Object. The authors investigated the ramifications of producing diffuse axo
nal injury (DAI) by lateral head rotation in a rat model.
Methods. Using a special injury-producing device, the rat's head was rapidl
y rotated 90 degrees in the coronal plane at an angular velocity of at leas
t 753.13 rad/second and an angular acceleration of at least 1.806 x 10(5) r
ad/second(2); the rotation was complete within 2.09 msec. There were no sta
tistically significant changes in PO2, PCO2, pH, or blood pressure values a
t 5, 15, or 60 minutes after head rotation compared with their respective p
reinjury baseline values. The rats exhibited posttraumatic behavior suppres
sion for an average of 12.6 minutes. The mortality rate was 17%. The rats t
hat survived had diffuse subarachnoid hemorrhage around the brainstem and u
pper cervical cord, but no obvious brain contusion. In sections stained wit
h 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 postinjur
y. The axonal injuries were most severe in the brainstem and were accompani
ed by parenchymal bleeding. The density of bulblike axonal protrusions peak
ed 6 hours postinjury in the medulla oblongata and 24 hours postinjury in t
he midbrain.
Conclusions. Rapid lateral head rotation can produce DAI characterized by s
evere damage to the rat brainstem.