Premium
In vivo viscoelastic properties of the brain in normal pressure hydrocephalus
Author(s) -
Streitberger KasparJosche,
Wiener Edzard,
Hoffmann Jan,
Freimann Florian Baptist,
Klatt Dieter,
Braun Jürgen,
Lin Kui,
McLaughlin Joyce,
Sprung Christian,
Klingebiel Randolf,
Sack Ingolf
Publication year - 2011
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/nbm.1602
Subject(s) - normal pressure hydrocephalus , viscoelasticity , brain tissue , medicine , ageing , hydrocephalus , cardiology , disease , surgery , materials science , dementia , composite material
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. Copyright © 2010 John Wiley & Sons, Ltd.