8,12,25,29,33,38,52,60]. The tibial nerve can be damaged by an acute or chronic stretch [34,66,67]; the severity of the injury is dependent on the magnitude of the force and the rate of deformation [67]. Over time, chronically injured nerves become stiffer because of fibrosis within the epineurium [68] and are unable to compensate for tension as easily as normal nerves; this makes them more susceptible to ischemia and injury.
Clinical presentation The diagnosis of tarsal tunnel syndrome is difficult and often is undiagnosed or misdiagnosed [1,4,8,16,18,19,23,25,30,38,65]. The symptoms can be diffuse and poorly localized [18,25].
History Tarsal tunnel usually presents with an insidious onset of pain or paresthesia that is located diffusely on the plantar aspect of the foot. Initially, symptoms are intermittent and then become constant [26]. The pain is characterized as a burning, tingling, or numb type of pain and its location will varies depending on which nerves are involved. The pain can radiate distally along the involved nerve branches. In one third of patients who have severe compression of the nerve, the pain migrates proximally along the medial aspect of the leg; this is called the Valleix phenomenon [4 –6,25,59]. Patients who have tarsal tunnel syndrome may have a history of significant or trivial trauma that precipitates the pain. Some patients complain of pain with each step [12,38]. Generally, the
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amount of burning and aching pain is proportional to the patient’s activity level [6,8,18,25,26,56,69]. The pain is relieved by rest, elevation, and loose shoes. Some patients have nocturnal pain that is severe enough to wake the patient and is relieved by walking [3,5,6,19,26,30,38,42]. This may be due to venostasis and engorgement of the tibial veins at night [19].
Physical examination The foot is examined for any significant hindfoot varus or valgus deformity [3– 5,8,12,16,25,33,38,52,59]. The course of the tibial nerve and its branches is palpated for any evidence of thickening or swelling, which may be indicative of a space-occupying lesion [5,8,18,30,34,70]. The range of motion of the ankle, subtalar, and transverse tarsal joints is documented. Although patients may complain of dysesthesia and numbness, it is difficult to define areas of numbness on the plantar aspect of the foot [8,25,30]. The earliest sign of this condition is decreased two-point discrimination on the plantar aspect of the foot [30]; with disease progression, hypoesthesia to pinprick occurs in the distribution of the involved nerve. Motor power is assessed by testing plantarflexion of the toes, especially the lateral toes to indicate weakness of the intrinsic muscles of the foot. Motor weakness is a common finding and is difficult to assess [18,25,38]. In the advanced stages, atrophy of the abductor hallucis or abductor digiti minimi may be observed. Paradoxically, the medial arch may appear full because of an accessory abductor hallucis muscle that compresses the nerve [16]. Objective physical findings of tarsal tunnel syndrome are found by exacerbating tibial nerve compression or tension to reproduce symptoms. Palpation of the tibial nerve and its branches can cause tenderness and reproduce symptoms. Tinel’s sign, the reproduction of pain by pressure on the tibial nerve behind the medial malleolus, is a specific finding [4,5,25,30– 32,38,70] and also may produce proximal migration of the pain into the leg. The cuff test involves inflating a pneumatic pressure cuff around the leg which acts as a venous tourniquet and causes venous engorgement; this increases local ischemia and reproduces symptoms [6,16,19,26,30,31,38,59]. Increasing the tension on the tibial nerve by forcing the ankle into maximal dorsiflexion [50,62] or the heel into eversion [4,6,16,25 –27,56,71] may aggravate symptoms. Some investigators believe that placing the heel into inversion relieves symptoms by reducing tibial nerve tension [4,6,26,27], whereas others believe that this maneuver reproduces symptoms by reducing the cross-sectional area of the tunnel, and hence, compressing the tibial nerve [16,18,19,30,56]. These apparently conflicting findings can be explained when one considers the cause of the tarsal tunnel syndrome. Because tibial neuropathy can result from nerve compression or tension, the physical maneuver that exacerbates the causative factor reproduces symptoms. Thus, in a tibial nerve that is under tension, heel eversion reproduces symptoms, whereas heel inversion reduces nerve tension and relieves symptoms. Although heel inversion reduces the cross-
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sectional area of the tunnel, the nerve is able to accommodate the reduction in volume without any deleterious effects. In the case of tarsal tunnel syndrome that results from a compression, the nerve cannot accommodate any further reduction in tarsal tunnel cross-sectional area and so inversion of the heel reproduces symptoms.
Diagnosis Because the history and physical examination for tarsal tunnel syndrome may not be conclusive, investigations, such as electrodiagnostic studies and radiologic imaging, may aid in clarifying the diagnosis of tarsal tunnel syndrome.
Electrodiagnostic studies Electrodiagnostic studies measure nerve function and can be classified into motor, sensory, or mixed compound nerve tests. There is controversy about which test is the most sensitive and specific for diagnosis of tarsal tunnel syndrome [2,7,23,25,35,65,69,72]. Mixed motor and sensory action potentials are much larger than sensory potentials alone and more sensitive for detecting early change [73]. Galardi et al [23] studied the sensitivity and specificity of distal motor latencies, sensory conduction velocities, and mixed motor and sensory conduction velocities. They concluded that distal motor latencies were insensitive (21.5%) but that sensory conduction velocities were too sensitive (92.8% –100%); sensory conduction velocity was abnormal in 8% of normal controls who were tested. Mixed motor and sensory conduction velocities were abnormal in 85.7% of patients who had tarsal tunnel syndrome, but there were no abnormalities in asymptomatic limbs or normal controls [25]. Abnormal conduction velocities in sensory and mixed motor and sensory action potentials increases the sensitivity and specificity for the diagnosis of tarsal tunnel syndrome. Studies must include the tibial nerve proximal to the tarsal tunnel and the opposite leg so as to exclude double crush phenomenon and peripheral neuropathy as causes. The relevance of electrodiagnostic studies is controversial. Pfeiffer and Cracchiolo [27] reported no correlation between results of electrodiagnostic studies and clinical results. Cimino [16] calculated the false negative rate of electrodiagnostic studies to be at least 9.5% and stated that a negative test did not preclude the diagnosis. Mann and Baxter [8] recommended that tarsal tunnel syndrome be diagnosed only when the following triad exists: pain and paresthesia in the foot, positive Tinel’s sign, and positive electrodiagnostic studies. A suggested algorithm is one that considers Mann and Baxter’s three findings. If all three are present, the patient has tarsal tunnel syndrome. If only two findings are present, the patient probably has tarsal tunnel syndrome and should be followed carefully. If only one finding is present, the patient does not have tarsal tunnel syndrome and other diagnoses should be entertained.
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Radiologic investigations Radiologic investigations are important in defining the anatomy within the tarsal tunnel. Plain radiograph Plain radiograph examination of the foot identifies displaced or malunited fractures, accessory ossicles, or bony exostoses within the vicinity of the tarsal tunnel. Weight-bearing radiographs of the foot and ankle also are useful for determining the presence of a foot deformity. Venography Venography may be indicated in patients who have a positive cuff test [74]. MRI In the absence of a abnormality on plain radiographs, MRI is the most effective method for assessing the contents of the tarsal tunnel, the flexor retinaculum, and the branches of the tibial nerve [51,75 –77]. It can image the foot and ankle in all three orthogonal planes and allows one to define any lesion in terms of size, site origin, and relation to the tibial nerve [51,75 – 77]. In failed tarsal tunnel syndrome surgery, MRI allows one to define the tarsal tunnel when considering inadequate decompression [76]. In a study of 29 feet that had electrodiagnostically-proven tarsal tunnel syndrome, 88% had a lesion identified by MRI. The lesions included tenosynovitis, varicosities, masses, and scar tissue. MRI is recommended in children who tend to have neoplastic mass lesions [75].
Treatment and results The treatment of tarsal tunnel syndrome is classified into nonoperative and operative methods. Except in acute cases, operative treatment should not be considered until after an adequate trial of nonoperative therapy. Nonoperative treatment The nonoperative treatments that are recommended in tarsal tunnel syndrome are rest, immobilization, orthotics, oral nonsteroidal anti-inflammatory drugs (NSAIDs), local corticosteroid injections, physiotherapy, stockings, and weight loss [6– 8,10,12,19,28,33,34,42,52,53,55,56,59,78]. Immobilization and orthotics The immobilization methods include ankle-foot orthosis [7], and, occasionally, a walking cast [8,42,74]. Orthotics to maintain a neutral foot position are effective if the foot deformity is flexible [12,16,19,59]. In flexible valgus heel, medial longitudinal arch supports and medial heel wedges have been used with success [12,19]. In more severe deformities, University of California Biome-
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chanics Laboratory –type inserts, which hold the calcaneus in neutral alignment and force the abducted forefoot into neutral, can be used [79]. More control can be gained by supplementing with a polypropylene ankle foot orthosis. Lateral heel wedges effectively treat flexible varus heels, whereas medial arch supports aggravate symptoms and should be avoided [59]. In patients who have symptoms that are reproduced by dorsiflexion, a 1-inch heel lift helped by decreasing tension on the tibial nerve [50,62]. Anti-inflammatory medication Oral NSAIDs and local corticosteroid injections into the region may have a transient effect in many cases [6,7,12,27]. In inflammatory conditions where tenosynovitis is a factor, however, such as rheumatoid arthritis or ankylosing spondylitis, NSAIDs have proven to be effective treatments [10,27,50,52, 53,55,56]. Physiotherapy Physiotherapy to strengthen the intrinsic muscles of the feet—the flexor digitorum longus, flexor hallucis longus, and tibialis posterior—was recommended to help restore the medial longitudinal arch and to stabilize the foot in a neutral position [12,34,55,61]. In runners who had ‘‘jogger’s foot,’’ where a hyperpronated foot stretches the tibial nerve, retraining to toe-in slightly and strike the lateral aspect of the foot helped to decrease the deformity [61]. Other treatment In patients who have varices, stockings are used to decrease the amount of swelling in the leg and the amount of venous stasis present [8,19,34,42]. In obese patients, some investigators recommend weight loss [6,61].
Summary of non-operative treatment Although nonoperative therapy is the first line of treatment, patients should be warned that it is effective in the presence of specific etiologic factors that are amenable to therapy, such as flexible foot deformities, tenosynovitis, and inflammatory arthritis. Nonoperative treatments have no significant effects on space-occupying lesions within the tarsal tunnel [16,27,28]. In Cimino’s review [16], only 16% of patients were treated nonoperatively. Orthotic management was successful in 34% of patients, all of whom had flexible deformity. Spontaneous resolution or corticosteroid injection was successful in 24%. Although nonoperative therapy is the recommended initial treatment, many investigators believe that it provides transient relief and that surgery is the only effective treatment [6,28,31,38].
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Operative treatment When tarsal tunnel syndrome results from a space-occupying lesion, surgical treatment provides predictably good results [6,8,18,19,27,28,42,70]. Surgical treatment was described by Lam [30]; it consists of release of the flexor retinaculum; neurolysis of the medial and lateral plantar nerves as far distally as possible; and surgical treatment of any etiologic factors, such as repairing fractures to restore normal spatial arrangement, excising a mass lesion, or resecting synovium. The tibial nerve is exposed proximal to the flexor retinaculum through a curved medial incision that starts 10 cm proximal to the medial malleolus and 2 cm posterior to the margin of the tibia and extends toward the talonavicular joint. The flexor retinaculum is divided completely and the tibial nerve is mobilized along its course as far distally as possible. The medial and lateral plantar nerves must be decompressed adequately—at least 2 cm distally into the sole of the foot. The medial plantar nerve is followed distally as it passes in its fibrous tunnel inferior to the talonavicular joint. The lateral plantar nerve travels behind the abductor hallucis muscle; part of the origin of the abductor hallucis may have to be released to expose the nerve adequately. Postoperatively, the patient remains nonweight bearing for 3 weeks; thereafter, weight bearing is permitted as tolerated and active and passive range of motion is encouraged. Failure to recognize the proximal extent of the flexor retinaculum and to decompress the distal tarsal tunnel can result in failure of therapy [13,76]. In a review of the literature, 65% of patients required surgical treatment; 91% had good or improved results [16]. This corresponds with surgical results from the literature, which have 79% to 95% good results [2,6,7,30,31,38,59]. Surgical results were better when: (1) patients were younger [28], (2) surgery was performed early in the disease process before motor involvement [28,30], and (3) a localized lesion was identified [6,8,18,19,27,28,42,70,80]. Takakura et al [28] reported that coalition and tumors gave the best surgical results, whereas idiopathic causes and trauma were associated with the poorest results; hemorrhage associated with trauma was believed to produce adhesions within the tarsal tunnel. More recently, Sammarco and Chang [81] stated that even without a discrete lesion or with symptoms that had been present for more than a year, a predictable improvement could be gained after surgery. Considering the excellent results in the literature from operative treatment and the poor results from nonoperative treatment methods, many investigators have advocated surgical therapy for lasting results in tarsal tunnel syndrome [6,8, 19,38]. A recent study, however, cast doubt on the long-term effectiveness of surgery [27]. Only 44% of 30 patients benefited markedly from surgical treatment. This discrepancy can be explained by the use of more precise and stringent subjective questionnaires and a minimum follow-up of 24 months (average 31 months), which is considerably longer than many earlier studies [2,6,7, 30,38,59]. Pfeiffer and Cracchiolo noted that early results of surgery were encouraging but results deteriorated. They concluded that ‘‘unless there is an associated lesion near or within the tarsal tunnel preoperatively, decompression of
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the posterior tibial nerve should be considered with caution,’’ and that patients who had undergone previous surgery for pain in the foot, plantar fasciitis, or symptoms of systemic inflammatory disease should be managed conservatively. A recent study examined 60 patients with 68 operations; subjective and objective outcomes were examined after return-to-normal function. Although objectively there was 85% symptom relief, subjectively, only 51% of patients had symptom relief [82]. Further investigation with similar studies is required.
Summary Tarsal tunnel syndrome is an uncommon condition whose signs and symptoms are ill-defined, this has lead to under- and misdiagnosis of the disorder. A high degree of suspicion, combined with a thorough history and physical examination, is required to make the diagnosis. Investigations, such as electrodiagnostic studies and MRI, improve diagnostic accuracy. Most patients warrant initial nonoperative therapy. Operative treatment is indicated in those who have acute onset or a definite space-occupying lesion. Results have been reported as excellent after surgery, but recent work suggests that long-term outcomes may not be so favorable. The worst results of operative treatment are found in patients who have posttraumatic or idiopathic etiology. Operative treatment after tarsal tunnel decompression is warranted only in those patients in whom an inadequate release can be identified.
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