Supraglottal Hyperadduction in an Individual With Parkinson Disease
Stefanie Countryman, Jennifer Hicks, Lorraine Olson Ramig, and Marshall E. Smith
American Journal of Speech-Language Pathology
Vol. 6, 74–84, DOI:10.1044/1058-0360.0604.74
Recent treatment for voice problems associated with idiopathic Parkinson disease has primarily focused on increasing reduced vocal loudness and improving true vocal fold hypoadduction, common voice deficits observed in these individuals. This study presents an individual with reduced vocal loudness and supraglottic hyperadduction accompanying Parkinson disease and the outcome following a course of the Lee Silverman Voice Treatment (LSVT). Posttreatment observations included increased vocal loudness, decreased supraglottic hyperadduction, and improved intonation and overall voice quality when compared with pretreatment observations. These results suggest that in this individual, supraglottic hyperadduction was due to a secondary compensatory behavior resulting from mild true vocal fold hypoadduction that responded positively to adduction therapy (LSVT). This study also demonstrates the use of a continuum of observations ranging from functional ratings to physiological measures to evaluate the impact of intensive voice treatment and identify mechanisms underlying treatment-related change in an individual with Parkinson disease.
Common neurological disorders, such as Parkinson disease, are often characterized by laryngeal abnormalities that result in voice disorders (Aronson, 1990; Brin, Fahn, Blitzer, Ramig, & Stewart, 1992; Darley, Aronson, & Brown, 1975; Logemann, Fisher, Boshes, & Blonsky, 1978). These disorders may contribute to reductions in vocal loudness, vocal quality, and overall speech intelligibility (Aronson, 1990; Kent et al., 1990; Ramig, 1992). Recently, Ramig and Scherer (1992) and Smith and Ramig (1995) developed an approach to planning behavioral treatment for voice disorders associated with neurological disease. This approach focuses on the disordered laryngeal function in combination with the neurological etiology and is designed to maximize improvement in overall intelligibility as efficiently as possible.
In this approach, the disordered voice is considered in relation to problems of adduction or phonatory instability (Ramig & Scherer, 1992). Disorders of hypoadduction are distinguished from those of hyperadduction. Disorders of hypoadduction are characterized by inadequate true vocal fold closure, reduced loudness, and breathy, hoarse vocal quality. Hypoadduction may accompany a variety of neurological disorders but is typically associated with lower motor neuron (flaccid) disorders, multiple sclerosis (Beukelman, Kraft, & Freal, 1985; Darley, Brown, & Goldstein, 1979; Jensen, 1960), some cases of closed head injury (Vogel & Von Cramon, 1982; Von Cramon, 1981), and Parkinson disease (Hanson, Gerratt, & Ward, 1984; Perez, Ramig, Smith, & Dromey, 1996; Smith, Ramig, Dromey, Perez, & Samandarii, 1995). The type and extent of vocal fold hypoadduction may be associated with the site and extent of the related neurological damage (Aronson, 1990)...