Mani Racheed, Basem Jade, Yang Liu, Shirdel Abdolmaleki Nahid, Ravishankar Anand, Fiore Susan, Djuric Petar, Egnor Michael
Department of Neurology, Stony Brook University Hospital, Stony Brook, NY, United States.
Department of Neurological Surgery, Stony Brook University Hospital, Stony Brook, NY, United States.
Front Neurol. 2025 May 1;16:1591275. doi: 10.3389/fneur.2025.1591275. eCollection 2025.
Normal pressure hydrocephalus (NPH) is characterized by ventriculomegaly without elevations in intracranial pressure (ICP). One way of viewing hydrocephalus is as a disorder of the cerebral windkessel. The cerebral windkessel is the system that dampens the arterial blood pressure (ABP) pulse in the cranium, transmitting this pulse from arteries to veins via the cerebrospinal fluid (CSF) path, bypassing the microvasculature to render capillary flow smooth. When the windkessel is physiologically tuned, windkessel effectiveness () is given by: =/, where represents CSF path inertance (pulse magnitude), is CSF path elastance, and is resistance in the CSF path. In NPH, we posit that there is a combination of arteriosclerosis (blunting the CSF pulse in the SAS- lowering ), and age-related softening of brain tissue (decreasing the elastance of subarachnoid CSF pathways- lowering ).
To model the windkessel, we utilize a tank circuit with parallel inductance and capacitance to simulate the pulsatile flow of blood and CSF as alternating current (AC), and smooth flow as direct current (DC). We model NPH as a disorder of windkessel impairment by decreasing windkessel inertance (reflecting diminished CSF pulsatility in the SAS from arteriosclerosis) and decreasing intracranial elastance (reflecting age-related brain atrophy). We simulate ventriculomegaly and shunting by lowering the resistance of this circuit.
In simulating NPH using this circuit, we found significant elevations in the amplitude and power of AC in the CSF and capillary paths when inertance and elastance were decreased. Conversely, this pulse power decreased with decreased resistance in the CSF path from ventriculomegaly and shunting.
Simulations of NPH demonstrated increased amplitude and power of AC in the CSF and capillary paths due to windkessel impairment. We posit that this pulsatility is redistributed from the SAS to the ventricular CSF path, exerting pulsatile stress on the periventricular leg and bladder fibers, which may explain NPH symptomatology. Ventriculomegaly may represent an active adaptation to improve windkessel effectiveness by decreasing CSF path resistance to mitigate decreased CSF path inertance and parenchymal elastance. Shunting provides a low resistance, accessory windkessel to obviate adaptive ventriculomegaly. This has significant implications in understanding this paradoxical condition.
正常压力脑积水（NPH）的特征是脑室扩大而颅内压（ICP）不升高。看待脑积水的一种方式是将其视为脑弹性腔室系统的紊乱。脑弹性腔室系统是一种在颅骨内缓冲动脉血压（ABP）脉搏的系统，它通过脑脊液（CSF）路径将该脉搏从动脉传递到静脉，绕过微血管以使毛细血管血流顺畅。当弹性腔室系统处于生理调节状态时，弹性腔室效率（）由下式给出：=/，其中表示脑脊液路径惯性（脉搏幅度），是脑脊液路径弹性，是脑脊液路径中的阻力。在NPH中，我们假定存在动脉硬化（使蛛网膜下腔间隙（SAS）中的脑脊液脉搏变钝 - 降低）和与年龄相关的脑组织软化（降低蛛网膜下腔脑脊液路径的弹性 - 降低）的组合。
为了对弹性腔室进行建模，我们使用具有并联电感和电容的 tank 电路来模拟血液和脑脊液的脉动流作为交流电（AC），以及平稳流作为直流电（DC）。我们将NPH建模为弹性腔室功能障碍的一种疾病，通过降低弹性腔室惯性（反映由于动脉硬化导致的SAS中脑脊液脉动性降低）和降低颅内弹性（反映与年龄相关的脑萎缩）。我们通过降低该电路的电阻来模拟脑室扩大和分流。
在使用该电路模拟NPH时，我们发现当惯性和弹性降低时，脑脊液和毛细血管路径中交流电的幅度和功率显著升高。相反，随着脑室扩大和分流导致脑脊液路径阻力降低，该脉搏功率降低。
NPH的模拟显示，由于弹性腔室功能障碍，脑脊液和毛细血管路径中交流电的幅度和功率增加。我们假定这种脉动性从SAS重新分布到脑室脑脊液路径，对脑室周围腿部和膀胱纤维施加脉动应力，这可能解释了NPH的症状学。脑室扩大可能代表一种主动适应，通过降低脑脊液路径阻力来提高弹性腔室效率，以减轻脑脊液路径惯性和实质弹性的降低。分流提供了一个低阻力的辅助弹性腔室，以避免适应性脑室扩大。这对理解这种矛盾的病症具有重要意义。
