Abstract

We aimed to determine the value of the paired-pulse inhibition (PPI) in the auditory cortex in patients with Parkinson's disease (PD) and analyze its dependence on clinical characteristics of the patients. The central (Cz) auditory evoked potentials were recorded in 58 patients with PD and 22 age-matched healthy subjects. PPI of the N1/P2 component was significantly (P < .001) reduced for interstimulus intervals 500, 700, and 900 ms in patients with PD compared to control subjects. The value of PPI correlated negatively with the age of the PD patients (P < .05), age of disease onset (P < .05), body bradykinesia score (P < .01), and positively with the Mini Mental State Examination (MMSE) cognitive score (P < .01). Negative correlation between value of PPI and the age of the healthy subjects (P < .05) was also observed. Thus, results show that cortical inhibitory processes are deficient in PD patients and that the brain's ability to carry out the postexcitatory inhibition is age-dependent.

Highlights

  • Parkinson’s disease (PD) is a neurodegenerative disorder primarily related to pathology in the substantia nigra pars compacta dopaminergic neurons that results in the development of the brain dopamine deficit

  • The aim of this study was to analyze the dependence of the paired-pulse inhibition (PPI) value of the N1/P2 component of auditory cortical evoked potentials on the clinical parameters of the PD patients: age, sex, disease duration, age at disease onset, Hoehn and Yahr stage, duration of the Levodopa intake, Levodopa dosage, and indices of motor and cognitive functions determined by using Unified Parkinson’s Disease Rating Scale (UPDRS) and Mini Mental State Examination (MMSE)

  • The main result of this study showed that PD patients had significantly reduced PPI of the N1/P2 component of evoked potentials in the auditory cortex for interstimulus intervals (ISIs) 500, 700, and 900 ms compared to the healthy age-matched subjects

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Summary

Introduction

Parkinson’s disease (PD) is a neurodegenerative disorder primarily related to pathology in the substantia nigra pars compacta dopaminergic neurons that results in the development of the brain dopamine deficit. The first mechanism is the decrease in release probability of excitatory neurotransmitters from terminals of afferent axons [13,14,15] This effect is likely the result of an inhibition of calcium influx through presynaptic receptors which play a causal role in the release of glutamate from synaptic vesicles on afferent stimulation [16]. Another possible mechanism of the decrement of the second response on paired stimulation is connected with synaptically released GABA from terminals of inhibitory interneurons [17,18,19]. As the paired-pulse facilitation, PPI is considered to be a form of a short-term synaptic plasticity [20, 21]

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