Virginia Research Day 2025

Medical Student Research Biomedical

13 The Effects of Blast-Induced Spinal Cord Injury on Myelination Over Time

Christine Lewis 1 ; Jazmin Rio 1 ; Carly Norris 2,3 ; Susan Murphy 3 ; Pamela VandeVord 3,4 ; Kelly C.S. Roballo 1,5 Corresponding author: jrio@vcom.vt.edu 1 Edward Via College of Osteopathic Medicine - VCOM Virginia 2 School of Biomedical Engineering and Sciences, Virginia Tech, Blacksburg, VA, United States 3 Department of Biomedical Engineering and Mechanics, Virginia Tech, Blacksburg, VA, United States 4 Veterans Affairs Medical Center, Salem, VA, United States

Chronic neuropathic pain is an unfortunate type of pain that many adults in the United States live with every day. For many patients, palliative care is the standard of treatment as there is a lack of research for definitive care. Blast-induced spinal cord injury (bSCI) causes neuropathic pain through the induction of widespread oligodendrocyte death, resulting in loss of myelin maintenance and myelin production. Remyelination occurs, but it is currently unknown what the extent of remyelination is and its effectiveness at regaining function. An important factor in the degree of remyelination and myelin degradation is the timing of the bSCI. This study aimed to identify the time frame of the bSCI and the progression of the degradation injury on the

myelin. Understanding the timeline of nerve injury progression could correlate to the progression of chronic neuropathic pain, providing a more individualized treatment regimen. We propose that 24 48 hours is a critical period for myelin regeneration to occur. 24 Sprague Dawley rats underwent a blast injury. Following blast exposure, spinal cord sections were isolated at 24, 48, and 72 hours, and myelin density was analyzed. The blast mice averaged 16, 24, and 17 on greyscale intensity for the 24, 48, and 74 hours respectively. The control mice averaged 23, 18, and 24 on greyscale intensity for the 24, 48, and 74 hours respectively. The blast mice had higher greyscale intensity than the control mice at

48 hours, suggestive of remyelination in the blast mice. However, with a p<0.05, the t-test showed that the results were insignificant. Although the null hypothesis cannot be rejected, it shows the importance of timing in the process of myelin degradation and remyelination, which can be applied towards target therapy for those with chronic neuropathic pain. To determine if there is significance, we will be repeating this study larger population size. In addition to investigating myelin after a bSCI, another avenue future research could explore would be the biochemical pathways involved in bSCI that result in oligodendrocyte death. This could reveal targets for intervention to halt the progression of bSCI.

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