4.5 Article

Compound Motor Action Potential Duration and Latency Are Markers of Recurrent Laryngeal Nerve Injury

期刊

LARYNGOSCOPE
卷 127, 期 8, 页码 1855-1860

出版社

WILEY
DOI: 10.1002/lary.26531

关键词

Recurrent laryngeal nerve; CMAP duration; CMAP latency; vocal fold paralysis

资金

  1. National Institutes of Health [R01 DC010884, T32 DC000022]

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Objective: Compound motor action potential (CMAP) can quantitatively evaluate innervation following injury to the recurrent laryngeal nerve (RLN) in canines. CMAP duration (the total time of CMAP) and latency (the time between the nerve impulse and the onset of action potentials) have not been assessed following RLN injury. Study Design: Animal study. Methods: Twelve canine hemilaryngeal preparations were investigated. Baseline CMAP duration and latency were derived. Group A (n = 5) underwent RLN stretch injury, and group B (n = 7) underwent RLN transection/repair. The change in CMAP duration and latency was assessed between the baseline and 6-month measurements using receiver operator characteristic (ROC) curves for each group individually and combined. Results: Six months following injury, transection/repair injuries had the most significant increase in CMAP duration (2.8 +/- 0.6 ms vs. 4.2 +/- 0.8 ms, difference 1.4 ms 95% confidence interval [CI]: 0.43 to 2.40) and latency (2.6 +/- 0.5 ms vs. 5.6 +/- 1.5 ms, difference 3.0 ms 95% CI: 1.65 to 4.38). Stretch injuries also caused an increase in CMAP duration (2.3 +/- 0.8 ms vs. 3.0 +/- 0.6 ms, difference 0.7 ms 95% CI: -0.49 to 1.77) and latency (2.5 +/- 0.8 ms vs. 4.7 +/- 1.5 ms, difference 2.3 95% CI: 0.76 to 3.80). Using ROC curves, CMAP duration and latency differentiated between the baseline control and RLN injury at 6 months (area under the curve = 0.78 and 0.98, respectively). Conclusion: CMAP duration and latency are both quantitative measures that may have clinical utility as markers of RLN injury. CMAP latency had superior discrimination between injured and uninjured RLNs. Increased CMAP duration and latency may be explained by incomplete myelination and focal conduction block.

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