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Parkinson’s disease (PD) is a progressive, degenerative disorder that affects 10 million people worldwide. More than 90% of individuals with PD develop hypokinetic dysarthria, a motor speech disorder that impairs vocal communication and quality of life. Despite the prevalence of vocal deficits in this population, very little is known about the pathological mechanisms underlying this aspect of disease. As such, effective treatment options are limited. Rat models have provided unique insights into the disease-specific mechanisms of vocal deficits in PD. This review summarizes recent studies investigating vocal deficits in 6-hydroxydopamine (6-OHDA), alpha-synuclein overexpression, DJ1-/-, and Pink1-/- rat models of PD. Model-specific changes to rat ultrasonic vocalization (USV), and the effects of exercise and pharmacologic interventions on USV production in these models are discussed.

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Purpose Individuals with Parkinson disease (PD) present with complex and variable symptoms, with recent findings suggesting that the etiology of PD extends beyond the involvement of just the basal ganglia. These symptoms include significant impairments in the speech and swallowing domains, which can greatly affect quality of life and therefore require therapeutic attention. This research-based update reviews the neurophysiological basis for swallowing and speech changes in PD, the effectiveness of various types of treatments, and the implications for symptom evaluation and management. Conclusion The mechanisms responsible for swallowing and speech symptoms in PD remain largely unknown. Dopaminergic medication and deep brain stimulation do not provide consistent benefits for these symptoms, suggesting a nondopaminergic network is involved. Importantly, evidence suggests that symptoms of dysphagia and hypokinetic dysarthria may be early indications of PD, so it is critical to investigate the cause of these changes.