Abstract
Spinal lesions substantially impair ambulation, occur generally in young and otherwise healthy individuals, and result in devastating effects on quality of life. Restoration of locomotion after damage to the spinal cord is challenging because axons of the damaged neurons do not regenerate spontaneously. Body-weight-supported treadmill training (BWSTT) is a therapeutic approach in which a person with a spinal cord injury (SCI) steps on a motorized treadmill while some body weight is removed through an upper body harness. BWSTT improves temporal gait parameters, muscle activation patterns, and clinical outcome measures in persons with SCI. These changes are likely the result of reorganization that occurs simultaneously in supraspinal and spinal cord neural circuits. This paper will focus on the cortical control of human locomotion and motor output, spinal reflex circuits, and spinal interneuronal circuits and how corticospinal control is reorganized after locomotor training in people with SCI. Based on neurophysiological studies, it is apparent that corticospinal plasticity is involved in restoration of locomotion after training. However, the neural mechanisms underlying restoration of lost voluntary motor function are not well understood and translational neuroscience research is needed so patient-orientated rehabilitation protocols to be developed.
Highlights
Spinal cord injuries (SCIs) cause substantial social, economic, and health burdens
The soleus H-reflex amplitude was enhanced after 3 week isometric maximal plantar flexion training when measured at 20% and 60% of maximal voluntary contraction (MVC) [102], with similar results to be reported after 14 week of resistance training that involved heavy weight-lifting exercises for the leg muscles with reflexes measured during maximal isometric ramp contractions [103]
spinal cord injury (SCI) changes the human body homeostasis leading to myriad changes of multiple systems
Summary
Spinal cord injuries (SCIs) cause substantial social, economic, and health burdens. In the majority of cases, the spinal cord is not completely severed and some fiber tracts and segmental spinal cord circuits remain intact [1], which determine the preserved functions and provide the basis for functional restoration. Treadmill training increases axonal regrowth and collateral sprouting proximal to the lesion site in mice [20], phosphorylation of Erk1/2 in the motor cortex as well as the spinal cord injury area [21], expression of brain-derived neurotrophic factor (BDNF) in the spinal cord [22], ameliorates muscle atrophy in moderate contused SCI rats [23], and alters properties of spinal motor neurons [24] These changes are only a small representation of activity-dependent plasticity located at the synaptic terminals of a variety of systems, that involves physiological, structural, and biochemical changes (see more in [25, 26]).
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