抄録
Translational acceleration impact was applied to elicit cerebral concussion and contusion in subhuman primates (12 Japanese monkeys and 2 baboons) using a HYGE sled and a slider-impactor system.
All animals were concussed more than 15 seconds by force ranging from 240 to 960 G (duration; 17.5-3.5 msec.) in average head accelerations. Five monkeys among 8 with frontal impact died within 27 minutes. This well correlated with thoracic trauma, including rib fracture and small mediastinal hemorrhage. Only one animal (baboon) among 6 with occipital impact died immediately and the cerebro-spinal junction was found traumatically severed. Bradycardia, apnea, systemic hypotension and depression of EEG activity occurred immediately after impact in every animal. No visible intracranial pathology, such as brain contusion, subdural hematoma, or intracerebral hematoma was noticed. Microscopic examination revealed central chromatolysis of nerve cells and degeneration of Purkinje cells. However, these findings did not correlate with the post-impact state of the animals nor with biomechanical data.
Our experiment suggests that translational acceleration impact to the brain does not usually cause gross morphological changes. Secondly, the so-called brain concussion might be the result of the cumulative effect of, 1) transient medullary paralysis, 2) cardio-respiratory depression of cervical cord origin, as well as, 3) cardiocirculatory insufficiency due to thoracic impact (primary shock). If severe, these factors would generate a vicious cycle to lead to a state of circulatory catastrophe which ends in death only.