Modulation of vocal pitch is a key speech feature that conveys important linguistic and affective information. Auditory feedback is used to monitor and maintain pitch. We examined induced neural high gamma power (HGP) (65–150 Hz) using magnetoencephalography during pitch feedback control. Participants phonated into a microphone while hearing their auditory feedback through headphones. During each phonation, a single real‐time 400 ms pitch shift was applied to the auditory feedback. Participants compensated by rapidly changing their pitch to oppose the pitch shifts. This behavioral change required coordination of the neural speech motor control network, including integration of auditory and somatosensory feedback to initiate change in motor plans. We found increases in HGP across both hemispheres within 200 ms of pitch shifts, covering left sensory and right premotor, parietal, temporal, and frontal regions, involved in sensory detection and processing of the pitch shift. Later responses to pitch shifts (200–300 ms) were right dominant, in parietal, frontal, and temporal regions. Timing of activity in these regions indicates their role in coordinating motor change and detecting and processing of the sensory consequences of this change. Subtracting out cortical responses during passive listening to recordings of the phonations isolated HGP increases specific to speech production, highlighting right parietal and premotor cortex, and left posterior temporal cortex involvement in the motor response. Correlation of HGP with behavioral compensation demonstrated right frontal region involvement in modulating participant's compensatory response. This study highlights the bihemispheric sensorimotor cortical network involvement in auditory feedback‐based control of vocal pitch.
Hearing one’s own voice is critical for fluent speech production as it allows for the detection and correction of vocalization errors in real time. This behavior known as the auditory feedback control of speech is impaired in various neurological disorders ranging from stuttering to aphasia; however, the underlying neural mechanisms are still poorly understood. Computational models of speech motor control suggest that, during speech production, the brain uses an efference copy of the motor command to generate an internal estimate of the speech output. When actual feedback differs from this internal estimate, an error signal is generated to correct the internal estimate and update necessary motor commands to produce intended speech. We were able to localize the auditory error signal using electrocorticographic recordings from neurosurgical participants during a delayed auditory feedback (DAF) paradigm. In this task, participants hear their voice with a time delay as they produced words and sentences (similar to an echo on a conference call), which is well known to disrupt fluency by causing slow and stutter-like speech in humans. We observed a significant response enhancement in auditory cortex that scaled with the duration of feedback delay, indicating an auditory speech error signal. Immediately following auditory cortex, dorsal precentral gyrus (dPreCG), a region that has not been implicated in auditory feedback processing before, exhibited a markedly similar response enhancement, suggesting a tight coupling between the 2 regions. Critically, response enhancement in dPreCG occurred only during articulation of long utterances due to a continuous mismatch between produced speech and reafferent feedback. These results suggest that dPreCG plays an essential role in processing auditory error signals during speech production to maintain fluency.
more » « less- Award ID(s):
- 1912286
- NSF-PAR ID:
- 10487892
- Editor(s):
- Bizley, Jennifer K.
- Publisher / Repository:
- Plos Biology
- Date Published:
- Journal Name:
- PLOS Biology
- Volume:
- 20
- Issue:
- 2
- ISSN:
- 1545-7885
- Page Range / eLocation ID:
- e3001493
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Abstract Hum Brain Mapp 37:1474‐1485, 2016 . © 2016 Wiley Periodicals, Inc. -
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Differences in prosody (e.g., intonation, rhythm) are among the most obvious language‐related impairments in autism spectrum disorder (ASD), and significantly impact communication. Subtle prosodic differences have also been identified in a subset of clinically unaffected first‐degree relatives of individuals with ASD, and may reflect genetic liability to ASD. This study investigated the neural basis of prosodic differences in ASD and first‐degree relatives through analysis of feedforward and feedback control involved in the planning, production, self‐monitoring, and self‐correction of speech by using a pitch‐perturbed auditory feedback paradigm during sustained vowel and speech production. Results revealed larger vocal response magnitudes to pitch‐perturbed auditory feedback across tasks in ASD and ASD parent groups, with differences in sustained vowel production driven by parents who displayed subclinical personality and language features associated with ASD (i.e., broad autism phenotype). Both ASD and ASD parent groups exhibited increased response onset latencies during sustained vowel production, while the ASD parent group exhibited decreased response onset latencies during speech production. Vocal response magnitudes across tasks were associated with prosodic atypicalities in both individuals with ASD and their parents. Exploratory event‐related potential (ERP) analyses in a subgroup of participants during the sustained vowel task revealed reduced P1 ERP amplitudes in the ASD group, with similar trends observed in parents. Overall, results suggest underdeveloped feedforward systems and neural attenuation in detecting audio‐vocal feedback may contribute to ASD‐related prosodic atypicalities. Importantly, results implicate atypical audio‐vocal integration as a marker of genetic risk to ASD, evident in ASD and among clinically unaffected relatives.
Autism Res 2019, 12: 1192–1210Autism Research published by International Society for Autism Research published by Wiley Periodicals, Inc.Lay Summary Previous research has identified atypicalities in prosody (e.g., intonation) in individuals with ASD and a subset of their first‐degree relatives. In order to better understand the mechanisms underlying prosodic differences in ASD, this study examined how individuals with ASD and their parents responded to unexpected differences in what they heard themselves say to modify control of their voice (i.e., audio‐vocal integration). Results suggest that disruptions to audio‐vocal integration in individuals with ASD contribute to ASD‐related prosodic atypicalities, and the more subtle differences observed in parents could reflect underlying genetic liability to ASD.
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Abstract Speech production involves the careful orchestration of sophisticated systems, yet overt speech errors rarely occur under naturalistic conditions. The present functional magnetic resonance imaging study sought neural evidence for internal error detection and correction by leveraging a tongue twister paradigm that induces the potential for speech errors while excluding any overt errors from analysis. Previous work using the same paradigm in the context of silently articulated and imagined speech production tasks has demonstrated forward predictive signals in auditory cortex during speech and presented suggestive evidence of internal error correction in left posterior middle temporal gyrus (pMTG) on the basis that this area tended toward showing a stronger response when potential speech errors are biased toward nonwords compared to words (Okada et al., 2018). The present study built on this prior work by attempting to replicate the forward prediction and lexicality effects in nearly twice as many participants but introduced novel stimuli designed to further tax internal error correction and detection mechanisms by biasing speech errors toward taboo words. The forward prediction effect was replicated. While no evidence was found for a significant difference in brain response as a function of lexical status of the potential speech error, biasing potential errors toward taboo words elicited significantly greater response in left pMTG than biasing errors toward (neutral) words. Other brain areas showed preferential response for taboo words as well but responded below baseline and were less likely to reflect language processing as indicated by a decoding analysis, implicating left pMTG in internal error correction.
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Abstract Objective: Acoustic distortions to the speech signal impair spoken language recognition, but healthy listeners exhibit adaptive plasticity consistent with rapid adjustments in how the distorted speech input maps to speech representations, perhaps through engagement of supervised error-driven learning. This puts adaptive plasticity in speech perception in an interesting position with regard to developmental dyslexia inasmuch as dyslexia impacts speech processing and may involve dysfunction in neurobiological systems hypothesized to be involved in adaptive plasticity. Method: Here, we examined typical young adult listeners ( N = 17), and those with dyslexia ( N = 16), as they reported the identity of native-language monosyllabic spoken words to which signal processing had been applied to create a systematic acoustic distortion. During training, all participants experienced incremental signal distortion increases to mildly distorted speech along with orthographic and auditory feedback indicating word identity following response across a brief, 250-trial training block. During pretest and posttest phases, no feedback was provided to participants. Results: Word recognition across severely distorted speech was poor at pretest and equivalent across groups. Training led to improved word recognition for the most severely distorted speech at posttest, with evidence that adaptive plasticity generalized to support recognition of new tokens not previously experienced under distortion. However, training-related recognition gains for listeners with dyslexia were significantly less robust than for control listeners. Conclusions: Less efficient adaptive plasticity to speech distortions may impact the ability of individuals with dyslexia to deal with variability arising from sources like acoustic noise and foreign-accented speech.more » « less
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Abstract Accurate integration of sensory inputs and motor commands is essential to achieve successful behavioral goals. A robust model of sensorimotor integration is the pitch perturbation response, in which speakers respond rapidly to shifts of the pitch in their auditory feedback. In a previous study, we demonstrated abnormal sensorimotor integration in patients with Alzheimer’s disease (AD) with an abnormally enhanced behavioral response to pitch perturbation. Here we examine the neural correlates of the abnormal pitch perturbation response in AD patients, using magnetoencephalographic imaging. The participants phonated the vowel /α/ while a real-time signal processor briefly perturbed the pitch (100 cents, 400 ms) of their auditory feedback. We examined the high-gamma band (65–150 Hz) responses during this task. AD patients showed significantly reduced left prefrontal activity during the early phase of perturbation and increased right middle temporal activity during the later phase of perturbation, compared to controls. Activity in these brain regions significantly correlated with the behavioral response. These results demonstrate that impaired prefrontal modulation of speech-motor-control network and additional recruitment of right temporal regions are significant mediators of aberrant sensorimotor integration in patients with AD. The abnormal neural integration mechanisms signify the contribution of cortical network dysfunction to cognitive and behavioral deficits in AD.
- Free Publicly Accessible Full Text
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Accepted Manuscript1.0
- Journal Article:
- https://doi.org/10.1371/journal.pbio.3001493
