Speech and motor deficits are highly prevalent (>70%) in individuals with the 600 kb BP4-BP5 16p11.2 deletion; however, the mechanisms that drive these deficits are unclear, limiting our ability to target interventions and advance treatment. This study examined fundamental aspects of speech motor control in participants with the 16p11.2 deletion. To assess capacity for control of voice, we examined how accurately and quickly subjects changed the pitch of their voice within a trial to correct for a transient perturbation of the pitch of their auditory feedback. When compared to controls, 16p11.2 deletion carriers show an over-exaggerated pitch compensation response to unpredictable mid-vocalization pitch perturbations. We also examined sensorimotor adaptation of speech by assessing how subjects learned to adapt their sustained productions of formants (speech spectral peak frequencies important for vowel identity), in response to consistent changes in their auditory feedback during vowel production. Deletion carriers show reduced sensorimotor adaptation to sustained vowel identity changes in auditory feedback. These results together suggest that 16p11.2 deletion carriers have fundamental impairments in the basic mechanisms of speech motor control and these impairments may partially explain the deficits in speech and language in these individuals.
Objectives To evaluate differences in vocal motor control and central auditory processing between treated unilateral vocal fold paralysis (UVFP) and healthy control cohorts. Study Design Cross‐sectional. Methods Ten UVFP study patients treated by type I thyroplasty with stable voices were compared to 12 control subjects for vocal motor control using a pitch perturbation response task and central auditory processing performance using a battery of complex sound intelligibility assays that included adverse temporal and noise conditions. Standard clinical evaluations of voice production and peripheral audiometric sensitivity were performed. Results Vocal motor control was impaired in treated UVFP. The UVFP cohort exhibited a 32.5% reduction in the instantaneous, subconscious compensatory response to pitch feedback perturbation in the interval between 150 ms and 550 ms following onset (P < 0.0001, linear mixed effects model). This impairment cannot simply be ascribed to vocal motor capacity insufficiency in the UVFP cohort because both cohorts demonstrated comparable functional capacity to perform the vocal motor task. The UVFP cohort also showed greater propensity for central auditory processing impairment (P < 0.05), notably for temporal compression and added noise challenges. Conclusion Combined central vocal motor control and auditory processing impairments in treated UVFP highlight reciprocal interdependency of sensory and motor systems. This pilot study suggests that peripheral motor impairment of the larynx can degrade central auditory processing, which in turn may contribute to vocal motor control impairment. A more complete restoration communicative function in UVFP will require deeper understanding of sensory, motor, and sensorimotor aspects of the human communication loop. Level of Evidence 3b Laryngoscope, 129:2112–2117, 2019
NA Laryngoscope, 126:2785-2791, 2016.
Our findings suggest that compared to survivors with only CIN, survivors with CIN/HL/TIN are at increased risk for the most severe symptom burden, significant problems associated with sensory loss and changes in balance, as well as significant decrements in all aspects of QOL.
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