In a prospective study, we repeatedly recorded fast goal-directed wris
t movements of 8 patients who had experienced an acute cerebellar hype
rmetria due to a stroke and who had subsequently recovered clinically.
Movements and the associated agonist and antagonist electromyographic
(EMG) activities were recorded before and after addition of inertial
loads. Four stages characterized the recovery process. At stage 1, hyp
ermetria was present in the basal state and was not modified by the ad
dition of inertial loads. At stage 2, hypermetria, which was present i
n the basal state, was enlarged by mass addition. At stage 3, hypermet
ria was absent in the basal state, but was revealed by an inertial loa
d increase. At stage 4, as in healthy subjects, there was no hypermetr
ia without or with addition of inertial loads. At stage 1, the patient
s presented several defects. (1) Facing an increased inertia, they cou
ld not increase their agonist EMG activity. (2) The onset latency of t
heir antagonist EMG activity was delayed. (3) Facing an increased iner
tia, they could not increase their antagonist EMG activity. Among thes
e three defects, the first disappeared at stage 2, the second at stage
3, and the third at stage 4.