Conner E S, Foley L, Black P M
J Neurosurg. 1984 Aug;61(2):322-7. doi: 10.3171/jns.1984.61.2.0322.
This research was directed at the pathophysiology of normal-pressure hydrocephalus. The experimental method consisted of accurate and simultaneous measurement of the pressure within the ventricle and over the cerebral convexity in cats with hydrocephalus but normal ventricular pressure. Hydrocephalus was induced by the intracisternal injection of kaolin. Prior to the induction of hydrocephalus, the difference between the ventricular pressure and the pressure over the convexity (the transmantle pressure) was small (0.27 +/- 0.31 cm saline, mean +/- standard deviation). After the induction of normal-pressure hydrocephalus in seven animals, there was a statistically significant elevation of the transmantle pressure to 3.4 +/- 3.9 cm saline (p less than 0.05, Student's paired t-test). There was no similar increase in animals injected with lactated Ringer's solution. This finding supports the theory that it is the transmantle pressure, and not the ventricular pressure, that is the physiological determinant of ventricular dilatation. The theory explains why hydrocephalus can develop and persist despite normal ventricular pressure.
本研究针对正常压力脑积水的病理生理学。实验方法包括精确且同时测量脑积水但脑室压力正常的猫的脑室内压力和脑凸面压力。通过脑池内注射高岭土诱导脑积水。在诱导脑积水之前，脑室内压力与脑凸面压力之间的差值（跨脑压）较小（0.27±0.31厘米盐水柱，平均值±标准差）。在七只动物诱导出正常压力脑积水后，跨脑压在统计学上显著升高至3.4±3.9厘米盐水柱（p<0.05，学生配对t检验）。注射乳酸林格液的动物没有类似的升高。这一发现支持了这样一种理论，即跨脑压而非脑室压力是脑室扩张的生理决定因素。该理论解释了为什么尽管脑室压力正常，脑积水仍会发生并持续存在。
