Assessment of association between velopharyngeal insufficiency and voice problems in children: cross-sectional study

Abstract Background Velopharyngeal insufficiency (VPI) often triggers secondary laryngeal compensations in children due to hyperfunctional phonation habits. Aim This study aimed to investigate the prevalence and clinical characteristics of various vocal fold lesions in children presenting with VPI of different etiologies compared to control groups. Methods A comparative cross-sectional study was conducted. Group I (study Group) included23 children diagnosed with VPI of various etiologies, with the diagnosis confirmed by comprehensive perceptual speech evaluation and flexible nasoendoscopy. Group II (control group) included23 typically developing children with no history of speech, language, or voice disorders. Visual assessment of the vocal folds to detect and characterize any structural lesions was thoroughly performed for all participants in both groups using rigid and flexible nasoendoscopy. Results Correlation between speech findings and the presence of nodules among cases (n=23). demonstrates a statistically significant association between vocal fold nodules and compensatory speech behaviors. Glottal stops were more frequent in cases with nodules (61.5%) compared to those without nodules (20.0%) (P=0.046). Similarly, pharyngealization was more prevalent among cases with nodules (61.5%) than those without (30.0%), with a significant association detected (Fisher’s exact test, P=0.014). Conclusions The main hypothesis is that vocal fold lesion formation in patients with velopharyngeal insufficiency occurs as a result of laryngeal compensation associated with VPI. The findings suggest that vocal fold lesions in children with velopharyngeal insufficiency may occur secondary to compensatory laryngeal behaviors. However, due to the limited sample size, these results should be interpreted with caution, and further large-scale, longitudinal investigations are recommended to confirm this potential pathogenic mechanism.