Tarsal Tunnel Syndrome
Introduction
Tarsal tunnel syndrome -- tarsal:
meaning the lower ankle area of the foot -- is a condition that usually affects
the medial (inside) aspect of the ankle. There are many structures that run
through this area, including tendons, veins, arteries and nerves. Tarsal Tunnel
Syndrome occurs when the posterior tibial nerve, as
it courses under the ligament at the ankle, becomes inflamed for a variety of
reasons, namely: excessive pronation, arthritic
problems such as rheumatoid arthritis, trauma, and even obesity.
The symptoms that are characteristic of this disease are persistent burning
pain, pain that radiates down to the toes and/or up to the lower leg, and pain
that is usually unremitting, in that is does not subside after weight has been
removed from the foot.
A nerve compression syndrome is the ìÖmechanical impingement of one or more
of the peripheral nerves about the foot and ankleî (Holmes, 1994, p.184).
Tarsal tunnel syndrome has been defined as an extrinsic or intrinsic
compression neuropathy of the posterior tibial nerve
or one of its branches (Frey and Kerr, 1993 and Bailie
and Kelikian, 1998). The condition was first
described by Keck and Lam in 1962 (As cited in Mahan, Rock and Hillstrom, 1996) and pertained to the entrapment within the
tarsal tunnel. The posterior tibial nerve becomes
impinged as it passes under the deep fascia of the leg and the abductor hallucis muscle (Frey and Kerr, 1993). Tarsal tunnel
syndrome is analogous to the carpal tunnel
syndrome seen in the wrist, however far less common (Laing,
1995). Mahan, Rock and Hillstrom (1996, p.84)
consider the tarsal tunnel syndrome in perspective to ìthe myriad of potential
etiologies and different diagnostic techniques, there is no clear decision
process that a clinician may use to guarantee an accurate diagnosis.
Furthermore, the specific etiology for a given patientís tarsal tunnel syndrome
may remain unknown and the treatment plan may
yield outcomes ranging from excellent to poorî. The following paper endeavours to present the current aetiologies,
diagnostic modalities and treatment regimes available to the podiatric
practitioner in the clinical management of the tarsal tunnel syndrome.
Overview
The flexor retinaculum
constitutes the roof of the tarsal tunnel and is formed by the deep fascia of
the leg and the deep transverse fascia (Richli,
Roger, Carrasco, Charnsangavej, Rosenthal and
Wallace, 1993). The proximal and inferior borders of the tunnel are
formed by inferior and superior margins of the flexor retinaculum
(Holmes, 1994). The floor of the tunnel is formed by the superior aspect of the
calcaneus, the medial wall of the talus, and the
distal-medial aspect of the tibia (Holmes, 1994). The remaining fibro-osseus canal is termed the Richetís
or the tibiocalcaneal
tunnel (Holmes, 1994). The tendons of the flexor hallucis
longus muscle, flexor digitorum
longus muscle, tibialis
posterior muscle, the posterior tibial nerve and the
posterior tibial artery pass through the tarsal tunnel
Table 1: Posterior Tibial Nerve Branches and
Their Innervation.
|
Branch |
Innervation |
|
|
|
|
Calcaneal |
medial and posterior aspects of the heel |
|
|
|
|
Medial Plantar |
cutaneous branches to plantar medial aspect foot |
|
|
motor branches to abductor hallucis muscle and flexor digitorum brevis muscle |
|
|
branches to talonavicular joint and calcaneonavicular joint |
|
|
|
|
Lateral Plantar |
motor branches to abductor digit quinti, quadratus plantae |
|
|
cutaneous nerve to the 5th digit |
|
|
4th common digital nerve |
|
|
motor branches to lumbricals, 2nd,3rd,4th interossei |
|
|
branches to transverse head adductor hallucis and muscles of 1st interosseous space |
There are an array of aetiologies that have been associated with the tarsal tunnel syndrome, resulting in the constriction of the posterior tibial nerve or one of its branches within the tarsal canal (Steinbock, 1990). Space occupying lesions as a causative factor of tarsal tunnel syndrome are well documented in the literature. Frey and Kerr (1993) suggest these lesions may be the result of post-traumatic, neoplastic or inflammatory factors. Variscosities, tenosynovitis, cysts and neurilemmoma are examples of space occupying lesions that are frequently mentioned in the literature (Boc and Hatef, 1995 and Mahan, Rock and Hillstrom, 1996). Boc and Hatef (1995) consider lipomas and neurofibromas to be rare examples of space occupying lesions producing the tarsal tunnel syndrome. Jaffe, Wade, Chivers and Siegal (1995) alert practitioners to the notion that although malignant soft tissue tumours of the foot are rare, they can exist. Jaffe et al.(1995) report on an unusual case where a woman coincidentally sustained multiple ant bites to the medial aspect of her foot parallel to the development of her tarsal tunnel symptoms. The resulting soft tissue swelling was considered a secondary response to the initial trauma, however further diagnostic imaging revealed the rare extraskeletal osteosarcoma. In 1993 Frey, Naritoku, Kerr and Halikus reported an unusual space occupying lesion case where a woman underwent bilateral calf liquid silicone injections for cosmetic enlargement purposes. The silicone migrated from the flexor hallucis longus tendon to eventuate in the tarsal tunnel region leading to the compression of the posterior tibial nerve and the resulting tarsal tunnel symptomatology.
Post-traumatic factors include bone fractures resulting in tibial nerve compression (Stefko and Lauerman, 1994). Holmes (1994, p.189) states ìÖhalf of the patients who present with tarsal tunnel syndrome relate a history of a previous sprain, ankle fracture, crush injury, flatfoot or fracture dislocation about the foot or ankleî. Myerson and Berger (1995) report on a case where a nonunion fracture of the sustentaculum tali migrated superiorly to cause tibial nerve impingement. Other fracture sites associated with tarsal tunnel symptomatology documented include; malleolar, calcaneal and the medial tubercle of the posterior process of the talus (Stefko and Lauerman, 1994).
Sammarco and Conti (1994) report on hypertrophic or accessory muscles that are positioned within the tarsal tunnel and result in the compression of the tibial nerve. These muscles include the abductor hallucis muscle, the flexor digitorum longus muscle and the tibiocalcaneus internus muscle. Sammarco and Conti (1994) conclude that the anomalous muscle may not necessarily be the underlying causative factor of the syndrome due to asymptomatic patients possessing anomalous muscles in the tarsal tunnel.
Recent studies have involved the use of animal models and cadaveric specimens to investigate tibial nerve tension as a potential causative factor. Daniels, Lau and Hearn (1998) investigated this phenomenon and concluded that tibial nerve tension increases within a surgically created cadaveric pes planus foot. Flanigan, Cassell and Saltzman (1997) investigated the vascular supply of the nerves in the tarsal tunnel and believe studies suggest the lateral plantar nerve is more commonly symptomatic as it is subjected to a greater tension than the medial plantar nerve. The increased tension within the nerve is proposed to interfere with neural transmission due to the diminishing intrinsic vascular supply (Flanigan, Cassell and Saltzman, 1997).
Many authors conclude that the underlying
causative factor of tarsal tunnel syndrome is often idiopathic (Bailie and Kelikian, 1998 and Stefko, and Lauerman, 1994).
An array of symptoms described as insidious in onset (Sammarco
and Conti, 1994) have been documented, these include; longitudinal arch pain,
plantar anaesthesia or paraesthesia
(Sammarco and Conti, 1994) or a sharp electric shock
type of pain (Mahan, Rock and Hillstrom,
1996). The pain may radiate distally from the ball of the foot to
the medial-posterior aspect of the leg (Sammarco and
Conti, 1994) or may be localised to the
plantar-medial aspect of the heel (Frey and Kerr, 1993). The pain may be present at rest but often the patient describes a
pain that exacerbates with activity (Belding, 1993) or post
prolonged ambulation (Boc and Hatef,
1995). Mann (1993) as cited in Laing
(1995) report night pain and proximal radiation of pain into the calf region (Valleix phenomenon).
Objective Diagnosis
The most widely recognised clinical sign prevalent in the literature is the positive Tinelís sign (Frey and Kerr, 1993; Frey et al., 1993, and Mahan, Rock and Hillstrom, 1996). The Tinelís sign is defined as ìa tingling sensation in the distribution of the posterior tibial nerve that is elicited by gentle localised percussion over the area of the nerve entrapmentî (Frey and Kerr, 1993, p.159). The Valleix sign is an alternate neurological test that involves palpation of the posterior tibial nerve that elicits pain directly, or if percussed refers pain proximally into the leg (Mahan, Rock and Hillstrom, 1996).
Other clinical signs the podiatric practitioner should be attentive to are; decreased pedal plantar sensation, weak intrinsic muscles, ìfullness of the longitudinal archî and swelling in the tarsal tunnel region (Sammmarco and Conti, 1994, p. 1308). Dependent on the aetiology, several cases report a palpable mass in the medial malleolar region (Boc and Hatef, 1995; Frey et al., 1993 and Myerson and Berger, 1995). Mahn, Rock and Hillstrom (1996) cite the tourniquet test performed by Mandel which elicits pain within five minutes upon inflation of a pneumatic cuff (from 30mm to 60mm of mercury pressure) superior to the ankle joint which Mandel proposes to be indicative of tarsal tunnel syndrome due to the presence of variscosities.
Electrodiagnostic studies have been commonly employed to identify tarsal tunnel syndrome (Frey and Kerr, 1993; Pfeiffer and Cracchiolo, 1994; Sammarco, Chalk and Feibel, 1993). Nerve conduction studies can examine ìthe latency, amplitude, and velocity of the posterior tibial nerve and associated plantar branchesî (Mahan, Rock and Hillstrom, 1996, p. 83). There are three parameters of electrodiagnostic studies that Holmes (1994) recommends need to be evaluated in the diagnosis of the tarsal tunnel syndrome, these include;
… I posterior tibial nerve conduction velocity
… II terminal latency of the medial plantar nerve to abductor hallucis muscle (>6.2msec)
… III terminal latency of the lateral plantar nerve to the abductor digiti quinti (>7msec)
Holmes (1994, p.189) suggests that if parameters II and III are met in addition to ìthe difference in the terminal latency of the medial and lateral plantar nerves should be greater than 1msec î then one may confirm the tarsal tunnel diagnosis. It is vital to note that many authors suggest electrodiagnostic studies are not a means of absolute diagnostic measure as it is possible to have tarsal tunnel syndrome in the absence of motor and sensory nerve deficiencies (Frey and Kerr, 1993; Mahan,Rock and Hillstrom, 1996, and Steinbock, 1990).
Radiography, computed tomography and magnetic
resonance imaging have been successfully used to determine any bony or
soft tissue etiologies for tarsal tunnel syndrome
A posterior tibial nerve block with local anaesthetic may be employed as a diagnostic tool to assess tarsal tunnel symptomatology relief upon injection (Mahan, Rock and Hillstrom, 1996).
Carrel, Davidson and Goldstein (1994) report on secondary signs that aid
clinical diagnosis that are consistent with prolonged cases of tarsal tunnel
syndromes which include; muscle atrophy supplied by the motor portion of the
affected nerve and cutaneous sensory changes supplied
by the sensory portion of the affected nerve.
Mahan, Rock and Hillstrom (1996) believe gaining a definitive diagnosis of tarsal tunnel syndrome is difficult, due to the complexities of the tarsal tunnel anatomy. The podiatric practitioner must be aware of the multitude of conditions with similar presenting symptoms to the tarsal tunnel syndrome
Table 3: Differential Diagnoses of the Tarsal Tunnel Syndrome.
|
Radiculopathy |
Drug reaction |
|
Neuropathy |
Diabetes mellitus |
|
Flexor tenosynovitis |
Gout |
|
Neuroma |
Peripheral vascular disease |
|
Plantar fasciatis |
Reflex sympathetic dystrophy |
|
Heel spur syndrome |
Lupus |
|
Sciatica |
Spondylitis |
|
Neuritis |
Prolapsed metatarsal heads |
|
Metatarsalgia |
Plantar callosities |
|
Herniated disc |
Intractable plantar keratoses |
|
Plantar fibromatosis |
Rheumatoid arthritis |
|
Sub-acute degeneration of the spinal cord |
Sinus tarsi syndrome |
The podiatric practitioner may implement conservative measures in the initial treatment stages of a suspect tarsal tunnel syndrome case, and later seek referral for surgical intervention if symptoms persist. The timeline of the initial conservative treatment plan varies considerably in the literature. The documented duration of conservative treatment failure ranges from six weeks (Holmes, 1994) to six months (Bailie and Kelikian, 1998) before surgical intervention is advocated. Bailie and Kelikian, (1998, p.65) comment on those authors that argue that conservative treatment is often ìÖmore warrantedî due to the limited success rates seen with surgical management. Non surgical treatment includes; orthotic therapy, physical therapy modalities, non steroidal anti-inflammatories and corticosteroid injections (Bailie and Kelikian, 1998). Holmes (1994) suggests a trial period of reduction in activity in conjunction with casting and splinting may be beneficial. Holmes (1994, p.190) suggests the period of conservative treatment allows the practitioner to observe the patients response to alternative conservative treatments, whilst employing the entire spectrum of diagnostic modalities available but ultimately enables the patient to use the time ìÖ to gain a full appreciation of the complex nature of this syndromeî.
Mahan, Rock and Hillstrom (1996, p.84) report on the three most common types of surgical procedures performed. The first is the surgical incision and release of the flexor retinaculum. The second is the release of the abductor fascia in the opening of the abductor hallucis muscle (the region where the posterior tibial nerves and vessels enter the plantar aspect of the foot). The third is the release of the posterior tibial nerve and/or its branches from ìsurrounding entrapmentsî (eg, variscosities). Alternative documented procedures include; ìÖexcision of bony or soft tissue masses, epineural release, and excision of the posterior tibial nerve with or without the associated plantar branchesî (Mahan, Rock and Hillstrom, 1996, p.84).
Mahan, Rock and Hillstrom (1996) conducted a retrospective study and documented 71.7% of the patients studied demonstrated at least a moderate improvement in symptoms following surgical intervention. Pfieffer and Cracchiolo (1994) reported only 44% of their patients had a an excellent or good result following surgical intervention. Pfieffer and Cracchiolo (1994) studied thirty two patients over an average duration of thirty-one months and conclude in advocating the avoidance of surgical intervention in the exception of a diagnosed space occupying lesion in or near the tarsal tunnel. Novotny, Kay and Parker (1996, p.641) attribute the failure of surgical intervention to weight gain, pronator deformities, ìÖincorrect initial diagnosis, incomplete release of retinaculum at surgery, nerve entrapment elsewhere or postoperative scarringî. Lau and Daniels (1998) propose a proportion of those failures could be accounted to a further increase in tibial nerve tension following surgical intervention involving tarsal tunnel release in the pes planus foot type, as seen in their in vitro cadaveric study.
There is little evidence in the literature of the clinical outcomes
following revision or re-release of the tibial nerve
following recurrent tarsal tunnel syndrome post surgical intervention (Skalley, Schon, Hinton and
Myerson 1994). Mahan, Rock and Hillstrom (1996, p.87)
suggest ìÖit is a difficult condition to manage successfully. It is unknown why
some patients develop recurrence of tarsal tunnel syndrome after surgical
releaseî. Novotny, Kay and Parker (1996) have attempted to address this
issue by incorporating a radial forearm
free flap (graft) in addition to the re-release of the retinaculum,
and the excision of evident scar tissue which they propose appears to limit
further scar tissue formation which in turn predisposes the tarsal tunnel
syndrome reoccurrence. ìThe posterior tibial nerve
was covered by a soft, pliable radial forearm flap. The radial artery and venae comitantes were anastomosed end
to side to the posterior tibial artery and venae comitantesî (Novotny, Kay
and Parker 1996, p.642). Campbell, Schon and Burkhardt (1998) have recently
reported a similar surgical technique that involves autogenous saphenous vein graft
wrapping of the tibial nerve which they propose
appears to show potential success in preventing external scar formation.