 So, this is a presentation on the imaging in cellar and supracellar lesions. I will begin with embryology followed by normal anatomy, a few anatomical variants and then we will talk about cellar and supracellar masses including solid as well as cystic lesions. This is by no means a comprehensive overview but more of a case-based review of a few interesting cases which would help us to see that the problems we face in day-to-day the whole thing. So, starting with embryology, the pituitary gland lies in the cellar, it has two parts, the anterior pituitary or the adenohypophysis and the posterior pituitary. Both these parts of the pituitary gland arise from the ectoderm but they have different origins. The adenohypophysis is formed from the erathcase pouch which is a superior imagination from the primitive oral cavity. This is ectodermal obviously and the posterior pituitary arises from the neuro ectoderm as you can see. So, the anterior pituitary wraps around the optic chiasm and the buroepophysis comes from the neuro ectoderm. This pituitary gland lies in the cellar, here we see the cellar which is a bony concave cavity. Anteriorly here we see the tuberculum cellae, posteriorly we see the dorsum cellae. The cellar is very closely related to the sphenoid sinus. So, any abnormality in this sphenoid sinus for example sinusitis or in mucosilin in this sphenoid sinus should be reported in our reporting of the cellar pathologies. This is the pituitary gland where we see the adenohypophysis which has a superiorly concave order normally. When we note the height of the adenohypophysis, the height may be increased in physiological conditions like puberty or pregnancy or immediate postpartum period. Posterior to the adenohypophysis we see a hyperintensity even on non-contrast even weighted sequences. So, this hyperintensity is the posterior pituitary bright spot. Superior to the adenohypophysis we see the infundibulum at the top of the infundibulum is the tuberosinidium. Where we see the optic chiasm, superior to the optic chiasm is the chiasmatic recess and the lamina terminalis of the corpus callusin. In the infundibulum is the infundibular recess, superiorly we see the region of the mammillary body, the hypothalamus which lies in relation to the mammillary body and the interpedicular system posteriorly to the cellar. Posteriorly the cellar is also related to the cliasis. So, the first we will talk about the cellar. The size of the cellar, any enlargement or erosion is typically seen on CT. Previously it used to be seen on X-rays but now very few of us actually see hardly any X-rays of the skull are being done. So, on the sagittal X-ray of the skull we can see and on the sagittal tomogram of the CT also we can see the cellar and we can note the size whether it is small or whether it is enlarged and there is there any erosion in the cellar. Nowadays with multi-planar CT being available with multiple slices 128 to 56 slice CTs being available for that matter even with a 16 slice CT we can reformat the axial CT images we can take thin sections and reformat it into sagittal to see the size of the cellar as I will be showing in one of the cases. Okay, so the cellar this is the normal size of the cellar please note it down for future difference. The cellar can be small as a congenital variant or it can be seen small cellar can be seen in dystopia maritonica or if the patient has received radiotherapy previously enlarged cellar can be seen in patients with for example normal variant like double cellar floor or if there is destruction of the anterior clientoid process or if there is any erosion of the cellar itself the cellar may be enlarged in patients with cellar masses or in patients who are having raised intracranial pressure for example any other intracranial mass or long-standing intracranial mass can be laid to raise dystopia or even idiopathic intracranial hypertension may lead to slight enlargement of the cellar. The normal height of the idino-hypophysis is typically measured on the coronal images here we are seeing the superiorly concave order of the idino-hypophysis which is the normal variant. The Elster's rule is very well known in infants and children the height should not be more than 6 millimeters in men and post-menopausal women it should be 8 millimeters in women it is slightly larger up to 10 millimeters and in late pregnancy and in the immediate postpartum period may be still further enlarged physiologically that can be up to 12 millimeters in height. Here we have a 7 year old girl with early puberty and hyper cortisolism MRI was performed to rule out any cellar mass so here we saw the superior convex border of the idino-hypophysis and the height was increased for a 7 year old the height should not be more than 6 millimeters but the height here measured 8 millimeters and it was unchanged over the next on a follow up scan it was suspected to be a pituitary adenoma but this is actually just a pituitary hyperplasia. Another variant that is seen is the hyperintensity of the idino-hypophysis in neonates. Here is a 5 day old infant which shows hyperintensity even on the non-contrast sequence in the idino-hypophysis as well as the posterior pituitary bright spot and this hyperintensity in the idino-hypophysis resolves over time this is a normal 4 month old pituitary idino-hypophysis which shows the normal signal like the rest of the brain. And the posterior pituitary bright spot is still seen. So how do we approach the differential diagnosis first we identify the cellar and the pituitary both the idino-hypophysis and the anterior pituitary bright spot so this is the cellar and the idino-hypophysis then we determine the epicenter of the lesion is it in above below or lateral to the pituitary and whether the lesion is solid cystic or mixed solid cystic heterogeneous is there any calcification are there any flow voids in the lesion. So here we have the pituitary gland and the lesions are predominantly in the cellar or in the pituitary gland and the differentials of pituitary idino-hypophysis or radkis cleft cyst or cranioferringioma may be considered this is these are lesions which are centered in the cellar lesions may be centered in the supra cellar lesion or may be involving the pituitary stop these lesions are typically germinomas, eosinophary granulomas, metastasis, lymphomas, etc. Superior to the infundibulum we see the optic chiasm on the coronal images it looks like an like the figure of 8 appearance which is laying on its side so this is the optic chiasm and we see that the signal intensity of the optic chiasm is just like the normal white matter if the optic chiasm is hyper intense or bulky then the differentials of demyelination or glioma should be considered or if the lesion is centered in the region of the optic chiasm or in the supra cellar system then these differentials should be considered. Superior to the optic chiasm we will see the region of the hypothalamus lesions involving the hypothalamus are the optic chiasmatic or the hypothalamus gliomas, hamartomas, germinomas, eosinophary granulomas etc. Lateral to the cellar we see the paracellar region in the paracellar region we see the cavernous sinuses and we see the flow void of the cavernous ICA. As we note in this patient for example the left cavernous ICA flow void is very much enlarged as compared with the right cavernous ICA so the differentials of aneurysm ectasia of the ICA or carotidocavernous pistula should be considered in this setting. So just to recap again if we are having cellar supra cellar masses they can be like typical masses itself which are microidonomas, macroidonomas, merengiomas, cranioferringiomas or invasion by any skull based tumours or metastasis. These are the most commonly seen cellar masses, cellar supra cellar masses. Any mass-like lesion in the pituitary may also be non-neoplastic for example a pituitary hyperplasia, apoplexy, pituitary abscess aneurysms, ratcase cleft cyst or infundibular non-neoplastic thickening by eosendiferic granuloma LCH or sarcoidosis. So this is just a quick recap. So patient comes for evaluation for pituitary microidonoma. Typical is that clinical profile will read as amenorrhea or galactoria and often we will see in the history that you have provided only one line, elevated prolactin but we don't know how much it has been elevated. Is it just like 30, 40, 50 or is it very high? So sometimes prolactin may be slightly elevated and this can be because of involvement of his talk or medications but if the prolactin is elevated more than 200 then we have to strongly suspect microidonoma and look for a microidonoma. Sometimes in 20 to 30% of the patients who undergo dedicated imaging of the pituitary lesion, we may see incidental microidonomas in the adenohypophysis. So when we are imaging for a microidonoma, we have to look for any asymmetry in the gland if there is any slight bulkiness or bumpiness on one side. If there is any shift in the stock for example if we are suspecting a microidonoma on the right side, the shift should be towards the left side, should be on the contralateral side because of slight mass effect. We have to also evaluate carefully the dynamic post contrast sequence which is a very important sequence when we are evaluating for a pituitary microidonoma. So why is this dynamic sequence so important? The pituitary gland does not have a blood-brain barrier like the rest of the brain. So if we inject contrast, the pituitary gland will enhance brilliantly. So any small tumor in it like a microidonoma which is less than 1 cm in height may be missed on routine delayed post-frontar scan. But in the early phase of the enhancement, while the pituitary gland will enhance brilliantly immediately, the adenoma will take some time to enhance and will tend to enhance later in time than the normal pituitary parenchyma. Hence we may be able to pick up the delayed enhancing adenoma on the dynamic imaging much better than the delayed post contrast scan when the entire gland including the adenoma will enhance uniformly. Hence dynamic post contrast sequence which is typically a spinico sequence is performed in all patients in whom microidonoma is performed. Just to note, this dynamic sequence is not required if we are having a very large, obviously bulky cellar, supracellar mass and we want to say, is it an adenoma? Is it a craniopharyngeoma? Is it LCH or is it something else? We don't need to do this dynamic sequence for any other lesions. Only if we are suspecting a pituitary mass and the scan looks relatively normal and we want to rule out a microidonoma which will not be seen on other sequences then we do this spinico sequence. Contrast is injected in the rapid bolus preferably using a pressure injector if available and then multiple sequences are acquired to get this time intensity curve. So we are seeing this multiple acquisitions. This is the pre-contrast sequence and as contrast is injected we see how contrast initially enhances the impendable and the central part of the gland and then the contrast enhancements press to the peripheral part of the gland as time passes. Alright? So I will show the same thing in a video. Great. So it played. We can see the enhancement of the pituitary gland on the delayed sequence. Okay? I have replayed it. Just to note the resolution of this sequence is good. This is a very thin sequence but the signal to noise ratio may not be good. So this is very good for looking for some small microidonomials that are missed on the routine post-contrast sequences. We can hardly make it out now that we know that it is there on the dynamic sequence. We can see some differential enhancement on this. Otherwise, we would have very easily missed it on the routine T1 coronal images. The signal to noise ratio is much better on the routine T1 coronal images but resolution is same on both these sequences. We need thin sequences evaluation of the pituitary whether it is for a micro or a microidonoma, two or three millimeter thick sequences. So this same microidonoma again I have shown on the dynamic sequence that this enhancement is seen and I have marked out the size also around four millimeters in diameter and it is hardly seen on the T2 weighted sequence. Here we have another patient, a 27 year old female with a tiny microidonoma on the left side of the adenohyepophysis. Then we have a 51 year old lady with a headache. Here we see that the cell is mildly enlarged and the adenohyepophysis is bulky measuring more than one centimeter in height. So this is a macro adenoma and for this patient we really don't need the dynamic sequence. The mass is well seen. Anything that is more than one centimeter in height actually for a post menopausal woman anything more than eight millimeters in height will be classified as a micro adenoma. This lesion is just a button B optic chiasm. Here we have another patient with a large homogenous lesion with post contrast enhancement and binding of the cellar seen on the CT. And on MRI again we can see the snowman or the figure of eight appearance of the cellar. There is not much involvement of the paracellar regions. The lesion is not extending into the cavernous sinuses nor is it encasing the ICA more than 180 degrees on the left side. On the right side there is some invasion into the cavernous sinus and we can see almost 270 degrees involvement of the cavernous ICA. So this suggests that there is extension into the paracellar region. All these findings are important when the surgeon is planning to operate this patient. Also we note that the cellar is enlarged and the lesion is extending towards the phenoid sinus. So maybe even trans phenoidal approach may be used for this surgery of this patient. When we are reporting this cellar, supracelar lesions, especially macro adenomas which are probably going to be treated by surgery, diffusion sequence and DTI sequence plays a very important role because in the DTI sequence we will see the anisotropy of the lesion and this will show how hard the lesion actually is and how easy it will be. Is it succable,cusable and on surgery or will it be a large hard unyielding lesion that will be very difficult to remove on surgery. So this is the role of diffusion tensor imaging in patients with macro adenomas. Here we have another patient of 43 year old with a sudden onset headache and decreased vision. So we see a cellar, supracelar mass which is hyper intense on T2 weighted images and note that even on T1 weighted images it is mildly hyper intense. On flare also it is hyper intense and we can see a slight fluid level on T2 weighted and flare images. I hope you can appreciate it. So this is a patient with a macro adenoma, macro adenoma with pituitary apoplexy. Here we have another patient, a 7 year old girl who presented with precocious puberty and primary hypothyroidism. Her TSH was elevated, it was 156. So that's very high. Patient had precocious puberty with thalarki and menarki and she had short stature. When we did imaging of the cellar of the pituitary gland, we saw that the pituitary gland was grossly enlarged and showed intense homogeneous enhancement. Initially we thought it was a pituitary macro adenoma. On follow up scan with treatment, TSH normalized. We can see TSH came back to 15 and the pituitary gland also reduced in size with medical management. So this was not a macro adenoma. A macro adenoma will not resolve the treatment of the hypothyroidism and so this patient actually had a just a pituitary hyperplasia and not a macro adenoma in this condition with juvenile hypothyroidism with isosexual precocious puberty. Also delayed bone age, this patient had delayed bone age and high TSH and multi-cystic ovaries is known as one with grim back syndrome. So any patient with hypothyroidism and precocious puberty, we should not think of a macro adenoma. These patients can have pituitary hyperplasia which will resolve a treatment. This is one with grim back syndrome. This patient also had multi-cystic ovaries. We can see the multiple system the ovaries and bulky ovaries. Here we have another pediatric patient, another pediatric case, two-month-old child with a failure to thrive and hyperbillirubinidia. We can see how yellow the kid is. Images are used with permission of the patient. Bera should severe hearing loss. Here we are seeing that the cochlea are grossly enlarged in size and with cystic dilatation. The pituitary gland is also hyperplastic. I don't know, hypoporosis is very small. Hypoplasia of the anterior pituitary which is well seen on the blown-up images. So this was basically, this patient is having jaundice, this typical faces with a hook-like nose, failure to thrive. Also there was pancreatic lipomythosis, hypoplastic adenomyopysis and enlarged cochlea. So this is another esoteric syndrome, joints and blizzards syndrome. No radiology presentation is complete without a couple of these esoteric syndromes. So I couldn't resist putting these cases, but they are very rare. So that's all right just for clinical interest. All right, coming back to the more commonly seen pathologies. So here we have a patient with a T2 hypo intense and a T1 hypo intense lesion between the adenomyopysis and the posterior pituitary, not enhancing. So this is a rat cases, this is a typical rat cases. So we should distinguish a rat cases from a cystic adenoma. If the patient is having any endocrine dysfunction like increased prolactin levels or hyperpartisalism or off midline location, we'll think of a cystic adenoma. Rat case cleft cysts are typically in the midline and hypo intense on T2 weighted images. These are characteristic features of a rat case cleft cyst or a pass-intermediate cyst. Often they can have T2 hypo intensity with T1 hyper intensity. On T2 sequence, if this is just slightly big, we can see as intracystic nodule. Honestly, I have never noticed this intracystic T2 hypo intense module. And the rat cases may also vary in size without treatment. So that's the interesting part. Coming back to a paracellar extension of the pituitary tumors. So here we have a patient with a macro adenoma. We are seeing it as abutting those optic chiasm. So this is what needs to be reported. And also the cavernous ICA is encased by more than 270 degrees. Here it is encased by around 180 degrees. So on the right side, there is no cavernous extension. But on the left side, there is extension into the cavernous sinus. So there is paracellar extension. And there is almost complete encasement of the cavernous ICA. Point to be noted, the flow void of the cavernous ICA is maintained. It is not compressed. And for example, had it been a para cavernous meninjuma or any other para cavernous lymphoma or any other para cavernous mass, the ICA flow void would also have reduced in size because of the mass effect. But typically because pituitary tumors or pituitary macro adenomas are not very, very hard lesions, they will encase the pituitary, but the flow void will be well maintained. Another sign is the tentorial enhancement of the pituitary. Here we can see there is some slight enhancement of the tentorium, which is a sign of cavernous sinus involvement. Very well seen on the actual images. Another differential is a supracellar cavernous ICA or a supraclinoid ICA aneurysm, which can be mistaken for an adenoma. On MRI, it is very difficult. I mean, we can see that this is a flow void. Obviously, this is an aneurysm. But especially a non-contrast CT, when the flow void is looking slightly hyper dense, it can be missed out from the non-contrast CT. So, always, always, always rule out an aneurysm. If we miss this diagnosis, if we miss a supracellar aneurysm and report it as an adenoma, it will be a disaster. Okay. From the mass lesions, they are going to a reality cellar syndrome. Cellar is mildly enlarged, but there is hardly any pituitary parent schema seen. Okay. Coming to supracellar non-pituitary masses. Macro adenomas are very common, but if we are seeing a pituitary gland adeno-hypophysis, which is separate from the supracellar tumor, then this is not a macro adenoma. This is something else. Now, what is it? We will see the differentials. Always, always, always, if it is not a macro adenoma, we will see the differential enhancement of the adeno-hypophysis or some slight differential signal on T2 weighted sequences. So, here we see a supracellar cystic lesion, which is hyper intense on T1 weighted images and which shows slight blooming on gradient sequence. This is a 65-year-old lady with headache and loss of vision. So, we are seeing a supracellar cystic lesion with T1 hyper intensity. This is a cranioferringioma. Cranioferringioma can also show multiple tiny cysts with heterogeneous enhancement. And we can see calcification, tiny specks of calcification in the cellar supracellar region. Cranioferringioma is sometimes associated with other pathologies. Here, we had a patient in Shri Chitra. This is a patient with Radke's cleft cyst, who also had an associated cranioferringioma. And we can see this fluid level vary well on the sagittal images. Coming back to the case we saw previously, this is a child adenuropophysicine separately from the supracellar heterogeneous solid cystic lesion. What is this? Is it a cranioferringioma? No. This is an optico-chiasmatic glioma. Another patient with an optico-chiasmatic glioma, in which we show that the optic chiasm is enhancing with a paracellar solid cystic mass lesion. So, this is another optico-chiasmatic glioma. Another patient with a supracellar lesion with blooming, extensive blooming on gradient sequence. So, is it calcium? Is it blood? It is hyper intense on T1 weighted images also. This is actually a supracellar mass with hemorrhage within. This patient is a patient pylomexoid astrocytoma with URAF mutation positive. Another supracellar mass is a hypothalamic hamartoma, apart from a hypothalamic and optico-chiasmatic glioma. Okay, here is a quiz question. A 55-year-old patient came with headache. We did a CT. CT was normal except for enlargement of the cellar. This enlargement of the cellar was well seen on the coronal reformatted image. Enlargement and slight erosion of the cellar. So, we performed an MRI which shows this mass. So, is it a macro adenoma? This was thought to be a macro adenoma, but no. Here we see that the adenomyopoiesis is enhancing separately from this mass. And the slight differential signal intensity is also seen on the P2 sagittal images. Here again we see that the adenomyopoiesis is enhancing differentially from this mass on post contrast images. So, this was not an adenoma. This was actually a meningeoma, cellar meningeoma. This patient was biopsied through the transfenoid approach. Here is another supracellar meningeoma. The adenomyopoiesis is separate and we are seeing the supracellar meningeoma with a classic dual tail. Another patient on CT, fat intensity with calcification, supracellar lesion, fat intensity with calcification. This is a supracellar dermoid. And we know that this has pre-contrast images itself. We are seeing it is hyper intense and we are seeing hyper intensities along the cell side. This gives us a clue that this dermoid is actually ruptured. And other tiny supracellar fat intensity is seen on the coronal non-contrast T1 weighted images. So, this could be a lipoma or a tiny dermoid. CSF intensity supracellar lesion is a supracellar arachnoid cyst which shows no enhancement. What about this lesion? Supracellar and paracellar lesion. This is rhododermin disease. Okay, coming to children with short stature. Typically, children with short stature come for imaging. We will see ectopic posterior pituitary. The posterior pituitary should actually lie behind the, I don't know, hypophysis. So, here we see that the posterior pituitary is ectopic and the anterior pituitary is also hypoplastic. Other findings that we can see in these patients can be septuoptic dysplasia or corpus callosal agenesis or single central incisor. Then we have another patient with short stature. We see the anterior pituitary is hypoplastic but posterior pituitary is in correct location. Then we have a patient with hypogonadotropic hypogonadism in which the olfactory bulbs are not visualized. This is colman syndrome. Here we have a patient with a single central incisor well seen on the actual images. The anterior pituitary is small with a tiny cyst within. The clivus is also hypoplastic. This is a spectrum of imaging findings that we may see in patients with short stature. Here we have another patient with short stature. I don't know, hypophysis is hypoplastic. And we also see that the right optic tract is not myelinated as compared with the left optic tract which is well myelinated, which is well seen on the DTI images also. There is differential intensity of the both the optic tracts, the right optic tract and radiation is different in signal intensity. Here we have a patient with diabetes and it is supposed to be a pituitary right spot may not be seen or they can show intense enhancement of the infundibulum in patients with hypophysitis. This is an interesting paper from KEM Hospital in the pituitary journal on the different imaging spectrum of hypophysitis. On T2 weighted images, we can see T2 is a hypo intense signal in the periphery in autoimmune hypophysitis. Here we have another patient with LCH, Langer and Cells Histrocytosis with a child with signal abnormality in the cerebellum. The pituitary gland looks fine but there is slight thickening of the infundibulum. It measured 4 millimeters in size. It should not be more than 3 millimeters. Other differentials apart from these supracelon masses are non-neoplastic pathologies like abscesses, infective etiologies and other tumors like unusual tumors like granular cell tumors. To conclude, these pituitary masses are quite commonly seen. We have to localize the lesion. Is it in the cellar or is it paracelar, supracelar, what is the center of the lesion and then describe the lesion which will give us a good differential diagnosis. Clinical profile is a very important role. Dynamic sequence especially for patients with microidinoma will play an important role and if you have to remember only one thing remember this. If you can see the idonohycophisis it is not a pituitary idonoma it is some other lesion.