Brain Mapping of Voice Control

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. Objectives: 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.