The LSVT Story…
Nearly ninety percent of the six million individuals with Parkinson disease (PD) worldwide have a speech or voice disorder . Neuropharmacological and neurosurgical treatments for PD, do not make a positive or lasting impact on speech in PD at this time (Schultz and Grant, 2000). Given recent neuroscience breakthroughs (e.g., Fisher, Petzinger, Nixon et al., 2004; Tillerson, Cohen, Philhower et al., 2001), there are great opportunities in rehabilitation today for speech treatment to be a routine, integral part of disease management in PD. Efficacious speech treatment offers the opportunity to improve quality of life in individuals with PD beyond what neurosurgical and neuropharmacological treatments offer.Today LSVT® (Lee Silverman Voice Treatment) is the speech and voice treatment for PD with Level 1 evidence (Pinto et al., 2004; Trail et al, 2005; Yorkston, Spencer, & Duffy, 2003) and it is being delivered by speech clinicians in over 40 countries around the world. The LSVT differs from previous forms of speech treatment for PD in both the treatment target and the mode of treatment delivery. The fundamental principles of LSVT are based upon the pathological mechanisms hypothesized to underlie voice and speech disorders in people with PD (Fox, Morrison, Ramig, & Sapir, 2002) : (1) an overall amplitude scale down of speech motor output (reduced amplitude of neural drive to the muscles of the speech mechanism) that may result in reduced vocal loudness (hypophonia), reduced pitch inflection (hypoprosodia) and reduced range of articulatory movements (hypokinetic articulation) (Albin, Young, & Penny, 1989; Penny & Young, 1983: Barbeau et al., 1962); and (2) problems in sensory perception of vocal effort and speech movements that prevent a person with PD from accurately regulating (internal cueing/scaling) the optimal amount of effort to produce adequate loudness (Demirci, Grill, McShane, & Hallet, 1995; Stelmach et al., 1991).
LSVT targets amplitude training (increased vocal loudness) as a single motor control parameter. It incorporates: (1) enhancing the voice source, which is consistent with improving the carrier in the classic engineering concept of signal transmission (Titze, 1993); (2) using vocal loudness as a trigger for distributed system-wide effects across the speech production system; (3) recalibration of vocal loudness and effort so individuals with PD integrate improved loudness into functional communication; and (4) training the individual to rely on his own resources (internal cueing and self-monitoring) to independently control and sustain adequately scaled speech motor output. The result is reduction or elimination of hypophonia, hypoprosodia, and hypokinetic articulation characteristics of the dysarthria associated with PD (Sapir, Ramig and Fox, 2008).
It is critical to recognize that the loudness target in LSVT is a healthy increase in vocal loudness. Patients are not trained to ‘yell or scream or to use pressed voice', rather the speech clinician trains a voice that has improved loudness with healthy voice quality.
On the surface, the simplicity of a single, simple over learned treatment target for patients “be LOUD” may make it feasible for these individuals with cognitive and learning challenges to successfully improve functional speech production in daily living (Fox et al., 2002). Beneath the surface simplicity of the target “be LOUD”, the speech clinician is delivering a well-integrated training program which is designed to directly address the complexity underlying the speech problem experienced by patients with PD (Sapir et al., 2008).
The mode of delivery of LSVT also differs from traditional forms of speech treatment. It requires intensive, high effort speech exercise combined with a simple, redundant and salient treatment target to facilitate transfer of loudness into functional daily living. The standardized protocol for LSVT embodies many of the fundamental principles of exercise and motor training that have been shown to promote neural plasticity and brain reorganization in animal models of PD (Fisher et al., 2004) and human stroke-related hemiparesis (Liepert et al., 1998). Our ability to embrace these principles and integrate them into the mode of delivery of treatment will be essential for advancing rehabilitation science in parallel with neuroscience. While the standardized protocol for LSVT was developed before these recent neuroscience investigations, it adheres to key principles of neural plasticity ( intensity, complexity, saliency, use it or lose it, and use it and improve it ) which are likely additional explanations for why LSVT has been successful (Fox et al., 2006; Farley, Fox, Ramig and McFarland, in press).
What is the story of LVT? How did we get to where we are today?
In 1983, Dr. Wilbur Gould walked into the acoustics lab at the Recording and Research Center of the Denver Center for the Performing Arts and said to me, “Lori, I have a friend who has a Parkinson disease (PD) treatment program and he needs a speech therapist, can you help him?” At the time, I was an Assistant Professor on a tenure track in the Department of Speech, Language and Hearing Science at the University of Colorado-Boulder and the Recording and Research Center in Denver was my primary research lab. I was working diligently to develop a fundable research program which would allow me to study “my current passion”: acoustic analysis of voice in aged individuals and those with neurological diseases.Of course I followed Dr. Gould's advice and met his friend in Estes Park , Colorado at the location of his PD treatment program. It was here that I had my very first encounter with individuals with PD. Shortly thereafter, during one of my monthly trips to Estes Park , I was introduced to a group of professionals who were developing a PD treatment program in Scottsdale , Arizona . They invited me to visit Scottsdale and to meet the family who was initiating the program in honor of their wife and mother, Mrs. Lee Silverman, who had been diagnosed with PD.
“If only we could hear and understand her” wished Mr. Ray Silverman and his adult children Tom and Carol regarding Mrs. Silverman, when I first met them in Scottsdale . At the time, speech treatment for patients with PD was considered to be unsuccessful. The consensus among the professional communities was “changes in the speech treatment disappear on the way to the parking lot” and while nearly 90% of patients with PD had a speech problem, only 4% received speech treatment.
The Silverman family found their inability to communicate with Mrs. Silverman most difficult. They challenged me to develop a speech treatment to help their mother communicate and invited me to set up a speech treatment program at their newly evolving “ Lee Silverman Center for Parkinsons” in Scottsdale . The Lee Silverman Center program was designed to be a month long, daily multi-disciplinary program to include medical care, physical therapy, occupational therapy, speech therapy, family support, nutrition and recreation.
Because the Silverman family was particularly concerned about speech in PD, they agreed to my request to fund a speech research lab within the clinical facility and hired a student of mine (Carolyn Mead Bonitati), a recent graduate of the University of Colorado-Boulder, to be the speech clinician in residence. My role was to design the speech treatment program and collect and analyze once a month pre-, post- and follow-up speech treatment data.
In 1985, the ‘seeds were sown' for what is known today as LSVT. At the time, most speech treatment approaches for PD focused on the classic articulation and rate problems in these patients. However, since I came from the world of voice, my instinct was to treat the voice disorder which included soft volume, monotone, hoarseness and breathiness. We developed a physiologically-based treatment program that we thought (naively at the time) focused primarily on laryngeal function. Our target was vocal fold adduction as an avenue to improve vocal loudness and quality. In order to motivate patients, we designed the treatment to be a high effort exercise program which combined voice exercises and generalization in to speech production. The treatment was designed to continuously push patients to new vocal effort levels (e.g., “louder, longer”). As a result, patients were highly engaged in physical exercise of their voices for 60 minutes a day within treatment sessions and had daily assignments to use their newly trained louder voice outside of the treatment room. As a part of the Lee Silverman multi-disciplinary program, the treatment was delivered at an intense dosage of four to five hours a week. High effort physical exercise and intense dosage of delivery remain fundamental elements of what is known as LSVT today .
Our initial approach to speech treatment focused on the motor symptoms underlying the disordered voice in these individuals with PD. However, very soon into the delivery of treatment, we noticed the significant sensory problems that challenged these patients. Soft talking individuals with PD would deny that they were too soft, but claim “my spouse needs a hearing aid”. When they were stimulated to
increase loudness to a normal level, they would complain, “I feel like I am shouting”. Thus, we enhanced the treatment to address these sensory problems. We referred to these sensory retraining activities as “calibration”. Today we recognize that this sensory mismatch together with deficits in internal cueing are two of the most challenging aspects of successfully treating speech in people with PD.
In 1985-86, I was traveling to Scottsdale once a month clinically evaluating the speech and voice in these patients as well as gathering outcome data. I found the Parkinson treatment work extremely satisfying but I was becoming concerned about the time that I was spending on this project in relation to my goal of establishing a fundable research program in my tenure track position. One day I was discussing this with Ron Scherer, a voice scientist at the Recording and Research Center . I got a significant piece of advice from Ron, “Lori, make the treatment your research!” A light bulb went on and I took this advice to heart!
At that time, speech treatment research was in its infancy. Our field was unaware of the paradigms for scientifically documenting behavioral treatment effects that are well-known today (e.g., Robey and Schultz, 1998). In 1988, we presented our first treatment outcome research paper (which would today be considered Phase 1 work) and first video tape of two individuals with PD pre to post-treatment to a group of expert researchers and clinicians at the Motor Speech conference in San Diego and received “mixed reviews”. One of the pillars in our field said to me, “Well Lori, you may have stumbled on to something” and another pillar said, “You have clearly measured all the wrong variables.” When our idea of intensively teaching patients with PD to increase vocal loudness reached the professional voice community, they universally were certain that we would provoke an outbreak of vocal hyperfunction in the PD community. We however remained extremely interested in what we were seeing clinically and our next step was to study it scientifically.
Our first federal research grant was awarded in 1989 by the National Institute of Disability and Rehabilitative Research (NIDRR), followed soon after in 1990 by our first R01 from the National Institutes of Health, National Institutes of Deafness and other Communicative Disorders (NIH-NIDCD). This year, 2007, we were fortunate enough to be awarded our fourth R01 from NIH-NIDCD to continue our studies until the year 2012.
The Recording and Research Center (known from 1994-2000 as the Wilbur James Gould Voice Research Center ) and since 2000 as the National Center for Voice and Speech (NCVS)) became the home for these studies. New team members were added including speech clinicians Stefanie Countryman and Annette Pawlas as well as otolaryngologist Marshall Smith. Between 1994 and 1995 we collected data at the University of Arizona-Tucson and added Cynthia Fox to the team. Jennifer Spielman (a University of Colorado graduate student at the time) began working with us as well. Shortly thereafter we added speech clinician, Angela Halpern and later speech clinician, Jill Petska. We learned very quickly the value of a team that combines scientific knowledge and passion with ‘real world' delivery of treatment and clinical knowledge. Today, we view the ability to span this ‘clinical to science' continuum as an essential element in the world of treatment research. Over the years we have observed consistently that ‘treatment outcomes can guide basic understanding of neurological condition'.
We designed two randomized control trials (RCT), one to study the efficacy of intensive respiratory treatment compared to intensive respiratory and laryngeal treatment and another to evaluate treatment outcomes with an untreated PD and healthy age-matched control groups. We wanted to address three questions: 1) which treatment (respiratory or respiratory and laryngeal) would make the biggest impact in patients with Parkinson disease, 2) would treatment effects be lasting and 3) what physiologic changes accompany successful treatment. Some of the outcomes of our work have been included in this volume:
Ramig, L., Sapir, S., Countryman, S., Pawlas, A., O'Brien, C., Hoehn, M., and Thompson, L. (2001) Intensive voice treatment (LSVT) for individuals with Parkinson disease: a two-year follow-up. J. Neurology, Neurosurgery and Psychiatry . 71, 493-498.
Smith, M., Ramig, L., Dromey, C., Perez, K., and Samandari, R. (1995) Intensive voice treatment in Parkinson's disease: laryngostroboscopic findings. J. Voice , 9, 453-459.
Of particular interest were the videostroboscopic data documenting for the first time the physiologic basis for improved vocal loudness in PD following what was then known as respiratory and laryngeal treatment compared to respiratory treatment alone. We concluded after this series of studies that respiratory and laryngeal treatment had more consistent, significant and lasting effects on speech production in individuals with PD in the short and long-term than did respiratory treatment alone.
The data published in 2001 (Ramig, Sapir, Countryman, et al., 2001) reported on patients followed for two years after one month of treatment and have been considered the first Level 1 evidence for a speech treatment for PD (Goetz, 2005). The second RCT (Ramig, Sapir, Fox, et al., 2001) reported that respiratory and laryngeal treatment resulted in significant increases in SPL post treatment and at 6 months follow-up when compared with pre-treatment levels. No significant changes were observed over the same period in an untreated PD control group and untreated age-matched healthy control group.
By this time, the Lee Silverman Center for Parkinsons no longer existed. Nevertheless, I asked Mr. Silverman's permission to name the speech treatment in honor of Mrs. Silverman, who by that time had passed away. From that point on the “respiratory and laryngeal” treatment has been known as the Lee Silverman Voice Treatment or LSVT, in honor of Mrs. Silverman.
In 1995 our team wanted to address the underlying mechanism of the laryngeal disorder in PD as well as the neural bases of treatment-related change. We began our collaboration with physiologists Erich Luschei , Shimon Sapir and Kristin Larson Baker as well as the University of Texas San Antonio imaging Center and the group lead by Peter Fox, MD. The outcomes of those studies are been summarized in these publications:
Baker, K., Ramig, L., Luschei, E., and Smith, M., (1998). Thyroarytenoid muscle activity associated with hypophonia in Parkinson disease and aging. Neurology . 51:6, 1592-1598.
Luschei, E., Ramig, L., Baker, K., and Smith, M. (1999) Discharge characteristics of laryngeal single motor units during phonation in young and older adults and individuals with Parkinson disease. J. Neurophysiology . 81, 2131-2139.
Liotti, M., Vogel, D., Ramig, L., New, P., Cook, C., Ingham, R., Ingham, J., and Fox, P. (2003) Hypophonia in Parkinson disease: neural correlates of voice treatment revealed by PET. Neurology . 60, 432-440.
Our physiologic findings supported the idea of reduced amplitude in laryngeal muscles of individuals with PD pre-treatment when compared with a healthy aged matched control group and were consistent with our treatment goal of scaling up amplitude to the speech mechanism.
Of particular interest were the neural imaging findings. Preliminary studies of PET related changes pre post LSVT documented treatment-dependent functional reorganization in people with PD. These findings included recruitment of the right hemisphere, and activation of central sensorimotor regions in the left hemisphere, such as the thalamus and pre-supplementary motor area (Liotti et al., 2003) These were the first data to identify the neural bases of treatment-related change following LSVT. A second study (Narayana et al., 2005) has confirmed these findings.
In 1998, I went on a sabbatical to New York City to spend time in the medical world of neurolaryngology. I was based at Mt. Sinai Medical Center and Columbia University .
This experience opened my eyes to a bigger world of medical neurology. The perspectives I gained through working with Mitchell Brin, Andy Blitzer, Ira Sanders and Don Wiesz among others helped us develop new ways of thinking about fundamentals of LSVT at peripheral as well as central levels. It was during this time that I met neuropsychologists Chris Morrison and Joan Borod. Chris helped us understand the value of the simple, redundant nature of LSVT as a feasible way for individuals with Parkinson disease with neuropsychological challenges to actually learn a new behavior (Fox et al., 2002). Joan's insight in to facial analysis helped motivate our documentation of the effects of LSVT that went well beyond the larynx.
While our initial treatment focus was to target vocal loudness through laryngeal function,
by 2000 it had become increasingly clear from our research and ongoing clinical experiences, that loudness training, was making a significant impact across the speech production mechanism to positively effect articulation and facial expression as well. In fact, we have now generated pilot data that LSVT effects generalize beyond vocal loudness to make a positive impact on swallowing, articulation, communicative gestures, facial expression, and neural functioning (Duncan, 2002; El Sharkawi et al., 2002; Liotti et al., 2003; Spielman, Borod and Ramig, 2003; Sapir et al, 2007).
Today, we are actively conducting randomized controlled trials (RCT) and are further examining this transfer of effects by (1) evaluating and comparing the system-wide generalized impact of two therapies [voice (LSVT-LOUD) and articulation (LSVT-ENUNCIATE)] on speech articulation, facial expression, swallowing in PD, and the system-wide generalized impact of these two therapies on limb gesture and limb motor functioning in PD. Functional imaging investigations (PET) of these two treatments will be used to identify changes in neural connectivity and functioning and identify any differences associated with these different treatment targets. Results from these studies will further clarify the neural bases for voice and speech disorders in people with PD as well as guide development and modifications for optimal speech treatment approaches for this population. We hypothesize that LSVT LOUD will recruit a wider network of brain regions than is normally seen during speech production, including enhanced basal ganglia function, phylogenetically old brain regions (including the insula and anterior cingulate gyrus) and right (non-dominant) hemisphere regions associated with amplitude scaling, emotive vocalization and prosody. In contrast, we hypothesize that LSVT ENUNCIATE will recruit pre-motor (chiefly of the left (dominant) hemisphere) and primary motor (M1) regions chiefly of the left (dominant) hemisphere in a pattern typical of normal speech production, and will not demonstrate recruitment of non-motor regions or right-hemispheric regions which are hypothesized for LSVT LOUD. We speculate that these changes will be associated with differential changes in behavior. We are fortunate to have a core team that includes researchers in speech treatment, physiology, swallowing, facial expression, communicative gesture, neuropsychology, neurology and otolaryngology to help us address these issues.
LSVT has evolved over the years through the wisdom of colleagues and collaborators who have enlightened our vision from a laryngeal loudness focus, to address sensory and neuropsychological elements of treatment and to today embrace the realities of neural plasticity. As we learn more, our perspectives on LSVT are further enhanced. Our ongoing research is addressing a range of topics including application of LSVT beyond PD to other adult and pediatric neurological conditions (e.g., multiple sclerosis, ataxia, cerebral palsy and stroke) (Sapir, Spielman et al., 2003; Sapir, Pawlas et al., 2001; Fox, Boliek et al., 2005; Mahler, 2007) , the application of principles of LSVT to physical therapy in PD (LSVT BIG) (Farley and Koshland, 2005) the hybrid treatment of combined LSVT BIG and LOUD (Farley, Fox, et al., in press), development of an animal model to evaluate the potential neuroprotective effects of physical and voice exercise (Ciucci, Ma, Fox et al., 2007) and use of technology to make delivery of intensive treatment dosage feasible globally (Halpern, Matos et al., 2005).
The potential of speech treatment to make an important impact on quality of life in individuals with Parkinson disease and other neurological disorders, while providing insight into the neural bases of these disorders and the underlying mechanism of treatment-related change, is a world that continues to offer humbling challenges and great satisfaction. We continue to be motivated to address this request for patients around the world:
“if only we could hear and understand her.”—family of Mrs. Lee Silverman
Funding acknowledgments and disclosures: Dr. Ramig is a Professor at the University of Colorado-Boulder, a Senior Scientist at the National Center for Voice and Speech ( Denver ) and an Adjunct Professor, Columbia University , New York City. The research reported in this article has been supported in part by funding from NIH-NIDCD R01 DC001150, NIH-NIDCD R21 DC 05583 and NIH-NINDS R21 NS043711.
Disclosure Statements: Dr. Ramig receives a lecturer and travel honorarium from the LSVT Foundation (non-profit organization), a consulting honorarium from the Kinetics Foundation (non-profit organization), receives a lecture honorarium and has intellectual property rights and ownership interest in LSVT Global LLC (for-profit organization that delivers training courses and sells products related to LSVT).
References
Albin , R. L., Young, A. B., & Penny, J. B. (1989). The functional anatomy of basal ganglia disorders. Trends in Neuroscience, 12, 366-375.
Barbeau A. , Sourkes T. L., & Murphy C. F. (1962). Les Catecholamines de la Maladie de Parkinson's. In J. Ajuriaguerra (Ed.), Monoamines et Systeme Nerveux Central (pp. 247–262) . Geneve: George, 1962.
Ciucci, M.R., Ma, T.S., Fox, C.M., Kane, J., Ramig, L. & Schallert, T. (2007) Qualitative changes in ultrasonic vocalization in rats after unilateral dopamine depletion or haloperidol: A preliminary study. Behavioural Brain Research, 182 , 284-289.
Demirci, M. , Grill, S., McShane, L., & Hallet, M. (1995). Impairment of kinesthesia in Parkinson's disease. Neurology, 45 , A218.
Duncan , S . (2002, September). Preliminary data on effects of behavioral and levadopa therapies o speech-accompanying gesture in Parkinson's disease. Presentation at the ICSLP meeting, Denver , CO .
El Sharkawi, A. , Ramig, L.O., Logemann, J.A., Pauloski, B.R., Rademaker, A.W., & et al. (2002). Swallowing and voice effects of Lee Silverman Voice Treatment (LSVT®): A pilot study. Journal of Neurology, Neurosurgery, and Psychiatry, 71 , 31-36.
Farley, B., Fox, C., Ramig, L. and McFarland, D. (in press). Intensive amplitude-specific therapeutic approaches for Parkinson disease: toward a neuroplasticity-principled rehabilitation model. Topics in Geriatric Rehabilitation .
Farley, B. & Koshland, G. (2005) Training BIG to move faster: the application of the speed-amplitude relation as a rehabilitation strategy for people with Parkinson disease. Exp Brain Res. 167(3): 462-7.
Fisher, B., Petzinger, G., Nixon, K., Hogg, E., Bremmer, S., Meshul, C., & Jakowec, M. (2004). Exercise-induced behavioral recovery and neuroplasticity in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse basal ganglia. J Neurosci Res., 77 , 378-390.
Fox, C., Boliek, C. and Ramig, L. (2005) The impact of intensive voice treatment (LSVT) on speech intelligibility in children with spastic cerebral palsy. Movement Disorders. 20 (10), p.S149.
Fox, C. M. , Morrison, C. E., Ramig, L. O., & Sapir, S. (2002). Current perspectives on the Lee Silverman Voice Treatment (LSVT) for people with idiopathic Parkinson's disease. American Journal of Speech-Language Pathology, 11 , 111-123.
Fox, C., Ramig, L., Ciucci, M., Sapir, S., McFarland, D., and Farley, B. (2006) The Science and Practice of LSVT®LOUD:Neural Plasticity-Prinicpled Approach to Treating Individuals with Parkinson Disease and Other Neurological Disorders. Seminars in Speech Language. 27 :283-299.
Goetz, C. (2003) Personal communication.
Halpern, A. , Matos, C., Ramig, L., Petska, J., Spielman, J., & Bennett, J. (2005). LSVTC- A PDA supported speech treatment for Parkinson's disease . Presented at the 9 th International Congress of Parkinson's Disease and Movement Disorders, New Orleans , LA.
Liepert, J., Miltner, W., Bauder, H., Sommer, M., Dettmers, C., Taub, E., & Weiller, C. (1998). Motor cortex plasticity during constraint-induced movement therapy in stroke patients. Neuroscience Letters, 250 , 5-8.
Liotti, M., Ramig, L.O., Vogel, D., New, P., Cook, C.I., Ingham, R.J., Ingham, J.C., & Fox, P.T. (2003). Hypophonia in Parkinson's disease. Neural correlates of voice treatment revealed by PET. Neurology, 60, 432-440.
Luschei, E., Ramig, L., Baker, K., and Smith, M. (1999) Discharge characteristics of laryngeal single motor units during phonation in young and older adults and individuals with Parkinson disease. J. Neurophysiology. 81 , 2131-2139.
Mahler, L. (2007) The effects of intensive voice therapy (LSVT) on motor speech disorder secondary to stroke. Unpublished dissertation. University of Colorado .
Narayana, S. , Vogel, D., Brown, S., Franklin, C., Zhang, W., Lancaster , W. J., & Fox P. (2005). Mechanism of action of voice therapy in Parkinson's hypophonia—A PET study . Poster presented at the 11 th Annual Meeting of the Organization for Human Brain Mapping, Toronto , Ontario , Canada .
Penny, J. B. , & Young, A. B. (1983). Speculations on the functional anatomy of basal ganglia disorders, Annual Review of Neuroscience, 6 , 73-94.
Pinto, S. , Ozsancak, C., Tripoliti, E., Thobois, S., Limousin-Dowsey, P., & Auzou, P. (2004). Treatments for dysarthira in Parkinson's disease, Lancet, 3 , 547-56.
Ramig, L., Sapir, S., Countryman, S., Pawlas, A., O'Brien, C., Hoehn, M., and Thompson, L. (2001) Intensive voice treatment (LSVT) for individuals with Parkinson disease: a two-year follow-up. J. Neurology, Neurosurgery and Psychiatry. 71 , 493-498.
Ramig, L. O., Sapir, S., Fox, C. (2001). Changes in vocal loudness following intensive voice treatment (LSVT) in individuals with Parkinson's disease: a comparison with untreated patients and normal age-matched controls. Movement Disorders, 16, 79-83.
Sapir, S., Ramig, L. and Fox, C. (2008) Voice, Speech and Swallowing Disorders. In Factor, S. and Weiner, W (eds.) Parkinson's Disease: Diagnosis and Clinical Management. Demos: New York , pp. 77-97.
Sapir, S., Spielman, J., Countryman, S., Ramig, L., Hinds, S., Fox, C., and Story, B. (2003) Phonatory and articulatory changes in ataxic dysarthria following intensive voice therapy with LSVT®: a single subject study. American J. Speech-Language Pathology , 12, 387-399.
Sapir, S., Spielman, J., Ramig, L., Story, B. & Fox, C. (2007) Effects of intensive voice treatment (LSVT ® )) on vowel articulation in dysarthric individuals with idiopathic Parkinson's disease: Acoustic and perceptual findings. J. Speech Language and Hearing Research, 50, 899-912.
Smith, M., Ramig, L., Dromey, C., Perez, K., and Samandari, R. (1995). Intensive voice treatment in Parkinson's disease: laryngostroboscopic findings. J Voice. 9, 453-459.
Stelmach , G.E. (1991). Basal ganglia impairment and force control. In J. Requin & G.E. Stelmach (Eds.), Tutorial in Motor Neuroscience (pp.147-158). Netherlands : Kluwer Academic Publishers.
Tillerson, J., Cohen, A., Philhower, J., Miller, G., Zigmond, M., & Schallert, T. (2001). Forced limb-use effects on the behavioral and neurochemical effects of 6-hydroxydopamine. Journal of Neuroscience, 21, (12), 4427-4435.
Titze, I. (1993). Vocal fold physiology: Frontiers in basic science. San Diego , CA : Singular Publishing Group Inc.
Trail, M., Fox, C., Ramig, L., Sapir, S., Howard, J. and Lai, E. (2005). Speech treatment for people with Parkinson's disease. Neurorehabilitation . 20, 205-221.
Yorkston, K. M. , Spencer, K.A., & Duffy, J.R. (2003). Behavioral management of respiratory/phonatory dysfunction from dysarthria: a systematic review of the evidence. Journal of Medical Speech-Language Pathology , 11 , xiii – xxxviii.