Reduced speaking-induced suppression of auditory evoked-potentials in early Parkinson’s disease suggests deficits in monitoring self-produced speech

Speech deficits are a common symptom of Parkinson’s disease (PD), but the neural mechanisms that cause them are not well understood. Paradoxically, the patients may not subjectively notice their own speech deficits such as hypophonic speech. We hypothesized that this reflects an impairment in monitoring self-produced speech: updating the internal speech model may malfunction in PD, which could explain their speech deficit. We measured evoked EEG responses to self-produced and passively heard phonemes in PD patients (N=17) with mild speech impairment and age-matched controls (N=18). When the speech sounds are self-produced, the amplitude of the evoked response is lower when compared to the condition where the same sounds are passively heard. This effect is known as speaking-induced suppression, and it reflects the modulation of sensory cortical processing through top-down corollary discharge predictions. We observed that the speaking-induced suppression was significantly reduced in PD patients, suggesting of abnormally high prediction errors (when compared to healthy controls). In addition, source reconstruction showed that activity in auditory cortex was stronger in PD patients than control participants already -200 ms before phonation as well as during a later time period (400500 ms after phonation). We conclude that altered internal monitoring of speech may underlie speech deficits in PD.