 Hello everyone. I'm going to I'm Dr Suhas. I'm a junior resident in radio diagnosis and I'm presenting this paper on spectrum of intracranial lipomas case series. The aim is to present a pictographic review or spectrum of intracranial lipoma presentations and to describe associated anomalies and features. Retrospectively, cases with CT MRI reports dating intracranial lipomas were taken from the departmental parks in Dr. D. Y. Partial Medical College. Key key key imaging characteristics related to intracranial lipoma and associated anomalies were recorded. Coming to our first case. Here we see that the genu and rostrum of the corpus callosum are well visualized in the body, extremus and spleenium are not. So, it has partial agenesis of the corpus callosum. In this region, we see a large T1 hyperintensity and it is communicating extractively through a tract and defect in the frontal bone. We see a few other similar appearing tracks as well. On T2 coronary image, it appeared bright and it showed and it appears hypo intense on T1 FS. So, it is likely it's a system of a fat containing lesion. It is causing displacement of the fibers as seen on the DTT. On the flare image, the lesion appeared hypo intense and we can also see dilatation of the posterior horns of bilateral ventricles. To summarize, our case has partial agenesis of the corpus callosum and the corpus callosum lipoma, which is showing extracranial extension. We can also see colpocephaly in this case. The same patient showed signal dropout on SW images and the pre and the post contrast T1 SS images show peripheral contrast enhancement. On CT, we see a hypo dense lesion corresponding to hypo dense lesion, which is extending extracranially through a small defect in the frontal bone. The same scene on the coronary CT image. Coming to our second case, this case too has partial agenesis of the corpus callosum. The last pericallosal inter hemispheric lipoma is noted inter hemispheric lesion showing T1 hyper intensity and suppression on fat on FS images as seen. The lesion is also showing intracranial extension of the lipoma. A third case has a pericallosal high T1 hyper intensity as seen in transverse as seen in societal and transverse images. Corresponding low at low high point in the area is seen in the same region on CT images. So we come to a conclusion of pericallosal lipoma. Here we can also see a soft tissue density, which is extending through a defect in the basal part of the frontal bone, likely to be a meningoencephalocene. Coming to our fourth case, it has a T1 hyper intensity along the pericallosal region in the entire extent of the corpus callosum. It shows signal dropout and FWI and correspondingly appears bright on face. Our fifth case is similar and it shows pericallosal T1 hyper intensity along the entire extent. In our sixth case, in the Fox region, we see a hypodense lesion, which is likely to be a Fox lipoma. In the seventh case, we have a T1 hyper intensity as seen in the action and societal images, likely to be quadrothermal late lipoma. In this image, we see a T1 hyper intensity in the region of the cribriform plate, likely to be a cribriform plate lipoma. To summarize the findings, to summarize our cases, our first case had a corpus callosal lipoma with extracranial extension. It was associated with partial lazinesses of the corpus callosum and corpus apalli. Our second case had pericallosal inter hemispheric lipoma and it also showed partial lazinesses of the corpus callosum along with intraventricular extension of the lipoma. Our third case was that had carvelinia lipoma in the posterior portion of the corpus callosum. It was associated with frontal meningoencephalosine. Our fourth case had carvelinia pericallosal lipoma along the entire corpus callosum. Our fifth case had a lipoma of corpus callosum and KVM septum pellicidum. Our sixth case had Fox lipoma. Seventh case was that of quadrothermal plate lipoma. Eighth was that of piriform plate lipoma. And our last four cases were not associated with any associated anomalies. Discussion. Intracranial lipomas are not tumors as such, but rather a result of abnormal differentiation of embryonic menix primitiva. They are frequently associated with abnormal development of adjacent structures. Location. Intracranial lipomas are widely distributed in the intracranial compartment. Although they are found easily anywhere, certain regions are characteristic. Pericallosal lipomas comprise 45% of all intracranial lipomas and they are usually associated with the adenosis of the corpus callosum in approximately 50% of the cases. They are divided morphologically into tubular nodular and curvilinear types. 25% of intracranial lipomas are quadrothermal system lipomas. They are associated with underdevelopment of the inferior corniculus. 15% are supracellar system lipomas. 10% are cerebellopontine angle lipomas. These lipomas often have facial nerve and vestibular cochlear nerve coursing through the lipoma. 5% are sylvanes tissue lipomas and rarely they can even be coratlexus lipomas. Imaging characteristics on CT, they typically appear as non-enhancing masses with uniform fat density, hence negative CT attenuation values. It has a lopinated soft appearance conforming to the adjacent anatomy. Some peripheral calcifications may be present. On MRI, MRI with and without fat saturation are able to make the diagnosis easily. In the absence of fat saturated images, then chemical shift artifact may be useful. Signal characteristics are that of fat, T1 hyperintensity, T2 hyperintensity, T1 with contrast enhanced gadolinium image shows no enhancement. Fat saturated sequences show low signal. On SWDI, they can produce blooming due to susceptibility artifacts. Differential diagnosis. The differential is essentially that of masses which contain fat and therefore include intracranial dermoid if ruptured will also have multiple droplets scattered throughout the subarachnoid space, usually in the midline. Differential teratoma, lipomatous transformation of neoplasm, such as in peanut epindymomas or gliomas. On MRI, if no fat saturated sequences are available, then a number of other possibilities should be entertained, which also have high T1 signal. On thrombose baryoneurism, often will have a calcified rim and hemo-sidrin-staining on gradient echo or SWI sequences, white epitomoid, rare and will restrict on DWI. These are my references. Thank you.