Department of Neurosurgery, Ajou University School of Medicine, Suwon 443-721, Republic of Korea.
Med Hypotheses. 2013 Aug;81(2):199-201. doi: 10.1016/j.mehy.2013.05.003. Epub 2013 Jun 2.
Many theories have been postulated to date regarding mechanisms involved in intracranial hypertension in patients with long-term, shunt-induced slit ventricle syndrome (SVS), but it still seems difficult to define this entity more clearly. Many hypotheses have attempted to explain the causes of SVS as chronic or intermittent catheter obstruction, brain compliance change, and ventricular herniation and distortion, but this theory does not explain clearly the reason why extraventricular pressure (EVP) is increased and intraventricular pressure (IVP) is low or frequently negative. The authors attempt to postulate a hypothesis by addressing new concept of capillary absorption laziness which results in dissociation of EVP with IVP. We, the authors, propose a concept of 'capillary absorption laziness', which is a tendency of the brain parenchymal extracellular fluid (ECF) not to be absorbed through the brain parenchymal capillary absorption system (BPCAS) that results from the bypass of ECF to shunt in the low or even negative ECF pressure and IVP. If this continues for a prolonged period, the tendency not to be absorbed through the BPCAS, even when the IVP and extracellular fluid pressures increases more than the intracranial pressure (ICP), may be established. This leads to situations of the brain such as parenchymal accumulation of the ECF which results in brain edema or swelling, and eventually distortion or herniation which can act as a functional obstruction and consequent dissociation between the IVP and EVP. Hypothesis of capillary absorption laziness may explain several common phenomena of the SVS such as low or even negative IVP in coexistence with high EVP and high ICP, and in these cases, we expect serious complications of SVS such as brain distortion and herniation. From this hypothesis we attempt to find new shunt management protocols to prevent long-term shunt induced complications.
目前已经提出了许多关于长期、分流诱导的狭缝脑室综合征（SVS）患者颅内高压相关机制的理论，但似乎仍然难以更清楚地定义这种情况。许多假说试图解释 SVS 的原因，如慢性或间歇性导管阻塞、脑顺应性改变以及脑室疝和变形，但该理论并不能清楚地解释为什么脑室外压（EVP）升高而脑室内压（IVP）降低或经常为负。作者试图通过探讨新的毛细血管吸收惰性概念来提出一个假说，从而导致 EVP 与 IVP 的分离。我们作者提出了“毛细血管吸收惰性”的概念，这是一种脑实质细胞外液（ECF）通过脑实质毛细血管吸收系统（BPCAS）吸收减少的趋势，这种趋势是由于 ECF 通过分流转移到低 ECF 压力和 IVP 甚至负压力的部位，导致 ECF 绕过 BPCAS。如果这种情况持续很长时间，即使 IVP 和细胞外液压力增加超过颅内压（ICP），也可能会出现不通过 BPCAS 吸收的趋势。这会导致脑实质 ECF 积聚，从而导致脑水肿或肿胀，最终导致变形或疝形成，这些都可能成为功能性阻塞，导致 IVP 和 EVP 之间的分离。毛细血管吸收惰性假说可以解释 SVS 的一些常见现象，如 IVP 低甚至负与 EVP 和 ICP 高同时存在，在这些情况下，我们预计 SVS 会出现严重的并发症，如脑变形和疝形成。从这个假说出发，我们试图寻找新的分流管理方案来预防长期分流诱导的并发症。
