RESUMO
Involuntary interruptions of upper limb movements, referred to as "upper limb freezing" (ULF) belong to the most disabling symptoms of Parkinson's disease (PD). Our study aimed to explore the cortical neuronal mechanisms underlying the reinstation of regular movement after a freezing episode and to control them by voluntary stops. We hypothesized that this movement recovery after a freeze would be accompanied by a decrease of beta power (13-30 Hz) over the primary sensorimotor cortex (electrode "C3"). We recorded a 62-channel surface EEG in 14 PD patients during a repetitive finger tapping task. After performing time-frequency analysis of the EEG data we segmented it to i) regular finger taps, ii) ULF episodes, and iii) voluntary movement stops (VS). We analysed cortical activity during each movement modality and later focused on the last 500 ms of ULF and VS and the first half of the following regular tap. At the beginning of regular finger taps we found decreased alpha power (6-12 Hz) over C3 (P = 0.01). During ULF, there was no significant activity modulation in the alpha and beta frequency bands, whereas beta power increased over C3 during VS (P = 0.0038). When tapping was reinstated after a freeze, we found that 100 ms before movement onset beta power decreased first present over C3, followed by fronto-central electrodes and then reaching the ipsilateral right fronto-temporal electrodes when reinstating regular tapping (P = 0.0256). Initiating movement after a VS showed a different pattern with a decrease of parieto-occipital beta activity 200 ms prior to the first tap (P = 0.044). Our findings suggest that PD freezers make use of different cortical pathways when re-initiating movement after ULF or VS. This includes either fronto-central or parieto-occipital pathways. These findings may help to customize novel neuromodulation strategies to counteract freezing behaviour.