IntroductionPeri-Ventricular Hyperintensity (PVH) as the name connotes refers to homogenous high signals contiguous to lateral ventricles on T2 weighted (T2W), Fluid Attenuated Inversion Recovery (FLAIR), and Proton Density (PD) images, without prominent hypointensity on T1 weighted (T1W) MR images [1][2][3][4][5]. They are differentiated from infarcts as they are not usually evident on T1W MR images and they do not follow specific vascular territories [2]. PVH is a qualitative evaluation of white mater lesions in brain Magnetic Resonance Imaging (MRI) [1].Regional localizations to peri-ventricular areas equate to white mater which is known to contain nerve fibres. White mater is dichotomized into deep (central) and subcortical (peripheral) white maters of either cerebral or cerebellar hemisphere [6,7]. This accounts for 60% of the total brain volume [6]. Major commissural tracts, cortical association fibres and cortical afferent/ efferent fibres are the constituents of the deep white mater. These nerve fibres consist of neuronal axons with myelin envelopes [6]. Others are supporting cells, interstitial spaces and vascular structures [6]. The supporting cells (neuroglia) are either oligo-dendrocytes or astrocytes [6].Oligodendrocytes produce and maintain myelin which functions as axonal insulators and facilitates rapid impulse transmission [6].The presence of normal myelin confers characteristic MRI intensity on normal brain MR images. Myelin has relatively short T2 and T1 relaxation times primarily owing to its lipid content. Normal myelin is therefore hypointense on T2W and hyperintense on T1W. If a disease decreases the myelin content, the white mater becomes less hydrophobic and takes on more water causing prolongation of T1 and T2 relaxation times. This leads to high signal on T2W, FLAIR and low signal on T1W as seen in PVH [6]. AbstractBackground: Peri-Ventricular Hyperintensity (PVH) refers to bright signal adjacent to lateral ventricles on T2