Hardik Kothare, Sarah Schneider, Katherine Yung, Leighton Hinkley, Danielle Mizuiri, Susanne Honma, Coleman Garrett, Molly Naunheim, Mark Courey, Srikantan Nagarajan, John Houde

Spasmodic dysphonia (SD) is a debilitating disorder of voicing where the laryngeal muscles are intermittently in spasm and are dystonic. This prevents the vocal folds from vibrating efficiently and results in involuntary interruptions during speech. The underlying causes of SD remain largely unknown. Prior imaging studies have found aberrant activity in the CNS during SD phonation. However, these studies could not resolve whether SD involves impairment of preparatory, feedforward aspects of vocal control or instead involves abnormal processing of sensory feedback during phonation. To investigate this question, we used Magnetoencephalography (MEG) to monitor neural activity and associated behavioural responses time-locked to glottal onset, phonation onset, and onset of pitch feedback perturbations in adductor SD (AdSD) patients and matched controls.

MEG scanning was performed in 17 patients and 12 controls. Four additional patients participated only in speech psychophysics studies without imaging. Data from 2 patients and 1 control had to be excluded because of large dental or movement artefacts. During scanning, subjects were prompted to start vocalising the vowel /ɑ/ and hold it for the duration of the prompt (2.4 s). Glottal onset was recorded using surface electromyography of pre-phonatory laryngeal muscular activity. On every trial, between 200ms and 500ms after voice onset, the pitch of their auditory feedback was briefly perturbed by +/- 100 cents for a period of 400ms and vocal responses to this change were recorded. We examined induced beta-band (12-30 Hz) neural oscillations over sensorimotor cortices in patients and controls and performed non-parametric statistical tests to observe group differences.

Patients showed an elongated interval between laryngeal movement onset and phonatory onset as well as abnormal pitch perturbation responses. Prior to glottal onset, patients showed reduced task-induced beta band suppression over the left laryngeal motor cortex, left ventral premotor cortex and left inferior frontal gyrus, and enhanced suppression bilaterally in the parietal lobe, especially around the angular gyrus . This abnormal activity in patients near the angular gyrus persisted after glottal onset. Additionally, after phonation onset, patients had increased bilateral suppression around the postcentral gyrus. Following the onset of an auditory feedback perturbation, patients showed increased bilateral frontal lobe suppression. The results suggest that AdSD patients not only have abnormal responses to sensory feedback during phonation, but also have impaired feedforward, preparatory vocal control prior to phonation.