Objective: Speech deficits are common in Parkinson's disease, and behavioural findings suggest that the deficits may be due to impaired monitoring of self-produced speech. The neural mechanisms of speech deficits are not well understood. We examined a well-documented electrophysiological correlate of speech self-monitoring in patients with Parkinson's disease and control participants. Methods:We measured evoked electroencephalographic responses to self-produced and passively heard sounds (/a/ phonemes) in age-matched controls (N=18), and Parkinson's disease patients who had minor speech impairment, but reported subjectively experiencing no speech deficits (N=17).Results: During speaking, auditory evoked activity 100 ms after phonation (N1 wave) was less suppressed in Parkinson's disease than controls when compared to the activity evoked by passively heard phonemes. This difference between the groups was driven by increased amplitudes to selfproduced phonemes, and reduced amplitudes passively heard phonemes in Parkinson's disease. Conclusions:The finding indicates that auditory evoked activity is abnormally modulated during speech in Parkinson's patients who do not subjectively notice speech impairment. This mechanism could play a role in producing speech deficits in as the disease progresses.

ObjectiveSpeech deficits are common in Parkinson’s disease, and behavioural findings suggest that the deficits may be due to impaired monitoring of self-produced speech. The neural mechanisms of speech deficits are not well understood. We examined a well-documented electrophysiological correlate of speech self-monitoring in patients with Parkinson’s disease and control participants.MethodsWe measured evoked electroencephalographic responses to self-produced and passively heard sounds (/a/ phonemes) in age-matched controls (N=18), and Parkinson’s disease patients who had minor speech impairment, but reported subjectively experiencing no speech deficits (N=17).ResultsDuring speaking, auditory evoked activity 100 ms after phonation (N1 wave) was less suppressed in Parkinson’s disease than controls when compared to the activity evoked by passively heard phonemes. This difference between the groups was driven by increased amplitudes to self-produced phonemes, and reduced amplitudes passively heard phonemes in Parkinson’s disease.ConclusionsThe finding indicates that auditory evoked activity is abnormally modulated during speech in Parkinson’s patients who do not subjectively notice speech impairment. This mechanism could play a role in producing speech deficits in as the disease progresses.