Laryngospasm (LS) is a well-described, vagally-mediated reflex response of the larynx to noxious stimuli, with the afferent limb supplied by the superior laryngeal nerve and the efferent limb by the recurrent laryngeal nerve (RLN). It is believed that stimulation of taste bud—like supraglottic chemoreceptors are responsible for triggering the afferent limb of the reflex and that central connections in the brain stem (in the vagal nuclei) are responsible for triggering the efferent limb of the LS response. This leads to repetitive excitatory “after discharges” of the RLN manifesting as sustained tonic adduction of the vocal cords. Thus, the LS response can be recorded with electromyographic (EMG) electrodes placed into the thyroarytenoid muscle.
Clinically, LS is characterized by sudden-onset hyperadduction of the vocal cords with inspiratory stridor and airway obstruction; gastroesophageal reflux (GER) has been implicated as one of its causes. Reflux-induced LS is a distressing, potentially life-threatening condition that occurs in both adult and pediatric patients. Adult patients with GER-induced LS usually have paroxysmal stridor and choking episodes. In addition, GER has been implicated as a possible cause of sudden infant death syndrome (SIDS), perhaps by causing fatal LS.
In animal models, water, milk, weak acids, and other test substances instilled in the supraglottic larynx have been shown to cause LS and/or central apnea; however, the effects of experimental reflux (of acid and pepsin) as a cause of LS have not been previously investigated. In addition, on the basis of previous studies, some animal models appear to be more similar to human neuroanatomy than others; the canine model appears to be the most comparable in terms of vagally mediated laryngeal responses. The purpose of this study was to investigate the effects of experimental reflux on the LS response in adult dogs to determine whether the LS response is acid related (or pepsin related) and to ascertain whether the afferent limb of the LS response is triggered by supraglottic chemoreceptors.
Christopher J. Loughlin, MD; Jamie A. Koufman, MD; David B. Averill, PhD; Michelle M. Cummins, MD; Yong-Jae Kim, MD; John P. Little, MD; Inglis J. Miller, Jr., PhD; J. Wayne Meredith, MD