By definition, tarsal tunnel syndrome is extrinsic, intrinsic, or a combination compression of the tibial nerve that presents in the lower extremity tarsal tunnel. Within the literature, there are results ranging from 44% to 95% success rates after a primary neurolysis of the tibial nerve at the level of the tarsal tunnel.1 Success rates are even less promising for patients who undergo revisional procedures. After a failed tarsal tunnel procedure, it is crucial to determine why the primary surgery failed and subsequently treat the correct underlying cause. In this chapter, the authors discuss how to identify tibial nerve injuries, determine the correct etiology for tarsal tunnel syndrome, and evaluate clinically and discuss revisional tarsal tunnel and tibial nerve surgical procedures.
The Tibial Nerve and Injuries
The Tibial Nerve
The tibial nerve originates from the lumbar and sacral plexus and is a continuation from the sciatic nerve. It contains fibers from L4, L5, S1, S2, and S3, providing both motor and sensory function to the lower extremity. The nerve provides motor function to the posterior muscle group of the lower extremity and sensory function to the posterior, medial, and lateral plantar regions of the leg and foot. Anatomically, the tibial nerve crosses the popliteal fossa and travels between the medial and lateral heads of the gastrocnemius muscle. Moving distally, the tibial nerve crosses below the upper level of the fibrous arch of the soleus muscle. Descending toward the ankle, the tibial nerve travels beneath the flexor retinaculum and enters the tarsal tunnel at the level of the medial malleolus. The distal tibial nerve then divides into 4 terminal branches. The medial and lateral calcaneal nerves are purely sensory and supply sensation to the heel of the foot. The medial and lateral plantar nerves contain both motor and sensory fibers.2 The site of division is variable, particularly for the calcaneal nerve, and can occasionally occur proximally or distally to the tarsal tunnel. Studies have shown that the medial and lateral plantar nerves can branch 5% to 7% of the time above the level of the tarsal tunnel. The medial and lateral plantar nerves enter the plantar foot by passing deep to the abductor hallucis muscle below the level of the tarsal tunnel. The calcaneal nerve branches 35% of the time above the level of the tarsal tunnel, 34% of the time within the tunnel, and 16% to 25% of time from the lateral plantar nerve.3–5 It is important to consider all variations of the tibial nerve.
Seddon and Sunderland are the commonly utilized classification for nerve injuries. It is essential to understand what degree of nerve injury is present in a patient prior to surgical intervention.6–8
Neuropraxia is the result of pressure, compressive trauma, entrapment, or contusion. The nerve conduction study will show decreased nerve conduction velocity and normal amplitudes past the zone of injury. The myelin is damaged, but axons are intact.
Axonotmesis is usually caused by traction injuries as seen in severe joint dislocations and intraneural neuromas. In a second-degree injury there is axonal discontinuity and Wallerian degeneration. The endoneurium, perineurium, and epineurium remain intact, but the axons are damaged. The nerve conduction study shows decreased nerve conduction velocity and absent amplitude.
A third-degree injury includes second-degree injury plus endoneurium disruption.
Neurotmesis is associated with fractures, crush traumatic injuries, and surgical trauma when the nerve is completely severed. This forms an end neuroma. The nerve conduction study shows total absence of nerve conduction velocities and amplitude. It is a total disruption of the nerve.8
Etiology of Recurrent Tarsal Tunnel Syndrome
There are 5 major etiologies that patients with recurrent tarsal tunnel symptoms fall under: incorrect diagnosis, an incomplete neurolysis or decompression, adhesive neuritis, intraneural damage, and double crush syndromes.1,9
Incorrect Initial Diagnosis
After a failed tarsal tunnel surgery, it is possible that initially the wrong diagnosis was made. Differential diagnosis of tarsal tunnel syndrome includes, but is not limited to, space-occupying lesions, underlying mechanical components, posterior tibial tendon dysfunction, hypertrophic or accessory muscles, and proliferative synovitis.1
Tarsal tunnel syndrome can be caused by varicose vascular structures, and patients who have this syndrome may show characteristic symptoms. If varicose veins are in the tarsal tunnel and if a foot deformity is present, a diagnosis of tarsal tunnel syndrome due to varicose vascular structures compression should be considered.10
Kumai et al. reported that patients suddenly feel foot pain whenever they soak a foot in hot water. This specific symptom occurs because of dilatation of the varicose vascular structures in the tarsal tunnel.11
Tarsal tunnel ganglia arise from the adjacent joints or tendon sheaths and compress the tibial nerve. Ganglia are the cause of tarsal tunnel syndrome in up to 8% of cases.12,13
A lipoma is a benign tumor composed of fatty tissue.
Schwannomas are rare, benign tumors originating in the Schwann cells of the peripheral nervous system. Although presentation is rare in the foot and ankle, the posterior tibial nerve is the most common nerve affected.14 Plexiform neurofibromas are rare in the foot and ankle but have been reported. This benign nerve tumor arises as a diffuse mass from the nerve trunk and causes overgrowth of cutis and subcutis structures.15
Hypertrophic or Accessory Muscles
Hypertrophy of the abductor hallucis muscle is a rare condition but is present several times within the literature. Although the accessory soleus resides outside the tarsal tunnel, it has been implicated in tarsal tunnel syndrome, likely related to extrinsic compression.16
Inflammation of the synovial membrane, or proliferative synovitis, can cause compression of the tibial nerve.1
Underlying Mechanical Component
Underlying rearfoot and ankle deformities can potentiate tarsal tunnel syndrome. A hindfoot valgus deformity may potentiate the symptoms of tarsal tunnel syndrome because the deformity may increase tension owing to an increase in eversion and dorsiflexion.1,17 It is therefore on high suspicion in the patient with significant flatfoot.
External scarring around the previously released nerve can limit the gliding of the nerve, which leads to neuritic pain and recurrent entrapment. Adhesive neuritis can occur secondary to postoperative hemorrhage and hematoma formation, infection, prolonged swelling, delayed wound healing, and hypertrophic and keloid scarring. Patient noncompliance can also contribute to adhesive neuritis.1,9
Nerve “tethering” in the surgical scar is a main cause of perineural fibrosis pain; it reduces nerve gliding, which is necessary for nerve function, and interferes with intraneural microcirculation leading to neural ischemia and degeneration. These damaging conditions lead to further compression, neurogenic pain, and possible neuroma formation.21–25
A nerve with intraneural damage, or axonal disruption, must be identified and areas of damage treated accordingly. Intraneural damage can result from traction, crush injury, ischemia, systemic disease, or biomechanical and pharmacologic factors (Table 20.1).1,17
Mechanism of Injury and Injury Examples That Can Lead to Intraneural Damage
Mechanism of Injury
Ankle sprain, fracture, and dislocation/subluxation
Can occur from extrinsic compression or vascular disease
Double crush syndromes, diabetes mellitus
Changes to tarsal tunnel volume due to hindfoot position
Double crush syndrome can occur when there is a proximal and a distal nerve entrapment, whether by neuronal injury, compression, tension, or systemic disease.1 With double crush syndrome, each site of compression may not individually cause neuralgia, but the 2 sites of compression or the “double crush” together produce symptoms. Examples of double crush syndromes are radiculopathy, lumbosacral plexopathy, higher levels of compression in lower extremity such as at soleal sling, and systemic diseases (diabetes mellitus, hypothyroidism, multiple sclerosis, human immunodeficiency virus, Lyme disease, etc).1,9
History, Physical Examination, and Diagnostics
It can be overwhelming treating a patient with tibial nerve palsy, or recurrent symptoms, after a failed tarsal tunnel surgery. A patient with a history of failed tarsal tunnel surgery presents in 1 of 3 ways: no improvement after surgery, partial improvement, or temporary relief with recurrence of symptoms. Determining the initial and current presentation of the patient is the first step in treating the patient correctly. Once the surgeon understands the underlying etiology of the failed tarsal tunnel surgery and how patients present themselves, we can correlate these together to form the correct diagnosis.1,9 Below is a chart with patient presentation and which etiology you may expect (Table 20.2).1,9 When performing revisional procedures, the surgeon must take into account the “zone of injury,” or the area where the soft tissue is damaged. This can be divided into 2 categories: nonreconstructable and reconstructable (Table 20.3 and Figure 20.2).
Description of Reconstructable and Nonreconstructable Zone of Injury
Reconstructable Zone of Injury
Non-reconstructable Zone of Injury
Adequate blood flow
Poor blood flow
Vascularized nerve bed
Devascularized nerve bed
Adequate skin tissue envelope
Poor skin tissue envelope
History and Physical Examination
The history of the nature and quality of pain should be the first line of questions followed by the onset and progression. History of presentation is very important in the diagnosis of tibial nerve entrapment, or injury, and the literature shows that 43% of patients who have tibial nerve palsy have a history of trauma including events such as ankle sprains.5 Physical examination should include a dermatological, vascular, and musculoskeletal examination. Musculoskeletal examination is essential to determine if motor function has been affected and for biomechanical evaluation. A thorough neurological examination including Semmes-Weinstein monofilament, 2-point discrimination, sharp-dull sensation, presence of Tinel sign, and point of maximum tenderness should be performed.