 Hello everyone, my name is Dr. Mohit Ammaltam of Kovala, 2nd year PG resident at Krishna Vishwavithya pit. I will be presenting paper on intracranial ring enhancing lesions. Most common lesions found in the non-urimaging are ring enhancing lesions, these can be caused by variety of infections, neoplastic, inflammatory and vascular diseases, aims and objectives to analyze and evaluate ring enhancing appearance as a sign in the differential diagnosis of neurological lesions in the brain. To distinguish between neoplastic and non-neoblastic peripheral ring enhancing or ring-like lesions on MRI, Materials and Methods, Study Design, Retrospective, Observational Study, Study Location, Department of Radio Diagnosis Games Karan, from January 2023 to December 2023, Study Population and Sample Size, 17 patients were included in retrospective study conducted at Department of Radio Diagnosis Games Karan, Study Period, January 2023 to December 2023, Cerebral Obsesses, 11-year female with history of high-grade fever and seizure episode, pyogenic abscesses, late-end capsulation stage, a well-defined thin wall-lobulid and smooth margin lesion noted in the 11-year ganglion capsular region involving thalamus extending superiorly to the coronary data and inferiorly to the mid-bend, heterogeneously hypointense on T1, T2 hyperintense showing thick uniform capsule and dual ring, getting suppressed on flat, showing peripheral complete ring enhancement with central non-enhancing component, peripheral effusion restriction with areas in center also showing diffusional restriction, mild peridational vasogenic edema is seen in the lab ganglion capsular region on emaspectroscopy, elevated lipid lectic pain with normal pollen and creatinine pig snoutin, cuba echeloma, a 60-year-old female with history of fevers and spiders, multifocal nodular and ring-enhancing lesion seen in right cerebellar hemisphere and peridational edema, effusing adjoining circular spaces, few of them are conglomerate the lesion is causing mild mass effect on fourth ventricle on right side, iso-to-hypointense on T2 flare and T1, no diffusional restriction, no blooming on GRE, no abnormal leptomanin gel or pecky manin gel enhancements in neurocystic cuff circuses, this is occur in 4-6 stages of vesicular stage, colloidal stage, granular stage, tassified stage, 12-year female with history of seizure, here the neurocystic circuses in granular nodular stage was noted, few well-defined lesions in the left parafell sign, parietal region in close proximity to the subarachnospheres, hyperintense on T2 weighted images and flare, and a beryfila hypointense ring and hypointense dot, likely spolier. isointense to hypointense on T1 weighted images showing areas of diffusional restriction in the beryfila, ring enhancement on post-contrast images, print metastasis. In a known case of infesive ductal carcinoma of the left breast, multiple ill-defined interaxial and extraction lesions are wearing it, involving bilateral cerebral hemisphere with surrounding edema, causing mass effect on fourth ventricle and brainstem with effacement of Cp-angle and medullary systems. Similar small lesion in parafell, several extra axial locations of right frontal region with no surrounding edema were noted. On T2 weighted images, it was iso2 hypointense, T2 weighted and flare, iso2 mildly hyperintense, and diffusional weighted on ADC, mildly patchy diffusional restriction was noted, on hemonoevidence of looming, and T1 post-contrast images, homogenous enhancement was noted, glioblastoma. 42 years female with history of headache, a high-grade gliolneoblastoma like glioblastoma, WHO grade 4 was noted, large ill-defined irregular area in right parietal, poxipetal, and part of temporal lobes involving splenium of corpus callism and callism must not crossing the midline, appearing iso2 hypointense on T1 weighted images and heterogeneously hyperintense on T2 weighted images with areas of cystic changes within. Peripheral remains central patchy areas of diffusional restriction and multifocal peripherals surrounding perillational edema with midline shift and central areas of looming and GRE sequences. On post-contrast T1 weighted images, heterogeneous predominantly peripheral enhancement with central non-enhancing areas were noted. Emma spectroscopy level increased cooling peak and reduced NAA peak with increased cooling to NNA ratio of 6.0, cooling to creatine ratio is 4.2, multiple sclerosis. 40-year female with history of headache, presented with an MRI patchy focal areas along both callosoceptal interface perpendicular to the corpus callism that is the loss and fingers. Similar lesion also seen in bilateral white matter of temporal lobe and left half of cerebral pedendal. Hypersink intensities on flare and T2, this lesion show no post-contrast enhancement and diffusion restriction. Patchy areas of ultra-signal intensity seen in this cervical spine predominantly at the C2, C3, C4, C5, C6 and T1 level. Hypointensity on T1 and T2's are hyperintensity noted. Few of these lesions are showing ring-like enhancement. So, as a result, where there were 4 cases of cerebral abscesses, 4 cases of tuberculomas, 2 cases of neurocyste circuses, 3 cases of metastasis, 2 cases of glioblastoma and 2 cases of multiple sclerosis. Cerebral ring enhancing lesions are defined as an area of hypointensity in MRI of brain tissue surrounded by a rim of enhancing tissue after contrasting injection. Various characteristics like number of lesions, location, margins, wall thickness, complete or incompleting enhancement from a peripheral edema are taken into consideration to reach the diagnosis. MR spectroscopy also helps in evaluating various ring-enhancing lesions. On concluding the paper, MRI along with MR spectroscopy has been the most sensitive modality in the characterization of intracranial ring-enhancing lesions. These were the references used in this paper. Thank you.