Sensorimotor control of vocal pitch production in Parkinson's disease

• Cantonese individuals with PD produced larger vocal compensation for pitch shifts than healthy participants.
• Pitch variability was predictive of the magnitude of vocal compensation for individuals with PD.
• Abnormal sensorimotor integration of voice F0 control in PD may be caused by the increased weighting of auditory feedback.

The present study was designed to investigate the sensorimotor control of voice fundamental frequency (F0) in individuals with Parkinson's diseases (PD). Fifteen Cantonese individuals with PD, and fifteen age- and sex-matched healthy Cantonese individuals participated in the experiment. Participants were asked to vocalize a vowel sound while hearing their voice auditory feedback unexpectedly pitch-shifted upwards or downwards through headphones. The size of pitch shifts varied from 50, 100, to 200 cents. One novel averaging method was used to categorize the individual trials such that only those trials that opposed the perturbation direction were averaged to generate an overall response. The results showed that Cantonese individuals with PD produced significantly larger magnitudes of vocal compensation for pitch perturbations than healthy participants. Both groups showed systematic changes in compensation magnitude as a function of perturbation size and direction: larger perturbation size or upward direction elicited greater compensation magnitude. Moreover, pitch variability indexed by the standard deviations of the baseline F0 was significantly correlated with the magnitude of vocal compensation in individuals with PD, whereas this correlation failed to reach significance for healthy participants. This study presents the first data demonstrating the abnormal processing of auditory feedback in the sensorimotor control of voice F0 for Cantonese individuals with PD. It is suggested that the abnormal sensorimotor integration of voice F0 control in PD may be caused by the increased weighting of auditory feedback control resulting from dysfunction of feedforward control and somatosensory feedback caused by the impairment of the basal ganglia.