Disordered laryngeal function has been documented in a number of videoendo-scopic and videostroboscopic studies. Hansen et al. (22) reported vocal fold bowing resulting in poor glottic closure in 94% of 32 PD patients, together with greater amplitude of vibration and laryngeal asymmetry. Smith et al. (41), using videostro-boscopic observations, found that 57% of 21 PD patients had a form of glottal incompetence (bowing, anterior or posterior chink) on fiberoptic examination. Perez et al. (42) observed laryngeal tremor in 55% of 29 PD patients. The primary site of tremor was vertical laryngeal motion; however, the most striking stroboscopic findings in this study were abnormal phase closure and phase asymmetry.
Additional data to support the laryngeal closure problems in PD come from analyses of EGG signals. Gerratt et al. (43) reported abnormally large speed quotient and poorly defined closing period in PD patients. Blumin et al. (44) used videostro-boscopy and fiberoptic endoscopic techniques, as well as a voice handicap index (VHI) questionnaire, to assess laryngeal function in 15 individuals with severe PD. Of these individuals, 13 (87%) had significant vocal fold bowing and 14 (93%) self-reported significant voice handicap. These observations were consistent with the slow vocal fold opening relative to the rate of closure and incomplete closure of the vocal folds.
EMG studies of the laryngeal muscles provided further information regarding laryngeal pathology in PD. Hirose and Joshita (45) studied the EMG data from the thyroarytenoid (TA) muscles in an individual with PD who had limited vocal fold movement. They observed no reduction in the number of motor unit discharges and no pathologic discharge patterns. They did find loss of reciprocal suppression of the TA during inspiration and interpreted this finding as evidence of deterioration in the reciprocal adjustment of the antagonist muscles. Their finding is consistent with deficits in sensory gating characteristics of PD (45). Luschei et al. (46) studied single motor unit activity in the TA muscle in individuals with PD and found a decreased firing rate in TA in male PD subjects. They interpreted these findings to suggest that PD affects rate and variability in motor unit activation (firing) in the laryngeal musculature. Baker et al. (21) found that absolute TA amplitudes during a loudness level task in individuals with PD were lower than that of young normal adults and normal aging adults. Gallena et al. (47) used TA EMG and nasoendoscopy to compare laryngeal physiology during speech of individuals with PD with and without lev-odopa and controls. Some patients were observed to have higher levels of laryngeal muscle activation, more vocal fold bowing, and greater impairment in voice onset and offset control with levodopa than without levodopa as well as in comparison to the controls.
The seemingly conflicting reports of excessive and reduced TA activity may represent a common problem underlying laryngeal motor control, namely a deficit in sensorimotor gating.
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