Exercise after spinal cord injury as an agent for neuroprotection, regeneration and rehabilitation
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- Exercise is neuroprotective after SCI by preventing neuropathic pain.
- The number of injured neurons that regenerate their axon increases with exercise.
- Exercise affects the molecular, cellular and physiological make-up of the injured spinal cord.
Basics of spinal cord injury
An SCI can be described in two phases, the initial mechanical trauma to neurons, glial cells and their surrounding vasculature followed by a secondary expansive phase, which results in invasive degeneration of the surrounding spinal cord tissue. Events at the cellular level include apoptosis of neurons and glial cells (particularly oligodendrocytes), axon retraction, glial scarring, and recruitment of inflammatory cells, demyelination and subsequent exposure of myelin-associated inhibitory molecules, and aberrant sprouting /plasticity of spared nerve fibers/pathways Biochemical changes, such as excitotoxicity, alterations to the electrophysiological properties of neurons, and the release of proinflammatory factors also are initiated once an injury has been incurred. The severity and degree of permanence of the motor and/or sensory deficits is dependent upon the location and extent of damage to the spinal cord tissue. If the initial injury is a contusion or bruising of the spinal cord, which is the most common form of SCI, then there may be some tissue sparing which can result in the retention of function. This form of injury is called an incomplete SCI. A transection through the spinal cord results in a complete interruption or separation between spinal segments causing total loss of motor and sensory function and is a model of complete SCI.
Spinal cord injury (SCI) is a traumatic event from which there is limited recovery of function, despite the best efforts of many investigators to devise realistic therapeutic treatments. Partly this is due to the multifaceted nature of SCI, where there is considerable disarray and dysfunction secondary to the initial injury. Contributing to this secondary degeneration is neurotoxicity, vascular dysfunction, glial scarring, neuroinflammation, apoptosis and demyelination. It seems logical that addressing the need for neuroprotection, regeneration and rehabilitation will require different treatment strategies that may be applied at varied stages of the post-injury response. Here we focus on a single strategy, exercise/physical training, which appears to have multiple applications and benefits for an acute or chronic SCI.
Exercise has been demonstrated to be advantageous at cellular and biochemical levels, as well as being of benefit for the whole animal or human subject. Data from our lab and others will be discussed to further elucidate the many positive aspects of implementing exercise following injury and to suggest that rehabilitation is not the sole target of a training regimen following SCI.
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All the manuscripts published by Journal of Brain Research are available freely online immediately after publication without any subscription charges or registration.
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