Phonatory and Articulatory Changes Associated With Increased Vocal Intensity in Parkinson Disease: A Case Study
Christopher Dromey, Lorraine Olson Ramig, and Antonia B. Johnson
Journal of Speech, Language, and Hearing Research
Vol. 38, 751–764, DOI: 10.1044/jshr.3804.751
This study examined changes in voice and speech production in a patient with Parkinson disease as he increased vocal intensity following 1 month of intensive voice treatment. Phonatory function and articulatory acoustic measures were made before and after treatment as well as 6 and 12 months later. Pre- to post-treatment increases were documented in sound pressure level in sustained phonation, syllable repetition, reading, and monologue. Consistent with mechanisms of intensity change reported in normal speakers, corresponding improvements were measured in estimated subglottal pressure, maximum flow declination rate, laryngeal airway resistance, open quotient, EGGW-25, harmonic-spectral slope, and maximum vowel duration. Measures of phonatory stability in sustained phonation and semitone standard deviation in reading and speaking showed changes accompanying increased vocal intensity. In addition, changes were measured in articulatory acoustic parameters (vowel and whole word duration, transition duration, extent and rate, and frication duration and rise time) in single-word productions. These findings indicate that this patient increased his vocal intensity using phonatory mechanisms that have been associated with the nondisordered larynx. In addition, the increased vocal intensity led to changes in articulation that were not targeted in treatment.
Vocal intensity is a key variable in the production of intelligible speech (Moore, 1946; Pickett, 1956; Ramig, 1992). Subglottal air pressure (Isshiki, 1964), vocal fold adduction (Scherer, 1991; Titze & Sundberg, 1992), and vocal tract shape (Gauffin & Sundberg, 1989; Scherer, 1991) have been associated with the control of vocal intensity. Maximum flow declination rate (MFDR), which reflects the interaction of subglottal air pressure and vocal fold adduction, and is an index of the speed of glottal flow “shut-off,” correlates highly with vocal intensity (Titze & Sundberg, 1992). The mechanism of intensity control has been described in normal (Holmberg, Hillman, & Perkell, 1988; Stathopoulos & Sapienza, 1993, 1993) and hyperfunctional voices (Hillman, Holmberg, & Perkell, 1989; Sapienza & Stathopoulos, 1994), but has not been studied following treatment designed to improve intensity in patients with vocal hypofunction...