02092nas a2200217   4500008004100000022001400041245009800055210006900153260001200222300001100234490000700245520143300252653001301685653001501698653002301713653002701736653002001763100002201783700002101805856004801826       2015                        eng d  a1089-409800aRestoring walking after spinal cord injury: operant conditioning of spinal reflexes can help.0 aRestoring walking after spinal cord injury operant conditioning   c04/2015  a203-150 v213 a<p>People with incomplete spinal cord injury (SCI) frequently suffer motor disabilities due to spasticity and poor muscle control, even after conventional therapy. Abnormal spinal reflex activity often contributes to these problems. Operant conditioning of spinal reflexes, which can target plasticity to specific reflex pathways, can enhance recovery. In rats in which a right lateral column lesion had weakened right stance and produced an asymmetrical gait, up-conditioning of the right soleus H-reflex, which increased muscle spindle afferent excitation of soleus, strengthened right stance and eliminated the asymmetry. In people with hyperreflexia due to incomplete SCI, down-conditioning of the soleus H-reflex improved walking speed and symmetry. Furthermore, modulation of electromyographic activity during walking improved bilaterally, indicating that a protocol that targets plasticity to a specific pathway can trigger widespread plasticity that improves recovery far beyond that attributable to the change in the targeted pathway. These improvements were apparent to people in their daily lives. They reported walking faster and farther, and noted less spasticity and better balance. Operant conditioning protocols could be developed to modify other spinal reflexes or corticospinal connections; and could be combined with other therapies to enhance recovery in people with SCI or other neuromuscular disorders.</p>10aLearning10aLocomotion10aspinal cord injury10aspinal cord plasticity10aspinal reflexes1 aThompson, Aiko, K1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2463695402145nas a2200217   4500008004100000022001400041245008500055210006900140260001200209300000700221490000600228520150000234653001301734653002401747653001501771653002301786653002701809100002201836700002101858856004801879       2014                        eng d  a1662-514500aOperant conditioning of spinal reflexes: from basic science to clinical therapy.0 aOperant conditioning of spinal reflexes from basic science to cl  c03/2014  a250 v83 aNew appreciation of the adaptive capabilities of the nervous system, recent recognition that most spinal cord injuries are incomplete, and progress in enabling regeneration are generating growing interest in novel rehabilitation therapies. Here we review the 35-year evolution of one promising new approach, operant conditioning of spinal reflexes. This work began in the late 1970's as basic science; its purpose was to develop and exploit a uniquely accessible model for studying the acquisition and maintenance of a simple behavior in the mammalian central nervous system (CNS). The model was developed first in monkeys and then in rats, mice, and humans. Studies with it showed that the ostensibly simple behavior (i.e., a larger or smaller reflex) rests on a complex hierarchy of brain and spinal cord plasticity; and current investigations are delineating this plasticity and its interactions with the plasticity that supports other behaviors. In the last decade, the possible therapeutic uses of reflex conditioning have come under study, first in rats and then in humans. The initial results are very exciting, and they are spurring further studies. At the same time, the original basic science purpose and the new clinical purpose are enabling and illuminating each other in unexpected ways. The long course and current state of this work illustrate the practical importance of basic research and the valuable synergy that can develop between basic science questions and clinical needs.10aH-Reflex10alearning and memory10aLocomotion10aspinal cord injury10aspinal cord plasticity1 aThompson, Aiko, K1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/24672441