Altered laryngeal sensation: a potential cause of apnea of infancy

Ann Otol Rhinol Laryngol. 2005 Apr;114(4):258-63. doi: 10.1177/000348940511400402.

Abstract

Delayed maturation of respiratory control of breathing and the laryngeal adductor reflex (LAR) are commonly implicated in infant apnea. A swallow response occurs to remove the stimulus from the pharynx to prevent aspiration once the glottis reopens. Induction of apnea by poorly cleared endogenous upper airway secretions has been postulated to be a potential cause of infant apnea. Our purpose was to determine whether alteration in the LAR, an indicator of laryngeal sensation, and the presence of secretions influenced the responsiveness of the LAR in infants with apnea. The LAR was induced in 20 infants with apnea (median gestational age, 36.5 weeks) by application of air pulses of controlled duration (50 ms) and intensity (2.5 to 10 mm Hg) to the aryepiglottic fold. Twenty infants evaluated for upper respiratory tract anomalies were used as a comparison group (median gestational age, 39 weeks). The infants with apnea required higher-intensity stimuli (p < .001) to induce the LAR (6.2 +/- 1.6 mm Hg) than did the comparison group (4.3 +/- 1.0 mm Hg) and demonstrated poorer clearance of secretions (p < .001). These findings were significant even when we adjusted for postconceptional age at the time of the test (p = .007). The findings of this study suggest that decreased laryngeal sensitivity results in poor endogenous secretion clearance and that it may induce a prolonged glottic closure event to prevent aspiration. This closure may play a role in infant apnea.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Air Movements
  • Case-Control Studies
  • Female
  • Gestational Age
  • Humans
  • Infant
  • Laryngeal Mucosa / metabolism
  • Laryngeal Muscles / physiopathology*
  • Laryngoscopy
  • Male
  • Physical Stimulation
  • Reaction Time
  • Reflex, Abnormal / physiology*
  • Sensory Thresholds / physiology
  • Sleep Apnea Syndromes / physiopathology*