Project Summary Vocal hyperfunction (VH) is a highly prevalent feature in the 3 – 9% of the U.S. population with voice disorders. Characterized by excessive and/or incoordinated laryngeal and perilaryngeal tension, its pathophysiology has been attributed to many potential etiologies, such as poor vocal hygiene, psychological factors, reflux, and atypical autonomic nervous system (ANS) function. Our central hypothesis, supported by our recent findings, is that auditory-motor function is impaired in some individuals with VH: we found impairments in speakers' auditory acuity to differences in recordings of their own voice fundamental frequency (fo) and their adaptive responses to artificial shifts in their own voice fo. In this cycle we propose to further elucidate the etiologic role of disrupted auditory-motor function in VH and to evaluate measures of auditory-motor function that have clinical applicability. In Aim 1, individuals with VH and controls will participate in tasks to derive fo adaptive responses with and without a simultaneous cognitive stressor to elicit ANS arousal. Converging evidence suggests that atypical ANS function is a potential etiologic factor in VH, and that the level of ANS arousal may be associated with impairments in auditory-motor function. Thus, we will directly assess whether disrupted ANS and auditory-motor function represent a shared endophenotype (related predisposing factors) in the etiology of VH. In Aim 2, fo acuity and adaptive responses will be investigated longitudinally in VH. Our pilot data indicate that many individuals with VH and atypical auditory-motor features show improvement in their adaptive responses immediately after voice therapy. This may represent normalization of an underlying etiologic factor. Conversely, voice therapy may provide strategies to improve vocal quality, without addressing the underlying neural vulnerability of individuals to develop VH, with changes in auditory-motor adaptation that are secondary. We anticipate that individuals with atypical auditory-motor features immediately post-therapy will have poorer long-term responses to therapy, with the implication that disrupted auditory-motor control is an etiologic factor in the development and persistence of VH. The fo perturbation methods employed in Aim 1 and Aim 2 require precise calibration of instrumentation and well-controlled acoustic environments, limiting their clinical viability. Therefore, in Aim 3, potential “clinic-friendly” correlates (auditory acuity to shifts in the fo of a standard voice and production of speech before, during, and after being exposed to a noisy environment to induce a Lombard response) will be psychometrically evaluated in terms of their concurrent validity and test-retest reliability. Successful completion of these Aims will provide theoretical and clinical insight, contributing directly to all Center Aims: delineation of the etiology and pathophysiology of VH, more specific phenotyping of VH, an...