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Some voice disorders are caused by uncontrolled muscle actions that affect the larynx or voice box.
The purpose of this study is to understand 1) how the brain controls voice production; 2) how changes in sensation within the voice box affect brain control of the voice box; 3) how the central nervous system is affected when people have motor or sensory abnormalities that affect the voice box; and 4) whether patients with voice disorders differ from people without voice disorders in the way the brain controls the voice box. By better understanding these concepts, researchers hope to develop improved treatments for patients with voice disorders.
Forty-five healthy adult volunteers and 90 patients with voice disorders will participate in this study. Participants must be between the ages of 20 and 70. The study will involve two visits to the Clinical Center. During the first visit, participants will undergo a medical history and physical exam. During the second visit, investigators will perform the following procedures on study participants: 1) look at the voice box with a nasolaryngoscope, a fine tube through the nose; 2) use MRI [magnetic resonance imaging] to record brain activity while participants use their voice to speak; 3) changing sensation in the voice box by dripping a topical anesthetic onto the vocal folds; and 4) using MRI to again record brain activity during speech immediately after applying the topical anesthetic.
Participants will receive up to $700 in compensation for their involvement in this study.
The neural organization of laryngeal motor and somatosensory function will be investigated in adults with idiopathic voice disorders using functional magnetic resonance imaging. Brain activation will be compared in normal volunteers and patients with spasmodic dysphonia (SD), muscle tension dysphonia (MTD) and vocal tremor. While each voice disorder is characterized by strained vocalization, the disorders are distinguished by other differences in voice symptoms. Accordingly, the brain correlates of vocalization in these disorders may both differ from each other and that of normal vocal function. Because sensory feedback has been identified as a factor in SD, the role of afferent input in vocalization will be investigated by comparing brain activation before and after topical anesthesia of the laryngeal mucosa. The afferent blockade is expected to significantly suppress dysphonic symptoms in SD patients for the duration of the block. The change in symptomatology may be associated with a temporary but significant change in central sensorimotor patterns in these patients. The block is not expected to alter MTD, vocal tremor or normal vocal function. The brain activation changes that accompany symptom relief in SD patients will determine alterations in central neural control that have a role in symptom generation in SD. Identifying these differences in central sensorimotor control between the disorders will provide insight into their differences in pathophysiology.
1. To determine if emotional vocalization and linguistic vocalization involve different cortical and sub-cortical functional networks in normal adults.
2. To determine if only the brain activation network active for linguistic vocalization network differs between normal controls and dysphonia patients during equivalent voice production effort.
3. To determine if patients with dysphonia differ from controls during the performance of non-vocal laryngeal gestures when patients are asymptomatic.
4. To determine if a reduction in sensation during topical anesthesia alters linguistic vocalization in dysphonia but not in controls.
National Institutes of Health Clinical Center, 9000 Rockville Pike
National Institutes of Health Clinical Center (CC)
Published on BioPortfolio: 2014-08-27T03:55:00-0400
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