scholarly journals Triangular body-cover model of the vocal folds with coordinated activation of the five intrinsic laryngeal muscles

2022 ◽  
Vol 151 (1) ◽  
pp. 17-30
Author(s):  
Gabriel A. Alzamendi ◽  
Sean D. Peterson ◽  
Byron D. Erath ◽  
Robert E. Hillman ◽  
Matías Zañartu
1996 ◽  
Vol 39 (2) ◽  
pp. 329-348 ◽  
Author(s):  
Anne Smith ◽  
Margaret Denny ◽  
Lauren A. Shaffer ◽  
Ellen M. Kelly ◽  
Minoru Hirano

The goal of the present experiment was to determine if stuttering is associated with unusually high levels of activity in laryngeal muscles. Qualitative and quantitative analyses of thyroarytenoid and cricothyroid recordings from 4 stuttering and 3 nonstuttering adults revealed the following: Compared to periods of fluent speech, intervals of disfluent speech are not typically characterized by higher levels of activity in these muscles; and when EMG levels during conversational speech are compared to maximal activation levels for these muscles (e.g., those observed during singing and the Valsalva maneuver), normally fluent adults show robust and sometimes near maximal recruitment during conversational speech. The adults who stutter had a lower operating range for these muscles during conversational speech, and their disfluencies did not produce relatively high activation levels. In summary, the present data require us to reject the claim that adults with a history of chronic stuttering routinely produce excessive levels of intrinsic laryngeal muscle activity. These results suggest that the use of botulinum toxin injections into the vocal folds to treat stuttering should be questioned.


1992 ◽  
Vol 43 (3) ◽  
pp. 227-235
Author(s):  
Ryuichi Aibara ◽  
Hiroshi Okamura ◽  
Toshihiro Mori ◽  
Yuji Kawamura ◽  
Seiji Kawakita

1985 ◽  
Vol 50 (1) ◽  
pp. 54-59 ◽  
Author(s):  
Thomas Shipp ◽  
Krzysztof Izdebski ◽  
Charles Reed ◽  
Philip Morrissey

EMG activity from four intrinsic laryngeal muscles (thyroarytenoid, posterior cricoarytenoid, interarytenoid, and cricothyroid) was obtained from one female spastic dysphonia patient while she performed a variety of speech and nonspeech tasks. These tasks were performed before and during a period of temporary unilateral laryngeal muscle paralysis. In the nonparalyzed condition, adductory muscle activity showed intermittent sudden increases that coincided with momentary voice arrests. These muscle patterns and accompanying voice interruptions were not present either when speech was produced in falsetto register or at anytime during the paralysis condition. The data suggest that individuals with this type of spastic dysphonia have normal morphology of recurrent laryngeal nerves and intrinsic laryngeal muscles, which means that the triggering mechanism(s) for spastic dysphonia symptoms must be located at some point neurologically upstream from the larynx.


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