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Neurology 2003;60:432-440
© 2003 American Academy of Neurology

Hypophonia in Parkinson’s disease

Neural correlates of voice treatment revealed by PET

M. Liotti, MD PhD, L.O. Ramig, PhD, D. Vogel, PhD, P. New, MD, C.I. Cook, MS, R.J. Ingham, PhD, J.C. Ingham, PhD and P.T. Fox, MD

From the Research Imaging Center (Drs. Liotti and Fox, C.I. Cook) and the Departments of Medicine (Neurology) (Drs. Liotti, Vogel, New, and Fox) and Radiology (Drs. Liotti and Fox), University of Texas Health Science Center at San Antonio; The Department of Speech, Language and Hearing Science (Dr. Ramig), University of Colorado at Boulder; The Wilbur James Gould Voice Center (Dr. Ramig), Denver, CO; The Department of Speech Communication Disorders (Dr. Vogel), Our Lady of the Lake University, San Antonio, TX; and The Department of Speech and Hearing Sciences (Drs. R.J. Ingham and J.C. Ingham), University of California, Santa Barbara.

Address correspondence and reprint requests to Dr. Mario Liotti, Division of Psychiatry, School of Community Health Sciences, University of Nottingham, A Floor, South Block, Queens Medical Centre, Nottingham NG7 2UH, UK; e-mail: mario.liotti{at}nottingham.ac.uk

Objective: To investigate the neural correlates of hypophonia in individuals with idiopathic PD (IPD) before and after voice treatment with the Lee Silverman Voice Treatment method (VT) using 15O-H2O PET.

Methods: Regional cerebral blood flow (rCBF) changes associated with overt speech–motor tasks relative to the resting state were measured in the IPD subjects before and after VT, and in a group of healthy control volunteers.

Results: Behavioral measures of voice loudness significantly improved following treatment. Before VT, patients had strong speech-related activations in motor and premotor cortex (M1-mouth, supplementary motor cortex [SMA], and inferior lateral premotor cortex [ILPm]), which were significantly reduced post-VT. Similar to the post-treatment session, premotor activations were absent (SMA) or below statistical threshold (M1-mouth) in the healthy control group. In addition, following VT treatment, significant right-sided activations were present in anterior insular cortex, caudate head, putamen, and dorsolateral prefrontal cortex (DLPFC). Finally, the VT-induced neural changes were not present with transient experimenter-cued increases of loudness in VT-untreated patients.

Conclusions: Effective improvement of IPD hypophonia following voice treatment with VT was accompanied by a reduction of cortical motor–premotor activations, resembling the functional pattern observed in healthy volunteers and suggesting normalization, and additional recruitment of right anterior insula, caudate head, putamen, and DLPFC. This treatment-dependent functional reorganization suggests a shift from an abnormally effortful (premotor cortex) to a more automatic (basal ganglia, anterior insula) implementation of speech–motor actions.




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