Perspective
THEMED ARTICLE y Parkinson’s disease
Intensive voice treatment in
Parkinson’s disease: Lee
Silverman Voice Treatment
Expert Rev. Neurother. 11(6), 815–830 (2011)
of
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Department of Communication,
Sciences and Disorders, University of
Haifa, Mount Carmel, 31905, Israel
2
University of Colorado Boulder,
CO, USA
3
National Center for Voice and Speech,
CO, USA
†
Author for correspondence:
Tel.: +972 508 594 700
Fax: +972 482 495 07
[email protected]
ho
1
Advances in neuroscience have led to an expanded and improved understanding of neurobiological
changes associated with rehabilitation and exercise in Parkinson’s disease (PD). This knowledge
has led to a direct clinical impact of increased referral for early and continuous exercise programs
for individuals with PD (physical, occupational, speech therapy and general exercise programs)
and an increased research focus on the impact of such approaches in humans with PD. The
purpose of this article is to examine the role of speech therapy in the landscape of exercise-based
interventions for individuals with PD. We will specifically focus on the intensive voice treatment
protocol, Lee Silverman Voice Treatment, as an example therapy. This article will briefly review
the literature on the characteristics and features of speech and voice disorders in individuals
with PD, and will discuss the impact of pharmacological and surgical treatment techniques on
these disorders. This will be followed by a focus on behavioral speech treatment, specifically
Lee Silverman Voice Treatment, including development of the treatment approach, documenting
efficacy, discovery of unexpected outcomes and insights into the mechanism of speech disorders
in PD gained from treatment-related changes. This research will be placed in the context of
other previous and current speech treatment approaches in development for individuals with
PD and will highlight future directions for research.
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Shimon Sapir1,
Lorraine O Ramig2,3
and Cynthia M Fox3
Keywords : Lee Silverman Voice Treatment • LSVT • neural plasticity • Parkinson’s disease
• speech and voice disorders • swallowing disorders
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It is a stunning time to be in rehabilitation today.
The basic science evidence for the value of exercise
in Parkinson’s disease (PD) has been documented
in animal models of the disease and is being
increasingly explored in humans with PD [1–3] .
In addition, research has identified key principles
of exercise that drive activity-dependent neural
plasticity (modifications in the CNS in response
to physical activity) [4–5] . These collective data
have elevated the role of exercise and/or rehabilitation in the overall management of PD beyond a
reactive referral for secondary impairments (e.g.,
aspiration due to swallowing impairments or hip
fracture due to falling) to a legitimate therapeutic
option prescribed early, upon diagnosis, that may
slow or halt symptom progression [2,6] . As a result
of this basic science evidence, there has been a
steady increase in the number of physical therapy
trials in individuals with PD from 1980 through
2010 [7] , and the practice variables that have been
documented to be effective in the animal models
(e.g., intensity and specificity) are being reported
in human trials of PD and stroke [1,3] .
www.expert-reviews.com
10.1586/ERN.11.43
The purpose of this article is to examine this
new paradigm of exercise-based interventions and
activity-dependent neural plasticity in PD in relation to literature in speech treatment, with a focus
on the Lee Silverman Voice Treatment (LSVT)
as an example therapy. We will begin with a brief
overview of the characteristics and features of
speech and voice disorders in individuals with
PD, discuss the impact of pharmacological and
surgical treatment techniques on these disorders,
and highlight possible underlying neural mechanisms of the dysarthria in PD. This will be followed by a focus on behavioral speech treatment,
specifically LSVT, including development of the
treatment approach, treatment efficacy, discovery of unexpected outcomes, and insights into
the mechanisms of speech disorders in PD gained
from treatment-related changes. This research will
be placed in the context of other previous and current speech treatment approaches in development
for individuals with PD. The key fundamentals
of the treatment approach will be discussed and
future directions for research will be highlighted.
© 2011 Expert Reviews Ltd
ISSN 1473-7175
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Sapir, Ramig & Fox
terms of magnitude and long-term maintenance of treatment outcomes. While some studies have documented dopamine-induced
improvement in speech motor function [23,34–38] , other studies
have failed to show systematic changes or clinically significant
improvement in the speech of individuals with PD following
levodopa treatment [33,39–42] . These findings suggest that neurochemical or neurobehavioral factors other than, or in addition to
dopamine deficiency may play a significant role in hypokinetic
dysarthria associated with PD, as will be discussed later [32,41] .
Neurosurgical procedures such as deep brain stimulation (DBS)
of the thalamus, pallidum or subthalamic nucleus, ablative surgeries (pallidotomy and thalamotomy) and fetal cell implantation
have been demonstrated to result in dramatic improvement in
limb motor function, yet these procedures have yielded contradictory results on speech functions in individuals with PD [42–45] .
The most common neurosurgical approach used today is DBS
of either the subthalamic nucleus (STN) or the internal segment of the globus pallidus (GPi). Although there have been
reports of improvements in components of speech production
with STN-DBS [46–49] , the impact on functional speech intelligibility remains unclear [50–51] . Adverse effects of STN-DBS
on speech have received increasing attention in the neurology
and speech literature in recent years [52–54] . Explanations for the
negative effects of STN-DBS on speech include high-frequency
stimulation [55] , location of electrode contacts and amplitude of
stimulation in the STN [51] , the spread of current to nearby fiber
tracts such as the cerebellothalamic fibers [56] and/or lesions of a
neural network that mediates sensorimotor speech control [57] .
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Parkinson’s disease affects 1–2% of individuals over the age of
60 years, as well as younger individuals in their 30s and 40s [8] .
Nearly 90% of these individuals are likely to develop speech disorders during the course of their illness [9] . These disorders, collectively called hypokinetic dysarthria [10] , may include any or a
combination of the following: reduced vocal loudness and abnormal vocal decay [11] ; a breathy, hoarse, or harsh voice quality [12] ;
imprecise consonants and vowels due to reduced range of articulatory movements, with the tendency of these movements to decay
and/or accelerate toward the end of a sentence [13–15] ; reduced
voice pitch inflections, or monotone; and rushed, dysfluent or
hesitant speech [13–16] . Other less frequently occurring speech
abnormalities may include palilalia and stuttering-like dysfluencies [17] . These speech problems have been traditionally attributed to muscle rigidity and hypokinesia secondary to dopamine
deficiency [18] . However, as we will discuss, additional factors,
such as deficits in scaling and maintaining movement amplitude,
internal cueing, high-level sensory processing, neuropsychological
functions (attention to action and vocal vigilance), along with
nondopaminergic or special dopaminergic mechanisms, may provide a more comprehensive or complimentary explanation for the
etiology of the dysarthria.
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Hypokinetic dysarthria in PD
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Perspective
Physiologic abnormalities associated with voice
& speech disorders in PD
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Studies of vocal function in individuals with PD have documented
poor vocal fold closure; reduced amplitude, asymmetrical or slow
vibratory patterns of the vocal folds and voice tremor (the latter
might be a form of essential tremor) [19–20] . Respiratory studies of
individuals with PD have documented a reduction or abnormalities in vital capacity, chest wall movements, respiratory muscle
activation patterns, amount of air expended during maximum
phonation tasks and intraoral air pressure during consonant/vowel
productions [21] . Electromyographic (EMG) studies of individuals
with PD revealed a reduction of neural drive to the laryngeal muscles [22] , abnormally elevated laryngeal muscle activity [23] or poor
reciprocal suppression of laryngeal and respiratory muscles [24] .
Kinematic and EMG studies of orofacial movements during various speech tasks in individuals with PD have indicated 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 [25–30] . These studies, which have included healthy control
subjects for comparison, suggest that hypokinetic speech movements in PD may be associated with abnormal neural drive to
the speech periphery and abnormal sensorimotor gating and may
be a major cause of the speech movement abnormalities in PD.
Medical treatment for voice & speech disorders in PD
Pharmacological treatments with dopamine-replacement therapy (levodopa or dopamine agonists) has marked therapeutic
effects on rigidity, akinesia, bradykinesia and tremor in the limb
motor system [31] ; however, its effects on hypokinetic dysarthria
in individuals with PD have yielded variable findings [32–33] in
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Hypotheses regarding neural mechanisms underlying
voice & speech disorders in PD
It has been suggested that some motor disorders in PD, including
hypokinetic dysarthria, may be partially related to abnormal nondopaminergic or special dopaminergic mechanisms, which impair
several high-level processes that are important for the regulation
and control of speech movements [16,32–33,53–54] . We will briefly
present four high-level processes we hypothesize to be impaired
and to underlie hypokinetic dysarthria in PD. These include scaling movement amplitude, sensory processing, internal cueing and
vocal vigilance.
Scaling movement amplitude
One likely cause of hypokinetic dysarthria in PD is reduced
amplitude of output (hypokinesia) and abnormal scaling and
maintenance of movement amplitude. Reduced range (hypo­
kinesia) of respiratory, laryngeal and orofacial movements during speech sound production in individuals with PD, with the
tendency of the amplitude of the movements to decay (become
more hypokinetic) within and across utterances, have been documented in various studies [11,14,25,58–59] . This reduction may manifest as a systematic reduction and decay of vocal loudness, pitch
intonation and precision of vowels, consonants and other sounds
of speech [14–15,58,60–62] , and may be attributed to the inability
of individuals with PD to scale and/or maintain movement
amplitude, force or related parameters [63–68] .
Expert Rev. Neurother. 11(6), (2011)
Intensive voice treatment in Parkinson’s disease: Lee Silverman Voice Treatment
provided with dots or lines on the paper, and asked to write so that
the letters touch the dots or the lines (external cues) [90] . The use
of external cueing has also been demonstrated to positively impact
gait in PD, with long-term retention, when cueing strategies were
systematically trained over several weeks’ time [91] .
Vocal vigilance
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A fourth factor is impairment in self monitoring and self regulation of voice and speech motor output due to deficits in attention
to action or vocal vigilance. There is evidence that attention to
action is impaired in individuals with PD, and that this impairment may contribute to the abnormal control of movements in
PD [92,93] . By inference, impaired vocal vigilance in individuals
with PD may have an adverse effect on motor speech control,
which may partially account for the hypokinetic dysarthria in
these individuals [54] . Importantly, it has been shown that attention to action in individuals with PD can be improved significantly
by intensive training [80,94] . As will be discussed later, the LSVT
treatment regimen, which has been designed to train individuals
with PD to pay attention to their speech output and to monitor
the effort to produce this output, has been shown to be effective
in the long-term maintenance of treatment outcome [87,95] .
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A second factor is abnormality in sensory processing. Behavioral
and physiological studies of speech and nonspeech oral and head
and neck functions in individuals with PD have documented
sensory abnormalities, manifested as errors on tasks of kinesthesia [69–71] ; difficulties with orofacial perception, including
decreased jaw proprioception, tactile localization on tongue, gums
and teeth, and targeted and tracking head movements to perioral
stimulation [72] ; problems utilizing proprioceptive information
for normal movement [70,72] ; abnormal higher order processing
of afferent information as demonstrated by abnormal reflex and
voluntary motor responses to proprioceptive input [27,73–75] ; and
abnormal sensory processing of voice and speech in individuals
with PD [25,76–80] . Laryngeal sensorimotor deficits in PD have
also been documented [81,82] . These sensorimotor abnormalities
may account, at least partially, for the deficits in scaling and
maintaining speech movement amplitude.
One aspect of sensory processing deficits in individuals with PD
is misperception of self-produced voice and vocal effort. Individuals
with PD are often unaware of the magnitude of their reduced vocal
loudness and will report, ‘my voice is fine, but my spouse needs
a hearing aid’ [83] . This is similar to the inaccurate perception of
body awareness and lack of self corrections of smaller and slower
movements in everyday living, even in early PD [2] . Furthermore,
when individuals with PD and hypokinetic dysarthria are asked to
produce ‘loud’ speech (i.e., increase amplitude of motor output),
they typically increase their speech to a normal conversational
volume level, yet they complain that this louder voice is ‘way too
loud’. This phenomenon has been documented experimentally by
Ho and colleagues [79] . These researchers found that even though
individuals with PD spoke with a softer voice than healthy controls, they nevertheless perceived their own speech to be louder
than that judged by the healthy controls. In addition, individuals
with PD overestimated the loudness of their speech during both
reading and conversation. Furthermore, sensorimotor abnormaities
in auditory–vocal feedback and feed-forward mechanisms have
been indirectly demonstrated in individuals with PD by behavioral [84] and neuro­physiological [85] studies. Finally, Ramig and
colleagues [86–88] have shown that addressing problems of sensory
processing deficits is an important therapeutic goal for a successful
treatment of hypokinetic dysarthria in individuals with PD [86–88] .
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Sensory processing
Perspective
Internal cueing
A third factor is deficits in internal cueing. One of the most striking characteristics of hypokinetic dysarthria in individuals with
PD is the dramatic improvement in voice and speech when these
individuals are externally cued or instructed to speak loudly and
or clearly. The improvement in voice and speech with external
cueing is most likely a compensatory response to deficits in internal cueing [89] . This conclusion is empirically supported by a series
of experimental studies conducted by Ho and colleagues [77–79] .
It is also consistent with the phenomenon of micrographia (the
abnormally small handwriting) in individuals with PD, which
tends to improve dramatically (though transiently) when these
individuals are verbally instructed to ‘write big’ or when they are
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Summary of origins of speech & voice disorders in PD
To summarize, the neural mechanisms underlying speech disorders in individuals with PD appear to be complex and not well
delineated. Additional research is needed to explore these deficits
and their interaction and contribution to the speech disorders
observed in individuals with PD. Given this complexity, it is not
surprising that traditional medical and behavioral treatments
have had only limited success in managing these problems and
in improving speech in the long term. New insights about the
nature of speech disorders in PD have been gained from testing
new hypotheses regarding the pathogenic mechanisms under­lying
these disorders and from studies of treatment effects, such as those
induced by the LSVT regimen.
Behavioral speech treatment for individuals with PD
Historically, speech and voice disorders in individuals with PD
were thought to be resistant to behavioral speech therapy [96–99] .
This view of speech therapy mirrored the view of physical therapy
and exercise in that it was perceived as not helpful (see [2] for full
historical physical therapy review). In the mid 1980s and early
1990s there began to be a shift in the view of both physical and
speech therapy for individuals with PD. In speech treatment,
studies in the UK and the USA reported on speech treatment protocols that documented positive impact on voice and speech outcomes [100–103] (see [33] for more detailed review). Two consistent
features of these studies emerged and were later recommended as
key treatment components to focus on in speech therapy in PD:
high dosage of the therapy (almost daily therapy for 2–4 weeks)
and a focus on improving the voice either through exercise of
prosody, loudness or a combination of these [104] . To our knowledge, of these published initial promising studies, only the Ramig
et al. protocol (known today as LSVT) was standardized and
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Sapir, Ramig & Fox
The Lee Silverman Voice Treatment
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Initial development of the LSVT began in the late 1980s under
the direction of Lorraine Ramig and her former student Carolyn
Bonitati at the Lee Silverman Center for Parkinson’s disease in
Scottsdale (AZ, USA). Initial Phase I and II studies were completed where the protocol of LSVT was established and tested
in clinical conditions. These initial data were reported in 1988
by Ramig and colleagues [106] and the standardized protocol
was introduced as the LSVT in honor of Mrs Lee Silverman, a
woman with PD. These initial data sets were the foundation for the
Phase III efficacy studies that were conducted in the 1990s. Two
randomized controlled trials were completed. The first study compared two treatments, both designed to improve vocal loudness in
people with PD. One treatment focused on increasing respiratory
drive and vocal fold adduction (known today as LSVT) and the
other treatment focused on increasing respiratory support only.
Both treatments were matched for intensity of dosage, positive
reinforcement from the clinicians, and homework and carryover
assignments. Additional details can be found in Ramig et al. [86] .
Subject groups were studied immediately before treatment, after
treatment and at 6, 12 and 24 months after treatment (with no
additional therapy). Multiple acoustic, perceptual, aerodynamic
and neuropsychological measures were collected. These data were
published in a series of studies [87–88,103,107] . The primary treatment
outcome variable from these studies was vocal sound pressure level
(vocSPL). In this series of studies, LSVT was superior in improving
vocal loudness and vocSPL over the alternative treatment approach.
In the second randomized controlled trial, LSVT was compared
with an untreated group of individuals with PD and an age- and
sex-matched healthy control group at three time points: before
treatment, after treatment and at 6 months after treatment. This
study was published in 2001 [88] . We have summarized the primary outcome variable of vocSPL across this series of studies and
added effect size values in Table 1. As can be seen, in most studies,
the effect size was larger than 0.80, indicating that the changes
induced by the LSVT are clinically highly significant [108] .
disorders. In addition, it became clear that it is important to distinguish between acute responses to a single episode of physical activity (i.e.. stimulating increased loudness) from chronic effects associated with long-term adaptation accompanying repetitive physical
exercise (i.e., training increased loudness) [112] . Across a series of
stimulated vocal loudness studies, we have documented short-term
improvements in a number of voice, respiratory and articulatory
measures in nondisordered and disordered speakers [113–115] , as
have other authors examining stimulated vocal loudness [116,117] .
However, Liotti et al. documented that changes in brain activation
in five subjects with idiopathic PD occurred only following training vocal loudness (LSVT) for 1 month [118] . These changes were
not observed before treatment with brief stimulated increases in
loudness, as will be discussed later. Will et al. also documented a
difference between stimulated and trained loudness, reporting that
only in the trained condition (not the stimulated condition) did
significant acoustic differences in vowel space accompany increased
loudness in individuals with PD [119] . Taken together, these findings suggest that while stimulating loudness does impact speech
production in the short term [120] , lasting changes in speech–motor
coordination and neural reorganization appear to require intensive
training. This is consistent with basic research studies that suggest there is a need for continued practice of a new motor skill
(e.g., intensive training) for long-term structural changes in neural
functioning [121] . Acquisition alone is not sufficient for sustained
neural plasticity (i.e., resistance to decay) nor may it be sufficient
for transfer and carryover outside the therapeutic environment.
Brain imaging studies using O15 PET have also documented
marked changes in brain function in conjunction with speech
improvement following LSVT [85,118,122,123] . Specifically, while
stimulated loud phonation prior to the administration of LSVT
activated cortical premotor areas, particularly the supplementary
motor area (SMA), after LSVT, SMA activity was normalized,
and increased activity in the basal ganglia (right putamen) suggested a shift from abnormal cortical motor activation to normal
subcortical organization of speech-motor output. The excessive
activity in the auditory cortex before LSVT and its reduction
to a normal level after LSVT, as discussed earlier, also suggests
improvement in brain function. The post-LSVT changes also
indicated an increase in activity in right anterior insula and right
dorsolateral prefrontal cortex, suggesting that LSVT may recruit a
phylogenetically old, preverbal communication system involved in
vocalization and emotional communication (consistent with the
multisystem effects of LSVT). Finally, the shift in brain activity
from left to right hemisphere and in regions that involve attention
to action and self-monitoring of action [122] indicates that the longterm maintenance of treatment outcomes may, at least partially,
be related to improvement in vocal vigilance.
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further researched to assess treatment efficacy in the short and
long term. Today, there are more than 20 years of research on
the development and research process of the LSVT program for
people with PD. Thus, the study of LSVT has provided a unique
opportunity to examine a behavioral treatment regimen through
the various phases of efficacy research [105] , as well as to improve
our understanding of motor speech disorders in PD and their
neurophysiologic underpinnings.
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Perspective
Review of secondary studies/outcomes
In the process of documenting treatment efficacy, there were a series
of secondary studies and discoveries that occurred. Most notably,
the recognition of the distributed effects across the speech production system following LSVT that extended beyond vocal loudness
[20] to include improved articulation [15,61,109] , facial expression [110]
and swallowing efficiency [111] . These distributed effects have been
of great interest, given the potential clinical efficacy of a single
treatment target (vocal loudness) to improve multiple speech system
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Fundamentals of LSVT: target, mode & calibration
Lee Silverman Voice Treatment is a PD-specific, standardized,
research-based approach and differs from the way in which traditional speech therapy was delivered at the time LSVT was
developed. Table 2 highlights these key differences. The LSVT
regimen is unique in a number of key ways. First, the target
Expert Rev. Neurother. 11(6), (2011)
Intensive voice treatment in Parkinson’s disease: Lee Silverman Voice Treatment
Perspective
Table 1. Summary of vocal sound pressure level data from a series of Lee Silverman Voice
Treatment studies.
Ramig et al. LSVT
26
Ramig et al. RESP
19
SPL ‘AH’
SPL Rainbow
Before After
Effect
size
Before After
Effect
size
68.2
81.2
2.78
66.3
74.33
1.81
64.67
69.17
1.20
[103]
4.7
4.65
4.02
4.83
3.37
4.1
69.32
68.01
65.68
68.16
64.66
66.24
0.67
[103]
5.05
4.31
2.68
3.33
2.58
2.11
-0.28
Before Follow-up Effect
12 mo
size
Before Follow-up Effect
12 mo
size
1.73
66.44
0.85
65.26
3.93
3.09
3.06
2.84
-0.29
65.73
65.94
0.06
65.13
63.3
2.72
4.34
2.59
3.13
68.44
4.61
4.49
Ramig et al.† RESP
13
69.69
68.12
5.26
5.43
76.31
Before Follow-up Effect
24 mo
size
12
68.26
76.5
4.45
4.1
69.19
70.12
5.31
7.01
14
Ramig et al. UNTX
69.1
82.4
5.1
3.9
69.3
70.5
4.1
4.4
ut
14
A
Ramig et al. LSVT
15
ho
Before After
Ramig et al. LSVT
Ramig et al. UNTX
15
1.93
0.15
69.46
67.18
0.65
[175]
-0.64
[175]
Before Follow-up Effect
24 mo
size
Before Follow-up Effect
24 mo
size
66.18
64.7
67.02
2.56
1.87
64.72
65.71
2.76
4.32
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Ramig et al.† RESP
0.82
Before Follow-up Effect
12 mo
size
22
21
Ref.
Effect
size
Ramig et al.† LSVT
Ramig et al.† LSVT
SPL Monologue
Before After
of
Treatment Subjects
groups
(n)
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Study
69.78
3.79
3.19
65.79
66.49
2.6
5.54
1.03
0.16
1.03
[87]
0.27
[87]
Effect
size
Before After
Effect
size
Before After
Effect
size
2.93
71.3
77.9
1.77
69
74.5
1.45
[88]
3.2
4.2
3.6
4
71.6
71.9
69.3
69.4
0.03
[88]
3.6
4.1
3.9
3.9
0.28
0.08
Before Follow-up Effect
6 mo
size
Before Follow-up Effect
6 mo
size
Before Follow-up Effect
6 mo
size
69.1
79.3
71.3
76.1
69
72.7
5.1
3.7
3.2
3.2
3.6
3.6
69.3
70.6
71.6
71.9
69.3
69.5
4.1
4.1
3.6
4.1
3.9
3.2
2.29
0.32
1.50
0.08
1.03
[88]
0.06
[88]
Note the total subject numbers for Monologue or Rainbow passage are reduced across both treatments in some studies.
The data include the number of subjects in each treatment group, the mean (SD) vocal sound pressure level (in dB) before treatment, after treatment and at
follow-up, and the effect size measure of the difference between before and after, or before and follow-up.
According to Cohen [108] effect size >0.80 is considered a highly significant difference (clinically speaking), a value of 0.50 indicates medium difference, and a value
0.20 indicates a small difference. Note the large effect size values for the LSVT and the small effect size values for the other treatment (RESP) or no treatment (UNTX).
There are some exceptions to the subject numbers given in the table, and these are as follows: Ramig et al. [175]: Monologue LSVT 13, RESP 8; Ramig et al. [87]:
Rainbow passage RESP 11; Monologue LSVT 12, RESP 6.
LSVT: Lee Silverman Voice Treatment; mo: Month; RESP: Speech therapy with the same schedule and intensity as LSVT, but with emphasis only on respiratory effort,
rather than on respiratory–phonatory effort, which is the basis of the LSVT regimen; SPL: Sound pressure level; UNTX: The group of individuals with Parkinson’s
disease who did not receive speech therapy at the time of the study.
†
of treatment is the voice. Specifically, LSVT trains amplitude
(increased vocal loudness) as a single motor control parameter.
Second, the mode of treatment delivery is intensive and requires
high effort, consistent with principles that drive activity-dependent neural plasticity [124] , theories of motor learning [125] and
skill acquisition [126] . Third, calibration addresses the sensory,
internal cueing and neuropsycological deficits (e.g., impaired
www.expert-reviews.com
attention to action or vocal vigilance) that can make generalization and lasting treatment effects difficult to obtain for
individuals with PD.
Target: vocal loudness (amplitude)
We hypothesize that training-induced increases in movement amplitude (i.e., vocal loudness) target the proposed
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Perspective
Sapir, Ramig & Fox
Table 2. Traditional speech therapy versus Lee Silverman Voice Treatment LOUD therapy for individuals
with Parkinson’s disease.
LSVT LOUD
Ramig et al. [87–88,103]
Traditional speech therapy
e.g., Till et al. [176]
Intensity
Standardized
Variable
Dosage
4 days per week for 4 weeks (16 sessions in 1 month)
Twice per week for 4–16 sessions over several months
Repetitions
Minimum 15 repetitions per task
Variable per task
Push for maximum patient-perceived effort each day (8 or 9 on scale of 1–10
with 10 being the most)
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Effort
Moderate to low exertion; reactive to patient response to
treatment
Focus
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Daily tasks
Complex focus:
Voice, respiration, articulation, rate, posture, resonance,
orofacial movement, pacing, intonation
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Simple focus:
LOUD
Increased movement amplitude directed predominately to respiratory/
laryngeal systems
• Variable from therapist to therapist – no standardized
protocols
• Variable from day to day (e.g., one session focus on
voice loudness and intonation, next session focus on
pacing, next session orofacial movements and posture)
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First half of the treatment session (25 min)
Task 1: maximum sustained movements:
• 15 reps: sustain ‘ah’ in good-quality, loud voice as long as possible
Task 2: directional movements:
• 15 reps each: say ‘ah’ in loud good-quality voice going high in pitch
• 15 reps each: say ‘ah’ in loud good-quality voice going low in pitch
Task 3: functional movements:
• Patient self-identifies ten phrases or sentences he/she says daily in
functional living (e.g., ‘Good morning’), five reps of the list of ten phrases.
Read phrases using same effort/loudness as you did during the long ‘ah’
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Hierarchy
A
• Speech practice often does not relate back to CORE
Second half of the treatment session (25 min)
exercises focused on rescaling effort, strength or some
• Designed to train rescaled amplitude/effort of movement achieved in CORE
other movement variable
exercises from daily tasks into context-specific and variable speaking
• Progression across treatment sessions of increasing
activities
complexity of speech tasks, often starting with speech
• Incorporate multiple repetitions with a focus on high effort (e.g., list of
that is more complex than single words
20 phrases/sentences repeated ten times for 200 repetitions)
•
Diffuse focus during practice, for example, think about
• Tasks increase complexity across weeks (words > phrases > sentences >
taking a deep breath, articulate, increase loudness and/
reading > conversation) and can be tailored to each subject’s goals and
or slow down
interests (e.g., golf vs cooking)
• Tasks progress in difficulty by increasing duration (maintain LOUD for longer
periods of time), amplitude (loudness – within normal limits) and
complexity of tasks (dual processing, background noise and attentional
distracters)
Shaping techniques
• Train vocal loudness that is healthy (i.e., no unwanted strain or excessive
vocal fold closure).
• Shape the quality and voice loudness through use of modeling (‘do what I
do’) or tactile/visual cues.
• Minimal cognitive loading: behavior is not achieved through extensive
instructions or explanations (that are often too complex for patient to
generalize outside of treatment room) but through modeling
• Typically use extensive verbal explanations, modeling
behavior, biofeedback
• Complex for patient
LSVT: Lee Silverman Voice Treatment.
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Intensive voice treatment in Parkinson’s disease: Lee Silverman Voice Treatment
Perspective
Table 2. Traditional speech therapy versus Lee Silverman Voice Treatment LOUD therapy for individuals
with Parkinson’s disease.
LSVT LOUD
Ramig et al. [87–88,103]
Traditional speech therapy
e.g., Till et al. [176]
Sensory calibration
Treatment: focus attention on how it feels and sounds to talk LOUD
Carryover activities: start day 1; daily assignments (treatment and
nontreatment days); use loud voice in real-life situations; difficulty of the
assignment matches the level of the hierarchy where the person is working;
make patient accountable and look for comments from patient that people in
their daily living have said, such as, ‘I can hear you better’
• No systematic approach to sensory problems associated
with speech disorders in Parkinson’s disease
• Carryover activities are typically used as a part of
generalization. They do not typically start the very first
day of treatment; rather after some period of
acquisition of the trained skill
Homework
regulation of vocal loudness for speech may involve a system
that has been adapted, through learning, for speech audibility
and intelligibility purposes [142–143] . Physiologic evidence suggests that the three subsystems of speech – respiration, phonation and articulation – are involved in vocal loudness regulation
in a highly orchestrated, integrated, quasi-automated manner
[134,144,145] . The central mechanism underlying this regulatory
system is not clear. We have hypothesized that this system
involves a phylo­genetically old neural network that regulates
emotive vocalization and that is subjugated to higher neural networks involving linguistically driven motor control [146] . Indeed,
brain lesions and/or brain stimulation in monkeys and humans
indicate that the emotive limbic system and its connections
to the medial prefrontal cortex, thalamic, parathalamic, basal
ganglia, periaqueductal gray and reticular formation networks
are involved in the regulation or mediation of vocal intensity
control [138,143,147–150] .
It is important to point out that LSVT aims to produce healthy
vocal loudness and speech clinicians are trained to increase vocal
loudness without any strain or hyperfunction. de Swart et al.
have claimed that the LSVT results in vocal hyperfunction [151] .
However, their claim is not substantiated empirically as they did
not study the effects of LSVT on the voice; rather, they tested
a single session of loud voice, which is far from the 16 carefully
planned sessions of training of healthy phonation in the LSVT
regimen [152] . In fact, post-LSVT videostroboscopic data [20]
and perceptual ratings of voice [12] indicate improved laryngeal
function and voice quality rather than vocal hyperfunction or
deterioration following treatment. These multilevel findings
(physiological, acoustic and perceptual) support healthy vocal
loudness in patients who receive LSVT. This is achieved by
teaching LSVT clinicians how to increase loudness in patients
with PD without causing any vocal strain or hyperfunction. See
Table 2 for a description of the shaping techniques that are inherent in LSVT exercises and prevent any hyperfunctional behaviors
during treatment.
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pathophysiological mechanisms underlying bradykinesia/hypokinesia – that is, inadequate muscle activation [127] . The muscleactivation 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
[66,127] . In addition to increasing movement amplitude, the distributed effects of vocal loudness training on articulation, facial
expression and swallowing are consistent with the concept of
global parameters [128–130] . The neurological bases of such global
motor effects are not known; however, vocal loudness might be
regulated, or at least influenced, by a biomechanical and neurophysiologic linkage between the articulatory and phonatory systems [15,131–135] .Specifically, articulatory positions or movements
have been shown to influence laryngeal muscle activity, vocal fold
closure, laryngeal tension, transglottal air flow, maximum air flow
declination rate, and air pressure, with some of these adjustments
also correlating strongly with vocSPL or vocal loudness level [131–
135] . Whether these articulatory influences on laryngeal function
are intentional is not clear [132] . In singers, at least, it appears that
articulatory adjustments are intentionally used to influence laryngeal function; for example, in the control of vibrato, vocal loudness and pitch, as argued elsewhere [135,136] . Additional evidence
of the orofacial articulatory–laryngeal interaction is provided by
a study showing that treatment of hypertensive voice disorders
in otherwise healthy individuals improves both phonation and
vowel articulation [137] .
Another explanation for the distributed and lasting impact of
LSVT is that the target involves and stimulates phylogenetically
old neural systems, especially the emotive brain, which play an
important role in vocalization and the intensity of vocalization,
both important parts of the survival mechanism [138] . As noted
earlier, speech production is a learned, highly practiced motor
behavior, with many of its movements regulated in a quasiautomatic fashion; loudness scaling is a task that both animals
and humans engage in all their lives [77,79,139–141] . Thus, the
of
LSVT: Lee Silverman Voice Treatment.
Homework exercises are typically provided. Frequency
and accountability for doing homework varies
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Start day 1: daily assignments to practice at home (daily tasks and hierarchy
exercises); treatment days (one other time for 5–10 min); nontreatment days
(two times for 10–15 min); homework book provided and patient made
accountable
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Sapir, Ramig & Fox
LSVT specifically trains individuals with PD to ‘recalibrate’ their
motor and perceptual systems so that they are less inclined to
downscale (reduce amplitude) speech movement parameters. In
addition, it is geared toward overcoming or compensating for
deficits in internal cueing, vocal vigilance and self-regulation of
vocal effort during speech production. We hypothesize that LSVT
retrains amplitude scaling via intensive sensorimotor training that
teaches patients to recognize the effort for louder speech, and
use it during everyday living. By directly addressing this sensory
mismatch, LSVT teaches subjects with PD to re­calibrate their
perception of normal loudness and vocal effort so that by the
end of 1 month of therapy, they spontaneously speak with greater
vocal loudness. A few examples of specific treatment tasks related
to calibration include recording the patient’s voice while reading with a louder voice that they self-perceive as ‘too loud’ and
then playing it back to them. They recognize and comment when
they hear the audiotapes that what felt and sounded too loud to
them while reading actually sounds within normal limits (or in
some cases still too soft) when played on the tape. In addition,
carryover activities are assigned daily that require patients to use
their louder voice in a specific communication setting outside of
the treatment room, such as, order dinner at the restaurant, or
greet coworkers. Convincing patients to speak in a voice that they
previously perceived is too loud and having positive reactions and
communication in their daily living, help convince them that the
louder voice is actually within normal limits. This improvement
may be due to some restoration of the internal cueing mechanism, and/or compensation through vocal vigilance. Although
the treatment delivery is complex for the clinician who is administering the therapy, the focus for the individual with PD is kept
purposefully simple and redundant (think loud, speak louder),
which may maximize the ability of individuals with PD to learn
this one target. If one treatment target can make an impact across
the speech production system, this may allow us to improve the
efficiency and effectiveness of treatment.
To date, LSVT is the behavioral therapy with the most data to
support positive outcomes addressing the type of speech impairments experienced by individuals with PD, as judged by the
members of the USA Academy of Neurologic Communications
Disorders and Sciences (ANCDS) [157] and others [158] . Specifically,
the LSVT has been shown to significantly improve (statistically,
and in terms of effect size measures) laryngeal function, vocal loudness, voice quality, prosodic voice fundamental frequency (and its
perceptual correlate pitch), inflection, vowel articulation, speech
quality and overall speech intelligibility (e.g., [12,15,20,61, 87–88,95,159] ;
see also reviews in [53,54]). Furthermore, the LSVT has been
shown to improve facial expression, swallowing and tongue function [110–111,160] . In addition, these LSVT-induced changes in
speech and nonspeech orofacial functions have been shown to
be associated with improved brain function [159,161,162] . Moreover,
improvement in vocal function owing to LSVT has been shown to
be maintained over months and up to 2 years of follow-up [87,95] .
The effectiveness of the LSVT program may be variably compromised by several factors, including atypical Parkinsonism,
coexisting dystonia, depression, dementia, abulia and adverse
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The mode of delivery of LSVT is intensive and high effort. It is consistent with theories of motor learning, skill acquisition and principles that drive activity-dependent neural plasticity. The LSVT
dosage involves 60-min individual treatment sessions, 4 days a week
for 4 consecutive weeks. In addition, there are daily homework
practice and carryover assignments on all 30 days of the month.
Within each treatment session, the first half of the session is spent
on three daily tasks, which are core exercises designed to rescale the
amplitude of motor output. These daily tasks are completed with
multiple repetitions (e.g., minimum of 15 repetitions per task per
day), and continually increased requirements for effort, consistency
and accuracy of vocal loudness [86] . The second half of the session is
spent on the speech hierarchy. The rescaled vocal loudness achieved
in the daily tasks is now systematically trained into speech. Across
the weeks of the hierarchy the duration of time that a person needs
to keep their voice loud and the complexity of the speech task
increase from words/phrases, to sentences, continuous reading and
finally, conversational speech.
Within the structured setting of the LSVT treatment sessions, many elements of exercise that promote activity-dependent neural plasticity are embedded [4–5] . Tables 2 & 3 highlight
these elements. Key elements of exercise that promote neural
plasticity, neural protection and neural restoration in animal
models included intensive training of motor tasks, increased
practice of motor tasks, active engagement or salience of tasks,
complexity of tasks, saliency, and the sensory experience of the
motor task [153,154] . In LSVT, for example, intensive treatment is
achieved both across and within treatment sessions. The dosage
across treatment sessions is four individual, 1-h treatment sessions 4 consecutive days a week for 4 weeks. Within treatment
sessions, patients are pushed to high vocally nonabusive intensity levels through increased repetitions of treatment tasks (e.g.,
minimum of 15 repetitions per task), driving high effort and continuous motor speech exercise (e.g., patients report self-perceived
high effort during tasks), and increasing accuracy requirements
as treatment progresses for achieving target goals. While the
LSVT protocol is standardized, saliency is achieved by tailoring
speech materials and homework and carryover assignments to
each individual’s interests, hobbies and communication goals.
Saliency is important because the more meaningful or rewarding
a task, the greater potential impact on neural plasticity [155,156] .
Complexity of tasks is built into the speech hierarchy exercises,
moving from simple reading of words and phrases from paper,
to carrying on conversational speech outside of the treatment
room in a noisy environment (e.g., cafeteria). Finally, the sensory experience of increasing vocal loudness is a major focus of
calibration, as discussed later.
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Mode: intensive, high-effort therapy
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Perspective
Calibration: sensory, internal cueing & neuropsychological
barriers to generalization
As discussed earlier, the etiology of the speech and voice disorder
in individuals with PD is complex. It appears that addressing the
motor deficit in isolation is not sufficient for lasting treatment
outcomes that generalize beyond the treatment room [83] . Thus,
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Expert Rev. Neurother. 11(6), (2011)
Intensive voice treatment in Parkinson’s disease: Lee Silverman Voice Treatment
Perspective
Table 3. Translation of some of the proposed principles underlying neural plasticity to proposed deficits in
Parkinson’s disease and the corresponding rationale and task in Lee Silverman Voice Treatment/LOUD.
Principle
Deficit specific to PD
LSVT/LOUD
Intensive, high-effort training can be
difficult in PD due to sensory deficits,
force control, fatigue, depression and
progressive loss of cardiac sympathetic
innervation
Train intensively 1 h per day, 4 days per week,
for 4 weeks; multiple repetitions (15 or more);
increase resistance, amplitude (within healthy
range) effort, accuracy; and daily homework
exercises. Train maximum perceived effort
As basal ganglia pathology progresses,
there is a loss in automaticity, requiring
greater conscious attention to task.
When required to perform dual tasks,
insufficient attentional resources results
in the decrement in one or both of the
concurrent tasks
Train complexity of movement with single
patient focus (LOUD) to multiple, motor tasks.
Retrain automaticity of amplitude (LOUD) in
familiar movements. Progress complexity over
4 weeks by varying contexts, adding dual
cognitive/motor loads and increasing duration
and difficulty of speech tasks (progress from
words to conversation)
People with early PD may experience lack
of awareness of subtle motor deficits,
depression, loss of motivation and a
feeling of ‘helplessness’. Thus, they do
not feel they need, or would not benefit
from speech therapy
We train salient familiar movements (core
patterns) of speech promoting success. We
provide homework tasks that reinforce success
of LOUD in emotionally salient social
interactions. We provide extensive positive
feedback
Intensity
Intensive practice is important for maximal
plasticity. Intensity can be increased via
frequency, repetitions, force/resistance,
effort and accuracy. Intensity increases
activation of corticostriatal terminals,
inducing synaptic plasticity in striatum
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Complex movements or environmental
enrichment have been shown to promote
greater structural plasticity (spine density,
protein expression/synapse number) in
adjacent and remote interconnected regions
than in simple movements
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Complexity
Practicing rewarding tasks (success/
emotionally salient) activates basal ganglia
circuitry. Rewards are associated with phasic
modulation of DA levels critical to induction
of striatal plasticity and learning/relearning
in PD
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Saliency
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Use it or lose it/use it & improve it
Timing matters
Deficits are subtle – not ‘red flag’ to seek
speech therapy. Getting early PD patients
to recognize need for exercise and then
convincing them to continually exercise is
challenging. Decreased physical activity
may be a catalyst in degenerative process
Educate people with PD on subtle deficits and
improve motor function that directly impacts
real life
Retrain a new way of speaking in everyday life
(LOUD or ENUNCIATE); thus, normal activity
offers continuous exercise
People with early PD have subtle physical
underactivity (small movements/soft
voice). This may be coupled with a lack
of awareness or self-correction, leading
to further inactivity
Train people with early PD when they may not
have deficits in all systems (laryngeal and
orofacial). Train strategies to raise awareness/
avoid neglect and increase muscle activation
for normal effort/amplitude required for
within-normal-limits vocal loudness
ut
Spared, but compromized DA neurons highly
vulnerable to bouts of inactivity/activity.
Inactivity may accelerate deficits.
Post-exercise intervention, there may be a
minimum use requirement to maintain
positive effects
A
Early exercise has the potential to: rescue DA
neurons, prevent chronic disuse, promote
system-wide plasticity and halt disease
progression – particularly to the
asymptomatic side
DA: Dopamine; ENUNCIATE: Speech therapy with the same schedule and intensity as LSVT, but with emphasis on effortful and precise enunciation of consonants
and other phonemes; PD: Parkinson’s disease; LSVT: Lee Silverman Voice Treatment.
Data taken from [83].
neurosurgical effects. Although data have been reported documenting improvements in individuals after thalamotomy [163] ,
fetal cell transplant and DBS [164–166] , as well as in individuals with multisystem atrophy, progressive supranuclear palsy
and Parkinson’s plus syndromes [167] , these outcomes may not
be of the same magnitude as in idiopathic PD and may require
follow-up treatment sessions to maintain improvements over time.
Nevertheless, the functional impact for individual patients can be
quite significant in these more advanced or complicated cases of
PD. There are a number of ongoing studies examining the impact
of alternative cues for speech in PD (e.g., clear speech) and the
use of external auditory devices to either cue vocal loudness or
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improved speech fluency [158] . It may be that for more complicated
speech disorders associated with PD, a combination of approaches
will be the most effective.
Ongoing research with the LSVT & speech treatment
in PD
The aforementioned findings and recent pilot data indicate
that training to increase vocal loudness with the LSVT regimen generalizes beyond laryngeal function to improve speech
articulation [15,61] , tongue function [160] , swallowing [111] , communicative gestures [168] , facial expression [110] and neural functioning [61,85,118,123] . Randomized controlled studies are ongoing to
823
Sapir, Ramig & Fox
of
treatment. We hypothesize that neither dopamine deficiency nor
rigidity are sufficient to account for the speech abnormalities in
PD, and that additional factors involving nondopaminergic or
special dopaminergic mechanisms, as well as deficits in scaling
movement amplitude, sensory processing, internal cueing and
self-regulatory mechanisms, add to the speech disorders in PD.
We present the LSVT as a scientifically proven effective treatment for speech disorders in PD, most likely because it addresses
the aforementioned deficits and because its mode of delivery is
consistent with principles that drive activity-dependent neural
plasticity. Neural imaging has provided preliminary evidence for
neural plasticity induced by the LSVT. We argue that intensive
treatment such as the LSVT should be administered at early
stages of the disease. Early intervention may potentially slow
speech symptom progression and can be administered before
adverse conditions such as depression, fatigue or dementia occur,
thus allowing optimal treatment outcomes. The feasibility of
intensive treatment can be enhanced by technology (telepractice
and software) to improve accessibility and to support continued
practice. Research studies are needed to improve our understanding of the neural mechanisms underlying the speech abnormalities in PD, as well as the neural changes that are induced by
LSVT and other modes of treatment.
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examine this spread of effects and its treatment specificity. Studies
are also planned to assess the reasons for the heterogeneous speech
outcomes following DBS-STN. Such studies may involve simultaneous quantitative measures of pre- and post-surgical speech
functioning and details of surgical and stimulator optimization.
Knowledge gained from these studies is likely to facilitate the
development of rehabilitative speech treatment approaches for
speech problems in people with DBS-STN either before surgery
(as preventative) or after surgery (as rehabilitation).
We are presently assessing the effectiveness of technology-­
supported delivery of LSVT to increase accessibility of treatment,
promote home practice, augment the effects of LSVT, reduce
clinician time, cut costs of treatment and support long-term practice. Telepractice delivery of LSVT allows a patient to receive
LSVT online (e.g., at home or in their office). Published data
have documented that LSVT delivered online has comparable
outcome data as LSVT delivered in the clinic [161,169] . In addition,
a study by Tindall et al. completed a cost ana­lysis comparing
live, traditional delivery of LSVT versus a telehealth delivery of
LSVT [162] . The computed mean amount of patient time and
money across these two modes of delivery were strikingly different. The live delivery mode required 51 h for 16 visits (travel
and therapy time), US$953.00 on fuel/mileage expenses and
US$269.00 for other expenses (e.g., food). By contrast, the telepractice delivery option required 16 h of time (therapy and no
travel) and no additional costs for fuel/mileage or other expenses.
Recent advances in software allow patients to carry out LSVT
sessions with software support. The LSVT COMPANION™ is
programmed to collect acoustic data and provide feedback as it
guides the patient through the LSVT exercises. Outcome data
document that treatment effects are comparable when half of the
sessions were delivered by software [159] .
Another area of research is the role of sensory and perceptual
functions in speech and voice disorders and rehabilitation. As discussed earlier, it appears that self-perception of voice in individuals with PD is defective but the nature of this defect is not well
understood. Therefore, by experimentally altering the patient’s
sidetone (his own voice/speech fed back to his auditory system
as he speaks) and simultaneously recording the response of the
patient to this manipulation we can gain insight into the nature
of the auditory–vocal mechanism underlying Parkinsonian speech
in general [84] , and in response to treatment in particular. Using
this method, we have collected pilot data on one patient with
PD and found that auditory–vocal responses to experimental
manipulation were absent prior to LSVT but present, as is normally observed [170] , after LSVT. However, these findings must
be replicated in order to ascertain their generalization to other
patients with PD before and after LSVT.
ro
Perspective
Expert commentary
Speech disorders are highly common in individuals with PD,
producing adverse effects on communication, health and quality of life. Traditionally, these disorders have been attributed
to dopamine deficiency and rigidity and have been considered
highly resistant to medical, surgical and behavioral forms of
824
Five-year view
In the next 5 years, it is expected that the following developments
will take place:
• The significant therapeutic impact of LSVT on voice, speech
and other orofacial functions, as well as on brain reorganization
in individuals with a progressive disease, provides a means to
explore the brain mechanisms underlying the unique symptoms
of PD and the mechanisms underlying the improvement of
these symptoms, including neural plasticity and, possibly, neural protection. Future studies with the LSVT or other behavioral treatments should therefore be designed to explore the
role of non-dopaminergic and special dopaminergic mechanisms in voice and speech disorders, and in other motor disorders that are only partially or completely unresponsive to
dopamine treatment;
• Explore animal models that may help us understand vocal
motor deficits related to dopamine depletion in disorders such
as PD. Two emerging models of vocal motor deficits following
dopamine depletion in rodents [171] and songbirds [172] offer
promise for the feasibility and value of these models;
• Explore the specific role of internal cueing, sensorimotor gating,
temporal processing, motor-to-sensory (vocal-to-auditory) gating, perceptual mechanisms, vocal vigilance and self-regulation
on voice and speech functions in general, and in individuals
with PD in particular;
• Explore the impact of combined treatments and tasks, such as
speech and gait, on functional recovery and treatment efficacy.
Preliminary evidence suggests that individuals with PD trained
Expert Rev. Neurother. 11(6), (2011)
Intensive voice treatment in Parkinson’s disease: Lee Silverman Voice Treatment
to increase gait amplitude (LSVT BIG) and speech loudness
(LSVT) can perform both tasks simultaneously without interference from the other task and while maintaining therapeutic
gains [173] ;
• Explore the interactions between behavioral treatment and
neurosurgical or neuropharmacologic treatments;
• Explore the impact of computer-based technology (e.g., internet, virtual clinician, web camera and videophones) on treatment efficacy and availability to patients. Preliminary studies
suggest that such technology is highly effective in the delivery
of LSVT in individuals with PD [161–162,174] .
Perspective
Financial & competing interests disclosure
This research has been funded by the NIH grant R01 DC1150 from the
National Institutes of Deafness and Other Communication Disorders.
Lorraine O Ramig and Cynthia M Fox receive lecture honoraria and have
ownership interest in LSVT Global, Inc. They have disclosed any conflict of
interest and their conflict of interest management plan has been approved
by the Office of Conflict of Interest and Commitment at the University of
Colorado, Boulder. 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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Key issues
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• Between 85 and 90% of individuals with Parkinson’s disease (PD) develop voice and speech disorders during the course of their illness.
These disorders, along with reduced facial expression and hand gestures, adversely affect communication and quality of life.
• Neurosurgical and levodopa treatments for PD have yielded minimal, inconsistent or adverse effects on voice and speech functions.
Traditional speech therapy has also yielded modest outcomes, in terms of both magnitude and long-term effects.
• To date, the most efficacious behavioral method to improve voice and speech and related orofacial functions such as swallowing and
facial expression is the Lee Silverman Voice Therapy (LSVT): an intensive, 1-month treatment regimen that emphasizes upscaling speech
movement amplitude and self-perception and regulation of vocal effort and loudness.
• Follow-up studies indicate that therapeutic effects of the LSVT are maintained up to 2 years after treatment.
• We suggest that voice and speech disorders in PD are related, at least partially, to complex, high-level mechanisms, reflected by deficits
in scaling amplitude of speech movement patterns, sensorimotor gating, internal cueing, self-perception and regulation of vocal output
and vocal vigilance. These high-level deficits are probably mediated through non-dopaminergic or special dopaminergic mechanisms.
We also argue that the LSVT is effective, in part because it specifically addresses these high-level deficits, and in part because it adheres
to principles of neural plasticity and motor learning.
• Brain imaging studies provide preliminary evidence for LSVT-induced changes toward normality in cortical and subcortical activation
patterns and in basal ganglia dopamine activity, as well as top-down improvement in vocal vigilance, as right hemisphere activation.
These findings, along with the intensive, repetitive and cognitively nondemanding features of the LSVT, suggest that this behavioral
treatment can potentially play an important role in neural plasticity. However, the small number of subjects included in the
aforementioned brain imaging studies of LSVT, and the lack of follow-up imaging studies of the effects of the LSVT, deems the brain
imaging findings and their interpretation tentative; thus, there is an urgent need for a more extensive research to delineate the neural
mechanisms underlying the short- and long-term effects of the LSVT.
• Present studies are being conducted to assess the impact of LSVT on non-speech functions, and the impact of a combined speech
therapy and physiotherapy (LSVT HYBRID) on speech and limb functions by emphasizing loud phonation and big limb movements,
respectively. Preliminary findings indicate that the combined approach, which is a dual task, yields results similar to those obtained with
each of the treatments administered alone.
• Computer-based technology (e.g., virtual clinician treatment delivery via portable devices) and telephone and internet communication
systems (e.g., remote clinician treatment delivery via Skype™) are being developed to avail treatment, enhance the effects of LSVT and
to allow home practice. Preliminary findings support the use of such technology, both in terms of its therapeutic effects and its
cost–effectiveness and potential availability to a large number of individuals suffering from PD.
• It has been our clinical experience that individuals with early stages of PD respond better than individuals at a later stage of PD to LSVT.
In part, the advantage of early versus late intervention seems to be related to intervening factors such as severity of the disease, motor
impairment, depression, cognition, motivation and fatigue, which are likely to increase as the disease progresses. Therefore, an
important goal would be to study early intervention with LSVT as a means to improve communication and quality of life, optimize
neural plasticity and perhaps help decelerate the disease process with regard to neural protection.
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