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

BackgroundParkinsons 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. ObjectiveDeep 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. MethodsOn two consecutive days, we applied single-pulse transcranial magnetic stimulation over both primary motor cortices in 20 PD patients treated with bilateral STN-DBS (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. ResultsAdvanced 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. ConclusionOur study provides evidence of altered corticospinal dynamics during movement preparation in advanced PD patients treated with STN-DBS. Consistent with results in earlier-stage 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.