Our goal is to improve the treatment and prevention of voice, speech and swallowing disorders. For this purpose, the Section conducts research both on the neural control of the larynx for voice, speech and swallowing as well as the pathogenesis and pathophysiology of neurogenic idiopathic voice and speech disorders. In addition, new treatment methods are being developed for persons with chronic pharyngeal dysphagia. Significant advances have been made during the last year in several areas. Our Section is particularly interested in the role of sensation in idiopathic voice disorders such as spasmodic dysphonia. First, however, we must determine what types of sensory feedback play a role in laryngeal motor control in humans. Speakers may use laryngeal sensory feedback to adjust vocal fold tension and length prior to initiating voice when auditory feedback becomes available. One of the questions we have is what sensors are used to provide feedback for vocal fold movement prior to voice initiation. Others have proposed that the thyroarytenoid muscles within the vocal folds contain muscle spindles that provide proprioceptive feedback. The possible role of stretch receptors in the larynx is controversial given the absence of muscle spindles in the laryngeal muscles in other mammals and conflicting findings regarding their existence in humans. We evaluated whether rapid changes in vocal fold length modulate laryngeal muscle contraction in humans during voicing. Mechanical perturbation was applied with a servomotor to first stretch the cricothyroid muscle by indenting the thyroid cartilage followed by a rapid release, stretching the thyroarytenoid muscle. Although servomotor displacements produced consistent changes in the subjects' voices, demonstrating changes in vocal fold length and tension, no simultaneous electromyographic reponses to stretch occurred in the thyroarytenoid or cricothyroid muscles inside the larynx. Instead, short-latency responses occurred in the sternothyroid muscle, an overlying strap muscle known to contain spindle afferents, The absence of intrinsic laryngeal muscle responses to stretch is consistent with a lack of spindles in these muscles and suggests that other sensory receptors, such as mucosal mechanoreceptors, are more likely to provide proprioceptive feedback for voice control in humans. Developmental speech disorders often occur in isolation and are idiopathic. The rate of spontaneous recovery from such developmental disorders is high, however, because no predictors of recovery are available, all children receive speech therapy. We are completing a series of studies of adults who have not recovered from developmental speech disorders to identify which factors are associated with poor recovery from developmental speech disorders. All of the adults studied had a persistent familial developmental speech disorder without language impairment. They were compared with unaffected adults on tasks requiring the discrimination of fine acoustic cues for word identification and on measures of verbal and nonverbal short-term memory. Significant group differences were found in the slopes of the discrimination curves for formant transitions for word identification and on tests of nonverbal rhythm and tonal memory, and verbal short-term memory. No group differences occurred in the use of stop gap durations for word identification, however, demonstrating that only selective deficits were present in auditory processing and memory. We are now examining whether specific auditory processing and short term memory disorders occur in those children who fail to recover from developmental multiple articulation disorders. Dysphagia is a significant health problem affecting many aging adults who suffer from neurological disorders and diseases. These swallowing disorders usually stem from central nervous system injury, leaving the peripheral control of muscles intact but without appropriate central control. We are studying the feasibility of using intramuscular electrical stimulation to augment airway protection by hyolaryngeal elevation during swallowing to reduce the risk of aspiration in those with chronic dysphagia. One of the difficulties is to trigger the onset of electrical stimulation so that it is coordinated with attempts to swallow. Patients must synchronize functional electrical stimulation (FES) with their reflexive swallowing and not adapt to FES by reducing the amplitude or duration of their own muscle activity. We first studied this in healthy adults by assessing whether they could learn to manually synchronize FES with hyolaryngeal muscle activity during swallowing, and whether they modified their patterns of muscle activity in response to FES of the same muscles during discrete swallows. Hooked-wire electrodes were used to record from the mylohyoid and thyrohyoid muscles on one side of the neck while delivering FES to the same muscles on the other side during swallowing. After performing baseline swallows, volunteers were instructed to trigger FES with a thumb switch in synchrony with their swallows for a series of trials. On the last trial, FES was disabled creating a foil. From the outset, volunteers synchronized FES with the onset of swallow-related thyrohyoid activity (about 225 ms after mylohyoid activity onset), preserving the normal sequence of muscle activation. When the baseline and foil trials were compared, no significant adaptive changes occurred in the amplitude, duration, or relative timing of activity in either muscle, indicating that the central pattern generator for hyolaryngeal elevation is immutable with short term stimulation that augments laryngeal elevation during the reflexive, pharyngeal phase of swallowing. In the last year, we have started using the same techniques in persons with chronic dysphagia aimed at determining if they can learn to coordinate FES with their own attempts to swallow. Our long term goal is to determine if FES can be used to reduce the risk of aspiration in chronic pharyngeal dysphagia.
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