Abstract
Abstract
Background
Concussion is the most common type of TBI, yet reliable objective measures related to these injuries and associated recovery processes remain elusive, especially in military personnel. The purpose of this study was to characterize the relationship between cytokines and recovery from acute brain injury in active duty service members. Inflammatory cytokines (IL-6, IL-10, and TNFα) were measured acutely in blood samples within 8 h following a medically diagnosed concussion and then 24 h later.
Methods
Participants (n = 94) were categorized into two groups: 1) military personnel who sustained provider-diagnosed concussion, without other major medical diagnosis (n = 45) and 2) healthy control participants in the same deployment environment who did not sustain concussion or other illness or injuries (n = 49). IL-6, IL-10, and TNFα concentrations were measured using an ultrasensitive single-molecule enzyme-linked immunosorbent assay. Differences in cytokine levels between concussed and healthy groups were evaluated at two time points (time point 1 ≤ 8 h after injury; time point 2 = 24 h following time point 1).
Results
At time point 1, IL-6 median (IQR) concentrations were 2.62 (3.62) in the concussed group, which was greater compared to IL-6 in the healthy control group (1.03 (0.90); U = 420.00, z = − 5.12, p < 0.001). Compared to healthy controls, the concussed group did not differ at time point 1 in IL-10 or TNFα concentrations (p’s > 0.05). At time point 2, no differences were detected between concussed and healthy controls for IL-6, IL-10, or TNFα (p’s > 0.05). The median difference between time points 1 and 2 were compared between the concussed and healthy control groups for IL-6, IL-10, and TNFα. Change in IL-6 across time was greater for the concussed group than healthy control (− 1.54 (3.12); U = 315.00, z = − 5.96, p < 0.001), with no differences between groups in the change of IL-10 or TNFα (p’s > 0.05).
Conclusion
Reported here is a significant elevation of IL-6 levels in concussed military personnel less than 8 h following injury. Future studies may examine acute and chronic neurological symptomology associated with inflammatory cytokine levels, distinguish individuals at high risk for developing neurological complications, and identify underlying biological pathways to mitigate inflammation and improve outcomes.
Funder
National Institute of Nursing Research Intramural Program
US Army Medical Research and Development Command
Publisher
Springer Science and Business Media LLC
Subject
Clinical Neurology,General Medicine
Reference48 articles.
1. Jones E, Fear NT, Wessely S. Shell shock and mild traumatic brain injury: a historical review. Am J Psychiatry. 2007;164(11):1641–5.
2. DePalma RG. Frontiers in Neuroengineering.Combat TBI: History, Epidemiology, and Injury Modes. In: Kobeissy FH, editor. Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects. Boca Raton: CRC Press/Taylor & Francis.(c) 2015 by Taylor & Francis Group, LLC; 2015.
3. Prieto DA, Ye X, Veenstra TD. Proteomic analysis of traumatic brain injury: the search for biomarkers. Expert Rev Proteomics. 2008;5(2):283–91.
4. Meerlo P, Sgoifo A, Suchecki D. Restricted and disrupted sleep: effects on autonomic function, neuroendocrine stress systems and stress responsivity. Sleep Med Rev. 2008;12(3):197–210.
5. Ritenour AE, Baskin TW. Primary blast injury: update on diagnosis and treatment. Crit Care Med. 2008;36(7 Suppl):S311–7.
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