Letter to the Editor. Before surgical sural nerve neurolysis, study neighboring sensory nerves

TO THE EDITOR: We read with interest the article by Matsubara et al.¹ who reported on a 67-year-old male diagnosed with right sural nerve entrapment at the level behind the right lateral malleolus, confirmed by magnetic resonance imaging (MRI) and sensory nerve conduction studies (Matsubara M, Yagi K, Hemmi S, et al. Surgical treatment of sural nerve entrapment aided by imaging- and electrography-based diagnosis: illustrative case. J Neurosurg Case Lessons. 2023;5[24]:CASE2387). The patient underwent surgical neurolysis, which resulted in significant pain reduction over a follow-up period of 10 months.¹ The study is impressive but has limitations that should be discussed.

We disagree that fourth and fifth toe pain is associated with sural nerve lesion.¹ The pain modality in the fourth and fifth toes is usually conducted via the superficial peroneal nerve.² Therefore, we should know whether there was a slowing in conduction velocity or a reduction in sensory nerve action potential (SNAP) amplitude of the superficial peroneal nerve. In addition, the lateral sole is sensitively supplied by the lateral plantar nerve, and the heel is sensitively supplied by a sensory branch of the tibial nerve. Therefore, we should also know the results of conduction studies of the lateral plantar nerve. Against this background, the usefulness of surgical neurolysis is quite questionable and the reduction in pain could also be a spontaneous event.

A limitation of the study is that the results of nerve conduction studies performed on the index patient were not presented. Sural nerve conduction is usually measured by stimulation and recording proximal to the lateral malleolus and thus proximal to the entrapment site. How do the authors explain the decreased SNAP amplitude proximal to the entrapment site? Was there imaging evidence of anterograde axonal degeneration? Is it conceivable that not the entrapment but a proximal lesion at the level of the spinal cord, plexus, thigh, or lower extremity was responsible for the reduced SNAP amplitude?

There is a discrepancy between the imaging findings and the nerve conduction studies regarding the portion of the sural nerve proximal to the entrapment site. MRI shows no impairment, but nerve conduction reveals decreased SNAP. How can this discrepancy be explained?

Another limitation of the study is that nerve conduction studies were not repeated after surgery. As the clinical manifestations improved, it is expected that the SNAP amplitude would also increase again.

A third limitation is that alternative causes of foot pain have not been adequately ruled out. Of particular interest are the results of lumbar spine MRI, lumbosacral plexus MRI, and routine blood tests for detecting secondary causes of polyneuropathy. Has Morton’s neuralgia been ruled out? Have all the orthopedic causes of foot pain been adequately ruled out?

There is no mention of what medications were used before surgery and whether they were effective. We should know if the patient has benefited from nonsteroidal anti-inflammatory drugs (NSAIDs), gabapentin, pregabalin, or opioids?

The visual analog scale (VAS) usually rates pain as 1 to 10 and with no dimension. What do the authors mean with a value of 70 mm? Does this correspond to a VAS score of 7?

In summary, the interesting study has limitations that call the results and their interpretation into question. Addressing these issues would strengthen the conclusions and could improve the status of the study. Before heel and lateral foot pain can be traced back to entrapment of the sural nerve, differential causes of symptoms must be sufficiently ruled out. In addition, impairment of the sensory fibers of the superficial peroneal nerve, lateral plantar nerve, and tibial nerve must be ruled out before sural nerve entrapment can be held responsible for heel and lateral foot pain.