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Rotational Accelera...
Rotational Acceleration Closed Head Flexion Trauma Generates More Extensive Diffuse Brain Injury than Extension Trauma
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- Krave, Ulrika, 1973 (författare)
- Chalmers tekniska högskola,Chalmers University of Technology
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- Al-Olama, Mohamed (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för biomedicin,Institute of Biomedicine
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- Hansson, Hans-Arne, 1939 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi,Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
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(creator_code:org_t)
- Mary Ann Liebert Inc, 2011
- 2011
- Engelska.
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Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert Inc. - 1557-9042 .- 0897-7151. ; 28:1, s. 57-70
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Abstract
Ämnesord
Stäng
- Our aim was to investigate if seemingly identical head and neck trauma would generate differing types of braindamage. We experimentally evaluated induced brain injuries immediately after trauma exposure, and at 1 weekpost-injury. Anesthetized rabbits were exposed once to a sagittal rotational acceleration head and neck injury ateither a high or a low load level, using either flexion or extension. A high-load extension trauma induced scatteredmeningeal petechial hemorrhages and no deaths, in contrast to a flexion trauma of the same level, which resultedin extensive parenchymal and meningeal hemorrhages, and all animals succumbed immediately. A low-levelflexion trauma induced scattered meningeal petechiae, but no gross damage, while extension at the same forcegenerated no macroscopically visible acute brain injury. Immunohistochemical investigations carried out at 7 daysdisclosed that a low-level flexion trauma, as well as both low- and high-level extension exposures, all induceddiffuse brain injuries in the cerebral cortex and white matter, corpus callosum, hippocampus, brainstem, andcerebellum, as revealed by abnormal distribution of neurofilaments, a prevalence of b-amyloid precursor protein,and astrogliosis. The diffuse brain injury seen after a low-level flexion trauma was equal to or more extensive thanthat seen after a high-level extension trauma. A low-level extension trauma induced only minor histopathologicalabnormalities. We conclude that a sagittal rotational acceleration trauma of the head and neck induced diffusebrain injury, and that flexion caused more extensive damage than extension at the same applied load.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Neurosciences (hsv//eng)
Nyckelord
- mild traumatic brain injury
- astrocytosis
- b-amyloid precursor protein
- diffuse axonal injury
- astrocytosis; b-amyloid precursor protein; diffuse axonal injury; mild traumatic brain injury
Publikations- och innehållstyp
- art (ämneskategori)
- ref (ämneskategori)
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