 The topic for my paper presentation is diagnostic approach to basal ganglia hyperintensities in infants. The basal ganglia receive projections from almost every region of the cerebral cortex which enables them to integrate extra pyramidal motor activity. This process demands high ATP energy, internal mandates, rich blood supply and high concentration of trace metals. Unfortunately, these same features make basal ganglia vulnerable to systemic conditions both in long term and short term. There is true susceptibility to damage during childhood when the metabolic need for basal ganglia is much higher. MRI imaging is a useful tool in assessing the acute and chronic changes of basal ganglia in systemic diseases and neurological diseases. The aim of my strategy is to characterize the imaging findings in infants with basal ganglia abnormalities using different sequences on MRI and to correlate these findings with the clinical history, clinical examination and biochemical markers. Material and methods in retrospective study was done on 15 children under the age of 2 years who presented with the various signs and symptoms and are referred for MRI. Imaging was performed on a 1.5 Tesla Siemens MRI. All conventional sequences were performed on all children. Post contrast and advanced imaging techniques were performed in selected cases based on findings on conventional imaging and clinical suspicion. The first case is it is comes under vascular etiology. Here we can see flare hyper intensities which shows diffusion restriction in right lentiform, quartet nuclei in corona radiator and right frontal parietal cortex. Also, we can see foci of blumine which is noted in the M2 and M3 segments of the right MCA. This is a case of acute infarct and right MCA territory which is secondary to right MCA thrombus. The second case in vascular etiology, here we can see flare heterogeneously hyper intense area which shows peripheral diffusion restriction on DWI with few areas showing blooming on span segments. And mild peripheral enhancement and post-contract imaging is also noted in the right thalamus and mild perillational edema is also noted in the mid-bred and right lentiform nucleus. Filling defects which are noted in the right internal cerebral vein, vein of galleon and inferior cervical sinus and straight sinus which suggests the thrombus. This is a case of venous infarct with hemorrhagic transformation in the right thalamus secondary to the venous thrombosis. In case of metabolic etiology, here is a case of five months old child with hypoglycemia. Here we can see bilateral symmetrical T2 hyper intensities, bilateral quartet nuclei and putamen which shows diffusion restriction. This is a case of hypoglycemic encephalopathy. This is another case of newborn which presents it by both asphyxia. Here we can see bilateral symmetrical flare hyper intensities showing diffusion restriction in the bilateral putamen. This is a case of hypoxic encephalopathy. This is another case of infine which shows bilaterally symmetric spelling T2 prolongation and restricted diffusion in basal ganglia, insular cortex and singulate gyrus. On MR spectroscopy, we can see a combination of a toxic metabolic peak of glutamate and glutamine at short TA times. This is a case of hypatic encephalopathy. In case of congenital etiology, there is a case of canavans disease which shows subquarticle deep and periventricular white matter of the bilateral cerebral hemisphere showing T2 hyper intensity and T1 hypointense which suggests dismarination. There is symmetrical involvement of bilateral globus pallidus, subthalamic nuclei which demonstrates the restricted diffusion with characteristic sparing of the posterior limb of the internal capsule. This is also mild T2 hyper intensity in the bilateral quartet nuclei and putamen. On MR spectroscopy, we can see an elevated NEAA peak and the NEA to creatine ratio is also not elevated. This is a case of canavans disease. The second case in congenital etiology, here we can see bilateral symmetrical T2 or flare hyper intensities which shows diffusion restriction and decrease ADC values in corded and lentiform nuclei. Few focal flare hyper intensities are also noted in the periapidactyl gray matter, substantia nigra and braced stem. On MR spectroscopy, we can see lactate peak and decreased NEAA by toline ratio. This is a case of bleak syndrome. Observations and discussion. In 15 children, acute cases causes of basal ganglia hyper intensities like hypoxia, hypoglycemia and encephalitis was seen in 6 children. Other cases includes infarction in 2 children, infarct with hemorrhagic transformation secondary to venous sinus thrombosis in 2 children, leach disease, canavans disease and hepatic encephalopathy in 1 children, hypoxic encephalopathy in 2 children. Bilaterally symmetric diffuse abnormalities involving the lentiform nucleus, corded nucleus in the entirely typically suggest systemic or metabolic causes as per sense a central cause whereas the lesion is asymmetric, focal or discrete involving only a part of basal ganglia it indicates the involvement by infection or by a neoplastic etiology. However, there is often an overlap and atypical features of systemic diseases such as the unilateral involvement may sometimes cause confusion. Conclusion systemic and metabolic abnormalities often involve the basal ganglia on both sides and careful assessment of brain abnormalities occurring simultaneously outside these structures is important, especially MR spectroscopy imaging should be included in the protocol. Imaging with T1 diffusion material imaging MR angiography MR spectroscopy are often helpful in narrowing down to differential diagnosis. Oftentimes however the diagnosis is not straightforward and the correlation of typical imaging features with especially the clinical history the laboratory data can have make the diagnosis clear and correct. These are my references. Thank you.