Nelson Roy1, Maria Dietrich2, Michael Blomgren3, Amanda Heller3, Daniel R Houtz4, James Lee5. 1. Department of Communication Sciences and Disorders, The University of Utah, Salt Lake City, Utah. Electronic address: nelson.roy@health.utah.edu. 2. Department of Communication Science and Disorders, University of Missouri, Columbia, Missouri. 3. Department of Communication Sciences and Disorders, The University of Utah, Salt Lake City, Utah. 4. Voice Disorders Center, University of Utah Healthcare, Salt Lake City, Utah. 5. Imaging and Neurosciences Center, The University of Utah, Salt Lake City, Utah.
Abstract
Primary muscle tension dysphonia (pMTD) is a voice disorder that occurs in the absence of laryngeal pathology. Dysregulated activity of the paralaryngeal muscles is considered the proximal cause; however, the central origin of this aberrant laryngeal muscle activation is unclear. The Trait Theory (Roy and Bless, 2000a,b) proposed that specific personality traits can predispose one to laryngeal motor inhibition and pMTD, and this inhibition is mediated by a hyperactive "behavioral inhibition system (BIS)" composed of limbic system structures (and associated prefrontal connections). This case study used functional magnetic resonance imaging to detect brain activation changes associated with successful management of pMTD, thereby evaluating possible neural correlates of this poorly understood disorder. METHOD: A 61-year-old woman with moderate-to-severe pMTD underwent functional magnetic resonance imaging scans before and immediately after successful treatment using manual circumlaryngeal techniques. Experimental stimuli were blocks of repeated vowel production and overt sentence reading. RESULTS: Significantly greater activation was observed pre- versus posttreatment in all regions of interest during sentence production, that is, periaqueductal gray, amygdala, hypothalamus, anterior cingulate cortex, hippocampus, dorsolateral prefrontal cortex, Brodmann area 10, and premotor and inferior sensorimotor cortex. CONCLUSIONS: Our findings are compatible with overactivation of neural regions associated with the BIS (cingulate cortex, amygdala, hypothalamus, periaqueductal gray) and motor inhibition networks (eg, [pre-]supplementary motor area) along with the dorsolateral prefrontal cortex and medial prefrontal cortex. Heightened input from limbic regions combined with dysfunctional prefrontal regulation may interfere with laryngeal motor preparation, initiation, and execution thereby contributing to disordered voice in pMTD.
Primary muscle tension dysphonia (pMTD) is a voice disorder that occurs in the absence of laryngeal pathology. Dysregulated activity of the paralaryngeal muscles is considered the proximal cause; however, the central origin of this aberrant laryngeal muscle activation is unclear. The Trait Theory (Roy and Bless, 2000a,b) proposed that specific personality traits can predispose one to laryngeal motor inhibition and pMTD, and this inhibition is mediated by a hyperactive "behavioral inhibition system (BIS)" composed of limbic system structures (and associated prefrontal connections). This case study used functional magnetic resonance imaging to detect brain activation changes associated with successful management of pMTD, thereby evaluating possible neural correlates of this poorly understood disorder. METHOD: A 61-year-old woman with moderate-to-severe pMTD underwent functional magnetic resonance imaging scans before and immediately after successful treatment using manual circumlaryngeal techniques. Experimental stimuli were blocks of repeated vowel production and overt sentence reading. RESULTS: Significantly greater activation was observed pre- versus posttreatment in all regions of interest during sentence production, that is, periaqueductal gray, amygdala, hypothalamus, anterior cingulate cortex, hippocampus, dorsolateral prefrontal cortex, Brodmann area 10, and premotor and inferior sensorimotor cortex. CONCLUSIONS: Our findings are compatible with overactivation of neural regions associated with the BIS (cingulate cortex, amygdala, hypothalamus, periaqueductal gray) and motor inhibition networks (eg, [pre-]supplementary motor area) along with the dorsolateral prefrontal cortex and medial prefrontal cortex. Heightened input from limbic regions combined with dysfunctional prefrontal regulation may interfere with laryngeal motor preparation, initiation, and execution thereby contributing to disordered voice in pMTD.
Authors: Kristina Simonyan; Julie Barkmeier-Kraemer; Andrew Blitzer; Mark Hallett; John F Houde; Teresa Jacobson Kimberley; Laurie J Ozelius; Michael J Pitman; Robert Mark Richardson; Nutan Sharma; Kristine Tanner Journal: Neurology Date: 2021-04-15 Impact factor: 11.800