Laryngopharyngeal reflux (LPR) is defined as the retrograde flow of gastric contents into the laryngopharynx, leading to a constellation of symptoms and signs distinct from classic gastroesophageal reflux disease (GERD).¹ While GERD is characterized by heartburn and regurgitation, LPR typically manifests with throat clearing, globus pharyngeus, chronic cough, and dysphonia.² The laryngeal mucosa is highly susceptible to damage from pepsin and acid, resulting in inflammation, edema, and ultimately, vocal dysfunction.

Voice disorders represent a significant burden on quality of life and professional efficacy. The etiological diagnosis of dysphonia is complex, with LPR being a frequently implicated but sometimes controversial contributor.³ Previous studies have established an association, yet the strength of the correlation and the specific profile of LPR-related dysphonia lack comprehensive characterization in a standardized clinical cohort⁴.

The primary aim of this study was to determine the prevalence of LPR in a consecutive series of patients presenting to a voice clinic with dysphonia. Secondary objectives were to compare acoustic, perceptual, and patient-reported voice outcomes between dysphonic patients with and without LPR, and to identify the most common laryngoscopic findings associated with reflux-related voice pathology⁵.

A prospective cohort study was conducted at Government Medical College Datia, M.P., over a 12-months period. The study protocol was approved all participants provided written informed consent.

Inclusion criteria: One hundred consecutive adult patients (>18 years) presenting with a primary complaint of dysphonia persisting for a minimum of 4 weeks were enrolled.

Exclusion criteria: a history of laryngeal surgery, active laryngeal infection, neurologic voice disorders (e.g., Parkinson's disease, spasmodic dysphonia), thyroid disorders, current smoking, and use of proton pump inhibitors or H2-receptor antagonists within the 4 weeks prior to evaluation.

Clinical and Instrumental Assessment

All patients completed a comprehensive evaluation in a single visit:

1. Symptom Assessment:The Reflux Symptom Index (RSI), a validated 9-item self-administered questionnaire (score range 0-45, with >13 considered abnormal).
2. Voice Handicap Assessment:The Voice Handicap Index-10 (VHI-10), a 10-item questionnaire assessing the psychosocial impact of dysphonia (score range 0-40).
3. Laryngoscopic Examination:A flexible transnasal laryngoscopy was performed by a single, blinded otolaryngologist. Findings were quantified using the 8-item Reflux Finding Score (RFS), with a score >7 indicative of LPR.⁶ Specific findings like vocal fold edema, diffuse laryngeal edema, and posterior commissure hypertrophy were recorded.
4. Acoustic Voice Analysis:Patients sustained the vowel /a/ at a comfortable pitch and loudness for 5 seconds. The mean of three trials was used to calculate perturbation measures (jitter %, shimmer %) and the harmonic-to-noise ratio (HNR) using the PRAAT software (version 6.3.04).
5. Perceptual Voice Analysis:A certified speech-language pathologist, blinded to patient grouping, rated a recorded speech sample using the GRBAS scale (Grade, Roughness, Breathiness, Asthenia, Strain), each on a 4-point scale (0=normal, 3=severe).⁷ The overall Grade (G) score was used for analysis.

Diagnostic Criteria for LPR

A diagnosis of LPR was made based on a combination of symptomatic and laryngoscopic criteria: an RSI score >13 and an RFS score >7. Patients meeting both criteria were classified as the LPR-positive dysphonia group (LPR+). Those failing to meet both criteria constituted the non-LPR dysphonia group (LPR-).

Statistical Analysis

Data were analyzed using SPSS Statistics version 28.0. Continuous variables were expressed as mean ± standard deviation (SD) and compared using the independent samples t-test or Mann-Whitney U test, as appropriate. Categorical variables were expressed as percentages and compared using the Chi-square or Fisher’s exact test. A p-value of <0.05 was considered statistically significant.

The study cohort comprised 100 patients (62 females, 38 males) with a mean age of 48.7 ± 12.3 years. Based on the diagnostic criteria, 68 patients were classified as LPR+ and 32 as LPR-.

Table 1: Demographic and Baseline Characteristics of the Study Cohort

Table 2: Prevalence of Individual Laryngoscopic Findings (RFS Components)

Table 3: Acoustic, Perceptual, and Patient-Reported Voice Outcomes

The prevalence of LPR in this dysphonic cohort was 68%. As shown in Table 1, the LPR+ group had a significantly longer duration of dysphonic symptoms (9.2 vs. 6.7 months, p=0.048). Table 2 details the laryngoscopic findings, with vocal fold edema (95.6%), posterior commissure hypertrophy (88.2%), and erythema (85.3%) being the most prevalent signs in LPR+ patients.

Voice analysis revealed significant differences between groups (Table 3). The LPR+ group exhibited markedly worse acoustic stability, with higher jitter and shimmer and a lower HNR. Perceptual voice quality (GRBAS-G) was rated as significantly more severe, and the psychosocial impact (VHI-10) was nearly 10 points higher in the LPR+ group.

This study confirms a high prevalence (68%) of LPR among patients seeking treatment for dysphonia, aligning with the upper range of previously reported estimates.¹,³ The findings robustly demonstrate that dysphonia in the context of LPR is not merely a subjective complaint but is associated with objectively quantifiable vocal deterioration.

The acoustic analysis provides compelling evidence of the destabilizing effect of LPR on phonation. The significant elevation in jitter and shimmer in the LPR+ group indicates increased cycle-to-cycle variability in pitch and amplitude, hallmarks of an inefficient and strained vocal fold vibration.⁸ The reduced HNR further suggests a voice source plagued by increased turbulent noise, likely stemming from the edematous and irregular vocal fold margins observed on laryngoscopy. These objective measures correlate strongly with both the RFS and the patient's own perception of vocal handicap (VHI-10), creating a cohesive triad of diagnostic evidence.

The laryngoscopic profile observed dominant findings of vocal fold edema, posterior commissure hypertrophy, and erythema is classic for LPR and provides a visual explanation for the acoustic findings.⁹ Chronic inflammation leads to increased mass and stiffness of the vocal fold cover, disrupting the delicate biomechanics required for clear phonation. The strong correlation between RFS and VHI-10 scores underscores that the visible pathology directly translates to functional impairment.

The significantly higher VHI-10 scores in the LPR+ group highlight the profound psychosocial and professional burden of this condition. Patients reported greater limitations in social interaction and occupational performance, emphasizing that LPR-related dysphonia extends beyond the larynx to affect overall quality of life.¹⁰

Limitations
This study has limitations. The diagnosis of LPR was based on clinical tools (RSI/RFS) rather than the gold standard of 24-hour dual-probe pH-impedance monitoring, which was not feasible in this clinical setting. However, RSI and RFS remain the most widely used and validated clinical instruments. The study design was observational and cross-sectional, demonstrating association but not causation. A longitudinal study assessing voice outcomes following anti-reflux treatment is the logical next step.

In a cohort of 100 patients with dysphonia, laryngopharyngeal reflux was identified as a highly prevalent etiological factor. Patients with LPR presented with a distinct profile characterized by significantly worse acoustic voice parameters, more severe perceptual voice quality, and greater patient-reported vocal handicap compared to dysphonic patients without LPR. The strong correlations between reflux scores and voice metrics solidify the link between the disease and its functional sequelae. This study reinforces the imperative for otolaryngologists and voice specialists to include a systematic evaluation for LPR in the diagnostic work-up of every patient with dysphonia. Early identification and management of LPR may prevent chronic laryngeal changes and lead to more effective restoration of vocal function

1. Koufman JA. The otolaryngologic manifestations of gastroesophageal reflux disease (GERD): a clinical investigation of 225 patients using ambulatory 24-hour pH monitoring and an experimental investigation of the role of acid and pepsin in the development of laryngeal injury. Laryngoscope. 1991;101(4 Pt 2 Suppl 53):1-78.
2. Lechien JR, Akst LM, Hamdan AL, et al. Evaluation and management of laryngopharyngeal reflux disease: state of the art review. Otolaryngol Head Neck Surg. 2019;160(5):762-782.
3. Ford CN. Evaluation and management of laryngopharyngeal reflux. JAMA. 2005;294(12):1534-1540.
4. Belafsky PC, Postma GN, Koufman JA. Validity and reliability of the reflux symptom index (RSI). J Voice. 2002;16(2):274-277.
5. Rosen CA, Lee AS, Osborne J, Zullo T, Murry T. Development and validation of the voice handicap index-10. Laryngoscope. 2004;114(9):1549-1556.
6. Belafsky PC, Postma GN, Koufman JA. The validity and reliability of the reflux finding score (RFS). Laryngoscope. 2001;111(8):1313-1317.
7. Hirano M. Clinical examination of voice. New York: Springer-Verlag; 1981.
8. Teixeira JP, Oliveira C, Lopes C. Vocal acoustic analysis – jitter, shimmer and HNR parameters. Procedia Technology. 2013;9:1112-1122.
9. Ylitalo R, Ramel S. Extraesophageal reflux in patients with contact granuloma: a prospective controlled study. Ann Otol Rhinol Laryngol. 2002;111(5 Pt 1):441-446.
10. Spantideas N, Drosou E, Bougea A, Alabdulqader A. Laryngopharyngeal reflux impact on the quality of life of patients with chronic rhinosinusitis. Eur Arch Otorhinolaryngol. 2022;279(7):3515-3522.