Supraglottic Activity

Evidence of Vocal Hyperfunction or Laryngeal Articulation?

sursvs{at}gwumc.edu

False vocal fold (FVF) adduction and compression of the arytenoid cartilages to the petiole of the epiglottis in an anterior to posterior (A-P) direction have been thought to characterize voice disorders with abnormally increased muscle tension or effort, often termed hyperfunctional voice disorders. To further evaluate the association between hyperfunctional voice disorders and supraglottic activity, we compared the incidence of static and dynamic supraglottic activity in individuals with normal laryngeal mucosa, normal voice quality, and no voice complaints to two populations: subjects with vocal fold nodules and subjects with complaints of dysphonia without visible vocal fold lesions, glottal incompetence, or impairment of arytenoid cartilage motion ("hyperfunctional" group). Thirty-two subjects were assigned to one of these three groups (10 control, 12 nodule, and 10 hyperfunctional). Laryngeal movements were recorded using flexible videoendoscopy while a subject was performing speech tasks such as sustained phonation, syllable repetitions, sentence imitations, and conversation. Samples were randomized by subject and task and rated for presence or absence of A-P and FVF compression. Statistically significant group differences were found for FVF compression across speech tasks (chi-square, p < 0.001). The control group had the smallest incidence (45%), nodule patients the next larger incidence (68%), and hyperfunctional patients the largest incidence (80%). Statistically significant group differences were found for A-P compression across speech tasks (chi-square, p < .05). The control group had the smallest incidence (74%), nodule patients the next larger incidence (78%), and hyperfunctional patients the largest incidence (92%). Statistically significant task differences were found for the presence of FVF compression in control subjects (chi-square, p < .005), hyperfunctional patients (chi-square, p < .025), and nodule patients (chi-square, p < .001), but not for A-P compression for any of the groups. A higher incidence of FVF compression was present for the speech tasks that included glottal stops. This context-specific variation in supraglottic activity suggested a dynamic component to FVF compression and also explained the high proportion of FVF compression in the control group. Each video sample was also rated for consistency of FVF or A-P compression to explore the static and dynamic nature of supraglottic activity. For samples on which raters agreed, A-P compression was typically present consistently, suggesting a static component, and FVF compression inconsistently, suggesting a dynamic component, for all three groups (chi-square, p < .001). These findings do not support previous suggestions that supraglottic activity may be a precursor to developing vocal fold nodules, as the nodule patients did not exhibit a higher incidence or consistency of A-P or FVF compression than patients with hyperfunctional voicing patterns in this study. Subjects in the hyperfunctional voice group were found to have static components of FVF and A-P compression. The presence of FVF compression in speech tasks that included glottal stops in the control group suggests an articulatory function at the laryngeal level.

KEY WORDS: false vocal fold compression, anterior-posterior compression, videoendoscopy, hyperfunction, supraglottic activity

Submitted on October 5, 1998
Accepted on July 6, 1999

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