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CHAPTER 4 allodynia/hyperalgesia (Bryce, 2009; Finnerup et al., 2009; Gwak et al., 2012; Hulsebosch et al., 2009; Jensen and Finnerup, 2014; Widerstrom-Noga et al., 2014). Although changes at the spinal and the supraspinal level have been correlated with the development of these two distinct pain phenotypes, the exact underlying mechanism remains unclear (Hari et al., 2009; Jensen and Finnerup, 2014; Siddall et al., 2003; Wrigley et al., 2009). While there was an overall treatment effect (Figure 4.2), 670 nm did not change the mechanical sensitivity of hypersensitive animals from 1 to 5-dpi (Figure 4.4). The failure to reach a significant difference between the hypersensitive subpopulations at 7-dpi (p = 0.10) is likely to have resulted from the high variability in mechanical sensitivity in combination with an insufficient number of animals developing hypersensitivity at 7-dpi. In support of this, it has been previously demonstrated that a significant difference existed between light-treated and untreated groups in a study with a larger sample size following a mild/moderate hemicontusion spinal cord injury (Hu et al., 2016). Furthermore, the observation from the present study, of a significant difference in the trajectory of pain development (i.e. at the below level regions) between the two injured groups over the 5 and 7-day recovery periods, further supports the notion of light-induced changes in the hypersensitive population from 7-dpi. Mechanical testing over the 7-day period is unlikely to desensitize the animals to the stimulus, which is supported by the lack of a time effect in sham-injured animals. By definition, the mechanical sensitivity observed in normosensitive SCI animals is within the range of uninjured animals, and therefore indicates a lack of pain. However, their sensitivity scores were significantly elevated compared to the shamSCI normosensitive population, suggesting that some degree of discomfort may be experienced in the normosensitive SCI group. Interestingly, 670 nm light reduces mechanical sensitivity in normosensitive spinal cord injured animals, as well as sham-injured animals (Figure 4.3c and Figure 4.5). As previously shown, the reduction in sensitivity is not due to reduced functional integrity of the dorsal column pathway (Hu et al., 2016), suggesting it arises from the anterolateral system. Following the surgery, bradykinins are released which elicits pain/sensitisation in the skin, while endogenous opioids such as endorphins are produced to control the pain (Stein et al., 2009). Photobiomodulation has been shown to decrease bradykinins while increasing endorphins (Chaves et al., 2014; Lins et al., 2010), therefore the effect of red light in the present study may result from alterations to bradykinins and/or endogenous opioids, leading to an overall reduction in sensitivity across all groups. Further studies pursuing this line of reasoning would be of great interest. Following spinal cord injury, pro-inflammatory cytokines are secreted by activated glial cells, both microglia/macrophages and astrocytes. During the post-injury period, astrocytes, together with microglia/macrophages, are activated through a combination of different mechanisms that involve neuro-inflammation, ionic imbalance and cytokines/chemokines (Gwak et al., 2012). Regional and global increases in GFAP expression have been documented from 2 hours and to 106PDF Image | Effects of Red Light Treatment on Spinal Cord Injury
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