Peripheral immune cells including macrophages, neutrophils and T cells can initiate the inflammatory response after SCI and finally can be higher level within few days. Macrophages and neutrophils can cause the growth of lesion and lead to damage tissue. By releasing cytokines (TNF, IL-1, IL-6, IL-10), macrophages and microglia can involve in the inflammatory reaction and secondary pathological changes. At the lesion site, inflammatory mediators including bradikynin, prostaglandins, leu-kotrienes, platlet suppressing factors and serotonin can be stored. Central nervous system inflammatory response may be promoted by cytokines, chemokines, nitric oxides, oxygen also expression of nitrogen species. From the animal model, after 30 minutes by the administration of IL-10, the inflammation is decreased. IL0-10 which is neuroprotective can develop motor function.
The generation of free radicals that is a vital issue to maintain the viability o
...f cells. The activity of anti-oxidants was reduced by aging which is most vital role to cause the SCI. From the experimental studies, Cyclosporin A, Vitamin E, Selenium proved to be effective for SCI. Also from other studies, lipid peroxidation process is inhibited by melatonin, mexiletine, thiopental, and propofol after the SCI.
There is a directory influence in excitatory neurotransmitter in the spinal card by NMDA receptors. A study prove that the blockade of NMDA receptor which have good protective activity in the secondary damage to the traumatic also ischemic animal models. NMDA antagonists can significantly improve neurological functions and decrease the occurring chance of edema. Magnesium ions can block this type of receptors. Study shows that injured area is reduced and functional improvement is occurred by the administration of AMPA antagonist. Glutamate which is major excitatory neurotransmitter located in the central nervou
system. Study detected that the neuronal damage occurred due to over activation of glutamate receptors. After SCI, Excitatory amino acids, glutamate and aspirates are peak up within few minutes. In the spinal cord, the concentration of extracellular excitatory amino acid arrived to the toxic level within 15 minutes till 120 minutes. However, extracellular excitatory amino acids have much toxic effect for the neurons during the SCI.
Apoptosis is found after SCI in human being which is accelerated due to the release of cytokines, inflammation, free radicals as well as excitotoxicity. After 3 hours to 8 weeks in traumatic SCI, the death of apoptotic cell is seen. From the experimental studies, after a few week of injury occurring of dimyelinization was intensified by apoptosis in oligodentrocytes. Crow et.al showed that oligodentrocytic changes in SCI for the initial period.
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