Monkeys were trained to perform simple motor habits including phasic movement and maintained limb positions before receiving bilateral lesions of the cerebellar dentate and interpositus nuclei. The frequency, relative amplitude, and duration of oscillations, measured by an accelerometer worn on the limb, varied with the limb's position, being slower and wider (ataxia) with more extended-abducted positions, faster and smaller (tremor) with more flexed-adducted postures. Changes with time showed a progressive conversion of ataxic oscillations to tremor as reflex and locomotor performance improved. At any time, limb fixation combined with phasic movement initiated the oscillations, whereas a fixed position by itself could be maintained, or a phasic movement without a fixed end point performed without tremor or ataxia. Analysis of these data suggests that the cerebellum provides a timing device for movement which matches limb fixation with phasic (usually distal) movement so that the limb fixation stops at the right moment for the phasic component to begin. The timing of these two components may have separate mediation by the interpositus (fixation) and dentate (phasic-distal) nuclei. During recovery, loss of internal feed-forward cerebellar circuits is compensated for by external feedback loops involving the dorsal root afferents and cerebral cortex.