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The pathophysiology of traumatic brain injury at a glance
Open accessAbstract
Summary: Traumatic brain injury (TBI) is defined as an impact, penetration or rapid movement of the brain within the skull that results in altered mental state. TBI occurs more than any other disease, including breast cancer, AIDS, Parkinson’s disease and multiple sclerosis, and affects all age groups and both genders. In the US and Europe, the magnitude of this epidemic has drawn national attention owing to the publicity received by injured athletes and military personnel. This increased public awareness has uncovered a number of unanswered questions concerning TBI, and we are increasingly aware of the lack of treatment options for a crisis that affects millions. Although each case of TBI is unique and affected individuals display different degrees of injury, different regional patterns of injury and different recovery profiles, this review and accompanying poster aim to illustrate some of the common underlying neurochemical and metabolic responses to TBI. Recognition of these recurrent features could allow elucidation of potential therapeutic targets for early intervention.
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“We counted brainstem neurons in a blinded manner using the same stereological procedures as previously described.9”
From Damage to Arousal-Promoting Brainstem Neurons with Traumatic Brain Injury (2016) · cites this paper as [9]
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“Additional factors that may protect the brainstem include lower metabolic requirements and a blood supply less likely to be damaged by direct traumatic forces.9”
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Recent Advances in Pathophysiology of Traumatic Brain Injury
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“The primary injury of TBIs, caused by trauma to the head which for example might stretch, compress or tear blood vessels and axons, is not the only reason why patients die or are disabled (Prins et al., 2013).”
BackgroundThe synapse in traumatic brain injury
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“The mechanical injury (primary insult) causes instantaneous tissue damage, which is followed by multiple secondary injury processes (Prins et al., 2013).”
BackgroundThe NLRP3 inflammasome in traumatic brain injury: potential as a biomarker and therapeutic target
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Metadata
- Authors
- Prins, M., Greco, T., Alexander, D., & Giza, C. C.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Prins, Mayumi
- Venue
- Disease Models & Mechanisms
- Publisher
- The Company of Biologists
- Published
- 2013-01-01
- Volume
- 6
- Issue
- 6
- Pages
- 1307-15
- ISSN
- 1754-8403 (ISSN-L)
- 1754-8411
- PMC
- PMC3820255
- OpenAlex
- W2141923055
- Cited by
- 426
- References
- 114
- Citations by year
- 2026: 7 · 2025: 29 · 2024: 37 · 2023: 40 · 2022: 41 · 2021: 55 · 2020: 55 · 2019: 40 · 2018: 46 · 2017: 27 · 2016: 14 · 2015: 24 · 2014: 8 · 2013: 3
- FWCI
- 10.37
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Disease Models & Mechanisms (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute of Neurological Disorders and Stroke (NS-058489, P01NS058489)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Physical Sciences › Engineering › Biomedical Engineering › Automotive and Human Injury Biomechanics
- Keywords
- traumatic brain injury, pathophysiology, brain metabolism, altered mental status, injury patterns, recovery profiles, therapeutic target, TBI epidemiology
- MeSH terms
- Brain, Brain Injuries, Free Radicals, Glucose, Humans, Mitochondria
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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