脑震荡鼠细胞组织病理学研究

目的：作为轻型颅脑损伤的脑震荡，一向认为是脑功能的一过性功能障碍，而无形态变化，近来的一些研究对这一观点提出了挑战，为深入探讨脑震荡发病机理特设计本研究．方法：用清醒Wister大鼠，在自制单摆式脑损伤复制仪上制备脑震荡模型．符合诊断者随机分为10组(n≥5)．于伤后64d内定时乙醚麻醉，心腔灌注10％甲醛液处杀固定，恒定在大脑、脑干与小脑取材4块，常规HE,Nissel染色．结果：(1)皮质第二、三层部分神经元变性和不完全性坏死，并呈现早期与延迟性损伤两个高峰性变化，伴淤血水肿与胶质细胞增生，病变以纵裂旁、脑底与近脑底区为著，左右半球不对称．海马损伤以CA1-CA2区与皮质明显病变相对应的部位为重；(2)皮质下核团少部分神经元变性坏死，并以中线区、下丘脑、脑室旁和脉络裂旁为重；(3)脑干、小脑少部分神经元变性坏死，并以浦氏细胞、第四脑室旁网状核团及延颈髓交界区为著．结论：本模型所致脑震荡存在有弥漫性的早期与延迟性神经元变性坏死等形态改变．文章对病变的空间分布特点及早期与延迟性损伤机理进行了讨论．

Histocyte Pathological Research of Cerebral Concussion in Rats

Cerebral concussion is usually considered to be a form of mild head injury without significant histopathology or other secondary sequelae. However, recent evidence challenges this idea. Our goal is to study the mechanisms of cerebral concussion so that we may determine how to interrupt the secondary insult after injury and thus preserve functional outcome. Briefly, a cerebral concussion was produced in rats using a simple pendulum device model. One control and ten experimental groups were used (n=5 in each group). The cerebral concussion groups were assigned to sacrifice times ranging from 3 hours to 64 days after injury. Under ether anesthesia, each rat was perfused through the heart with 10% formalin. Four samples were taken from the cerebrum through the optic chiasm, infundibular, brain stem, and cerebellum. Paraffin sections were stained with HE and Nissl. The results showed (1) degeneration and incomplete necrosis in some neurons in the second and third layers of cortex, with accompanying edema and gliacyte hyperplasia. This pathological change was observed at 2 and 8 days after trauma indicating two injury peaks. The histopathological change of the cortex was asymmetrical; located on both sides of the interhemispheric fissure, in the vicinity of the cerebrum bottom, and CA 1 to CA 2 sectors of the hippocampus. (2) Neuronal degeneration and necrosis were observed in cortical intermediate areas, hypothalamus, brain stem and cerebellum, especial in Purkinje cells, the reticular formation, and other nerve nuclei in the side of the fourth ventricle and the combining site of oblongata and neck medullas. Conclusion: (1) There was some diffuse neuronal degeneration and necrosis from the cortex to oblongata after concussion. The secondary insult of neurons after brain concussion appeared in early and late phases suggesting two histopathological peaks. That morphological change may construct the pathological basis of cerebral concussion and post-concussional syndrome. (2) The two injury peaks after concussion may be relevant to secondary injury - especially microcirculation disorder. (3) The distribution feature of the injury in this model may be explained by biomechanics.