Abstract

Signs of both motor and sensory nervous lesions have previously been shown in the upper airway of patients with OSA and habitual snorers. Snoring per se may damage all upper airway neurons over time, thereby causing progression to manifest sleep apnea. To test this hypothesis, nonsnoring subjects, untreated snorers, and CPAP-treated patients underwent repeated sensory testing of the soft palate in a prospective long-term study. Cold detection threshold (CDT) testing at the soft palate and lip with a thermode and nocturnal respiratory recordings were performed in 2008 to 2009 with retesting 6 to 7 years later. In 25 untreated snorers, palatal CDT worsened from a median (25th-75th percentile range) 4.2°C (3.2-5.9) to 11.0°C (7.0-17.4) (P< .001). The apnea-hypopnea index increased from a median 7.0 to 14.0 events/h (P< .05). There was no significant correlation between changes in CDT and the apnea-hypopnea index. In 21 nonsnoring control subjects, palatal CDT increased from a median 3.2°C to 5.6°C (P< .005). In 19 CPAP-treated patients, palatal CDT did not significantly change; eight patients had improved values. CDTs worsened significantly more in the snorers group than in the control subjects (P< .05) and the CPAP-treated patients (P< .001). There was no significant difference between control subjects and CPAP-treated patients. CDT worsened considerably over time in untreated snorers, significantly more than in nonsnoring control subjects and CPAP-treated patients. Untreated snorers therefore risk developing poor sensitivity in the upper airway. In contrast, efficient treatment of OSA seems to protect the sensory innervation, as the CPAP-treated group maintained their sensitivity to cold and, in some cases, the sensitivity even improved.

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