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CHAPTER 1 Regeneration Limited regeneration is observed following spinal cord injury due to two main reasons: the limited endogenous regenerative ability of central nervous system (CNS) neurons and the presence of various inhibitors in the cellular microenvironment (Lee and Zheng, 2008). Up-regulation of intrinsic growth factors is limited in CNS neurons (Huebner and Strittmatter, 2009). In fact, axons can start to regenerate 6 hours after injury (Kerschensteiner et al., 2005). Some of them may form correct connections due to neural plasticity through collateral sprouting (Onifer et al., 2011). The rest will fail due to the lack of navigation and the presence of inhibitors. Endogenous oligodendrocyte progenitor cells are also attracted to the injured site for remyelination, but most fail to do so, also due to the presence of inhibitors (Levine et al., 2001). These inhibitors are mainly present in the myelin or the glial scar. Chondroitin sulphate proteoglycan, secreted by reactive astrocytes, is the main inhibitor (reviewed in Morgenstern et al., 2002; Siebert et al., 2014). It has been shown to inhibit both neurite growth and oligodendrocyte progenitor cells (Fawcett and Asher, 1999; Siebert and Osterhout, 2011). Another important inhibitor is Nogo-A, which is present in the myelin. Together with other myelin-associated inhibitors, Nogo-A inhibits axonal growth (Huebner and Strittmatter, 2009). An increase of the regenerative ability of neurons and oligodendrocytes and removal of inhibitors would be largely beneficial to the long-term regeneration following spinal cord injury. These above-mentioned events cause immediate and prolonged changes in the cellular environment which lead to functional deficits. 1.1.1.2 Functional deficits Sensory and motor function of the periphery is maintained and controlled by the spinal cord. Upon spinal cord injury, functional deficits may occur in motor control and/or sensory feedback. Pain (Page 11) is also present and can persist following spinal cord injury (in > 50% of patients). Spinal cord injured patients may also suffer from autonomic dysfunction and paralysis/paresis at, and below, the neurological level of injury. Some cardiovascular and respiratory dysfunction can be life-threatening in the acute phase, and some of these symptoms may continue into the chronic phase (reviewed in Karlsson, 2006). The current section will only focus on the somatic system by providing an overview of the arrangement of the motor and sensory pathways, and changes to these pathways following spinal cord injury. Motor pathways and functional deficits The motor pathways (Figure 1.1) are responsible for both voluntary (corticospinal and corticobulbar tracts) and involuntary (extrapyramidal tracts) movement of all skeletal muscles in the body. All motor tracts consist of upper motor neurons which communicate indirectly, via interneurons or rarely via direct contacts with lower motor neurons that reside in the brainstem or spinal cord. 7PDF Image | Effects of Red Light Treatment on Spinal Cord Injury
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