Mechanical Deformation Distribution in the White Matter Tracts of the Corona Radiata in Normal Pressure Hydrocephalus

Introduction: The origins of the clinical manifestations in normal pressure hydrocephalus (NPH) remain obscure. It has been postulated that ventricular dilation generates tangential shearing forces on the paracentral fibers of the corona radiata, hence interfering with their function and producing the clinical triad of gait apraxia, dementia, and incontinence. The identification and analysis of white matter of the corona radiata displacement and deformation in NPH may clarify the relationship between physiopathology and clinical manifestations.

Method: Based on a healthy 60-year-old male cerebral MRI examination, we used finite element (FE) analysis to simulate ventricular dilation in three dimensions (3-D) and calculate the strain and deformation of the surrounding parenchyma. The latter was modeled as a poroelastic material saturated by interstitial fluid developed in a previous article by the authors. Magnetic resonance diffusion-tensor imaging-based white matter tractography was then applied to integrate the stress exerted along the projections of the corona radiata.

Results: We used analysis of variance (ANOVA) to analyze the data of our simulation. We separated the internal capsule of each cerebral hemisphere into anterior and posterior limb. We calculated medians and standard deviations for relative elongation, maximal relative elongation, mean displacement, and maximal displacement for each limb on both sides. We considered the difference to be statistically significant with a p value of >0.01.

On both sides, we found that mean and maximal deformation were significantly higher in the posterior limb. Furthermore displacement of the white matter tracts was higher in the posterior limb.

Conclusion: Our simulation demonstrates that ventricular dilation does not have a homogeneous effect on periventricular fiber tracts. Correlating our findings to functional anatomy, we can suppose that motor symptoms of NPH could be due to corticospinal tract elongation and displacement. Hence, ventricular dilation could be considered the primum movens of NPH gait symptoms. However, further physiopathological explanations may remain valuable such as ischemia or metabolic toxicity.