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Cited by 462Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchAutomotive and Human Injury Biomechanics

Animal models of head trauma

Open access
Cernak, Ibolja·2005·NeuroRX
DOI 10.1602/neurorx.2.3.410PMC PMC1144485
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Abstract

Animal models of traumatic brain injury (TBI) are used to elucidate primary and secondary sequelae underlying human head injury in an effort to identify potential neuroprotective therapies for developing and adult brains. The choice of experimental model depends upon both the research goal and underlying objectives. The intrinsic ability to study injury-induced changes in behavior, physiology, metabolism, the blood/tissue interface, the blood brain barrier, and/or inflammatory- and immune-mediated responses, makes in vivo TBI models essential for neurotrauma research. Whereas human TBI is a highly complex multifactorial disorder, animal trauma models tend to replicate only single factors involved in the pathobiology of head injury using genetically well-defined inbred animals of a single sex. Although such an experimental approach is helpful to delineate key injury mechanisms, the simplicity and hence inability of animal models to reflect the complexity of clinical head injury may underlie the discrepancy between preclinical and clinical trials of neuroprotective therapeutics. Thus, a search continues for new animal models, which would more closely mimic the highly heterogeneous nature of human TBI, and address key factors in treatment optimization.

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  • Experimental animal models are critical in understanding the links between clinical outcomes of TBI and cellular/molecular dysfunction resulting in neuroendocrine dysfunction.

    “They are critical in understanding the links between the clinical outcomes of TBI and some cellular/ molecular dysfunction resulting in neuroendocrine dysfunction (193).”

    From Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach (2015) · cites this paper as [193]

    The Introduction and Conclusion describe animal TBI models as important for relating injury outcomes to cellular and molecular mechanisms. Neither passage establishes that those mechanisms result in neuroendocrine dysfunction; searches for neuroendocrine and endocrine terms did not find support for that part of the claim. (LLM, conf=0.85)

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Research works printed but not linked: 1

  1. [2]2. Lighthall JW, Anderson TE. In: The neurobiology of cenral ner- vous system trauma (Salzman SK, Faden AI, eds), pp 3-12. New York/Oxford: Oxford University Press, 1994.

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Authors
Cernak, I.
Venue
NeuroRX
Publisher
Springer Science and Business Media LLC
Published
2005-07
Volume
2
Issue
3
Pages
410-422
ISSN
1545-5343 (ISSN-L)
DOI
10.1602/neurorx.2.3.410
PMC
PMC1144485
OpenAlex
W2056804957
Semantic Scholar
05857a6126f1be753c6b0c93d060bf3ee85f30ce
Cited by
462
References
210
Citations by year
2026: 5 · 2025: 8 · 2024: 21 · 2023: 15 · 2022: 15 · 2021: 21 · 2020: 16 · 2019: 30 · 2018: 26 · 2017: 31 · 2016: 41 · 2015: 36 · 2014: 37 · 2013: 29 · 2012: 31
FWCI
1.51
Type
journal article
Language
en
Open access
Locations
  • NeuroRx (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • WBI Studies Repository (submittedVersion)
Topics
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Automotive and Human Injury Biomechanics
Keywords
traumatic brain injury, animal models, neuroprotection, secondary injury mechanisms, blood-brain barrier, neuroinflammation, preclinical to clinical translation
MeSH terms
Animals, Brain, Brain Injuries, Disease Models, Animal, Craniocerebral Trauma, Humans, Head Injuries, Closed, Head Injuries, Penetrating

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