Guinea-pigs were used to study plastic changes of the nervous system associated with spinal decompensation (postural asymmetry). This phenomenon is elicited by a lesion or blockade to the spinal cord of an animal that has compensated to a unilateral vestibular neurectomy. Spinal preparations of compensated animals were monitored for the return of spinal reflex activity and then given a postbrachial spinal transection or a lumbar plexus blockade with 2% xylocaine. No decompensation asymmetry was measureable in passive resistance to stretch or in ongoing forelimb extensor and neck electromyographic activity. In other experiments integrated multiunit activity of the vestibular nuclei of ‘intact’ and ‘compensated’ animals was measured to determine the effects of cool blocks performed at spinal T-7. For a given locus, the net multiunit activity of the vestibular nuclei either did not change, decreased or increased in response to the T-7 cold block. In the 31 loci studied that proved to be in the descending vestibular nuclei (14 loci in 5 ‘intact’, and 17 loci in 5 ‘compensated’ animals), the mean response (to the block at T-7) in the descending vestibular nuclei of ‘intact’ animals was a 0.3% increase in spontaneous activity, while in the ‘compensated’ animals there was a mean 27.7% decrease in activity. This difference is statistically highly significant. Three mechanisms are proposed to account for this result and it is concluded that compensatory changes confined to the spinal cord are unlilely to account for body postural decompensation. Vestibular compensation involves the establishment of a tonic facilitatory influence of the spinal cord upon the descending vestibular nucleus ipsilateral to a vestibular neurectomy.