 Hello everyone. Myself Dr. Vishwabhi Singh, I am a junior resident, third year from Dr. D. Y. Patel Medical College and today I will be presenting a case series on intercranial lipomas which are prepared under the guidance of Dr. Jacob Deeson, assistant professor D. Y. Patel Medical College. So the aim is to present a pictographic review of the spectrum of intercranial lipoma and to describe other associated anomalies and features with it. The method was retrospectively, we took cases with CT MRI reports stating intercranial lipomas from a PAX and the key magic characteristics related to intercranial lipoma and associated anomalies were recorded. So starting with my first case on T1's cycle section, we see a well defined lesion in the frontal area. This appears T1 hyper intense, T2 hyper intense and appears hyper intense on T1 fat set. The lesion is causing posterior displacement of the association fibres and we can see on flare that there is ventricleomegaly. So here the corpus callusum in T1's arch is not well visualized, we can only see the gostrum and genu and the body isthomas and sphenium cannot be visualized. We can see multiple linear hyper intensities extending from the lipoma through a small boony defect in the frontal bone to the superficial or subcutaneous plane which shows another T1 weighted hyper intensity lipoma and here we see it to be a partial adhesive of the corpus callusum with extra cranial extension and we see corpus felae. The same lesion on SWI shows peripheral signal dropout. On pre and post contrast there is no enhancement and on CT imaging we see that is the lesion is hypodense corresponding to low-city attenuation value of fat. Case 2, we see another lesion in the intramasphiric vision with extension into the right ventricle as seen on T1 core images. The corpus callusum is not well visualized and on fat side imaging it shows hyper intensity. There is glooming seen on GRE sequence which can be due to pericylic calcification. So here we see a pericylocal intramasphiric fat containing lipoma which could be a dermoid with calcification with associated partial urge visis disdinesis of the corpus callusum with associated intramintal lipoma or fat droplets due to rupture of dermoid. Coming to Case 3, here on T1 SAG and transfer section we can see a curvilinear lipoma in the posterior portion of the corpus callusum here and on transfer section we see curvilinear lipoma in the posterior portion of the corpus callusum. We can see another soft tissue density extending from the small bony defect which could be a meningoencephalocene. On CT attenuation we can see that the region corresponds to low CT attenuation value of fat. Case 4, we can see T1 weighted hyper density along the corpus callusum and in feed to the spleenium the same on axial section can be seen in the corpus callusum region. It shows signal dropout on SWI images and correspondingly guide images on face. Case 5, again we see another pericylocal linear hyperintensity which shows hyperintense signal on transfer section as well and signal dropout on SWI images. Case 6, we see a well defined hypodense lesion in the false cerebri which is a false lipoma. Then again in case 7 we can see a well defined hyperintense signal in the right cortygeminal system corresponding to cortygeminal plate lipoma. Then in case 8 we can see a triangular shaped hyperintensity, well defined hyperintensity in the cribriform plate which is a corresponding to cribriform lipoma. We have a case summary and in this we can see that the first three cases in the first which we saw corpus callusum lipoma with excreta extension. There was partial adgenesis of corpus callusum along with corpus epheli then in the second case periclosal inter hemispheric lipoma with partial adgenesis of corpus callusum and intravetricular lipoma. Then in third we saw curviline lipoma with meninguensia phyllocea and the other cases did not have any associated abnormally. Coming to the discussion part we know that inter canal lipomas are tumors as such are not tumors as such but rather result of abnormal differentiation of the embryology, embryological meninges primitive they are frequently associated with abnormal development of adjacent structures and location wise these can be distributed anywhere but there are certain regions which are more characteristic. For example periclosal lipoma 45% of the times which is associated with adgenesis of the corpus callusum as we saw in the first two cases and it can be divided into two types morphologically that is tubonodular and curvilinear. Then we have cortigeminal cisterns 25% of the cases then we have supracellous cistern lipoma 15% in cerebellum pontine angle lipomas there is facial nerve and vestibular nerve start traversing through the lipoma and there are sylvian and porat praxis lipoma which is which are quite rare. So on CT they typically appear as a non enhancing mass with uniform fat density as they have negative CT innovation value it has a low belated soft mass appearance conforming to adjacent anatomy and there might be some peripheral classification. On MRI it appears as a MRI T1 hyper intense T2 hyper intense and there is no enhancement on post contrast on fat set it is hyper intense and they might be blooming on SWI sequencing due to susceptibility artifact. Differential diagnosis is essentially those masses which are fat for example intracranial dermoid, intracranial teratoma or there is lipomatous transformation of neoplasms like P net which is primitive in user endocrine tumor appendymoma or glaioma. On MRI if fat set is not available then we will have to consider other possibilities which have high T1 signal for example thombost baryanodism or white epitome white which is rare and will give diffusion restriction on DWI images. These are my references. Thank you.