4.6 Article

Traumatic brain injuries

期刊

NATURE REVIEWS DISEASE PRIMERS
卷 2, 期 -, 页码 -

出版社

NATURE PUBLISHING GROUP
DOI: 10.1038/nrdp.2016.84

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资金

  1. US Department of Defense [WH81XWH-14-2-0018]
  2. US National Institute of Neurological Disorders and Stroke [R21 NS086714-01]
  3. US Department of Veterans Affairs
  4. Veterans Affairs Biorepository [CSP 501]
  5. National Institute of Neurological Disorders and Stroke [1U01NS086659-01]
  6. US National Institute of Ageing Boston University Alzheimer disease Disease Center [P30AG13846, 0572063345-5]
  7. Department of Defense [W81XWH-13-2-0064, WXWH-13-2-0095, VA I01 RX 002170]
  8. National Operating Committee on Standards for Athletic Equipment
  9. Concussion Legacy Foundation
  10. Andlinger Foundation
  11. World Wrestling Entertainment
  12. National Football League

向作者/读者索取更多资源

Traumatic brain injuries (TBIs) are clinically grouped by severity: mild, moderate and severe. Mild TBI (the least severe form) is synonymous with concussion and is typically caused by blunt non-penetrating head trauma. The trauma causes stretching and tearing of axons, which leads to diffuse axonal injury - the best-studied pathogenetic mechanism of this disorder. However, mild TBI is defined on clinical grounds and no well-validated imaging or fluid biomarkers to determine the presence of neuronal damage in patients with mild TBI is available. Most patients with mild TBI will recover quickly, but others report persistent symptoms, called post-concussive syndrome, the underlying pathophysiology of which is largely unknown. Repeated concussive and subconcussive head injuries have been linked to the neurodegenerative condition chronic traumatic encephalopathy (CTE), which has been reported post-mortem in contact sports athletes and soldiers exposed to blasts. Insights from severe injuries and CTE plausibly shed light on the underlying cellular and molecular processes involved in mild TBI. MRI techniques and blood tests for axonal proteins to identify and grade axonal injury, in addition to PET for tau pathology, show promise as tools to explore CTE pathophysiology in longitudinal clinical studies, and might be developed into diagnostic tools for CTE. Given that CTE is attributed to repeated head trauma, prevention might be possible through rule changes by sports organizations and legislators.

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