Voice Disorders Clinical Trial
Official title:
Functional Brain Mapping of Laryngeal Sensorimotor Control in Voice Disorders
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.
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.
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