Auditory feedback control of vocal intensity during speech and sustained-vowel production

Purpose Individuals with cerebellar ataxia (CA) caused by cerebellar degeneration exhibit larger reactive compensatory responses to unexpected auditory feedback perturbations than neurobiologically typical speakers, suggesting they may rely more on feedback control during speech. We test this hypothesis by examining variability in unaltered speech. Previous studies of typical speakers have demonstrated a reduction in formant variability (centering) observed during the initial phase of vowel production from vowel onset to vowel midpoint. Centering is hypothesized to reflect feedback-based corrections for self-produced variability and thus may provide a behavioral assay of feedback control in unperturbed speech in the same manner as the compensatory response does for feedback perturbations. Method To comprehensively compare centering in individuals with CA and controls, we examine centering in two vowels (/i/ and /ɛ/) under two contexts (isolated words and connected speech). As a control, we examine speech produced both with and without noise to mask auditory feedback. Results Individuals with CA do not show increased centering compared to age-matched controls, regardless of vowel, context, or masking. Contrary to previous results in neurobiologically typical speakers, centering was not affected by the presence of masking noise in either group. Conclusions The similar magnitude of centering seen with and without masking noise questions whether centering is driven by auditory feedback. However, if centering is at least partially driven by auditory/somatosensory feedback, these results indicate that the larger compensatory response to altered auditory feedback observed in individuals with CA may not reflect typical motor control processes during normal, unaltered speech production.

Download Full-text

Auditory Feedback Control Mechanisms Do Not Contribute to Cortical Hyperactivity Within the Voice Production Network in Adductor Spasmodic Dysphonia

Journal of Speech Language and Hearing Research ◽

10.1044/2019_jslhr-19-00325 ◽

2020 ◽

Vol 63 (2) ◽

pp. 421-432 ◽

Cited By ~ 2

Author(s):

Ayoub Daliri ◽

Elizabeth S. Heller Murray ◽

Anne J. Blood ◽

James Burns ◽

J. Pieter Noordzij ◽

...

Keyword(s):

Feedback Control ◽

Auditory Feedback ◽

Brain Activity ◽

Spasmodic Dysphonia ◽

Control Mechanisms ◽

Planum Temporale ◽

Resting State Functional Connectivity ◽

Adductor Spasmodic Dysphonia ◽

Cortical Regions ◽

Auditory Feedback Control

Purpose Adductor spasmodic dysphonia (ADSD), the most common form of spasmodic dysphonia, is a debilitating voice disorder characterized by hyperactivity and muscle spasms in the vocal folds during speech. Prior neuroimaging studies have noted excessive brain activity during speech in participants with ADSD compared to controls. Speech involves an auditory feedback control mechanism that generates motor commands aimed at eliminating disparities between desired and actual auditory signals. Thus, excessive neural activity in ADSD during speech may reflect, at least in part, increased engagement of the auditory feedback control mechanism as it attempts to correct vocal production errors detected through audition. Method To test this possibility, functional magnetic resonance imaging was used to identify differences between participants with ADSD ( n = 12) and age-matched controls ( n = 12) in (a) brain activity when producing speech under different auditory feedback conditions and (b) resting-state functional connectivity within the cortical network responsible for vocalization. Results As seen in prior studies, the ADSD group had significantly higher activity than the control group during speech with normal auditory feedback (compared to a silent baseline task) in three left-hemisphere cortical regions: ventral Rolandic (sensorimotor) cortex, anterior planum temporale, and posterior superior temporal gyrus/planum temporale. Importantly, this same pattern of hyperactivity was also found when auditory feedback control of speech was eliminated through masking noise. Furthermore, the ADSD group had significantly higher resting-state functional connectivity between sensorimotor and auditory cortical regions within the left hemisphere as well as between the left and right hemispheres. Conclusions Together, our results indicate that hyperactivation in the cortical speech network of individuals with ADSD does not result from hyperactive auditory feedback control mechanisms and rather is likely related to impairments in somatosensory feedback control and/or feedforward control mechanisms.

Download Full-text