Berke, Gerald S.

ObjectiveTo identify research priorities to increase understanding of the pathogenesis, diagnosis, and improved treatment of spasmodic dysphonia.Study Design and SettingA multidisciplinary working group was formed that included both scientists and clinicians from multiple disciplines (otolaryngology, neurology, speech pathology, genetics, and neuroscience) to review currently available information on spasmodic dysphonia and to identify research priorities.ResultsOperational definitions for spasmodic dysphonia at different levels of certainty were recommended for diagnosis and recommendations made for a multicenter multidisciplinary validation study.ConclusionsThe highest priority is to characterize the disorder and identify risk factors that may contribute to its onset. Future research should compare and contrast spasmodic dysphonia with other forms of focal dystonia. Development of animal models is recommended to explore hypotheses related to pathogenesis. Improved understanding of the pathophysiology of spasmodic dysphonia should provide the basis for developing new treatment options and exploratory clinical trials.SignificanceThis document should foster future research to improve the care of patients with this chronic debilitating voice and speech disorder by otolaryngology, neurology, and speech pathology.

Glottic phonatory parameters have been studied in constant flow models; however, the lung‐thorax system is better viewed as a constant pressure source. Adjusting the driving pressure and recurrent laryngeal nerve stimulation as independent variables, rather than as dependent variables, may provide a more physiologic understanding of laryngeal function and glottic parameters, including subglottic pressure, airflow, fundamental frequency, and glottic area. In three dogs subglottic pressure and airflow were measured in two separate conditions: with constant recurrent laryngeal nerve stimulation and varying driving pressure, and with constant driving pressure and varying recurrent laryngeal nerve stimulation. Videostroboscopic measures on four dogs assessed glottic areas with constant recurrent laryngeal nerve stimulation at different driving pressures. With constant recurrent laryngeal nerve stimulation, increasing driving pressure had no effect on glottic areas, whereas subglottic pressure, fundamental frequency, and airflow increased significantly. However, changes in subglottic pressure were minimal in comparison with changes in driving pressure. At constant driving pressure, increasing recurrent laryngeal nerve stimulation increased subglottic pressure and fundamental frequency and decreased airflow. These findings suggest that during phonation subglottic pressure is primarily dependent on recurrent laryngeal nerve stimulation and laryngeal muscular contraction, but not on lung driving pressure.