Tarsal Tunnel Syndrome Workup

• Electromyography (EMG) and nerve conduction velocity (NCV) studies may be a useful initial tool in evaluating suspected cases of tarsal tunnel syndrome and in confirming the presence of neuropathy. Additionally, the type of nerve fiber (sensory, motor, or both) and the pathophysiology (axonal vs demyelinating and symmetric vs asymmetric) can be differentiated with the information obtained from EMG and/or NCV. A physiatrist or neurologist who is experienced in extremity EMG and NCV studies can best perform these tests.

  • EMG studies may demonstrate prolonged posterior tibial distal nerve latency to the abductor hallucis or abductor digiti quinti muscles. This finding may also be accompanied by low motor amplitude or absent responses in either of these muscles. Early on, medial and/or lateral plantar sensory action potentials may be affected with prolonged latency, slowed velocity, and decreased amplitude. Sensory action potentials may be unobtainable in advanced cases of tarsal tunnel syndrome.
  • Needle examination of the abductor hallucis and/or abductor digiti quinti muscles may show denervation and active and/or chronic changes. To ensure that this finding is not an S1 root lesion, the posterior tibial muscles above the tarsal tunnel (posterior tibialis) or muscles other than the posterior tibial muscles (extensor digitorum brevis) should demonstrate sparing. The lumbosacral paraspinal muscles should be intact.
  • EMG and NCV testing values include the following:
    • Prolonged distal motor latency: Terminal latencies of the abductor digiti quinti muscle (lateral plantar nerve) longer than 7.0 ms are abnormal.
    • Terminal latencies of the abductor hallucis muscle (medial plantar nerve) longer than 6.2 ms are abnormal.
    • Fibrillations in the abductor hallucis muscle may be present.
  • Repeat EMG studies that are performed 6 months after surgery may aid in assessing the physiologic success of the decompression procedure in patients who had positive results. Decreases may be noted in the distal latencies.
  • Results of NCV studies may be normal in patients with small fiber neuropathies. Additionally, lower-extremity sensory responses may be absent in normal elderly patients. Therefore, electrodiagnostic testing should not be a substitute for a good clinical examination.
• Diabetes mellitus produces a distal, symmetric sensory and motor polyneuropathy. This is an axonal neuropathy due to degeneration of distal axons. Diabetes also produces a neuropathy due to microangiopathy, which results in a proximal, asymmetric mononeuropathy (primarily motor nerves). The initial evaluation should include urinalysis and tests of the fasting serum glucose level, hemoglobin A1C (HbA1C/HgA1C), blood urea nitrogen (BUN), creatinine, complete blood cell count (CBC), erythrocyte sedimentation rate (ESR), and vitamin B12 levels.
• The arthritis that is associated with Reiter syndrome typically affects the knees, ankles, and feet, causing pain and swelling; wrists, fingers, and other joints are less often affected. Patients with Reiter syndrome commonly develop inflammation where the tendon attaches to the bone, a condition called enthesopathy. Enthesopathy may result in heel pain and the shortening and thickening of fingers and toes. Some patients who are affected with Reiter syndrome also develop heel spurs that are associated with chronic or long-lasting foot pain.
• Men between the ages of 20 and 40 years are most likely to develop Reiter syndrome. It is the most common type of arthritis that affects young men; among men younger than 50 years, about 3.5 per 100,000 develop Reiter syndrome each year. Approximately 3% of all men with a sexually transmitted disease develop Reiter syndrome. Women can also develop this disorder, though less often than men, with features that are often milder and more subtle.

  • About 80% of affected patients are positive for human leukocyte antigen (HLA) - B27. Only 6% of people who do not have Reiter syndrome have the HLA-B27 gene.
  • In performing a rule-out workup of underlying systemic arthritic conditions, ESR, rheumatoid factor (RF), and antinuclear antibody (ANA) serology should be performed.
  • Typically, patients with rheumatic diseases, including Reiter syndrome, have an elevated ESR. However, in Reiter syndrome, results of RF and ANA testing are negative; therefore, HLA-B27 typing may be useful in differentiating this seronegative arthropathy from other arthritides.
• Generalized amyloidosis can cause a peripheral neuropathy due to pressure atrophy of nerve fibers. The central nervous system is not affected except in areas that lack a blood-brain barrier, such as the choroid plexus and pineal gland. Nerve biopsy is helpful in specific cases to diagnose leprosy, amyloid neuropathy, sarcoidosis, and leukodystrophies.

• Magnetic resonance imaging (MRI) and ultrasonography may be useful modalities in suspected cases of soft-tissue masses and other space-occupying lesions in the tarsal tunnel. Additionally, MRI is useful in assessing for flexor tenosynovitis and unossified subtalar joint coalitions.^[13]
• Plain radiography is useful in evaluating the patient's underlying foot structure, fractures, bony masses, osteophytes, and subtalar joint coalition.

• See Lab Studies and Imaging Studies

Regarding neuroma in continuity, in most cases, the nerve has an intact perineural sheath. This entity may result from chronic nerve compression and irritation, which causes nerve swelling. The proliferation of fibrous tissue causes nerve compression; therefore, this type of entity must be decompressed, and the fibrous tissue may need to be removed.

Ganglion cysts that cause compressive peripheral neuropathies are unusual, but when combined, they are not an uncommon etiology. The source and cause of ganglion cysts remain unsettled issues; one theory was fibrillar degeneration of collagen, with accumulation of intracellular and extracellular mucin. If encountered during surgery, these lesions need to be removed en toto as part of thorough nerve decompression.