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Nat Rev Dis Primers. 2016 Nov 17;2:16084. doi: 10.1038/nrdp.2016.84.

Traumatic brain injuries.

Author information

1
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, SE-43180 Mölndal, Sweden.
2
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Gothenburg, Sweden.
3
Department of Neurology, Washington University School of Medicine in Saint Louis, St. Louis, Missouri, USA.
4
Department of Critical Care Medicine, Safar Center for Resuscitation Research, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
5
Department of Physical Medicine and Rehabilitation, Baylor College of Medicine, Houston, Texas, USA.
6
Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas, USA.
7
Department of Veterans Affairs, VA Boston Healthcare System, Boston, Massachusetts, USA.
8
Departments of Neurology and Pathology &Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts, USA.
9
Department of Rehabilitation Medicine, Erasmus University Medical Centre, Rotterdam, The Netherlands.
10
Rijndam Rehabilitation Center, Rotterdam, The Netherlands.
11
Departments of Psychiatry, Neurology, Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, California, USA.
12
Department of Veterans Affairs, San Francisco Veterans Affairs Medical Center, San Francisco, California, USA.
13
Institute of Neurology, University College London, London, UK.

Abstract

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.

PMID:
27853132
DOI:
10.1038/nrdp.2016.84
[Indexed for MEDLINE]

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