An investigation of motor memory deficits in Parkinson’s disease

People with Parkinson’s disease (PD) display motor memory deficits when tested on motor adaptation tasks involving visuomotor rotations, while the process of adaptation itself seems largely unaffected. Other forms of adaptation are unexplored and the mechanisms underlying their motor memory deficits unknown. Previous research has suggested reinforcement mechanisms to be affected in PD, but whether defective reinforcement is underlying motor memory impairments has never been directly investigated. Firstly, we investigated if the motor memory deficits shown by earlier studies also hold for force-field adaptation, where the participant learns to compensate for a perturbation caused by an external force acting on the limb. We then explored if adaptation to such force-fields was possible when adaptation was dependent on contextual cues, i.e. if people with PD were able to make context-motor associations, and in addition we investigated whether augmentation of reward and punishment improved reinforcement in PD. To increase our understanding of the effect of reward and punishment feedback on context-dependent motor learning their separate effects were investigated in a group of young adults. Results showed intact recall of the learned adapted state in people with PD, suggesting intact consolidation, but motor memory as tested with interference, where memory of the initial adaptation impairs learning of an opposite adaptation, to be strongly reduced in PD. We found evidence that people with PD were less able to learn context-motor associations in comparison to older Controls and these deficits became more pronounced when success-based feedback was strengthened suggesting reduced sensitivity to augmentation of reward and/or punishment. In young adults, reward and punishment feedback did not influence context-dependent motor adaptation itself, but it had some effect on movement velocity. We conclude that PD pathology leads to weaker context-motor associations and defective reinforcement processes, which may be underlying impaired recall of certain motor states

Surprise disrupts cognition via a fronto-basal ganglia suppressive mechanism

Surprising events markedly affect behaviour and cognition, yet the underlying mechanism is unclear. Surprise recruits a brain mechanism that globally suppresses motor activity, ostensibly via the subthalamic nucleus (STN) of the basal ganglia. Here, we tested whether this suppressive mechanism extends beyond skeletomotor suppression and also affects cognition (here, verbal working memory, WM). We recorded scalp-EEG (electrophysiology) in healthy participants and STN local field potentials in Parkinson's patients during a task in which surprise disrupted WM. For scalp-EEG, surprising events engage the same independent neural signal component that indexes action stopping in a stop-signal task. Importantly, the degree of this recruitment mediates surprise-related WM decrements. Intracranially, STN activity is also increased post surprise, especially when WM is interrupted. These results suggest that surprise interrupts cognition via the same fronto-basal ganglia mechanism that interrupts action. This motivates a new neural theory of how cognition is interrupted, and how distraction arises after surprising events