Anna Latorre (United Kingdom)
UCL Queen Square Institute of Neurology Department of Clinical and Movement NeurosciencesAuthor Of 1 Presentation
MOTOR CORTICAL NETWORK EXCITABILITY IN PARKINSON’S DISEASE: A TRANSCRANIAL MAGNETIC STIMULATION-ELECTROENCEPHALOGRAPHY STUDY
- Giorgio Leodori (Italy)
Abstract
Background and Aims:
Bradykinesia in Parkinson’s disease (PD) reflects changes in the basal ganglia-thalamocortical circuit converging on the primary motor cortex (M1) and supplementary motor area (SMA). We investigated changes in M1 and SMA excitability in PD patients and their relation to dopaminergic status and bradykinesia.
Methods:
In a sham-controlled study, we compared transcranial magnetic stimulation (TMS)-evoked cortical potentials (TEPs) from the M1 and SMA between 15 PD patients tested OFF and ON medication and 12 healthy controls (HCs) and investigated correlations between TEPs and clinical bradykinesia.
Results:
PD patients OFF compared to HCs showed reduced P30 amplitude from the M1s contralateral and ipsilateral to the most bradykinetic side, reduced N45 from the M1 contralateral to the most bradykinetic side, and increased N40 from the SMA. In PD patients OFF, reduced P30 from the M1 contralateral to the most affected side was associated with reduced N40 from SMA. Dopaminergic therapy normalized M1 P30 contralateral and ipsilateral to the most bradykinetic side and SMA N40. We found a direct correlation between M1 P30 amplitude and bradykinesia only for the most affected side in PD patients OFF.
Conclusions:
Changes in M1 P30 and SMA N40 in PD suggest decreased M1 excitability and increased SMA excitability. The effect of dopaminergic therapy and the clinical correlation suggest that changes in the excitability of these motor areas reflect abnormal basal ganglia-thalamocortical activity related to bradykinesia. The N45 reduction in PD patients suggests additional excitability changes of the most affected M1, which are dopamine independent and not correlated with bradykinesia.