Karki Pragalv, Sincomb Stephanie, Murphy Matthew C, Gunter Jeffrey L, Senjem Matthew L, Graff-Radford Jonathan, Jones David T, Botha Hugo, Cutsforth-Gregory Jeremy K, Elder Benjamin D, Huston John, Cogswell Petrice M
Department of Radiology, Mayo Clinic, Rochester, MN, USA.
Department of Mechanical and Aerospace Engineering, University of California - San Diego, La Jolla, USA.
Brain Multiphys. 2024 Dec;7. doi: 10.1016/j.brain.2024.100101. Epub 2024 Oct 1.
Idiopathic normal pressure hydrocephalus (iNPH) is a cerebrospinal fluid (CSF) dynamics disorder as evidenced by the delayed ascent of radiotracers over the cerebral convexity on radionuclide cisternography. However, the exact mechanism causing this disruption remains unclear. Elucidating the pathophysiology of iNPH is crucial, as it is a treatable cause of dementia. Improving the diagnosis and treatment prognosis rely on the better understanding of this disease. In this study, we calculated the pulsatile transmantle pressure and investigated the phase lag between this pressure and the volumetric CSF flow rate as a novel biomarker of CSF dynamics disruption in iNPH.
44 iNPH patients and 44 age- and sex-matched cognitively unimpaired (CU) control participants underwent MRI scans on a 3T Siemens scanner. Pulsatile transmantle pressure was calculated analytically and computationally using volumetric CSF flow rate, cardiac frequency, and aqueduct dimensions as inputs. CSF flow rate through the aqueduct was acquired using phase-contrast MRI. The aqueduct length and radius were measured using 3D T1-weighted anatomical images.
Peak pressure amplitudes and the pressure load (integrated pressure exerted over a cardiac cycle) were similar between the groups, but the non-dimensionalized pressure load (adjusted for anatomical factors) was significantly lower in the iNPH group ( , Welch's t-test). The phase lag between the pressure and the flow rate, arising due to viscous drag, was significantly higher in the iNPH group ( ).
The increased phase lag is a promising new biomarker for quantifying CSF dynamics dysfunction in iNPH.
The exact mechanism causing the disruption of CSF circulation in idiopathic normal pressure hydrocephalus (iNPH) remains unclear. Elucidating the pathophysiology of iNPH is crucial, as it is a treatable cause of dementia. In this study, we provided an analytical and a computational method to calculate the pulsatile transmantle pressure and the phase lag between the pressure and the volumetric CSF flow rate across the cerebral aqueduct. The phase lag was significantly higher in iNPH patients than in controls and may serve as a novel biomarker of CSF dynamics disruption in iNPH.
特发性正常压力脑积水（iNPH）是一种脑脊液（CSF）动力学障碍，放射性核素脑池造影显示放射性示踪剂在脑凸面的上升延迟可证明这一点。然而，导致这种破坏的确切机制仍不清楚。阐明iNPH的病理生理学至关重要，因为它是痴呆的可治疗病因。改善诊断和治疗预后依赖于对这种疾病的更好理解。在本研究中，我们计算了搏动性跨脑压，并研究了该压力与脑脊液体积流速之间的相位滞后，将其作为iNPH中脑脊液动力学破坏的一种新型生物标志物。
44例iNPH患者和44例年龄及性别匹配的认知未受损（CU）对照参与者在3T西门子扫描仪上接受了MRI扫描。使用脑脊液体积流速、心率和导水管尺寸作为输入，通过分析和计算得出搏动性跨脑压。使用相位对比MRI获取通过导水管的脑脊液流速。使用3D T1加权解剖图像测量导水管长度和半径。
两组之间的峰值压力幅度和压力负荷（一个心动周期内施加的积分压力）相似，但iNPH组的无量纲压力负荷（根据解剖因素调整）显著更低（ ，韦尔奇t检验）。由于粘性阻力导致的压力与流速之间的相位滞后在iNPH组中显著更高（ ）。
增加的相位滞后是一种很有前景的新型生物标志物，可用于量化iNPH中的脑脊液动力学功能障碍。
特发性正常压力脑积水（iNPH）中导致脑脊液循环破坏的确切机制仍不清楚。阐明iNPH的病理生理学至关重要，因为它是痴呆的可治疗病因。在本研究中，我们提供了一种分析方法和一种计算方法来计算搏动性跨脑压以及跨脑导水管的压力与脑脊液体积流速之间的相位滞后。iNPH患者的相位滞后显著高于对照组，可能作为iNPH中脑脊液动力学破坏的一种新型生物标志物。
