Neurophysiology of the Superior Laryngeal Nerve in an In Vivo Rat Model

Objective: The superior laryngeal nerve (SLN) is fundamental in laryngeal sensation, cough reflex, and pitch control. SLN injury has substantial consequences including altered sensation, aspiration, and dysphonia. To date, in vivo measurement of the SLN remains elusive. The purpose of this study was to assess the feasibility of recording motor and sensory evoked potentials in a rat SLN model.

Methods: Twenty-two rat hemi-laryngeal preparations (n = 11) were obtained from 4-month-old Sprague-Dawley rats and included in this study. Compound motor action potentials (CMAPs) and motor unit number estimation (MUNE) were calculated by stimulating the SLN at the point of medial extension near the carotid artery and by placing a recording electrode on the cricothyroid muscle. Sensory response was determined through stimulation of the SLN and laryngoscopic visualization of a laryngeal adductor reflex (LAR). SLN and cricothyroid muscle cross-sections were stained and histologic morphometrics were quantified.

Results: Laryngeal evoked potentials were successfully obtained in all trials. Mean CMAP latency and negative durations were 0.99 ± 0.57 ms and 1.49 ± 0.57 ms, respectively. The median MUNE was 2.06 (IQR 1.88, 3.51). LAR was induced with a mean intensity of 0.69 ± 0.20 mV. Mean axon count, myelin thickness, and g-ratio were 681 ± 192.2, 1.72 ± 0.26, and 0.45 ± 0.04, respectively.

Conclusions: This study demonstrates the feasibility of recording evoked response potentials following SLN stimulation. We hypothesize that this work will provide a tractable animal model to study changes in laryngeal sensation and cricothyroid motor function with aging, neurodegenerative disease, aspiration, or nerve injury.

Level of evidence: NA Laryngoscope, 134:1778-1784, 2024.