4.7 Article

Exploratory associations with Tumor Necrosis Factor-α, disinhibition and suicidal endorsement after traumatic brain injury

Journal

BRAIN BEHAVIOR AND IMMUNITY
Volume 41, Issue -, Pages 134-143

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2014.05.020

Keywords

Brain injury; Depression; Inflammation; Suicide; Tumor Necrosis Factor-Alpha; Disinhibition; Impulsivity

Funding

  1. CDC [R49 CCR 323155]
  2. DOD [W81XWH-071-0701]
  3. University of Pittsburgh's Women's Studies Faculty Research Fund
  4. NIDRR [H133A120087]
  5. UPMC Rehabilitation Institute

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Purpose: To examine the relationship of Tumor Necrosis Factor (TNF)-alpha to disinhibition and suicidal endorsement after traumatic brain injury (TBI). Participants: Adults with moderate to severe TBI (acute serum levels: n = 48, n = 543 samples; acute CSF levels: n = 37, n = 389 samples; chronic serum levels: n = 48, n = 326 samples). Main measures: TNF alpha levels (CSF, Serum) from time of injury to 12 months post-injury; Frontal Systems Behavior Scale - Disinhibition Subscale at 6 and 12 months post-injury; Patient Health Questionnaire at 6 and 12 months post-injury. Results: Participants with TBI had significantly higher CSF and serum TNF alpha levels than healthy controls (p < 0.05). Acute and chronic serum TNF alpha was significantly associated with disinhibition at 6 months post-injury (p = 0.009, p = 0.029 respectively), and 6 month disinhibition was associated with suicidal endorsement at both 6 and 12 months (p = 0.045, p = 0.033 respectively) and disinhibition at 12 months post-injury (p < 0.001). Conclusion: These preliminary data suggest a biological to behavioral pathway of suicidality after TBI, from TNF alpha to disinhibition to suicidal endorsement. Future investigation is warranted to validate these findings and clarify what biological mechanisms might underlie these relationships. (C) 2014 Elsevier Inc. All rights reserved.

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