Effects of Red Light Treatment on Spinal Cord Injury

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CHAPTER 3 freshly sacrificed rats (each dot represents the mean of triplicate readings). Readings shown are taken at the light source (through the Perspex restraining box, intensity at dorsal surface) and at the ventral surface of the spinal cord as shown by the white arrow in b (intensity at ventral surface). Black arrow indicates proportion of light absorbed and/or scattered by intervening tissues. (d) Spectral analysis of the light source indicating central frequency of 675 nm. 3.4.2 Surface temperature changes following light treatment The surface temperature of rats was measured directly before, and 2 minutes after treatment. 27 readings from sham-treated, and 25 readings from light-treated animals were acquired from 4 animals in each group over consecutive days of treatment. While there was no significant difference in the surface temperature of sham-treated animals (before, 33.6 ± 0.23 °C; after, 33.6 ± 0.25 °C) there was a small, but significant increase following light treatment (before, 32.8 ± 0.36 °C; after, 33.5 ± 0.22 °C; p = 0.038, paired t-test). 3.4.3 Red light reduces allodynia following spinal cord injury To examine the effect of red light on the development of neuropathic pain, allodynia was assessed on 6 regions over the rat dorsum using a T10 hemicontusion spinal cord injury model that results in clear development of hypersensitivity in most animals within 7 days. The T10 spinal hemicontusion resulted in 63% of animals (n = 12) developing hypersensitivity in both sham- treated (SCI, n = 19) and light-treated (SCI+670, n = 19) groups at 7 days post-injury. The hypersensitive subpopulation of rats from the SCI group had a mean CSS (SCI, CSS: 25.3 ± 4.5) that was 3.7 × the hypersensitive threshold (Figure 3.2a). The mean CSS was significantly reduced by 40% (SCI+670, CSS: 14.5 ± 1.6; 2.1 × the hypersensitivity threshold) in the hypersensitive subpopulation of rats from the SCI+670 group. Light treatment significantly reduced At- (T9-T12 dermatomes) and Below- (L2-L5 dermatomes) LSSs, which arose from contralateral At-Level and both ipsi-and contralateral Below-Level regions (Figure 3.2b). Compared to the uninjured control group (control, Figure 3.2c), sham injury without light treatment (shamSCI, n = 8) had no significant effect on LSS or RSS despite two sham-injured animals developing At-Level hypersensitivity. Light treatment of sham-injured animals (shamSCI+670, n = 10) resulted in significant reductions of At- and Below-LSS compared to the shamSCI group (Figure 3.2c). Thus, while the incidence of hypersensitivity was not altered by red light, the level of hypersensitivity was markedly reduced At- and Below-levels in T10 contused light-treated allodynic animals. Red light also caused a significant reduction in sensitivity in 670-treated sham-injured animals (shamSCI+670, CSS: 0.8 ± 0.5) compared to uninjured control animals (control, CSS: 2.8 ± 0.8) as well as normosensitive spinal cord injured animals (SCI, CSS: 3.5 ± 0.9), even though these animals were not hypersensitive. 64

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