Voice and Speech in Atypical Parkinsonian Disorders

Abstract

Background

Motor speech disorders are early, common, and functionally limiting features of atypical parkinsonian disorders (APDs) such as progressive supranuclear palsy (PSP), corticobasal syndrome (CBS), and multiple system atrophy (MSA). These impairments are underrecognized and undertreated in neurology clinics.

Objectives

This review aims to characterize speech impairment in APDs, offer practical guidance for clinical evaluation, highlight the role of Speech‐Language pathologists (SLPs) in diagnosis and management, and outline current and emerging management strategies.

Methods

A narrative review was conducted by the Diagnosis and Treatment Working Group of CurePSP's Centers of Care, integrating literature and clinical experience to summarize evaluation, diagnosis, and treatment of motor speech disorders in APDs.

Results

Speech changes in APDs are often mixed dysarthrias with hypokinetic, spastic, and/or ataxic components, and may include apraxia of speech; these are frequently more severe and progress quicker than in Parkinson's disease. These features can assist in differential diagnosis and should prompt early referral to SLPs. Despite the high prevalence of speech and voice changes, comprehensive assessment of motor speech disorders is uncommon in neurology clinics. Current evidence regarding the efficacy of interventions is mixed. Digital acoustic analysis and neuromodulation offer promising directions for diagnosis and treatment.

Conclusions

Early, collaborative management of motor speech impairment elevates care in APDs. Neurologists and SLPs must work together to improve recognition, diagnosis, and care. Future research should focus on objective biomarkers and personalized therapies to support communication, autonomy, and quality of life for individuals living with APDs.

Voice and speech (ie, motor speech) impairments typically appear early and are nearly universal in atypical parkinsonian disorders (APDs) such as progressive supranuclear palsy (PSP), corticobasal syndrome (CBS), and multiple system atrophy (MSA). The presence of specific speech patterns may aid diagnosis and predict disease severity. ¹ In addition, speech and communication difficulties profoundly affect quality of life in APDs, given their frequency, severity, impact on social interactions and self‐advocacy, and their correlation with dysphagia. ² , ³ Changes in voice and speech in APDs also contribute to care partner burden due to impairments in communication between disease‐affected individuals and their families. ⁴ Despite these facts, the understanding of the prevalence, assessment, characterization, and management of speech impairments in the APDs remains underdeveloped by neurologists. ⁵

Our collective experience as the Diagnosis and Treatment Working Group of CurePSP's Centers of Care suggests that among the reasons for this limitation are (1) insufficient literature on how to evaluate and best address speech and communication changes in APDs in the neurology clinic, and (2) delays in involving speech‐language pathologists (SLPs). The evaluation of verbal communication encompasses voice, speech, language, and cognition; however, this practical review focuses primarily on the first two. Language and cognitive issues can play a significant role in speech impairment but require a separate dedicated review. The group of authors, comprising neurologists and speech‐language pathologists, hopes that this comprehensive overview of voice and speech symptoms related to APDs and strategies for management will help neurology professionals feel more confident in their care for individuals with PSP, CBS, and MSA.

Motor Speech Disorders

Pathophysiology and Syndromes

Understanding motor speech production and how impairments develop are critical to a comprehensive assessment and tailored symptom management. ⁶ Voice and speech production rely on the coordination of five key subsystems: respiration (which is used in the literature to refer to ventilation, rather than the formal definition of gas exchange), phonation, resonance, articulation, and prosody. ⁷ Respiration provides the airflow from the lungs, serving as the energy source for speech, which powers phonation. ⁸ Phonation occurs as the vocal folds in the larynx vibrate to create a voiced sound. ⁸ Resonance reflects the shaping of sound as it travels through the vocal tract, including the throat, oral cavity, and nasal passages. Articulation involves the precise movements of the tongue, lips, jaw, and other parts of the vocal tract to form distinct speech sounds. Finally, prosody adds rhythm, pitch, and loudness variation, giving speech emotional expressiveness. ⁷

Neurological impairments can affect individual features of movement, such as strength, symmetry, range, tone, steadiness, speed, and accuracy, which occur in each of the motor speech subsystems. ⁷ The taxonomy of motor speech production impairment parallels that of body and limb movements, including spasticity, rigidity, hypokinesia, incoordination, and tremor. ⁷ The term “motor speech disorders” encompasses both dysarthria, characterized by disruptions in neuromuscular execution that affect voice and speech, and apraxia of speech (AOS), which involves difficulties in planning and programming motor speech. ⁹

The nature and localization of the motor speech disorder can be recognized based on the distinct perceptual features noted by the examiner. These features form the basis for classifying dysarthria, as proposed by Darley, Aronson, and Brown. ¹⁰ This classification proposes six types of dysarthria, characterized by distinct clusters of motor speech profiles across different subsystems associated with distinct localizations, including the basal ganglia, cerebellar networks, and motoneurons (see Table 1, with further explanations of some terms in Table S1). The understanding of the neurological mechanisms underlying the pathophysiology of various dysarthria clusters remains very limited, particularly with regard to APDs.

TABLE 1.

Motor speech characteristics and suspected neuroanatomical correlates by dysarthria type and apraxia of speech

Subdomain a	Hypokinetic	Hyperkinetic	Ataxic	Spastic	Flaccid	Apraxia of speech
Vocal loudness	Reduced Loudness decay	Variable	Excess loudness variation	Reduced	Reduced	No characteristic changes
Voice quality	Hoarse/Harsh Runs out of air when speaking	Hoarse Vocal tremor Pitch instability and/or breaks Transient breathiness Voice stoppage	Monopitch Pitch instability Intermittent hyponasality	Strained Strangled Pitch breaks Hypernasality	Breathy Strained Hoarse Pitch breaks Pitch instability Diplophonia Hypernasality	No characteristic changes
Rate of speech	Fast Short rushes of speech	Variable	Slow/Variable	Slow Short phrases	No characteristic changes	Slow Reduced syllables per breath group
Flow/fluency and cadence	Stuttering‐like dysfluencies Delayed initiation	Speech interruptions (abnormal noises) Prolonged intervals between words Prolonged sounds	Prolonged sounds Irregular breakdowns	Effortful	Effortful	Groping Restarts Distorted substitutions/additions Syllable segregation Prolonged intervals between and within multisyllabic words Prolonged sounds
Articulation accuracy	Imprecise	Imprecise (inconsistent errors) Distorted vowels	Imprecise (inconsistent errors) Distorted vowels Telescoping	Imprecise (consistent errors) Distorted vowels	Imprecise (consistent distortion) Distorted vowels	Imprecise (inconsistent errors) Distorted vowels Articulatory groping Sound sequencing errors
Word and phrasal stress and intonation	Monopitch Monoloudness Reduced stress Inappropriate silences	Inappropriate silences/pauses	Excess/equal stress	Monopitch Monoloudness	Monopitch Monoloudness	Excess/equal stress Atypical silences/pauses Errors in placing stress
Localization	Basal ganglia	Basal ganglia	Cerebellum and/or cerebellar circuitry	Bilateral upper motor neurons	Lower motor neurons	Supplementary motor cortex

^a Impairments in multiple domains can lead to certain characteristics. In order to make the table more accessible, we have placed features that may correspond to different subdomains into a single category.

In bold, the characteristics that tend to be distinctive or more severely impaired when compared to other dysarthria types. Adapted from Duffy. ⁷

In addition to dysarthria, AOS needs to be considered when evaluating motor speech. ⁹ AOS is characterized by impaired planning and programming of speech movements, often resulting in inconsistent articulation errors and disrupted prosody, despite preservation of muscle strength. ⁹ AOS tends to have relatively isolated disturbances of articulation and/or prosody. ¹¹ , ¹²

This approach provides a helpful first step in characterizing motor speech. However, in APDs, multiple systems are affected simultaneously, and features of different types of dysarthria and AOS may co‐occur. ¹³ Careful evaluation and description of the various features can guide both diagnosis and treatment.

Motor Speech Disorders in APDs

Dysarthria is common in APDs, appearing earlier, with greater severity, and with more rapid progression than in Parkinson's disease (PD). ¹⁴ This feature can help distinguish APDs from PD. ¹⁵ In addition, there are qualitative differences. In PD, voice and motor speech changes most commonly present as hypophonia, or a hypokinetic dysarthria, characterized by reduced loudness and a harsh voice quality. ¹⁶ Speech is usually fast in rate and/or with short rushes of speech due to decreased range of motion, leading to articulatory imprecision. ¹⁶ , ¹⁷ In addition, there is a lack of modulation in speech and loudness (ie, a uniformity in syllabic stress and overall low volume described as monotone speech and monoloudness). ¹⁶ The presence of features of other types of dysarthria, such as spastic or ataxic, with or without features of hypokinetic dysarthria, warrants concern for an APD (Table 1). ⁵

In PSP, dysarthria can be the presenting symptom, and less intelligible or incomprehensible speech is often the first significant disability patients experience. ⁵ The voice and speech profile in PSP is variable. Hypokinetic dysarthria is the most common type of dysarthria, followed by a mixed hypokinetic‐spastic type with predominant hypokinetic features. ¹⁸ The hypokinetic features of dysarthria in PSP may be similar to those seen in PD (ie, reduced loudness, hoarse/harsh voice quality, rapid rate with rushes of speech, articulation imprecision, monopitch and monoloudness) but more severe in nature and emerging at earlier stages. ¹⁸ In addition, PSP often presents with elements of voice spasticity, such as a strained or strangled vocal quality and hypernasality. ⁵ The rate of speech in PSP may be particularly slow, monotone, and effortful (sometimes described as “robotic”), rather than fast and/or accelerating, as in hypokinetic dysarthria in PD. ¹⁶ If elements of ataxic dysarthria are present, these usually include scanning speech (ie, slow and deliberate speech characterized by inappropriate breakdown of words into syllables with varying loudness), prolonged speech pauses, distorted vowels, and articulatory imprecision. ¹⁹ The latter sometimes leads to telescoping (ie, inappropriate omission or collapsing of syllables). In advanced cases, patients may become severely hypophonic or anarthric (ie, the most severe form of dysarthria and/or apraxia of speech), unable to initiate voicing or articulation due to the severity of the motor speech disorder. ²⁰

AOS can also be present as an initial symptom of PSP or begin later. ¹⁸ AOS frequently occurs with dysarthria, and less frequently in isolation. ¹⁸ Most descriptions of dysarthria in PSP predate the establishment of PSP variants and describe the typical speech in PSP‐Richardson's syndrome. ²¹ In contrast, the recently defined PSP‐speech language variant (PSP‐SL) is characterized by the presence of progressive AOS or agrammatic aphasia. ²² However, AOS may also be present—though not as prominently—in PSP subtypes other than PSP‐SL, such as PSP‐Richardson's syndrome or PSP‐parkinsonism. ¹⁸ Other features, such as stuttering, freezing of speech, and palilalia (ie, repetition of syllables, words, or phrases that were just said), can be present in PSP, and their presence should increase the likelihood of PSP in the differential diagnosis. ⁵ Echolalia, which refers to the repetition of words said by others, usually immediately, is a less common phenomenon. ²³

CBS presents with similar patterns of speech deficits as PSP, with AOS and a non‐fluent/agrammatic variant of primary progressive aphasia as possible initial manifestations in dominant hemisphere‐onset cases. ²⁴ While speech changes can be observed in almost a quarter of cases at onset, they can occur in up to half of cases throughout the course of the disease. ²⁴ In the context of CBS, which is generally due to either a 4R‐tauopathy or Alzheimer's disease, or less commonly TDP‐43 proteinopathy, the presence of dysarthria and/or AOS is suggestive of a 4R‐tauopathy, particularly corticobasal degeneration (CBD). ²⁵ , ²⁶

Speech impairment within 3 years of the onset of motor symptoms is a supportive feature in the diagnosis of MSA. ²⁷ Additionally, the degree of speech severity correlates with the severity of the disease. ²⁸ MSA subtypes include MSA with predominant parkinsonism (MSA‐P) and MSA with cerebellar features (MSA‐C). MSA‐P typically has mixed hypokinetic‐spastic features, whereas MSA‐C has more predominant ataxic features. ²⁹ , ³⁰ However, it can have a spastic component, which is less common at least during earlier stages. ²⁹ Features unique to MSA include inspiratory sighs (ie, a breath characterized by a deep inhalation, often followed by a prolonged exhalation) and stridor. ³¹ Notably, the presence of stridor is associated with a poor prognosis and increased mortality in MSA. ³² Other features of the parkinsonian variant of MSA, such as vocal flutter and vocal cord immobility due to either paresis or dystonia, may present and may give the characteristic of a croaky, quivering, and irregular voice quality. ³³ , ³⁴ , ³⁵

Evaluation

Clinical Evaluation

The clinical evaluation of voice and speech relies on three complementary components: (1) clinical history, (2) perceptual evaluation of voice and speech features, and (3) voice and speech mechanisms during non‐speech tasks. ⁷

History

A thorough history can help guide diagnostic decision‐making. The timeframe of the onset of voice and speech changes in isolation and in the context of other symptoms, as well as their progression, is relevant, as they tend to present earlier and more severely in APDs. Patients or their families may describe changes in the quality of voice (eg, softer, lower, deeper), speech clarity (eg, mumbled or slurred), or rate (eg, faster or slower), as well as the progression of physical symptoms. Although patients may report, “I have trouble speaking,” pointed questions can help identify the specific aspects of speech that are affected for that individual, thereby differentiating a language disorder from a motor speech disorder. A list of helpful questions and their corresponding clinical correlates is presented in the Table S2.

Communication abilities vary widely, and what is normal for one person may represent a major departure from baseline for another. The impact of motor speech changes also differs across individuals with APDs. Thus, patient and care‐partner perspectives on voice and speech changes—and their effect on quality of life—are essential. Standardized questionnaires such as the Communicative Participation Item Bank (CPIB) ³⁶ and the NeuroQol – Communication battery ³⁷ are brief and valuable, but have not yet been validated in APDs. ³⁸

Clinician's Perceptual Evaluation of Speech

Perceptual evaluation describes voice and speech during spontaneous and task‐specific speaking. Connected speech (ie, set(s) of connected utterances providing a message) is the most important task because it best reflects everyday communication. The relevant aspects of voice and speech associated with common tasks are summarized in Table 2, including the features that can help differentiate between PD and APDs. Additional tasks may allow for more specificity in the evaluation. We have provided sample videos of the motor speech evaluation in patients with PD (Video 1), PSP (Videos 2 and 3), MSA‐C (Video 4), CBS (Video 5), and primary progressive apraxia of speech (Video 6), along with detailed descriptions in the video legends.

TABLE 2.

A practical voice and speech examination approach to aid in differentiating various APDs

Task	Features assessed	PD	PSP/CBS	MSA‐P	MSA‐C	PSP/CBS with AOS
Spontaneous speech	All Dysarthria type and apraxia of speech	Hypokinetic dysarthria	Mixed Hypokinetic Spastic Ataxic	Mixed Hypokinetic Ataxic	Ataxic	Slow Effortful False starts
Sustained vowel	Vocal loudness Vocal quality	Reduced loudness Fades Harsh Hoarse	Reduced loudness Strangled Strained	Hypophonic Irregular High‐pitched	Variable Irregular High‐pitched	Variable
Alternating and sequential motion rates	Rate of speech Fluency and cadence Accuracy	Slow	Slow	Slow	Abnormal breakdown Imprecise	Slow Imprecise Worse performance in SMR
Repetition of sentences	Rate of speech Fluency and cadence Accuracy Stress and intonation	Monopitch Monoloudness	Monopitch Monoloudness	Monopitch Monoloudness	Abnormal breakdown	Abnormal breakdown. Increased difficulty with longer sentences
Additional features		None	Echolalia palilalia	Inspiratory sighs Stridor	Inspiratory sighs Stridor	Orobuccal apraxia

Abbreviations: AOS, apraxia of speech; CBS, corticobasal syndrome; MSA‐C, multiple system atrophy—cerebellar type; MSA‐P, multiple system atrophy—parkinsonian type; PD, Parkinson's disease; PSP, progressive supranuclear palsy.

Video 1.

Download video file ^{(44.6MB, mp4)}

Patient with Parkinson's disease and hypokinetic dysarthria. He exhibits reduced vocal loudness and a hoarse vocal quality with intermittent breathiness and flutter. He speaks in short phrases with rushes of speech. Occasional word‐finding difficulties and repeated words are noted. There is a lack of variation in his pitch (ie, monopitch). His voice quality improves with sustained phonation. Slight imprecisions are noted in his alternating motion rates (AMRs) and sequential motion rates (SMRs).

Video 2.

Download video file ^{(49.7MB, mp4)}

Patient with progressive supranuclear palsy and apraxia of speech—prosodic subtype with additional features of spastic dysarthria. He exhibits a harsh voice quality with excess loudness variation. His speech is slow with decreased words per breath and excess pausing between words. Sound distortions are noticed in connected speech. Speech is monopitch and monoloud. His alternating motion rates (AMRs) and sequential motion rates (SMRs) are slow.

Video 3.

Download video file ^{(39.3MB, mp4)}

Patient with progressive supranuclear palsy and hypokinetic dysarthria with neurogenic stuttering. She exhibits a fast speech rate with stuttering (repeated sounds), imprecision, and decreased excursions of articulators (resulting in a mumbling quality). Speech is monopitch and monoloud. Imprecisions due to decreased excursion of articulators are noticed in alternating motion rates (AMRs) and sequential motion rates (SMRs).

Video 4.

Download video file ^{(39.8MB, mp4)}

Patient with multiple system atrophy‐type C and mixed ataxic and hypokinetic dysarthria. She exhibits reduced vocal loudness with a high‐pitched voice quality. She speaks in short phrases with short rushes of speech. There is an irregular articulatory breakdown. Stridor is present in connected speech. Vocal unsteadiness is noticed in sustained phonation, and slight imprecisions are noticed in alternating motion rates (AMRs) and sequential motion rates (SMRs).

Video 5.

Download video file ^{(45.1MB, mp4)}

Patient with corticobasal syndrome and apraxia of speech. He also exhibits a hoarse voice quality. His rate of speech is slow with decreased words per breath group. In addition, he has segmentation between and within words, articulatory imprecision, prolonged phonemes, and false starts. Stress and intonation are equal and excessive. His sequential motion rates (SMRs) are slow.

Video 6.

Download video file ^{(38.8MB, mp4)}

Patient with primary progressive apraxia of speech. She exhibits slow, effortful speech with articulatory errors, primarily with consonants. The speech is also monopitch. The alternating motion rates (AMRs) and sequential motion rates (SMRs) were imprecise with sound distortions, and sequencing in SMRs was impaired.

The first step in the evaluation is the description of connected speech. Connected speech can be unprompted (eg, describing symptoms during a clinical visit) or prompted (eg, open‐ended questions or describing a picture). ³⁹ Reading a passage (eg, The Rainbow Passage or The Grandfather Passage) can be helpful in certain circumstances, such as when a person is experiencing apathy or anxiety. ⁷ When evaluating reading, impairment in oculomotor function needs to be considered, as well as literacy and baseline reading fluency. By evaluating connected speech, the clinician can gather an overall impression of the patient's voice and speech, including its intelligibility (ie, ease of understanding of words), comprehensibility (ie, ease of understanding of the message), and abnormal features. ⁴⁰

The second step is the evaluation of voice loudness, pitch, and quality. This can be done by asking the patient to take a deep breath and saying “ah” for as long and as steadily as possible until they run out of air. ⁷ The duration of the phonation and its variability (or lack thereof) should be noted. This task can be particularly helpful in highlighting the presence of a strangled or strained voice quality, as noted in PSP, or the variability in loudness and/or high‐pitched quality of voice, as noted in MSA. Vocal tremor is often revealed on sustained phonations, but is not typical of APDs.

The third step is to ask patients to repeat certain syllables as quickly and steadily as possible. In rapid alternating motion rates (AMRs), patients are asked to take a deep breath and repeat the syllable “puh” as quickly and steadily for as long as they can. This task is repeated with the syllables “tuh” and “kuh.” This is followed by sequential motion rates (SMRs) where patients are asked to sequence the syllables “puh‐tuh‐kuh.” The clinician needs to provide an accurate example by repeating the syllables at a rate of six syllables per second. Here, the rate of production (syllables per second) along with the presence of articulation errors should be noted. These can help differentiate the rapid rushes of speech observed in PD and PSP from the slower production with abnormal breakdowns seen in MSA‐C. The presence of sound distortions in the context of a slow and effortful rate warrants considering the presence of apraxia of speech, particularly if these become more evident during SMRs compared to AMRs. ⁴¹

Depending on the situation, additional testing can be considered. If hypernasality is considered, patients can be asked to repeat sentences that include plosive sounds (ie, b, d, and p, such as “The big, black dog bit the big, black bear”) with and without manually occluding their nostrils. If a change is heard, then hypernasality can be suspected. ⁷ Intonation and stress (ie, prosody) can be evaluated by asking the patient to repeat a sentence as a statement or a question (eg, “I did that” or “These pretzels are making me thirsty”). ⁷ If motor planning/programming (ie, AOS) is being considered as a possibility, additional tasks, including repetition of words and sentences with increasing length and complexity (eg, cat/catnip/catapult/catastrophe), along with tasks that place minimal demands on language, such as singing a well‐known tune (eg, Happy Birthday) or naming the days of the week, should be considered. ¹¹ , ⁴²

In addition, the oral motor exam provides insight into the structural integrity and function of muscles utilized for speech by examining for symmetry, strength, speed, range of motion, and coordination in spontaneous and volitional movements; this allows for judgments about the presence of weakness, spasticity, rigidity, reduced habitual excursion, adventitious movements, and/or incoordination. ⁷ In the context of APDs, other factors, including the presence of dystonia, which can be present in APDs, plus the presence of vocal fold paralysis or impaired motion, or orofacial dyskinesias due to levodopa, which can be seen in MSA, should be considered. ⁴³ If AOS is being considered, additional testing, including oro‐buccal tasks not related to voice or speech (eg, puffing cheeks, licking lips, pantomime drinking with a straw), is warranted. ⁹

Sampling a patient's speech multiple times may also be helpful. Recording the evaluation is usually recommended, as it allows for later review as well as comparison to baseline over the disease progression.

Additional Considerations

Other factors can influence speech characteristics. For example, low vocal intensity and a hoarse voice may reflect reduced physiologic effort due to apathy, depression, or a comorbid medical condition, rather than a neurologic disturbance of the motor speech system. ⁷ , ⁴⁴ Medications, such as benzodiazepines and other sedatives, can be a cause or contributor to effortful or slurred speech, and antipsychotics can lead to stuttering. ⁴⁵ Levodopa may cause orofacial dyskinesias in MSA; however, little is known about the impact of levodopa on speech in APDs. ⁴³ Similarly, cognitive and behavioral changes (eg, impulsivity) can impact performance on specific speech tasks. ⁴⁶ For instance, a patient may have sequencing errors on SMRs due to difficulty with task comprehension or disinhibition; however, in the absence of articulatory deficits in conversation, there would be a low suspicion for AOS. Documenting any variables that may influence performance (eg, sedating medications, fatigue) is always recommended.

Standardized measures for assessing the clinical features of dysarthria and diagnosing types are limited and geared towards SLPs. They may be burdensome to incorporate into the neurological examination. Specific scales widely used by neurologists, such as the MDS‐Unified Parkinson's Disease Rating Scale (MDS‐UPDRS), the Progressive Supranuclear Palsy Rating Scale (PSPRS), and the Unified Multiple System Atrophy Rating Scale (UMSARS), include single questions regarding changes in speech, which combine intelligibility, voice, and articulation as one element. ⁴⁷ , ⁴⁸ , ⁴⁹ This limits the characterization and understanding of the elements contributing to speech severity, potentially missing more subtle abnormalities.

Management

Fundamentals of interventions for voice and speech impairments with APDs are early recognition, characterization of deficits, and a clear definition of expectations and goals. Therapeutic options should focus on restoring lost function, promoting the use of residual function, and employing compensatory strategies.

Education of patients and families is a crucial first step to management. This is done by explaining the nature of the deficits and emphasizing the importance of strategies to maximize comprehensibility of the speech in context. Examples include avoiding distractions and multitasking, as well as ensuring that the topic of conversation is clearly conveyed and understood from the outset. ⁵⁰

Referral to Speech‐Language Pathology

The complex and disabling nature of motor speech impairments in APDs underscores the importance of neurologists and SLPs working together in the assessment and interventions for this patient population. The SLP evaluation in the context of parkinsonism can serve different complementary purposes: (1) in‐depth characterization of voice, speech, and communication changes and their mechanical substrates; (2) evaluation and management of dysphagia, which may be present in the context of dysarthria; (3) therapy for voice and speech deficits and (4) recommendations regarding alternative/assistive communication devices and voice banking (Table S3). Regular reassessments and adjustments to therapy are essential to address the evolving needs of individuals with APDs, given their rapidly progressive nature. ⁵¹ Delayed clinical diagnosis of APDs frequently results in advanced symptom presentation by the time of referral to SLPs, further complicating care. An early SLP referral assists in educating patients and care partners about the current and anticipated impacts of the disease and providing therapies designed to maintain and enhance speech, voice, cough, and swallowing functions. Additionally, SLPs play a crucial role in managing these impairments through targeted interventions. It is worth emphasizing the importance of defining the deficits within each subsystem and how they relate to one another, as this will inform the hierarchical approach to therapy (ie, which subsystem should be addressed first). An example of this is imprecise articulation in the context of parkinsonism, which may be driven by reduced ventilatory support or laryngeal weakness, each warranting a different approach (Table 3).

TABLE 3.

Selected speaker‐oriented therapeutic options by subsystem impairment

Subsystem	Therapeutic options
Respiration	Increasing respiratory support exercises Inspiratory and expiratory strength training Posture adjustments and prosthetics (eg, abdominal binders) Inspiratory checking and biofeedback
Phonation	Vocal fold augmentation injection Botulinum toxin for vocal fold dystonia Feedback devices (eg, SpeechVive) Portable voice amplifier Changes in pitch Voice therapy Botulinum toxin for dystonia
Resonance	Palatal lift Palatal injection augmentation Nasal occlusion (ex. with nasal plug)
Articulation	Botulinum toxin injection for dystonia Strengthening, stretching and relaxation of muscles involved in articulation Articulation biofeedback Articulation therapy (eg, traditional approach, clear speech, intelligibility drills) Delayed auditory feedback Pacing techniques (eg, pacing boards, finger tapping, rhythmic cueing) Voice therapy targeting improved anterior resonance or loudness, with indirect impact on articulation
Prosody	Breath group therapy Chunking utterances Contrastive stress tasks

Evaluations by SLPs can provide a more nuanced assessment of voice and speech, capture more subtle abnormalities, and characterize the type of dysarthria. The assessment by an SLP serves as a complement to the neurologist's evaluation in the differential diagnosis of parkinsonian conditions. To do this, SLPs often use different dysphonia and dysarthria evaluations and outcomes. Evaluation frameworks include the Mayo Clinic Motor Speech Assessment and the Frenchay Dysarthria Assessment, among others. ⁷ , ⁵² , ⁵³ Outcomes may include performance‐based outcomes (eg, maximum phonation time), clinician‐reported outcomes (eg, Apraxia of Speech Rating Scale), and patient‐reported outcomes (eg, Voice Handicap Index‐10) (Table S4). ⁵⁴ , ⁵⁵ Beyond the ability to identify and adequately describe voice and speech abnormalities, evaluations by SLPs provide further insight into defining which key subsystems (ie, respiration, phonation, resonance, articulation, prosody) are involved in the patient's dysarthria. This is relevant as understanding the impaired mechanics can help in tailoring therapy.

Motor speech impairment is usually associated with impairments in swallowing and coughing, which can be life‐threatening in APDs and are associated with shorter survival. ⁵¹ , ⁵⁶ , ⁵⁷ , ⁵⁸ For example, in PSP, those exhibiting features of spasticity are more likely to have dysphagia, and those with more motor speech disorders had more severe dysphagia. ⁵⁶ , ⁵⁹ Early dysphagia, along with motor speech impairments, is a hallmark features that more strongly suggest an APD compared to PD. ¹⁵ , ²¹ Patients and families may underreport these. ⁶⁰ , ⁶¹ An SLP evaluation, which includes a bedside screening of swallowing abilities, may uncover the issue and lead to a more formal referral for a baseline or recurring modified barium swallow evaluation or fiberoptic endoscopic evaluation of swallowing. ⁶¹

Given the multifaceted nature of dysarthria in APDs, further assessment of phonatory and airway function may be warranted. Visual examination of laryngeal structure and function—such as flexible nasolaryngoscopy with or without videostroboscopy—performed by a laryngologist, otolaryngologist, or specially trained SLP, can help identify laryngeal impairment, including reduced mobility, paralysis, or focal dystonia. Individuals with MSA, particularly MSA‐P, are especially susceptible to stridor and upper airway obstruction, with up to 30% experiencing multi‐factorial airway compromise, and may benefit from early examination of laryngeal structure and function. ³³ , ⁶² When dysphonia is disproportionately severe or inconsistent with the commonly seen APD presentation, laryngeal imaging is indicated to rule out neoplasm, benign lesions, or other etiologies. ⁶³ Referral for pulmonary function testing may also be indicated to quantify respiratory involvement, especially in MSA, where laryngeal dysfunction may significantly impact ventilation and contribute to stridor. ³²

Therapeutic Interventions

The evidence for therapeutic interventions for voice and speech impairments in APDs is limited. The current practice is based on the knowledge gained from the treatment of other conditions with overlapping features of APDs, such as PD and amyotrophic lateral sclerosis (ALS). ⁶⁴ Although these conditions may share features and subsystem impairment, to what extent the benefit of a specific therapy translates from one condition (eg, PD, ALS) to APDs remains to be determined.

One widely studied SLP approach for PD is LSVT LOUD®, a structured program that incorporates intensive, high‐effort vocal exercises to increase vocal intensity and enhance speech clarity. While LSVT LOUD has demonstrated efficacy in managing hypokinetic dysarthria in PD, ⁶⁵ , ⁶⁶ , ⁶⁷ its effectiveness in APDs remains inconclusive. In PSP, research findings have been mixed. One study reported a significant improvement in vocal intensity following LSVT LOUD, but found no corresponding gains in voice quality or articulation. ⁶⁸ Conversely, another study reported no significant post‐treatment improvements in vocal intensity, sustained vowel duration, or speech intelligibility. ⁶⁹ In MSA, post‐treatment improvements in vocal intensity have been reported in both the Parkinsonian (MSA‐P) ⁷⁰ and cerebellar (MSA‐C) subtypes ⁷¹ ; however, small sample sizes limit the generalizability of these findings.

Other interventions may also be considered to support speech intelligibility and functional communication. For patients exhibiting rapid speech patterns, rate control strategies such as pacing boards, ⁷² rhythmic auditory entrainment, ⁷³ , ⁷⁴ and delayed auditory feedback ⁷⁵ , ⁷⁶ have been shown to effectively regulate speech tempo and improve intelligibility in individuals with PD. Only one study has evaluated the role of speech cueing in PSP and MSA, showing no immediate effects on speech severity ratings. ¹³ This study revealed that APDs tend to increase their speech rate when asked to speak clearly, different from what is observed in PD and controls, who tend to slow down. ¹³ However, the effectiveness of these techniques in modulating speech rate in APDs remains largely unknown to date. While expiratory muscle strength training (EMST) has been studied for its impact on cough function and swallowing safety in other neurological diseases, such as PD, its effectiveness as a speech and voice intervention remains unclear. ⁷⁷ Current evidence suggests that EMST may not significantly improve key speech parameters, such as articulation and intelligibility. ⁷⁸ However, its feasibility in APDs is beginning to be explored. ⁷⁹

Additionally, compensatory strategies play an essential role in supporting communication as symptoms progress. In earlier stages of disease progression with APDs, personal voice amplifiers can increase speech volume, ⁸⁰ enhance speech intelligibility, ⁸⁰ and improve communicative participation while minimizing respiratory and vocal fatigue. ⁸¹ In addition, augmentative and alternative communication methods, such as alphabet or pictorial visual displays, writing devices, text‐to‐speech applications, and speech‐generating devices, may be used to augment communication or serve as the primary mode of communication. Some speech‐generating devices can be controlled through movement, such as head or eye movements, which may be an option depending on the individual's motor limitations. The progressive nature of these conditions and the current absence of disease‐modifying therapies prompt consideration of voice banking, which uses the individual's own voice through a tablet or other devices ⁸² (Table 3).

Finally, other factors either associated with or not related to APDs may contribute to voice and speech issues and warrant treatment. Examples of this include jaw or vocal cord dystonia, for which botulinum toxin should be considered, and oculomotor abnormalities, which can affect reading, and for which prisms may be helpful. ⁵⁰ In addition, cognitive impairment and apathy limit the participation and potential benefit of these therapeutic strategies. It is essential to recognize the impact of the diagnosis of a neurodegenerative disease on the patient's willingness to engage in treatment. Additionally, the limitations in communication affect the quality of life for patients and their care partners. ² This highlights the relevance of incorporating counseling and mental health support as part of the management plan.

Future Avenues

Although the clinical presentation of motor speech disorders in APDs is relatively well characterized, our understanding of the underlying pathophysiology and treatment options is primarily derived from studies in PD and warrants further evaluation in people with APDs.

Digital speech biomarkers offer a promising avenue for diagnosing and monitoring APDs. ⁸³ , ⁸⁴ , ⁸⁵ The most established method is acoustic analysis, which utilizes open‐source software (eg, Praat 5) to extract several variables from voice samples. These objective metrics, such as jitter, shimmer, and cepstral peak prominence, can reveal abnormalities that may not be apparent to the ear and have the potential to enhance diagnosis, differentiate among APDs, and serve as prognostic factors. ⁸⁶ , ⁸⁷ Acoustic analysis provides quantitative baselines that could track changes over time. ⁸⁸ In PD, there is preliminary evidence on the successful application of machine learning to voice spectrograms for categorizing individuals with and without PD, compared to traditional acoustic analysis. ⁸⁹ , ⁹⁰ While these findings show great promise, application of acoustic speech biomarkers as a clinical diagnostic tool and a marker of progression in APDs remains under investigation.

Non‐invasive brain stimulation techniques, such as transcranial magnetic stimulation (TMS), show promise in early‐stage studies in APDs. Two studies focusing on cerebellar rTMS showed improvements in dysarthria. ⁹¹ , ⁹² The placebo effect, however, is a concern in both studies, as one study was open‐label, and the other had a patient‐detected sham arm. Both studies also had a limited sample size, making it difficult to extend the results to clinical therapy at this time.

Conclusions

Motor speech disorders are a common symptom and substantially affect communication and daily functioning in APDs. This practical review can serve as a guide for clinicians, highlighting the importance of timely assessment and management of the voice and speech function of patients with PSP, CBS, or MSA. Although the prevalence, diagnostic techniques, and prognostic value of motor speech problems in APDs are relatively well understood, evidence for effective treatments remains grossly understudied. The development of digital biomarkers holds promise for improving the diagnosis and monitoring of disease progression. Further development of patient‐tailored therapies, such as neuromodulation, is needed. We recommend close collaboration between neurologists and SLPs in the care of people with PSP, CBS, and MSA. Not only do the two specialties provide complementary expertise necessary to improve the timely diagnosis, communication, quality of life, and even survival for this patient population, but together they can pursue the future development of best practices and evidence‐based interventions. Future research should prioritize multicenter trials of targeted therapies, the validation of digital biomarkers, and the integration of patient‐reported outcomes to enhance care for individuals with APDs.

Author Roles

(1) Research project: A. Conception, B. Organization, C. Execution; (2) Statistical Analysis: A. Design, B. Execution, C. Review and Critique; (3) Manuscript Preparation: A. Writing of the first draft, B. Review and Critique.

F.R.P.: 1A, 1B, 1C, 3A.

F.A.: 1C, 3B.

M.B.: 1C, 3B.

H.D.C.: 1C, 3B.

R.D.: 3C.

K.D.P.: 1C, 3B.

L.I.G.: 1C, 3B.

L.S.H: 1C, 3B.

N.H.: 1C, 3B.

K.K.: 3C.

S.K.: 1C, 3B.

G.L.: 1C, 3B.

N.R.M.: 1C, 3B.

M.M.: 1C, 3B.

L.M.K.: 3C.

A.P.: 3C.

J.P.: 1C, 3B.

H.P.: 1C, 3B.

L.P.V.: 1C, 3B.

K.R.: 1C, 3B.

J.S.: 3B.

M.T.: 1C, 3B.

R.L.U.: 1C, 3B.

K.V.C.: 1C, 3B.

T.V.: 1C, 3B.

A.M.W.: 3C.

Disclosures

Ethical Compliance Statement: The authors confirm that the approval of an institutional review board was not required for this work. FRP obtained patient consent, and all patients signed the video consent. We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this work is consistent with those guidelines.

Funding Sources and Conflict of Interest: No specific funding was received for this work.

The authors declare that there are no conflicts of interest relevant to this work.

Financial Disclosures for the Previous 12 Months: FRP has received funding from the NIH (R21DC019749), serves as a rater for Biovie and receives royalties from Cambridge University Press. FA has received funding from the NIH. MB has received research grant support from Michael J. Fox Foundation, Parkinson's Foundation, Center for Pacific Innovations, Knowledge, and Opportunities (PIKO), and CurePSP. LG disclosures include: consulting on clinical trial design for AI Therapeutics, Amylyx, Aprinoia, Ferrer, Mitochon, and NextCure. Intellectual property license fee sharing via Rutgers University for the PSP Rating Scale and related services. Royalties for single‐author book: Golbe LI. A Clinician's Guide to Progressive Supranuclear Palsy. (2019) Rutgers University Press, New Brunswick, NJ. SK has received funds from Eli Lilly, the Institute for Clinical and Economic Review and My Concierge MD KR received research support from the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health. The authors declare that there are no additional financial disclosures to report. MT has received grant funds from the NIH(NINDS, NS126319) and royalties from MedBridge, Inc. The rest of the authors report no relevant disclosures.

Financial Disclosures and Conflicts of Interest

Author disclosures are available in the Supporting Information.

Supporting information

Data S1. Coi_Disclosure.

TABLE S1. Definition of selected perceptual features

TABLE S2. Features of motor speech disorders, history, and correlates

TABLE S3. Goals of speech‐language pathology referral

TABLE S4. Selected outcome measures used by Speech‐Language pathologists (SLPs)

Appendix A.

Diagnosis and Treatment Working Group, CurePSP Center of Care Network members.

Farwa Ali, MBBS, Michiko Bruno, MD, Timothy Chang, MD, Rohit Dhall, MD, Kimiko Domoto‐Reilly, MD, Lawrence I. Golbe, MD, Ihtsham Haq, MD, Lawrence S. Honig, MD, PhD, Sarah Kremen, MD, Guillaume Lamotte, MD, MSc, Zoltan Mari, MD, Nikolaus R. McFarland, MD, PhD, Leila Montaser‐Kouhsari, MD, PhD, Alexander Pantelyat, MD, Federico Rodriguez‐Porcel, MD, Junaid Siddiqui, MD, Jessica Shurer, MSW, LCSW, Christopher Spears, MD, Tuhin Virmani, MD, PhD, Anne‐Marie Wills, MD.

Data Availability Statement

Data sharing not applicable to this article as no datasets were generated or analysed during the current study.