title: Sensorimotor function of the upper-airway muscles and respiratory sensory processing in untreated obstructive sleep apnea.
abstract: Numerous studies have demonstrated upper-airway neuromuscular abnormalities during wakefulness in snorers and obstructive sleep apnea (OSA) patients. However, the functional role of sensorimotor impairment in OSA pathogenesis/disease progression and its potential effects on protective upper-airway reflexes, measures of respiratory sensory processing, and force characteristics remain unclear. This study aimed to gain physiological insight into the potential role of sensorimotor impairment in OSA pathogenesis/disease progression by comparing sensory processing properties (respiratory-related evoked potentials; RREP), functionally important protective reflexes (genioglossus and tensor palatini) across a range of negative pressures (brief pulses and entrained iron lung ventilation), and tongue force and time to task failure characteristics between 12 untreated OSA patients and 13 controls. We hypothesized that abnormalities in these measures would be present in OSA patients. Upper-airway reflexes (e.g., genioglossus onset latency, 20 ± 1 vs. 19 ± 2 ms, P = 0.82), early RREP components (e.g., P1 latency 25 ± 2 vs. 25 ± 1 ms, P = 0.78), and the slope of epiglottic pressure vs. genioglossus activity during iron lung ventilation (-0.68 ± 1.0 vs. -0.80 ± 2.0 cmH(2)O/%max, P = 0.59) were not different between patients and controls. Maximal tongue protrusion force was greater in OSA patients vs. controls (35 ± 2 vs. 27 ± 2 N, P < 0.01), but task failure occurred more rapidly (149 ± 24 vs. 254 ± 23 s, P < 0.01). Upper-airway protective reflexes across a range of negative pressures as measured by electromyography and the early P1 component of the RREP are preserved in OSA patients during wakefulness. Consistent with an adaptive training effect, tongue protrusion force is increased, not decreased, in untreated OSA patients. However, OSA patients may be vulnerable to fatigue of upper-airway dilator muscles, which could contribute to disease progression.
authors: Brigham and Women's Hospital, Div. of Sleep Medicine, Sleep Disorders Program, Boston, MA 02115, USA. deckert@rics.bwh.harvard.edu
authors: Danny J
authors: DJ
authors: Eckert
authors: Yu L
authors: YL
authors: Lo
authors: Julian P
authors: JP
authors: Saboisky
authors: Amy S
authors: AS
authors: Jordan
authors: David P
authors: DP
authors: White
authors: Atul
authors: A
authors: Malhotra
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D004576:Electromyography; D005071:Evoked Potentials; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D017286:Polysomnography; D011597:Psychomotor Performance / Q000502:physiology; D012018:Reflex / Q000502:physiology; D012121:Respiration, Artificial; D012132:Respiratory Muscles / Q000503:physiopathology*; D020181:Sleep Apnea, Obstructive / Q000503:physiopathology* / Q000628:therapy; D014059:Tongue / Q000503:physiopathology; D015919:Ventilators, Negative-Pressure; D014851:Wakefulness / Q000502:physiology