Objective: To study motor compensation mechanisms in Parkinson’s disease.

Background: Whereas akinesia in Parkinson’s disease (PD) is linked to dopaminergic neurons death and striatal dopamine depletion, discrepancies between the degree of nigro-striatal denervation and the severity of akinesia were observed leading to the hypothesis of motor compensation. Several mechanisms underlying this compensation both at the striatal dopaminergic synapse level and at the network level have been described but never investigated in vivo in PD patients.

Method: 65 early PD patients, 24 iRBD patients and 24 controls were included. Every subjects had clinical assessment, a 123I-FP-CIT-SPECT  and multi-modal 3T MRI (3DT1, DTI, T1 neuromelanin and resting-state fMRI) under medication. SPECT data were  segmented in striatal anatomical and functional subregions. DTI data were transformed into OD, ICVF and FW maps. fMRI data were transformed into ReHo and ALFF maps and were used for simple functional  and effective connectivity  analyses. Neuromelanin alteration was quantified using a hybrid intensity x volume measure. Motor compensation was estimated through an adjusted motor severity index (aMSI), i.e. a ratio between the degree of akinetic motor severity and the degree of neuromelanin nigral alteration. Related Z-Scores were created according to a non-parametric approach. Significant correlations were entered into a stepwise ascending multiple regression.

Results: PD and iRBD patients had a significant decrease of 123I-FP-CIT-SPECT fixation in all the subareas of the striatum and a significant alteration of the neuromelanin intensity x volume value. In the multiple regression analysis,  aMSI was negatively correlated (suggesting protective mechanisms) to the simple functional connectivity between the sensorimotor striatum and the associative parietal cortex, the ReHo within the cerebellar lobules VII and VIII and within the associative parietal cortex. It was positively correlated (suggesting inefficient mechanisms) to the simple functional connectivity between the cerebellar lobules V and VI and the primary motor cortex and to the simple functional connectivity between the cerebellar lobules V and VI and the superior parietal lobule.

Conclusion: New or more active dopaminergic synapses, reorganization of motor and cognitive subcortical loops and of the associative areas of the cerebellum are the main motor compensation mechanisms in human early PD.

« Back to 2019 International Congress

MDS Abstracts - https://www.mdsabstracts.org/abstract/motor-compensation-in-parkinsons-disease-a-multimodal-neuroimaging-study/