Pathophysiology of bradykinesia in Parkinson's disease

Bradykinesia means slowness of movement and is one of the cardinal manifest ations of Parkinson's disease. Weakness, tremor and rigidity may contribute to but do not fully explain bradykinesia. We argue that bradykinesia resul ts from a failure of basal ganglia output to reinforce the cortical mechani sms that prepare and execute the commands to move. The cortical deficit is most apparent in midline motor areas. This leads to particular difficulty w ith self-paced movements, prolonged reaction times and abnormal pre-movemen t EEG activity. Movements are often performed with normally timed EMG burst s but the amount of EMG activity is underscaled relative to the desired mov ement parameters. There are also abnormalities in sensory scaling and senso rimotor integration. The brain appears to be able to compensate to some deg ree for the basal ganglia deficit. There is overactivity in the lateral pre motor areas during task performance and movements can be speeded by giving sensory cues. Attention to movement is also beneficial. However, we propose that the engagement of compensatory processes may also lead to reduced per formance in other tasks. For example, patients' problems in performing more than one task at the same time could result from lack of sufficient resour ces both to compensate for their basal ganglia deficit and to run two tasks simultaneously. Surgical therapies are unlikely to work solely by normaliz ing basal ganglia output to that seen in healthy individuals. It seems more plausible that surgery removes an interfering signal that allows more effi cient compensation by other structures.