Pathogenetic mechanism of cerebral concussion due to rotational angular acceleration impact.

Abstract

The pathophysiological response and morphological damage from concussion caused by rotational angular acceleration impact were studied. In all monkeys tested, concussion syndromes were induced by impact in the range of 26.5 ?? 136.4×103 rad/sec2 with a duration of 1.03 ?? 9.09 msec. The morphological findings revealed two types of brain damage. One was a sharply demarcated vital dye-stained lesion which represented an ischemic lesion with occlusion of small vessels at the base of the lesion in the frontal lobe on the side opposite the impact site. The other consisted of scattered cellular damage in the lower medulla and medullospinal junction without staining by vital dye, which was observed on the monkey suffered from concussion by linear acceleration impact.20) In the vital dye-stained lesions, the local cerebral blood flow was reduced and the partial oxygen pressure decreased until 2 hours after impact. Lactic acid increased, ATP content decreased and there was no increase in free radicals. In the border zone of the lesions, local cerebral blood flow decreased in the first 1 hour, but increased 1.5 hrs after impact. Also, free radicals increased in the border zone despite the lack of change in lactic acid and ATP contents compared with the vital dye-stained lesions themselves. There was no variation in amplitude or latency of the brain stem response to auditory stimulation, but the somatosensory response at the sensory cortex changed to a low amplitude of elongation of the latency in the concussion caused by the rotational acceleration impact. These findings clearly suggest that there are two types of brain damage in concussions caused by rotational acceleration impact.