Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2021
The short-latency R1 response of the electrical laryngeal adductor reflex contributes to airway protection by initiating glottic closure.
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Téllez Maria J, Sinclair Catherine F, Díaz-Baamonde Alba, Peláez-Cruz Roberto, Ulkatan Sedat
Аннотация
OBJECTIVE: The fundamental role of the short-latency (R1) laryngeal adductor reflex (LAR) response remains unclear with conflicting reports in the literature. This study's primary aim was to objectively determine whether the bilateral R1 response, which was elicited by electrical stimulation of the supraglottic mucosa, triggered bilateral glottis closure.
METHODS: Video recording of the LAR in a prospective case series of patients undergoing trans-oral rigid laryngoscopy. The LAR was elicited by electrical stimulation of supraglottic mucosa. The LAR R1 and long-latency (R2) responses in laryngeal adductor musculature were correlated with mechanical vocal fold (VF) adduction in a time-locked manner. A high-speed camera recording 1057 frames per second was used to determine where in the LAR contractile closure the electrical R1 component occurred.
RESULTS: Five patients were prospectively enrolled. The R1 response was present in all trials for all patients. The R2 response was recorded in four patients (80%). As assessed by the latency of the R1 response, electrical activation of the adductor muscles always preceded the mechanical onset of VF movement. VF adduction began near the middle of the R1 response in all trials for all patients. The R2 response of the LAR began after visible VF adduction for all patients.
CONCLUSIONS: This study provides the first objective evidence that the bilateral R1 response of the electrically elicited LAR is the electrical event that initiates reflex airway closure.
SIGNIFICANCE: These results suggest that under total intravenous anesthesia, the larynx preserves its capacity to elicit a LAR, thereby maintaining some protective functions that can prevent airway penetration.
METHODS: Video recording of the LAR in a prospective case series of patients undergoing trans-oral rigid laryngoscopy. The LAR was elicited by electrical stimulation of supraglottic mucosa. The LAR R1 and long-latency (R2) responses in laryngeal adductor musculature were correlated with mechanical vocal fold (VF) adduction in a time-locked manner. A high-speed camera recording 1057 frames per second was used to determine where in the LAR contractile closure the electrical R1 component occurred.
RESULTS: Five patients were prospectively enrolled. The R1 response was present in all trials for all patients. The R2 response was recorded in four patients (80%). As assessed by the latency of the R1 response, electrical activation of the adductor muscles always preceded the mechanical onset of VF movement. VF adduction began near the middle of the R1 response in all trials for all patients. The R2 response of the LAR began after visible VF adduction for all patients.
CONCLUSIONS: This study provides the first objective evidence that the bilateral R1 response of the electrically elicited LAR is the electrical event that initiates reflex airway closure.
SIGNIFICANCE: These results suggest that under total intravenous anesthesia, the larynx preserves its capacity to elicit a LAR, thereby maintaining some protective functions that can prevent airway penetration.