THEMED ARTICLE y Parkinson’s disease Perspective

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Intensive voice treatment in

Parkinson’s disease: Lee
Silverman Voice Treatment
Expert Rev. Neurother. 11(6), 815–830 (2011)
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Shimon Sapir†1, Advances in neuroscience have led to an expanded and improved understanding of neurobiological
Lorraine O Ramig2,3 changes associated with rehabilitation and exercise in Parkinson’s disease (PD). This knowledge
and Cynthia M Fox3 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)
1
Department of Communication,
Sciences and Disorders, University of
and an increased research focus on the impact of such approaches in humans with PD. The
Haifa, Mount Carmel, 31905, Israel purpose of this article is to examine the role of speech therapy in the landscape of exercise-based
2
University of Colorado Boulder, interventions for individuals with PD. We will specifically focus on the intensive voice treatment
CO, USA protocol, Lee Silverman Voice Treatment, as an example therapy. This article will briefly review
3
National Center for Voice and Speech,
CO, USA the literature on the characteristics and features of speech and voice disorders in individuals
†
Author for correspondence: with PD, and will discuss the impact of pharmacological and surgical treatment techniques on
Tel.: +972 508 594 700 these disorders. This will be followed by a focus on behavioral speech treatment, specifically
For personal use only.

Fax: +972 482 495 07 Lee Silverman Voice Treatment, including development of the treatment approach, documenting
[email protected]
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.

Keywords : Lee Silverman Voice Treatment • LSVT • neural plasticity • Parkinson’s disease
• speech and voice disorders • swallowing disorders

It is a stunning time to be in rehabilitation today. The purpose of this article is to examine this
The basic science evidence for the value of exercise new paradigm of exercise-based interventions and
in Parkinson’s disease (PD) has been documented activity-dependent neural plasticity in PD in rela-
in animal models of the disease and is being tion to literature in speech treatment, with a focus
increasingly explored in humans with PD [1–3] . on the Lee Silverman Voice Treatment (LSVT)
In addition, research has identified key principles as an example therapy. We will begin with a brief
of exercise that drive activity-dependent neural overview of the characteristics and features of
plasticity (modifications in the CNS in response speech and voice disorders in individuals with
to physical activity) [4,5] . These collective data PD, discuss the impact of pharmacological and
have elevated the role of exercise and/or rehabili- surgical treatment techniques on these disorders,
tation in the overall management of PD beyond a and highlight possible underlying neural mecha-
reactive referral for secondary impairments (e.g., nisms of the dysarthria in PD. This will be fol-
aspiration due to swallowing impairments or hip lowed by a focus on behavioral speech treatment,
fracture due to falling) to a legitimate therapeutic specifically LSVT, including development of the
option prescribed early, upon diagnosis, that may treatment approach, treatment efficacy, discov-
slow or halt symptom progression [2,6] . As a result ery of unexpected outcomes, and insights into
of this basic science evidence, there has been a the mechanisms of speech disorders in PD gained
steady increase in the number of physical therapy from treatment-related changes. This research will
trials in individuals with PD from 1980 through be placed in the context of other previous and cur-
2010 [7] , and the practice variables that have been rent speech treatment approaches in development
documented to be effective in the animal models for individuals with PD. The key fundamentals
(e.g., intensity and specificity) are being reported of the treatment approach will be discussed and
in human trials of PD and stroke [1,3] . future directions for research will be highlighted.

www.expert-reviews.com 10.1586/ERN.11.43 © 2011 Expert Reviews Ltd ISSN 1473-7175 815

 Perspective Sapir, Ramig & Fox

Hypokinetic dysarthria in PD terms of magnitude and long-term maintenance of treatment out-

Parkinson’s disease affects 1–2% of individuals over the age of comes. While some studies have documented dopamine-induced
60 years, as well as younger individuals in their 30s and 40s [8] . improvement in speech motor function [23,34–38] , other studies
Nearly 90% of these individuals are likely to develop speech dis- have failed to show systematic changes or clinically significant
orders during the course of their illness [9] . These disorders, col- improvement in the speech of individuals with PD following
lectively called hypokinetic dysarthria [10] , may include any or a levodopa treatment [33,39–42] . These findings suggest that neuro-
combination of the following: reduced vocal loudness and abnor- chemical or neurobehavioral factors other than, or in addition to
mal vocal decay [11] ; a breathy, hoarse, or harsh voice quality [12] ; dopamine deficiency may play a significant role in hypokinetic
imprecise consonants and vowels due to reduced range of articula- dysarthria associated with PD, as will be discussed later [32,41] .
tory movements, with the tendency of these movements to decay Neurosurgical procedures such as deep brain stimulation (DBS)
and/or accelerate toward the end of a sentence [13–15] ; reduced of the thalamus, pallidum or subthalamic nucleus, ablative surger-
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voice pitch inflections, or monotone; and rushed, dysfluent or ies (pallidotomy and thalamotomy) and fetal cell implantation
hesitant speech [13–16] . Other less frequently occurring speech have been demonstrated to result in dramatic improvement in
abnormalities may include palilalia and stuttering-like dysfluen- limb motor function, yet these procedures have yielded contradic-
cies [17] . These speech problems have been traditionally attrib- tory results on speech functions in individuals with PD [42–45] .
uted to muscle rigidity and hypokinesia secondary to dopamine The most common neurosurgical approach used today is DBS
deficiency [18] . However, as we will discuss, additional factors, of either the subthalamic nucleus (STN) or the internal segment
such as deficits in scaling and maintaining movement amplitude, of the globus pallidus (GPi). Although there have been reports
internal cueing, high-level sensory processing, neuropsychological of improvements in components of speech production with
functions (attention to action and vocal vigilance), along with STN-DBS [46–49] , the impact on functional speech intelligibility
nondopaminergic or special dopaminergic mechanisms, may pro- remains unclear [50,51] . Adverse effects of STN-DBS on speech
vide a more comprehensive or complimentary explanation for the have received increasing attention in the neurology and speech lit-
etiology of the dysarthria. erature in recent years [52–54] . Explanations for the negative effects
of STN-DBS on speech include high-frequency stimulation [55] ,
For personal use only.

Physiologic abnormalities associated with voice location of electrode contacts and amplitude of stimulation in the
& speech disorders in PD STN [51] , the spread of current to nearby fiber tracts such as the
Studies of vocal function in individuals with PD have documented cerebellothalamic fibers [56] and/or lesions of a neural network
poor vocal fold closure; reduced amplitude, asymmetrical or slow that mediates sensorimotor speech control [57] .
vibratory patterns of the vocal folds and voice tremor (the latter
might be a form of essential tremor) [19,20] . Respiratory studies of Hypotheses regarding neural mechanisms underlying
individuals with PD have documented a reduction or abnormali- voice & speech disorders in PD
ties in vital capacity, chest wall movements, respiratory muscle It has been suggested that some motor disorders in PD, including
activation patterns, amount of air expended during maximum hypokinetic dysarthria, may be partially related to abnormal non-
phonation tasks and intraoral air pressure during consonant/vowel dopaminergic or special dopaminergic mechanisms, which impair
productions [21] . Electromyographic (EMG) studies of individuals several high-level processes that are important for the regulation
with PD revealed a reduction of neural drive to the laryngeal mus- and control of speech movements [16,32,33,53,54] . We will briefly
cles [22] , abnormally elevated laryngeal muscle activity [23] or poor present four high-level processes we hypothesize to be impaired
reciprocal suppression of laryngeal and respiratory muscles [24] . and to underlie hypokinetic dysarthria in PD. These include scal-
Kinematic and EMG studies of orofacial movements during vari- ing movement amplitude, sensory processing, internal cueing and
ous speech tasks in individuals with PD have indicated a reduc- vocal vigilance.
tion in the size and peak velocity of jaw movements, increased
levels of tonic resting and background neuromuscular activity, Scaling movement amplitude
and loss of reciprocity between agonist and antagonistic muscle One likely cause of hypokinetic dysarthria in PD is reduced
groups [25–30] . These studies, which have included healthy control amplitude of output (hypokinesia) and abnormal scaling and
subjects for comparison, suggest that hypokinetic speech move- maintenance of movement amplitude. Reduced range (hypo­
ments in PD may be associated with abnormal neural drive to the kinesia) of respiratory, laryngeal and orofacial movements during
speech periphery and abnormal sensorimotor gating and may be a speech sound production in individuals with PD, with the ten-
major cause of the speech movement abnormalities in PD. dency of the amplitude of the movements to decay (become more
hypokinetic) within and across utterances, have been documented
Medical treatment for voice & speech disorders in PD in various studies [11,14,25,58,59] . This reduction may manifest as a
Pharmacological treatments with dopamine-replacement ther- systematic reduction and decay of vocal loudness, pitch intona-
apy (levodopa or dopamine agonists) has marked therapeutic tion and precision of vowels, consonants and other sounds of
effects on rigidity, akinesia, bradykinesia and tremor in the limb speech [14,15,58,60–62] , and may be attributed to the inability of indi-
motor system [31] ; however, its effects on hypokinetic dysarthria viduals with PD to scale and/or maintain movement amplitude,
in individuals with PD have yielded variable findings [32,33] in force or related parameters [63–68] .

816 Expert Rev. Neurother. 11(6), (2011)

 Intensive voice treatment in Parkinson’s disease: Lee Silverman Voice Treatment Perspective

Sensory processing the letters touch the dots or the lines (external cues) [90] . The use
A second factor is abnormality in sensory processing. Behavioral and of external cueing has also been demonstrated to positively impact
physiological studies of speech and nonspeech oral and head and gait in PD, with long-term retention, when cueing strategies were
neck functions in individuals with PD have documented sensory systematically trained over several weeks’ time [91] .
abnormalities, manifested as errors on tasks of kinesthesia [69–71]; dif-
ficulties with orofacial perception, including decreased jaw proprio- Vocal vigilance
ception, tactile localization on tongue, gums and teeth, and targeted A fourth factor is impairment in self monitoring and self regula-
and tracking head movements to perioral stimulation [72] ; problems tion of voice and speech motor output due to deficits in attention
utilizing proprioceptive information for normal movement [70,72] ; to action or vocal vigilance. There is evidence that attention to
abnormal higher order processing of afferent information as dem- action is impaired in individuals with PD, and that this impair-
onstrated by abnormal reflex and voluntary motor responses to pro- ment may contribute to the abnormal control of movements in
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prioceptive input [27,73–75]; and abnormal sensory processing of voice PD [92,93] . By inference, impaired vocal vigilance in individuals
and speech in individuals with PD [25,76–80] . Laryngeal sensorimotor with PD may have an adverse effect on motor speech control,
deficits in PD have also been documented [81,82] . These sensorimo- which may partially account for the hypokinetic dysarthria in
tor abnormalities may account, at least partially, for the deficits in these individuals [54] . Importantly, it has been shown that atten-
scaling and maintaining speech movement amplitude. tion to action in individuals with PD can be improved significantly
One aspect of sensory processing deficits in individuals with PD by intensive training [80,94] . As will be discussed later, the LSVT
is misperception of self-produced voice and vocal effort. Individuals treatment regimen, which has been designed to train individuals
with PD are often unaware of the magnitude of their reduced vocal with PD to pay attention to their speech output and to monitor
loudness and will report, ‘my voice is fine, but my spouse needs the effort to produce this output, has been shown to be effective
a hearing aid’ [83] . This is similar to the inaccurate perception of in the long-term maintenance of treatment outcome [87,95] .
body awareness and lack of self corrections of smaller and slower
movements in everyday living, even in early PD [2] . Furthermore, Summary of origins of speech & voice disorders in PD
when individuals with PD and hypokinetic dysarthria are asked to To summarize, the neural mechanisms underlying speech disorders
For personal use only.

produce ‘loud’ speech (i.e., increase amplitude of motor output), in individuals with PD appear to be complex and not well delin-
they typically increase their speech to a normal conversational eated. Additional research is needed to explore these deficits and
volume level, yet they complain that this louder voice is ‘way too their interaction and contribution to the speech disorders observed
loud’. This phenomenon has been documented experimentally by in individuals with PD. Given this complexity, it is not surprising
Ho and colleagues [79] . These researchers found that even though that traditional medical and behavioral treatments have had only
individuals with PD spoke with a softer voice than healthy con- limited success in managing these problems and in improving speech
trols, they nevertheless perceived their own speech to be louder in the long term. New insights about the nature of speech disorders
than that judged by the healthy controls. In addition, individuals in PD have been gained from testing new hypotheses regarding the
with PD overestimated the loudness of their speech during both pathogenic mechanisms under­lying these disorders and from studies
reading and conversation. Furthermore, sensorimotor abnormaities of treatment effects, such as those induced by the LSVT regimen.
in auditory–vocal feedback and feed-forward mechanisms have
been indirectly demonstrated in individuals with PD by behav- Behavioral speech treatment for individuals with PD
ioral [84] and neuro­physiological [85] studies. Finally, Ramig and Historically, speech and voice disorders in individuals with PD were
colleagues [86–88] have shown that addressing problems of sensory thought to be resistant to behavioral speech therapy [96–99] . This
processing deficits is an important therapeutic goal for a successful view of speech therapy mirrored the view of physical therapy and
treatment of hypokinetic dysarthria in individuals with PD [86–88] . exercise in that it was perceived as not helpful (see [2] for full his-
torical physical therapy review). In the mid 1980s and early 1990s
Internal cueing there began to be a shift in the view of both physical and speech
A third factor is deficits in internal cueing. One of the most strik- therapy for individuals with PD. In speech treatment, studies in
ing characteristics of hypokinetic dysarthria in individuals with the UK and the USA reported on speech treatment protocols that
PD is the dramatic improvement in voice and speech when these documented positive impact on voice and speech outcomes [100–103]
individuals are externally cued or instructed to speak loudly and (see [33] for more detailed review). Two consistent features of these
or clearly. The improvement in voice and speech with external studies emerged and were later recommended as key treatment
cueing is most likely a compensatory response to deficits in inter- components to focus on in speech therapy in PD: high dosage of
nal cueing [89] . This conclusion is empirically supported by a series the therapy (almost daily therapy for 2–4 weeks) and a focus on
of experimental studies conducted by Ho and colleagues [77–79] . improving the voice either through exercise of prosody, loudness or
It is also consistent with the phenomenon of micrographia (the a combination of these [104] . To our knowledge, of these published
abnormally small handwriting) in individuals with PD, which initial promising studies, only the Ramig et al. protocol (known
tends to improve dramatically (though transiently) when these today as LSVT) was standardized and further researched to assess
individuals are verbally instructed to ‘write big’ or when they are treatment efficacy in the short and long term. Today, there are
provided with dots or lines on the paper, and asked to write so that more than 20 years of research on the development and research

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 Perspective Sapir, Ramig & Fox

process of the LSVT program for people with PD. Thus, the study from chronic effects associated with long-term adaptation accom-
of LSVT has provided a unique opportunity to examine a behav- panying repetitive physical exercise (i.e., training increased loud-
ioral treatment regimen through the various phases of efficacy ness) [112] . Across a series of stimulated vocal loudness studies, we
research [105] , as well as to improve our understanding of motor have documented short-term improvements in a number of voice,
speech disorders in PD and their neurophysiologic underpinnings. respiratory and articulatory measures in nondisordered and dis-
ordered speakers [113–115] , as have other authors examining stimu-
The Lee Silverman Voice Treatment lated vocal loudness [116,117] . However, Liotti et al. documented
Initial development of the LSVT began in the late 1980s under that changes in brain activation in five subjects with idiopathic
the direction of Lorraine Ramig and her former student Carolyn PD occurred only following training vocal loudness (LSVT) for
Bonitati at the Lee Silverman Center for Parkinson’s disease in 1 month [118] . These changes were not observed before treatment
Scottsdale (AZ, USA). Initial Phase I and II studies were com- with brief stimulated increases in loudness, as will be discussed
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pleted where the protocol of LSVT was established and tested later. Will et al. also documented a difference between stimulated
in clinical conditions. These initial data were reported in 1988 and trained loudness, reporting that only in the trained condition
by Ramig and colleagues [106] and the standardized protocol (not the stimulated condition) did significant acoustic differences
was introduced as the LSVT in honor of Mrs Lee Silverman, a in vowel space accompany increased loudness in individuals with
woman with PD. These initial data sets were the foundation for the PD [119] . Taken together, these findings suggest that while stimulat-
Phase III efficacy studies that were conducted in the 1990s. Two ing loudness does impact speech production in the short term [120] ,
randomized controlled trials were completed. The first study com- lasting changes in speech–motor coordination and neural reorgani-
pared two treatments, both designed to improve vocal loudness in zation appear to require intensive training. This is consistent with
people with PD. One treatment focused on increasing respiratory basic research studies that suggest there is a need for continued
drive and vocal fold adduction (known today as LSVT) and the practice of a new motor skill (e.g., intensive training) for long-term
other treatment focused on increasing respiratory support only. structural changes in neural functioning [121] . Acquisition alone
Both treatments were matched for intensity of dosage, positive is not sufficient for sustained neural plasticity (i.e., resistance to
reinforcement from the clinicians, and homework and carryover decay) nor may it be sufficient for transfer and carryover outside
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assignments. Additional details can be found in Ramig et al. [86] . the therapeutic environment.
Subject groups were studied immediately before treatment, after Brain imaging studies using O15 PET have also documented
treatment and at 6, 12 and 24 months after treatment (with no marked changes in brain function in conjunction with speech
additional therapy). Multiple acoustic, perceptual, aerodynamic improvement following LSVT [85,118,122,123] . Specifically, while
and neuropsychological measures were collected. These data were stimulated loud phonation prior to the administration of LSVT
published in a series of studies [87,88,103,107] . The primary treatment activated cortical premotor areas, particularly the supplementary
outcome variable from these studies was vocal sound pressure level motor area (SMA), after LSVT, SMA activity was normalized,
(vocSPL). In this series of studies, LSVT was superior in improving and increased activity in the basal ganglia (right putamen) sug-
vocal loudness and vocSPL over the alternative treatment approach. gested a shift from abnormal cortical motor activation to normal
In the second randomized controlled trial, LSVT was compared subcortical organization of speech-motor output. The excessive
with an untreated group of individuals with PD and an age- and activity in the auditory cortex before LSVT and its reduction
sex-matched healthy control group at three time points: before to a normal level after LSVT, as discussed earlier, also suggests
treatment, after treatment and at 6 months after treatment. This improvement in brain function. The post-LSVT changes also
study was published in 2001 [88] . We have summarized the pri- indicated an increase in activity in right anterior insula and right
mary outcome variable of vocSPL across this series of studies and dorsolateral prefrontal cortex, suggesting that LSVT may recruit a
added effect size values in Table 1. As can be seen, in most studies, phylogenetically old, preverbal communication system involved in
the effect size was larger than 0.80, indicating that the changes vocalization and emotional communication (consistent with the
induced by the LSVT are clinically highly significant [108] . multisystem effects of LSVT). Finally, the shift in brain activity
from left to right hemisphere and in regions that involve attention
Review of secondary studies/outcomes to action and self-monitoring of action [122] indicates that the long-
In the process of documenting treatment efficacy, there were a term maintenance of treatment outcomes may, at least partially,
series of secondary studies and discoveries that occurred. Most be related to improvement in vocal vigilance.
notably, the recognition of the distributed effects across the speech
production system following LSVT that extended beyond vocal Fundamentals of LSVT: target, mode & calibration
loudness [20] to include improved articulation [15,61,109] , facial Lee Silverman Voice Treatment is a PD-specific, standardized,
expression [110] and swallowing efficiency [111] . These distributed research-based approach and differs from the way in which tradi-
effects have been of great interest, given the potential clinical effi- tional speech therapy was delivered at the time LSVT was devel-
cacy of a single treatment target (vocal loudness) to improve mul- oped. Table 2 highlights these key differences. The LSVT regimen
tiple speech system disorders. In addition, it became clear that it is unique in a number of key ways. First, the target of treatment
is important to distinguish between acute responses to a single is the voice. Specifically, LSVT trains amplitude (increased vocal
episode of physical activity (i.e.. stimulating increased loudness) loudness) as a single motor control parameter. Second, the mode

818 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.
Study Treatment Subjects SPL ‘AH’ SPL Rainbow SPL Monologue Ref.
groups (n)
Before After Effect Before After Effect Before After Effect
size size size
Ramig et al. LSVT 26 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

Ramig et al. RESP 19 69.32 68.01 -0.28 65.68 68.16 0.82 64.66 66.24 0.67 [103]

5.05 4.31 2.68 3.33 2.58 2.11

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Before Follow-up Effect Before Follow-up Effect Before Follow-up Effect

12 mo size 12 mo size 12 mo size
Ramig et al.† LSVT 22 68.44 76.31 1.73 66.44 69.46 0.85 65.26 67.18 0.65 [175]

4.61 4.49 3.93 3.09 3.06 2.84

Ramig et al.† RESP 13 69.69 68.12 -0.29 65.73 65.94 0.06 65.13 63.3 -0.64 [175]

5.26 5.43 2.72 4.34 2.59 3.13

Before Follow-up Effect Before Follow-up Effect Before Follow-up Effect
24 mo size 24 mo size 24 mo size
Ramig et al.† LSVT 21 68.26 76.5 1.93 66.18 69.78 1.03 64.7 67.02 1.03 [87]

4.45 4.1 3.79 3.19 2.56 1.87

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Ramig et al. RESP

†
12 69.19 70.12 0.15 65.79 66.49 0.16 64.72 65.71 0.27 [87]

5.31 7.01 2.6 5.54 2.76 4.32

Before After Effect Before After Effect Before After Effect
size size size
Ramig et al. LSVT 14 69.1 82.4 2.93 71.3 77.9 1.77 69 74.5 1.45 [88]

5.1 3.9 3.2 4.2 3.6 4

Ramig et al. UNTX 15 69.3 70.5 0.28 71.6 71.9 0.08 69.3 69.4 0.03 [88]

4.1 4.4 3.6 4.1 3.9 3.9

Before Follow-up Effect Before Follow-up Effect Before Follow-up Effect
6 mo size 6 mo size 6 mo size
Ramig et al. LSVT 14 69.1 79.3 2.29 71.3 76.1 1.50 69 72.7 1.03 [88]

5.1 3.7 3.2 3.2 3.6 3.6

Ramig et al. UNTX 15 69.3 70.6 0.32 71.6 71.9 0.08 69.3 69.5 0.06 [88]

4.1 4.1 3.6 4.1 3.9 3.2

†
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.
dB: Decibels; 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 delivery is intensive and requires high effort, consis- Target: vocal loudness (amplitude)
tent with principles that drive activity-dependent neural plastic- We hypothesize that training-induced increases in movement
ity [124] , theories of motor learning [125] and skill acquisition [126] . amplitude (i.e., vocal loudness) target the proposed pathophysi-
Third, calibration addresses the sensory, internal cueing and neu- ological mechanisms underlying bradykinesia/hypokinesia – that
ropsycological deficits (e.g., impaired attention to action or vocal is, inadequate muscle activation [127] . The muscle-activation defi-
vigilance) that can make generalization and lasting treatment cits that occur in bradykinesia are believed to result from inad-
effects difficult to obtain for individuals with PD. equate merging of kinesthetic feedback, motor output and context

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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 Traditional speech therapy
Ramig et al. [87–88,103] 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
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Minimum 15 repetitions per task Variable per task

Effort
Push for maximum patient-perceived effort each day (8 or 9 on scale of 1–10, Moderate to low exertion; reactive to patient response to
with 10 being the most) treatment
Focus
Simple focus: Complex focus:
LOUD Voice, respiration, articulation, rate, posture, resonance,
Increased movement amplitude directed predominately to orofacial movement, pacing, intonation
respiratory/laryngeal systems
Daily tasks
First half of the treatment session (25 min) • Variable from therapist to therapist – no standardized
Task 1: maximum sustained movements: protocols
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• 15 reps: sustain ‘ah’ in good-quality, loud voice as long as possible • Variable from day to day (e.g., one session focus on
Task 2: directional movements: voice loudness and intonation, next session focus on
• 15 reps each: say ‘ah’ in loud good-quality voice going high in pitch pacing, next session orofacial movements and posture)
• 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’
Hierarchy
Second half of the treatment session (25 min) • Speech practice often does not relate back to CORE
• Designed to train rescaled amplitude/effort of movement achieved in CORE exercises focused on rescaling effort, strength or some
exercises from daily tasks into context-specific and variable speaking other movement variable
activities • Progression across treatment sessions of increasing
• Incorporate multiple repetitions with a focus on high effort (e.g., list of complexity of speech tasks, often starting with speech
20 phrases/sentences repeated ten times for 200 repetitions) that is more complex than single words
• Tasks increase complexity across weeks (words > phrases > sentences > • Diffuse focus during practice, for example, think about
reading > conversation) and can be tailored to each subject’s goals and taking a deep breath, articulate, increase loudness
interests (e.g., golf vs cooking) and/or slow down
• 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 • Typically use extensive verbal explanations, modeling
vocal fold closure) behavior, biofeedback
• Shape the quality and voice loudness through use of modeling (‘do what I • Complex for patient
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
LSVT: Lee Silverman Voice Treatment.

820 Expert Rev. Neurother. 11(6), (2011)

 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 Traditional speech therapy
Ramig et al. [87–88,103] e.g., Till et al. [176]
Sensory calibration
Treatment: focus attention on how it feels and sounds to talk LOUD • No systematic approach to sensory problems associated
Carryover activities: start day 1; daily assignments (treatment and with speech disorders in Parkinson’s disease
nontreatment days); use loud voice in real-life situations; difficulty of the • Carryover activities are typically used as a part of
assignment matches the level of the hierarchy where the person is working; generalization. They do not typically start the very first
make patient accountable and look for comments from patient that people in day of treatment; rather after some period of
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their daily living have said, such as, ‘I can hear you better’ acquisition of the trained skill
Homework
Start day 1: daily assignments to practice at home (daily tasks and hierarchy Homework exercises are typically provided. Frequency
exercises); treatment days (one other time for 5–10 min); nontreatment days and accountability for doing homework varies
(two times for 10–15 min); homework book provided and patient made
accountable
LSVT: Lee Silverman Voice Treatment.

feedback within the basal ganglia, that is necessary to select and involved in vocal loudness regulation in a highly orchestrated,
reinforce an appropriate gain in the motor command [66,127] . integrated, quasi-automated manner [134,144,145] . The central
In addition to increasing movement amplitude, the distributed mechanism underlying this regulatory system is not clear. We
effects of vocal loudness training on articulation, facial expression have hypothesized that this system involves a phylo­genetically
and swallowing are consistent with the concept of global param- old neural network that regulates emotive vocalization and that
For personal use only.

eters [128–130] . The neurological bases of such global motor effects is subjugated to higher neural networks involving linguistically
are not known; however, vocal loudness might be regulated, or at driven motor control [146] . Indeed, brain lesions and/or brain
least influenced, by a biomechanical and neurophysiologic link- stimulation in monkeys and humans indicate that the emotive
age between the articulatory and phonatory systems [15,131–135] . limbic system and its connections to the medial prefrontal cortex,
Specifically, articulatory positions or movements have been shown thalamic, parathalamic, basal ganglia, periaqueductal gray and
to influence laryngeal muscle activity, vocal fold closure, laryngeal reticular formation networks are involved in the regulation or
tension, transglottal air flow, maximum air flow declination rate, mediation of vocal intensity control [138,143,147–150] .
and air pressure, with some of these adjustments also correlating It is important to point out that LSVT aims to produce healthy
strongly with vocSPL or vocal loudness level [131–135] . Whether vocal loudness and speech clinicians are trained to increase vocal
these articulatory influences on laryngeal function are intentional loudness without any strain or hyperfunction. de Swart et al.
is not clear [132] . In singers, at least, it appears that articulatory have claimed that the LSVT results in vocal hyperfunction [151] .
adjustments are intentionally used to influence laryngeal func- However, their claim is not substantiated empirically as they did
tion; for example, in the control of vibrato, vocal loudness and not study the effects of LSVT on the voice; rather, they tested
pitch, as argued elsewhere [135,136] . Additional evidence of the a single session of loud voice, which is far from the 16 carefully
orofacial articulatory–laryngeal interaction is provided by a study planned sessions of training of healthy phonation in the LSVT
showing that treatment of hypertensive voice disorders in oth- regimen [152] . In fact, post-LSVT videostroboscopic data [20]
erwise healthy individuals improves both phonation and vowel and perceptual ratings of voice [12] indicate improved laryngeal
articulation [137] . function and voice quality rather than vocal hyperfunction or
Another explanation for the distributed and lasting impact of deterioration following treatment. These multilevel findings
LSVT is that the target involves and stimulates phylogenetically (physiological, acoustic and perceptual) support healthy vocal
old neural systems, especially the emotive brain, which play an loudness in patients who receive LSVT. This is achieved by
important role in vocalization and the intensity of vocalization, teaching LSVT clinicians how to increase loudness in patients
both important parts of the survival mechanism [138] . As noted with PD without causing any vocal strain or hyperfunction. See
earlier, speech production is a learned, highly practiced motor Table 2 for a description of the shaping techniques that are inher-
behavior, with many of its movements regulated in a quasi-auto- ent in LSVT exercises and prevent any hyperfunctional behaviors
matic fashion; loudness scaling is a task that both animals and during treatment.
humans engage in all their lives [77,79,139–141] . Thus, the regulation
of vocal loudness for speech may involve a system that has been Mode: intensive, high-effort therapy
adapted, through learning, for speech audibility and intelligibility The mode of delivery of LSVT is intensive and high effort. It
purposes [142,143] . Physiologic evidence suggests that the three sub- is consistent with theories of motor learning, skill acquisition
systems of speech – respiration, phonation and articulation – are and principles that drive activity-dependent neural plasticity.

www.expert-reviews.com 821
 Perspective Sapir, Ramig & Fox

The LSVT dosage involves 60-min individual treatment ses- speech movement parameters. In addition, it is geared toward
sions, 4 days a week for 4 consecutive weeks. In addition, there overcoming or compensating for deficits in internal cueing,
are daily homework practice and carryover assignments on all vocal vigilance and self-regulation of vocal effort during speech
30 days of the month. Within each treatment session, the first production. We hypothesize that LSVT retrains amplitude scal-
half of the session is spent on three daily tasks, which are core ing via intensive sensorimotor training that teaches patients
exercises designed to rescale the amplitude of motor output. to recognize the effort for louder speech, and use it during
These daily tasks are completed with multiple repetitions (e.g., everyday living. By directly addressing this sensory mismatch,
minimum of 15 repetitions per task per day), and continually LSVT teaches subjects with PD to re­c alibrate their percep-
increased requirements for effort, consistency and accuracy of tion of normal loudness and vocal effort so that by the end of
vocal loudness [86] . The second half of the session is spent on the 1 month of therapy, they spontaneously speak with greater vocal
speech hierarchy. The rescaled vocal loudness achieved in the loudness. A few examples of specific treatment tasks related to
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daily tasks is now systematically trained into speech. Across the calibration include recording the patient’s voice while reading
weeks of the hierarchy the duration of time that a person needs with a louder voice that they self-perceive as ‘too loud’ and then
to keep their voice loud and the complexity of the speech task playing it back to them. They recognize and comment when
increase from words/phrases, to sentences, continuous reading they hear the audiotapes that what felt and sounded too loud
and finally, conversational speech. to them while reading actually sounds within normal limits
Within the structured setting of the LSVT treatment ses- (or in some cases still too soft) when played on the tape. In
sions, many elements of exercise that promote activity-depen- addition, carryover activities are assigned daily that require
dent neural plasticity are embedded [4,5] . Tables 2 & 3 highlight patients to use their louder voice in a specific communication
these elements. Key elements of exercise that promote neural setting outside of the treatment room, such as, order dinner at
plasticity, neural protection and neural restoration in animal the restaurant, or greet coworkers. Convincing patients to speak
models included intensive training of motor tasks, increased in a voice that they previously perceived is too loud and having
practice of motor tasks, active engagement or salience of tasks, positive reactions and communication in their daily living, help
complexity of tasks, saliency, and the sensory experience of the convince them that the louder voice is actually within normal
For personal use only.

motor task [153,154] . In LSVT, for example, intensive treatment is limits. This improvement may be due to some restoration of
achieved both across and within treatment sessions. The dosage the internal cueing mechanism, and/or compensation through
across treatment sessions is four individual, 1-h treatment ses- vocal vigilance. Although the treatment delivery is complex for
sions 4 consecutive days a week for 4 weeks. Within treatment the clinician who is administering the therapy, the focus for the
sessions, patients are pushed to high vocally nonabusive inten- individual with PD is kept purposefully simple and redundant
sity levels through increased repetitions of treatment tasks (e.g., (think loud, speak louder), which may maximize the ability of
minimum of 15 repetitions per task), driving high effort and con- individuals with PD to learn this one target. If one treatment
tinuous motor speech exercise (e.g., patients report self-perceived target can make an impact across the speech production system,
high effort during tasks), and increasing accuracy requirements this may allow us to improve the efficiency and effectiveness
as treatment progresses for achieving target goals. While the of treatment.
LSVT protocol is standardized, saliency is achieved by tailoring To date, LSVT is the behavioral therapy with the most data to
speech materials and homework and carryover assignments to support positive outcomes addressing the type of speech impair-
each individual’s interests, hobbies and communication goals. ments experienced by individuals with PD, as judged by the
Saliency is important because the more meaningful or rewarding members of the USA Academy of Neurologic Communications
a task, the greater potential impact on neural plasticity [155,156] . Disorders and Sciences (ANCDS) [157] and others [158] . Specifically,
Complexity of tasks is built into the speech hierarchy exercises, the LSVT has been shown to significantly improve (statisti-
moving from simple reading of words and phrases from paper, cally, and in terms of effect size measures) laryngeal function,
to carrying on conversational speech outside of the treatment vocal loudness, voice quality, prosodic voice fundamental fre-
room in a noisy environment (e.g., cafeteria). Finally, the sen- quency (and its perceptual correlate pitch), inflection, vowel
sory experience of increasing vocal loudness is a major focus of articulation, speech quality and overall speech intelligibility
calibration, as discussed later. (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, swallow-
Calibration: sensory, internal cueing & neuropsychological ing and tongue function [110,111,160] . In addition, these LSVT-
barriers to generalization induced changes in speech and nonspeech orofacial functions
As discussed earlier, the etiology of the speech and voice have been shown to be associated with improved brain func-
disorder in individuals with PD is complex. It appears that tion [159,161,162] . Moreover, improvement in vocal function owing
addressing the motor deficit in isolation is not sufficient for to LSVT has been shown to be maintained over months and up
lasting treatment outcomes that generalize beyond the treat- to 2 years of follow-up [87,95] .
ment room [83] . Thus, LSVT specifically trains individuals The effectiveness of the LSVT program may be variably com-
with PD to ‘recalibrate’ their motor and perceptual systems promised by several factors, including atypical Parkinsonism,
so that they are less inclined to downscale (reduce amplitude) coexisting dystonia, depression, dementia, abulia and adverse

822 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
Intensity
Intensive practice is important for maximal Intensive, high-effort training can be Train intensively 1 h per day, 4 days per week,
plasticity. Intensity can be increased via difficult in PD due to sensory deficits, for 4 weeks; multiple repetitions (15 or more);
frequency, repetitions, force/resistance, force control, fatigue, depression and increase resistance, amplitude (within healthy
effort and accuracy. Intensity increases progressive loss of cardiac sympathetic range) effort, accuracy; and daily homework
activation of corticostriatal terminals, innervation exercises. Train maximum perceived effort
inducing synaptic plasticity in striatum
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Complexity
Complex movements or environmental As basal ganglia pathology progresses, Train complexity of movement with single
enrichment have been shown to promote there is a loss in automaticity, requiring patient focus (LOUD) to multiple, motor tasks.
greater structural plasticity (spine density, greater conscious attention to task. Retrain automaticity of amplitude (LOUD) in
protein expression/synapse number) in When required to perform dual tasks, familiar movements. Progress complexity over
adjacent and remote interconnected regions insufficient attentional resources results 4 weeks by varying contexts, adding dual
than in simple movements in the decrement in one or both of the cognitive/motor loads and increasing duration
concurrent tasks and difficulty of speech tasks (progress from
words to conversation)
Saliency
Practicing rewarding tasks People with early PD may experience lack We train salient familiar movements (core
(success/emotionally salient) activates basal of awareness of subtle motor deficits, patterns) of speech promoting success. We
ganglia circuitry. Rewards are associated with depression, loss of motivation and a provide homework tasks that reinforce success
For personal use only.

phasic modulation of DA levels critical to feeling of ‘helplessness’. Thus, they do of LOUD in emotionally salient social
induction of striatal plasticity and learning/ not feel they need, or would not benefit interactions. We provide extensive
relearning in PD from speech therapy positive feedback
Use it or lose it/use it & improve it
Spared, but compromized DA neurons highly Deficits are subtle – not ‘red flag’ to seek Educate people with PD on subtle deficits and
vulnerable to bouts of inactivity/activity. speech therapy. Getting early PD patients improve motor function that directly impacts
Inactivity may accelerate deficits. to recognize need for exercise and then real life
Post-exercise intervention, there may be a convincing them to continually exercise is Retrain a new way of speaking in everyday life
minimum use requirement to maintain challenging. Decreased physical activity (LOUD or ENUNCIATE); thus, normal activity
positive effects may be a catalyst in degenerative process offers continuous exercise
Timing matters
Early exercise has the potential to: rescue DA People with early PD have subtle physical Train people with early PD when they may not
neurons, prevent chronic disuse, promote underactivity (small movements/soft have deficits in all systems (laryngeal and
system-wide plasticity and halt disease voice). This may be coupled with a lack orofacial). Train strategies to raise awareness/
progression – particularly to the of awareness or self-correction, leading avoid neglect and increase muscle activation
asymptomatic side to further inactivity for normal effort/amplitude required for
within-normal-limits vocal loudness
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; LSVT: Lee Silverman Voice Treatment; PD: Parkinson’s disease.
Data taken from [83].

neurosurgical effects. Although data have been reported docu- improved speech fluency [158] . It may be that for more complicated
menting improvements in individuals after thalamotomy [163] , speech disorders associated with PD, a combination of approaches
fetal cell transplant and DBS [164–166] , as well as in individu- will be the most effective.
als with multisystem atrophy, progressive supranuclear palsy
and Parkinson’s plus syndromes [167] , these outcomes may not Ongoing research with the LSVT & speech treatment
be of the same magnitude as in idiopathic PD and may require in PD
follow-up treatment sessions to maintain improvements over time. The aforementioned findings and recent pilot data indicate
Nevertheless, the functional impact for individual patients can be that training to increase vocal loudness with the LSVT regi-
quite significant in these more advanced or complicated cases of men generalizes beyond laryngeal function to improve speech
PD. There are a number of ongoing studies examining the impact articulation [15,61] , tongue function [160] , swallowing [111] , commu-
of alternative cues for speech in PD (e.g., clear speech) and the nicative gestures [168] , facial expression [110] and neural function-
use of external auditory devices to either cue vocal loudness or ing [61,85,118,123] . Randomized controlled studies are ongoing to

www.expert-reviews.com 823
 Perspective Sapir, Ramig & Fox

examine this spread of effects and its treatment specificity. Studies treatment. We hypothesize that neither dopamine deficiency nor
are also planned to assess the reasons for the heterogeneous speech rigidity are sufficient to account for the speech abnormalities in
outcomes following DBS-STN. Such studies may involve simul- PD, and that additional factors involving nondopaminergic or
taneous quantitative measures of pre- and post-surgical speech special dopaminergic mechanisms, as well as deficits in scaling
functioning and details of surgical and stimulator optimization. movement amplitude, sensory processing, internal cueing and
Knowledge gained from these studies is likely to facilitate the self-regulatory mechanisms, add to the speech disorders in PD.
development of rehabilitative speech treatment approaches for We present the LSVT as a scientifically proven effective treat-
speech problems in people with DBS-STN either before surgery ment for speech disorders in PD, most likely because it addresses
(as preventative) or after surgery (as rehabilitation). the aforementioned deficits and because its mode of delivery is
We are presently assessing the effectiveness of technology-­ consistent with principles that drive activity-dependent neural
supported delivery of LSVT to increase accessibility of treatment, plasticity. Neural imaging has provided preliminary evidence for
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promote home practice, augment the effects of LSVT, reduce neural plasticity induced by the LSVT. We argue that intensive
clinician time, cut costs of treatment and support long-term prac- treatment such as the LSVT should be administered at early
tice. Telepractice delivery of LSVT allows a patient to receive stages of the disease. Early intervention may potentially slow
LSVT online (e.g., at home or in their office). Published data speech symptom progression and can be administered before
have documented that LSVT delivered online has comparable adverse conditions such as depression, fatigue or dementia occur,
outcome data as LSVT delivered in the clinic [161,169] . In addition, thus allowing optimal treatment outcomes. The feasibility of
a study by Tindall et al. completed a cost ana­lysis comparing intensive treatment can be enhanced by technology (telepractice
live, traditional delivery of LSVT versus a telehealth delivery of and software) to improve accessibility and to support continued
LSVT [162] . The computed mean amount of patient time and practice. Research studies are needed to improve our understand-
money across these two modes of delivery were strikingly dif- ing of the neural mechanisms underlying the speech abnormali-
ferent. The live delivery mode required 51 h for 16 visits (travel ties in PD, as well as the neural changes that are induced by
and therapy time), US$953.00 on fuel/mileage expenses and LSVT and other modes of treatment.
US$269.00 for other expenses (e.g., food). By contrast, the tele-
For personal use only.

practice delivery option required 16 h of time (therapy and no Five-year view

travel) and no additional costs for fuel/mileage or other expenses. In the next 5 years, it is expected that the following developments
Recent advances in software allow patients to carry out LSVT will take place:
sessions with software support. The LSVT COMPANION™ is
• The significant therapeutic impact of LSVT on voice, speech
programmed to collect acoustic data and provide feedback as it
and other orofacial functions, as well as on brain reorganization
guides the patient through the LSVT exercises. Outcome data
in individuals with a progressive disease, provides a means to
document that treatment effects are comparable when half of the
explore the brain mechanisms underlying the unique symptoms
sessions were delivered by software [159] .
of PD and the mechanisms underlying the improvement of
Another area of research is the role of sensory and perceptual
these symptoms, including neural plasticity and, possibly, neu-
functions in speech and voice disorders and rehabilitation. As dis-
ral protection. Future studies with the LSVT or other behav-
cussed earlier, it appears that self-perception of voice in individu-
ioral treatments should therefore be designed to explore the
als with PD is defective but the nature of this defect is not well
role of nondopaminergic and special dopaminergic mecha-
understood. Therefore, by experimentally altering the patient’s
nisms in voice and speech disorders, and in other motor disor-
sidetone (his own voice/speech fed back to his auditory system
ders that are only partially or completely unresponsive to
as he speaks) and simultaneously recording the response of the
dopamine treatment;
patient to this manipulation we can gain insight into the nature
of the auditory–vocal mechanism underlying Parkinsonian speech • Explore animal models that may help us understand vocal
in general [84] , and in response to treatment in particular. Using motor deficits related to dopamine depletion in disorders such
this method, we have collected pilot data on one patient with as PD. Two emerging models of vocal motor deficits following
PD and found that auditory–vocal responses to experimental dopamine depletion in rodents [171] and songbirds [172] offer
manipulation were absent prior to LSVT but present, as is nor- promise for the feasibility and value of these models;
mally observed [170] , after LSVT. However, these findings must
be replicated in order to ascertain their generalization to other • Explore the specific role of internal cueing, sensorimotor gating,
patients with PD before and after LSVT. temporal processing, motor-to-sensory (vocal-to-auditory) gat-
ing, perceptual mechanisms, vocal vigilance and self-regulation
Expert commentary on voice and speech functions in general, and in individuals
Speech disorders are highly common in individuals with PD, with PD in particular;
producing adverse effects on communication, health and qual-
ity of life. Traditionally, these disorders have been attributed • Explore the impact of combined treatments and tasks, such as
to dopamine deficiency and rigidity and have been considered speech and gait, on functional recovery and treatment efficacy.
highly resistant to medical, surgical and behavioral forms of Preliminary evidence suggests that individuals with PD trained

824 Expert Rev. Neurother. 11(6), (2011)

 Intensive voice treatment in Parkinson’s disease: Lee Silverman Voice Treatment Perspective

to increase gait amplitude (LSVT BIG) and speech loudness Financial & competing interests disclosure
(LSVT) can perform both tasks simultaneously without inter- This research has been funded by the NIH grant R01 DC1150 from the
ference from the other task and while maintaining therapeutic National Institutes of Deafness and Other Communication Disorders.
gains [173] ; Lorraine O Ramig and Cynthia M Fox receive lecture honoraria and have
ownership interest in LSVT Global, Inc. They have disclosed any conflict of
• Explore the interactions between behavioral treatment and interest and their conflict of interest management plan has been approved
neurosurgical or neuropharmacologic treatments; by the Office of Conflict of Interest and Commitment at the University of
• Explore the impact of computer-based technology (e.g., inter- Colorado, Boulder. The authors have no other relevant affiliations or finan-
net, virtual clinician, web camera and videophones) on treat- cial involvement with any organization or entity with a financial interest
ment efficacy and availability to patients. Preliminary studies in or financial conflict with the subject matter or materials discussed in the
suggest that such technology is highly effective in the delivery manuscript apart from those disclosed.
Expert Review of Neurotherapeutics Downloaded from informahealthcare.com by Northwestern University on 02/09/15

of LSVT in individuals with PD [161,162,174] . No writing assistance was utilized in the production of this manuscript.

Key issues
• 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
For personal use only.

and vocal vigilance. These high-level deficits are probably mediated through nondopaminergic 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.

References Parkinson’s disease. Eur. J. Phys. Rehabil. damage. J. Speech Lang. Hear. Res. 51,
Med. 45, 215–229 (2009). S225–S239 (2008).
1 Fisher BE, Wu AD, Salem GJ et al.
The effect of exercise training in improving 3 Petzinger G, Fisher B, Van Leeuwen J-E 5 Kleim J, Jones T, Schallert T. Motor
motor performance and corticomotor et al. Enhancing neuroplasticity in the basal enrichment and the induction of plasticity
excitability in people with early Parkinson’s ganglia: the role of exercise in Parkinson’s before or after brain injury. Neurochem.
disease. Arch. Phys. Med. Rehabil. 89(7), disease. Mov. Disord. 25, S141–S145 (2010). Res. 11, 1757–1769 (2003).
1221–1229 (2008). 4 Kleim JA, Jones TA. Principles of 6 Zigmond MJ, Cameron JL, Leak RK
2 Hirsch MA, Farley BG. Exercise and experience-dependent neural plasticity: et al. Triggering endogenous
neuroplasticity in persons living with implications for rehabilitation after brain neuroprotective processes through

www.expert-reviews.com 825
 Perspective Sapir, Ramig & Fox

exercise in models of dopamine Yorkston KM, Beukelman DR, Bell KR 32 Goberman A. Correlation between acoustic
deficiency. Parkinsonism Relat. Disord. (Eds.). A College-Hill Publication, Little, speech characteristics and non-speech
1553, 542–545 (2009). Brown and Co., CA, USA, 19–58 (1988). motor performance in Parkinson disease.
7 Keus S, Munneke M, Nijkrake M, 19 Perez K, Ramig LO, Smith M, Dromey C. Med. Sci. Monit. 11, CR109–CR116
Kwakkel G, Bloem B. Physical therapy in The Parkinson larynx: tremor and (2005).
Parkinson’s disease: evolution and future videostroboscopic findings. J. Voice 10, 33 Trail M, Fox C, Ramig LO, Sapir S,
challenges. Mov. Disord. 24, 1–14 (2009). 354–361 (1996). Howard J, Lai EC. Speech treatment for
8 de Lau LM, Breteler MM. Epidemiology of 20 Smith M, Ramig LO, Dromey C, Perez K, Parkinson’s disease. NeuroRehabilitation
Parkinson’s disease. Lancet Neurol. 5(6), Samandari R. Intensive voice treatment in 20, 205–221 (2005).
525–535 (2006). Parkinson’s disease: laryngostroboscopic 34 De Letter M, Santens P, Van Borsel J.
9 Ho A, Iansek R, Marigliani C, findings. J. Voice 9, 453–459 (1995). The effects of levodopa on word
Bradshaw JL, Gates S. Speech impairment Solomon N, Hixon TJ. Speech breathing in intelligibility in Parkinson’s disease.
Expert Review of Neurotherapeutics Downloaded from informahealthcare.com by Northwestern University on 02/09/15

21
in a large sample of people with Parkinson’s Parkinson’s disease. J. Speech Hear. Res. 36, J. Commun. Disord. 38, 187–196 (2005).
disease. Behav. Neurol. 11, 131–137 (1998). 294–310 (1993). 35 Goberman A, Coelho C, Robb M.
10 Darley F, Aronson A, Brown J. Hypokinetic 22 Baker K, Ramig LO, Luschei E, Smith M. Phonatory characteristics of Parkinsonian
Dysarthria. In: Motor Speech Disorders. Thyroarytenoid muscle activity associated speech before and after morning
Saunders, PA, USA (1975). with hypophonia in Parkinson disease medication: the ON and OFF states.
and aging. Neurology 51, 1592–1598 J. Commun. Disord. 35, 217–239 (2002).
11 Ho A, Iansek R, Bradshaw JL. Motor
instability in Parkinsonian speech intensity. (1998). 36 Jiang J, Lin E, Wang J, Hanson DG.
Neuropsychiatry Neuropsychol. Behav. 23 Gallena S, Smith PJ, Zeffiro T, Ludlow CL. Glottographic measures before and after
Neurol. 14, 109–116 (2001). Effects of levodopa on laryngeal muscle levodopa treatment in Parkinson’s disease.
activity for voice onset and offset in Laryngoscope 109, 1287–1294 (1999).
12 Baumgartner C, Sapir S, Ramig LO. Voice
quality changes following phonatory- Parkinson disease. J. Speech Hear. Res. 44, 37 Sanabria J, Ruiz PG, Gutierrez R et al.
respiratory effort treatment (LSVT®) versus 1284–1299 (2001). The effect of levodopa on vocal function in
respiratory effort treatment for people with 24 Vincken W, Gauthier SG, Dollfuss RE, Parkinson’s disease. Clin. Neuropharmacol.
Parkinson disease. J. Voice 14, 105–114 Hanson RE, Parauay CM, Cosio MG. 24, 99–102 (2001).
For personal use only.

(2001). Involvement of upper-airway muscles in 38 Cahill L, Murdoch BE, Theodoros DG,

13 Adams S. Hypokinetic dysarthria in extrapyramidal disorders, a cause of airflow Triggs EJ, Charles BG, Yao AA. Effect of
Parkinson’s disease. In: Clinical Management limitation. N. Engl. J. Med. 7, 438–442 oral levodopa treatment on articulatory
of Sensorimotor Speech Disorders. McNeil (1984). function in Parkinson’s disease:
MR (Ed.). Thieme, NY, USA (1997). 25 Ackermann H, Ziegler W. Articulatory preliminary results. Motor Control 2,
deficits in parkinsonian dysarthria. 161–172 (1998).
14 Forrest K, Weismer G, Turner G.
Kinematic, acoustic and perceptual analysis J. Neurol. Neurosurg. Psychiatry. 54, 39 Kompoliti K, Wang QE, Goetz CG,
of connected speech produced by 1093–1098 (1991). Leurgans S, Raman R. Effects of central
Parkinsonian and normal geriatric adults. 26 Ackermann H, Konczak J, Hertrich I. dopaminergic stimulation by apomorphine
J. Acoust. Soc. Am. 85, 2608–2622 (1989). The temporal control of repetitive on speech in Parkinson’s disease. Neurology
articulatory movements in Parkinson’s 54, 458–462 (2000).
15 Sapir S, Spielman, J, Ramig LO, Story BS,
Fox C. Effects of intensive voice treatment disease. Brain Lang. 56, 312–319 (1997). 40 Larson K, Ramig LO, Scherer RC.
(the Lee Silverman Voice Treatment 27 Caligiuri M, Abbs JH. Response Acoustic and glottographic voice analysis
[LSVT]) on vowel articulation in properties of the perioral reflex in during drug-related fluctuations in
dysarthric individuals with idiopathic Parkinson’s disease. Exp. Neurol. 98, Parkinson’s disease. J. Med. Speech Lang.
Parkinson disease: acoustic and perceptual 563–572 (1987). Pathol. 2, 211–226 (1994).
findings. J. Speech Lang. Hear. Res. 50, 28 Hirose H. Pathophysiology of motor speech 41 Skodda S, Visser W, Schlegel U. Short- and
899–912 (2007). disorders (dysarthria). Folia Phoniat. Basel long-term dopaminergic effects on
16 Sapir S, Pawlas AA, Ramig LO et al. Voice 38, 61–88 (1986). dysarthria in early Parkinson’s disease.
and speech abnormalities in Parkinson J. Neural Transm. 117, 197–205 (2010).
29 Leanderson R, Persson A, Ohman S.
disease: relation to severity of motor Electromyographic studies of the function 42 Spencer K, Morgan K, Blond E.
impairment, duration of disease, of the facial muscles in dysarthria. Acta Dopaminegic medication effects on the
medication, depression, gender, and age. Otolaryngol. 263, 89–94 (1970). speech of individuals with Parkinson’s
J. Med. Speech Lang. Pathol. 9, 213–226 disease. J. Med. Speech Lang. Pathol. 17,
30 Leanderson R, Meyerson B, Persson A. Lip
(2001). 125–144 (2009).
muscle function in Parkinsonian
17 Benke T, Hohenstein C, Poewe W, dysarthria. Acta Otolaryngol. 74, 350–357 43 Biary N, Pimental PA, Langenberg PW.
Butterworth B. Repetitive speech (1972). A double-blind trial of clonazepan in the
phenomena in Parkinson’s disease. treatment of parkinsonian dysarthria.
31 Radad K, Gille G, Rausch W. Short review
J. Neurol. Neurosurg. Psychiatry. 69, Neurology 38, 255–258 (1988).
on dopamine agonists: insight into clinical
319–324 (2000). 44 Ghika J, Ghika-Schmid F, Fankhauser H
and research studies relevant to Parkinson’s
18 McClean M. Neuromotor aspects of speech disease. Pharmacologic Rep. 57, 701–712 et al. Bilateral contemporaneous
production and dysarthria. In: Clinical (2005). posteroventral pallidotomy for the treatment
Management of Dysarthric Speakers. of Parkinson’s disease: neuropsychological

826 Expert Rev. Neurother. 11(6), (2011)

 Intensive voice treatment in Parkinson’s disease: Lee Silverman Voice Treatment Perspective

and neurological side effects, report of four 57 Tommasi G, Krack P, Fraix V et al. 70 Jobst EE, Melnick ME, Byl NN,
cases and review of the literature. Pyramidal tract side effects induced by Dowling GA, Aminoff MJ. Sensory
J. Neurosurg. 91, 313–321 (1999). deep brain stimulation of the subthalamic perception in Parkinson’s disease. Arch.
45 Krack P, Batir A, VanBiercom N et al. nucleus. J. Neurol. Neurosurg. Psychiatry 79, Neurol. 54, 450–454 (1997).
Five-year follow-up of bilateral stimulation 813–819 (2008). 71 Klockgether T, Borutta M, Rapp H,
of the subthalamic nucleus in advanced 58 Rosen K, Kent RD, Duffy JR. Task-based Spieder S, Dichgans J. A defect of
Parkinson’s disease. N. Engl. J. Med. 345, profile of vocal intensity decline in kinesthesia in Parkinson’s disease. Brain
1925–1934 (2003). Parkinson’s disease. Folia Phoniat. Logoped. 120, 460–465 (1997).
46 Gentil M, Garcia-Ruiz P, Pollak P, 57, 28–37 (2005). 72 Schneider S, Diamond SG, Markham CH.
Benabid A-L. Effect of stimulation of the 59 Caligiuri M. The influence of speaking rate Deficits in orofacial sensorimotor function
subthalamic nucleus on oral control of on articulatory hypokinesia in in Parkinson’s disease. Ann. Neurol. 19,
patients with Parkinsonism. J. Neurol. Parkinsonian dysarthria. Brain Lang. 36, 275–282 (1986).
Expert Review of Neurotherapeutics Downloaded from informahealthcare.com by Northwestern University on 02/09/15

Neurosurg. Psychiatry 67, 329–333 (1999). 493–502 (1989). 73 Diamond SG, Schneider JS, Markham CH.
47 Gentil M, Garcia-Ruiz P, Pollak P, Benabid 60 Liss JM, Spitzer SM, Caviness JN, Adler C. Oral sensorimotor defects in people with
A-L. Effect of bilateral deep-brain The effects of familiarization on Parkinson’s disease. Adv. Neurol. 45,
stimulation on oral control of patients with intelligibility and lexical segmentation in 335–338 (1987).
Parkinsonism. Eur. Neurol. 44, 147–152 hypokinetic and ataxic dysarthria. 74 Rickards C, Cody FW. Proprioceptive
(2000). J. Acoust. Soc. Am. 112, 3022–3030 control of wrist movements in Parkinson’s
48 Gentil M, Chauvin P, Pinto S, Pollak P, (2002). disease. Brain 120, 977–990 (1997).
Benabid A-L. Effect of bilateral stimulation 61 Sapir S, Ramig LO, Spielman JL, Fox C. 75 Schneider JS, Lidsky TI. Basal Ganglia and
of the subthalamic nucleus on Parkinsonian Formant centralization ratio: a proposal for Behavior: Sensory Aspects of Motor
voice. Brain Lang. 78, 233–240 (2001). a new acoustic measure of dysarthric Functioning. Hans Huber, Toronto, Canada
49 Gentil M, Pinto S, Pollak P, Benabid A-L. speech. J. Speech Lang. Hear. Res. 53, (1987).
Effect of bilateral stimulation of the 114–125 (2010).
76 Graber S, Hertrich I, Daum I, Spieker S,
subthalamic nucleus on Parkinsonian 62 Skodda S, Visser W, Schlegel U. Vowel Ackermann H. Speech perception deficits
dysarthria. Brain Lang. 85, 190–196 (2003). articulation in Parkinson’s disease. J. Voice in Parkinson’s disease: underestimation of
For personal use only.

50 Pinto S, Gentil M, Krack P et al. Changes DOI: 10.1016/j.jvoice.2010.01.009 (2010) time intervals compromises identification
induced by levodopa and subthalamic (Epub ahead of print). of durational phonetic contrasts. Brain
nucleus stimulation on Parkinsonian speech. 63 Bartels AL, Leenders KL. Parkinson’s Lang. 82, 65–74 (2002).
Mov. Disord. 20 (11), 1507–1515 (2005). disease: the syndrome, the pathogenesis 77 Ho AK, Bradshaw JL, Iansek R,
51 Tripoliti E, Zrino L, Martinez-Torres I and pathophysiology. Cortex 45, 915–921 Alfredson R. Speech volume regulation in
et al. Effects of contact location and voltage (2009). Parkinson’s disease: Effects of implicit cues
amplitude on speech and movement in 64 Demirci M, Grill S, McShane L, and explicit instructions. Neuropsychologia
bilateral subthalamic nucleus deep brain Hallet M. Impairment of kinesthesia in 37. 1453–1460 (1999).
stimulation. Mov. Disord. 23, 2377–2383 Parkinson’s disease. Neurology 45, A218 78 Ho AK, Iansek R, Bradshaw JL.
(2008). (1995). Regulations of parkinsonian speech volume:
52 Romito LM, Albanese A. Dopaminergic 65 Desmurget M, Grafton ST, Vindras P, the effect of interlocuter distance. J. Neurol.
therapy and subthalamic stimulation in Gréa H, Turner RS. Basal ganglia network Neurosurg. Psychiatry 67, 199–202 (1999).
Parkinson’s disease: a review of 5-year mediates the control of movement 79 Ho A, Bradshaw JL, Iansek T. Volume
reports. J Neurol. 257(Suppl. 2), amplitude. Exp. Brain Res. 153, 197–209 perception in Parkinsonian speech. Mov.
S298–S304 (2010). (2003). Disord. 15, 1125–1131 (2000).
53 Ramig LO, Fox C, Sapir S. Speech 66 Desmurget M, Grafton ST, Vindras P, 80 Solomon NP, Robin DA, Lorell DM,
treatment for Parkinson’s disease. Expert Gréa H, Turner RS. The basal ganglia Rodnitzky RL, Luschei ES. Tongue
Rev. Neurother. 8, 297–309 (2008). network mediates the planning of function testing in Parkinson’s Disease:
54 Sapir S, Ramig L, Fox C. Speech and movement amplitude. Eur. J. Neurosci. 19, indicators of fatigue. In Motor Speech
swallowing disorders in Parkinson’s disease. 2871–2880 (2004). Disorders: Advances in Assessment and
Curr. Opin. Otolaryngol. Head Neck Surg. 67 Hallet M. Sensorimotor integration and Treatment. Till JA, Yorkston KM,
16, 205–210 (2008). mys­terious sensory phenomena in Beukelman R (Eds). Paul H Brooks, MD,
55 Törnqvist AL, Schalén L, Rehncrona S. movement disorders. In: Motor Control. USA, 147–160 (1994).
Effects of different electrical parameter Hallet M (Ed.) American Academy of 81 Hammer MJ. Design of a new
settings on the intelligibility of speech in Neurology, MN, USA (1997). somatosensory stimulus delivery device for
patients with Parkinson’s disease treated 68 Morris M, Iansek R, Matyas T, Summers J. measuring laryngeal mechanosensory
with subthalamic deep brain stimulation. Abnormalities in the stride length-cadence detection thresholds in humans. IEEE Trans.
Mov. Disord. 20, 416–423 (2005). relation in Parkinsonian gait. Mov. Disord. Biomed. Eng. 56(4), 1154–1159 (2009).
56 Astrom M, Tripoliti E, Hariz MI et al. 13, 61–69 (1998). 82 Hammer MJ, Barlow SM. Laryngeal
Patient-specific model-based investigation 69 Demirci M, Grill S, McShane L, Hallett somatosensory deficits in Parkinson’s
of speech intelligibility and movement M. A mismatch between kinesthetic and disease: implications for speech respiratory
during deep brain stimulation. Stereotach. visual perception in Parkinson’s disease. and phonatory control. Exp. Brain Res.
Funct. Neurosurg. 88, 224–233 (2010). Ann. Neurol. 41, 781–788 (1997). 201(3), 401–409 (2010).

www.expert-reviews.com 827
 Perspective Sapir, Ramig & Fox

83 Fox C, Morrison C, Ramig L, Sapir S. 94 Morris ME, Iansek R, Matyas TA, 108 Cohen J. Statistical Power Analysis for the
Current perspectives on the Lee Silverman Summers JJ. Stride length regulation in Behavioral Sciences (2nd Edition). Lawrence
Voice Treatment (LSVT®). Am. J. Speech Parkinson’s disease. Normalization Erlbaum, NY, USA (1988).
Lang. Pathol. 11, 111–123 (2002). strategies and underlying mechanisms. 109 Dromey C, Ramig L, Johnson A.
84 Kiran S, Larson C. Effect of duration of Brain 119(2), 551–568 (1996). Phonatory and articulatory changes
pitch-shifted feedback on vocal responses in 95 Sapir S, Ramig L, Hoyt P, O’Brien C, associated with increased vocal intensity in
patients with Parkinson’s disease. J. Speech Hoehn M. Phonatory-respiratory effort Parkinson disease: a case study. J. Speech
Lang. Hear. Res. 44, 975–987 (2001). (LSVT®) vs. respiratory effort treatment for Hear. Res. 38, 751–763 (1995).
85 Liotti M, Vogel D, Sapir S, Ramig L, hypokinetic dysarthria: comparing speech 110 Spielman J, Borod J, Ramig L. Effects of
New P, Fox P. Abnormal auditory gating in loudness and quality before and 12 months intensive voice treatment (LSVT) on facial
Parkinson’s disease before & after LSVT. after treatment. Folia Phoniatr. 54, expressiveness in Parkinson’s disease:
Presented at: The Annual Meeting of the 296–303 (2002). preliminary data. Cog. Behav. Neurology 16,
Expert Review of Neurotherapeutics Downloaded from informahealthcare.com by Northwestern University on 02/09/15

American Speech, Language and Hearing 96 Allan CM. Treatment of non-fluent speech 177–188 (2003).
Association. Washington DC, USA, resulting from neurological disease: 111 El-Sharkawi A, Ramig LO, Logemann JA
16–19 November (2000). treatment of dysarthria. Br. J. Disord. et al. Swallowing and voice effects of Lee
86 Ramig L, Pawlas A, Countryman S. Comm. 5, 3–5 (1970). Silverman Voice Treatment (LSVT®):
The Lee Silverman Voice Treatment (LSVT): 97 Greene HCL. The Voice and Its Disorders. a pilot study. J. Neurol. Neurosurg.
a Practical Guide to Treating the Voice and Pitman Medical, London, UK (1980). Psychiatry 71, 31–36 (2002).
Speech Disorders in Parkinson Disease. 98 Sarno MT. Speech impairment in 112 Dishman RK, Berthoud HR, Booth FW
National Center for Voice and Speech, IA, Parkinson’s disease. Arch. Phys. Med. et al. Neurobiology of exercise. Obesity
USA (1995). Rehabil. 49(5), 269–275 (1968). 14(3), 345–356 (2006).
87 Ramig L, Sapir S, Countryman S et al. 99 Weiner WJ, Lang AE. Movement Disorders: 113 Dromey C, Ramig L. Intentional changes
Intensive voice treatment (LSVT®) for A Com­prehensive Survey. Futura, NY, USA in sound pressure level and rate: their
individuals with Parkinson disease: (1989). impact on measures of respiration,
a two-year follow-up. J. Neurol. Neurosurg. phonation, and articulation. J. Speech Lang.
100 Scott S, Caird FL. Speech therapy for
Psychiatry 71, 493–498 (2001). Hear. Res. 41, 1003–1018 (1998).
Parkinson’s disease. J. Neurol. Neurosurg.
For personal use only.

88 Ramig L, Sapir S, Fox C, Countryman S. Psychiatry. 46, 140–144 (1983). 114 Kleinow J, Smith A, Ramig L. Speech
Changes in vocal intensity following stability in idiopathic Parkinson disease:
101 Robertson S, Thompson F. Speech therapy
intensive voice treatment (LSVT®) in effects of rate and loudness manipulations.
in Parkinson’s disease: a study of efficacy
individuals with Parkinson disease: J. Speech Lang. Hear. Res. 44(5), 1041–1051
and long term effects of intensive
a comparison with untreated patients and (2001).
treatment. Br. J. Disord. Commun. 19,
normal age-matched controls. Mov. Disord.
213–224 (1984). 115 Ramig L, Sapir S, Baker K et al. The ‘big
16, 79–83 (2001).
102 Johnson J, Pring T. Speech therapy and picture’ on the role of phonation in the
89 Cunnington R, Iansek R, Bradshaw JL. treatment of individuals with motor speech
Parkinson’s disease: a review and further
Movement-related potentials in Parkinson’s disorders: Or ‘what’s up with loud?’
data. Br. J. Disord. Comm. 125, 183–194
disease: external cues and attentional Presented at: The Tenth Biennial Conference
(1990).
strategies. Mov. Disord. 14, 63–68 (1999). on Motor Speech. San Antonio, TX, USA,
103 Ramig L, Countryman S, Thompson L,
90 Oliveira RM, Gurd JM, Nixon P, 2–6 February (2000).
Horii, Y. A comparison of two forms of
Marshall JC, Passingham RE. 116 Tjaden K, Wilding GE. Rate and loudness
intensive speech treatment for Parkinson
Micrographia in Parkinson’s disease: the manipulations in dysarthria: acoustic and
disease. J. Speech Hear. Res. 38, 1232–1251
effect of providing external cues. J. Neurol. perceptual findings. J. Speech Lang. Hear.
(1995).
Neurosurg. Psychiatry. 63, 429–433 (1997). Res. 47(4), 766–783 (2004).
104 Speech therapy in Parkinson’s disease. Mov.
91 Rochester L, Rafferty D, Dotchin C, 117 Watson PJ, Hughes D. The relationship of
Disord. 17(4), S163–S166 (2002).
Msuya O, Minde V, Walker RW. The effect vocal loudness manipulation to prosodic F0
of cueing therapy on single and dual-task 105 Robey RR, Schultz MC. A model for
and durational variables in healthy adults.
gait in a drug naïve population of people conducting clinical-outcome research: an
J. Speech Lang. Hear. Res. 636–644 (2006).
with Parkinson’s disease in northern adaptation of the standard protocol for use
in aphasiology. Aphasiology 12, 787–810 118 Liotti M, Ramig LO, Vogel D et al.
Tanzania. Mov. Disord. 25, 906–911
(1998). Hypophonia in Parkinson’s disease.
(2010).
Neural correlates of voice treatment
92 Bohnen NI, Kaufer DI, Hendrickson R 106 Ramig L, Mead C, Scherer R, Horii Y,
revealed by PET. Neurology 60, 432–440
et al. Cognitive correlates of cortical Larson K, Kohler D. Voice therapy and
(2003).
cholinergic denervation in Parkinson’s Parkinson’s disease: a longitudinal study of
efficacy. Presented at: The Clinical 119 Will L, Spielman J, Ramig L. Stimulated
disease and Parkinsonian dementia.
Dysarthria Conference. San Diego, CA, or trained loudness: is there a difference
J. Neuro. 253, 242–247 (2006).
USA, 4–7 February (1988). and does it matter? Presented at: The
93 Rowe J, Stephan KE, Friston K, Conference on Motor Speech Disorders.
Frackowiak R, Lees A, Passingham R. 107 Ramig L, Dromey C. Aerodynamic
Austin, TX, USA, 23–26 March 2006.
Attention to action in Parkinson’s disease: mechanisms underlying treatment-related
changes in vocal intensity in patients with 120 Schulman R. Articulatory dynamics of
impaired effective connectivity among
Parkinson disease. J. Speech Hear. Res. 39, loud and normal speech. J. Acoust. Soc. Am.
frontal cortical regions. Brain. 125,
798–807 (1996). 85, 295–312 (1989).
276–289 (2002).

828 Expert Rev. Neurother. 11(6), (2011)

 Intensive voice treatment in Parkinson’s disease: Lee Silverman Voice Treatment Perspective

121 Kleim JA, Napper RMA, Swain RA, 134 McClean MD, Tasko SM. Association of 147 Jürgens U, Zwirner P. The role of the
Armstrong KE, Jones TA, Greenough WT. orofacial with laryngeal and respiratory periaqueductal grey in limbic and
Selective synaptic plasticity in the motor output during speech. Exp. Brain neocortical vocal fold control. Neuroreport
cerebellar cortex of the rat following Res. 146, 481–489 (2002). 7, 2921–2923 (1996).
complex motor learning. Soc. Neurosci. 135 Sapir S. The intrinsic pitch of vowels: 148 Meissner I, Sapir S, Kokmen E, Stein SD.
Abstr. 20(2), 1435 (1994). theoretical, physiological, and clinical The paramedian diencephalic syndrome:
122 Narayana S, Fox PT, Zhang W et al. considerations. J. Voice 3, 44–51 (1989). a dynamic phenomenon. Stroke 18,
Neural correlates of efficacy of voice 136 Sapir S, Larson KK. Supralaryngeal muscle 380–385 (1987).
therapy in Parkinson’s disease identified by activity during sustained vibrato in four 149 Sapir S, Campbell C, Larson C. Effect of
performance-correlation analysis. Hum. sopranos: surface EMG findings. J. Voice 7, geniohyoid, cricothyroid and sternothyroid
Brain Mapp. 31, 222–236 (2010). 213–218 (1993). muscle stimulation on voice fundamental
123 Narayana S, Vogel D, Brown S et al. Roy N, Nissen SL, Dromey C, Sapir S. frequency of electrically elicited phonation
Expert Review of Neurotherapeutics Downloaded from informahealthcare.com by Northwestern University on 02/09/15

137
Mechanism of action of voice therapy in Articulatory changes in muscle tension in rhesus macaque. Laryngoscope 91,
Parkinson’s hypophonia – a PET study. dysphonia: evidence of vowel space 457–468 (1981).
Presented at: The 11th Annual Meeting of expansion following manual 150 West RA, Larson CR. Neurons of the
the Organization for Human Brain circumlaryngeal therapy. J. Commun. anterior mesial cortex related to faciovocal
Mapping. Toronto, Ontario, Canada, 12–16 Disord. 42, 124–135 (2009). activity in the awake monkey.
June (2005). J. Neurophysiol. 74, 1856–1869 (1995).
138 von Cramon D, Jürgens U. The anterior
124 Fox C, Ramig L, Ciucci M et al. cingulate cortex and the phonatory control 151 de Swart BJ, Willemse SC, Maassen BA,
The science and practice of LSVT/LOUD: in monkey and man. Neurosci. Biobehav. Horstink MW. Improvement of voicing in
neural plasticity-principled approach to Rev. 7, 423–425 (1983). patients with Parkinson’s disease by speech
treating individuals with Parkinson disease therapy. Neurology 60(3), 498–500
139 Jürgens U, Kirzinger A, von Cramon D.
and other neurological disorders. Semin. (2003).
The effects of deep-reaching lesions in the
Speech Lang. 27, 283–299 (2006).
cortical face area on phonation. 152 Liotti M, Ramig L. Improvement of
125 Ofer-Noy N, Dudai Y, Karni A. Skill A combined case report and experimental voicing in patients with Parkinson’s disease
learning in mirror reading: how repetition monkey study. Cortex 18, 125–130 by speech therapy. Neurology 61(9),
For personal use only.

determines acquisition. Cog. Brain Res. 17, (1982). 1316–1317 (2003).

507–521 (2003).
140 Kitchen DM, Cheney DL, Seyfarth RM. 153 Tillerson J, Cohen AD, Philhower J,
126 Tillerson J, Miller G. Forced limb-use and Male chacma baboons (Papio hamadryas Miller GW, Zigmond MJ, Schallert T.
recovery following brain injury. ursinus) discriminate loud call contests Forced limb-use effects on the behavioral
Neuroscientist 8, 574–585 (2002). between rivals of different relative ranks. and neurochemical effects of
127 Berardelli A, Rothwell JC, Thompson PD, Anim. Cogn. 8, 1–6 (2005). 6-hydroxydopamine. J. Neuroscience 21,
Hallett M. Pathophysiology of bradykinesia 141 Leinonen L, Laakso ML, Carlson S, 4427–4435 (2001).
in Parkinson’s disease. Brain 124, Linnankoski I. Shared means and 154 Tillerson J, Caudle WM, Reveron ME,
2131–2146 (2001). meanings in vocal expression of man and Miller GW. Exercise induces behavioral
128 Allen, G. Segmental timing control in macaque. Logoped. Phoniatr. Vocol. 28, recovery and attenuates neurochemical
speech production. J. Phon. 1, 219–237 53–61 (2003). deficits in rodent models of Parkinson’s
(1973). 142 Jürgens U. Neuronal control of mammalian disease. Neuroscience 119, 899–911 (2003).
129 Dromey C, Ramig L. The effect of lung vocalization, with special reference to the 155 Alexander GE, Crutcher MD. Functional
volume on selected phonatory and squirrel monkey. Naturwissenschaften 85, architecture of basal ganglia circuits: neural
articulatory variables. J. Speech Lang. Hear. 376–388 (1998). substrates of parallel processing. Trends
Res. 41, 491–502 (1998). 143 Sapir S, Aronson AE. Aphonia after closed Neurosci.13, 266–271 (1990).
130 Gandour J, Dechongkit S, Ponglorpisit S, head injury: aetiologic considerations. 156 Graybiel AM. The basal ganglia and
Khunadorn F. Speech timing at the Br. J. Disord. Commun. 20, 289–296 chunking of action repertoires. Neurobiol.
sentence level in Thai after unilateral (1985). Learn. Mem. 70, 119–136 (1998).
brain damage. Brain Lang. 46, 419–438 144 McClean M, Tasko S. Association of 157 Yorkston K, Spencer KA, Duffy JR.
(1994). orofacial muscle activity and movement Behavioral management of respiratory/
131 Cookman S, Verdolini K. Interrelation of during changes in speech rate and intensity. phonatory dysfunction from dysarthria:
mandibular laryngeal functions. J. Voice J. Speech Lang. Hear. Res. 46, 1387–1400 a systematic review of the evidence. J. Med.
13, 11–24 (1999). (2003). Speech Lang. Pathol. 11, xiii–xxxviii (2003).
132 Higgins MB, Netsell R, Schulte L. 145 Wohlert A, Hammen V. Lip muscle activity 158 Yorkston KM, Hakel M, Beukelman DR,
Vowel-related differences in laryngeal related to speech rate and loudness. Fager S. Evidence for effectiveness of
articulatory and phonatory function. J. Speech Lang. Hear. Res. 43, 1229–1239 treatment of loudness, rate, or prosody in
J. Speech Lang. Hear. Res. 41, 712–724 (2000). dysarthria: a systematic review. J. Med.
(1998). 146 Sapir S, Ramig L, Fox C. The Lee Speech Lang. Pathol. 15(2), xi–xxxvi
133 Larson KK, Sapir S. Orolaryngeal reflex Silverman Voice Treatment for voice, (2007).
responses to changes in affective state. speech and other orofacial disorders in 159 Halpern A, Matos C, Ramig LO, Petska J,
J. Speech Lang. Hear. Res. 38, 990–1000 patients with Parkinson’s disease. Future Spielman J. LSVTC – a PDA supported
(1995). Neurol. 1, 563–570 (2006). speech treatment for Parkinson’s disease.

www.expert-reviews.com 829
 Perspective Sapir, Ramig & Fox

Presented at: The 9th International Congress 165 Sapir S, Halpern A, Spielman J, Ramig L, 171 Ciucci MR, Ma ST, Fox C, Kane JR,
of Parkinson’s Disease and Movement Gilley P. Speech Treatment for individuals Ramig LO, Schallert T. Qualitative
Disorders. New Orleans, LA, USA with idiopathic Parkinson’s disease post changes in ultrasonic vocalization in rats
2–5 March (2005). DBS-STN: LSVT-DBS. Presented at: after unilateral dopamine depletion or
160 Ward E, Theodoros D, Murdoch B, The Second International Symposium on haloperidol: a preliminary study. Behav.
Silburn P. Changes in maximum capacity Basal Ganglia Speech Disorders and Deep Brain Res. 182(2) 284–289 (2007).
tongue function following the Lee Brain Stimualtion. Aix en Provence, France, 172 Miller JE, Burkett ZD, White SA.
Silverman Voice Treatment program. 29 June–1 July (2010). Birdsong as a model system for early
J. Med. Speech Lang. Pathol. 8, 331–335 166 Tassorelli C, Buscone S, Sandrini G et al. detection of Parkinson disease. Presented
(2000). The role of rehabilitation in deep brain at: Annual Society for Neuroscience Meeting,
161 Howell S, Tripoliti E, Pring T. Delivering stimulation of the subthalamic nucleus for Chicago, IL, USA, 21–27 October (2009).
the Lee Silverman Voice Treatment Parkinson’s disease: a pilot study. 173 Fox CM, Farley BG, Ramig LO,
Expert Review of Neurotherapeutics Downloaded from informahealthcare.com by Northwestern University on 02/09/15

(LSVT) by web camera: a feasibility study. Parkinsonism Relat Disord. 15, 675–681 McFarland D. An integrated speech and
Int. J. Lang. Commun. Disord. 44, 287–300 (2009). physical therapy approach for Parkinson
(2009). 167 Countryman S, Ramig L, Pawlas A. Speech disease: Training BIG and LOUD. Mov.
162 Tindall LR, Huebner RA, Stemple JC, and voice deficits in Parkinsonian Plus Disord. 22 (Suppl. 16), S98–S99 (2007)
Kleinert HL. Videophone-delivered voice syndromes: can they be treated? J. Med. 174 Constantinescu GA, Theodoros DG,
therapy: a comparative analysis of outcomes Speech Lang. Pathol. 2(3), 211–225 (1994). Russell TG, Ward EC, Wilson SJ,
to traditional delivery for adults with 168 Duncan S. Preliminary data on effects of Wootton R. Home-based speech treatment
Parkinson’s disease. Telemed. J. E Health behavioral and levodopa therapies of for Parkinson’s disease delivered remotely:
14, 1070–1077 (2008). speech-accompanying gesture in a case report. J. Telemed. Telecare 16,
163 Countryman S, Ramig L. Effects of Parkinson’s disease. Presented at: 100–104 (2010).
intensive voice therapy on voice deficits The ICSLP Meeting. Denver, CO, USA, 175 Ramig L, Countryman S, O’Brien C,
associated with bilateral thalamotomy in 16–20 September (2002). Hoehn M, Thompson L. Intensive speech
Parkinson’s disease: a case study. J. Med. 169 Theodoros DG, Constantinescu G, treatment for individuals with Parkinson’s
Speech Lang. Pathol.1, 233–250 (1993). Russell TG et al. Treating the speech disease: short- and long-term comparison
For personal use only.

164 Halpern A, Spielman J, Ramig L, Down I, disorder in Parkinson’s disease online. of two techniques. Am. Acad. Neurol. 47,
Gilley P. Speech Treatment for Individuals J. Telemed. Telecare. 12, S3, 88–91 (2006). 1496–1504 (1996).
with IPD Post Deep Brain Stimulation: 170 Bauer J, Mittal J, Larson C, Hain T. Vocal 176 Till JA, Yorkston KM, Beukelman R.
LSVT-DBS. Presented at: The 15th responses to unanticipated perturbations in Motor Speech Disorders: Advances in
Biennial Conference on Motor Speech. voice loudness feedback: an automatic Assessment and Treatment. Paul H Brooks,
Savannah, GA, USA, 3–7 March 2010 mechanism for stabilizing voice amplitude. Baltimore, MD, USA (1994).
(2010). J. Acous. Soc. Am. 119, 2363–2371 (2006).

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