Relationship between Outcome Following Traumatic Brain Injury and Allostatic Load

Wainman-Lefley, J. and McMillan, T. (2016) Relationship between Outcome Following Traumatic Brain Injury and Allostatic Load. The International Brain Injury Association’s Eleventh World Congress on Brain Injury, The Hague, The Netherlands, 02-05 Mar 2016.

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Objectives: There is an association between traumatic brain injury (TBI) and an increased risk of death, for up to 13 years after injury, which is independent of gender, age and social deprivation. The allostatic load (AL) model proposes that stressors cause multi-systemic physiological deregulation, the damage from which accumulates and contributes to disease trajectories. Higher AL is associated with poorer physical and cognitive outcomes in the general population, but has not been investigated systematically in people with TBI. This study investigates relationships between AL and TBI soon after injury and at 6 months follow-up. Methods: AL is a composite construct of anthropometric, cardiovascular, immune, metabolic and neuroendocrine functioning. Data were collected from patients in hospital after a severe TBI and a comparison group matched for age, gender and social deprivation. The primary outcome measure was the Glasgow Outcome at Discharge Scale (GODS) in hospital and outcome at 6 month follow-up on the Glasgow Outcome Scale-Extended (GOSE) if in the community or the GODS if in inpatient rehabilitation. Results: The AL of 36 TBI participants was not significantly different from matched comparison participants at hospital discharge (Wilcoxon signed rank test, z = –1.73, p > 0.05, r = 6.19) or at 6-month follow-up (z = 0.06, p > 0.05, r = 6.55). There was no significant association between AL and the GODS at hospital discharge (Spearman rho = –0.03, p > 0.05) or at 6 month follow-up (GOSE or GODS) (rho = –0.08, p > 0.05). Components of AL (anthropometric, rho = –0.08, p > 0.05; cardiovascular, rho = –0.22, p > 0.05; immune, rho = 0.22, p > 0.05 or metabolic, rho = –0.04, p > 0.05) at hospital discharge did not predict disability outcome at 6 months except for neuroendocrine (rho = –0.45, p < 0.05), where lower levels of dehydroepiandrosterone and higher levels of aldosterone at hospital discharge were associated with poorer ratings on the Glasgow Outcome scales at follow-up. Conclusions: There was no evidence to support the view that cumulative life stress as assessed by allostatic load explains the heterogeneity in outcome after TBI. Greater neuroendocrine system deregulation at hospital discharge was associated with disability outcome at 6 months. Neuroendocrine dysfunction could have significant implications for recovery from TBI and rehabilitation. A better understanding of this relationship is a potential area of future research.

Item Type:Conference or Workshop Item
Glasgow Author(s) Enlighten ID:McMillan, Professor Tom and Wainman-Lefley, Ms Jessica
Authors: Wainman-Lefley, J., and McMillan, T.
College/School:College of Medical Veterinary and Life Sciences > School of Health & Wellbeing > Mental Health and Wellbeing

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