After spinal cord injury (SCI), various sensorimotor functions can recover, ranging from simple spinal reflexes to more elaborate motor patterns, such as locomotion. Locomotor recovery after complete spinalization (complete SCI) must depend on the presence of spinal circuitry capable of generating the complex sequential activation of various leg muscles. This is achieved by an intrinsic spinal circuitry, termed the central pattern generator (CPG), working in conjunction with sensory feedback from the legs. After SCI, different changes in cellular and circuit properties occur spontaneously and can be promoted by pharmacological, electrical, or rehabilitation strategies. After partial SCI, hindlimb locomotor recovery can result from regeneration or sprouting of spared pathways, but also from mechanisms observed after complete SCI, namely changes within the intrinsic spinal circuitry and sensory inputs.

Recovery of Locomotion After Spinal Cord Injury: Some Facts and Mechanisms

Small lesions of the adult central nervous system (CNS) often have a good prognosis with extensive functional recovery based in part on spontaneous neuritic sprouting and rearrangements of projections. This is well documented for the cortex, but these changes can also occur in the spinal cord. Nogo-A is a protein present in CNS myelin that inhibits neurite growth. Models of spinal cord injury (SCI) in rats and macaque monkeys demonstrate that treatment with function-blocking antibodies of Nogo-A results in an upregulation of growth-specific proteins, enhanced regenerative and compensatory sprouting of fibers, and the formation of new functional connections in the spinal cord. In animals with unilateral sensorimotor cortex lesions followed by Nogo-A antibody treatment, fibers from the intact corticofugal system crossed the midline, supplying innervation to the denervated brain stem or spinal cord. Behavioral tests showed marked improvements of functional recovery in the Nogo-A antibody treated spinal cord- or brain-injured animals. A Phase I clinical trial applying anti-Nogo-A antibody to subjects with acute SCI has been successfully conducted and a multicentric, multinational Phase II trial is currently in preparation.

Anti-Nogo on the go: from animal models to a clinical trial.

A Sensitized IGF1 Treatment Restores Corticospinal Axon-Dependent Functions

Distinct Contributions of Mesencephalic Locomotor Region Nuclei to Locomotor Control in the Freely Behaving Mouse

https://opus.lib.uts.edu.au/bitstream/10453/128482/1/1-s2.0-S0301008217300357-main.pdf

And yet it moves: Recovery of volitional control after spinal cord injury.

Stimulation in the Neonatal Rat Spinal Cord In Vitro Locomotor Rhythm Evoked by Ventrolateral Funiculus

Modificationsof Neurons in Area 4 During Voluntary Gait Corticoreticular Pathways in the Cat. II. Discharge

This chapter reviews a number of experiments on the recovery of locomotion after various types of spinal lesions and locomotor training mainly in cats. We first recall the major evidence on the recovery of hindlimb locomotion in completely spinalized cats at the T13 level and the role played by the spinal locomotor network, also known as the central pattern generator, as well as the beneficial effects of locomotor training on this recovery. Having established that hindlimb locomotion can recover, we raise the issue as to whether spinal plastic changes could also contribute to the recovery after partial spinal lesions such as unilateral hemisections. We found that after such hemisection at T10, cats could recover quadrupedal locomotion and that deficits could be improved by training. We further showed that, after a complete spinalization a few segments below the first hemisection (at T13, i.e., the level of previous studies on spinalization), cats could readily walk with the hindlimbs within hours of completely severing the remaining spinal tracts and not days as is usually the case with only a single complete spinalization. This suggests that neuroplastic changes occurred below the first hemisection so that the cat was already primed to walk after the spinalization subsequent to the hemispinalization 3 weeks before. Of interest is the fact that some characteristic kinematic features in trained or untrained hemispinalized cats could remain after complete spinalization, suggesting that spinal changes induced by training could also be durable. Other studies on reflexes and on the pattern of "fictive" locomotion recorded after curarization corroborate this view. More recent work deals with training cats in more demanding situations such as ladder treadmill (vs. flat treadmill) to evaluate how the locomotor training regimen can influence the spinal cord. Finally, we report our recent studies in rats using compressive lesions or surgical complete spinalization and find that some principles of locomotor recovery in cats also apply to rats when adequate locomotor training is provided.

The "beneficial" effects of locomotor training after various types of spinal lesions in cats and rats.

Locomotion is a very robust motor pattern which can be optimized after different types of lesions to the central and/or peripheral nervous system. This implies that several plastic mechanisms are at play to re-express locomotion after such lesions. Here, we review some of the key observations that helped identify some of these plastic mechanisms. At the core of this plasticity is the existence of a spinal central pattern generator (CPG) which is responsible for hindlimb locomotion as observed after a complete spinal cord section. However, normally, the CPG pattern is adapted by sensory inputs to take the environment into account and by supraspinal inputs in the context of goal-directed locomotion. We therefore also review some of the sensory and supraspinal mechanisms involved in the recovery of locomotion after partial spinal injury. We particularly stress a recent development using a dual spinal lesion paradigm in which a first partial spinal lesion is made which is then followed, some weeks later, by a complete spinalization. The results show that the spinal cord below the spinalization has been changed by the initial partial lesion suggesting that, in the recovery of locomotion after partial spinal lesion, plastic mechanisms within the spinal cord itself are very important.

Chapter 16--spinal plasticity in the recovery of locomotion.

After a complete spinal section, quadruped mammals (cats, rats, and mice) can generally regain hindlimb locomotion on a treadmill because the spinal cord below the lesion can express locomotion through a neural circuitry termed the central pattern generator (CPG). In this review, we propose that the spinal CPG also plays a crucial role in the locomotor recovery after incomplete spinal cord injury.

https://www.physiology.org/doi/pdf/10.1152/physiol.00042.2008

Re-expression of Locomotor Function After Partial Spinal Cord Injury

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