Expression of atrophy-related transcription factors in the process of intrinsic laryngeal muscle atrophy after denervation

2014 ◽  
Vol 272 (1) ◽  
pp. 137-141 ◽  
Author(s):  
Hirofumi Sei ◽  
Aki Taguchi ◽  
Naoya Nishida ◽  
Naohito Hato ◽  
Kiyofumi Gyo
2003 ◽  
Vol 54 (4) ◽  
pp. 270-276 ◽  
Author(s):  
Akihiro Katada ◽  
Satoshi Nonaka ◽  
Isamu Kunibe ◽  
Masaaki Adachi ◽  
Hiroshi Shigyo ◽  
...  

1996 ◽  
Vol 203 (1) ◽  
pp. 45-48 ◽  
Author(s):  
Yasuo Hisa ◽  
Shinobu Koike ◽  
Toshiyuki Uno ◽  
Nobuhisa Tadaki ◽  
Masaki Tanaka ◽  
...  

1999 ◽  
Vol 31 (Supplement) ◽  
pp. S219
Author(s):  
J. R. Rodman ◽  
L. E. Gosselin ◽  
P. Horvath ◽  
D. Megirian ◽  
G. A. Farkas

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.


2004 ◽  
Vol 14 (3) ◽  
pp. 395-403 ◽  
Author(s):  
Trevor N. Stitt ◽  
Doreen Drujan ◽  
Brian A. Clarke ◽  
Frank Panaro ◽  
Yekatarina Timofeyva ◽  
...  

2018 ◽  
Vol 61 (7) ◽  
pp. 1525-1543 ◽  
Author(s):  
Leah B. Helou ◽  
Clark A. Rosen ◽  
Wei Wang ◽  
Katherine Verdolini Abbott

Purpose Research suggests that abnormal levels of intrinsic laryngeal muscle (ILM) contraction is a potential causal factor in stress-induced voice disorders. This study seeks to characterize the ILM stress response in a cohort of vocally healthy women. Method The authors used an unblinded, nonrandomized, repeated-measures design. Forty vocally healthy female adults were subjected to a stressful speech preparation task. Measurements of heart rate, blood pressure, trapezius muscle (positive control) activation, and tibialis muscle (negative control) activation were obtained from 37 participants before and during stressor exposure, in a nonvoice and nonspeaking task paradigm, to confirm physiological stress response compared to baseline. Fine wire electromyography of the ILMs (posterior cricoarytenoid, thyroarytenoid/lateral cricoarytenoid muscle complex, and cricothyroid) was performed simultaneously so that the activity of these muscles could be measured prior to and during stressor exposure. Results The protocol successfully elicited the typical and expected physiological stress responses. Findings supported the hypothesis that, in some individuals, the ILMs significantly increase in activity during stress reactions compared to baseline, as do the control muscles. Conclusions This study characterizes ILM responses to psychological stress in vocally healthy participants. Some of the female adults in this study appeared to be “laryngeal stress responders,” as evidenced by increased activity of the ILMs during a silent (i.e., nonvocal, nonspeech) speech preparation task that they considered to be stressful.


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