Acoustic Intensity and Speech Breathing Kinematics in a Patient with Parkinson’s Disease

Abstract

Parkinson’s disease (PD) is a neurodegenerative disease which affects the basal ganglia control circuit (Duffy, 2013). The motor speech disorder most strongly associated with PD is hypokinetic dysarthria, which presents with distinctive speech characteristics including reduced loudness and the inability to adequately maintain loud speech (Darley, Aronson, & Brown 1969; Duffy 2013). This is due to the variable kinematics for speech breathing associated with PD, which may result in abnormal muscular excursions, reduced vital capacity, and irregular breathing cycles (Duffy, 2013). The impaired ventilatory control can be attributed to the rigidity of muscles of inhalation and exhalation, as well as bradykinesia and hypokinesia. The study aimed to evaluate whether a patient with PD was able to manipulate their acoustic intensity, and if such intensity changes were accompanied by changes in speech breathing kinematics in a novel intraoperative environment. The study’s data were collected intra-operatively during surgery for deep brain stimulation and recordings from the subthalamic nucleus and cortex. The patient was instructed to modulate acoustic intensity while repeating three syllable CV triplets. Speech breathing kinematics of the rib cage were obtained using a Piezo Crystal Effort Sensor with a double buckle band throughout speech production. The speech breathing kinematics of interest were duration, displacement, and peak velocity of inhalation, peak velocity of exhalation, and duration from onset of exhalation to onset of speech, as well as a descriptive comparison between tidal breathing and speech breathing. Spearman Rho correlations indicated that there were weak to no relationships observed between speech breathing kinematics and intensity in this specific participant. However, a medium effect size (Hedge’s g) was observed between tidal and speech breathing for inhalation duration, and small to medium effect size for inhalation displacement and peak velocity. While previous literature suggests that people with PD can manipulate intensity when cued as a result of kinematic modulations for speech breathing, the current study does not support these findings for this one patient. However, previously reported differences between tidal and speech breathing were supported. Potential explanations for the lack of intensity modulation are explored, including constraints induced by the intra-operative environment

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