Motor Cortical Network Excitability in Parkinson's Disease

• DOI: 10.1002/mds.28914
• Publication Date: 2022-01-10T07:20:29Z
• Authors: Giorgio Leodori; Maria Ilenia De B...; Andrea Guerra; Andrea Fabbrini; Lorenzo Rocchi; Anna Latorre; Giulia Paparella; Daniele Belvisi; Antonella Conte; Kailash P. Bhatia; John C. Rothwell; Alfredo Berardelli
• Keywords: bradykinesia; motor cortex; Parkinson's disease; supplementary motor area; transcranial magnetic stimulation-electroencephalography; TRANSCRANIAL MAGNETIC STIMULATION; CORTEX; TMS-EEG; Parkinson's disease; transcranial magnetic stimulation-electroencephalography; INHIBITION; Hypokinesia; 03 medical and health sciences; supplementary motor area; 0302 clinical medicine; motor cortex; OSCILLATIONS; Humans; BRAIN; Parkinson's disease; Bradykinesia; Motor cortex; Supplementary motor area; Transcranial magnetic stimulation-electroencephalography; Motor Cortex; Parkinson Disease; Evoked Potentials, Motor; Transcranial Magnetic Stimulation; REACTIVITY; FALSE DISCOVERY RATE; bradykinesia; NEURONAL-ACTIVITY; EFFECTIVE CONNECTIVITY; Parkinson's disease; bradykinesia; motor cortex; supplementary motor area; transcranial magnetic stimulation-electroencephalography.

AbstractBackgroundMotor impairment 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). Previous studies assessed M1 excitability in PD using transcranial magnetic stimulation (TMS)‐evoked electromyographic activity. TMS‐evoked electroencephalographic activity may unveil broader motor cortical network changes in PD.ObjectiveThe aim was to assess motor cortical network excitability in PD.MethodsWe compared TMS‐evoked cortical potentials (TEPs) from M1 and the pre‐SMA between 20 PD patients tested off and on medication and 19 healthy controls (HCs) and investigated possible correlations with bradykinesia.ResultsOff PD patients compared to HCs had smaller P30 responses from the M1s contralateral (M1+) and ipsilateral (M1–) to the most bradykinetic side and increased pre‐SMA N40. Dopaminergic therapy normalized the amplitude of M1+ and M1– P30 as well as pre‐SMA N40. We found a positive correlation between M1+ P30 amplitude and bradykinesia in off PD patients.ConclusionsChanges in M1 P30 and pre‐SMA N40 in PD suggest that M1 excitability is reduced on both sides, whereas pre‐SMA excitability is increased. The effect of dopaminergic therapy and the clinical correlation suggest that these cortical changes may reflect abnormal basal ganglia‐thalamocortical activity. TMS electroencephalography provides novel insight into motor cortical network changes related to the pathophysiology of PD. © 2022 International Parkinson and Movement Disorder Society