 Good evening, everyone. I'm Dr. Akshay Gangi, JR3 in department of radio diagnosis in Grand Government Medical College and Sir JJ group of hospitals. Today, my topic for presentation is MRI imaging in tuberous sclerosis. Tuberous sclerosis, also known as tuberous sclerosis complex TSC, is a rare genetic disorder characterized by growth of non-cancerous tumors in various organs of the body involving brain, kidney, heart, lungs, eyes, skin and other organs. It affects multiple systems and provides a wide range of symptoms and complications. It is caused by mutation in one of two genes, TSC-1 or TSC-2, which instruct for making proteins that regulate cell growth and proliferation. Neurological symptoms such as seizures, developmental delay, intellectual disability, behavioral problem, and autism spectrum disorders are seen. The metallurgical symptoms such as facial angiofibromas, chagrin patches and hypermelanotic macaoles. Renal symptoms in the form of renal angiomyelipomas and renal cysts which may cause bleeding, cleaning, dysfunctional, hypertension. Cardiac symptoms that is cardiac rhabdomyomas, milituorhythmias, or heart failure. Pulmonary symptoms, TSC can cause lymphangioleomyomatosis which cause pulmonary symptoms. Ophthalmic symptoms such as retinal hematomas or other eye abnormalities. Diagnosis, it is diagnosed based on clinical features, imaging and genetic testing. There is a criteria for diagnosing TSC set by international tuberous sclerosis complex consensus conference in 2012, which includes both major and minor features. The diagnosis requires two major features or one major feature plus two more more minor features. Genetic testing will also aid in the conformation of diagnosis. Facial angiofibromas or forehead plaques, we are talking about major features now. Non-traumatic angiol or periangol fibromas, hypermelanotic macaoles, chagrin patch, cortical tuber, subepanenominal nodule, subepanenominal giant cell, astrocytoma that is SEGA, cardiac abdomen, renal angiomyloepoma. These are major features. Minor features are multiple randomly distributed pits in dental enamel, hematoma, cervical polypons, cerebral vertebrae, radiative migrations lines, gengival fibromas, non-renal hematoma, retinal acromic patch. Role of MRI and diagnosing TSC. MRI plays a crucial role in diagnosing TSC. Brain imaging provides us with diagnosis of cortical tuber subepanenominal nodules and SEGA. It can also be used to monitor SEGA over time. Renal angiomyloepomas are detected in abdominal imaging. Also cardiac imaging helps us to pick up cardiac graftomyoma aims to provide corroboratory findings in case of clinical suspicion of TSC. Also to raise suspicion of TSC in case the clinician has missed the findings and stigmata. Also in known cases of TSC, we can serially monitor the disease progression and guide further management. Protocols we do brain imaging in axial T1, T2 flare, gradient imaging and susceptibility weighted imaging. Renal imaging is done in routine abdominal protocol using fat suppress sequences, T1, T2 weighted sequences and cardiac imaging. Now here is the case we have T2 flare diffusion weighted imaging and susceptibility actual images of brain showing large ill-defined lobulated solid cystic intraventricular lesion epicentered in foremen of Monroe extending into supracellar region. The lesion appears heterogeneously hyper intense on T1, T2 flare imaging with no diffusion restriction on DWI and shows multiple foci of blooming on susceptibility imaging with heterogeneous post-contrast enhancement feature solicit of sub-epidemial giant cell astrocytoma SEGA. Postoperative HPE proved this to be SEGA and further work up confirmed diagnosis of TSC. Another we have images axial and coronal T2 flare, T1 pretty post-contrast diffusion and susceptibility images. Few sub-epidemial nodules are noted in bilateral lateral ventricles showing heterogeneous intensity on T2 weighted and T1 weighted imaging and show mild post-contrast enhancement and blooming on SWI and do not show any diffusion restriction. On CT correlation these nodules were calcifications features solicit of sub-epidemial nodules. Here is another case axial T2 weighted flare diffusion weighted imaging and susceptibility imaging of brain. Multiple foci of T2 weighted flare hyper intense signal in bilateral frontal parietal regions, right temporal and left occipital regions are noted which are limited to cortical surface with cortical thickening and blurring of gravid matter differentiation. They do not show diffusion restriction, do not show blooming. Few of these show flare hyper intense signal extending from cortex towards the ventricle that is trans mantle sign features solicit of focal cortical dysplasias. Another patient which was known case of tuberous sclerosis came to us for the diagnosis of renal angiomyel hypomas. We did an abdominal CT but on the thorax section we were able to pick up this hyper dense area which was void of contrast filling. The patient was suspected for rhabdomyoma, cardiac rhabdomyoma and on 2D eco findings are consistent with cardiac rhabdomyoma. Another patient which we have axial T2 weighted flare diffusion and ADC images of brain. Multiple scattered non-enhancing areas appearing T2 weighted hyper intense and T1 iso intense with no evidence of restricted diffusion bilateral cerebral hemispheres are noted which are suggested of cortical tubers and SEGA. We have CT findings as well in this patient. Agile sections of CECT thorax shows us sub-centimeter size nodules in both the lungs, multiple scattered and thin wall lung cyst in sub pleural region of left lower lobe. This was a case of lympho angiomyomatosis in a known case of tuberous sclerosis. Another patient came to us for the workup. The patient had a gross abdominal distinction. Agile sections of CECT abdomen were taken in arterial and venous phases. This is also a known case of tuberous sclerosis. Multiple large well-defined lesions arising from bilateral kidneys are noted which showing both soft tissue and fat at innovation with significant internal vascularity during arterial and venous phases. Features suggested of renal angiomyloepomas. Also the maximum intensity projection image that is MIP image shows us arterial analgesms noted within the lesion in left kidney. Clinical considerations we are always always taking account clinical stigmata, clinical findings along with imaging findings to reach diagnosis of TSC in previously unknown cases. We can also use MRI to monitor the growth of SEGA, renal angiomyloepomas and other lesions. MRI thus helps in guiding treatment decisions such as surgical intervention for symptomatic lesions. We cannot ignore limitations of MRI. There is difficulty in distinguishing between TSC related lesions from malignant tumors on MRI and also it needs a certain level of expertise in interpreting MRI findings in context of TSC. Conclusion MRI plays a crucial role in diagnosing, monitoring and managing tuberous sclerosis complex relative manifestations yet continued research and advancements are required for enhancing our understanding and treatment of TSC. These are my references. Thank you.