Reduced Intracortical Facilitation to TMS in Both Isolated REM Sleep Behavior Disorder (RBD) and Early Parkinson's Disease with RBD

Giuseppe Lanza, Filomena Irene Ilaria Cosentino, Bartolo Lanuzza, Mariangela Tripodi, Debora Aricò, Michela Figorilli, Monica Puligheddu, Francesco Fisicaro, Rita Bella, Raffaele Ferri, Manuela Pennisi, Giuseppe Lanza, Filomena Irene Ilaria Cosentino, Bartolo Lanuzza, Mariangela Tripodi, Debora Aricò, Michela Figorilli, Monica Puligheddu, Francesco Fisicaro, Rita Bella, Raffaele Ferri, Manuela Pennisi

Abstract

Background: a reduced intracortical facilitation (ICF), a transcranial magnetic stimulation (TMS) measure largely mediated by glutamatergic neurotransmission, was observed in subjects affected by isolated REM sleep behavior disorder (iRBD). However, direct comparison between iRBD and Parkinson's disease (PD) with RBD is currently lacking.

Methods: resting motor threshold, contralateral cortical silent period, amplitude and latency of motor evoked potentials, short-interval intracortical inhibition, and intracortical facilitation (ICF) were recorded from 15 drug-naïve iRBD patients, 15 drug-naïve PD with RBD patients, and 15 healthy participants from the right First Dorsal Interosseous muscle. REM sleep atonia index (RAI), Mini Mental State Examination (MMSE), Geriatric Depression Scale (GDS), and Epworth Sleepiness Scale (ESS) were assessed.

Results: Groups were similar for sex, age, education, and patients for RBD duration and RAI. Neurological examination, MMSE, ESS, and GDS were normal in iRBD patients and controls; ESS scored worse in PD patients, but with no difference between groups at post hoc analysis. Compared to controls, both patient groups exhibited a significantly decreased ICF, without difference between them.

Conclusions: iRBD and PD with RBD shared a reduced ICF, thus suggesting the involvement of glutamatergic transmission both in subjects at risk for degeneration and in those with an overt α-synucleinopathy.

Keywords: REM sleep behavior disorder; cortical excitability; neurotransmitters; parkinsonian syndrome; transcranial magnetic stimulation.

Conflict of interest statement

The authors declare no conflict of interest.

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