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letter
. 2025 Sep 2;10:348–349. doi: 10.1016/j.cnp.2025.08.005

Asymptomatic tarsal tunnel syndrome in rheumatoid Arthritis: An electrophysiological perspective with insights into clinical and laboratory correlates

Hosna Elshony a,b,⁎, Mohamed H Aly b, Abdelgaffar Mohammed b, Abdulrahman M Hassan c, Abdulrahman A Alshehri b, Mohamed Hedak b, Rakan Almuhanna b, Abdulaziz Al-Ghamdi b, Rasha Elsaadawy a
PMCID: PMC12450557  PMID: 40985008

Dear Editor,

We appreciate the authors’ interest in our study and the opportunity to clarify points raised in their letter. Their comments on the diagnostic terminology and methodological scope highlight important aspects of electrophysiological research in rheumatoid arthritis (RA)–related neuropathies.

With regard to terminology, we acknowledge that in its classical sense, tarsal tunnel syndrome (TTS) is a clinical diagnosis characterized by sensory disturbances in the distribution of the posterior tibial nerve or its branches, confirmed by physical examination and supported by electrodiagnostic studies. However, the phrase “subclinical TTS” has been used in the neurophysiology and rheumatology literature to describe objective electrophysiological abnormalities localized to the tarsal tunnel in patients without overt symptoms, particularly in systemic conditions such as diabetes mellitus, hypothyroidism, and RA (Ibrahim et al., 2019, Kalçık et al., 2021, Martinez-Lopez et al., 2023). Our use of this term followed that precedent, aiming to emphasize both the anatomical localization and the potential clinical trajectory of such findings. We agree that “tibial neuropathy at the tarsal tunnel” is an accurate descriptive alternative, but believe “subclinical TTS” conveys the early stage of a process that may progress to symptomatic entrapment, underscoring the importance of early recognition.

Regarding the absence of comparative nerve conduction studies of other peripheral nerves, our study was deliberately focused on the posterior tibial nerve and its branches, as our primary objective was to investigate the prevalence of localized entrapment at the tarsal tunnel in RA. To reduce the likelihood that the abnormalities represented a diffuse neuropathy, we applied strict exclusion criteria for common causes of generalized nerve involvement, including diabetes, thyroid dysfunction, vitamin B12 deficiency, chronic kidney disease, neurotoxic medication exposure, and significant lower limb deformities unrelated to RA. We also employed age-, sex-, and BMI-matched healthy controls and used laboratory-specific normative data to ensure accurate localization. While multi-nerve testing could provide additional information about systemic versus focal patterns, it was beyond our study’s original scope and resources. We agree with the correspondents that future multicentre studies should incorporate more extensive nerve conduction protocols to address this question.

We would also like to emphasise that our use of the term “subclinical” was intended precisely to avoid conflating electrophysiological abnormalities with a symptomatic syndrome. We did not recommend treatment based solely on nerve conduction study results. Rather, we suggested that such findings, when present in RA patients with high disease activity or joint deformities, may warrant closer clinical monitoring given the potential risk of progression. In our view, the identification of early, localized conduction changes in the posterior tibial nerve is clinically relevant, as timely recognition offers an opportunity for preventive strategies—mechanical, pharmacological, or surgical—before functional impairment occurs.

In conclusion, we welcome the discussion generated by our study and agree that precision in terminology and careful methodological design are essential in this area. Whether referred to as “subclinical TTS” or “asymptomatic tibial neuropathy at the tarsal tunnel,” the presence of localized conduction abnormalities in asymptomatic RA patients deserves attention, as it may inform future screening strategies aimed at preserving mobility and quality of life. We hope that this exchange encourages further research that combines comprehensive nerve conduction assessments with longitudinal follow-up to clarify the natural history and optimal management of these early neurophysiological changes.

1. Availability of data and material

Data available from correspondence author upon reasonable request.

Ethical statement

Written informed consent was obtained from the patient for publication of this case report and any accompanying images.

Funding sources

No funding from any governmental or nongovernmental sources.

Declaration of Competing Interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

References

  1. Ibrahim S., El-Sherif A.M., El-Kafrawy A., et al. Electrophysiological evaluation of tarsal tunnel syndrome in rheumatoid arthritis patients. Egypt Rheumatol. 2019;41(1):23–30. [Google Scholar]
  2. Kalçık Ü.M., Ardıçoğlu Ö., Pıhtılı Taş N., et al. Assessment of the frequency of tarsal tunnel syndrome in rheumatoid arthritis. Turk J Phys Med Rehab. 2021;67(4):421–427. doi: 10.5606/tftrd.2021.6797. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Martinez-Lopez J., Lopez-Mendez A., Garcia-Garcia M., et al. Synovial hypertrophy in the tarsal tunnel as a predictor of electrophysiological abnormalities in rheumatoid arthritis. Rheumatology. 2023;62(1):123–131. [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

Data available from correspondence author upon reasonable request.


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