Could bradykinesia in Parkinson's disease simply be compensation?

Even normal movements can be slow and hesitant. To distinguish between bradykinesia and the simple slow inefficiency sometimes seen in normal movement, we matched the movement durations of 12 patients with Parkinson's disease (PD) and 12 age-matched controls and examined end-point accuracy, number of submovements, force inefficiency, and relative duration of acceleration and deceleration phases of movement. Subjects used an electronic pen which sampled pen-tip position at 200 Hz, and performed a sequence of drawing movements to nine targets (0.5, 1, or 2 cm diameter) upon a WACOM SD420 graphics tablet. Patients could be trained to move at the preferred speed of controls (and vice versa). When moving at the same fast speed as controls, patient's movements were less accurate (increased end-point spread). Even when moving at their own preferred speed, patients' movements were less efficient (more submovements, more zero crossings in acceleration function) than controls moving at the same speed. If bradykinesia simply reflected increased caution and visual guidance, we would expect patients to exhibit prolongeddecelerative phases of movement associated with terminal guidance. However, patients consistently required prolongedaccelerative phases of movement, suggesting that there was a problem in generating appropriate movement forces to produce the required end-point accuracy. It is hypothesised that bradykinesia is not simply a compensation for defective preparatory processes, but may reflect a defective internal cue in PD which disrupts and impairs the outflow of motor responses.