 So I'm talking about common, perhaps, and not so common pathologies in the cellar and supracelar location. The cellar region houses the mastoidal and pituitary, its top, and hypothalamus, and it's a complex anatomic location with MRI being the most important modality for evaluation. Pituitary adenomas of picnic compromise 90% of the diagnosed cellar regions while the remaining uncommon or less typical at primarily intracelar or supracelar location include the inflammatory pathologies like lymphocytic hypofisitis, neuropsychoidosis, neoplastic like bad case lapses, astrocytomas, primary CNS lymphomas, meningeoma, germ cell tumors, or metastasis, and a vasculinoration like aneurysm, hemangioma, and at the point of discussion here where errors in immune differentiation are relatively common. It is necessary to consider the possibility of occurrence of these regions as it can alter the course of management like using a totally different approach to surgery in gliomas or possibly even avoid surgery like in case of hypofisitis. Diagnostic approach and accurate correlation with history is of prime importance. 33-year-old female, presenting with gyrochlorion, opresional headaches, no menstrual review of bad case, with increased levels of prolactin, T2 weighted images show an isointense mass with a hyperintense volume within. On post contrast, it is shown heterogeneous enhancement with non-enhancing hormone. The stock is thickened of approximately 6.1 of them. History of pituitary bright spot is preserved on treatment images. Now, pituitary adenoma or hypofisitis. I have closed my book here. If there is asymmetrical enlargement of the glioma, it is pointing towards adenomas. If there is symmetrical enlargement, it points towards hypofisitis. Features like widening of cell atarsica, heterogeneous enhancement point towards adenomas. While features like stop thickening, posterior pituitary bright spot lost and parasol are dark, T2 sign is present points towards hypofisitis. In this patient, a young female with obvious stop thickening, symmetrical enlargement and intense post contrast enhancement. A diagnosis of lymphocytic hypofisitis was made. Patient was started on steroid and on follower were marked showed regression of cells. Case 2 is a for 29-year-old female, presenting with amenorrhea, infertility and loss of weight since 6 months. History of diminishing of vision and bilateral eyes present. The anterior pituitary hormones are low, high CRP and ESR levels are noted. Lactin cortisol is normal. On T2 T1 weighted images, there is a cellar mass with a hypointense nodule within. T2 is hyper intense. On post contrast tissue, homogeneous enhancement with stop thickening of approx. 5 mm. The posterior pituitary bright spot is not seen on T1 weighted images. But there is a striking nodular enhancement of the thalamus triad vessels in the granular capsular formation. On diffusion weighted images, there is no restriction in diffusion scene. And the left optic nerve is showing a signal of normal T2 hyper intense signal. In the super-chiasmatic part, and no packet meningeal enhancement is however seen. There were two differentials of neurosurpoidosis and lymphoma based on few studies that have described neurosurpoidosis presenting as neural lymphoma process. The features considered were homogeneous contrast enhancement, stop thickening nodular perivascular enhancement and the left optic nerve signal. Angiocentric lymphoma was also considered going to nodular perivascular enhancement and the optic nerve environment. But there was no diffusion restriction and that would help us roll out. However, typical features of neurosurpoid like packet meningeal enhancement, diffusion restriction with significant drop on ADC or absinthe, more high-level lymphoenopathy or lung-perantival environment on atrocity. A transplant-ordered YFC optimization was done which conformed to diagnostic neurosurpoidosis. Case 3 is of a 25-year-old male presenting with gradual onset of mood-opening headache and blood vision since 5 months. On T1 societal images, we can see a heterogeneous solid cystic T1 iso intense mass. Which is hyper-intense on T2 with cystic areas within showing intense enhancement on contrast. On MR spectroscopy, showed polina and anilopetes, the pituitary gland and the distal stock are seen separately from the lesion. It is seen to compress the lateral ventricle with a certain hydrocephalus and dilatation of ventricles. On T1 and flare images, if we compare the size of the lesion on T1 and on flare is approximately the same. They are showing that it is showing a non-infiltrative pattern. There is abutment of the chiasma anteriorly. However, no new non-new within a cystocyan is seen here. It is a high-grade or a low-grade glioma. It is important to distinguish because in adults, it is uncommon to have a pylocytic astrocytema in that location. However, a non-infiltrative pattern, intense enhancement and no dissemination in the pod, points towards low-grade gliomas like pylocytic astrocytema. Plastic features of a cystic mask with a neural nodule is absent. This was confirmed on Hystopath and tumor resected with 3 nutrients. T4 is of a 31-year-old male, presenting with chronic headache, not really with symptomatic treatment. No other symptoms are present. On T1 sagittal images, we can see a figure of 8 opiations here, which is iso-intense to brain data. On T2 weighted images, which is iso-intense, but there is a high-point-intense nodule within the vision. On post-contrast sequences, we can see that the normal pituitary is seen compressed against the celloposteriorine. The chiasma and the tracts are normal. This is a claw sign that has been described here. Now, again, there are two differentials, macro-arynomers or ratcase-clepsis. Now, macro-arynomers were present with fluid levels. Intrastic nodule is common in ratcase-clepsis. T2 intensities can be variable owing to the different protein conference. Pituitary and its top is seen separately and usually compressed posteriorly, then it points towards ratcase-clepsis. Here, an intracistic nodule is there. There are no obvious endocrine symptoms and a peripherally-enhancing limb, that is the claw sign seen. So, it points towards ratcase-clepsis. Case 5 is of a 14-year-old male child, presenting with short stature, features of apoconadism, low levels of T3, potassium, acetate, GH was low and so was normal. Here, we can see that the anterior pituitary is small in size, the stalk is absent and there is an abnormal location of the posterior pituitary bright spot seen at the base of the third ventricle. Is it an ectopic posterior pituitary? It would point towards pituitary stalk interruption syndrome, which is a rare syndrome with incidence of 0.5 per 1 lakh light-froats with a tride of MRI findings of interupted pituitary stalk, hypoplastic, anterior pituitary and ectopic posterior pituitary bright spot. This patient fits into this diagnosis. However, the occurrence of bright spot is diagnostic and should not be missed. How do we approach this cellular and supracellar pathologies? Identify the cellular tersica and the gland. Determine epicenter of the lesion, whether it is cellular, paracellar or supracellar. Analyse the lesion morphology, cellular intensity, solid cystic, low voice, bone environment, calcification enhancement. Then, come down to specific characters like paracera, dark pituitary sign, flaw sign, nodular vascular enhancement, pactive manager enhancement, which would confirm the diagnosis and surgical planning. There is a quick summary of the mimicers of this not-so-common pathologies where differentiated characteristics are listed with the common mimicers of these pathologies. In conclusion, we can say that MRI can be accurately used to identify the origin of the lesion whether it is coming from the pituitary or it is separate. The type of enhancement, enlargement of the cellar, stalk thickening, presence of the bright spot, intracystic nodule, leptomanageal environment, complete systemic evaluation are important differentiators in diagnosis. Classic features like T2, dark sign, diffusion restriction, neural nodule venous sign, figure of atronification may be absent or even if it is present, it can be misleading. When lesions are large, like ratkiss, leptomanageoma, they may displace or obliterate the gland itself, making differentiation of the merinomas and determine whether it is a cellar or extracellular pathology difficult. History is of prime importance in arriving at the diagnosis. Thank you.