Abstract
Simple SummarySpinal cord injury results in a decreased quality of life and impacts hundreds of thousands of people in the US alone. This review discusses the underlying cellular mechanisms of injury and the concurrent therapeutic hurdles that impede recovery. It then describes the phenomena of neural plasticity—the nervous system’s ability to change. The primary focus of the review is on the impact of cervical spinal cord injury on control of the upper limbs. The neural plasticity that occurs without intervention is discussed, which shows new connections growing around the injury site and the involvement of compensatory movements. Rehabilitation-driven neural plasticity is shown to have the ability to guide connections to create more normal functions. Various novel stimulation and recording technologies are outlined for their role in further improving rehabilitative outcomes and gains in independence. Finally, the importance of sensory input, an often-overlooked aspect of motor control, is shown in driving neural plasticity. Overall, this review seeks to delineate the historical and contemporary research into neural plasticity following injury and rehabilitation to guide future studies.Neuroplasticity is a robust mechanism by which the central nervous system attempts to adapt to a structural or chemical disruption of functional connections between neurons. Mechanical damage from spinal cord injury potentiates via neuroinflammation and can cause aberrant changes in neural circuitry known as maladaptive plasticity. Together, these alterations greatly diminish function and quality of life. This review discusses contemporary efforts to harness neuroplasticity through rehabilitation and neuromodulation to restore function with a focus on motor recovery following cervical spinal cord injury. Background information on the general mechanisms of plasticity and long-term potentiation of the nervous system, most well studied in the learning and memory fields, will be reviewed. Spontaneous plasticity of the nervous system, both maladaptive and during natural recovery following spinal cord injury is outlined to provide a baseline from which rehabilitation builds. Previous research has focused on the impact of descending motor commands in driving spinal plasticity. However, this review focuses on the influence of physical therapy and primary afferent input and interneuron modulation in driving plasticity within the spinal cord. Finally, future directions into previously untargeted primary afferent populations are presented.
Highlights
The negative consequences of spinal cord injury (SCI) arise from far more than the loss of directly damaged grey matter and neural pathways
Following an overview of the term “neuroplasticity,” this review will focus on the plasticity that occurs naturally following SCI, and how rehabilitative strategies enhance recovery of upper extremity or forelimb function through afferent driven and interneuron-mediated local plasticity in the spinal cord
Neuroplasticity is defined as the potential for functional and anatomical changes of the nervous system in response to stimuli during learning or in response to injury [34]
Summary
The negative consequences of spinal cord injury (SCI) arise from far more than the loss of directly damaged grey matter and neural pathways These dead and dying neurons release death signals which exacerbate the injury. In an effort to mitigate secondary injury, reactive astrocytes physically limit the spread of inflammation, compensate for a leaky blood brain barrier, and reduce lesion expansion by forming a glial scar [7,8,9] This physical barrier may prevent axonal regeneration through the lesion. Wallerian degeneration of the distal axons and myelin results in debris releasing Nogo, OMGp, and MAG, which have all been shown to inhibit regeneration and sprouting [18] These impediments limit the efficacy of spontaneous recovery. Following an overview of the term “neuroplasticity,” this review will focus on the plasticity that occurs naturally following SCI, and how rehabilitative strategies enhance recovery of upper extremity or forelimb function through afferent driven and interneuron-mediated local plasticity in the spinal cord
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