 Myself, Dr. Nandish, I am from Vishnu Vishnu Vijapit, by two authors being Dr. Pramu Chalb and Dr. Amal Govindy. I will be presenting case 3 of Krenoparenjama. Krenoparenjama is a benign neoblasm which is created as a double-edged ribbon. They are thought to arise from the pituitous remnants of plastic spots that occur in cellar and supercellar regions and can be seen anywhere from the flow of the red-brick to the pituitary gland. Cellar and supercellar repression compromise of 70% and supercellar cruelty 20%, purely intracellar 10%. Representing symptoms include signs of increased intracranial pressure, secondary to obstructive hyperlipidosis, and more common in children. Visual disturbances or hypothalamic pituitary access dysfunction may occur and children may also present with throat failure. Histological findings are comprised of chords of polymer or spramus epithelium keratin formation. This slide with epithelium cells in loose connection tissue or glass stroma may be formed in the tumor. This is very in colour and viscosity and may contain cholesterol crystals or MRA. Krenoparenjama is further divided as adamantino matters which is more common in pituitary and tapillary. So the common findings of the both include adamantino matters that are multi-librated and partially solid, mostly cystic. Whereas tapillary, they are discreetly encapsulated mass with a smooth margin, often solid, with a cauliflower-like configuration. And adamantino matters, they are said often contain dark viscous machinery oil fluid rich in cholesterol crystals. So tapillary, if they contain cysts, their fluid will be clear, unlike the machinery oil-type fluid in case of adamantino matters. The surface of adamantino matters of Krenoparenjama are often irregular and repetitive, adhering to the adjacent structures such as hypothermia. Whereas in case of papillary, it has a smooth surface and does not adhere to the adjacent brain. Calcification is usually present in case of adamantino matters and calcification and common outlay in case of papillary. And it is seen to give a wet keratin nodules characteristic appearance in case of adamantino matter, which is absent in papillary. So the study information of the case being a 12-year-old boy who came to our hospital with complaints of headache, learning of vision, since one and a half years. There was no previous history of trauma or any documented evidence of mass vision. No previous imaging studies were available, CTL, cholesterol and marrow were done for the patient. Coming to the CT panel, a well-defined multi-librated solid cystic lesion measuring of 5.8 into 3.2 into 4.1 is noted in the suppressor region. The soft tissue density component of the lesion near the seas of density with cystic component is seen. We can also note the extensive peripheral and chunky central areas of calcification. Extensions of the lesion superiorly, the lesion is causing mass effect on the adamantino with a marked enhancement of the bilateral adamanticals with perimetrical curves. Inferiorly, the lesion is causing mass effect on the pituitary gland and its cordial displacement. Hostiorly, the lesion is causing effacement of the interpedantular and pre-pontent systems with mass effect of the bones and lipid with epidermal stenosis causing hydrocephalus. Coming to the mRNA findings, a well-defined multi-librated solid cystic lesion is noted in the suppressor region. The solid component of the lesion appears high source to hypo on T1 and the cystic component shows variable signal intensity with high-pointage to high-soil density on T1. So, it appears heterogeneously hyper-intense on T2 or plate and the cystic component appears hyper-intense on T2 sections. SWI and phase analysis, they show extensive peripheral trendy in central areas of blooming which are indicative of calcification. Coming to the post-contest section, the solid component shows heterogeneous post-contest trends whereas the cystic component shows parallel compression engine. Case discussion, a well-defined multi-librated solid cystic region is noted in the suppressor region. The lesion shows soft tissue density, solid component and CSF density cystic component with calcifications on CT. The solid component of the lesion appears high source to hypo on T1 and the cystic component shows variable signal intensity with high-pointage to high-soil density on T1 and the cystic component shows peripheral and chunky central areas of blooming on the substrate's sensitivity of calcifications. The cystic component shows variable signal intensity with high-pointage to high-soil density on T1 high-pointing on T2 and shows peripheral contrast enhancement. The lesion is called in the last of it an acute obstructive edifice as described slightly adamantinal matters, cranial pharyngeal one. So the difference has been that here's what's left sits on CT. Non-contrast, it appears typically not classified and shows homogenous lower tension and commonly it may be off-mixed and so too lower tension or contains mal-calculated calcifications in ball. On post-contest images, they typically are non-enhancing although the cyst ball may enhance in some cases. Coming to the MRI findings, T1 50% are hyperventilized and 50% are high-covalent. T2 majority of them are hyperventilized. Coming to the post-contest, there is no contrast enhancement of the cystine however it's been enhancing the frame of the tunneling or compressed pituitary tissue may be equivalent. The second difference will be pituitary macroderma. The CT findings of macroderma are usually eye-students with a grey matter but cysts and hemorrhage might be seen. Calcifications are made and moderate but heterogeneous enhancement of the macroderma is typically on CT. MMR findings, macroderma are usually eye-students with cortex but the procedure pituitary bright spot is absent or dispressed into the supra-diplomatic system on T1 meter. Small cysts and hemorrhage hopefully are seen and hemorrhage generally eye-students with grey matter on T2. Hyperintensity along with optic infarctis on T2 layer occur in 15-20% of the cases. Hemorrhage, cardinomas, fibrum on T2 weighted. Most of the macroderma can then strongly participate in this thing on contrast. Subtle durous thickening is present in 5-10% of the cases. The next difference will be hypothermia plioma. On T1 it appears high-sointense relative to the brain-barricana and on T2 it appears high-sointense to hyperintense relative to the brain-barricana and it shows homogenous spot contrast enhancement. The next difference will be intrapidermoid cyst which appears hypodensone CT and on MR, isotope slightly high-sointense compared to CSF on both T1 and T2 weighted sequences and it does not suppress on place. Hypothelium comartoma. On T1 it appears high-sointense relative to the grey matter and on T2 it appears high-sointense relative to the grey matter and it does not show any post-contact enhancement. The last attention will be intrapidermoid teratoma. On CT, the majority of the intrapidermoid teratomas demonstrate at least some fat and some calcifications which is usually solid or clump-like. They usually have cystic or solid components contributing to a regular outline. Solid components demonstrate variable energy. On MRN T1 it shows high-sointense components due to fat and proteininsic lipidrate to fluid. Intimidate components of soft tissue and the high-sointense components due to calcifications and fat products. On CT, it shows our contrast enhancement. T2 it gives a mixed signal. These are the references. Thank you.