COULD BRADYKINESIA IN PARKINSONS-DISEASE SIMPLY BE COMPENSATION

Even normal movements can be slow and hesitant. To distinguish between bradykinesia and the simple slow inefficiency sometimes seen in norma l movement, we matched the movement durations of 12 patients with Park inson's disease (PD) and 12 age-matched controls and examined end-poin t accuracy, number of submovements, force inefficiency, and relative d uration of acceleration and deceleration phases of movement. Subjects used an electronic pen which sampled pen-tip position at 200 Hz, and p erformed a sequence of drawing movements to nine targets (0.5, 1, or 2 cm diameter) upon a WACOM SD420 graphics tablet. Patients could be tr ained to move at the preferred speed of controls (and vice versa). Whe n 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 sub movements, 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 prolo nged decelerative phases of movement associated with terminal guidance . However, patients consistently required prolonged accelerative phase s of movement, suggesting that there was a problem in generating appro priate movement forces to produce the required end-point accuracy. It is hypothesised that bradykinesia is not simply a compensation for def ective preparatory processes, but may reflect a defective internal cue in PD which disrupts and impairs the outflow of motor responses.