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  • Age as a Key Determinant of Inflammatory Response, Glial and Axonal Survival After Traumatic Spinal Cord Injury

    Final Number:
    154

    Authors:
    Julio C Furlan MD PhD MBA MSc; Yang Liu; Dalton Dietrich PhD; Michael Norenberg MD; Sydney Croul MD; Michael G. Fehlings MD PhD FRCSC FACS

    Study Design:
    Other

    Subject Category:

    Meeting: Congress of Neurological Surgeons 2014 Annual Meeting

    Introduction: This study examines whether age is a key determinant for inflammatory response, oligodendroglial apoptosis and axonal survival after traumatic spinal cord injury (SCI).

    Methods: This study includes post-mortem spinal cord tissue from 64 cases of SCI (at cervical or high-thoracic level) and 38 controls cases. Each group was subdivided into younger and elderly individuals (65 years of age or older). Alternating 6-microm sections from 2 to 3 segments caudal to the SCI and age/sex/level-matched segments from controls were stained for: (i) neuroinflammation (neutrophils, macrophages, cytotoxic-T/natural-killer cells, helper/regulator-T cells, B-cell lymphocytes); (ii) apoptotic oligodendrocytes; (iii) axons; (iv) extent of degeneration. The number of cells or axons was counted in the motor and sensory areas within the spinal cord using unbiased stereological techniques.

    Results: There were 25 women and 77 men with a mean age of 58.6 years (range from 16 to 90 years). Younger and elderly individuals had statistically similar number of neutrophils, macrophages, and lymphocytes in most of the stages after SCI. Yet, younger individuals showed significantly greater number of B-cell lymphocytes within the lateral corticospinal tracts in the subacute stage after SCI than elderly individuals. Younger and elderly individuals had statistically similar number of oligodendrocytes in apoptosis in all stages after SCI. The number of preserved axons did not significantly differ between younger and elderly individuals with SCI and without prior CNS injury. Extend of degeneration within the spinal cord white matter did not significantly differ between the two groups.

    Conclusions: Our results indicate that age at the time of injury does not adversely affect the cellular inflammatory response, oligodendroglial apoptosis and axonal survival after traumatic SCI. Those results are consistent with prior clinical studies that have shown no significant effects of age on neurological and functional recovery following traumatic SCI when data analysis is adjusted for potential confounders.

    Patient Care: The results of this study support the notion that elderly individuals can potentially have similar benefits of the ongoing translational studies focused on neuroprotective strategies based on modulation of neuroinflammation. Based on our study, protocols of future translational studies and clinical trials for neuroprotective strategies focused on oligodendrocyte preservation of adults with traumatic SCI should include elderly individuals.

    Learning Objectives: By the conclusion of this session, participants should be able to: 1) Describe the influence of age at the time of trauma on neuroinflammatory response to spinal cord injury, 2) Recognize the effects of age on oligodendrocyte preservation and axonal survival following traumatic spinal cord injury, and 3) Identify the importance of age as a potential confounder in future translational studies focused on neuroprotective strategies in the management of adults with traumatic spinal cord injury.

    References:

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