Department of Radiology, Charité - University of Medicine Berlin, Germany.
NMR Biomed. 2011 May;24(4):385-92. doi: 10.1002/nbm.1602. Epub 2010 Oct 7.
Nearly half a century after the first report of normal pressure hydrocephalus (NPH), the pathophysiological cause of the disease still remains unclear. Several theories about the cause and development of NPH emphasize disease-related alterations of the mechanical properties of the brain. MR elastography (MRE) uniquely allows the measurement of viscoelastic constants of the living brain without intervention. In this study, 20 patients (mean age, 69.1 years; nine men, 11 women) with idiopathic (n = 15) and secondary (n = 5) NPH were examined by cerebral multifrequency MRE and compared with 25 healthy volunteers (mean age, 62.1 years; 10 men, 15 women). Viscoelastic constants related to the stiffness (µ) and micromechanical connectivity (α) of brain tissue were derived from the dynamics of storage and loss moduli within the experimentally achieved frequency range of 25-62.5 Hz. In patients with NPH, both storage and loss moduli decreased, corresponding to a softening of brain tissue of about 20% compared with healthy volunteers (p < 0.001). This loss of rigidity was accompanied by a decreasing α parameter (9%, p < 0.001), indicating an alteration in the microstructural connectivity of brain tissue during NPH. This disease-related decrease in viscoelastic constants was even more pronounced in the periventricular region of the brain. The results demonstrate distinct tissue degradation associated with NPH. Further studies are required to investigate the source of mechanical tissue damage as a potential cause of NPH-related ventricular expansions and clinical symptoms.
在首次报道正常压力脑积水 (NPH) 近半个世纪后,该病的病理生理学病因仍不清楚。几种关于 NPH 病因和发展的理论强调了与疾病相关的脑力学特性改变。磁共振弹性成像 (MRE) 独特地允许在不干预的情况下测量活脑的粘弹性常数。在这项研究中,20 名特发性 (n = 15) 和继发性 (n = 5) NPH 患者接受了大脑多频 MRE 检查,并与 25 名健康志愿者 (n = 25;平均年龄 62.1 岁;10 名男性,15 名女性) 进行了比较。从存储和损耗模量的动力学中得出与脑组织刚度 (µ) 和微观机械连通性 (α) 相关的粘弹性常数,该动力学是在实验实现的 25-62.5 Hz 频率范围内获得的。在 NPH 患者中,存储和损耗模量均降低,与健康志愿者相比,脑组织的软化程度约为 20% (p < 0.001)。这种刚性的丧失伴随着 α 参数的降低 (9%,p < 0.001),表明在 NPH 期间脑组织的微观结构连通性发生了改变。这种与疾病相关的粘弹性常数降低在脑的脑室周围区域更为明显。研究结果表明,NPH 与组织退化有关。需要进一步的研究来探究机械组织损伤的来源,作为 NPH 相关脑室扩张和临床症状的潜在原因。