Bateman Grant A, Bateman Alexander R
Department of Medical Imaging, John Hunter Hospital, Newcastle, NSW 2310, Australia.
School of Medicine and Public Health, College of Health, Medicine and Wellbeing, Newcastle University, Callaghan Campus, Newcastle, NSW 2308, Australia.
Brain Sci. 2025 May 20;15(5):527. doi: 10.3390/brainsci15050527.
: Idiopathic intracranial hypertension (IIH) is, by definition, of unknown cause. Davson's equation indicates that the increased intracranial pressure (ICP) found in IIH could be due to an increase in the CSF formation rate (CSF), the CSF outflow resistance (R) or the venous sinus pressure. Studies simultaneously measuring the ICP and sagittal sinus pressures in IIH suggest that there is either a reduction in the R and/or the CSF. The latter suggests that the increased venous pressure can be the only variable causing this disease process. A study maintaining the ICP at zero showed a significantly elevated CSF in this disease. The purpose of the current study is to define the most feasible explanation for these findings and to suggest a viable pathophysiology for IIH. : A lumped parameter vascular model, originally developed to study normal pressure hydrocephalus, was extended to investigate IIH. The model used the simultaneously obtained ICP and sagittal sinus pressure measurements from five experiments published in the literature to estimate the CSF and the capillary transmural pressure (TMP). The assumptions made during this study were those of a normal mean arterial pressure, a normal total R and a normal blood flow rate. : When the CSF formation rates were plotted against the estimated capillary transmural pressures, a straight line was returned, suggesting that the CSF and capillary TMP are related. : The novel findings of this study suggest that the CSF in IIH varies with the capillary TMP. A reduced capillary TMP in IIH can moderate the ICP if there is net CSF absorption across the capillaries. This would require the blood-brain barrier (BBB) to be disrupted. The model suggests that drugs which stabilise the BBB may trigger IIH by blocking CSF absorption across the capillaries, increasing the apparent CSF formation rate back toward normal and increasing the ICP. Anaemia will promote IIH by increasing the cerebral blood flow, the capillary TMP and the CSF.
特发性颅内高压（IIH），顾名思义，病因不明。戴维森方程表明，IIH中发现的颅内压（ICP）升高可能是由于脑脊液生成率（CSF）增加、脑脊液流出阻力（R）或静脉窦压力增加所致。同时测量IIH患者ICP和矢状窦压力的研究表明，R和/或CSF存在降低。后者表明静脉压升高可能是导致该疾病过程的唯一变量。一项将ICP维持在零的研究显示，该疾病中CSF显著升高。本研究的目的是为这些发现确定最合理的解释，并提出IIH可行的病理生理学机制。
一个最初用于研究正常压力脑积水的集总参数血管模型被扩展用于研究IIH。该模型利用文献中发表的五项实验同时获得的ICP和矢状窦压力测量值来估计CSF和毛细血管跨壁压力（TMP）。本研究期间所做的假设是平均动脉压正常、总R正常和血流速率正常。
当将CSF生成率与估计的毛细血管跨壁压力作图时，得到一条直线，表明CSF与毛细血管TMP相关。
本研究的新发现表明，IIH中的CSF随毛细血管TMP而变化。如果存在跨毛细血管的CSF净吸收，IIH中降低的毛细血管TMP可使ICP降低。这将需要血脑屏障（BBB）被破坏。该模型表明，稳定BBB的药物可能通过阻断跨毛细血管的CSF吸收、使表观CSF生成率恢复正常并增加ICP而引发IIH。贫血将通过增加脑血流量、毛细血管TMP和CSF来促进IIH。
