1. health and fitness
2. disorders

Review
Speech treatment for
Parkinson’s disease
Expert Rev. Neurotherapeutics 8(2), 299–311 (2008)
KEYWORDS: dysarthria • hypokinetic • hypophonia • LSVT®• neural plasticity • Parkinson’s disease • speech and voice
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Author for correspondence
Department of Speech,
Language, Hearing Sciences,
University of Colorado,
Boulder, Campus Box 409,
Boulder, CO 80309, USA
Tel.: +1 303 492 3023
Fax: +1 303 499 6742
[email protected]
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†
Researchers estimate that 89% of people with Parkinson’s disease (PD) have speech and voice
disorders including disorders of laryngeal, respiratory and articulatory function. Despite the
high incidence of speech and voice impairment, studies suggest that only 3–4% of people
with PD receive speech treatment. Here, we review the literature on the characteristics and
features of speech and voice disorders in people with PD and the types of treatment
techniques available (medical, surgical and behavioral), with a focus on behavioral therapies.
We provide a summary of the current status of the field of speech treatment in PD and
recommendations for implementation of the current efficacy of treatment interventions.
Directions for future research, including a speculative viewpoint on how the field will evolve in
5 years time, are discussed.
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Lorraine O Ramig†,
Cynthia Fox and
Shimon Sapir
disorder • speech and voice treatment
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Oral communication is vital in education,
employment, social functioning and self-expression. The prevalence of disordered communication is particularly high (89%) in the nearly
seven million individuals worldwide with Parkinson’s disease (PD); however, only 3–4%
receive speech treatment [1–3]. Soft voice, monotone, breathiness, hoarse voice quality and
imprecise articulation, together with lessened
facial expression (masked faces), contribute to
limitations in communication in the vast majority of individuals with PD [4,5]. The reduced
ability to communicate is considered to be one
of the most difficult aspects of PD by many
people with the disease and their families [6].
Moreover, speech and language changes in PD
can have a negative impact upon individuals
with PD and their family-life long before frank
impairments of intelligibility are apparent [7].
Affected individuals often become disabled or
retire early, are forced to give up activities they
enjoy, incur substantial medical costs and have
increased mortality [8–10]. Based upon 2004 estimates, PD costs the USA US$34 billion annually in direct health-related expenses, disabilityrelated costs, and lost productivity [11,12]. As the
number of elderly people greater than 65 years
of age increases, these costs are expected to
exceed US$50 billion by 2040 [13]. The average
age of diagnosis of PD is 60 years, but in many
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10.1586/14737175.8.2.299
individuals the disease develops at a much
younger age. Given the relative slow progression
of the disease, improvement in the ability of
these individuals to communicate increases the
chance that they could maintain an improved,
productive quality of life, despite living out the
rest of their life with a chronic disease. Thus, the
value of an effective treatment for disordered
communication in this population is clear.
Although medical treatments, including neuropharmacological as well as neurosurgical
methods, may be effective in improving limb
symptoms, their impact on speech production
remains unclear [14–20]. Moreover, historically,
people with PD have been particularly resistant
to speech treatment [1,21–26]. Recently, however,
a speech treatment approach called Lee Silverman Voice Treatment (LSVT® LOUD) has generated efficacy data for successfully treating voice
and speech disorders in this population. The
purpose of this review is to:
• Provide a brief summary of speech and voice
characteristics associated with PD
• Discuss medical and behavioral speech treatment approaches for PD
• Summarize key components of speech treatment that seem to underlie positive outcomes
• Highlight ongoing and future research directions in speech treatment for PD
© 2008 Future Drugs Ltd
ISSN 1473-7175
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Ramig, Fox and Sapir
Physiologic abnormalities associated with speech & voice
disorders in PD
Physiologic (videolaryngostroboscopic and electroglottographic) studies of voice in people with PD have documented
voice tremor, poor vocal fold closure and reduced amplitude,
asymmetry or slow vibratory patterns of the vocal folds [62,63].
Respiratory studies in people with PD have documented reduction or abnormalities in vital capacity, amount of air expended
during maximum phonation tasks, intraoral air pressure during
consonant/vowel productions, chest wall movements and respiratory muscle activation patterns during speech breathing [64].
Electromyographic (EMG) studies of vocal function in people
with PD indicate either a reduction of neural drive to the laryngeal muscles [27] or abnormally elevated laryngeal muscle activity [65], and poor reciprocal suppression of laryngeal and respiratory muscles [66]. Kinematic and EMG studies of orofacial
movements during speech in PD indicate a reduction in the
size and peak velocity of jaw movements, increased levels of
tonic resting and background neuromuscular activity, and loss
of reciprocity between agonist and antagonistic muscle groups
[30,34,35,67–69]. Thus, these studies collectively suggest decreased
amplitude of speech movements in people with PD associated
with abnormal neural drive to the speech periphery and abnormal sensorimotor gating. Importantly, these studies also indicate that muscle rigidity is not a major cause of the speech
movement abnormalities in PD. Moreover, the severity of
speech disorders in PD may change markedly as the function of
the specific speech tasks being performed and in the absence or
presence of external cues, such as the instruction to speak
loudly and clearly [70,71]. These, and other findings to be
reviewed later, suggest that the neuropathological mechanisms
underlying speech disorders in PD probably involve high level
motor dysfunctions and sensory processing abnormalities.
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Disorders of laryngeal, respiratory and articulatory function
have been documented across a number of perceptual, acoustic
and physiological studies in people with PD [27–33]. The neural
mechanisms underlying these voice and speech disorders are
unclear [34–39]. Traditionally, they have been attributed to motor
signs of the disease such as rigidity, bradykinesia, hypokinesia
and tremor. Of particular importance to speech and voice disorders in people with PD are the proposed pathophysiological
mechanisms underlying bradykinesia/hypokinesia: inadequate
muscle activation [40]. The muscle activation deficits that occur
in bradykinesia are believed to result from inadequate merging
of kinesthetic feedback, motor output and context feedback
within the basal ganglia, that is necessary to select and reinforce
an appropriate gain in the motor command [40,41]. This is supported by single cell recording studies [42] and recent brain activation imaging studies [41] showing a correlation in activation of
neurons or muscle with increasing movement amplitude. In
addition to the mechanisms of bradykinesia/hypokinesia,
abnormal sensory processing [43–45] and impaired ability to initiate a motor response (problem with internal cueing) [46,47] play
an important role in speech and voice disorders.
Perceptually, speech and voice in people with PD are characterized by reduced loudness, monopitch, monoloudness,
reduced stress, breathy, hoarse voice quality, imprecise articulation, short rushes of speech, and hesitant and dysfluent speech
[48,49]. Collectively, these speech symptoms are called hypokinetic
dysarthria [50]. Voice problems are typically the first to occur,
with other problems, such as prosody, articulation and fluency,
gradually appearing as the speech disorder progresses [2,3,45].
Acoustic descriptions of voice characteristics of people with
PD have also been documented. Early studies varied in reporting a reduction in vocal sound pressure level (vocSPL) in these
people [51–55]. More recently, Fox and Ramig compared 29 people with PD with age- and gender-matched neurologically
healthy individuals (control group) and found that vocSPL was
2–4 decibels (at 30 cm) lower across a number of speech tasks
in the people with PD relative to the control group [6]. A 2–4
decibel change is equal to a 40% perceptual change in loudness
[6]. In addition to an overall low level of vocal loudness, Ho and
colleagues found that voice intensity in people with PD tend to
decay much faster than that observed in a control group during
various speech tasks [56]. Results related to the voice frequency
(an acoustic correlate of pitch) in the speech of people with PD
have consistently reported a reduced frequency range
[51–53,54–57]. These findings support the perceptual characteristics of monopitch or monotonous speech typically observed in
this patient population [3,48–49,58]. Acoustic correlates of disordered articulation have been studied and include problems
with timing of vocal onsets and offsets (voicing during normally voiceless closure intervals of voiceless stops), reduced
range of vowel articulation [59] and spirantization (presence of
fricative-like, aperiodic noise during stop closures) [34,60,61].
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Speech & voice characteristics in PD
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Sensory & internal cueing deficits associated with speech
& voice disorders in PD
It has been suggested that unlike certain limb motor disorders
in PD, which are strongly and directly related to dopamine
deficiency and rigidity, some motor disorders in PD, including
speech, may also involve abnormal nondopaminergic or special
dopaminergic mechanisms, which impair internal cueing, sensorimotor gating and scaling of movement parameters, thus
resulting in poor regulation and control of speech movement
initiation, amplitude and timing [71–73].
Numerous investigators documented sensorimotor deficits in
the orofacial system [67,74–76] and abnormal auditory, temporal,
and perceptual processing of voice and speech [34,43,44,46,75–78].
These abnormalities have been implicated as important etiologic
factors in the speech and voice impairment associated with PD
[79]. Behavioral evidence from limb and speech motor systems
for sensory processing disorders in PD include: errors on tasks of
kinesthesia [80–82]; difficulties with orofacial perception, including decreased jaw proprioception, tactile localization on tongue,
gums and teeth, and targeted and tracking head movements to
Expert Rev. Neurotherapeutics 8(2), (2008)
Speech treatment for Parkinson’s disease
understanding of the neuropathology of speech and voice disorders in PD. Current treatments for speech and voice disorders in people with PD consist of neuropharmacological therapies, neurosurgical procedures, behavioral speech therapy or a
combination thereof [85,86]. At this time, a combination of
medical therapy (e.g., optimal medication) with behavioral
speech therapy appears to offer the greatest improvement for
speech dysfunction [85]. There are a number of recent papers
that have reviewed the literature related to speech treatment in
PD including medical and behavioral interventions for this
population [73,86–90].
Medical treatment for speech and voice disorders in PD
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In contrast to the marked therapeutic effects of dopamine therapy (levodopa or dopamine agonists) on rigidity, akinesia,
bradykinesia and tremor in the limb motor system [91], the
magnitude, consistency, and long-term effects of levodopa or
dopamine agonist therapy on speech in PD are far from satisfactory [72,73]. Specifically, while several studies have documented dopamine-induced improvement in speech motor
function, such as a reduction in excessive laryngeal neuromuscular activity, better laryngeal control of voice onset and vocal
fold closure during speech [65], better speech intelligibility [92],
greater prosodic voice fundamental frequency (Fo) inflection,
greater vocSPL, better voice quality [93,94], enhanced lip function during speech and nonspeech tasks [95], and less voice
tremor [96], many other studies have failed to show systematic
changes or clinically significant improvement in speech with
levodopa [16,17,73]. These findings have led researchers to suggest
that voice and speech disorders in PD might be related to nondopaminergic or special dopaminergic mechanisms [45,72]. In
line with this suggestion, it has been shown that clonazepam, a
nondopaminergic agent, when given at 0.25–0.5 mg/day dosages, can significantly improve some aspects of speech, such as
imprecise consonants, short rushes of speech, and inappropriate
silences in an individual with PD [97].
Neurosurgical procedures such as deep brain stimulation
(DBS) of the thalamus, pallidum or subthalamic nucleus (STN),
ablative surgeries (pallidotomy and thalamotomy) and fetal cell
implantation, have also been shown to result in dramatic
improvement in limb motor function, but produce inconsistent
effects on speech, with some showing dramatic improvement,
others showing improvement, others no changes and still others
reporting dysarthria as a significant side effect of DBS in some
individuals [14,15,98–102]. The adverse effects on speech might be
related to voltage spread and/or lesions of a neural network that
mediates sensorimotor speech control [87]. In addition, stimulator placement and adjustments may play a key role in speech
outcomes [102]. The effects of different electrical parameter settings on the intelligibility of speech in patients with PD treated
with subthalamic DBS need further research [102].
Given that neuropharmacological and neurosurgical
approaches alone do not improve speech and voice consistently and significantly [85,87], behavioral speech therapy
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perioral stimulation [75]; problems utilizing proprioceptive information for normal movement [75,81]; and abnormal higher order
processing of afferent information as demonstrated by abnormal
reflex and voluntary motor responses to proprioceptive input
[83]. Thus, one aspect of hypokinetic dysarthria in PD might
include complex deficits in the utilization of specific sensory
inputs to organize and guide speech movements.
Additional insights into the sensory deficits affecting speech
and voice in people with PD have been provided by Ho and
colleagues [43,46]. People with PD demonstrated an abnormal
pattern of speech loudness modulation, and failed to increase or
decrease loudness in response to the auditory feedback and
background noise in the same manner as people in the control
group. When given explicit auditory cues to increase loudness,
the people with PD were able to increase their speech loudness.
These findings further suggest an impairment with online or
autophonic scaling of loudness in people with PD; an impairment that can be overridden, in the short term, with explicit
external cueing. This impairment is analogous to the micrographic handwriting in individuals with PD when asked to
write on a blank piece of paper. Once these individuals are provided with dots on the paper, and asked to write so that the letters touch the dots (external cues), or once they are provided
with the word “big” spoken to them (another external cue) the
handwriting improves dramatically, but only during the short
time that they are exposed to the cues and/or immediately after
the cue is given [84].
Review
Summary of PD-related speech & voice dysfunction
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In summary, perceptual, acoustic and physiological data have
documented varying degrees of dysfunction in different aspects
of speech in people with PD. The most common perceptual
speech characteristics are reduced loudness, monopitch, hoarse
voice and imprecise articulation. Acoustic studies of speech of
people with PD appear to parallel perceptual studies and have
shown evidence of reduced vocSPL, reduced vocSPL range,
reduced frequency range and abnormal articulatory acoustics.
Physiological studies of articulatory muscles have revealed
reduced amplitude and speed of movements from a kinematic
analysis, EMG activity and abnormal vocal fold closure patterns. In addition, studies of sensory aspects of PD have
revealed sensorimotor deficits that include errors on tasks of
kinesthesia, difficulties with orofacial perception, including
decreased jaw proprioception, tactile localization on tongue,
gums and teeth, and targeted and tracking head movements to
perioral stimulation. More research is needed to clarify the
impact of sensory processing and internal cuing deficits in
hypokinetic dysarthria associated with PD.
Treatment for speech & voice disorders in PD
Management of speech and voice disorders in people with PD
has been challenging for both medical and rehabilitation practitioners. This has been due, in part, to the lack of precise
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Behavioral speech & voice therapy for PD
Reviews of evidence-based practice (EBP) for behavioral speech
therapy for people with PD have been recently summarized by
Trail and colleagues [73]. Summary statements from that review
as well as additional reviews not included in that summary will
be discussed here including: Movement Disorders review [88],
Cochrane reviews [103,104], NICE PD treatment guidelines [105]
and the Academy of Neurology review [106]. These reviews used
the criteria of only including randomized controlled studies and
most analyzed the quality of the studies based on Consolidated
Standards of Reporting Trials (CONSORT) guidelines.
Summary findings from these reviews concluded that there
was insufficient evidence to conclude on the efficacy of speech
therapy in the following areas:
• Prevention of disease progression in PD
• As an adjunct treatment to medication and/or surgery
• In preventing motor complications in PD
• On motor and nonmotor complications of PD [88]
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The authors concluded there was insufficient evidence to
prove or disprove the benefit of speech and language therapy
for speech disorders in people with PD due to the methodological flaws, the small number of people examined and the possibility of publication bias (Cochrane). Furthermore, there was
insufficient evidence to determine if any specific speech therapy modality is superior to another [104,106]. The authors recommended future clinical research should include larger, randomized, prospective and controlled studies. In addition, the
use of functional neural imaging studies to examine people
with PD pre- and post-speech therapy to determine the functional and anatomic changes related to speech treatment was
suggested [88].
Although there was inconclusive evidence for one speech treatment over another, all reviews acknowledged the potential for
speech treatment to improve function in people with PD. More
specifically, all reviews proposed that behavioral speech therapies
should be intensive and focus on loudness (e.g., LSVT LOUD)
or prosody based on the evidence reviewed [106–109].
Since the publication of the Movement Disorders review,
other studies for speech therapy in PD have been published.
One study by Ramig and colleagues [110] was independently
reviewed by the primary author of the section responsible for
speech therapy and it was concluded to be of high-quality
Level I evidence [GOETZ C. PERS. COMM., 2003]. This paper was not
included in any of the other reviews listed above. Currently,
an update of information from the Cochrane review for
speech therapy and PD is taking place. The updated Cochrane
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Caveats to behavioral treatment evidence-based reviews
There are a few important considerations to keep in mind
regarding reviews of behavioral treatment literature, both those
presented here or encountered in the future. Montgomery and
Turkstra discuss the limitations of evidence-based medicine
(EBM), which is the standard for judging medical treatment
efficacy, and its counterpart, EBP, which is the growing standard for judging rehabilitative treatment efficacy [112]. While
these guidelines are helpful to understand and judge the quality
of clinical research, there are limitations to the information
they can provide. Three points for caution in interpreting data
from EBP guidelines discussed include [112]:
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• As a sole treatment in any indication of PD
review will include and analyze randomized controlled studies that have been published or are in progress from 2001 to
the present.
The UK NICE recently updated their national clinical guidelines for diagnosis and management of PD. As part of the
guidelines, they conducted a review of speech treatment literature including the Cochrane review discussed above as well as
several studies published after that review [110,111]. Their recommendations for clinical care were that speech and language
therapy should be available to people with PD. One of the specific recommendations from the NICE guidelines, consistent
with recommendations from other reviews, is that speech therapy should focus on improving vocal loudness and pitch range,
as in programs such as the LSVT LOUD.
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should be used to improve speech and voice even for optimally
medicated people with PD and for those who have undergone
neurosurgical procedures.
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Review
• Evidence that is “statistically significant” is not necessarily
“clinically meaningful”
• Group data will not always apply to the individual patient,
clinical judgment is also necessary
• Randomized controlled trials (RCTs), the current gold standard in EBM and EBP, may not be feasible or achievable for
answering many clinical questions
The authors summarized, “evaluations and recommendations
for clinical practice should not be based only on the amount of
RCT or other evidence but also on reasoned assessments of the
problems inherent in attributing treatment cause to experimental effect; the degree of generalizability; and the scientific,
social, and ethical implications of a decision in favor of or
against assessing a cause to an effect. Also, such evaluations and
recommendations should not discount the role of reasoned
judgments made by experienced clinicians” [112].
In line with the above comments, the Academy of Neurologic
Communication Disorders and Sciences (ANCDS) has offered
two additional reviews [89,113], These authors did not limit the
review to RCTs; rather they included case, single subject and
group designs. The first review examined evidence for behavioral management of respiratory and phonatory dysfunction
from dysarthria including studies of speech therapy for people
with PD [89]. The strength of evidence was based upon the following factors: type of study (e.g., case, single subject or group);
primary focus of treatment (e.g., biofeedback or LSVT LOUD);
Expert Rev. Neurotherapeutics 8(2), (2008)
Speech treatment for Parkinson’s disease
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treatment studies comparing various techniques, parameters of
treatment scheduling (e.g., intensity or dosage) and descriptions
of how optimal rate is selected and trained. Prosody studies also
included Phase I and II research. The current status indicates
that manipulating prosody may enhance linguistic information,
thus intelligibility. Future research needs to include areas such as
comparison of approaches, generalization of training, techniques
for perceptual ratings of prosody and documenting social validity. Finally, there were studies of general instructions, such as
instructions to speak “clearly.” The current status documents
that this type of approach may take advantage of compensatory
abilities and be applied to many types of dysarthria. Future
research should focus on larger groups of speakers, candidacy
issues for the approach and studying actual rather than simulated
communication breakdowns [113].
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Intensive voice treatment (LSVT LOUD) for PD
Given the large research base supporting training-increased
vocal loudness via LSVT LOUD, it is beneficial to examine this
specific treatment protocol in more detail as it pertains to current and future speech treatment research [73,87,89]. The fundamentals of LSVT LOUD are based upon the hypothesized features underlying voice disorders in people with PD [79]. These
features include:
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number of people, medical diagnosis, replicability, psychometric
adequacy (e.g., reliability), evidence for control, measures of
impairment, measures of activity or participation and study conclusions. For speech therapy related to PD this review included:
three studies of biofeedback devices totaling 39 people; five
studies with devices (e.g., delayed auditory feedback) totaling 16
people; 14 studies of LSVT LOUD totaling approximately
90 people; and three miscellaneous studies of group treatment.
For a table outlining details of these studies, see [89].
Conclusions from the review reported that LSVT LOUD has
the greatest number of outcome measures associated with any
speech treatment examined. Furthermore, the authors summarized that for the most part outcomes were positive and can be
interpreted with confidence [89]. Recommendations for future
research for biofeedback, devices and group treatment
approaches included having a larger number of people in studies, well-controlled replicable and reliable studies of welldefined populations and control or comparison group studies
(randomized controlled studies). Recommendations for future
research in LSVT LOUD included additional documentation
of long-term maintenance effects, large multisite effectiveness
studies (clinical trials), alternative modes of administration
(e.g., different dosages of intensity) and further study of treated
people with PD to better define predictors of success or failure
with the treatment.
The second, more recent review examined evidence for effectiveness of global treatment parameters including loudness, rate,
prosody or general instructions such as “clear” speech for individuals with dysarthria [113]. The evidence was characterized
based upon Phases of research as defined by Robey and Schultz
[114]. Phase I studies included experimental manipulations, typically a single dosage/session of loudness, rate or prosody manipulations. Phase II studies included treatment protocols carried
out in a speaker with dysarthria in case reports and small groups
with no control or treatment comparison. Phase III studies
included treatment protocols tested with single subject or group
designs with control groups or treatment comparisons. This
review included PD and other etiologies; however, the majority
of data were from individuals with PD. A full comprehensive
summary of findings can be found in Table 2 of the Yorkston
et al. review with brief summary statements below [113].
The strongest evidence regarding treatment effectiveness was
for modification of loudness, specifically the LSVT LOUD
protocol, in people with PD. This work demonstrated progression through all three phases of research, had a well-defined,
replicable protocol, measured multiple aspects of speech and
included a relatively large subject pool. Continued research
should focus on areas such as measures of outcomes in natural
social situations and examining factors to optimize learning
(e.g., dosage). Studies modifying rate included Phase I and II
research and revealed it may be a powerful technique for
improving intelligibility in some speakers with dysarthria.
There are a variety of techniques used across studies. Areas for
future research include examining generalization of techniques,
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• An overall amplitude scale down of the speech mechanism
(reduced amplitude of neural drive to the muscles of the
speech mechanism) that may result in a “soft voice that is
monotone” [115–117]
• Problems in sensory perception of effort that prevents a person with PD from accurately monitoring his/her vocal output
and results [116,118]
• The individual’s difficulty in independently generating (internal cueing/scaling) the right amount of effort to produce
adequate loudness [119,120]
The result is hypophonia, hypoprosodia and hypokinetic
articulation characteristics of the dysarthria associated with PD.
It is critical to recognize that the loudness target in LSVT
LOUD is a healthy increase in vocal loudness. Patients are not
trained to yell or scream or to use pressed voice, rather the
speech clinician trains a voice that is louder with appropriate
voice quality.
The mode of delivery of LSVT LOUD differs from traditional forms of speech treatment. It requires intensive, high
effort speech exercise combined with a simple, redundant and
salient treatment target to facilitate transfer of loudness into
functional daily living. The standardized protocol for LSVT
LOUD embodies many of the fundamental principles of exercise and motor training that have been shown to promote neural plasticity and brain reorganization in animal models of PD
[121] and human stroke-related hemiparesis [122]. Such intensive
training, especially when practiced continuously and at the
onset of the disease or following brain injury, has been shown
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As indicated previously, these neural systems are involved in
vocalization, loudness regulation and vocal learning, which collectively may account for the significant and long-term effects
of LSVT LOUD on speech in individuals with PD. This may
also help to explain how a cross-system, such as swallowing,
may also be affected by training vocal loudness. Perspectives
such as these elucidate why LSVT LOUD improves voice and
speech production in PD and other neural conditions, as compared with previous treatments that have focused on rate or
articulation, which involve primarily cortical, phylogenetically
newer neural centers.
Thus both mode of treatment delivery and target of the treatment approach are areas of study in future speech treatment
research.
Expert commentary & five-year view
Positive gains have been made over the years towards recognizing key variables for successful speech treatment outcomes in
people with PD. Ongoing and future investigations have the
potential to further clarify underlying mechanisms of speech
disorders in PD while addressing key variables for improving
speech treatment outcomes. Suggested areas for research related
to manipulations of loudness, rate, prosody and general instructions were summarized previously. Some areas of ongoing and
future research in our collaborative laboratories include:
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to impact molecular changes associated with cell survival, cell
growth and functional recovery in animal models of PD. These
changes reflect neural plasticity and brain reorganization
[121,123–126], and challenge the assumption that there is no
potential for recovery of function in PD or other neurodegenerative disorders. Thus, translation of the principles of
neural plasticity to therapeutic approaches will require a significant paradigm shift in rehabilitation sciences [127]. Our ability
to embrace these principles and integrate them into the mode
of delivery of treatment will be essential for advancing rehabilitation science in parallel with neuroscience. While the standardized protocol for LSVT LOUD was developed before these
recent neuroscience investigations, it adheres to key principles
of neural plasticity, such as intensity, complexity, saliency, use it
or lose it, and use it and improve it, which may explain, in part,
why it has been successful (for details, see [125]).
The target of training vocal loudness (increased amplitude of
motor output) may stimulate generalized neural motor activation across the speech production system and potentially other
motor systems. The improvements in articulation, facial expression, swallowing and limb movements are consistent with the
concept of global parameters, whereby a single treatment target
impacts common control mechanisms that, in turn, influence
motor behaviors beyond the specific targeted function [128–130].
The neurological bases of such global motor effects are not know.
However, McClean and Tasko reported evidence for neural coupling of orofacial muscles to neural systems of laryngeal and respiratory control in human studies [131]. These authors suggest
that a potential source of this observed neural coupling might be
from efferent drive from a common brain region to motor neurons innervating orofacial, laryngeal and respiratory muscles.
Such common neural structures and coupling may explain, in
part, the potential spread of effects from stimulation of increased
vocal effort and loudness (respiratory and laryngeal systems) to
orofacial muscles and swallowing function. Another explanation
for the distributed and lasting impact of LSVT LOUD is that it
involves and stimulates phylogenetically old neural systems, especially the emotive brain, which is an important part of the survival mechanism. Speech production is a learned, highly practiced motor behavior, with many of its movements regulated in a
quasiautomatic fashion [132,133]; loudness scaling is a task that
both animals and humans engage in all their lives [43,44,134–137].
Thus, the regulation of vocal loudness for speech may involve a
phylogenetically old system that has been adapted, through
learning, for speech production and comprehension purposes.
In summary, these findings suggest the effects of loud phonation may be uniquely pervasive across the speech production system by stimulating common neural mechanisms for speech and
other motor systems, and/or by stimulating neural systems that
mediate emotive vocalization via an integrated, phylogenetically
old neural mechanism.
Brain changes induced by LSVT LOUD as measured with
PET imaging [124,138] reflect improvements in the basal ganglia,
limbic system, prefrontal cortex and right hemisphere functions.
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• Comparative studies evaluating the impact of training vocal
loudness (LSVT LOUD) to matched treatment targeting
high effort articulatory exercise (ENUNCIATE), with neural
imaging of treatment-related changes [139]
• Systematically documenting the impact of DBS surgery on
speech in people with PD and their response to speech therapy
post-surgery
• Applying principles of successful speech therapy (LSVT
LOUD) to limb motor systems and creating a combined
amplitude-based speech and physical therapy program
• Evaluating the potential neuroprotective impact of exercisebased speech therapies in humans with PD
• Developing animal models of PD-like vocalization
• Increasing accessibility to speech treatment through technology
Published pilot data from training loudness (LSVT LOUD)
have documented that effects generalize beyond vocal loudness
to improve swallowing, speech articulation, communicative gestures, facial expression and neural functioning [59,124,140–143].
Ongoing randomized controlled studies are further examining
this spread of effects by evaluating and comparing the systemwide generalized impact of two therapies (voice [LSVT LOUD]
and articulation [ENUNCIATE]) on speech articulation, facial
expression and swallowing in idiopathic PD, and the systemwide generalized impact of these two therapies on limb gesture
and limb motor functioning in PD. Functional imaging investigations (PET) of these two treatments will identify changes in
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and 27% on quality of life (Parkinson’s Disease Questionnaire
[PDQ]-summary score). These data document that individuals
with early PD are able to improve beyond baseline levels. There
is a great need to simplify rehabilitation approaches for people
with PD owing to the progressive nature of the disorder, cognitive challenges that make motor learning difficult, and logistical
and financial burdens that intensive speech and physical therapies present. A whole body, amplitude-based treatment program may be one possible solution. This was a Phase I study
and further research is required.
Recent advances in neuroscience reveal that exercise and
motor training impacts molecular changes associated with cell
survival, cell growth and functional recovery in animal models
of PD. This challenges the assumption that there is no potential for recovery in PD or other neurodegenerative disorders.
Altogether, these background tenants emphasize the need for
human studies of exercise-based programs that are continuous,
immediately available at the time of diagnosis, and that promote neural plasticity and brain reorganization [79,124,126,144].
The translation of the principles of neural plasticity to therapeutic approaches will require a significant paradigm shift in
rehabilitation sciences [127]. Current rehabilitation approaches
are typically not developed specifically for the deficits in PD (or
other neural disorders), nor do they implement the principles
that promote plasticity in a standardized manner. Our ability to
embrace these principles and integrate them into the mode of
delivery of treatment will be essential for evolving rehabilitation
science in parallel with neuroscience. We need future studies to
specifically evaluate the impact of intensive behavioral speech
therapy on neuroplasticity and the potential for neuroprotection as measured by dopamine-related changes in imaging studies over time. These data would have the potential to facilitate
early referral to speech and physical therapies.
As discussed above, speech and voice deficits associated with
PD have been largely resistant to pharmacological and surgical
treatment, but have responded to intensive speech treatments.
The mechanism underlying this phenomenon is not well understood and is difficult to systematically test in human models.
Thus, we turn to the rodent as a model, which may be helpful,
especially if human and rodent vocalizations share similar
underlying neural events. Our underlying tenet for using the rat
model is that the impairment in voice and speech in individuals
with PD is at least partially related to phylogenically old neural
mechanisms subserving phonation [45]. Initial data suggest that
mild transient dopamine depletion with haloperidol or even
unilateral degeneration of dopamine neurons are associated with
changes in the ultrasonic vocalization (USV) acoustic signal,
such as decreased frequency bandwidth [149]. USV in the rodent
model of PD may be a useful model to study parkinsonian-like
vocalization deficits. This work sets the stage for future research
aimed at acquiring neurobiological and behavioral evidence on
the effects of vocal exercise in an animal model as a translational
approach from basic science to human clinical science in the
area of PD speech treatment. In addition, this model offers the
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neural connectivity and functioning and identify any differences associated with different treatment targets. Results from
these studies will further clarify the neural bases for voice and
speech disorders in people with PD as well as guide development and modifications for optimal speech treatment
approaches for this population.
While DBS-STN has been a valuable treatment for many
symptoms of PD, speech outcomes have been variable.
Reports range from improvements in selective aspects of
speech to severe problems in speech and swallowing following
DBS-STN [87]. People and families consistently rate problems
in speech and swallowing following DBS-STN as significant
and persistent. We need systematic studies of these heterogeneous speech outcomes following DBS-STN that include simultaneous quantitative measures of pre- and post-surgical speech
functioning and details of surgical and stimulator optimization. This careful definition of speech outcomes following
DBS-STN will provide guidance to surgical stimulation targets for speech. Furthermore, this knowledge will facilitate
development of rehabilitative speech treatment approaches for
speech problems in people with DBS-STN either pre-surgery
(as preventative) or post-surgery (as rehabilitation).
Currently, several research groups are undertaking these tasks.
The 1st International Symposium on Basal Ganglia Speech Disorders and Deep Brain Stimulation was held in 2007 at the
Institute of Neurology, Queen Square, London. This meeting
brought together researchers (neurosurgeons, neurologists,
speech scientists and speech-language pathologists) from
around the world to address the issues surrounding DBS surgery and changes in speech. Advances in surgical techniques,
stimulator settings and use of behavioral speech treatments will
likely emerge in the next 5 years given the concentrated focus
on this area of research.
Recently, the principles of LSVT LOUD were applied to limb
movement in people with PD. Training-increased amplitude of
limb and body movement (bigness) in people with PD has documented improvements in amplitude (trunk rotation/gait) that
generalized to improved speed (upper/lower limbs), balance and
quality of life [144,145]. In addition, people were able to maintain
these improvements when challenged with a dual task. The
extension of this work to a novel integrated treatment program
that simultaneously targets speech and limb motor disorders in
people with PD (big and loud) has been proposed. Results from
pilot work have been completed in 11 people with PD: nine
stage I (three de novo) and two stage II. Data revealed all subjects
increased vocSPL (loudness) during sustained vowels and reading (average 10 db SPL increase across both tasks), and increased
stride length/velocity during gait (average of 9 cm) [146,147]. The
gains in vocal SPL and gait stride length were comparable to previously published data from independently training LSVT
LOUD (speech; range 8–13 dB SPL) [110–148] or LSVT BIG
(limbs; range 9–30 cm) [145]. These changes in speech and gait
function had a positive impact of 28% on disease severity (Unified Parkinson’s Disease Rating Scale [UPDRS]-motor section)
Review
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305
Ramig, Fox and Sapir
Key issues
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• Speech and voice disorders negatively impact people with
Parkinson’s Disease (PD)
– Between 85 and90% of individuals with PD develop voice
and speech disorders during the course of their illness.
Many patients develop speech and voice problems early in
the course of their disease. These disorders, along with
reduced facial expression, adversely affect communication
and quality of life.
• There are limited effects of medication, neurosurgery, and
traditional speech on voice and speech disorders in PD
– Neurosurgical and levodopa treatments for PD have yielded
minimal, inconsistent or adverse effects on voice and
speech functions.
• Current reviews of speech treatment evidence suggest more
data are needed to clarify the most effective speech treatment
approach in PD.
• Criteria for reviewing behavioral treatment evidence may
differ from pharmacological studies owing to difficulties with
concealed placebo treatment. The use of comparison
treatments and statistical analysis with smaller sample sizes
may be warranted.
• Speech treatment that has a focus on vocal loudness and pitch
or increasing vocal effort and loudness is recommended for
people with PD.
• Effects of the Lee Silverman Voice Therapy have greatest
amount of data supporting impact on voice, speech and other
orofacial functions, as well as on brain reorganization.
• Future areas of research in treatment studies, neural imaging,
deep brain stimulation, neural plasticity and animal models of
vocalizations will help clarify neural basis of speech disorders in
PD and guide development and refinement of speech treatment
approaches, and support early referral to speech treatment.
306
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Advances in computer and web-based technology offer
potentially powerful solutions to the problems of delivering
an intensive efficacious dosage of treatment, treatment accessibility and long-term maintenance in rehabilitation. For
example, a computer training application for upper limb
motor deficits following stroke has been developed for delivery of constraint induced therapy, a program which requires
intensive motor training (e.g., 6 h/day for 2 weeks). This
computerized system, called AutoCITE, was documented to
result in comparable outcomes to live delivery of the therapy
[150]. Computer technology has also been developed for delivery of an intensive speech treatment (LSVT LOUD) and is
discussed below.
Halpern and colleagues [151,152] reported on the use of a personal digital assistant as an assistive device for delivering LSVT
LOUD to people with PD. The LSVT LOUD companion
(LSVT LOUD-C) is specially programmed to collect data and
provide feedback as it guides people through the treatment
exercises, enabling them to participate in therapy sessions at
home. A total of 15 people with PD participated in a study
during which nine voice treatment sessions were completed
with a speech therapist and seven sessions were completed
independently at home utilizing the LSVT LOUD-C. Data
revealed findings similar to previously published data on 16
face-to-face sessions both immediately post-treatment and at
6-month follow-up [151–152]. An evolution of the LSVT
LOUD-C has been the development of a virtual speech therapist (LSVT LOUD-VT). This is a perceptive animated character, modeled after expert LSVT speech therapists, that delivers
LSVT LOUD in a computer-based program [153]. A prototype
of the LSVT LOUD-VT has been developed and clinical testing has begun. In addition, delivery of intensive speech therapy, such as LSVT, via Telehealth systems or other web-enabled speech therapy systems have documented positive
outcomes in people with PD and will enhance accessibility to
the intensive sensorimotor training important for successful
speech outcomes.
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ability to evaluate issues of timing and medication confounds on
these neurobiological and behavioral outcomes, studies that
cannot be easily done in humans with PD. Thus, animal data
offer an important opportunity to advance our understanding
of speech motor control in neural diseases, such as PD.
It is recognized that there are practical challenges of delivering
speech treatment intensively (four individual sessions per week
for 4 weeks). In fact, any treatment regime (speech, physical or
occupational therapy) that is consistent with plasticity promoting principles and incorporates elements such as intensity and
multiple repetitions will require going beyond the one-to-one
(patient to clinician) classic paradigm of treatment delivery.
There are not enough therapists to deliver this efficacious dosage of treatment to all the people with PD in need; a need
which will only increase dramatically in the coming years with
the aging of the baby boomer population. Furthermore, continued exercise following the conclusion of speech treatment and
tune-up sessions may be needed for maintenance of vocal loudness as the disease progresses. Moreover, intensive treatment can
be costly, especially for the elderly, whose source of income
might be limited. Thus, there is a need for expanding service
delivery while containing costs and human resources.
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Review
Conclusion
The majority of people with PD experience speech and voice
disorders at some point during the disease course and these deficits impair their quality of life. Medical and surgical treatments alone have not sufficiently alleviated speech disorders for
people with PD, and in some cases have exacerbated or resulted
in voice and speech impairment. Thus a combination of behavioral speech therapy, specifically the LSVT LOUD approach,
in medically managed people with PD appears at present to be
the most effective type of speech intervention, though more
level I studies are needed. There are many exciting avenues of
ongoing and future speech research that will clarify our understanding of the underlying mechanism of speech disorders in
PD and impact development of rehabilitation strategies over
the next 5 years.
Expert Rev. Neurotherapeutics 8(2), (2008)
Speech treatment for Parkinson’s disease
Financial & competing interests disclosure
Lorraine Ramig is a Professor at the University of Colorado-Boulder, Senior
Scientist at the National Center for Voice and Speech (Denver) and Adjunct
Professor, Columbia University, New York City. Cynthia Fox is a Research
Associate at the National Center for Voice and Speech in Denver and Research
Lecturer in the Department of Neurology at the University of Arizona. Shimon
Sapir is an Associate Professor at the University of Haifa. This research has
been funded in part by NIH grants R01 DC1150 from National Institutes of
Deafness and other Communication Disorders (Ramig, Fox and Sapir).
Lorraine Ramig receives a lecturer and travel honorarium from the
LSVT Foundation (nonprofit organization), a consulting honorarium
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Papers of special note have been highlighted as:
• of interest
•• of considerable interest
from the Kinetics Foundation, receives a lecture honorarium and has
intellectual property rights and ownership interest in LSVT Global LLC
(for-profit organization that runs training courses and sells products
related to LSVT Treatment).
Cynthia Fox receives a lecturer and travel honorarium from the LSVT
Foundation (nonprofit organization), receives lecture honorarium and has
intellectual property rights and ownership interest in LSVT Global LLC.
The authors have no other relevant affiliations or financial involvement
with any organization or entity with a financial interest in or financial
conflict with the subject matter or materials discussed in the manuscript
apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
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••
••
This RCT evaluates the short- and
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••
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Affiliations
•
Lorraine O Ramig, PhD, CCC-SLP
Professor, Department of Speech,
Language, Hearing Sciences, University of
Colorado, Campus Box 409, Boulder, CO
80309, USA; Senior Scientist, National
Center for Voice & Speech, Denver Center
for the Performing Arts, Denver, Colorado;
Adjunct Professor, Columbia University,
New York City, NY, USA
Tel.: +1 303 492 3023
Fax: +1 303 499 6742
[email protected]
•
Cynthia Fox, PhD, CCC-SLP
Research Associate, National Center for
Voice and Speech, Denver, CO, USA;
Research Lecturer, Department of
Neurology, University of Arizona, Tucson
6133 E. Calle Ojos Verde, USA
Tucson, AZ 85750–1944
Tel.: +1 520 631 2996
Fax: +1 520 615 8559
[email protected]
•
Shimon Sapir, PhD, CCC-SLP
Associate Professor, Department of
Communication Sciences and Disorders,
Faculty of Social Welfare and Health
Sciences, University of Haifa, Haifa, Mount
Carmel, Haifa, 31905, Israel
Tel.: +972 4824 0517
Fax: +972 4824 9507
[email protected]
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Congress of Parkinson’s Disease and
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