Neuroreport ◽  
2020 ◽  
Vol 31 (4) ◽  
pp. 325-331
Author(s):  
Xiuqin Wu ◽  
Baofeng Zhang ◽  
Lirao Wei ◽  
Hanjun Liu ◽  
Peng Liu ◽  
...  

NeuroImage ◽  
2008 ◽  
Vol 39 (3) ◽  
pp. 1429-1443 ◽  
Author(s):  
Jason A. Tourville ◽  
Kevin J. Reilly ◽  
Frank H. Guenther

2009 ◽  
Vol 23 (14) ◽  
pp. 1849-1871 ◽  
Author(s):  
Jorge Solis ◽  
Koichi Taniguchi ◽  
Takeshi Ninomiya ◽  
Klaus Petersen ◽  
Tetsuro Yamamoto ◽  
...  

2020 ◽  
Vol 63 (2) ◽  
pp. 421-432 ◽  
Author(s):  
Ayoub Daliri ◽  
Elizabeth S. Heller Murray ◽  
Anne J. Blood ◽  
James Burns ◽  
J. Pieter Noordzij ◽  
...  

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.


2020 ◽  
Author(s):  
Muge Ozker ◽  
Werner Doyle ◽  
Orrin Devinsky ◽  
Adeen Flinker

AbstractAccurate and fluent production of speech strongly depends on hearing oneself which allows for the detection and correction of vocalization errors in real-time. When auditory feedback is disrupted with a time delay (e.g. echo on a conference call), it causes slowed and stutter-like speech in humans. Impaired speech motor control during delayed auditory feedback is implicated in various neurological disorders ranging from stuttering to aphasia, however the underlying neural mechanisms are poorly understood. Here, we investigated auditory feedback control in human speech by obtaining electrocorticographic recordings from neurosurgical subjects performing a delayed auditory feedback (DAF) task. We observed a significant increase in neural activity in auditory sites that scaled with the duration of feedback delay and correlated with response suppression during normal speech, providing direct evidence for a shared mechanism between sensitivity to altered feedback and speech-induced auditory suppression in humans. Furthermore, we find that when subjects robustly slowed down their speech rate to compensate for the delay, the dorsal division of the precentral gyrus was preferentially recruited to support articulation during an early time frame. This recruitment was accompanied by response enhancement across a large speech network commencing in temporal cortex and then engaging frontal and parietal sites. Our results highlight the critical components of the human speech network that support auditory feedback control of speech production and the temporal evolution of their recruitment.


1970 ◽  
Vol 13 (2) ◽  
pp. 298-303 ◽  
Author(s):  
James H. Abbs ◽  
Karl U. Smith

Proceeding from prior experimental evidence that better speech-sound identification most often occurs with right-ear presentation, an experiment was conducted to test for differences in speech production with right-ear and left-ear auditory feedback of one’s own speech. A hybrid-computer system and techniques of experimental programing were employed to control the intervals of aural delay. Presentation of delayed auditory feedback to the right ear during speech, with white noise masking the left ear, resulted in a significantly greater number of articulatory errors than did delayed feedback to the left ear with white noise masking the right ear. With a measure of total speaking time, however, similar differences between ears during delayed hearing were not found. The findings were interpreted as an indication of differences in aural function during auditory feedback control of speech. Such differences are consistent with aural laterality differences reported with speech identification.


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