Conclusions: Present findings suggest that F0 and intensity are controlled in an integrated fashion to maintain the contrast between stressed and unstressed words. When a cue is impaired through perturbation, speakers not only oppose the perturbation but enhance other prosodic cues to achieve emphatic stress.
Conclusions: The results suggest that both voice pattern and feedback condition influenced the stability of the LR data. Specifically, the pressed voice pattern may be more susceptible to auditory feedback influence because it was less stable than the breathy and the normal voice patterns. Future investigation should continue to explore the relevance of auditory feedback for theoretical and clinical issues surrounding voice.
Overreliance on auditory feedback may lead to sound/syllable repetitions: simulations of stuttering and fluency-inducing conditions with a neural model of speech production
This paper investigates the hypothesis that stuttering may result in part from impaired readout of feedforward control of speech, which forces persons who stutter (PWS) to produce speech with a motor strategy that is weighted too much toward auditory feedback control. Over-reliance on feedback control leads to production errors which, if they grow large enough, can cause the motor system to “reset” and repeat the current syllable. This hypothesis is investigated using computer simulations of a “neurally impaired” version of the DIVA model, a neural network model of speech acquisition and production. The model’s outputs are compared to published acoustic data from PWS’ fluent speech, and to combined acoustic and articulatory movement data collected from the dysfluent speech of one PWS. The simulations mimic the errors observed in the PWS subject’s speech, as well as the repairs of these errors. Additional simulations were able to account for enhancements of fluency gained by slowed/prolonged speech and masking noise. Together these results support the hypothesis that many dysfluencies in stuttering are due to a bias away from feedforward control and toward feedback control.
In an fMRI experiment, we tested experienced singers with singing tasks to investigate neural correlates of voluntary and involuntary vocal pitch regulation. We shifted the pitch of auditory feedback (±25 or 200 cents), and singers either: 1) ignored the shift and maintained their vocal pitch or 2) changed their vocal pitch to compensate for the shift. In our previous study, singers successfully ignored and compensated for 200-cent shifts; in the present experiment, we hypothesized that singers would be less able to ignore 25-cent shifts, due to a prepotent, corrective pitch-shift response. We expected that voluntary vocal regulation during compensate tasks would recruit the anterior portion of the rostral cingulate zone (RCZa) and posterior superior temporal sulcus (pSTS), as our earlier study reported; however, we predicted that a different network may be engaged during involuntary responses to 25-cent shifts. Singers were less able to ignore 25-cent shifts than 200-cent shifts, suggesting that pitch-shift responses to small shifts are under less voluntary control than responses to larger shifts. While we did not find neural activity specifically associated with involuntary pitch-shift responses, compensate tasks recruited a functionally connected network consisting of RCZa, pSTS, and anterior insula. Analyses of stimulus-modulated functional connectivity suggest that pSTS and intraparietal sulcus may monitor auditory feedback to extract pitch-shift direction in 200-cent tasks, but not in 25-cent tasks, which suggests that larger vocal corrections are under cortical control. During the compensate tasks, the pSTS may interact with the RCZa and anterior insula before voluntary vocal pitch correction occurs.