Dysphagia in Parkinson Disease: Part I – Pathophysiology and Diagnostic Practices

Abstract

Purpose of Review

Dysphagia affects the majority of individuals with Parkinson disease (PD) and is not typically diagnosed until later in disease progression. This review will cover the current understanding of PD pathophysiology, and provides an overview of dysphagia in PD including diagnostic practices, gaps in knowledge, and future directions.

Recent Findings

Many non-motor and other motor signs of PD appear in the prodrome prior to the manifestation of hall- mark signs and diagnosis. While dysphagia often presents already in the prodrome, it is not routinely addressed in standard neurology examinations.

Summary

Dysphagia in PD can result in compromised efficiency and safety of swallowing, which significantly contributes to malnutrition and dehydration, decrease quality of life, and increase mortality. The heterogeneous clinical presentation of PD complicates diagnostic procedures which often leads to delayed treatment. Research has advanced our knowledge of mechanisms underlying PD, but dysphagia is still largely understudied, especially in the prodromal stage.

Introduction

Parkinson disease (PD) is a progressive, degenerative, multi-system disorder. Signs of disease include the traditional hallmark motor signs – bradykinesia, resting tremor, rigidity, and postural instability – as well as multiple non-motor and ‘other’ motor signs such as orthostatic hypotension, cardiac dysautonomia, gastrointestinal dysmotility, and deficits in higher order functions such as communication, cognition, and affect [1]. Impaired swallowing, or dysphagia, is a significant concern in PD, as functional swallowing is controlled by multiple somatic and autonomic sensorimotor functions and requires appropriate cognitive function. Many non-motor or other motor signs including dysphagia manifest early in the disease process, and predate the emergence of hallmark motor disturbances by decades. Dysphagia affects over 90% of people with PD, significantly impacting health outcomes by contributing to malnutrition, dehydration, and increased mortality due to aspiration, which can lead to aspiration pneumonia [2–4]. Even though aspiration pneumonia is the leading cause of death in PD [4], dysphagia is not routinely identified until it is more severe, typically in the mid-to-late stages. Despite current research advancements, understanding of the prodromal and early stages of the disease process and the mechanisms underlying dysphagia in PD remains limited. Here, we briefly review pathophysiology, current diagnostic practices, gaps in knowledge, as well as future directions for PD-associated dysphagia research and clinical practice.

Classic Pathology

PD was originally described as a movement disorder characterized by progressive loss of dopaminergic neurons in the nigrostriatal pathway and aggregation of Lewy bodies in the remaining neurons [5]. The loss of dopaminergic neurons within the substantia nigra was thought to be the primary cause for cardinal motor signs such as rigidity, tremor, and bradykinesia, although other neurotransmitter systems appear to be affected as well [6]. Research has shifted the focus from motor signs to non-motor and ‘other’ motor features of PD, revealing that PD is a multi-system disease affecting the central as well as the peripheral nervous systems [1]. Current diagnostic practices, however, depend heavily on motor symptoms only, even though many non-motor signs manifest earlier in disease progression, which causes for tremendous delays in diagnosis and treatment. In fact, motor features are estimated to appear after 50-60% of dopaminergic neurons have already been lost [7]. However, hyposmia, sleep disruptions, constipation, and depression can precede dopamine deficiency related symptoms by years and mark the prodromal stage of disease [1]. Further, fatigue, diplopia, anxiety, and dysphagia might occur during mid-stage disease, often still prior to diagnosis [1]. PD-specific dementia and cognitive dysfunction occur much later and mark the late stages in the progression of PD [1]. Most motor and non-motor signs worsen over the time course of the disease. Cognitive deficits, although often present at diagnosis, worsen in the later years of the disease and with age [8]. Diagnosis is often delayed due to the broad spectrum of non-specific signs in the prodromal and early stages and occurs during mid-to late stage of disease progression, when hallmark motor signs appear. The duration of each stage of the disease is variable as well as the order of the appearance of non-motor symptoms [1]. However, non-motor signs can appear throughout the course of the disease and often worsen over time. Figure 1 shows a timeline by which non-motor PD features are expected to manifest [1].

Figure 1.

Schematic timeline of non-motor features of PD [1]

Pathophysiology

The etiology of PD is not yet fully understood, but there have been substantial advances in identifying risk factors, genetic contributions, and early pathophysiology. PD is heterogeneous in its presentation, and there may be several different subtypes of PD based on age of onset, clinical presentation, sex, genetics, and pathology [9]. The average age of diagnosis is 60–65 years [10] but diagnoses are sometimes made earlier (early onset-45 years) or later in elderly populations (late onset-75 years) [9,11]. PD can also be subtyped into cases that are tremor-dominant versus akinetic-rigid (sometimes referred to as the postural instability and gait dysfunction, PIGD, type) [12]. Further, the prevalence and wide array of non-motor signs often precede hallmark motor signs, suggesting a non-motor subtyping – those with non-motor-dominant phenotypes or those with a mixed motor and non-motor phenotype [13].

There are also sex-based differences in how PD manifests. Overall, males are twice as likely to develop PD, with earlier age of onset [14] and more severe clinical presentation compared to females [14,15]. Males and females also differ based on predominant signs of disease. Females are more likely to present with depression, constipation, and tremor-predominant phenotype [16,17], whereas males are more affected by deficits in verbal fluency, rigidity, and daytime sleepiness [16,17]. In the context of swallowing, those with PD have larger pharyngeal areas compared to healthy individuals, an indicator of pharyngeal muscle atrophy [18]. A recent study reported that this may be more pronounced in males, thereby contributing to worse swallowing function [19]. Another study reported that male sex is one predictive clinical risk factor for increased penetration and aspiration in PD [20]. However, further research is needed to confirm and analyze sex differences in PD-associated dysphagia.

Research on mechanisms underlying non-motor signs of PD have led to subtyping based on neurotransmitter systems, including cholinergic, noradrenergic, serotonergic, and mixed dopaminergic [1,9,13]. Additionally, while the vast majority of cases are still considered idiopathic, more than 20 genes have been identified in PD, including GBA, LRRK2, SNCA, PINK1, PRKN, and DJ-1 [21]. About 10% of individuals with PD carry a GBA mutation, and these carriers are more likely to have earlier symptom onset and a predominantly PIGD phenotype with non-motor signs including depression, anxiety, and cognitive impairment [22]. LRRK2, especially the G2019S mutation, is one of the most common genes linked to PD. Approximately 1% are associated with sporadic and 4% with familial PD [23]. Cases associated with LRRK2 have a slower decline in motor signs and a lack of cognitive impairment [24].

Post-mortem analyses, biopsy, and animal research suggest subdividing PD into a brain-first or body-first disorder, whereby pathology originates either first in the brain and spreads to other neural regions and periphery (brain-first), or originates in the periphery and spreads to the brain (body-first) [25]. The brain-first hypothesis posits that pathology originates in the brain prior to spreading elsewhere. In line with this directionality of spread hypothesis, some propose an “amygdala-centered” pattern, where pathology is most abundant in the center of the brain (amygdala, entorhinal cortex, and substantia nigra), compared to lower brainstem regions, spinal intermediolateral column, and neocortical regions. Borghammer and colleagues indicate that an amygdala-centered profile appears to be one of two common patterns of Lewy pathology, as evidenced by postmortem studies [25].

Another proposed pattern is a caudo-rostral pattern, which is consistent with the body-first hypothesis. The Braak staging system is in line with the body-first hypothesis [25,26] as pathology may originate outside of the brain (e.g. the gut or olfactory bulb). It also suggests that pathology propagates in a caudal-to-rostral direction, affecting lower brainstem regions before higher/cortical regions. More specifically, caudal brainstem regions such as the dorsal motor nucleus of the vagus (Braak stage 1) show Lewy body pathology earlier than the substantia nigra or cortex (Braak stage 3–6). Figure 2 illustrates the Braak’s proposed disease staging system. Interestingly, brainstem regions associated with swallow function are located in the caudal brainstem. For example, nucleus ambiguus nerve fibers provide motor innervation for swallowing, including muscles of the pharynx, upper esophagus, and intrinsic laryngeal muscles [27]. The nucleus tractus solitarius integrates sensory information from vagally-mediated peripheral regions such as the larynx, pharynx, and esophagus, and synchronizes peristaltic activity during swallowing [27]. These swallowing brainstem regions are heavily connected to caudal brainstem regions affected early in disease progression according to Braak staging. Clinical studies and animal models reveal that changes to swallowing often occur in the prodrome, prior to hallmark motor disturbances and nigrostriatal dopamine depletion [1,28–30].

Figure 2.

Braak’s proposed disease staging system [35]; List of abbreviations: co, coeruleus–subcoeruleus complex; dm, dorsal motor nucleus of the glossopharyngeal and vagal nerves; fc, first order sensory association areas, premotor areas, and primary sensory/motor field; hc, high order sensory association areas and prefrontal fields; mc, anteromedial temporal mesocortex; sn, substantia nigra.

Hallmark pathologic markers of PD are inclusion bodies known as Lewy Bodies or Lewy Neurites. A major component of these bodies is an aggregated form of the protein alpha-synuclein (α-syn). Abnormal α-syn aggregation is consistently seen throughout the nervous system in many different subtypes of PD. Pathologic aggregation of α-syn leads to soluble oligomeric and insoluble fibrillary forms. Although Lewy Bodies have traditionally been identified in the central nervous system, there is also peripheral involvement, including findings in the upper aerodigestive [31,32] and gastrointestinal tracts [33,34]. This supports the hypothesis that PD onset may manifest earliest, in many cases, within the periphery [34].

Although not all cases present uniformly, it is very likely that PD onset begins decades prior to diagnosis, and that dysfunction at time of diagnosis is not reflective of the full pathophysiology occurring earlier in the disease process. This is because diagnosis is heavily reliant on motor signs, response to dopamine replacement, and/or fluorodopa imaging studies [36–38]. Yet, earlier non-motor and other motor signs of disease, including dysphagia, do not respond to favorably to dopamine replacement [39,40]. Some of the earliest and most common signs of PD include hyposmia, depression, sleep disturbances, gastrointestinal dysfunction, diplopia, anxiety, hypophonia, and dysphagia [1]. Dysphagia ultimately affects over 90% of patients and is associated with reduced quality of life, increased medical costs, increased social isolation, poor patient outcomes, and complications such as malnutrition, dehydration, and mortality [3,4,41,42]. Deficits include impaired sensation and movement for the safe and efficient transport of food, liquid, and saliva from mouth to stomach. Compromised swallow function often results in residue and airway compromise, which increases risk for aspiration pneumonia – the leading cause of death in PD [4,43,44]. However, the pathophysiology underlying swallowing dysfunction in PD is poorly understood. Current understanding points to dopaminergic and non-dopaminergic mechanisms being impaired in PD-related swallow dysfunction, with noradrenergic and serotonergic systems being implicated sooner [1].

Dysphagia in Parkinson disease

Dysphagia is prevalent in PD, estimated in 40-80% of individuals worldwide – depending on the type of diagnostic procedure [44], and can occur across all stages of disease [45]. Even though dysphagia typically worsens over time and becomes more apparent in later stages, early signs can occur in the prodromal and early stages [1]. However, dysphagia typically remains undiagnosed until later in disease progression. The hallmark features of dysphagia in PD include festinated/repetitive tongue movement (also termed tongue pumping) [46,47], reduced mastication speed and coordination [48], significantly prolonged oropharyngeal transit time [46,49], pharyngeal ‘spillage’ [49], and delayed swallow initiation [50]. Additionally, studies report an increased number of swallows to clear the pharynx of residue [46], slowed hyolaryngeal movements [51], and esophageal dysmotility [52,53]. Due to deficits in proprioception across sensorimotor functions [54,55], many individuals with PD are unaware of their swallowing issues [4,56]. Further, reduced laryngeal sensation can contribute to silent aspiration [46,53] and aspiration pneumonia, which is a major cause of hospitalization in patients with PD [57,58]. Deficits in airway protection are also very commonly evidenced by decreased expiratory cough airflow rates [59–61], decreased cough reflex [56,60,61], airway sensory deficits [54,55], and upper airway obstruction [62]. Additionally, esophageal abnormalities, as well as achalasia [63] and reflux [64] are commonly seen in this population.

The consequences of impaired safety and efficiency of swallowing in PD significantly and adversely affect quality of life and can lead to economic burden. Weight loss, malnutrition, and dehydration, as well as an increased risk for aspiration contribute to increased mortality rates [65]. However, we currently do not fully understand how the incidence and prevalence of aspiration pneumonia contributes to morbidity and mortality. Müller and colleagues reported an estimated mean survival time of 24 months after onset of dysphagia symptoms [66]. Additionally, individuals with PD often experience salivary changes during disease progression, described below, which can impact swallowing function, overall health, and quality of life.

Saliva

Salivation plays a key role in oral health and swallowing physiology, including: (1) moistening and formation of the bolus [67], (2) coating and lubrication of dental and mucosal surfaces [68–71], and (3) clearance of food debris from the oral cavity [72,73]. The major structures associated with salivary secretion are the paired parotid, sublingual, and submandibular glands [74]. These glands produce more than 90% of the salivary volume [75], and produce varying volumes and compositions of saliva depending on age [76], medications [77], and gland size [78].

About 50% of individuals with PD experience hyposalivation [79,80] and xerostomia [79], and 50% experience sialorrhea [44,81]. These two phenomena may appear contradictory because drooling may suggest excessive production of saliva. However, PD largely reduces salivary flow [82]. This reduction in flow may result from the high density of α-syn aggregation within salivary glands [83]. Excessive drooling in PD does not correspond with hypersalivation, but rather unsuccessful clearance of saliva from the oral cavity, such as reduced spontaneous swallow frequency [84,85]. In fact, individuals with PD may spontaneously swallow 39% less frequently than younger healthy controls [86]. However, a reduction in swallow frequency alone does not capture the complexity of salivary dysfunction, given that individuals with PD who complain of drooling swallow significantly more often than those with no complaints of drooling [87]. Instead, the primary predictor of drooling is facial and oropharyngeal hypokinesia. Therefore, an increase in swallowing frequency may be a compensatory response to reduce drooling and improve swallow efficiency [87]. Additionally, drooling may have a cognitive component, as individuals with PD swallow less frequently and drool more often when cognitively distracted [88].

In addition to flow, salivary composition is also altered. Individuals with PD have salivary microbiota profiles distinct from healthy controls, suggesting that oral dysbiosis may precede a decline in oral health in PD [89]. These early changes to the oral microbiota may predispose individuals to dental caries and inflammation, thereby contributing to the oral health issues experienced by individuals with PD [79]. Further, oral dysbiosis in PD may be linked to the dysbiosis in the gut [90], and could also increase the risk for respiratory infection in those patients who aspirate due to oropharyngeal dysphagia [91].

Diagnosis and Disease Monitoring in PD

Diagnosis of PD

The heterogeneous clinical presentation of PD complicates the diagnostic procedure. Diagnosis is primarily based on the presence of hallmark motor signs (i.e. resting tremor, bradykinesia, muscle rigidity, postural instability), response to dopamine replacement [92], and brain imaging [38]. However, a definitive diagnosis can typically only be verified postmortem. As aforementioned, many non-motor and other motor features of PD, including swallowing dysfunction, manifest in the early stages and often remain undiagnosed until later in the disease process [1,28,64].

Disease Severity Rating Scales

Clinical differentiation among disease stages is difficult and various scales are used to evaluate disease progression and severity during the diagnostic process. The Unified Parkinson Disease Rating Scale (UPDRS) is the most common tool used to measure disease severity in PD. It consists of three subsections with multiple individually scored signs using a scale from 0 to 4 with the lowest number representing no dysfunction and the highest number representing severe dysfunction. The scale measures 1) mentation, behavior, and mood, 2) activities of daily living, and 3) motor control [93,94]. Unfortunately, the UPDRS has only one question focused on swallowing and one focused on salivation, which does not represent the full complexity or severity of dysphagia in PD. The Hoehn and Yahr Scale (H&Y) is another measure of disease severity based on the UPDRS to assess motor deficits in PD [95]. Five stages of injury and disability are defined by this scale as five stages of disease progression: from no signs of disease to wheelchair bound or bedridden, unless aided [96]. Because swallowing dysfunction appears early in the disease process prior to time of diagnosis, this scale also does not fully reflect the severity and complexity of swallowing deficits relative to staging. Early Braak Stages (1-2) encompass pathology prior to nigrostriatal dopamine depletion; however, this framework does not account for earlier peripheral involvement such as α-syn aggregation in muscles and organs [1,97–100]. Further, Braak staging is not used clinically and is more often reported in research. Although dysphagia generally worsens with disease progression, this is not linear nor is it often associated with a particular disease stage due to the inherent heterogeneous presentation of PD and the lack of clinical tools used in neurology that include robust measures of swallowing function across stages.

Diagnosis of Dysphagia in PD

Dysphagia is not routinely addressed in standard neurology consultations despite the fact that dysphagia may present as one of the first signs of PD [101,102]. However, only 20–40% of patients are aware of their swallowing issues, in part because laryngeal sensation is impaired [4,56], contributing to silent aspiration in this population. Deficits in proprioception across most sensorimotor functions are a major feature of PD [54,55]. Therefore, a comprehensive approach to diagnosis is paramount to identify PD-associated swallowing changes in the early stages of disease [64].

Clinical Screening and Evaluation

Standardized self-report questionnaires are helpful in the diagnosis of swallowing dysfunction in PD and can serve as an initial screening for swallowing impairment. Of all available questionnaires, the dysphagia-specific Swallowing Quality of Life Questionnaire (SWAL-QOL) is the most commonly used to assess the impact of dysphagia on quality of life within PD [103]. The SWAL-QOL has also been a useful tool in research and clinical trials [3,104–106]. Additionally, the Sydney Swallow Questionnaire, a 17-item visual-analog scale self-report questionnaire used to evaluate several areas of an individual’s swallowing performance, is often used clinically and in research [107] .

Clinical examinations of swallowing using trials with solid and liquid boluses are also paramount for diagnosis of dysphagia in PD [4]. Protocols such as the ‘standard water swallow test’ can screen for signs of penetration or aspiration [4]; however, instrumented assessments are required to specify the nature and degree of impairment in the general diagnosis of dysphagia in this population [56, 108,109].

Instrumented Evaluations

In contrast to clinical screens and evaluations, instrumented assessments allow for visualization of structures in the oropharynx and yield functional measurement of swallowing physiology impairments. With instrumented tools, swallowing dysfunction can be detected in more than 50% of asymptomatic PD patients [50]. The two most commonly used tools to evaluate oropharyngeal dysphagia are the Videofluoroscopic Swallow Study (VFSS) [4] and Fiberoptic Endoscopic Evaluation of Swallowing (FEES).

VFSS allows for examination of the swallow using video x-ray technology to observe the oral, pharyngeal, and esophageal stages of the swallow, including bolus passage through the upper esophageal sphincter [110–112]. Additionally, the entire esophagus can be visualized during VFSS to assess esophageal dysfunction such as achalasia [63]. This procedure is usually performed in radiology (although mobile units can be used at bedside), and involves small amounts of radiation [112]. Lateral and anterior/posterior views allow for identification of anatomic and physiologic impairments related to swallowing. Individuals with PD often develop oropharyngeal swallow deficits (see Table 1), that contribute to issues with bolus clearance [50], and airway compromise/aspiration [46,53].

Table 1.

Typical findings from a VFSS in PD.

Finding	Selection of Articles
Repetitive tongue elevations (pumping)	[46,47]
Reduced mastication speed and coordination	[48]
Prolonged oropharyngeal transit time	[46,49]
Pharyngeal spillage	[49,50]
Delayed swallow initiation	[50]
Increased number of swallows to clear pharynx	[46]
Slowed hyolaryngeal movement	[51]
Esophageal dysmotility	[52,53]

FEES uses a flexible endoscope that is inserted into the nasal passage and passes through the hypopharynx, allowing visualization of pharyngeal and laryngeal structures [113]. Swallow safety (penetration/aspiration/clearance after cough) and efficiency (pharyngeal residue), as well as the anatomy and physiology of the velopharynx, posterior pharyngeal wall, epiglottis, vocal folds, pyriform sinuses, and the tongue base, can be assessed. Further, secretions and respiration can be evaluated, and sensory testing can be performed. FEES is arguably more sensitive especially for penetration and aspiration than VFSS [114,115]. Table 2 shows major findings of FEES in individuals with PD.

Table 2.

Typical findings of FEES in PD.

Finding	Selection of Articles
Penetration/Aspiration	[116–123]
Pharyngeal Residue	[116,118,121,123]
Premature Spillage	[117,118]
Post-swallowing Residue	[117,118]
Velopharyngeal Incompetence	[122]
Cough Reflex	[122]

High-Resolution Manometry (HRM) is useful for assessing pressure and timing events in the pharynx and esophagus [124]. A catheter with circumferential pressure sensors is passed through the nasal cavity into the esophagus. Spatio-temporal pressure measurements along the aerodigestive pathway provide quantitative descriptions of pressure and timing differentials during a swallow. HRM is a useful tool in identifying subclinical swallowing impairment, especially in the early stages of PD [4]. A multimodal approach using HRM in combination with the Sydney Swallow Questionnaire, has shown to be a robust method for the identification of even subtle sub-clinical changes in swallowing function and could identify individuals with early-stage PD with the highest accuracy compared to VFSS findings [28]. Further, intraluminal impedance can detect speed and direction of bolus movements [125] and is, in combination with pressure measurements, an effective assessment tool for motility and flow luminal content [126]. A combination of manometry and impedance has been used to evaluate esophageal motility disorders [127] and for the assessment of pharyngeal swallow [127]. Overall, impedance is a highly reliable tool when combined with HRM pressure/timing measurements and can assess pharyngeal residue [128].

Deficits in airway protection often result in worsening of health outcomes impacting quality of life; therefore, cough function assessment, including thorough pulmonary and airway examination, is recommended for PD-associated dysphagia [129]. Table 3 shows major findings of airway examinations in individuals with PD.

Table 3.

Typical findings of airway examinations in PD.

Finding	Selection of Articles
Decrease in peak expiratory cough airflow rate	[59–61]
Decreased cough reflex	[56,60,61]
Impaired sequential cough	[130]
Airway sensory deficits	[54]
Upper airway obstruction	[62]
Reduced pulmonary function	[62]

For a detailed analysis of disturbances in the oral, pharyngeal, and esophageal phases of swallowing in PD, a combination of tools are often used [4], including thorough airway and cough examination. Frequent oral phase findings in PD-associated dysphagia are repetitive tongue pumping, oral residue, premature spillage, and piecemeal deglutition [131]. Findings in the pharyngeal stage are residue in vallecula and pyriform sinuses, penetration, aspiration, somatosensory deficits, and reduced swallow rate in spontaneous swallowing [132]. In the esophageal phase, PD patients often present with esophageal hypomobility, spasms, and contractions [133].

Existing Gaps in Knowledge and Future Directions

A challenge in the diagnosis of PD is the considerable overlap in disease presentation with other similarly presenting conditions, such as essential tremor, dementia with Lewy bodies, and Huntington’s, to name a few [134]. Additionally, disambiguating the normal aging process from PD-related changes in swallowing function is difficult [135]. Efforts have been made to improve differential diagnosis of PD with the use of biomarkers such as detection of α-syn in cerebral spinal fluid, blood, and saliva [136,137]. While currently there is no established laboratory test or single biomarker that provides adequate sensitivity and specificity to identify PD, particularly in the early stages, these methods show promise for future clinical utility.

Lastly, gaps in knowledge remain concerning potential differences in clinical presentation between sexes in terms of phenotype, age of onset, and disease progression, especially with regard to dysphagia. This minimizes the generalizability of research on standard diagnostic procedures that may be biased toward male subjects. Future basic and translational research in the prodromal stage, with particular attention to both sexes, is necessary to collectively advance diagnosis and treatment options of dysphagia in PD.

Conclusion

Parkinson disease is a complex progressive condition involving the central and peripheral nervous systems. Often, individuals with PD present with motor and non-motor signs besides the hallmark motor deficits which are the primary target of clinical diagnosis. Further, the heterogeneous clinical presentation of PD often complicates diagnosis. Changes in swallow function can occur in the prodromal stage and often present as one of the first signs; however, dysphagia is typically not addressed during initial clinical diagnostic practices, which can delay prevention and treatment of swallowing impairments. Early comprehensive swallow assessments that combine functional assessments, patient reported outcomes/questionnaires, and instrumented evaluations are highly recommended to asses PD-related swallowing changes – especially in the early stages of disease. Early monitoring, assessment, and treatment may help combat the devastating sequela of untreated dysphagia and broaden treatment options. Since biological sex may play a role in PD phenotype, disease progression, and age of onset, diagnostic practices might require re-evaluation and refinement in order to address these potential differences. Unfortunately, only few studies have investigated sex differences and more research is needed to address this gap in knowledge. The second article in this set – “Dysphagia in Parkinson disease: Part II – Treatment Practices and Contributions from Animal Research,” addresses current treatments for PD and PD-associated dysphagia, and discusses insights from animal research.