Parkinson's disease (PD) is a chronic, progressive and currently non-curable neurodegenerative disease associated with substantial morbidity, increased mortality, and high economic burden. Approximately 1.5 million Americans are currently diagnosed with PD at a cost of $23 billion dollars annually (Weintraub, Comella, & Horn, 2008) with a three to four fold increase in disease rate expected to occur over the next ten years (Tanner & Ben-Shlomo, 1999). Although PD is classically defined by the presence of general motor symptoms that include resting tremor, bradykinesia, rigidity, and postural instability, cranial motor deficits in the form of a hypokinetic dysarthria and dysphagia are reported to occur in 90% of PD patients (Sapir, Ramig, & Fox, 2008). These impairments have been documented to be associated with significant reductions in quality of life, social interactions and mental well-being (Plowman-Prine, Sapienza, et al., 2009). Alarmingly, aspiration pneumonia constitutes the leading cause of death in PD, resulting in a life expectancy ten years below the general population (Hely, Reid, Adena, Halliday, & Morris, 2008).
Speech and voice subsystems significantly affected in PD may include respiration, phonation, articulation, resonance, and prosody (Schulz & Grant, 2000). Hallmark perceptual characteristics of Parkinsonian speech include reduced loudness, monotony of pitch and loudness, reduced stress, variable rate, short rushes of speech, imprecise consonants, and a harsh and breathy voice (Darley et al., 1969, Plowman-Prine et al., 2009a and Ramig et al., 2008).
Swallowing impairments in PD are usually attributed to movement dysfunction of affected bulbar structures and include: lingual tremor, repetitive lingual pumping, anterior bolus leakage, slow or impaired mastication, mandible rigidity, reduced and delayed pharyngeal constrictor contraction, slow and reduced laryngeal excursion, slowing of true vocal fold closure, reduced epiglottic range of movement, reduced and delayed opening of the esophageal sphincter's, abnormal esophageal motility, and esophageal bolus redirection (Chou et al., 2007, Durham et al., 1993, Leopold and Kagel, 1996, Leopold and Kagel, 1997 and Nagaya et al., 1998). These bulbar movement abnormalities may contribute to functional swallowing deficits that include: poor oral bolus control, ineffective oral transit, increased oral transit time, oral buccal residue, premature spillage of the bolus into the valleculae, delay in the execution of the swallow reflex, stasis in the valleculae or pyriforms, penetration and/or aspiration, and gastroesophageal reflux (Pitts et al., 2008, Troche et al., 2008, Troche et al., 2010a and Troche et al., 2010b).
