Effect of Velopharyngeal Gap Size on Laryngeal Morphology and Vocal Function in Children With VPI

Overview

Speech production relies on the precise coordination of the respiratory, phonatory, resonatory, and articulatory systems . The velopharyngeal mechanism is essential in separating the oral and nasal cavities during speech and swallowing. Disruption of this mechanism leads to velopharyngeal insufficiency (VPI), which is characterized by the inability to achieve complete velopharyngeal closure due to structural or anatomical deficits. VPI is frequently associated with cleft palate, either repaired or unrepaired. It may also occur secondary to submucous cleft palate (CP), craniofacial syndromes, short palate, or post-adenoidectomy.

Although the primary communication problem in VPI is a resonance disorder, persistent velopharyngeal insufficiency may alter normal vocal behavior. To compensate for the loss of intraoral pressure, many children with VPI develop excessive laryngeal muscle tension, increased respiratory effort, abnormal vocal fold adduction, or other compensatory phonatory behaviors. Over time, this laryngeal hyperfunction and other compensatory behaviors may result in muscle tension dysphonia and cause morphological changes of the vocal folds, such as vocal nodules, inflammation, and edema. The reported prevalence of voice disorders in VPI patients ranges widely, from 5.5% based on a retrospective parent-reported hoarseness questionnaire to 72% in a prospective study employing perceptual voice assessment. This wide disparity primarily reflects methodological differences-such as indirect parental report versus direct perceptual evaluation, retrospective versus prospective designs, and heterogeneous patient samples-that profoundly influence prevalence estimates. Individuals with VPI may exhibit chronic hoarseness, forced, soft, strangled, or aspirated phonation. Additionally, children with CP ± lip (L) often have higher F0, jitter, and shimmer in their voices compared to typically developing children. Aydinli et al. have also shown that children with CP ± L who use glottal stops as a compensatory articulation strategy tend to have higher F0, shimmer, and jitter, indicating increased tension in their vocal cords affecting vocal fold vibration. Vocal nodules were the most common anatomical finding among individuals with CP and CP/L. The relationship between VPI severity and concomitant voice disorders has been the subject of abundant investigation, yet studies across all assessment modalities have yielded inconsistent results. At the subjective level, Deengam et al. reported a correlation between hypernasality severity and perceptual voice disorder ratings, whereas Fujiki and Thibeault found that children with severe hypernasal resonance were 78% less likely to present with laryngeal pathology. Further adding to the discrepancy, Hamming et al., using a history of speech surgery as an indicator for VPI severity in a retrospective design, found no significant association between VPI and hoarseness, suggesting that voice abnormalities may persist independently of severity. In an effort to resolve these inconsistencies, objective instrumental techniques-particularly nasoendoscopy-have been employed for precise VPI severity evaluation. However, reliance on the velopharyngeal closure pattern alone (e.g., closing, inconsistent, open) has not clarified the picture: D'Antonio et al. found no relationship between laryngeal/voice findings and velopharyngeal function, while McWilliams et al. reported that children with a borderline closure mechanism were more susceptible to voice changes. These persistent vocal abnormalities likely reflect chronic compensatory behaviors and laryngeal tissue changes driven by the pre-repair aerodynamic deficit, meaning a dynamic closure pattern does not reliably capture the cumulative vocal load imposed by the condition. A more direct anatomical metric-the velopharyngeal gap (VPG) size-should theoretically be a better predictor. Yet here too, findings diverge: Lehes et al. observed no significant association between VPI severity and acoustic voice parameters, implying that increasing gap size does not necessarily correlate with voice quality, while Villafuerte-Gonzalez et al. reported abnormal acoustic measures, including elevated shimmer, specifically in cases with moderate VPG. Critically, both VPG size studies were limited by extremely small sample sizes (≤18 patients), severely constraining generalizability and statistical power. Thus, the contradictory evidence across subjective and objective measures-including the most direct anatomical index-underscores a fundamental gap in the literature and highlights the urgent need for a large-scale, adequately powered investigation that systematically quantifies velopharyngeal gap size via nasoendoscopy and rigorously examines its correlation with both subjective and objective voice outcomes.