@article{39f9d9c91a6d41f5a6a50a297d937dfc,
title = "Compound motor action potential duration and latency are markers of recurrent laryngeal nerve injury",
abstract = "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. Level of Evidence: NA. Laryngoscope, 127:1855–1860, 2017.",
keywords = "CMAP duration, CMAP latency, Recurrent laryngeal nerve, vocal fold paralysis",
author = "Bhatt, {Neel K.} and Park, {Andrea M.} and Al-Lozi, {Mohammad T.} and Gale, {Derrick C.} and Paniello, {Randal C.}",
note = "Funding Information: Twelve canine hemilaryngeal preparations were used over the course of this study. The effect size, correlation, and variability were not known, preventing sample size calculation a priori. This study utilized socialized, purpose-bred, adult mongrel canines between 20 and 25 kg in weight. The animals were maintained in a facility approved by the American Association for Accreditation of Laboratory Animal Care. Only female canines were used. The National Institutes of Health (NIH) guidelines for animal care were strictly followed. This study was performed in accordance with the Public Health Service Policy on Humane Care and Use of Laboratory Animals, the NIH Guide for the Care and Use of Laboratory Animals, and the Animal Welfare Act (7 U.S.C. et seq.). The animal use protocol was approved by the Institutional Animal Care and Use Committees of Washington University School of Medicine. CMAP measurements were obtained at baseline and 6 months following injury. The CMAP data were computed using Nicolet Viking electromyography software and machine (Natus Medical Inc., Pleasanton, CA). Stimulation of the RLN in each hemilaryngeal preparation was achieved by placing a Harvard stimulating electrode onto the nerve 8 cm inferior to the cricothyroid joint. The active recording needle electrode was placed transcutaneously into the thyroarytenoid muscle. The reference electrode was placed into the dermis of the anterior neck, just superior to the larynx. The ground electrode was placed into the auricular skin. An initial voltage of 15 V was used to maximally stimulate the nerve. The stimulating voltage was decreased incrementally to the lowest possible voltage as to not cause diminution of the CMAP amplitude. CMAP measurements, including duration and latency, were collected. The software calculated the CMAP duration as the time interval between the first negative wave deflection and the return of the curve to 0 mV. The onset latency was generated from the time difference between the nerve stimulus and the first wave deflection. The canine body temperature was maintained above 36.0?C. General anesthesia was induced using intravenous thiopental sodium, and 2% isoflurane inhalant was used to maintain adequate anesthesia. A permanent tracheostomy was established. In all canine hemilaryngeal preparations, the preinjury CMAP was measured. Next, the RLN was injured by either stretch injury (group A) or complete transection and repair (group B). The type of injury and right versus left side were chosen randomly. The effectiveness of this randomization was not performed. Group A: Stretch Injury (n = 5). The RLN stretch injury was performed approximately 4 cm inferior to the cricothyroid joint. The stretch injury was accomplished by placing two 9-0 nylon epineural sutures on opposite sides of the injury site. As the sutures were pulled in opposite direction, the CMAP amplitude was lost. The CMAP amplitude was confirmed to be 0 mV following injury. Group B: Transection injury and repair (n = 7). The RLN was transected with straight microsurgical scissors approximately 4 cm inferior to the cricothyroid joint. Using an operating microscope, three to four interrupted 9-0 nylon sutures were used to immediately repair the transection. Six months following RLN injury, an awake, infraglottic exam through the tracheostomy was performed and recorded to assess the degree of spontaneous vocal fold motion recovery. The vocal fold motion was rated (Table). Given the lack of any well-known rating scale for vocal fold motion, the investigators developed this rating scale. Anesthesia was administered and the RLN was carefully dissected. CMAP measurements were performed, and the canine was sacrificed. The assessment of vocal fold movement was performed in a blinded fashion from the infraglottic video recording. The first author, who has experience rating canine vocal fold motion from previous studies, rated the vocal fold motion without knowledge of the type of injury administered to the RLN. Mean and standard deviation were used to describe the distribution of CMAP values, including amplitude, duration, and onset latency. Two-tailed, paired t test was used to calculate mean differences, confidence intervals (CI), and P values between the baseline and recovery data. Mean difference and 95% CI around it were used to report effect size. Receiver operative characteristic binary logistic regression was used to determine the AUC and discrimination for each CMAP measure (Microsoft Excel 2010, Redmond, WA). The baseline measurements (CMAP duration and latency) were compared to the 6-month CMAP measurements for both stretch and transection/repair injuries. In general, two sets of data that can be separated by a diagnostic test threshold will yield a higher sensitivity, specificity, and AUC. A diagnostic test with 100% sensitivity and 100% specificity would generate perfect discrimination and an AUC equal to 1. In this study, the AUC represented the ability for CMAP duration and CMAP latency to correctly classify the normal and abnormal values. To assess the impact of RLN injury on CMAP duration and latency, regardless of the specific type of mechanism, the stretch and transection/repair groups were pooled for post hoc analysis. The purpose of this analysis was to determine if CMAP latency and/or duration could be a useful diagnostic test to differentiation between preinjury and postinjury values. AUC CIs were calculated using Hanley and McNeil derivation of standard error. Sensitivity and specificity were calculated using binomial distributions. Publisher Copyright: {\textcopyright} 2017 The American Laryngological, Rhinological and Otological Society, Inc.",
year = "2017",
month = aug,
doi = "10.1002/lary.26531",
language = "English",
volume = "127",
pages = "1855--1860",
journal = "Laryngoscope",
issn = "0023-852X",
number = "8",
}