Article ID Journal Published Year Pages File Type
3043717 Clinical Neurophysiology 2015 10 Pages PDF
Abstract

•Stimulus rate-dependent amplitude suppression of the auditory P1/N1-complex is impaired in patients with advanced Parkinson’s disease.•Dopaminergic treatment has no effect on these auditory sensory gating characteristics.•Deep brain stimulation of the subthalamic nucleus restores a physiological P1/N1-amplitude attenuation profile and may improve early attentive filtering processes possibly at the level of the frontal cortex.

ObjectiveWhile motor effects of dopaminergic medication and subthalamic nucleus deep brain stimulation (STN-DBS) in Parkinson’s disease (PD) patients are well explored, their effects on sensory processing are less well understood. Here, we studied the impact of levodopa and STN-DBS on auditory processing.MethodsRhythmic auditory stimulation (RAS) was presented at frequencies between 1 and 6 Hz in a passive listening paradigm. High-density EEG-recordings were obtained before (levodopa ON/OFF) and 5 months following STN-surgery (ON/OFF STN-DBS). We compared auditory evoked potentials (AEPs) elicited by RAS in 12 PD patients to those in age-matched controls. Tempo-dependent amplitude suppression of the auditory P1/N1-complex was used as an indicator of auditory gating.ResultsParkinsonian patients showed significantly larger AEP-amplitudes (P1, N1) and longer AEP-latencies (N1) compared to controls. Neither interruption of dopaminergic medication nor of STN-DBS had an immediate effect on these AEPs. However, chronic STN-DBS had a significant effect on abnormal auditory gating characteristics of parkinsonian patients and restored a physiological P1/N1-amplitude attenuation profile in response to RAS with increasing stimulus rates.ConclusionsThis differential treatment effect suggests a divergent mode of action of levodopa and STN-DBS on auditory processing.SignificanceSTN-DBS may improve early attentive filtering processes of redundant auditory stimuli, possibly at the level of the frontal cortex.

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