Upper airway sensory function in children with obstructive sleep apnea syndrome

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Drug-Induced Sleep Endoscopy (DISE) with Target Controlled Infusion (TCI) and Bispectral Analysis in Obstructive Sleep Apnea
07:54

Drug-Induced Sleep Endoscopy (DISE) with Target Controlled Infusion (TCI) and Bispectral Analysis in Obstructive Sleep Apnea

Published on: December 6, 2016

Ignacio E Tapia1, Preetam Bandla, Joel Traylor

  • 1Sleep Center, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.

Sleep
|July 10, 2010
PubMed

Insights

Children with obstructive sleep apnea syndrome (OSAS) have reduced sensation in their tongue and palate. This impaired upper airway sensation may contribute to breathing issues during sleep.

Area of Science:

  • Pediatric Sleep Medicine
  • Neuroscience
  • Otolaryngology

Background:

  • Obstructive sleep apnea syndrome (OSAS) in children is linked to impaired physiological responses during sleep.
  • A potential contributing factor is dysfunction in the upper airway sensory pathway.

Purpose of the Study:

  • To investigate whether children with OSAS exhibit diminished upper airway sensation compared to healthy controls.
  • To explore the afferent limb of the upper airway sensory pathway in pediatric OSAS.

Main Methods:

  • A case-control study involving children aged 6-16 years with OSAS and age/BMI-matched controls.
  • Two-point discrimination (TPD) was measured using modified calipers on the anterior tongue, interior cheek, and hard palate during wakefulness.

Main Results:

  • Children with OSAS demonstrated significantly impaired TPD in the anterior tongue and hard palate compared to controls.
  • TPD in the interior cheek did not differ significantly between the OSAS and control groups.
  • The OSAS group had a significantly higher apnea-hypopnea index than the control group.

Conclusions:

  • Children with OSAS exhibit impaired tactile sensation in the anterior tongue and hard palate while awake.
  • This sensory deficit may stem from a primary sensory abnormality or be secondary to OSAS-related nerve damage or hypoxemia.
  • Further research is warranted to assess sensory function after OSAS treatment.
Abstract

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