Idris Zamzuri, Mustapha Muzaimi, Abdullah Jafri M
Department of Neurosciences, School of Medical Sciences, Universiti Sains Malaysia 16150, Kubang Kerian, Kelantan, Malaysia.
Asian J Neurosurg. 2014 Jan;9(1):7-13. doi: 10.4103/1793-5482.131058.
The pathogenesis underlying communicating hydrocephalus has been centered on impaired cerebrospinal fluid (CSF) outflow secondary to abnormal CSF pulsation and venous hypertension. Hydrodynamic theory of hydrocephalus fares better than traditional theory in explaining the possible mechanisms underlying communicating hydrocephalus. Nonetheless, hydrodynamic theory alone could not fully explain some conditions that have ventriculomegaly but without hydrocephalus. By revisiting brain buoyancy from a fresher perspective, called microgravity environment of the brain, introducing wider concepts of anatomical and physiological compensatory-decompensatory phases for a persistent raise in intracranial pressure, and along with combining these two concepts with the previously well-accepted concepts of Monro-Kellie doctrine, intracranial hypertension, cerebral blood flow, cerebral perfusion pressure, brain compliance and elasticity, cerebral autoregulation, blood-brain and blood-CSF barriers, venous and cardiopulmonary hypertension, Windkessel phenomenon, and cerebral pulsation, we provide plausible explanations to the pathogenesis for communicating hydrocephalus and its related disorders.
交通性脑积水的发病机制一直聚焦于继发于异常脑脊液搏动和静脉高压的脑脊液（CSF）流出受损。脑积水的流体动力学理论在解释交通性脑积水潜在机制方面比传统理论表现更佳。尽管如此，仅流体动力学理论无法完全解释一些存在脑室扩大但无脑积水的情况。通过从一个全新视角重新审视脑浮力，即脑的微重力环境，引入关于颅内压持续升高的解剖学和生理学代偿 - 失代偿阶段的更广泛概念，并将这两个概念与先前广为接受的孟罗 - 凯利学说、颅内高压、脑血流量、脑灌注压、脑顺应性和弹性、脑自动调节、血脑屏障和血脑脊液屏障、静脉和心肺高压、Windkessel现象以及脑搏动等概念相结合，我们对交通性脑积水及其相关病症的发病机制提供了合理的解释。
