CPL - Chalmers Publication Library
| Utbildning | Forskning | Styrkeområden | Om Chalmers | In English In English Ej inloggad.

Rotational Acceleration Closed Head Flexion Trauma Generates More Extensive Diffuse Brain Injury than Extension Trauma

Ulrika Krave (Institutionen för tillämpad mekanik, Fordonssäkerhet) ; Mohamed Al-Olama ; Hans-Arne Hansson
Journal of Neurotrama (0897-7151). Vol. 28 (2011), p. 57-70.
[Artikel, refereegranskad vetenskaplig]

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 b-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.

Nyckelord: astrocytosis; b-amyloid precursor protein; diffuse axonal injury; mild traumatic brain injury;

Denna post skapades 2011-02-23. Senast ändrad 2011-02-24.
CPL Pubid: 137232


Läs direkt!

Lokal fulltext (fritt tillgänglig)

Länk till annan sajt (kan kräva inloggning)

Institutioner (Chalmers)

Institutionen för tillämpad mekanik, Fordonssäkerhet (2005-2017)
Institutionen för biomedicin (GU)
Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi (GU)



Chalmers infrastruktur