Sanaz Khosravani1, Arash Mahnan2, I-Ling Yeh3, Peter J Watson4, Yang Zhang4, George Goding5, Jürgen Konczak2. 1. Human Sensorimotor Control Laboratory, School of Kinesiology, University of Minnesota, United States. Electronic address: khosr023@umn.edu. 2. Human Sensorimotor Control Laboratory, School of Kinesiology, University of Minnesota, United States. 3. Human Sensorimotor Control Laboratory, School of Kinesiology, University of Minnesota, United States; Department of Occupational Therapy, National University of Singapore, Singapore. 4. Department of Speech, Language, and Hearing Sciences, University of Minnesota, United States. 5. Department of Otolaryngology, University of Minnesota, United States.
Abstract
OBJECTIVE: Spasmodic dysphonia (SD) is a debilitating voice/speech disorder without an effective cure. To obtain a better understanding of the underlying cortical neural mechanism of the disease we analyzed electroencephalographic (EEG) signals of people with SD during voice production. METHOD: Ten SD individuals and 10 healthy volunteers produced 50 vowel vocalization epochs of 2500 ms duration. Two EEG features were derived: (1) event-related change in spectral power during vocalization relative to rest, (2) inter-regional spectral coherence. RESULTS: During early vocalization (500-1000 ms) the SD group showed significantly larger alpha band spectral power over the left motor cortex. During late vocalization (1000-2500 ms) SD patients showed a significantly larger gamma band coherence between left somatosensory and premotor cortical areas. CONCLUSIONS: Two atypical patterns of cortical activity characterize the pathophysiology of spasmodic dysphonia during voice production: (1) a reduced movement-related desynchronization of motor cortical networks, (2) an excessively large synchronization between left somatosensory and premotor cortical areas. SIGNIFICANCE: The pathophysiology of SD is characterized by an abnormally high synchronous activity within and across cortical neural networks involved in voice production that is mainly lateralized in the left hemisphere. Published by Elsevier B.V.
OBJECTIVE:Spasmodic dysphonia (SD) is a debilitating voice/speech disorder without an effective cure. To obtain a better understanding of the underlying cortical neural mechanism of the disease we analyzed electroencephalographic (EEG) signals of people with SD during voice production. METHOD: Ten SD individuals and 10 healthy volunteers produced 50 vowel vocalization epochs of 2500 ms duration. Two EEG features were derived: (1) event-related change in spectral power during vocalization relative to rest, (2) inter-regional spectral coherence. RESULTS: During early vocalization (500-1000 ms) the SD group showed significantly larger alpha band spectral power over the left motor cortex. During late vocalization (1000-2500 ms) SDpatients showed a significantly larger gamma band coherence between left somatosensory and premotor cortical areas. CONCLUSIONS: Two atypical patterns of cortical activity characterize the pathophysiology of spasmodic dysphonia during voice production: (1) a reduced movement-related desynchronization of motor cortical networks, (2) an excessively large synchronization between left somatosensory and premotor cortical areas. SIGNIFICANCE: The pathophysiology of SD is characterized by an abnormally high synchronous activity within and across cortical neural networks involved in voice production that is mainly lateralized in the left hemisphere. Published by Elsevier B.V.
Authors: Kristina Simonyan; Julie Barkmeier-Kraemer; Andrew Blitzer; Mark Hallett; John F Houde; Teresa Jacobson Kimberley; Laurie J Ozelius; Michael J Pitman; Robert Mark Richardson; Nutan Sharma; Kristine Tanner Journal: Neurology Date: 2021-04-15 Impact factor: 11.800