| Literature DB >> 33515333 |
Kim De Keyser1, Miet De Letter2, Patrick Santens3, Durk Talsma4, Dick Botteldooren5, Annelies Bockstael5.
Abstract
There is accumulating evidence for auditory dysfunctions in patients with Parkinson's disease (PD). Moreover, a possible relationship has been suggested between altered auditory intensity processing and the hypophonic speech characteristics in PD. Nonetheless, further insight into the neurophysiological correlates of auditory intensity processing in patients with PD is needed primarily. In the present study, high-density EEG recordings were used to investigate intensity dependence of auditory evoked potentials (IDAEPs) in 14 patients with PD and 14 age- and gender-matched healthy control participants (HCs). Patients with PD were evaluated in both the on- and off-medication states. HCs were also evaluated twice. Significantly increased IDAEP of the N1/P2 was demonstrated in patients with PD evaluated in the on-medication state compared to HCs. Distinctive results were found for the N1 and P2 component. Regarding the N1 component, no differences in latency or amplitude were shown between patients with PD and HCs regardless of the medication state. In contrast, increased P2 amplitude was demonstrated in patients with PD evaluated in the on-medication state compared to the off-medication state and HCs. In addition to a dopaminergic deficiency, deficits in serotonergic neurotransmission in PD were shown based on increased IDAEP. Due to specific alterations of the N1-P2 complex, the current results suggest deficiencies in early-attentive inhibitory processing of auditory input in PD. This interpretation is consistent with the involvement of the basal ganglia and the role of dopaminergic and serotonergic neurotransmission in auditory gating.Entities:
Keywords: Auditory event-related potentials; Auditory gating; Auditory processing; Intensity dependence of auditory evoked potentials; P1–N1–P2 complex; Parkinson’s disease
Year: 2021 PMID: 33515333 DOI: 10.1007/s00702-021-02305-3
Source DB: PubMed Journal: J Neural Transm (Vienna) ISSN: 0300-9564 Impact factor: 3.575