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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 \u03b2-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.<\/jats:p>","DOI":"10.1089\/neu.2010.1431","type":"journal-article","created":{"date-parts":[[2010,11,3]],"date-time":"2010-11-03T08:18:50Z","timestamp":1288772330000},"page":"57-70","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":18,"title":["Rotational Acceleration Closed Head Flexion Trauma Generates More Extensive Diffuse Brain Injury than Extension Trauma"],"prefix":"10.1177","volume":"28","author":[{"given":"Ulrika","family":"Krave","sequence":"first","affiliation":[{"name":"Chalmers University of Technology","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamed","family":"Al-Olama","sequence":"additional","affiliation":[{"name":"University of Gothenburg","place":["Sweden"]},{"name":"Sahlgrenska University Hospital","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans-Arne","family":"Hansson","sequence":"additional","affiliation":[{"name":"University of Gothenburg","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2011,1,1]]},"reference":[{"key":"e_1_3_3_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2008.10.013"},{"key":"e_1_3_3_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jbiomech.2005.02.014"},{"key":"e_1_3_3_4_1","first-page":"733","volume-title":"Trauma, in Greenfield's Neuropathology","author":"Blumbergs P.","year":"2008","unstructured":"Blumbergs P., , Reilly P., , Vink R. 2008. 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