Auditory Feedback Control Mechanisms Do Not Contribute to Cortical Hyperactivity Within the Voice Production Network...

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.