Animal studies suggest that the basal ganglia (BG) provide internal cu
es to trigger submovements in a movement sequence, with Parkinson's di
sease (PD) involving a deficiency in this cueing mechanism. However, i
t is not clear why defective internal cues can produce slow movements,
or the extent to which slow movements are indeed the basic movement a
bnormality or are perhaps a compensatory mechanism for some other prim
ary deficit. In this study we examined a number of the kinematic indic
es of matched fast movements between PD patients and age-matched contr
ols, 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 wi
th PD, and their matched controls, used an electronic pen, which sampl
ed pen-tip position at 200 Hz, and performed a sequence of drawing mov
ements to nine targets upon a WACOM SD 420 graphics tablet. Subjects w
ere trained to perform the movement sequence at a fast speed and were
then required to perform the same movement at the same speed with redu
ced visual cues. Kinematic analysis indicated that, when visual cues w
ere reduced, movements of PD patients became spatially and temporally
unstable as they were progressively performed down the sequence. The i
nstability 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 le
ads to problems synchronising preparatory activity, which then results
in abnormalities in movement forces which are characterised by unpred
ictable and inaccurate movement endpoints. When movements are strung t
ogether in a sequence the inaccuracy is additive leading to motor inst
ability.