Understanding the involvement of the central nervous system (CNS) in voice production is essential to incorporating principles of neuroplasticity into therapeutic practice for voice disorders. Early steps to attaining this goal require the identification of specific neural biomarkers of the changes occurring in the CNS from a voice disorder and its subsequent treatment. In the absence of an adequate animal vocalization model, the larynx has not been acutely and reversibly perturbed to concurrently examine the effect on both peripheral and central processing of the altered input/output.
Using a unique, reversible perturbation approach, it was the purpose of this study to perturb the larynx to mimic a voice disorder and study short-term neuroplastic response. Functional magnetic resonance imaging (fMRI) was the neuroimaging tool of choice for this study due to its superior spatial and temporal resolution. The voice was perturbed by anesthetizing the right recurrent laryngeal nerve, with a solution of lidocaine hydrochloride and epinephrine to induce a temporary right vocal fold paralysis. The paralysis lasted for approximately 90 minutes and had an overt presentation similar to that of a true vocal fold paralysis. Behavioral and fMRI data were obtained at three time points- baseline, during the vocal fold paralysis and one hour after recovery.
Patterns of activity on fMRI during the three time points were found to be distinct on both subjective examination and statistical analysis. The regions of interest examined had distinct trends in activity as a function of the paralysis. Interestingly, males and females responded differently to the paralysis and its subsequent recovery. Strong correlation was not observed between the behavioral measures and fMRI activity reflecting a disparity between the overt presentation and recovery of vocal fold paralysis and cortical activity as seen on fMRI.
The fictive paralysis model employed in this study provided a perturbation model for phonation that allowed us to examine behavioral and central neural correlates for disordered phonation in a controlled environment. Although this data is representative of acute changes from a transient paralysis, it provides an insight into the response of the cortex to sudden perturbation at the peripheral phonatory mechanism.
| Identifer | oai:union.ndltd.org:uky.edu/oai:uknowledge.uky.edu:gradschool_diss-1220 |
| Date | 01 January 2011 |
| Creators | Joshi, Ashwini |
| Publisher | UKnowledge |
| Source Sets | University of Kentucky |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | University of Kentucky Doctoral Dissertations |
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