Differential roles for the thyroarytenoid and lateral cricoarytenoid muscles in phonation

Laryngeal adductor muscle dysfunction is a common cause of voice disorders. Reconstitution of adductor muscle function is often the target of therapy, but the effects of these muscles on voice production remain to be fully understood. This study investigated the differential roles of thyroarytenoid (TA) and lateral cricoarytenoid (LCA) muscles on voice production.

Basic science study using an in vivo canine model of phonation.

The TA and LCA muscle nerve branches were stimulated to obtain seven graded levels of muscle activation, from threshold to maximal contraction. The effects of LCA muscle activation alone, TA muscle activation alone, and combined TA and LCA muscle activation on phonation onset parameters were investigated. Phonatory posture, phonation onset type, fundamental frequency (F0), phonation onset pressure, and airflow were evaluated.

LCA muscle activation closed the posterior glottis, but the midmembranous gap remained. TA muscle activation closed the membranous glottis, but the posterior gap remained. Complete glottal closure was obtained only with combined TA and LCA muscle activation. Phonation onset with the LCA muscle alone was characterized by multiple modes (soft, aperiodic, periodic), whereas with the TA muscle alone it was abrupt and periodic but had significant baseline noise. Combined muscle activation led to elimination of baseline noise with stable abrupt periodic onset of phonation. Combined muscle activation was also necessary for F0 variation. The LCA muscle assisted the TA muscle in increasing subglottal pressure while concurrently reducing phonation onset airflow.

The TA muscle is necessary for F0 variation, stable onset phonation, and increased subglottal pressure, but needs the LCA muscle for optimal effectiveness and to reduce airflow requirements with increased activation.

NA.