[Characteristics of genioglossus neuromuscular activity in patients with obstructive sleep apnea during drug-induced sleep].

Objective

To analyze genioglossus (GG) activation responses to the negative pressure of upper airway cavity during awake and different sleep stages in patients with different obstructive sleep apnea (OSA) graduation.

Methods

This prospective cohort study started from August 2019 to January 2021, recruited 42 male OSA patients aged from 21 to 59 (38.77±8.42) years. After completing whole night polysomnography (PSG) and upper airway CT, each subject underwent drug-induced sleep with simultaneous monitoring of genioglossal electromyography (GGEMG) and pressure of epiglottis (Pepi). Subjects were divided into three groups of mild OSA(7 males), moderate OSA(12 males), and severe OSA(23 males). The differences in upper airway CT measurements, parameters of GGEMG and Pepi during awake and induced sleep were compared. Statistical analysis was conducted by SPSS 21.0.

Results

There was no significant difference in the GGEMG parameters between the mild and moderate groups. In wakefulness, the peak phasic GGEMG of the severe group was higher than the mild group (t=1.249, P=0.025), with no statistically difference in the corresponding Pepi. In the sleep onset, the GGEMG parameters and Pepi in severe group were higher than the other two groups. Linear regression analysis of the maximum GGEMG and maximum Pepi at the end of obstructive apnea (OA) in all moderate plus severe patients (n=35) was shown nonlinear correlation (r=0.28, P=0.694). The airway length of the glossopharyngeal cavity was linearly correlated with the maximum Pepi of OA (r=0.468, R2=0.219, P=0.005).

Conclusions

The individual difference of GG activation in OSA patients is related to the severity of the disease (frequency of respiratory events) and negative pressure stimulation. In moderate and severe OSA patients, GG activity is not in harmony with the corresponding negative pressure stimulation, which may be one of the mechanisms leading to the aggravation of OSA.