Objective: Our objective was to investigate Motor Reserve (MR) in idiopathic Parkinson’s Disease (PD).

Background: MR is defined as the resilience mechanisms of the brain coping with neurodegeneration in PD. Several different mechanisms were proposed for MR, however it has never been investigated on PD with clinical unilateral signs and bilateral binding reduction at dopamine transporter (DAT) imaging using a rigorous neurophysiological method.

Method: In this cross-sectional study, we included 16 PD patients and 28 healthy control. Patients were included if presenting unilateral motor signs (Hoehn and Yahr stage=1/5, two independent raters) but DAT density ([123I]-Ioflupane-SPECT, DATQUANTTM) was significantly reduced in bilateral putamina (Putamen z-score>0.5). Subjects were extensively investigated using the Unified Parkinson’s Disease Rating Scale (part-III was videorecorded). Transcranial magnetic stimulation (TMS) was performed on primary motor cortices (M1) in presymptomatic (PH) and symptomatic hemispheres (SH) for patients and on dominant hemisphere for HC. TMS measured cortical excitability, associative plasticity and interhemispheric-inhibition (IHI). A Motor Reserve Coefficient (MRC) based on clinical and DAT data was defined to evaluate MR and its association with neurophysiology data.

Results: TMS testing revealed asymmetries in corticospinal excitability with higher values in the PH. SH demonstrated lower M1-plasticity (compared to the asymptomatic hemisphere). Finally, we found reduced IHI from PH to SH. Interestingly, reduced putamen binding was predicted by reduced intracortical facilitation (ICF) in SH and by higher plasticity and reduced IHI in PH. Reduced putamen binding was predicted by enhanced plasticity and reduced IHI in PH, and by reduced ICF in SH. Putamen/caudate ratio was directly associated with corticospinal excitability in PH and inversely associated with cortical plasticity in symptomatic hemisphere. MRC distinguished PH from SH (AUC 0.9844). It was associated in SH with plasticity increment, IHI and corticospinal excitability reduction.

Conclusion: Response to PD neurodegeneration involves a M1-putamen network, and cortico-M1 connections, responsible for excitability and plasticity changes, depending on caudate activity and becoming more effective with binding reduction in putamen. Further insight on PD MR networks is relevant for novel neuromodulation approaches, aimed at reducing motor burden in daily life.

References: Hoenig, M.C., Dzialas, V., Drzezga, A., van Eimeren, T., 2022. The Concept of Motor Reserve in Parkinson’s Disease: New Wine in Old Bottles? Mov. Disord. Off. J. Mov. Disord. Soc. https://doi.org/10.1002/mds.29266

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MDS Abstracts - https://www.mdsabstracts.org/abstract/neurophysiological-markers-of-motor-reserve-in-parkinsons-disease/