Kirchner J A
Acta Otolaryngol. 1977 Jan-Feb;83(1-2):163-9. doi: 10.3109/00016487709128828.
A previously reported experimental study demonstrated that the intermediate (partly abducted) position of a paralysed vocal cord may be due to physiological inactivation, rather than paralysis, of the cricothyroid muscle. This inhibition was shown to be caused by interruption of vagal afferent impulses originating in pulmonary pressure receptors. The case reported here offered an unusual opportunity of studying this condition by serial section of a human larynx. A patient's left vocal cord was paralysed by cancer in the left pulmonary hilum and apex. There was aspiration and loss of voice. The larynx was obtained at autopsy and studied by serial sections. These showed that the P.C.A- muscle on the paralysed side was, in fact, completely atrophic and degenerated, as were the other intrinsic muscles but that the cricothyroid muscle was morphologically normal. Invasion of both the recurrent laryngeal nerve and the vagus at the thoracic inlet interrupts afferent impulses and inactivates the cricothyroid muscle, with resultant glottic incompetence.
先前报道的一项实验研究表明，麻痹声带的中间（部分外展）位置可能是由于环甲肌的生理失活，而非麻痹所致。这种抑制作用被证明是由源自肺压力感受器的迷走传入冲动中断引起的。本文报道的病例提供了一个通过对人类喉部进行连续切片来研究这种情况的难得机会。一名患者的左声带因左肺门和肺尖部的癌症而麻痹。患者出现了误吸和失音症状。该喉部在尸检时获取并进行了连续切片研究。结果显示，麻痹侧的环杓后肌实际上完全萎缩和退化，其他固有肌肉也是如此，但环甲肌在形态上正常。喉返神经和迷走神经在胸廓入口处受到侵犯会中断传入冲动并使环甲肌失活，从而导致声门功能不全。
