Influences of laryngeal afferent blockade on laryngeal muscle activity during speech

Abstract

Problem: A previous study determined that sensory blockade reduced symptoms in spasmodic dysphonia. The purpose of this study was to determine how laryngeal afferent feedback blockade alters laryngeal muscle activity during speech, to explain this benefit in patients with spasmodic dysphonia. Methods: We used hooked wire electrodes to record from intrinsic laryngeal muscles (thyroarytenoid, cricothyroid, and posterior cricoarytenoid) during sentence production in subjects with either adductor and abductor spasmodic dysphonia before and after bilateral superior laryngeal nerve blockade with lidocaine. Prior to the block, sensory thresholds were determined for air puff stimuli presented to the mucosa overlying the arytenoid cartilages. Following the block, laryngeal muscle activity during production of the same sentences was recorded again and sensory testing confirmed blockade on both sides. Measures included the mean muscle activity during the first syllable of each sentence, syllable duration, and the pre-phonatory interval between muscle activity onset and voice onset for the first syllable of each sentence. Results: No changes occurred in mean muscle activity level following afferent blockade in all 3 muscles. Significant within-subject reductions were found in the duration of the first syllable of the sentence and in the pre-phonatory interval between thyroarytenoid muscle activity onset and vocalization onset for speech. The pre-phonatory interval decreased in 7 of the 8 subjects. No significant changes in pre-phonatory interval were found in the posterior cricoarytenoid or cricothyroid muscles. Conclusion: Symptom benefits following a reduction in afferent feedback are not a result of reduced muscle activity level but may reflect changes in central patterning of muscle activity in patients with spasmodic dysphonia. Significance: These results provide further understanding of the pathophysiology of symptom generation in spasmodic dysphonia. Support: The research was supported by the National Institute of Neurological Disorders and Stroke, 1 Z01 NS002980-05.