Rotational acceleration closed head flexion trauma generates more extensive diffuse brain injury than extension trauma.
Our aim was to investigate if seemingly identical head and neck trauma would generate differing types of brain damage. We experimentally evaluated induced brain injuries immediately after trauma exposure, and at 1 week post-injury. Anesthetized rabbits were exposed once to a sagittal rotational acceleration head and neck injury at either a high or a low load level, using either flexion or extension. A high-load extension trauma induced scattered meningeal petechial hemorrhages and no deaths, in contrast to a flexion trauma of the same level, which resulted in extensive parenchymal and meningeal hemorrhages, and all animals succumbed immediately. A low-level flexion trauma induced scattered meningeal petechiae, but no gross damage, while extension at the same force generated no macroscopically visible acute brain injury. Immunohistochemical investigations carried out at 7 days disclosed that a low-level flexion trauma, as well as both low- and high-level extension exposures, all induced diffuse brain injuries in the cerebral cortex and white matter, corpus callosum, hippocampus, brainstem, and cerebellum, as revealed by abnormal distribution of neurofilaments, a prevalence of β-amyloid precursor protein, and astrogliosis. The diffuse brain injury seen after a low-level flexion trauma was equal to or more extensive than that seen after a high-level extension trauma. A low-level extension trauma induced only minor histopathological abnormalities. We conclude that a sagittal rotational acceleration trauma of the head and neck induced diffuse brain injury, and that flexion caused more extensive damage than extension at the same applied load.
Division of Vehicle Safety, Applied Mechanics, Chalmers University of Technology, Göteborg, Sweden.
Ulrika
U
Krave
Mohamed
M
Al-Olama
Hans-Arne
HA
Hansson
D000054:Acceleration; D016564:Amyloid beta-Protein Precursor / Q000096:biosynthesis; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis; D016489:Head Injuries, Closed / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology*; D007150:Immunohistochemistry; D018613:Microscopy, Confocal; D016900:Neurofilament Proteins / Q000096:biosynthesis; D011817:Rabbits; D012399:Rotation
D016564:Amyloid beta-Protein Precursor; D005904:Glial Fibrillary Acidic Protein; D016900:Neurofilament Proteins