Subthalamic deep brain stimulation alleviates motor symptoms without restoring deficits in corticospinal suppression during movement preparation in Parkinson’s disease.

Wilhelm, Emmanuelle [UCL] Derosiere, Gerard [UCL] Quoilin, Caroline [UCL] Cakiroglu, Inci [UCL] Paço, Susana Raftopoulos, Christian [UCL] Nuttin, Bart Duque, Julie [UCL] et al.[show all]

Background: Parkinson’s disease (PD) patients exhibit alterations in neurophysiological mechanisms underlying movement preparation, especially the suppression of corticospinal excitability – called “preparatory suppression” – considered to propel movement execution by increasing motor neural gain in healthy individuals. Objective: Deep brain stimulation (DBS) of the subthalamic nucleus (STN) being an attractive treatment for advanced PD, we aimed to investigate the potential contribution of this nucleus to PD-related changes in such corticospinal dynamics. Methods: On two consecutive days, we applied single-pulse transcranial magnetic stimulation over both primary motor cortices in 20 PD patients treated with bilateral STNDBS (ON vs. OFF), as well as 20 healthy control subjects. Motor-evoked potentials were elicited at rest or during a left- or right-hand response preparation in an instructed-delay choice reaction time task. Preparatory suppression was assessed by expressing amplitudes of motor potentials evoked during movement preparation relative to rest. Results: Advanced PD patients exhibited a deficit in corticospinal suppression during movement preparation, limited to the responding hand (especially the most-affected), independently of STN-DBS. Significant links between preparatory suppression and clinical variables were found for least-affected hands only. Conclusion: Our study provides evidence of altered corticospinal dynamics during movement preparation in advanced PD patients treated with STN-DBS. Consistent with results in earlierstage patients, preparatory suppression deficits were limited to the responding hand and most pronounced on the most-affected side. STN-DBS did not restore this abnormality, which warrants further investigations into possible neuroanatomical sources of such corticospinal suppression, necessary to understand the consistent lack of this mechanism in PD patients.