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Open AccessAmerican Journal of Speech-Language PathologyViewpoint1 May 2002Current Perspectives on the Lee Silverman Voice Treatment (LSVT) for Individuals With Idiopathic Parkinson Disease Cynthia M. Fox, MA Chris E. Morrison, Lorraine Olson Ramig, and Shimon Sapir Cynthia M. Fox Contact author: Cynthia M. Fox, MA, Department of Speech and Hearing Sciences. PO Box 210071, University of Arizona, Tucson, AZ, 85721. E-mail: email protected University of Arizona, Tucson Google Scholar , Chris E. Morrison Mount Sinai Medical Center, New York, NY Google Scholar , Lorraine Olson Ramig University of Colorado, Boulder and Wilbur James Gould Voice Center, The Denver Center for the Performing Arts, Denver, CO Google Scholar and Shimon Sapir Wilbur James Gould Voice Center, The Denver Center for the Performing Arts, Denver, CO Google Scholar https://doi.org/10.1044/1058-0360(2002/012) SectionsAboutPDF ToolsAdd to favoritesDownload CitationTrack Citations ShareFacebookTwitterLinked In Successful treatment of speech disorders in individuals with progressive neuro logical diseases can be challenging. Hillman, Gress, Haugraf, Walsh, and Bunting (1990) stated that "voice treatment for disorders that are degenerative is controversial since there is no expectation for recovery of function or that any improvement secondary to speech language pathology intervention will be maintained in the long term" (p. 308). Individuals with idiopathic Parkinson disease (IPD) have been particularly resistant to speech treatment, with the conventional wisdom being summarized by the statement that changes observed in the treatment room disappear on the way to the parking lot (Allan, 1970; Aronson, 1985; Greene, 1980; Sarno, 1968; Weiner Oxtoby, 1982). The reduced ability to communicate is considered to be one of the most difficult aspects of IPD by many patients and their families. Soft voice, monotone, breathy, hoarse voice quality, and imprecise articulation (Darley, Aronson, Logemann, Fisher, Boshes, Kompoliti, Wang, Goetz, Leurgans, Larson, Ramig, Rigrodsky Solomon et al., 2000; Wang, Kompoliti, Jiang, Wolfe, Garvin, Bacon, this has shed light on the neural bases of IPD (Albin, 1995; Brooks, 1995; Hayes, Davidson, Keele, Mink, 1996; Wichmann Weiss, Stelmach, Chaiken, Oxtoby, 1982; Streifler Ramig, Countryman, Thompson, Ramig, Sapir, Countryman, Pawlas, O'Brien, Hoehn, Ramig, Sapir, Fox, Duffy, 1995; Froeschels, Kastein, Hardy, 1967; Rosenbek Yorkston, Beukelman, Boone Colton Stemple, 1993). LSVT integrates these concepts and techniques in a manner specifically designed for individuals with IPD. In addition, LSVT is administered in a manner consistent with principles of exercise science (Brown, McCartney, Frontera, Merredith, O'Reilly, Knuttgen, Yorkston et al., 1988). Treatment challenges and successes have guided our understanding of the basic mechanisms of voice and speech disorders in IPD and the development of our approach to treatment. The purpose of this paper is to share current perspectives on LSVT by integrating outcome data within an explanatory motor perspective supporting the role of phonation as an efficacious treatment approach for individuals with IPD and to suggest that sensory processing deficits, as well as neuropsychological changes, may be important considerations for speech treatment approaches with this population. Development and Outcomes of LSVT From a Motor Perspective Disordered voice and speech characteristics of individuals with IPD are frequently related to the motor signs of the disease (rigidity, bradykinesia, hypokinesia, tremor). Reduced amplitude of movement (hypokinesia) and slowed movement (bradykinesia), which are observed across motor systems in individuals with IPD, have been associated with reduced excitation of the cortical motor centers from the basal ganglia and subsequent reduced drive to motoneuron pools (Penny Hallet and Khoshbin, 1980; Tatton, Eastman, Bed-ingham, Verrier, Wisendanger Ramig, Countryman, et al., 1995; Ramig et al., 1996), which were maintained as long as 12 months posttreatment in some individuals with IPD (Sapir, Ramig, Hoyt, Sapir, Ramig, Hoyt, O'Brien, in review) for individuals who received LSVT but not an alternative treatment (see Smith et al., 1995). It is important to recognize that training increased loudness in individuals with IPD results in a loudness level within normal limits and with a healthy voice quality (i.e., not a pressed or shouted voice); therefore, there was no evidence of increased hyperfunction (ventricular hyperadduction or anterior-posterior foreshortening) posttreatment (Smith et al., 1995). In contrast, mild-to-moderate hyperfunction observed pre-treatment in some individuals with IPD—which was hypothesized to be compensation for hypoadduction of true vocal folds—resolved post-LSVT (Countryman, Hicks, Ramig, Smith et al., 1995). Finally, preliminary data from laryngeal EMG in two individuals with IPD have documented positive increases in thyroarytenoid (TA) muscle activity post-LSVT from a pretreatment reduction in TA activity—as compared to healthy aging individuals (Ramig, Sapir, et al., 2000). Taken together, these findings support the impact of intensive loudness training on the phonatory source for individuals with IPD and are consistent with the hypothesis that increasing drive to the respiratory and laryngeal systems increases amplitude of vocal output, thereby improving vocal loudness and quality. Additional outcome data from LSVT suggest that vocal loudness training may stimulate increased amplitude and coordination of motor output (beyond the phonatory system) to the orofacial system as well. Improvements in articulation have been documented following LSVT as reflected in measures of formant transition duration, rate and extent of movement (Dromey, Ramig, Ramig, Sapir, et al., 2000; Wohlert Caligiuri, 1989; Connor, Abbs, Cole, Forrest, Weismer, Turner, 1989; Leanderson, Meyerson, Netsell, Daniel, Eccles, 1980) and the vocal expression of emotion (Cummings, Benson, Houlihan, Jurgens Meyers, 1976; Porges, 1995). In addition, positive improvements in the nonspeech motor function of swallowing in eight individuals with IPD having a mild swallowing disorder (El Sharkawi et al., 1998, 2002) have been reported. El Sharkawi et al. (2002) documented a 51% reduction in swallowing motility disorders for these individuals on several bolus types. The swallow disorders that resolved with voice treatment were oral-tongue and tongue-base disorders. These swallowing observations may be considered in light of a recent report (Ward, Theodoros, loudness scaling is a task we engage in all our lives. For example, it is common to increase loudness to improve speech intelligibility when speaking against noise or when the listener is far away. Therefore, intensive loudness training may provide the stimulation needed for individuals with IPD to activate and appropriately modulate speech motor programs that are still intact. Accordingly, increasing loudness does not involve deautomatization of speech production by requiring individuals to focus on specific speech parameters such as rate, pauses, or articulatory precision; rather the speaker simply speaks louder (Dromey, 2000; Klienow et al., 2001; Ramig, Pawlas, et al., 1995). Furthermore, training loud phonation may modify vocal behavior by targeting an emotive, phylogenetically old neural system, which involves the limbic system, basal ganglia, thalamus, and periaquaductal gray and the circuits that interconnect these subsystems (Cummings et al., 1983) This observation is supported by recent PET work that demonstrated increased activity in paralimbic regions (left anterior insula and, to a lesser extent, anterior cingulate cortex) post-LSVT, suggesting a greater mobilization of corticolimbic circuits involved in emotional communication (Liotti et al., 1999, in review). The specificity of treatment effects to training vocal loudness versus alternative treatment goals, such as over articulate, remains to be determined Although studies of LSVT for individuals with IPD are promising, there are clearly limitations to our existing knowledge. 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