When treating patients with abnormal tone, I often find recurrent inhibition using a range of sensory modalities from cooling to electrical stimulation at low levels is very effective in some patients. Others respond best to reciprocal activity. Clearly, spasticity results from an inbalance of inhibitory and excitatory activity, but can we deduct or identify which? If so, does that have a direct influence on central or peripheral management of tone? While Botox and other end organ interventions work, I am looking for ways to alter the central activity related to the abnormal tone.