Del Bigio M R, da Silva M C, Drake J M, Tuor U I
Division of Neuropathology, Hospital for Sick Children, Toronto, Ontario, Canada.
Can J Neurol Sci. 1994 Nov;21(4):299-305. doi: 10.1017/s0317167100040865.
The neonatal cat model of kaolin-induced hydrocephalus is associated with progressive and severe ventriculomegaly. In this experiment we studied the evolution of the histopathological changes in hydrocephalic (n = 23) cats from 5-168 days after the induction of hydrocephalus along with age-matched controls (n = 10). In the periventricular white matter, extracellular edema and axonal damage were present within days of the onset of hydrocephalus. This was followed by reactive gliosis, white matter atrophy, and in some animals gross cavitation of the white matter. Even in the chronic, apparently compensated state there was ongoing glial cell death. Six cats were shunted an average of 23.6 +/- 6.5 days after the induction of hydrocephalus because they were no longer able to feed independently. In spite of clinical improvement the white matter changes persisted. Overt cortical changes were minimal except where areas of white matter destruction encroached upon the deep layers. The white matter changes are very similar to those seen in periventricular leukomalacia and suggest that ischemia plays a role in neonatal brain injury caused by hydrocephalus.
高岭土诱导的新生儿脑积水猫模型与进行性严重脑室扩大有关。在本实验中，我们研究了脑积水诱导后5至168天的脑积水猫（n = 23）以及年龄匹配的对照猫（n = 10）组织病理学变化的演变。在脑室周围白质中，脑积水发病数天内就出现细胞外水肿和轴突损伤。随后是反应性胶质增生、白质萎缩，在一些动物中还出现白质的明显空洞形成。即使在慢性、明显代偿状态下，也存在持续的神经胶质细胞死亡。6只猫在脑积水诱导后平均23.6±6.5天进行了分流，因为它们不再能够独立进食。尽管临床症状有所改善，但白质变化仍然存在。除了白质破坏区域侵犯深层的情况外，明显的皮质变化很少。白质变化与脑室周围白质软化所见非常相似，提示缺血在脑积水所致新生儿脑损伤中起作用。
