Xiao-Sheng H, Sheng-Yu Y, Xiang Z, Zhou F, Jian-ning Z
Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, Peoples Republic of China.
J Neurosurg. 2000 Oct;93(4):626-33. doi: 10.3171/jns.2000.93.4.0626.
The authors investigated the ramifications of producing diffuse axonal injury (DAI) by lateral head rotation in a rat model.
Using a special injury-producing device, the rat's head was rapidly rotated 90 degrees in the coronal plane at an angular velocity of at least 753.13 rad/second and an angular acceleration of at least 1.806 x 10(5) rad/second2; the rotation was complete within 2.09 msec. There were no statistically significant changes in PO2, PCO2, pH, or blood pressure values at 5, 15, or 60 minutes after head rotation compared with their respective preinjury baseline values. The rats exhibited posttraumatic behavior suppression for an average of 12.6 minutes. The mortality rate was 17%. The rats that survived had diffuse subarachnoid hemorrhage around the brainstem and upper cervical cord, but no obvious brain contusion. In sections stained with silver or hematoxylin and eosin, axonal swelling and bulblike protrusions at the axonal axis were observed in the medulla oblongata, midbrain, upper cervical cord, and corpus callosum between 6 hours and 144 hours postinjury. The axonal injuries were most severe in the brainstem and were accompanied by parenchymal bleeding. The density of bulblike axonal protrusions peaked 6 hours postinjury in the medulla oblongata and 24 hours postinjury in the midbrain.
Rapid lateral head rotation can produce DAI characterized by severe damage to the rat brainstem.
