Laryngeal muscle responses to mechanical displacement of the thyroid cartilage in humans

Laryngeal and Speech Section, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland Submitted 13 April 2004 ; accepted in final form 30 May 2005 Speakers may use laryngeal sensory feedback to adjust vocal fold tension and length before initiating voice. The mechanism for accurately initiating voice at an intended pitch is unknown, given the absence of laryngeal muscle spindles in animals and conflicting findings regarding their existence in humans. Previous reports of rapid changes in voice fundamental frequency following thyroid cartilage displacement suggest that changes in vocal fold length modulate laryngeal muscle contraction in humans. We tested the hypothesis that voice changes resulting from mechanical perturbation are due to rapid responses in the intrinsic laryngeal muscles. Hooked wire electrodes were used to record from the thyroarytenoid, cricothyroid, and sternothyroid muscles along with surface electrodes on the skin overlying the thyroid cartilage in 10 normal adults. Servomotor displacements produced consistent changes in the subjects’ vocal fundamental frequency at 70–80 ms, demonstrating changes in vocal fold length and tension. No simultaneous electromyographic responses occurred in the thyroarytenoid or cricothyroid muscles in any subjects. Instead, short-latency responses at 25–40 ms following stimulus onset occurred in the sternothyroid muscles, simultaneous with responses in the surface recordings. The sternothyroid responses may modulate long-latency changes in voice fundamental frequency ( 150 ms). The absence of intrinsic laryngeal muscle responses is consistent with a lack of spindles in these muscles. Our results suggest that other sensory receptors, such as mucosal mechanoreceptors, provide feedback for voice control. somatosensory; sternothyroid; thyroarytenoid; stretch reflex Address for reprint requests and other correspondence: T. M. J. Loucks, Laryngeal and Speech Section, Clinical Neurosciences Program, National Institute of Neurological Disorders and Stroke, Bldg. 10, Rm. 5D 38, 10 Center Drive, MSC 1416, Bethesda, MD 20892-1416 (E-mail: louckst{at}ninds.nih.gov )