Speech Rehabilitation in Parkinson¡¯s Disease
Armenuhi
V. Avagyan, Hasmik H. Mkrtchyan, Tigran R. Petrosyan
Armenuhi
V. Avagyan, Hasmik H. Mkrtchyan, Tigran R. Petrosyan, Department of Speech and Rehabilitation Therapy,
Armenian State Pedagogical University, Armenia
Correspondence to: T.R. Petrosyan, Department of Speech
and Rehabilitation Therapy, Armenian State Pedagogical University, 17 Tigran
Mets avenue, Yerevan, 0010, Republic of Armenia
Email: tigpetrosyan@mail.ru
Telephone: +37410597043
Fax: +37410597008
Received: May 12, 2015
Revised: July 29, 2015
Accepted: August 3, 2015
Published online: September 1, 2015
ABSTRACT
The
purpose of this review was to evaluate the different speech therapy approaches
for persons with Parkinson¡¯s Disease (PD). Treatment methods reviewed include
speech therapy (LSVT), pharmacological therapy and deep brain stimulation
(DBS). Recent research data show that speech therapy has proven to be the most
effective therapeutic strategy for improving voice and speech function.
Pharmacotherapy or DBS methods not combined with speech therapy do not appear
to significantly improve voice and speech function in PD across research
studies. Possible explanation for this results is that LSVT is the major tool
for speech rehabilitation in patients with PD. Research data comparing the
efficacy of LSVT LOUD and LSVT ARTIC have confirmed the advantages of LSVT LOUD
for the speech therapy in patients with PD
© 2015 ACT. All
rights reserved.
Key words: Parkinson's disease; speech disturbances; rehabilitation
strategies
Avagyan AV,
Mkrtchyan HH, Petrosyan TR. Speech Rehabilitation in Parkinson¡¯s
Disease. International Journal of Neurology Research 2015; 1(3): 158-162 Available from:
URL: http://www.ghrnet.org/index.php/ijnr/article/view/1197
Introduction
Parkinson¡¯s disease (PD) is a chronic progressive neurodegenerative
disorder with an increasing incidence worldwide. PD is characterized by the
idiopathic loss of dopaminergic neurons, primarily in the anterior part of the
substantia nigra[1]. The main symptoms of PD result from
significantly reduced activity of dopaminergic neurons in the pars compacta
region of the substantia nigra[2]. There are several pathways in the
brain connecting other brain areas with the basal ganglia: motor, oculmotor,
associative, limbic and orbitofrontal pathways, All these tracts are affected
in PD, and their dysfunction explains many of the symptoms of the disease since
these pathways are involved in different functions including motor activities,
attention and learning. The motor pathway has been examined more intensively
than other tracts. The model of motor pathway alteration in PD has been studied
extensively for the last three decades, although some aspects of the model and
the hypothesis as a whole have been challenged which have led to various
modifications. According to this model, the basal ganglia normally inhibits a
number of motor systems, preventing them from becoming inappropriately active.
When a motivation or decision is made to perform an action, inhibitory
influence is reduced for the target motor system, facilitating the activation.
Dopamine has a major role in such inhibition, so high levels of dopamine can
promote motor activity, whereas low levels of dopamine require greater effort
for any given movement. This mechanism- dopamine depletion is the cause of
hypokinesia and reduced motor output. Pharmacotherapy of PD is aimed to induce
excessive dopamine activity, prevent the activation of motor systems at
inappropriate times and thereby prevent dyskinesias.
Almost two
centuries ago, J. Parkinson first described the disease that bears his name.
There are various etiological factors in PD. Age is the most evident risk
factor and the genetic predisposition second. This explains the increase in prevalence
of Parkinson's disease with age. PD reduces the life expectancy and in few
decades the neurodegenerative disorders will be the main cause of mortality in
elderly, surpassing cancer.
Results of
clinical trials showed that PD has higher incidence after the age of 50. Less
than 10% of patients manifest symptoms before the age of 40[3]. On
the other hand the prevalence of the disease decreases after 65 years of age
and in persons over 80 is not more than 1%.
PD symptoms
are classified as motor and not motor. The motor symptoms include: resting
tremor, bradykinesia, muscular rigidity, and postural impairment. Non motor
(non-dopaminergic) symptoms of PD are various: disorders of mood, behavior,
cognition and a speech disorder characterized as hypokinetic dysarthria[4].
Sustained vowel phonation in PD is measured by the basic frequency or pitch of
vocal vibration, extent of voice range variability (jitter), the extent of
expiratory flow changes (shimmer), and the noise amplitude relative to normal speech
tone. Voice onset time (VOT) is also used to evaluate speech in PD. VOT is the
period from articualtion of a stop consonant to the pronunciation the following
vowel[5]. All these measures or parameters are changed in PD
differently and have specific alteration pattern.
The jitter or
extent of voice variation represents the variability of the speech basic
frequency (characterized also as pitch period) from one cycle to the next[5].
It could be characterized also as short-term perturbations (from cycle-to-cycle)
in the basic frequency of the voice[6].The shimmer is the extent of
expiratory flow variation typical for each vocal cycle. It is a cycle-to cycle,
short-term fluctuations in voice amplitude[7]. Resonance is defined
the selective augmentation of certain frequencies using induced vibrations in
the chest, pharynx, and head sinuses[8].
Speech
Parameters
Articulation is one of the main parameters in speech. It is the
pronunciation process of consonants and vowels, where lips, tongue, palate, and
pharynx have a key role. The process is controlled by the laryngeal stops and
initiation of phonation to pronounce voiced and unvoiced sounds[8].
The easiest method to analyze the articulation is the diadochokinetic (DDK)
task. The DDK task analyzes the ability to repeat a combination of a consonant
and a vowel (C-V combination) with both lips pursed. The patients have to
pronounce keeping the tongue against back of the upper teeth (alveolar), or
pronounce keeping the tongue against the soft palate (velar) in a rhythmic
manner. Subjects are required to repeat three-syllable item (usually
/pa/-/ta/-/ka/) as fast and long as possible.
Prosody is
another parameter studied in patients with PD. It is the variation in loudness,
pitch, and timing of the speech. 13 Prosodic parameters are characterized as
fundamental frequency, intensity (loudness), rate of articulation,
characteristics of pause, and the rhythm of speech.
Asthenia is
the measure of strength of voice. It is most often measured by the subjective
GRBAS scale (Grade of Dysphonia, Roughness, Breathiness, Asthenia, Strain)[9].
Changes of
speech parameters in PD
The vocal changes in PD are influenced by different factors. PD
patients usually speak in a soft, monotone. This monotone speech is perceived
as normal by the patients. The patients lack a feedback between speech and
muscular effort from chest wall and diaphragm[8]. Parkinsonian
dysarthria can affect up to 90% of patients in various stages of disease[10].
Phonatory
impairment is the primary impairment in PD and second more frequent impairment
is the articulation although PD patients usually manifest more speech
abnormalities. For example, alteration of prosody is another manifestation of
PD. Different components of Prosody can be altered, including speech rhythm and
velocity, rate of articulation and speech to pause ratio, intensity of speech,
and variation of pitch[10]. A number studies have confirmed that as
the disease progresses, the voice pitch starts to decrease. Other components
that are usually changed in patients are speech rate and characteristics of
pause. Defects of production were revealed almost in all PD patients, including
frequency reduction and fluctuations of intensity in reading tasks.
In a clinical
trial PD patients (without pharmacotherapy) were compared to the group of
healthy controls in voice functions (jitter, shimmer, noise to harmonics ratios
(NHR)) using sustained vowel phonation. The only phonation parameter that did
not show statistical significances between the study and control group was
pitch variations. Patients in early stages of PD usually don¡¯t have impaired
control of stationary voice pitch during sustained phonation. For all other
measurements of phonation significant differences were observed between the two
groups.
Voice change
such as hoarseness, hypophony, and tremolo are significantly different for all
types of shimmers, jitters, and NHR[5].
Another study has analyzed voice parameters compared to UPDRS scores.
According to the study results roughness, breathiness, and asthenia were more
expressed in patients with PD than in the controls. The obtained values were
higher for both males and females with PD. Males with PD also manifested a
significant increase in roughness. The authors concluded that that
pathophysiological changes in PD alter the voice, but only few significant
correlations were found between the UPDRS and traditional voice indices[9].
Alterations in the auditory system
and altered auditory-motor integration in PD may contribute both the perception
(self-perception) of voice and correspondingly speech production in patients.
An interesting study, that was focused on speech disturbances in PD, revealed
differences between spontaneous or regular speech and text reading. Altered
organization of speech gestures in hypokinetic dysarthria could be caused by
impaired motor planning and disorganization of internal model of motor actions.
This study was based on clinical observations as well as various reports that
cause dysfunction in basal ganglia affecting articulation and phonation, that
are expressed differently in spontaneous and repeated speech. For the
spontaneous speech an internal motor plan is required with consecutive
initiation, execution, and monitoring, and a template is created for repeated
speech, decreasing the load on motor system of speech control[11].
Comparative
efficacy of PD treatment based on voice and speech improvement in patients
Acoustical voice analyses can provide useful information for the
diagnosis of PD in different stages of the pathology, for continuous monitoring
of patients, but first of all, for providing a sound feedback in voice
treatment for therapists[5].
The
significant impact of task on speech motor parameters was evaluated. The task
used to analyze voice disturbance must be taken into account to identify motor
speech processes, and to understand the influence of brain dysfunction not only
on voice, but also on articulation[11].
A special
voice therapy called Lee Silverman Voice Treatment (LSVT) has been studied in
several trials and was shown to be an effective tool for the alleviation of
hypokinetic dysarthria. It affects the increased amplitude of motor output
during speech production by applying increased vocal cord efforts and loudness,
and in this way helps the patients to modulate their vocal output[12].
The trials have revealed statistically significant efficacy of this method on
speech pathology in individuals with various stages of PD. The effects of LSVT
usually last not less than 2-3 years. The obtained data showed that this
methodology improves also swallowing, articulation, improves communicative
gestures, neural functioning and facial expression[13]. Further
efforts of researchers are aimed to develop a computer-based LSVT program which
can increase the efficacy of treatment[14].
All mentioned
trials had derived some common conclusions and recommendations for the
application of LSVT in patients with PD. The first conclusion stated that LSVT
can yield long lasting effects on the speech of patients. The second conclusion
stresses that the method targets different systems that use the same muscles
and nerves to produce speech and ensure the swallowing. In this the method can
result in high efficacy for voice and swallowing recovery[15].
Deep brain
stimulation of the subthalamic nucleus (DBS-STN) results in dramatical
improvement of overall motor functions of the limbs. It effectively reduces
tremor, but shows not stable results in speech rehabilitation. several studies
that were focuses on the efficacy of DBS in patients with PD have shown
controversial results. Some of them have reported speech problems as side
effects in patient receiving DBS after implantation. Others mentioned no
changes in speech disturbances, and the third group has revealed an actual
improvement. This diversity of results are most likely secondary, such as
lesions induced by stimulating electrodes, difference in the stage of PD,
different disease pattern in studied patient groups[13].
The studies
have reported also high efficacy of DBS when changing the settings of
stimulation and selecting zones away from motor control centers. A number of
studies emphasize the differences within an individual in the effects of
stimulation on the two speech subsystems. These findings should temper global
statements about the effect of neurostimulatory implants on Parkinsonian
patients. They also emphasize how important careful consideration of individual
differences may have on the effect of deep brain stimulation on different
subsystems of speech[16]. DBS affects the respiratory and laryngeal
control not similarly. High-frequency stimulation results in respiratory overactivation which results
in excessive closure of vocal folds. On the contrary low frequency stimulation
has more beneficial influence. According to the statement of the authors the
most important aspects in the rehabilitation of PD patients are not only the
difference between high- versus low-frequency stimulation, but also between
speech and limb function[17].
Electrical
stimulation of the subthalamic nucleus aims to modulate the activity of the
basal ganglia. The method is rather effective in the motor recovery, but in
general does not affect the speech pattern. In the same way the pharmacological
therapies (levodopa) are not as effective for speech as they are for motor
functions.
These data
underline differences in the relationship between speech and nonspeech motor
control systems in PD and point out the complex input of these factors. DBS may
have different effects on different components of motor speech processes in
different and in some cases even in an opposite way. All these arguments make
it rather difficult to compare effects of DBS on various elements of motor
speech[18,19]. This difficulty is due to the complex pathogenesis of
PD as the brain tissue alteration progresses on different brain structures
based on their neurobiological characteristics rather than merely increasing
degeneration in a restricted neuroanatomical zone. This fact points to a
possibility that degeneration alters different transmitter systems.
Different drug
groups have been developed to treat PD. Some of these drugs potentiate (DA
agonists) or substitute (L-dopa) the DA in the brain of patients with PD.
Treatment options for the Parkinson's disease include: anticholinergic agents,
monoamine oxidase-B (MAO-B) inhibitors, and catechol-O-methyl transferase
(COMT) inhibitors[20,21]. Pharmacotherapy of PD was initiated with
anticholinergic agents which have been used for years. Blocking the action of
acetylcholine (ACh), they reduce tremor which is caused by the deficiency of DA[22].
Little improvement in articulation was observed after the administration of
anticholinergic agents[23]. MAO-B inhibitors such as Deprenyl stop
the degradation of DA and may potentiate the L-dopa action. Deprenyl has been
shown to improve speech in both subjective and objective measures of
articulation and respiration[24]. Articulatory improvements were
observed in oral motor diadochokinesis and respiratory improvements were
revealed in values of vital capacity and number of words pronounced per
exhalation[24]. Though speech improvement was not found to be as
significant as motor symptoms, the speech parameters were improved to a certain
level by L-dopa therapy¡±. Patients were evaluated by an oral reading task, and
speech rate, pauses, and rhythm were reported as the most improved[25].
Other studies
have studied labial kinematics and muscle physiological responses induced by
L-dopa. Labial movement study revealed a shorter period of time between the
initiation of labial movement and speech, and increased speed and symmetry of
labial activity[26]. This snowed that L-dopa normalizes the neuronal
control of labial movements contributing to the speech improvements in patients
with hypokinetic dysarthria[27]. More recent studies have not shown
significant difference in acoustic measures. Persons with PD had lower
intensity and variability of baseline frequency and intensity, and highly
expressed whisperiness and harshness in PD patients compared to healthy control
subjects and these data did not change after pharmacotherapy[28].
Thus,
presented strategies for the treatment of PD have different impact on speech
recovery. Being a special method of speech therapy LSVT has maximum positive
influence on speech recovery (Table 1). DBS-STN and pharmacotherapy result in
partial recovery of speech and must be followed by such a specialized method of
speech rehabilitation like LSVT (Figure 1). Various tasks have been applied
evaluating the stimulability of speech in Parkinson's disease. These tasks
include automatic speech tasks, maximum phonation time, maximum pitch range and
loud calling. Interesting specific pattern of speech recovery has been reported
by different authors. Partial recovery of speech in patients treated with
DBS-STN, pharmacotherapy and LSVT are presented in the table 1.
Computer based
technology helped to develop new effective
solutions for the treatment of dysarthria in patients with PD. These
technologies provide effective delivery of drugs, long term and high efficacy
of rehabilitation[29-31]. Recent studies have shown the impact of
telepractice and different software programs on treatment efficacy for LSVT
LOUD[32-35]. Tindall et al[105] conducted a cost
analysis comparing in-person effectiveness of LSVT LOUD versus the telepractice
application. The in-person treatment required 51 hours for 16 visits and
$1222.00 for total expenses, whereas the telepractice method required 16 hours
of time and $970.00.
A special
software program has been developed to register acoustic data and create an
interactive feedback for patients treated with LSVT LOUD exercises.
Telepractice and software programs will increase accessibility of LSVT method.
The use of this technology is not LSVT specific and has a potential to increase
accessibility, enhance effectiveness, and reduce financial burden of many
intensive rehabilitation programs for people with PD.
Animal models
of PD to study movement and exercise have been described and used in a large number
of studies but no analogous models were developed to study vocalization
deficits. Only recently new models were developed to study vocalmotor deficits
following dopamine depletion in rodents and songbirds[36-38].
Effective animal models can improve our understanding of voice/speech deficits
in PD and reveal the therapeutic value of these interventions to inhibit
voice/speech symptom progression in patients with PD.
Future
research will focus on the underlying mechanisms of treatment caused changes
that have a positive impact on speech and quality of life in patients with
Parkinson disease.
Our
Research Strategy
Our ongoing study in LSVT and combined treatment is focused on issues
related to the significance of comparing two treatment strategies: LSVT LOUD
which trains vocal loudness and LSVT ARTIC which is articulation training. LSVT
LOUD tries to reach the healthy level of vocal loudness using variety of speech
tasks: high/low vowels, sustained vowels, speech hierarchy and functional
phrases. LSVT ARTIC uses high-force articulation or pronunciation using special
speech tasks: diadochokinesis and functional phrases.
Preliminary
data that were obtained in one year period revealed better post-rehabilitation
results in LSVT LOUD. patients in both groups were evaluated by testing the
single-word intelligibility in noise conditions[39] and using the
Facial Action Coding System (FACS)[40].
Summarizing
the above data that present the etiology of dysarthria in pathients with
Parkinson's disease, we have underlined the most important aspect of that - the
dysarthria is not purely dopaminergic, and therefore traditional pharmacotherapy
or DBS for motor defects do not target the speech problems. Voice therapy can
be very helpful, especially for mild to moderate cases of PD. Other methods,
including electrical stimulation of the subthalamic nucleus or Deep Brain
stimulation have distributed controversial results. Application of DBS or
stimulation of the subthalamic nucleus requires individual approach and
detailed analysis of manifestations and various radiologic examination data in
patients with PD. LSVT LOUD remains as a better option for the speech therapy
in patients with PD.
CONFLICT OF INTERESTS
The authors have no conflicts of interest to declare.
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Peer reviewer: Gjumrakch
Aliev, President and Founder GALLY International Biomedical Research Institute.
Professor of Cardiovascular, Neuropathology and Gerontology, GALLY
International Biomedical research Inst., Inc., 7733 Louis Pasteur Drive, #330,
San Antonio, TX 78229, USA; Min Kong, Department of Neurology, Yan tai shan
Hospital, Shan dong Province, 264000, China.
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