 This was a one-year-old male who came with complaints of vomiting and altered sensorium. He had tonic-lionic type of movements and uprolling of eyes as well as frothing for mouth for few minutes. He did not have any significant past history. On examination his GCS was 9, the pupils were dilated and sluggish response to light was there. There was decreased power in all four limbs and the deep tendon reflexes were sluggish. So an MRI of the brain was advised. The diffusion-weighted MRI showed that there were restricted diffusion in most of the right cerebral hemisphere and part of the left cerebral hemisphere appearing bright on DW images and turning dark on ADC maps. There was no blooming scene in these areas on SWI and these regions appear subtly hyper intense on FLARE images. They were also subtly hyper intense on T2W images and nearly ISO intense on T1W images but the adjacent sulcal spaces were effaced and there was thickening of the cortex. On post-contrast study there was diffuse leptomaninjil enhancement. The patient kept worsening and hence an MRI was repeated after eight days which showed that there was increase in the FLARE hyper intensity more so on the right side. Also there was diffuse thickening of the cortex. On T1-weighted images now we could see cortical hyper intensities and post-contrast enhancement showed diffuse chiral enhancement more so on right side. The patient was worsening for few days and then he stabilized and this was an MRI which was repeated after a month which showed that there was no restricted diffusion in the present study but the T1-weighted images showed that there was diffuse chiral T1 hyper intensities on the right side and slight chiral hyper intensities on the left side also. Also there was diffuse cerebral atrophy which was seen in the form of dilatation of ventricular system and other CSF spaces. So to summarize in initial stages there were extensive areas of restricted diffusion mostly involving the cortex and sub-cortical white matter in bilateral cerebral hemispheres there was more on the right side. There was extensive cortical necrosis in the later stages involving predominantly the right cerebral hemisphere with gyreform enhancement. Also there was diffuse leptomaninjil enhancement suggestive of congestion. In the later stages there was dilatation of the ventricles and CSF spaces suggestive of early cerebral atrophy. Considering these imaging findings in the initial stages the differential diagnosis which were put forth were encephalitis because of the restricted diffusion hypoxic insult but the patient did not have status epilepticus to support prolonged hypoxia. Another differential diagnosis which was considered was malas due to restricted diffusion in multiple areas. In view of suspicion of encephalitis a neurotropic virus panel was run which was negative. CSF examination was done which did not reveal any obvious infective etiology. Also anti-neuronal antibody panel was run which showed that CSF anti-NMDA receptor antibodies were positive. So this is a case of anti-N methyl deaspartate acid receptor encephalitis. It is a form of autoimmune limbic encephalitis which is seen in young patients females being more affected than males. It is usually associated with some kind of a tumor mostly ovarian tiratoma. The typical presentation is of psychiatric symptoms but the patients can have varied symptoms. MRI findings are usually non-specific. MRI could be normal or we could see abnormal T2 or flare in hyper-intensities mostly involving the medial temporal lobe but any part of the brain can be involved. In later stages we see atrophy. Sometimes an FDG pet is done which shows hyper or hypometabolism in the affected regions depending on the stage of the disease. A pelvic USG should definitely be done in these cases to look for an ovarian tiratoma which may be associated with it which is seen as an heterogeneous adnexal mass having different components such as fat calcifications and soft tissue. Thank you.