Category: Parkinson's Disease: Pathophysiology
Objective: To test the hypothesis that motor cortex plasticity is maladaptive in Parkinson’s disease (PD) patients suffering from dyskinesias, as compared to non-dyskinetic patients.
Background: Levodopa-induced dyskinesias (LIDs) represent a common motor complication in PD, likely caused by maladaptive plasticity and disinhibition of both cortico-basal ganglia and cortico-cortical motor circuits. Whether the primary motor cortex (M1) is just a ‘passive integrator’ of subcortical and cortico-cortical abnormalities, or it also plays an active role in the pathophysiology of LIDs is not completely clear. Here we tested the hypothesis that M1 plasticity is maladaptive in dyskinetic patients OFF medication.
Method: We adopted a new perturbation strategy, by applying transcranial static magnetic field stimulation (tSMS) to M1 in two independent and parallel experiments. Experiment 1 was a randomized sham-controlled double-blind study (NCT02657681) in which we investigated the long-term effects (i.e. >24h) on cortical excitability – as measured by transcranial magnetic stimulation (TMS) – induced by 9 sessions of 30-min tSMS over two weeks in dyskinetic patients OFF medication (n=50 recruited, 42 completed the study, 35 with cortical excitability data). Experiment 2 was an open study in which we investigated the acute effects on cortical excitability induced by 10-min tSMS in dyskinetic (n=22) vs. non-dyskinetic patients (n=22) OFF medication. We also studied a group of de novo PD patients naïve to levodopa (n=21) and a group of aged healthy subjects (n=21).
Results: Experiment 1 showed that 9 sessions of real tSMS unexpectedly increased corticospinal excitability compared to sham, without significantly changing motor features OFF medication or the intensity of dyskinesias ON medication. Experiment 2 showed that 10-min tSMS induced maladaptive corticospinal potentiation in dyskinetic patients OFF medication, but not in non-dyskinetic patients nor in de novo PD patients, while inducing the expected corticospinal depression in healthy subjects.
Conclusion: These results suggest that M1 corticospinal plasticity is maladaptive in dyskinetic PD patients OFF medication and may contribute to the pathophysiology of LIDs.
To cite this abstract in AMA style:
M. Dileone, C. Ammann, V. Catanzaro, R. Piredda, M.G Monje, I. Navalpotro-Gómez, A. Bergareche, L. Vela, F. Alonso-Frech, M.J Catalán-Alonso, J.A Molina, N. López-Ariztegui, F. Hernández-Fernández, B. Fernández-Rodríguez, C. Gasca-Salas, J.U Máñez-Miró, R. Martínez-Fernández, A. Sánchez-Ferro, A. Oliviero, J.A Obeso, G. Foffani. Maladaptive motor cortex plasticity off medication in Parkinson’s disease patients with levodopa-induced dyskinesias [abstract]. Mov Disord. 2020; 35 (suppl 1). https://www.mdsabstracts.org/abstract/maladaptive-motor-cortex-plasticity-off-medication-in-parkinsons-disease-patients-with-levodopa-induced-dyskinesias/. Accessed June 15, 2025.« Back to MDS Virtual Congress 2020
MDS Abstracts - https://www.mdsabstracts.org/abstract/maladaptive-motor-cortex-plasticity-off-medication-in-parkinsons-disease-patients-with-levodopa-induced-dyskinesias/