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Abstract
Knowledge on brain networks subserving vocalization in vocally healthy individuals under various task conditions is scarce but paramount to understand voice disorders. The aims of our study were to determine (1) the effect of social-evaluative stress on the central neural control of phonation underlying speech production; and (2) the neural signature, personality profile, and aerodynamic vocal function in relation to salivary cortisol responses. Thirteen vocally healthy females underwent an event-related sparse-sampling fMRI protocol consisting of voiced and whispered sentence productions with and without exposure to the social-evaluative stressor public speaking anticipation. Participants completed a personality questionnaire, rating scales of negative emotional state, and provided salivary cortisol samples. In the total sample, the task contrast of voiced productions revealed that stressor exposure resulted in a peak activation in the right caudate with concomitant deactivations in the bilateral pgACC and aMCC, and right IFG, BA 9, BA 10, insula, putamen, and thalamus. There were individual differences in stressor-induced brain activations as a function of stress reactivity with greater cortisol reactivity linked with lower laryngeal motor cortex activity and lower scores on aspects of extraversion. Our data confirm that stress alters the phonatory control for speech production through limbic-motor interactions. The findings support the Trait Theory of Voice Disorders (Roy and Bless 2000) and help provide critical insights to the study of voice disorders such as primary muscle tension dysphonia.
Highlights
Phonatory control for speech operates under fluctuating cognitive and emotional states
The first three cortisol samples were not included in our analysis because of possible contamination by the participants’ experience in the mock scanner from which they would have recovered before stressor induction
The study showed that our fMRI stress reactivity and speech protocol was feasible and that pilot data were promising showing that (a) the key impact of stressor exposure on vocal control occurred in areas considered secondary to phonation control, deactivations in the anterior cingulate cortex (ACC), middle cingulate cortex (MCC), insula, putamen, and thalamus, and (b) there are individual differences in stressor-induced brain activations as a function of stress reactivity, as defined by salivary cortisol, with greater cortisol reactivity linked with lower laryngeal motor cortex activity and lower scores on aspects of extraversion
Summary
Phonatory control for speech operates under fluctuating cognitive and emotional states. While humans exert volitional control over phonation underlying speech production via primarily direct corticomotoneuronal pathways (Jürgens 2002), the direct or indirect impact of emotion on phonation for speech remains ambiguous at best. Primary vocal motor areas include the laryngeal motor cortex (LMC), premotor cortex, supplementary motor area (SMA), and lobule VI of the cerebellum, whereas secondary areas include the cingulate motor area, the ventral tier nuclei of the thalamus, the putamen, frontal operculum, and the anterior insula (Brown et al 2009). Primates regulate vocalizations through a limbic vocal motor pathway that relies on the anterior cingulate cortex (ACC) and periaqueductal gray (PAG) (Jürgens 2002). The analogous limbic vocal motor pathway plays a role in non-speech emotional vocalizations, such as crying or laughing (Ludlow 2005).
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