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Spinal Cord Injury Research Paper

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vThe spinal cord is well-protected anatomically with barriers, vertebra, muscles of the back, and the meninges. A considerable force is required to cause trauma to the neural tissue of the spinal cord. This can be laceration or maceration by a sharp penetrating object; contusion or compression, the most common form of spinal cord injury; or infarct by vascular insult. All of these injury forces begin the process of tissue destruction we term the primary injury.

These mechanical forces predominately damage the central grey matter, due to its softer and highly vascularised nature, causing massive loss of essential cells, including local neurons, astrocytes, oligodendrocytes and endothelial cells in the vicinity of the injury site (Dumont et …show more content…

The prolonged excitatory activation of ionotropic N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors as well as metabotropic glutamate receptor lead to neuronal cell death (Caccamo et al., 2004, Park et al., 2004). It is commonly accepted that ionotropic glutamate receptors are responsible for the harmful effect of excitotoxicity. The continued binding of excess glutamate to NMDA receptor induces the uncontrolled influx of calcium ions (Ca2+). This massive overload of intracellular Ca2+ leads to activation of calpain and mitochondrial oxidative phosphorylation which ultimately causes apoptosis (Caccamo et al., 2004, Choi, 1992, Lawson and Lowrie, 1998). The AMPA receptor is involved in regulating the influx of sodium ions (Na+). The continued activation of AMPA receptors, due to the unwarranted glutamate level, induces influx of Na+ which consequently leads to osmotic imbalance and swelling of the neurons (Caccamo et al., 2004). The excess swelling of neurons can leads to necrosis (Park et al., 2004). Consider as a therapeutic target, extracellular glutamate concentrations increase to neurotoxic levels within the first three hours after the injury (Liu et al., 1999, Liu and Bilkey, 1999, McAdoo et al., 1999), leaving a small time window for immediate treatment to prevent …show more content…

This protein has been shown to activate the epidermal growth factor receptor (EGFR) thereby inhibiting neurite outgrowth and axon regeneration (Schachtrup et al., 2007). In addition to plasma proteins, there is invasion of blood circulating inflammatory cells into the spinal cord through the disrupted BSB. Since spinal cord is considered as an immune-privileged or immunologically quiescent site, the sudden influx of immune cells dramatically alters the regulation of the inflammatory response in the injured spinal cord (Trivedi et al., 2006). This dysregulation of the inflammatory response plays a major role in enlargement of tissue damage in the secondary phase of the injury. As such, it is thought that the initial damage to the local blood vessels and BBB is decisive for the disruption events that cause the secondary phase of injury (Mautes et al., 2000a, Mautes et al.,

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