Abstract

To evaluate the effect of levodopa on cochlear dynamics and on the medial olivocochlear efferent pathway of idiopathic Parkinson's disease (PD) individuals. Individuals with and without PD, followed at a University Hospital, were submitted to Distortion Product Otoacoustic Emissions (DPOAE) and DPOAE Inhibitory Effect (OAEIE) in the presence of contralateral noise. Correlation measures between DPOAE and OAEIE results with Hoehn&Yahr (H&Y) stage, daily dose of levodopa and PD diagnosis period were established. Furthermore, electroacoustic measures were compared between individuals without and those with PD, stratified by dose of levodopa daily administered. Weak negative correlation between DPOAE amplitude and daily dose of levodopa was found, as well positive correlations between EIEOA with daily dose of levodopa and time of PD diagnosis, respectively. Higher DPOAE amplitude was found in individuals with PD using daily doses of levodopa ≤ 600 milligrams when compared to individuals without PD and those with PD using higher doses. EIEOA was lower in individuals using doses ≤ 600 milligrams, when compared to the other groups. Daily doses of levodopa up to 600 mg / day increase the cochlear mechanical-transducer responses in 2 and 3 kHz frequencies, while the action of olivocochlear efferent systems is reduced in this region.

Highlights

  • Idiopathic Parkinson’s disease (PD) is a chronic, neurodegenerative disease that presents classic movement disorder symptoms such as tremor, stiffness, bradykinesia and postural instability

  • Acting as a dopamine precursor, which can transpose the blood-brain barrier, levodopa is decarboxylated in neural tissues, being converted into dopamine, which is stored in presynaptic terminals of striatal neurons[3]

  • The results of the present study indicate that the magnitude of Distortion Product Otoacoustic Emissions (DPOAE) is greater in individuals with PD who use lower daily doses of levodopa

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Summary

Introduction

Idiopathic Parkinson’s disease (PD) is a chronic, neurodegenerative disease that presents classic movement disorder symptoms such as tremor, stiffness, bradykinesia and postural instability. The pathophysiology of the disease is related to the degeneration of dopaminergic neurons of the nigrostriatal system and to dopamine depletion[1]. With the progression of neuronal degeneration in PD, there is an increase in plasma levels of this neurotransmitter, which is stored in synaptic terminals of other tissues and structures[4]. This condition has been associated to the onset of motor complications in PD due to the chronic use of levodopa, such as fluctuation of motor signal control and dyskinesias[4,5,6]

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