Kotapka M J, Gennarelli T A, Graham D I, Adams J H, Thibault L E, Ross D T, Ford I
Division of Neurosurgery, University of Pennsylvania, Philadelphia.
J Neurotrauma. 1991 Winter;8(4):247-58. doi: 10.1089/neu.1991.8.247.
Traumatically induced subtotal hippocampal neuronal loss traditionally has been considered a consequence of intracranial hypertension and impaired cerebral perfusion. We have examined the frequency and distribution of hippocampal lesions in an acceleration model of brain injury in 54 anesthetized nonhuman primates undergoing physiologic monitoring and subjected postinjury to comprehensive neuropathologic examination. Hippocampal lesions occurred in 32/54 animals (59%). These lesions always involved the CA-1 hippocampal subfield and were bilateral in 24 animals. Hippocampal involvement was not associated with marked elevation of intracranial pressure or depression of cerebral perfusion pressure. These lesions occurred in the absence of involvement of other brain regions considered selectively vulnerable to hypoxic insults. Hippocampal damage occurred in 46% of animals with mild injury characterized by brief periods of unconsciousness and no residual neurologic deficit. Ninety-four percent of animals with severe injuries and prolonged posttraumatic coma had hippocampal involvement. Traumatically induced selective neuronal necrosis of the hippocampus is a specific lesion not explained by the conventional mechanistic theories of head injury. An alternative hypothesis, such as excitotoxicity involving glutamate or other neurotransmitters, may account for the lesions demonstrated in this study.
传统上，创伤性诱发的海马神经元部分缺失被认为是颅内高压和脑灌注受损的结果。我们在54只接受生理监测的麻醉非人灵长类动物的脑损伤加速模型中，研究了海马损伤的频率和分布，并在损伤后进行了全面的神经病理学检查。54只动物中有32只（59%）出现了海马损伤。这些损伤总是累及海马CA-1亚区，24只动物为双侧损伤。海马受累与颅内压显著升高或脑灌注压降低无关。这些损伤发生时，其他被认为对缺氧损伤有选择性易损性的脑区并未受累。46%有轻度损伤（表现为短暂昏迷且无残留神经功能缺损）的动物出现了海马损伤。94%有严重损伤和创伤后长期昏迷的动物有海马受累。创伤性诱发的海马选择性神经元坏死是一种特定的损伤，传统的头部损伤机制理论无法解释。一种替代假说，如涉及谷氨酸或其他神经递质的兴奋性毒性，可能解释本研究中所示的损伤。
