The Effects of Hard Voice Onset on Objective Voice Function in Patients With Laryngopharyngeal Reflux

OBJECTIVE:Laryngopharyngeal reflux (LPR) causes laryngopharyngeal hypersensitivity and laryngeal muscle hyperfunction, which may result in hard voice onset in patients with LPR. The purpose of this study is to examine the incidence of hard voice onset in patients with LPR and the effects of hard voice onset on objective voice function in patients with LPR. METHODS:Forty patients with confirmed LPR were enrolled in the LPR group, and 40 healthy subjects were enrolled in the non-LPR group. Subjects underwent laryngeal high-speed videoendoscopy, and the presence or absence of hard voice onset in each subject was determined by two experienced laryngologists based on whether glottal closure was complete or incomplete before vocal fold vibration. Based on the results, the subjects with LPR were divided into a hard voice onset group and a non-hard voice onset group. The voice onset time (VOT) was measured and compared between the hard and non-hard voice onset groups within the LPR group. Laryngeal aerodynamic assessment was also carried out on the LPR group, and subglottal pressure, phonation threshold pressure (PTP), glottal resistance, and mean flow rate were measured. The voice acoustic signals of subjects were additionally analyzed in the LPR group, and the fundamental frequency, jitter, shimmer, and noise-harmony ratio were determined. The kappa statistic, chi-square test and independent-samples t test in SPSS were used for statistical analysis. RESULTS:The two laryngologists had substantial inter-rater consistency on the evaluation of hard voice onset and non-hard voice onset, with a kappa statistic of 0.71. In the LPR group, 42.5% of patients had hard voice onset (17/40), significantly more than in the non-LPR group (8/40, 20%) (P < 0.05). The VOT in the LPR group was significantly longer than in the non-LPR group (P < 0.05). Within the LPR group, the VOT, PTP and shimmer were significantly greater in the hard voice onset group than in the non-hard voice onset group (all P < 0.05). The other laryngeal aerodynamic parameters and acoustic parameters were not significantly different between the hard voice onset group and the non-hard voice onset group (P > 0.05). CONCLUSION:Changes in vocal production may occur in LPR patients, causing them to be more susceptible to hard voice onset. The patients with hard voice onset require longer VOT and greater PTP to initiate phonation.