“…This growing body of evidence supports the hypothesis that longer duration beta bursts in subcortical structures, equating to longer periods of beta oscillations and synchrony, represent pathological or impaired sensorimotor processing in Parkinson's disease (Anidi et al, 2018;Cagnan et al, 2019;Deffains et al, 2018;Lofredi et al, 2019b;Tinkhauser et al, 2018Tinkhauser et al, , 2017aTinkhauser et al, , 2017b and that one mechanism of STN DBS is to remove pathological sensorimotor network processing, while leaving intact normal physiological processing (Anidi et al, 2018;Holt et al, 2019;Tinkhauser et al, 2017a;Torrecillos et al, 2018). The discovery that averaged beta band power was attenuated during increasing intensities of DBS led to its successful use as the control variable in closed loop DBS studies Eusebio et al, 2011;Little et al, 2016aLittle et al, , 2016bLittle et al, , 2013Piña-Fuentes et al, 2019Rosa et al, 2017Rosa et al, , 2015Syrkin-Nikolau et al, 2017;Velisar et al, 2019;Whitmer et al, 2012). Similarly, the accumulating evidence suggests that beta burst duration will be a functionally relevant, patient specific control variable for closed loop DBS.…”