 Let's discuss case series on skull-based lesions but before we jump into the skull-based pathology we should first understand the anatomy, various visors, buraminas and neurovascular structures that are associated. CT and MRI are the imaging modality of choice and they help not just in narrowing down the differential but also in pre-operative localization and its relationship with the adjacent neurovascular structure. So, we need to know that in MRI we should take even non-fat-sat sequence as extra-cranial fat are better appreciated which are located in the orbital cortex, teregopalate and posa in area medial to teregot muscle which get obiturated in infection, inflammation, tumor pathology. So the skull-based is divided into an anterior-middle and posterior cranial posa. This is an arbitrary division not a rigid. However, for ease of understanding the anterior skull-based is bounded anteriorly by the frontal bone posteriorly by the lettering host minoid. The anterior cranial posa is majority formed by the minoid bone anteriorly bounded by the tuberculum cellae anterior-cranial process posteriorly by the peterous bone and dorsum cellae and posterior-cranial posa bounded anteriorly by the clivus bone and posteriorly by the mastoid part of temporal bone and squamous occipital bone. So anterior-cranial posa we can see on sagittal and coronal sequence section of the CT where we can see the cribriform plate and the crista galle and olfactory nerve which will be better appreciated in MRI. Then we have axial section showing the optic canal in red and supereo-optalamic fissure in blue, optic canal giving passage to ophthalmic artery and optic nerve, supereo-optalamic fissure giving passage to third, fourth, V1 division and sixth cranial nerve. On axial section again on CT we can see foramine oval in blue and spanosome in red, oval giving passage to mandibular nerve, excisory meningiol artery, lecipetrosolam and emissary vein and foramine spanosome giving passage to medial meningiol artery. This is the coronal section showing the spinoid sinus and peregrine plate and then we have two openings laterally we have foramine red-tendum on red giving passage to mandibular nerve and infromidally we have median canal for the passage of median nerve and artery. In the axial section we can see median canal connected with the medial cranial posa via foramine laser. Then we have inferior-optalamic fissure which gives passage to inferior-optalamic vein and nerve and then on coronal section we have foramine oval, on axial section we have foramine rotundum and finally we have coronal section showing optic canal with optic struts separating it from supereo-optalum. Then we have posterior cranial posa where we can see the internal auditory canal giving passage to 70 cranial nerve along its labyrinth side artery. Then we have foramine magnum, lateral to it is the hypoglossal canal for the passage of 12 cranial nerve. Then we have carotid canal and medial to it is the jugular paramen for the passage of 9 cranial nerve through fars nervosa and internal jugular brain, 10th and 11 cranial nerve through fars vascularis. These are the fars of jugular foramine only separated just by fibrous tempa. Now this is the sequence of MRI. We can see olfactory nerve and olfactory nerve optic nerve. Then we have third cranial nerve oplomatria at the level of midbrain. Then we have thick cranial nerve at the level of fars which is trajamanal nerve and then we have vestibular copliar nerve and facial nerve at the level of cerebellar pontine angle passing through the internal auditory canal. So this was the case of 23-year-old woman presenting with nasal discharge with episodes of seizure and meningitis. MRA revealing a large defect in the grippy form plate with herniation of the CSF field stack that contains orbital frontal gyrus and gyrus rectus and meninges. The nasal cavity shows expansion and there is hypertrophy of the left inferior terminate. This was the case of frontal atmodal meningo enkypulocy. Usually it is congenital however it can be seen in urtus due to trauma or idrogenic force. This was the case of 45-year-old man presenting with sudden onset diplopia. MRA reveals due to hyper intense lesion with evident enhancement involving the spinoid bone and left hub of the lesser wing with extending extension into the orbital epics and displacement of the left optic nerve. Cities can reveal permeatory lysis and destruction of the spinoid and clivis bone epicenter in the spinoid atmodal fissure. So this was the case of controsarcoma. Its counterpart caudoma can be differentiated as caudoma is midline not off midline and it involves the clivis bone and controsarcoma usually has higher ADC values as compared to caudoma. Now this is the known case of rhododorferment disease. 27-year-old man presenting with proptosis swelling in the orbit with multiple fibrobenics swelling. The MRA reveals obliteration of the migratory sinus cavity with heterogeneous enhancement in the migratory bone spinoid and atmod bone. Cities can show the ground glass expansion of the medullary cavity with cortical thinning. Now other ancillary findings this patient had were the coreate plexus diploma, enlargement and T2 heterogeneous hyperenters of the Lycroman gland and multiple enlarged cervical lymph nodes in the city scan. So the teaching point was that in a known case of fibrous rhododorferment disease if you see such bony lesion it is associated with fibrous dysplasia. So this is the case of 27-year-old man presenting with facial deformity environment duration. You can see the clinical picture MRA is showing the T2 heterogeneous hyperenters lesion with obliterated margin. Involving the left half of the face, auron is the pharynx with bilateral processes. The lesion shows patchy areas of enhancement with diffusion restriction and areas of necrosis. On cities there is a lactic destruction of the spinoid bone, cryptophon plate, erygoid plate and left orbit. A provisional diagnosis of synonyms of carcinoma was made. However, the histopathology proved to be an adenoid cystic carcinoma. It is the second most common malignancy after mucoepidermal carcinoma affecting the minus livery gland. Lung metastasis is quite common which was seen in this case. 40-year-old woman presenting with insidious onset loss of vision on the left, MRA revealing T2 hyperenters lesion, lobulated, involving the intraorbital segment of the left optic nerve with heterogeneous enhancement showing diffusion restriction. This was the case of optic nerve glioma. Most of them are pylocytic astrocytoma, WHCN is grade 1. They are associated with NF type 1. However, in adults it can be aggressive. This is 16-year-old boy presenting with multiple episodes of frank nasal bead, MRA showing T2 hyperenters lesion with multiple provides giving salt and paper appearance. On post-conference sequence, there is avid enhancement, the lesion is represented in the left, teregopalatin fursa. This was the case, of course, a case of juvenile nasopharyngeal angiopibroma which is benign, but locally aggressive bascule tumor which is almost exclusively seen in meboids. Now we have three cases of shornoma. 61-year-old woman presenting with tinnitus headache, MRA revealing a solid cystic lesion, the solid component showing heterogeneous enhancement, the lesion is calling expansion of the internal auditory canal. So, this was the case of vestibular shornoma which is the most common intracranial and most common cerebellopontan cystinal mass associated with NF type 2. Shornomas passes through the porous acousticals while meningeoma doesn't. That's how we can differentiate if there is any lesion in the cerebellopontan angle. Now, this is the case of particular woman presenting with tinkling sensation in the left half of the face, MRA revealing low obliterate T2 hyperenters lesion in the left mechal scape showing heterogeneous enhancement causing mass effect in the form of obliteration of the cystinal space and displacement of the left hemipons. Trageminal was not seen separately on the left while on the right it is seen, so this was the case of Trageminal shornoma. It is the second most common site after vestibular cochlear nerve if there is a shornoma and sensory nerve are the most commonly affected as compared to pro-pure motor cranial nerve in shornoma. While olfactory nerves and optic nerves do not contain shell cells, these sensory nerves are never affected in shornoma. Now, this is 30-year-old man presenting with proposes, torses and diminishing of vision, MRA revealing a low obliterate dumbbell shaped T2 hyperenters lesion with heterogeneous enhancement and in the mechal cave extending into the orbit through orbital epics. This was the case of given division of Trageminal shornoma. So, two-third of the mechal cave given as shornoma, we have linking mechal sign in which the normal mechal cave is filled with CSF and appears bright. However, any lesion that fills this space will cause obliteration of this T2 hyperentersity and then contrast will be seen with the opposite bright side. Finally, last case, 70-year-old man presenting with type and dimities headache and left ear discharge. There was hyperintensity along the pitrus bone obliterate loss of flow by signal along the right ICI and T2 hyperintensity in the middle-year cavity. This was the case of skull-based hoistomalitis, which was a typical infection arising from the temporal bone and not from sinusitis or deep facial infection, which is a typical and usually involves the central skull-based. So, the take-home message is that both CT and MRA have the imaging mortality of choice for skull-based pathology. We need to have thorough knowledge of anatomy, apart from knowing various imaging characteristics of any particular lesion and our role of radiologist is not just limited to diagnosing it but also to describe the relation with the important structure and its extent. Thank you so much.