Poor laryngeal muscle coordination that results in abnormal glottal posturing is believed to be a primary etiologic factor in common voice disorders such as non-phonotraumatic vocal hyperfunction. An imbalance in the activity of antagonistic laryngeal muscles is hypothesized to play a key role in the alteration of normal vocal fold biomechanics that results in the dysphonia associated with such disorders. Current low-order models are unsatisfactory to test this hypothesis since they do not capture the co-contraction of antagonist laryngeal muscle pairs. To address this limitation, a scheme for controlling a self-sustained triangular body-cover model with intrinsic muscle control is introduced. The approach builds upon prior efforts and allows for exploring the role of antagonistic muscle pairs in phonation. The proposed scheme is illustrated through the ample agreement with prior studies using finite element models, excised larynges, and clinical studies in sustained and time-varying vocal gestures. Pilot simulations of abnormal scenarios illustrated that poorly regulated and elevated muscle activities result in more abducted prephonatory posturing, which lead to inefficient phonation and subglottal pressure compensation to regain loudness. The proposed tool is deemed sufficiently accurate and flexible for future comprehensive investigations of non-phonotraumatic vocal hyperfunction and other laryngeal motor control disorders.
翻译:眼下低级模型不能令人满意地测试这一假设,因为它们不能捕捉对立的喉咙肌肉配对的合拍。为了应对这一限制,引入了一种控制自我维持的三角身体覆盖模型,并带有内在肌肉控制功能。这种方法以先前的努力为基础,并能够探索对立的肌肉配对在幻灯中所起的作用。拟议办法的体现是,与先前的研究达成充分一致,使用有限的元素模型、精炼液和临床研究,持续和时间变化的声动姿态。对异常情景的模拟实验性模拟表明,监管不力和升级的肌肉活动导致更受绑架的心动肌肉控制前和后台压力分析。