Shipp T, Izdebski K, Reed C, Morrissey P
J Speech Hear Disord. 1985 Feb;50(1):54-9. doi: 10.1044/jshd.5001.54.
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.
从一名女性痉挛性发声障碍患者身上获取了四块喉内肌（甲杓肌、环杓后肌、杓间肌和环甲肌）的肌电图活动，该患者在执行各种言语和非言语任务时进行了此项监测。这些任务在暂时性单侧喉肌麻痹之前和期间进行。在非麻痹状态下，内收肌活动显示出间歇性突然增加，这与瞬间的声音停止同时出现。当用假声发声时或在麻痹状态下的任何时候，这些肌肉模式和伴随的声音中断都不存在。数据表明，患有这种类型痉挛性发声障碍的个体，其喉返神经和喉内肌形态正常，这意味着痉挛性发声障碍症状的触发机制一定位于喉部神经学上游的某个位置。
