John Huston

MR elastography (MRE) of the brain is a novel biomarker capable of measuring the stiffness of the brain noninvasively. MRE is a 3-step process whereby shear waves are introduced by a soft, pillowlike driver placed within a standard head coil. The 60-Hz vibration has been well tolerated in our practice and we have not encountered any patients who found the experience uncomfortable. A phase contrast like a pulse sequence is performed that includes 8 offsets to fully characterize the resulting shear waves within the brain tissue. Finally, a mathematic inversion is performed to create elastograms, which quantitatively report the parenchymal stiffness. Previous work has demonstrated the ability of MRE to characterize both the stiffness and adhesion to the normal brain of intracranial tumors. In this study, we applied the technique to the diffuse neurologic disorder normal pressure hydrocephalus (NPH).

NPH is typically characterized by cognitive impairment, urinary incontinence, and gait difficulty. Currently, NPH is considered the only treatable form of dementia. Conventional imaging can suggest the diagnosis when ventriculomegaly out of proportion to the size of the Sylvian fissure is present. However, currently a favorable response to a high-volume lumbar puncture is the most definitive criterion for diagnosis.

MRE demonstrated significant regional patterns of stiffening and softening of the brain in patients with NPH compared with healthy controls. The periventricular white matter and frontal lobe were softer, while stiffening was found in the occipital, parietal, and temporal lobes. Based on their unique stiffness patterns, NPH can be differentiated from other common forms of dementia. Additional work from our group demonstrated that neurodegenerative forms of dementia, such as Alzheimer disease (AD) and frontotemporal dementia (FTD), exclusively result in brain softening. FTD results in significant softening limited to the frontal and temporal lobes, while AD results additionally in parietal lobe softening. On the other hand, patients with dementia with Lewy bodies (DLB) have no detectable change in brain stiffness. These findings align with the pathophysiologic changes observed in these diseases. For instance, AD and FTD are associated with extensive cell death, as well as neuronal and synaptic loss. DLB is not associated with cell death and resulting structural changes, but impaired brain function results from alpha-synuclein accumulation.

MRE has demonstrated a unique pattern of mixed brain stiffening and softening in NPH. The pattern is in alignment with pathophysiologic theories of NPH, including periodic episodes of increased intracranial pressure, lower parenchymal compliance, and increased pulse pressure. MRE demonstrates unique patterns of brain viscoelastic change in the common forms of dementia and may in the future help identify those patients with NPH, the 1 treatable form of cognitive decline.

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