Aerodynamic Mechanisms Underlying Treatment-Related Changes in Vocal Intensity in Patients With Parkinson Disease

Aerodynamic Mechanisms Underlying Treatment-Related Changes in Vocal Intensity in Patients With Parkinson Disease

Lorraine Olson Ramig and Christopher Dromey

Journal of Speech, Language, and Hearing Research

Vol. 39, 798–807, DOI: 10.1044/jshr.3904.798

Excerpt

The purpose of this study was to document changes in aerodynamic and glottographic aspects of vocal function in patients with Parkinson disease who received two forms of high effort treatment. Previous reports (Ramig, Countryman, Thompson, & Horii, 1995) have documented increased sound pressure level (SPL) following treatment that trained phonation and respiration (Lee Silverman Voice Treatment: LSVT), but not for treatment that trained respiration only (R). In order to examine the mechanisms underlying these differences, measures of maximum flow declination rate (MFDR) and estimated subglottal pressure (Psub) were made before and after treatment. A measure of relative vocal fold adduction (EGGW) was made from the electroglottographic signal during sustained vowel phonation. Sound pressure level data from syllable repetition, sustained vowel phonation, reading, and monologue tasks were also analyzed to allow a more detailed understanding of treatment-related change in several contexts. Consistent with increases in SPL, significant increases in MFDR, estimated Psub, and EGGW were measured posttreatment in patients who received the LSVT. Similar changes were not observed following R treatment. These findings suggest that the combination of increased vocal fold adduction and subglottal pressure is a key in generating posttreatment increases in vocal intensity in idiopathic Parkinson disease (IPD).

The voices of patients with Parkinson disease are characterized by low vocal intensity, monotonicity, and hoarseness (Aronson, 1990; Logemann, Fisher, Boshes, & Blonsky, 1978), which may contribute to a reduction in speech intelligibility (Ramig, 1992; Maclay, 1992). These characteristics have been associated with reduced vocal fold adduction (Hanson, Gerratt, & Ward, 1984; Perez, Ramig, Smith, & Dromey, in press; Smith, Ramig, Dromey, Perez, & Samandari, 1995) and impaired respiratory function (Critchley, 1981; Murdoch, Chenery, & Bowler, 1989; Solomon & Hixon, 1993). Recently, posttreatment increases in vocal intensity (measured as the sound pressure level of a subject’s speech) and fundamental frequency variability have been reported in patients with Parkinson disease following one of two forms of intensive speech treatment (Ramig, Countryman, Thompson, & Horii, 1995). One type of treatment focused on increasing inspiratory and expiratory volumes for speech in order to increase subglottal air pressure, since greater passive recoil forces at high lung volumes can contribute to pressure increases (Hixon, 1973). This approach was termed the respiratory effort treatment (R). The other treatment focused on increasing both respiratory effort and vocal fold adduction and is known as the Lee Silverman Voice Treatment (LSVT). Posttreatment findings documented clinically and statistically significant increases in sound pressure level primarily for the subjects who received treatment designed to increase vocal fold adduction as well as respiratory volumes (Ramig et al., 1995). For example, the LSVT subjects increased on average 12 dB for sustained vowels, 6 dB for a reading passage, and 4 dB for a monologue task. On the other hand, subjects who received the respiratory treatment alone decreased on average 2 dB for sustained vowel phonation and increased 2 dB for reading and 1 dB for the monologue task (Ramig et al., 1995)...