The Section conducts research on the integrated neural control of laryngeal function for voice, speech and swallowing. Our purpose is to determine the normal control system as well as the pathogenesis and pathophysiology of neurogenic disorders affecting these functions. Building on this information 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 central gating of brain stem responses to laryngeal sensory stimulation in normalcy and in idiopathic voice disorders such as spasmodic dysphonia. In the last year we have examined how normal speakers modulate brain stem responses such as the early (R1) laryngeal adductor response during different motor control tasks such as speech in particular. We hypothesized that during phonation these brain stem responses are gated so that precise control can be maintained for phonation but that during non-phonatory tasks such as effort closure these responses would be increased because the laryngeal muscles are more active for sustained vocal fold closure. Electrical stimulation of the laryngeal afferents contained in the superior laryngeal nerve was presented during quiet inspiration, and during humming, phonation and effort closure in normal speakers. We measured the amplitude and frequency of the early R1 and later bilateral R2 responses during each of these tasks. Because the laryngeal motor neurons are firing at a more rapid rate during each of these tasks compared to inspiration, we hypothesized that the laryngeal adductor responses during these tasks would be equal to the responses at rest plus the mean increase in baseline activity during a task over the mean activity during inspiration. Not only were the laryngeal responses reduced relative to the hypothesized levels, these responses were reduced in amplitude relative to the responses occurring during respiration during all tasks. This suggests that when subjects are performing volitional laryngeal control tasks, these brain stem responses to sensory stimulation within the larynx are actively suppressed. We are now examining patients with spasmodic dysphonia to test the hypothesis that this gating of laryngeal sensory-motor responses is not normal in these patients. ? In mammals, the vocalization system includes the anterior cingulate, the periaquaductal grey and the integrative brain stem system to the motor neuron pools. Because electrical stimulation in the laryngeal cortex motor area only elicits vocalization in humans, it has been hypothesized that only humans have a cortically based vocalization system which is learned and involves direct corticobulbar pathways from the cortex to the brain stem. We tested this hypothesis by comparing brain activation on fMRI during vocalized syllables that only involved articulation at the larynx, such as repetition of the vowel ?ee?, with prolonged expiration without voice. We used event related neural imaging to examine specific regions of interest. An unexpected similar pattern of predominantly left hemisphere activation was found for both conditions with the only difference being auditory activation because of the greater feedback during the voiced task compared to prolonged expiration. The results indicate that a left hemisphere lateralized control system for volitional control of both prolonged exhalation and phonation are present in humans. However, in addition to activation in the left hemisphere pre-frontal and motor cortical regions, activity was also found in the supplementary motor area, the anterior cingulate and the putamen during both tasks. The findings indicate that the learned human system of voice and respiratory control for voice production is an integration of both the mammalian vocalization system and a cortically based control system. ? 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 innervation of muscles intact but without appropriate central nervous system control. We have been studying the feasibility of using intramuscular electrical stimulation to augment airway protection by increasing hyo-laryngeal elevation during swallowing to reduce the risk of aspiration in these patients. Recently, surface electrical stimulation was introduced for use in dysphagia therapy with claims that electrical stimulation on the surface of the throat could raise the hyo-laryngeal complex. To evaluate this claim we completed two studies of the effects of surface electrical stimulation on the position of the hyoid and larynx at rest and during swallowing using videofluoroscopy. The first study involved patients with chronic pharyngeal dysphagia. When stimulation was applied at rest, the hyoid bone was lowered in the neck on average by about 10 mm. During swallowing no benefit was found in these patients airway protection with stimulation in comparison to swallowing without stimulation. In the second study 10 different stimulation combinations of surface electrode placements were used in healthy volunteers and in all those placements over the laryngeal area the hyoid was lowered in the neck to the same degree on videofluoroscopy. In addition, submental surface stimulation did not elevate either the larynx or the hyoid bone. Finally, in the healthy subjects when stimulation was applied over the larynx significant reductions occurred in peak elevation of both the larynx and hyoid bone during stimulated swallows. The stimulated swallows were also judged less safe than non-stimulated swallows on a scale measuring penetration of liquid during swallowing in these healthy individuals. In conclusion, surface electrical stimulation not only did not benefit patients but may place patients at increased risk of aspiration because of increased resistance to hyoid elevation during swallowing. We have continued our studies of intramuscular stimulation to aid swallowing in patients with chronic pharyngeal dysphagia and a Phase II controlled trial comparing an implanted neuromuscular stimulator with sensory stimulation for the treatment of patients with chronic pharyngeal dysphagia is planned to start next year.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Intramural Research (Z01)
Project #
1Z01NS002980-08
Application #
7324560
Study Section
(MNB)
Project Start
Project End
Budget Start
Budget End
Support Year
8
Fiscal Year
2006
Total Cost
Indirect Cost
City
State
Country
United States
Zip Code
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