Animal studies suggest that the basal ganglia (BG) provide internal cues to trigger submovements in a movement sequence, with Parkinson's disease (PD) involving a deficiency in this cueing mechanism. However, it is not clear why defective internal cues can produce slow movements, or the extent to which slow movements are indeed the basic movement abnormality or are perhaps a compensatory mechanism for some other primary deficit. In this study we examined a number of the kinematic indices of matched fast movements between PD patients and age-matched controls, performed with and without reductions in visual cues for guidance, in order to delineate the relationship between the internal cue and the kinematic characteristics of these movements. Fourteen patients with PD, and their matched controls, used an electronic pen, which sampled pen-tip position at 200 Hz, and performed a sequence of drawing movements to nine targets upon a WACOM SD 420 graphics tablet. Subjects were trained to perform the movement sequence at a fast speed and were then required to perform the same movement at the same speed with reduced visual cues. Kinematic analysis indicated that, when visual cues were reduced, movements of PD patients became spatially and temporally unstable as they were progressively performed down the sequence. The instability was associated with an abnormal force profile increase in peak movement velocity and target overshoot, which became additive as the submovements progressed. We suggest that defective cue production is the basic deficit in parkinsonian hypokinesia. The defective cue leads to problems synchronising preparatory activity, which then results in abnormalities in movement forces which are characterised by unpredictable and inaccurate movement endpoints. When movements are strung together in a sequence the inaccuracy is additive leading to motor instability.