Parkinson’s disease (PD) is a neurodegenerative disorder marked by the degeneration of dopaminergic neurons and characterized by both motor and non-motor symptoms. While traditionally defined by motor dysfunction, language and speech impairments are equally significant. Hypokinetic dysarthria, the most common motor speech disorder in PD, affects phonation, articulation, prosody, resonance, and respiration (Sapmaz Atalar et al., 2023). Yet, beyond these motor aspects, PD involves cognitive–linguistic impairments spanning semantics, fluency, discourse, and pragmatics.
This review synthesizes current findings on speech–language alterations, their neurobiological underpinnings, neuropsychological profiles, and neuroimaging and electrophysiological evidence, while also integrating clinical and therapeutic applications. It further suggests that early linguistic markers could serve as biomarkers for cognitive decline in PD.
Language is a cornerstone of social communication, emotional expression, and cognitive representation. In Parkinson’s disease, the progressive loss of dopaminergic function impairs not only movement but also communication abilities, profoundly influencing social interaction and psychological health.
Symptoms such as bradykinesia and muscle rigidity hinder speech fluency, while higher-order linguistic functions — semantic processing, syntax, and pragmatic understanding — are also compromised. As these communication challenges intensify, patients often face depression, isolation, and decreased quality of life.
This paper integrates the motor speech impairments (especially hypokinetic dysarthria) with higher-order linguistic dysfunctions (semantic, discourse, pragmatic) to illuminate their neurological and neuropsychological foundations, offering clinical and rehabilitative implications.
1. Speech and Language Disorders in Parkinson’s Disease
1.1 Hypokinetic Dysarthria
Between 80–90% of PD patients develop hypokinetic dysarthria (Sapmaz Atalar et al., 2023). This condition is characterized by:
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Monotony in speech
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Reduced loudness (hypophonia)
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Decreased stress and intonation variation
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Rapid, repetitive phoneme production
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Imprecise articulation
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Episodes of “freezing of speech”
These symptoms stem from laryngeal and thoracic rigidity, resulting in insufficient respiratory support. Importantly, many patients exhibit limited self-awareness of reduced speech volume — a reflection of impaired auditory–sensory feedback (Ho et al., 2000; Liu et al., 2012).
Neuroimaging has revealed dysfunctions in the striatum and premotor cortex, disrupting auditory–motor integration (Huang et al., 2016). Thus, speech impairment in PD represents not only a motor deficit but a broader sensorimotor integration disorder.
1.2 Impairments in Verbal Fluency, Semantics, and Discourse
Beyond articulation and voice, PD patients display cognitive-linguistic disturbances, including:
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Reduced word retrieval, especially for verbs
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Decreased semantic fluency
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Difficulty processing complex or abstract language
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Reduced narrative coherence and increased redundancy
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Impaired comprehension of irony, humor, and indirect meanings
These impairments arise from dysfunctions across frontal–striatal, temporal, and parietal circuits (Montemurro et al., 2019), reflecting the interplay between executive and semantic systems in PD.
2. Neuropsychological Profiles
Assessment of language in PD must consider cognitive factors alongside linguistic measures. Common evaluation tools include:
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Verbal Fluency Tests (semantic and phonemic)
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Boston Naming Test
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Token Test
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Narrative and Discourse Tasks (e.g., picture descriptions)
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Trail Making, Stroop, and Hayling Tests for executive function
Patients with mild cognitive impairment (PD-MCI) exhibit reduced semantic fluency and executive control, whereas those with Parkinson’s disease dementia (PDD) show comprehensive deficits in comprehension and discourse (Miller et al., 2006).
These findings reinforce the role of fronto-striatal degeneration in mediating the cognitive–linguistic continuum of PD.
3. Brain Structure and Neuroimaging Findings
The dopaminergic degeneration initiating in the substantia nigra–striatum pathway extends to cortico–basal ganglia–cerebellar circuits, affecting both motor and linguistic domains (Sapmaz Atalar et al., 2023).
Key findings include:
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DTI (Diffusion Tensor Imaging): Disruption of white-matter tracts — especially the arcuate fasciculus, uncinate fasciculus, and superior longitudinal fasciculus — correlates with reduced linguistic performance.
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fMRI: Reveals hyperactivation of the striatum–SMA circuit and compensatory frontal recruitment during speech tasks.
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PET: Demonstrates that dopaminergic modulation directly influences semantic access and prosodic control (Behroozmand et al., 2015).
4. Electrophysiological Evidence (ERP)
Event-Related Potential (ERP) studies provide temporal insights into language processing:
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Delays and reduced amplitudes in the N400 component indicate slowed semantic integration.
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Abnormalities in prosody-related timing further support a cognitive–semantic slowing model parallel to motor dysfunction.
These findings highlight a shared neural timing deficit, aligning linguistic processing delays with motor symptoms in PD.
5. Clinical Applications and Therapeutic Implications
The Lee Silverman Voice Treatment (LSVT LOUD) remains the gold standard for hypokinetic dysarthria. Administered four times per week for four weeks, LSVT significantly enhances:
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Vocal loudness
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Speech intelligibility
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Articulatory precision (Ramig et al., 2018)
Complementary interventions include:
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SPEAK OUT!® and Expiratory Muscle Strength Training (EMST)
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Traditional articulation exercises
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Compensatory strategies such as pacing and gestural support
Pharmacologically, levodopa offers limited improvement and may even worsen speech fluency at high doses. Likewise, Deep Brain Stimulation (DBS) may improve motor symptoms while deteriorating speech parameters.
Thus, optimal management necessitates a multidisciplinary approach—integrating neurology, speech-language pathology, neuropsychology, and caregiver education (Sapmaz Atalar et al., 2023).
6. Future Research Directions
To advance understanding and treatment, future research should prioritize:
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Standardized PD-specific language assessment batteries
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Longitudinal, multimodal studies integrating ERP, fMRI, and acoustic analyses
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Exploration of early linguistic biomarkers for cognitive decline prediction
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Utilization of AI-driven speech analytics for continuous monitoring and early detection
Conclusion
Language impairments in Parkinson’s disease extend beyond motor speech to encompass semantic, syntactic, and pragmatic dysfunctions. These multifaceted deficits reflect widespread neural network disruption — particularly within cortico-striatal and temporo-prefrontal circuits.
Comprehensive clinical evaluation must therefore address both acoustic–speech and neurocognitive–linguistic domains. Effective management integrates pharmacological, behavioral, and technological interventions within an interdisciplinary framework.
Ultimately, future multimodal and neuropsychologically informed research will deepen our understanding of PD’s language profile and its role in tracking disease progression.
References
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Sapmaz Atalar, M., Oğuz, Ö., & Genç, G. (2023). Hypokinetic dysarthria in Parkinson’s disease: A narrative review. Medical Bulletin of Şişli Etfal Hospital, 57(2), 163–170.
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Miller, N., Noble, E., Jones, D., & Burn, D. (2006). Life with communication changes in Parkinson’s disease. Age and Ageing, 35(3), 235–239.
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Ramig, L. O., Fox, C., & Sapir, S. (2018). Speech treatment in Parkinson’s disease: Randomized controlled trial. Movement Disorders, 33(11), 1777–1791.
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Huang, X., Chen, X., Yan, N., et al. (2016). The impact of Parkinson’s disease on cortical mechanisms supporting auditory-motor integration. Human Brain Mapping, 37, 4248–4261.
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Montemurro, M., et al. (2019). Pragmatic processing in Parkinson’s disease. Frontiers in Psychology, 10, 1220.
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Behroozmand, R., Shebek, R., Hansen, D. R., Oya, H., Robin, D. A., Howard III, M. A., & Greenlee, J. D. (2015). Sensory–motor networks involved in speech production and motor control: An fMRI study. NeuroImage, 109, 418–428.