In our spinal deafferentation research (C2 to T12) we first dealt with severe issues of spinal stability due to the laminectomy. As we got around this problem, and put post op monkeys into gang cages rather than individual cages-- observing them therein on a 24 hrs basis until they recovered so that they not be injured by others, we found much more rapid recovery than when recovering alone in an individual cage with far less intervention needed over far less time than when recovering in a solo cage. The behavioral recovery was spectacular. More important, the initially ataxic and dysmetric movements recovered initially in post-op recovery. Later elaborate movements did not exhibit the same motoric pathology seen initially, even though these movements had not appeared previously post-op. Several "rules" or patterns seem to be characteristic:

1) hand brought in contact with mouth (usually lower jaw as seemingly purposeful self-touch of the face above was not seen) heralded the beginning of hand use in both bilat and unilat monkeys. This occurred before limb was used posturally in standing and quadrupedal ambulation. Sectioning of mental nerve at its root removed the predictability of arms use in deaff monkeys and greatly retarded recovery of arms function. Movements recovered before supportive power and sustained muscular contraction so the forelimbs can be of postural assistance. Indeed, recovery was ALWAYS distal to proximal. Lastly, the leaving of a rootlet intact (deliberate as in no case was it by accident) retarded rather than assisting in recovery of deaff arm use. A similar pattern was seen in monkeys deafferented as fetuses in second trimester, reinserted for vaginal birth at full gestation. 

Since recovery of purposeful movements appeared in a burst rather than gradually, much earlier in a gang cage setting than in a nursing situation, can we attribute post-spinal shock disuse, not to loss of sensorimotor coordination but to a loss of dopamine striatal suppression that once overcome, completely overwhelms loss of attention after deaff? And, would this constitute a phenomenon distinct from learned disuse and later rehabilitatory learned force re-use? In other words, movement sequences as in reach and grasp, do not need sensory input-- indeed,aberrant input from intact rootlet would be disruptive-- so that the brain at birth and certainty by second trimester has the neural access to limb muscles well mapped, using sensory input more for highly skilled fine movements and tonic postures rather than to guide the limb movements characteristic of monkey behavior. Lastly, has anyone looked at the effect of striatocortical and substantia nigra-striatal dopamine input as a factor in disuse and spontaneous recovery of the deafferented forelimb?

Perhaps older notions of segmented integrations needing sensory input need reconsideration, n'est pas?