Hydrocephalus (HCP) is a neurological disease characterised by enlarged ventricles resulting in compression of surrounding brain tissues¹. Conventional imaging techniques depict ventricle size accurately; however, they are less capable of detecting changes in brain microstructure. The aim of this work was to quantify changes in brain mechanical and diffusion properties during the development of hydrocephalus, using MR Elastography^2,3 and Diffusion Tensor Imaging (DTI)^4,5. Both imaging techniques are linked to tissue microstructure and, hence, may be fruitful in tracking microstructural changes as well as improving our understanding of neural injury in hydrocephalus and how neural microstructure changes during the course of the disease.This study was approved by the local animal care ethics committee. Hydrocephalus was induced in eight female Sprague-Dawley rats (4 weeks old) by injecting 30 μL suspension of kaolin (25% w/v in saline) into the cisterna magna. Six sham-injected rats were used as controls. MR imaging (9.4T, Bruker) was performed 1 day before, and at 3, 7 and 16 days post intervention. T2-weighted MR images were collected to quantify the ventricle size and brain anatomy. MR elastography at 800 Hz was used to measure brain tissue shear modulus (G*). DTI (32 gradient directions) was conducted to study changes in brain tissue microstructure, as reflected in the fractional anisotropy (FA) and mean diffusivity (MD) (Figure 1).In hydrocephalic rats, the ventricles enlarged significantly as early as 3 days post intervention, but not in controls. This ventricular enlargement was associated with an enlargement of the head of the rat, a decrease in cross-sectional area of the deep gray matter, and a decrease in thickness of the cortical gray matter (Figure 2). These changes in brain anatomy were associated with changes in tissue microstructure. In the deep gray matter, MD remained unchanged over time and FA increased, likely due to tissue compression. In the cortical gray matter, MD increased progressively and FA decreased and these are likely related to the emergence of oedema in the region. Even though both regions underwent different changes in tissue microstructure, G* of both regions was higher in hydrocephalic brains than in controls at 3 day post- injection. This changed in the later stages of hydrocephalus development and regional variations in mechanical properties reflect the alteration of the tissue microstructure and water content, e.g. seven days after hydrocephalus induction, G* in the oedematous cortical gray matter was lower than in controls (Figure 3). Changes in the mechanical and diffusion properties of brain tissue followed distinct time courses during the development of hydrocephalus. This study suggests that MR elastography and DTI provide complementary information, and their combination provides additional insight into the status of brain tissue during ventricular enlargement in hydrocephalus than either alone.