Andeweg J
Neuroradiology. 1996 Oct;38(7):621-8. doi: 10.1007/s002340050321.
For more than a century, available data concerning collateral venous outflow from the brain have received insufficient attention, as existing theories did not assign practical importance to them. Ideas concerning arterial blood supply and circulation of cerebrospinal fluid were considered more relevant. But available data afford a schematic model of cerebral venous outflow that does have important pathophysiological consequences. Principal outflow through the internal jugular veins can be substituted completely by the large vertebral plexuses, through communications at the cranial base. Emissary veins of the skull vault are small and few in number. Outflow from the deep venous system through the great vein of Galen can be substituted by choroidal, thalamic and striate anastomoses toward the basal vein. So-called intracerebral venous anastomoses through the centrum semiovale towards the convexity are nonexistent or negligible. Instead, a venous watershed exists separating paraventricular white matter from a layer of subcortical white matter. In most infants, the cavernous sinus is not yet connected to the cerebral veins. Once such communications have been formed, important collateral pathways exist through basal and Sylvian veins via the cavernous sinus to the pterygoid plexuses. Simultaneous hindrance of principal and collateral venous outflow will lead to elevated venous pressure and eventual insufficiency of cerebral blood flow (CBF). This will cause increased intracranial pressure, and ventricular enlargement due to periventricular atrophy. The slow phase of the two-compartment model of CBF coincides with the paraventricular white matter area of the deep venous system. In the neonate CBF was found to be still very low, and in the two compartments CBF increases at a different rate to a maximum in childhood. In hydrocephalus, measurement of CBF in the slow deep compartment, rather than the fast cortical one, will be most informative.
一个多世纪以来，有关大脑侧支静脉流出的现有数据未得到足够重视，因为现有理论未赋予它们实际重要性。有关动脉血液供应和脑脊液循环的观点被认为更具相关性。但现有数据提供了一个确实具有重要病理生理后果的脑静脉流出示意图模型。通过颈内静脉的主要流出可通过颅底的交通支被大的椎静脉丛完全替代。颅顶的导静脉细小且数量少。通过大脑大静脉从深部静脉系统流出可通过脉络丛、丘脑和纹状体吻合支向基底静脉替代。所谓通过半卵圆中心向脑凸面的脑内静脉吻合并不存在或可忽略不计。相反，存在一个静脉分水岭将室旁白质与一层皮质下白质分隔开。在大多数婴儿中，海绵窦尚未与脑静脉相连。一旦形成这种交通，就存在重要的侧支途径，通过基底静脉和大脑外侧裂静脉经海绵窦至翼静脉丛。主要和侧支静脉流出同时受阻将导致静脉压升高及最终脑血流量（CBF）不足。这将导致颅内压升高以及由于脑室周围萎缩引起的脑室扩大。CBF两室模型的缓慢期与深部静脉系统的室旁白质区域一致。在新生儿中发现CBF仍然很低，并且在两个室中CBF以不同速率增加，在儿童期达到最大值。在脑积水时，测量缓慢的深部室而非快速的皮质室的CBF将最具信息量。
