Effect of hyperthermia on the laryngeal closure reflex. Implications in the sudden infant death syndrome.

Abstract

A recent study with dogs has defined an age-related period of transient hyperexcitability in the laryngeal adductor neurons. This observation suggests that age-related neurologic instability of laryngeal mechanisms and abnormal laryngeal closure may be a cause of transient upper airway obstruction, inducing potentially fatal central apnea that could result in the sudden infant death syndrome. Since hyperthermia has been implicated as a cofactor in sudden and unexpected infant death, its effect on laryngeal excitability requires clarification. This investigation has found that both the latency and threshold of the laryngeal adductor reflex decreases during hyperthermia. Thus, hyperthermia effectively enhances this reflex during its age-related period of hyperexcitability, and is capable of triggering upper airway-induced central apnea of sufficient severity to result in death. The effect of temperature on latency is attributed to changes in axonal conduction and synaptic transmission velocities. Temperature-dependent changes in synaptic transmission are hypothesized as the cause of the observed threshold changes.