Impact and management of cognition on speech and swallow function in Parkinson's disease

Abstract

Parkinson's disease (PD) is a multisystem neurodegenerative disorder involving motor and nonmotor symptoms. Cognitive impairment, dysarthria, and dysphagia are common during disease progression and are associated with reduced quality of life, loss of functional independence with activities of daily living, and increased morbidity and mortality. While cognitive impairment, dysarthria, and dysphagia are each well-described in PD, the extent to which cognition influences speech and swallowing function in this population requires further study. This narrative review aims to synthesize current evidence on how cognitive impairment intersects with dysarthria and dysphagia in PD. Relevant literature was identified through targeted database searches and citation tracking, emphasizing correlational and dual-task studies on cognition in relation to speech and swallowing outcomes. Although findings vary across tasks, cognitive domains, and disease severity, the literature collectively suggests that speech and swallowing draw on higher-level cortical processes, particularly attention and executive function, and that cognitive decline and increased cognitive load impact speech and swallowing performance in PD. The burden on the cognitive system is often under-recognized in the context of dysarthria and dysphagia management in PD. Further research that deeply explores the needs of individuals with PD and their care partners across the continuum of cognitive decline is necessary to inform person-centered care, as well as treatment approaches that cooperatively target cognition and speech/swallow function. Finally, future research addressing cognition in the early or even prodromal phase of PD may offer opportunities to increase cognitive reserve and mitigate cognitive decline.

Plain language title

How thinking affects talking and swallowing in Parkinson's disease

Plain language summary

Parkinson's disease (PD) causes problems with movement, and it can also affect thinking, talking, and eating. People with PD may need more help with everyday tasks due to thinking problems, and they may become less involved in social activities due to difficulty talking, as daily interactions become harder and less enjoyable. Additionally, difficulty eating makes mealtimes longer and less enjoyable for people with PD and may also lead to serious health problems such as malnutrition, pneumonia, and even death. This review looked at research about how changes in thinking impact talking and eating in people with PD. Overall, the research suggests that thinking skills such as planning, paying attention, and multitasking are important for speech and swallowing. Therefore, people with PD may have more difficulty with talking and eating when thinking skills are more compromised or when they are asked to do more than one task at a time. In these situations, speech may become less clear and swallowing may become less efficient or less safe (i.e., food or liquid going into the airway instead of the esophagus). However, it is important to note that these effects are not the same for everyone. Some individuals experience greater difficulty during complex tasks, and others are less affected. The type of task and the severity of thinking problems appear to influence these outcomes. This variability shows that thinking problems may impact talking and eating in different ways across individuals with PD. More research is needed to better understand these challenges and find ways to support thinking skills, effective communication, safe eating, and improved participation in daily life for people with PD.

Overview

Parkinson's disease (PD) is a multisystem neurodegenerative movement disorder, currently affecting 11 million persons with projections suggesting that this number will double by 2050.^1,2 In addition to the motor symptoms of PD such as hallmark movement disturbances, widespread nonmotor dysfunction is also part of the disease process. Cognitive impairment is a significant nonmotor feature of PD, reflecting cortical degeneration in brain regions that also support critical functional activities, such as speech and swallowing. Dysarthria, a motor speech disorder characterized by reduced speech intelligibility and articulatory imprecision, affects nearly 90% of individuals with PD over the disease course and is associated with decreased social participation and quality of life (QoL).^3,4 Similarly, dysphagia, or swallowing dysfunction, develops in over 90% of this population. ⁵ Impaired airway protection and reduced oral intake secondary to dysphagia can reduce mealtime participation and impact quality of life, ⁶ as well as result in severe health complications including malnutrition, dehydration, and aspiration pneumonia which contribute to increased healthcare utilization and mortality risk. ⁵

Figure 1.

Cognitive and motor control mechanisms contributing to speech and swallowing dysfunction in Parkinson's disease (PD). PD is characterized by impaired motor automaticity, necessitating increased dependence on cognitive resources to support speech and swallowing. However, PD is also associated with cognitive impairment, resulting in a “double burden” on the speech and swallowing mechanisms. Under increased cognitive load, already limited cognitive resources may break down, leading to reduced speech and swallowing performance in addition to poorer functional outcomes.

Approximately 20–33% of individuals with PD have mild cognitive impairment (MCI) at the time of diagnosis and 60–83% develop Parkinson's disease dementia (PDD) during their disease course. 7 Primary deficits in memory (including working, episodic, visual, and prospective), executive function, and visuospatial processing reduce capacity to perform activities of daily living (ADLs) and contribute to loss of functional independence.^8–14 These cognitive changes in PD are associated with decreased life expectancy, increased care partner burden, and increased risk of nursing home placement. ⁷ While cognitive impairment, dysarthria, and dysphagia are each well-described in PD, the extent to which cognition influences speech and swallowing function in this population remains unclear.

This narrative review synthesizes current evidence on how cognitive impairment intersects with dysarthria and dysphagia in PD. Specifically, we review the pathophysiology, clinical presentation, and behavioral treatment of cognitive impairment, dysarthria, and dysphagia in PD; examine the influence of cognition on speech and swallowing functions; identify recurring themes across studies; and discuss future directions for research. Relevant literature was identified through PubMed using Medical Subject Headings (MeSH) related to cognition, speech, and swallowing in PD. Searches were limited to English-language studies and selected based on explicit examination of cognitive impairment or cognitive task demands in relation to speech or swallowing outcomes in PD. Correlational studies and dual-task paradigms were prioritized. To capture literature not consistently indexed under PubMed MeSH terms, additional relevant studies were identified through Google Scholar using the same keywords. Citation tracking served as a tertiary search strategy. Abstracts were screened for relevance, followed by full-text review. Study design, cognitive measures, speech and swallowing outcomes, and overall findings were extracted and compared across chosen studies. Two authors reviewed these findings and agreed upon the interpretation. Though this review primarily seeks to highlight recent publications, earlier foundational studies are also included to more robustly characterize current understanding of these concepts.

Review of cognitive impairment, dysarthria, and dysphagia in Parkinson's disease

Cognitive impairment

Pathophysiology

Cognitive impairment in PD arises from widespread neuropathological and neurochemical dysfunction, with abnormal collections of alpha-synuclein protein (Lewy bodies) propagating across the brainstem, limbic, and cortical regions and disrupting neurotransmitter systems essential for cognition.^12,15–17 Loss of dopamine within frontostriatal circuits impedes communication between the basal ganglia and prefrontal cortex, adversely impacting executive functions. ¹⁷ Additionally, cholinergic degeneration from the basal forebrain disrupts posterior cortical function and contributes to memory (primarily working and episodic memory) as well as visuospatial deficits.^12,15–17 Lewy body pathology in the locus coeruleus diminishes noradrenergic availability and leads to impaired attention and inhibition.^12,16 Superimposed Alzheimer's disease pathologies (beta-amyloid and tau) on PD synucleinopathy also exacerbate cognitive impairment, particularly episodic and semantic memory and visuospatial dysfunction.^12,15,16 Structural damage secondary to gray and white matter atrophy further disrupts functional connectivity in cortical and subcortical regions.^12,16

Clinical presentation

Cognitive decline in PD does not follow a consistent trajectory and may emerge at any stage. However, the likelihood of developing cognitive impairment increases as neurodegeneration progresses. ⁷ Despite individual variability, PD most commonly affects executive functions, attention, memory (including working, prospective, and episodic memory), and visuospatial perception, ¹⁶ making executing instrumental ADLs difficult. Executive dysfunction may include impaired cognitive flexibility, inhibition, planning, and problem-solving^7,18 while attentional deficits are most evident in tasks that involve alternating attention and resisting distraction. ¹⁹ Memory is likewise vulnerable and typically reflects deficits in working, prospective, episodic, and visual memory, with long-term and semantic memory remaining relatively preserved.^8–14 Visuospatial function including spatial orientation, perceptual discrimination, visuoconstruction, and visual memory that are needed for everyday tasks such as navigation, facial recognition, and reading/writing, impact the ability to maintain independence.^7,20 Clinically, PD-related cognitive impairment is categorized as either MCI or PDD, distinguished by the extent to which deficits interfere with ADLs. ⁷

Treatment

Treatment of cognitive impairment in PD is challenging due to its variable presentation, unpredictable trajectory, and interaction with psychiatric and motor symptoms. Moreover, evidence-based cognitive interventions for PD remain limited. Cognitive training involves structured, repeated practice of specific cognitive tasks to promote neuroplastic adaptation. ²¹ Although there have been conflicting findings regarding the benefit of cognitive training for individuals with PD,^22–24 there is a body of evidence suggesting that various aspects of cognition may improve following cognitive training programs,^23–25 especially in the domains of executive function and short- and long-term memory. ²⁴ Greater benefits for those with MCI (versus PDD) highlight the need for early intervention.^24,25 However, these approaches often comprise decontextualized pen-and-paper or computerized tasks that have limited generalization to everyday function and ADLs. ²⁰ Data have shown that, even when cognitive training yields improvements on cognitive tests, subjective experience and long-term outcomes may not improve.^26,27 More ecologically valid cognitive rehabilitation approaches are needed. Compensatory strategies to facilitate participation in ADLs are also frequently used in cognitive treatment for PD, especially later in the disease course, including external memory aids such as calendars, lists, and medication organizers. ²⁰ Technology, including phone alarms and activity trackers, have also become increasingly popular methods of supporting memory and executive functions in daily activities. ²⁰

Dysarthria

Pathophysiology

Hypokinetic dysarthria (HKD), the characteristic motor speech impairment in PD, primarily arises from basal ganglia dysfunction. Loss of dopamine in the substantia nigra degenerates the nigrostriatal pathway, disrupting striatal input to the basal ganglia motor circuit and dysregulating the initiation, amplitude, and speed of speech movements.^3,28 This degeneration also extends to non-dopaminergic pathways of the broader cortical-cerebellar-basal ganglia network underlying the motor control required for accurate speech production.^28–30 As a result, disruptions in sensory and temporal processing occur, impairing the initiation, timing, and amplitude of articulatory movements and reducing the clarity of voice and speech. ³⁰

Clinical presentation

HKD can occur at any stage of PD but is often most severe in the later stages.^28,29 Common features include reduced vocal intensity (i.e., loudness), monopitch and monoloudness, breathy or hoarse vocal quality, imprecise articulation, reduced respiratory-speech coordination, festinating speech, short utterances, irregular pauses, and dysfluencies.^3,28–30 HKD results in reduced intelligibility and diminished ability to communicate effectively, which are associated with negative self-perception, reduced participation in daily interactions, social withdrawal, and reduced QoL.^3,31 Spontaneous conversation, diadochokinetic tasks, and dual-task conditions (i.e., multitasking) tend to increase speaking difficulty due to increased cognitive and/or motor demands, whereas symptoms are typically less pronounced during simple, structured tasks (e.g., sustained vowel phonation, reading words), because they reduce internal monitoring demands. External cues to speak louder/slower also offload control from the impaired internal monitoring system and tend to be more effective when cognitive communication demands are low. ³⁰ Because individuals with PD often exhibit reduced awareness of speech deficits—due to deficits in sensorimotor processes, executive function, and self-monitoring—generalization to functional contexts remains a challenge.^29,30,32

Treatment

Multiple behavioral treatments for HKD exist, with the well-established Lee Silverman Voice Treatment LOUD (LSVT) being one of the most common approaches. ³³ LSVT targets increased amplitude of respiratory and laryngeal systems (“loudness”) and sensory recalibration (self-monitoring of loudness) through a prescriptive, structured, and intensive program. ³⁴ In addition to improving loudness, ¹⁵ studies have reported neuroplastic adaptations following LSVT, such as increased activation in the right hemisphere premotor and motor cortices as well as association and integration areas. ³⁵ Cross-system effects on articulation, pitch, and overall intelligibility^36,37 as well as long-term (6–24 month) maintenance of communication gains^37,38 have all been reported following LSVT. SPEAK OUT! is a comparable amplitude-focused intervention with a modest evidence base, ³⁹ and includes an optional group-based treatment format (The LOUD Crowd). ³⁹ Other behavioral treatments to improve speech in PD with less evidence to support their use include music therapy, traditional voice or articulation therapy, Pitch Limiting Voice Treatment, feedback-based methods (such as biofeedback and masking noise), delayed auditory feedback, expiratory muscle strength training, and coaching strategies. ³⁹

Dysphagia

Pathophysiology

The pathophysiology of dysphagia in PD is thought to involve both dopaminergic and non-dopaminergic pathways, yet exact mechanisms remain unclear.^5,40 Dopamine deficiency in the striatum may impair basal ganglia input to the supramedullary network that is active during volitional swallowing. ⁴⁰ Lewy body deposition in non-dopaminergic regions of the brainstem and cortex may further disrupt swallowing control. ⁴⁰ Beyond the central nervous system, post-mortem PD studies have identified alpha-synuclein pathology in peripheral nerves innervating pharyngeal muscles. ⁴¹ Peripheral neurodegeneration may contribute to pharyngeal muscle wasting, which aligns with reports of increased atrophic myofibers in pharyngeal muscles of individuals with PD-related dysphagia. ⁴² Collectively, current evidence suggests dysphagia in PD is complex, involving multi-regional pathology at the cortical, subcortical, and peripheral levels disrupting both sensory and motor aspects of swallowing.

Clinical presentation

Swallowing difficulty may occur at any point during PD progression. ⁴³ Despite evidence of early impairments, dysphagia is often not identified until symptoms are severe. ⁵ Clinical features of dysphagia include repetitive lingual movements (“tongue pumping”), slowed and disorganized mastication, lingual weakness, prolonged bolus transit, premature bolus spillage into the pharynx, delayed swallow initiation, impaired respiratory-swallow coordination, and an increased number of swallows to clear oropharyngeal residue (material left in the mouth/throat after the swallow).^5,44,45 These features often result in bolus errantly entering the laryngeal vestibule (penetration) or the airway (aspiration). Due to parallel degradation in cough sensory thresholds and motor effectiveness (i.e., dystussia), individuals with PD often do not sense and/or are unable to effectively eject penetrated/aspirated material.^46–48 Together, swallowing impairments, diminished laryngeal sensation, and reduced cough effectiveness contribute to silent aspiration and aspiration pneumonia, a primary cause of death in individuals with PD.^40,46,49 Sialorrhea (drooling) is another common symptom and reflects reduced frequency of spontaneous swallows rather than hypersalivation; in fact, PD is associated with hyposalivation. ⁵⁰ Furthermore, a combination of reduced sensorimotor proprioception and executive dysfunction may contribute to limited awareness of swallowing deficits. ³² Dysphagia in PD is associated with weight loss, malnutrition, dehydration, and aspiration, all of which contribute to increased morbidity and mortality in addition to reduced QoL and increased economic burden. ⁵

Treatment

Treatment for PD-related dysphagia is typically categorized into compensatory and rehabilitative approaches. Compensatory strategies aim to support safe and efficient swallowing through behavioral modifications; examples include taking small bites/sips, increasing sensory input (cold or sour boluses), alternating food and liquids, slowing rate of intake, postural techniques, and dietary modifications (i.e., altering the texture/consistency of food/liquid).^51,52 While compensations may temporarily improve swallowing ease and/or safety, they do not address the underlying impairment and do not mitigate the risk of aspirating secretions/saliva.^53,54 In contrast, rehabilitative approaches aim to improve swallowing physiology through targeted exercise. Expiratory muscle strength training (EMST), which requires forcefully exhaling against resistance into a pressure-calibrated device, has been shown to improve airway protection in individuals with PD.^40,51,52,55 Sensorimotor training for airway protection (smTAP) is an alternative skill-based treatment approach which aims to optimize cough strength and coordination through a task-specific coughing exercise. ⁵⁶ Additionally, LSVT has been shown to have cross-system improvements in swallowing despite its primary use for HKD.^57,58 Preliminary evidence suggests that lingual strengthening may enhance tongue pressure and suprahyoid muscle activation in PD but larger interventional trials are needed to examine impacts on swallowing outcomes. ⁵⁹ Targeted maneuvers—such as the effortful swallow, Mendelsohn maneuver, supraglottic swallow, and falsetto exercise—are also used to address specific physiologic components of the swallow, although there is limited evidence to support their efficacy in PD.^51,52,60,61 The pathophysiology, clinical presentation, and treatment of cognitive dysfunction, dysarthria, and dysphagia are summarized in Table 1.

Table 1.

Review of cognitive impairment, dysarthria, and dysphagia in Parkinson's disease.

	Cognitive impairment	Dysarthria	Dysphagia
Pathophysiology	Lewy body pathology; neurotransmitter dysfunction; beta amyloid and tau co-pathology; structural atrophy	Dopamine loss; basal ganglia dysfunction; cortico-cerebellar-basal ganglia pathway degeneration	Dopamine loss; Lewy body deposition; alpha-synuclein pathology; peripheral neurodegeneration
Clinical Presentation	Deficits in executive function, attention, memory, and visuospatial skills; difficulty performing ADLs	Reduced loudness; monopitch; breathiness; imprecise articulation; festinating speech; shorter utterances; dysfluencies	Tongue pumping; delayed initiation; impaired respiratory-swallow coordination; reduced cough effectiveness; penetration/aspiration; drooling
Treatment	Cognitive training via repeated practice; compensatory strategies (e.g., external memory aids)	Intensive, amplitude-focused interventions (e.g., Lee Silverman Voice Treatment; SPEAK OUT!)	Compensatory strategies (e.g., small bites/sips); rehabilitative approaches (e.g., expiratory muscle strength training; exercises such as effortful swallow or Mendelsohn maneuver)

Impact of cognitive decline in speech and swallowing in Parkinson's disease

Cognitive influences in speech

Baseline cognitive impairment and dysarthria

Dopamine depletion in fronto-striatal pathways that connect the basal ganglia with frontal and prefrontal cortices disrupts cognitive and motor processes that underlie speech production. Correlational studies have sought to describe baseline associations between cognitive decline and motor speech impairment in PD, with findings generally supporting a relationship between dysarthria and executive function, attention, and working memory. Sousa et al. (2023) compared cognitive status and dysarthria severity in individuals with and without HKD and found that those with HKD performed worse on assessments of executive function, especially divided and alternating attention, in comparison to the non-HKD group. ⁶² Additionally, the authors noted that individuals with HKD more frequently expressed concerns regarding cognition. ⁶² Barnish et al. (2017) found poorer performance on the Montreal Cognitive Assessment (MoCA) correlated to lower scores on measures of functional communication in participants with PD; however, cognitive status was not a predictor of intelligibility. ⁶³ In a cross-sectional, observational study by Liu et al. (2019), deficits in attention and memory were strong independent predictors of PD-related dysarthria, with participants in this group demonstrating lower ADL scores and a higher incidence of frontal and temporal lobe lesions. ⁶⁴ This pattern has also been observed in prosodic studies, with Thies et al. (2020) reporting that individuals with PD demonstrated impaired prominence marking (speech emphasis), which was linked to executive dysfunction and motor impairment. In contrast, Steurer et al. (2022) found no significant association between cognitive performance and speech production, though dysarthria was related to structural changes in cortical regions implicated in executive function. ⁶⁵ Overall, despite variations in effect sizes and study designs, executive and attentional dysfunction are frequently correlated with motor speech impairment in PD.

Cognitive demand in motor speech performance

Cognitive influences on speech production have conventionally been examined through dual-task studies, often under conditions of increased attentional demand, which highlight the interaction between the cognitive and motor speech systems and their vulnerability. Fournet et al. (2022) used a dual-task paradigm to examine attentional involvement in motor speech encoding. ⁶⁶ Participants with PD and mild to moderate HKD performed an automatic speech task (reciting days of the week) concurrently with either a computerized processing speed task (stimulus detection) or an inhibition task (stimuli discrimination). ⁶⁶ In the less demanding condition (processing speed), speech rate was relatively preserved at the expense of non-speech task performance. ⁶⁶ However, in the inhibitory condition, speech rate and non-speech task performance both declined, with dual-task costs greater in those with more severe HKD. ⁶⁶ Interestingly, set shifting, or cognitive flexibility, was associated with baseline motor speech function but did not predict greater dual-task costs. ⁶⁶

Whitfield and Goberman (2017) utilized a dual-task paradigm to investigate cognitive mechanisms specifically related to speech motor learning in young adults, healthy older adults, and individuals with PD. ⁶⁷ Participants learned and practiced a sequence of six nonwords; on the following day, they recited the nonword sequence while simultaneously completing a computerized visuomotor tracking task. ⁶⁷ Although individuals with PD were able to initially learn the nonword sequence at a similar level to age-matched controls, they demonstrated the greatest degree of mutual interference under dual-task conditions the following day, performing worse on both the speech and non-speech tasks compared to other groups. ⁶⁷ In contrast to attention-focused studies, Dragicevic et al. (2024) designed a Stroop-like dual task to investigate the effects of working memory demand on speech production in PD. ⁶⁸ Participants with PD and age- and sex-matched controls were recorded reading sentences embedded with names of colors and were instructed to state the color of the ink as opposed to the written color name. ⁶⁸ The PD group did not demonstrate greater speech deterioration under dual-task conditions than controls. ⁶⁸

Understanding the influence of cognition on motor speech production depends on how speech tasks are defined and the specific demands of the concurrent cognitive task. Individuals with PD may have difficulty dividing attention equally under dual-task conditions and instead may adopt a serial alternating attention strategy, as evidenced in a study where spontaneous speech afforded more flexibility for pausing to separate competition between tasks, and speech deficits were more evident during numerical recitation tasks due to the continuous nature of that task. ⁶⁹ This interpretation may appear to contradict evidence that individuals with PD experience greater communicative difficulty in conversation and struggle with alternating attention,^30,36 but may be attributed to the degree of task complexity (e.g., familiar topic) and opportunity for alternating attention. ⁶⁹ Fournet et al. (2022) found that speech performance was prioritized during the less-demanding stimulus detection task, while both speech and non-speech performance worsened when the concurrent task required response suppression. ⁶⁶ Together, findings suggest that motor speech production in PD may deteriorate when concurrent cognitive demands require sustained attentional control, reducing opportunities for compensatory prioritization or task separation.

Related limitations appear to occur during speech motor learning. Whitfield and Goberman (2017) proposed that learned utterances become increasingly automatic, with poorer performance in the PD group reflecting incomplete automatization and greater reliance on cortical processing. ⁶⁷ This interpretation parallels Ho et al. (2002) in which numerical recitation, an automatic speech task, deteriorated under increased attentional load, suggesting that speech production in PD remains dependent on cognitive resources. ⁶⁹ This may be explained by impairments in automatic processing and subsequent increased attentional resource allocation required for accurate speech production in PD.^70,71

While Dragicevic et al. (2024) ⁶⁸ centered their paradigm on working memory, the task had inherent executive demands, including inhibition and selective and sustained attention; however, in contrast to the aforementioned studies, speech performance was relatively preserved under these conditions. One possible interpretation is that participants in Dragicevic et al. (2024) ⁶⁸ benefitted from the external support offered by written sentences; whereas, dual tasks in the other studies required greater internal generation and regulation of speech output—which is impaired in PD. Thus, speech performance in PD may reflect the interplay between internal modulation capacity, external support availability, and cognitive load, rather than any single factor in isolation. Clinically, individuals with PD are often able to achieve greater loudness or speech clarity with cueing (external support), yet deficits in executive function, awareness, and self-monitoring ability (internal modulation) often limit the degree to which these treatments generalize to conversational contexts (increased cognitive load). Clinicians may consider treatment paradigms that integrate executive function skills with improving speech loudness/clarity to promote treatment gains that generalize to functional conversation.

Cognitive influences in swallowing

Baseline cognitive impairment and dysphagia

Correlational studies have aimed to identify interlinkages between cognition and swallowing in PD. Kim et al. (2015) found that executive function and verbal memory (immediate and delayed recall) deficits were associated with oral phase swallowing impairment, proposing that PD-related cognitive decline primarily disrupts volitional processes such as mastication and lingual movement, whereas the pharyngeal phase is more reflexive and less influenced by cortical dysfunction. ⁷² In contrast, Battista et al. (2025) found attentional and executive dysfunction in individuals with PD were associated with increased laryngeal penetration and pharyngeal residue, indicating a parallel decline or possible relationship between pharyngeal phase swallowing and cognitive decline. ⁷³

The relationship between cognition and swallowing has been further illustrated through research on dysphagia risk. A six-year longitudinal study by Wang et al. (2022) identified cognitive impairment as an independent predictor of dysphagia in PD ⁷⁴ ; while Pflug et al. (2018) reported that aspiration (Penetration-Aspiration Scale [PAS] score of 7 or 8) was more prevalent in individuals with PD-related cognitive deficits. ⁴³ Together, these correlational studies suggest cognitive impairment in PD may be associated with, and could possibly predict, dysphagia across oral and pharyngeal phases, confirming critical cortical involvement alongside brainstem modulation of swallow function.

Cognitive demand in swallowing performance

Further support for cognitive influences on swallowing in PD has emerged from dual-task research. Brodsky et al. (2012) investigated the role of divided attention in swallowing using a dual-task design. ⁷⁵ At the same time as swallowing a 5 mL bolus, participants were instructed to press a foot pedal when a target nonword was presented. ⁷⁵ Under this dual-task condition, slower responses to nonword stimuli were observed during the anticipatory phase (the period between reaching for the cup and bringing it to the mouth) but not during oropharyngeal swallowing, though interpretation was limited by lack of instrumental assessment. ⁷⁵ Similarly, Reynolds et al. (2018) examined divided attention using a dual-task paradigm in relation to sialorrhea in PD. ⁷⁶ The authors found that participants with PD swallowed less frequently and drooled more during a distracting task than at rest. ⁷⁶

Expanding on Brodsky et al. (2012), Troche et al. (2014) used videofluoroscopy to assess the impact of concurrent attentional load. Participants with PD-related dysphagia listened to a digit sequence, swallowed 10 mL thin liquid barium, and then recited the digits.^75,77 Swallowing safety, characterized by PAS scores, worsened under dual-task conditions in those with mild cognitive deficits but unexpectedly improved in those with more impaired cognition. ⁷⁷ A study by Labeit et al. (2020) employed a dual-task design using Fiberoptic Endoscopic Evaluation of Swallowing (FEES) in which participants with PD, with or without dysphagia, silently rehearsed a six-digit number while swallowing. ⁷⁸ Across the sample, the added attentional demand of the digit rehearsal task increased premature spillage and pharyngeal residue, with dual-task costs greater in participants with lower MoCA scores ⁷⁸ —in contrast to Troche et al.'s (2014) ⁷⁷ findings which suggested that dual-task costs were greater for those with higher cognition. Similarly, Ardenghi et al. (2021) found that pharyngeal residue increased during a manual digit opposition task in individuals with PD (but not controls) and that more severe dysphagia in the dual-task condition was linked to poorer performance on the MoCA. ⁷⁹

Findings from these studies indicate that increased cognitive load does not appear to uniformly affect swallowing function in PD. Under dual task conditions, Troche et al. (2014) ⁷⁷ reported that greater cognitive impairment may preserve swallowing safety whereas Labeit et al. (2020) ⁷⁸ and Ardenghi et al. (2021) ⁷⁹ found it was associated with reduced swallowing efficiency. One interpretation is that airway protection may be prioritized over bolus control and pharyngeal clearance under limited attentional capacity. In this context, the seemingly paradoxical findings from Troche et al. (2014) (wherein swallowing safety improved during the dual task in participants with more impaired cognition but worsened in those with only mild cognitive deficits) may point to a nonlinear relationship between attentional allocation and swallowing across stages of cognitive impairment. Increased mental arousal secondary to demanding dual-task conditions is another possible explanation. ⁷⁷ Additionally, methodological variation across studies (e.g., videofluoroscopy versus FEES) should be considered, as different assessment tools may be more sensitive to certain swallowing outcomes. While the variable findings are likely attributable to heterogeneity in research design, oropharyngeal swallowing appears to draw on attentional resources, and this relationship may depend on the severity of cognitive impairment.

Themes and future directions

This narrative review describes cognitive, speech, and swallowing impairments in PD. The current evidence suggests a complex relationship between cognitive decline and speech/swallowing decline in PD and highlights the shared neural substrates underlying these functions. Speech and swallowing are not purely motor behaviors; rather they rely heavily on top-down cortical control. Moreover, greater recruitment of cognitive resources is necessary to circumvent the degraded automatic system in PD. Yet, these very cognitive processes—attention, executive function, and working memory—are also disrupted in the disease process, limiting capacity to recruit compensatory strategies. This effect is highlighted through dual task studies which illustrate the degradation of speech intelligibility and swallow safety/efficiency when attention is divided or cognitive load increases. This creates a significant dual burden on the cognitive system and is often under-recognized in the context of dysarthria and dysphagia management in PD. Treatment approaches that synergistically target cognition and speech/swallow function are necessary.

Given the limited body of literature integrating these topics, a narrative format was chosen as a first step to conceptually explore the interrelationships among cognition, speech, and swallowing in PD. The next step in this work is to use the information generated to inform the design of a systematic or scoping review that will allow comparisons between studies and identification of gaps in the literature. It is important to note that the studies described in this review are cross-sectional and correlational in design and causation cannot be determined. Great heterogeneity in disease presentation and progression in PD preclude drawing largescale ubiquitous conclusions. Rather, there is a need to consider potential phenotypes and personalized management that integrates cognitive and speech/swallow training. Moreover, cognition has a moderating effect on treatment efficacy and should routinely be incorporated into speech/swallow evaluations to inform treatment selection. Speech/swallow treatments may be tailored to unique cognitive profiles and (1) include targeted cognitive rehabilitation that is functionally aligned with speech/swallow goals and (2) adapt treatment type (e.g., compensatory vs rehabilitative) and parameters (e.g., cueing, feedback, dosing, visual aids, external supports, spaced retrieval training, care partner involvement) based on cognition. Qualitative and mixed methods research that deeply explores the needs of patients with PD across the continuum of cognitive decline as well as their care partners, is critical to inform relevant and person-centered treatment design. Finally, future research may examine ways to address cognition in the early or even prodromal phase of PD, with the potential to increase cognitive reserve and delay or prevent cognitive decline.