Journal of Neurophysiology, Vol 60, Issue 4 1285-1302, Copyright © 1988 by APS

ARTICLES

Changes in motor cortex neural discharge associated with the development of cerebellar limb ataxia

J. Hore and D. Flament
Department of Physiology, University of Western Ontario, London, Canada.

1. The relation between changes in motor cortex neural (MCN) discharge and the development of limb ataxia during cerebellar dysfunction was studied in 4 Cebus monkeys. Elbow movements with decreased accelerations or with tremor were produced by reversible cerebellar nuclear cooling. Discharge from 160 neurons was analyzed in detail. 2. During cerebellar cooling 37 of 80 neurons that discharged before movement onset decreased their phasic, but not their tonic, activity. This could not be explained by decreased peak velocities during cerebellar cooling. It is suggested that this decreased phasic discharge is related to the less abrupt onset and smaller magnitude of agonist EMG activity, and to the decreased initial accelerations, without decreased peak velocities, observed in limb movements during cerebellar dysfunction. This view implies that the cerebellum is involved in some way in the generation of commands to agonist alpha-motoneurons. 3. No evidence was found that 3- to 4-Hz cerebellar intention tremor is driven by a purely central oscillator. All 28 neurons that discharged strongly in relation to cerebellar tremor in movements responded strongly and reciprocally to limb perturbations. 4. A number of changes were observed during cerebellar nuclear cooling in kinematically related neural discharge associated with disordered elbow movements: an increase in discharge of some velocity- and acceleration-like neurons, a decrease in (reciprocal) inhibition, and a shift from an acceleration-like to a velocity-like discharge in some neurons. 5. Fourteen of 29 neurons with muscle-like discharge patterns discharged in a servoassistance-like manner during cerebellar dysfunction that was consistent with them contributing to tremor. 6. The results indicate that a variety of disorders, i.e., in the generation of central commands that initiate movements and in the regulation of the gain and phase of proprioceptive feedback, contribute to the development of limb ataxia during cerebellar dysfunction.

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