 Hello everyone and welcome to this prelude session for the 20th MRI teaching course. The course is starting tomorrow that is 7th of August and this is a comprehensive extended course which we are going to have this year spread over 5 days, 7th, 8th, 14th, 15th of August and 22nd of August. Today in this prelude we will have two esteemed speakers with us, Dr. Divya Thahinvala Ma'am and Dr. Vardhan Joshi. Ma'am will be taking MRI in cell and supracellar pathologies and Dr. Joshi will be taking MRI in post-operative spine. So dear friends just a reminder the course is going to start tomorrow and you are still there to register so please the links are going to be shared on the chat box. Do register for the course. We will have the day one as topics related to physics and the day two that is 8th of August we will be covering detailed MRI anatomies topics. So tomorrow we are going to start at 6 p.m. and the lectures will cover basics and advanced MRI sequences, MRI artifacts, MRI safety and also physics behind advanced MRI sequences like perfusion and spectroscopy. 8th of August we are going to have anatomy topics covering from neuroanatomy in details then to musculoskeletal anatomy. After this we will have our neuro and MSK dedicated sessions on 14th of August and 15th of August. We are going to cover everything and all of these will be case based approach, practical approaches and also we will have polling sessions to have your interactions with our speakers. So the 15th of August session which will be of CNS imaging will start 9 a.m. sharp in the morning and will continue late evening till 7 p.m. And the last day will be on 22nd of August where we are going to cover body imaging topic. This session also starts at 8 a.m. and continues till evening 7 p.m. And we are going to cover everything including breast imaging with MRI cardiac imaging topics, imaging of liver lesions including focal liver lesions, benign and malignant. We are also going to take topics like MRI, infantriatic cystic lesions, renal lesion etc. And not only we have our nationally renowned speakers but also we do have faculty from abroad and thanks to the online platform and the flexibility it offers. So we are going to have lectures from esteemed speakers like Dr. Kaurang Shah, Dr. Asim Lahiri, Dr. Jim Gu, Dr. Rajanjay and Dr. Raj Kitar etc. Poster papers we are thankful to all your submissions and we have over 100 posters submission and over 75 paper submissions yesterday was the last day but you have requested for some corrections in your submission so that is allowed. Thank you once again for being a part of this event. This is our organizing committee, Dr. Shailendra Singh, Dr. Jagneesh Thakkar, Dr. Sanjeev Mani, Dr. Deepak Patkarsar who is the key person and force behind all these academic events. Myself, Dr. Matusha Verma, Dr. Gauri Aujha, my colleague and our main support to Mamta Patkar ma'am. We are thankful to all our educational partners including Sanrat, care stream players, Vivier, Aqfa and Fugipil for their constant support. So dear friends, now let's begin with the prelude the sessions and the first speaker for today is Dr. Vivita Hinwala. Mam is DM in Neuro radiology from the esteemed Shri Chitra Institute of Medical Sciences and she has several publications and book chapters to her credit. She is consultant neuro radiologist at NIH SRCC Children's Hospital and NM Medical Center mobile. She will take us to the topic of MRI cellar and supra cellar pathologies. We welcome you ma'am and let's begin with the talk. At the onset I would like to thank Patkarsar, Mitusha and the entire team of the MRI nanavati conference for having me here. It is a great pleasure and an honor to be here actually. Can you see my screen? You can open the main power pod. Great. So at the onset I would like to just, these are difficult times, very trying times and all of us have different struggles. So I was reading one of my favorite books from all time, Little Women by Luisa Mealkot and there was some lines in it that struck a chord. A year seems a very long time to wait but remind them this is for the girls. That while we wait we may all work and these, so that these hard days need not be wasted and all these webinars including this very prestigious conference play a very important role so that we are not wasting time while we are waiting for the world to get a little safer. I hope Mitusha, you can see my pointer. Yes ma'am. Is it? So I will start with the presentation. So this is a presentation on the imaging in cellar and supracelar lesions. I will begin with embryology followed by normal anatomy, a few anatomical variants and then we will talk about cellar and supracelar 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 will help us to see that the problems we may face in day-to-day reporting. All right. So starting with embryology. So the pituitary gland lies in the cellar. It has two parts, the anterior pituitary or the adenohipophysis and the posterior pituitary. Both these parts of the pituitary gland arise from the ectoderm but they have different origins. The adenohipophysis is formed from the rathcase pouch which is a superior imagination from the primitive oral cavity. This is ectodermal obviously. And the posterior pituitary arises from the neuroactoderm as you can see. So the anterior pituitary wraps around the optic chiasm and the neuroepophysis comes from the neuroepophysis comes from the neuroectoderm. This pituitary gland lies in the cellar. Here we see the cellar which is a bony cavity 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 the sphenoid sinus for example sinusitis or mucosilin the sphenoid sinus should be reported in our reporting of the cellar pathologies. This is the pituitary gland. Here we see the adenohipophysis which has a superior concave order normally. Then we note the height of the adenohipophysis. The height may be increased in physiological conditions like puberty or pregnancy or immediate postpartum period. Posterior to the adenohipophysis we see a hyperintensity even on non-contrast even weighted sequences. This hyperintensity is the posterior pituitary bright spot. Superior to the adenohipophysis we see the infundibulum and at the top of the infundibulum is the tubercine area. Here we see the optic chiasm. Superior to the optic chiasm is the chiasmatic recess and the lamina terminalis of the corpus callus. 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 clientus. 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. 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 multiplanar CT being available with multiple slices, 128-256 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 a case in one of the cases in the presentation. This is the normal size of the cellar. Please note it down for future reference. The cellar can be small as a congenital variant or small cellar can be seen in dystrophia myotonica or if the patient has received radiotherapy previously. Large 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 raised ICP or even idiopathic intracranial hypertension may lead to slight enlargement of the cellar. The normal height of the adenohypophysis is typically measured on the coronal images. Here we are seeing the superiorly concave order of the adenohypophysis 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 in adults it should be seen 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 it 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 hypercortisolism. MRI was performed to rule out any cellar mass. Here we saw the superior convex border of the adenohypophysis 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 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 adenohypophysis in neonates. Here is a 5-day old infant which shows hyperintensity even on the non-contrast sequence in the adenohypophysis as well as the posterior pituitary bright spot and this hyperintensity in the adenohypophysis resolves over time. This is a normal 4 month old pituitary adenohypophysis which shows the normal signal like the rest of the brain talent stigma 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 adenohypophysis and the anterior pituitary bright spot. So this is the cellar and the adenohypophysis. 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. The lesions are predominantly in the cellar or mixed in the pituitary gland. Then the differentials of pituitary adenoma or rathcase, cleft cyst or craniopharyngeoma may be considered. These are lesions which are centered in the cellar. Lesions may be centered in the supracellar lesion or may be involving the pituitary stop. These lesions are typically germinomas, eosinophilic granulomas, metastasis, lymphomas, etc. Superior to the infundibilum, we see the optic chiasm. On the coronal images, it looks like a figure of eight 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 difference of demalination or glioma should be considered. Or if the lesion is centered in the region of the optic chiasm or in the supracellar system, then these differences should be considered. Superior to the optic chiasm, we will see the region of the hypothalamus. Lesions involving the hypothalamus are the optical chiasmatic or the hypothalamic gliomas, hamartomas, germinomas, eosinophilic granulomas, etc. Lateral to the cellar, we see the paracellar region and we look at the... 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 carotico-cavernous pestula should be considered in this setting. So, just to recap again, if we are having cellar supracellar masses, they can be typical masses itself, which are microadenomas, macroadenomas, melangeomas, cardiopelangeomas or invasion by any skull-based tumors or metastasis. These are the most commonly seen cellar masses, cellar supracellar masses. Any mass-like lesion in the pituitary may also be non-neoplastic. For example, pituitary hyperplasia, apoplexy, pituitary apsis, aneurysms, ratcase cleft cyst or infundibular non-neoplastic thickening by eosiniferic granuloma, LCH or sarcoidosis. So, this is just a quick recap. So, patient comes for evaluation for pituitary microadenoma. Typically, the clinical profile will read as amenorrhea or galacturia. And often we will see in the history that we have been provided only one like 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 mildly elevated, slightly elevated and this can be because of involvement of the stock or medications. But if the prolactin is elevated more than 200, then we have to consider, we have to strongly suspect microadenoma and look for a microadenoma. Sometimes in 20 to 30% of the patients who undergo imaging of the pituitary, dedicated imaging of the pituitary lesion, we may see incidental macroadenomas in the adenohyepophysis. So, when we are imaging for a microadenoma, 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 microadenoma on the right side, the shift should be towards the left side, should be on the contralateral side because of slight mass effect. Or we have to also evaluate carefully the dynamic post-contrast sequence which is a very important sequence when we are evaluating for a pituitary microadenoma. 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 microadenoma which is less than 1 centimeter in height may be missed on routine delayed post-contrast 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 parankaima. Hence, we may be able to pick up the enhanced, 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 spinicosequence is performed in all patients in whom microadenoma is performed. Just to note, this dynamic sequence is not required if we are having a very large, obviously bulky, supercellar 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 microadenoma which will not be seen on other sequences, then we do this spinicosequence. Contrast is injected in a 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 impundibilment, the central part of the gland and then the contrast enhancements press to the peripheral part of the gland as time passes. So I will show the same thing in a video. I hope it plays great. So it played, we can see the enhancement of the pituitary gland on the delayed sequence. 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 microidinomas 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 for evaluation of the pituitary whether it is for a micro or a microidinoma two or three millimeter thick sequences. So this same microidinoma again I have shown on the dynamic sequence that this enhancement is seen and I have marked out the size also around 3.7 or 4.0 around 4 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 microidinoma 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 1 centimeter in height. So this is a macroidinoma and for this patient we really don't need the dynamic sequence. The mass is well seen. Anything that is more than 1 centimeter in height actually for a post menopausal woman anything more than 8 millimeters in height will be classified as a microidinoma. This lesion is just abutting the optic chiasm. Here we have another patient with a large homogenous lesion with post contrast enhancement and widening of the cell scene on the CT. And on MRI again we can see the snowman or the figure of 8 appearance of the cellar. There is not much involvement of the paracella regions. The lesion is not encasing the cavernous 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 paracella region. All these findings are important when the surgeon is planning to operate this patient. Also we note that the cellar is enlarged and extending the lesion is extending towards the sphenoid sinus. So maybe even trans-phenoidal approach may be used for this surgery of this patient. When we are reporting this cellar, supra-cellar lesions especially macroidinomas 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 acceptable, curable 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 macroidinomas. Here we have another patient of 43 year old with a sudden onset headache and decreased vision. So we see a cellar, supra-cellar mass which is hyper intense on T1 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 macroidinoma macroidinoma with pituitary apoplexy. Here we have another patient, a 7 year old girl who presented with precocious puberty and primary hypothyroidism. TSH was elevated, it was 156 so that is very high. Patient had precocious puberty with thalarki and menarki and he 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 homogenous enhancement. Initially we thought it was a pituitary macroidinoma. 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 macroidinoma. A macroidinoma will not resolve with involvement with treatment of the hypothyroidism and so this patient actually had just a pituitary hyperplasia and not a macroidinoma and this condition with juvenile hypothyroidism with precocious puberty also delayed bone age. Patient had delayed bone age and high TSH and multi-cystic ovaries is known as one with groomback syndrome. So any patient with hypothyroidism and precocious puberty we should not think of a macroidinoma these patients can have pituitary hyperplasia which will resolve with treatment. This is one with groomback 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 failure to thrive and hyperbillirubinemia. 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 hypoplastic the adenohypophysis is very small. Hypoplasia of the antidepituitary which is well seen on the blown up images. So this was basically the patient having jaundice, despicable faces with a hook like nose failure to thrive. Also there was pancreatic lecomatosis hypoplastic adenohypophysis 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. I couldn't resist putting these cases but they are very rare. So that's all right just for clinical interest. 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 adenohypophysis and the posterior pituitary not enhancing. So this is a rat cases. This is a typical rat cases. So we should distinguish rat cases from a cystic adenoma. If the patient is having any endocrine dysfunction like increased prolactin levels or hyper cortisolism 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 the cyst is just slightly big we can see as intracystic nodule. Honestly I have never noticed this intracystic P2 hypo intense nodule. And these rat cases may also vary in size without treatment. So that's the interesting part. Coming back to it. Paracellar extension of the pituitary tumors. So here we have a patient with a macro adenoma. We are seeing it is abutting this optic chiasm. So this is what we 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 para cavernous meningoma 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. And other sign is the tendorial enhancement of the pituitary. Here we can see there is some slight enhancement of the tendorium which is the sign of cavernous sinus involvement very well seen on the actual images. Unfortunately I do not have this. 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 on an it can be missed out of 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 Coming when a slight change of track from the empty cellar syndrome we are going towards from the mass lesions we are going towards the empty cellar syndrome cellar is mildly enlarged but there is hardly any pituitary parent karma seen. Okay coming to supracellar non-pituitary masses macro adenomas are very common but if we are seeing a pituitary gland adenoepophysis 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 if it is not a macro adenoma we will see the differential enhancement of the adenoepophysis 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 life blooming on gradient sequence this is a 65 year old lady with headache and loss of vision. So here we have a cystic lesion with T1 hyper intensity this is a craniopharyngeoma craniopharyngeoma can also show multiple tiny cysts with heterogeneous enhancement and we can see calcification tiny specks of calcification in the cellar supracellar region craniopharyngeoma 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 adenoma and we can see this fluid level very well on the surgical images. Coming back to the case we saw previously this is a child with us I don't know apophysis seen separately from the supracellar heterogeneous solid cystic lesion. What is this? Is it a craniopharyngeoma? No this is an optic charismatic glioma here we have another patient the optic another patient with an optic charismatic glioma in which we show that the optic chiasm is enhancing with the paracellar solid cystic mass lesion. So this is another optic chiasmatic glioma. Another patient with a supracellar lesion with 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 with it. This patient is a modified astrocytoma with virac mutation positive. Another supracellar mass is a hypothalamic hamartoma apart from a hypothalamic and optic charismatic glioma. Here is a twist 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 adenoepophysis is enhancing separately from this mass. And the slight differential signal intensity is also seen on the T2 sagittal images. Here again we see the adenoepophysis is enhancing it differentially from this mass. Of course contrast images. So this was not an adenoma. This was actually a meningeoma, cellar meningeoma. This patient was biopsied through the transfenoid approach. And this patient was a meningeoma not a macro adenoma. Here is another supra cellar meningeoma. The adenoepophysis is separate and we are seeing the supra cellar meningeoma with a classic neural tail. Another patient on CT. Fat intensity with calcification. Supra cellar lesion. Intensity with calcification. This is supra cellar dermoid. And we know that this has pre-contrast images itself. We are seeing it as 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 supra cellar intensity is seen on the coronal non-contrast T1 weighted images. Supra cellar intensity is seen. So this could be hypoma or a tiny dermoid. CSF intensity supra cellar lesion is a supra cellar arachnoid cyst. Which was no enhancement. What about this lesion? Supra cellar and paracelar lesion. This is rhododorsmen 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 would actually lie behind the hypo pisces. 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 septo-optic dysplasia or corpus callosal agencies or single central incisors. So coming back quickly then we have another patient with short stature. We see the anterior pituitary is hypoplastic and the posterior pituitary is in the correct location. Then we have a patient with hypo-gonadotropic hypo-gonadism 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 cli-verse 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. Pituitary is hypo I don't know, apophysis 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 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 hypo intense signal in the periphery in autoimmune hypophysitis. Here we have another patient with LCH Scytocytosis with signal abnormality a child with signal abnormality in the cerebellum. The pituitary gland looks fine but there is slight thickening of the infundibulum. It measured 4 mm in size. It should not be more than 3 mm. Other differentials apart from the supracelan masses are non-neoplastic pathologies like abscesses, infective etiologies and other tumors like unusual tumors like granular cell tumor. And this brings me to the end of my presentation. Couple of interesting papers I have shown to conclude this pituitary masses are quite commonly seen. We have to localize the lesion. Is it in the cellar or is it paracellar, supracellar what is the center of the lesion and then describe the lesion which will give us a good differential diagnosis. Clinical profile plays a very important role dynamic sequence especially for patients with microadenoma will play an important role and if you have to remember only one thing remember this. If you can see the adenohyepophysis it is not a pituitary adenoma it is some other lesion. If you can see the adenohyepophysis separately. This brings me to the end of my presentation. Thank you very much. Thank you ma'am for this wonderful talk and for taking this important topic. So simplified manner of approach and whatever questions we have you can please post them in the chat box and after the second talk we are going to take the questions. So now I would like to welcome our next speaker Dr. Vardhan Joshi sir who is the consultant and head of department of ideology at Sayazhi speciality hospital Pune and sir has a special interest in MSK as well as neuroimaging. He is a recognized DNB teacher and has several publications and lectures to his credits. Sir will be talking about post-operative spine role of MRI. So let's begin. Is that okay? The audio video both are good. Okay. Okay. Thanks Malini. So before we start reporting any post-operative spine case there is a sort of a checklist and the first point in that checklist is what was the primary clinical syndrome and diagnosis for which the patient was offered surgery. The next point is pertaining to the surgical details. That means exactly what has been done with the patient. What all things have been removed from his body and are there any added things which have been given to the patient like metallic hardware, metallic screws etc. The third point is very very important and that is what is the time interval between the surgery and the present imaging. Because the same post-operative finding can have a different implication in early post-op period and can have a different interpretation in late post-operative period. And last but not the least is what are the present signs and symptoms with which the patient has presented now. So once you go through all this checklist then we are supposed to go through the previous imaging and then start interpreting the scans. So maybe 15-20 years back the complications of the spinal surgeries were so much that many of these patients used to come back with post-operative signs and symptoms and therefore a separate terminology was used to describe this patient and that was called as fail-back surgery syndrome. And it is characterized by post-surgical intractable pain in the low back and lower extremities combined with varying degrees of functional incapacitation. And the incidence of the fail-back surgery syndrome has been reported variably in the literature from 10% to as high as 40%. However with the advent of newer and newer surgical techniques this incidence of complications has definitely gone down significantly. So the causes of fail-back surgery syndrome can be broadly grouped together into mechanical causes inflammatory or infective causes those which are surgically induced and those which are related to pre-operative diagnostic failure and these are all the list of causes in the early post-op and low post-op period which can contribute to the formation of fail-back surgery syndrome out of which one can just pay attention to the areas which have been highlighted in yellow. So recurrent disc herniation is one of the important mechanical causes in late post-operative period and the same thing applies to spinal canal stenosis and spinal instability. Inflammatory and infective causes are spondylo discitis or infection in the early post-operative period and epidural fibrosis and arachniditis in the late post-operative period and surgically induced cause is the dural tear with meningosal formation in early post-operative period. Rest of the causes are rare and one may encounter them occasionally in their clinical practice. So there are various imaging techniques by which one can image post-operative spine and is a plain X-rays and fluoroscopy CT MR. USG is basically reserved as a guidance tool for diagnostic aspiration or therapeutic aspiration of various collections and PET CT has also been introduced recently for post-operative spine. Plain radiographs do have a very specific role at the time of the surgery for placing the hardware and in the post-operative period it is used to assess the position of the hardware and to assess stability or instability of the spine and the same can be assessed dynamically by fluoroscopy. CT is an excellent modality in all those patients where MR is contraindicated that means all those patients were having pacemakers. The bony defects of laminectomy and laminotomy are better demonstrated on CT as compared to that on MR and the same thing holds true for textileoma or gossipibioma which refers to the granuloma formation because of a retained gauze piece which contains the barium impregnated gauze line. CT is very good for assessment of instrumentation and instability for assessment of spinal canal stenosis and for demonstration of early complications like infections and hematomas. Okejali you may be asked to do what is known as CT myelography in general CT is less accurate than MR for distinguishing between recurrent disc herniation and epidural fibrosis so MR remains the imaging modality of choice it is excellent for distinguishing between recurrent disc herniation and epidural fibrosis for assessment of canal stenosis it is as good as CT it is good for early complications like gauze and hematomas it is the only modality which can demonstrate us the bone marrow edema inflammation of the soft tissues enhancement of the nerve roots identification of subtle blood products and inflammation of the facet joints not all cases of post operative spine would need a gadolinium contrast so gadolinium is reserved for those patients where there is need to distinguish between epidural fibrosis and recurrent disc herniation for those cases which have got infection to demonstrate sterile arachnoditis or radicalitis or when the patient has been operated upon for neoplasm or infection so before we understand abnormal we should know what is normal in post operative spine and for that we just need to know little bit about the surgical techniques so laminate Tommy refers to removal of a single lamina that is unilateral laminate Tommy or both the laminate that is bilateral laminate Tommy sometimes instead of removal of the whole lamina only the inferior portion of the lamina is nibbled out and that is called as laminate Tommy and then that is combined with removal of the adjacent portion of ligament of phlegum which is also called as fenestration so laminate Tommy is laminate Tommy and fenestration form a part of open spinal surgeries a further advent or innovation in the open surgical technique has been the minimally invasive spinal surgery where a tubular retractor is placed into the patient's body and then through this retractor various instruments are advanced into the area of interest the advantage is obvious that the trauma to the normal spinal or paraspinal soft tissue is minimized so there is lesser injury to the surrounding structures and there is earlier post operative recovery a further innovation or advancement to minimally invasive spinal surgery has been the fully endoscopic spinal surgery where a small endoscope which is hardly 6 to 8 millimeters in diameter is introduced into the patient's body and then surgeries are performed so in the post operative period the bony defects of laminate Tommy and laminate Tommy are best demonstrated on T1 weighted MR images as compared to T2 the posterior spinal muscles and the fat would show asymmetry because of a handling of the soft tissues and the dural tube or the thickle sac has got a tendency to show focal expansion towards the site of the laminate Tommy and this should not be misinterpreted as pseudo meningo series at the time of the discate Tommy significant proportion of the nucleus pulposes is removed and therefore that results in reduction in the height of the disc space as seen in this particular image and that brings closer the adjacent vertebral end plates so there is increased friction along the vertebral end plates and there is marrow edema formation which appears high upon T1 and hyper on T2 weighted images and that exactly mimics for modic type 1 changes the posterior portion of the disc keeps on looking hyper intense on T2 weighted images because it is this portion which has been handled by the surgeon and if you end up giving contrast to these patients you would see some minimal enhancement in the posterior portion of the disc and sometimes along the vertebral end plates also so overall this appearance mimics for infection but actually there is no infection is absolutely fine in the post operative period and therefore it is referred to as aseptic spondylo discitis or chemical spondylo discitis and this imaging appearances can remain for a time period of about 6 months to 1 year after surgery so findings of feedback surgeries syndrome have to be distinguished from acceptable and expected post operative findings after a successful spinal surgery and one has to exercise extreme caution in first 6 to 8 weeks after the surgery so if you end up imaging the patient in the immediate post operative period what will happen is there is disruption of the annulus fibrosis there is a lot of edema there are a lot of blur products and there is beginning of formation of the granulation tissue so all this together will form a large soft tissue muck which mimics for pre operative disc herniation now subsequently the edema subsides the hemorrhage subsides and granulation tissue takes over which is a body's mechanism to attempt healing and the granulation tissue would last for a period of about 6 months beyond which the granulation tissue gets absorbed and what we get is epidural fibrosis now we come to a very important concept in imaging of post operative spine and that is epidural fibrosis is going to be a part and parcel of each and every spinal surgery so it is going to be seen in all 100% of the patients who have undergone a spinal surgery in all these patients the fibrosis is so minimal that it is clinically totally insignificant only in a certain small group of patients the fibrosis becomes very big and then it proliferates it can entrap the nerve roots and patients can get symptoms so with all this background now we will go on to various clinical scenarios so the first clinical scenario is that of a 51 year old male who show post operative improvement for a period of about 24 hours and then he started worsening after that so this is T2 axial and this is T1 axial for interpretation so what we see over here is that there is bilateral laminate Tommy and there is formation of a collection in the posterior spinal soft tissues and the collection is having lot of T1 hyper intensity within and that indicates that there are lots of blood products so we are dealing with a hematoma in the post operative period so post operative hematomas are rare they present within hours to days following surgery as a worsening corticoinase syndrome MR shows presence of mixed blood products and it is obviously more sensitive than CT for location for demonstrating the location as well as the extent of the hematomas the smaller hematomas can be treated conservatively but the larger hematomas need to be evacuated either by interventional radiologist or by the surgeon. Coming to another clinical scenario this was a 45 year old main who presented with severe pain and fever 2 weeks after the surgery the surgeon was suspecting infection and lab parameters were suggestive of leukocytosis elevated CRP and raised ESR so what we see here is a lot of marrow edema along the vertebral end plates which are appearing hyper on T1 and hyper on T2 weighted and stir images and there is reduction in the height of the disk space with some amount of hyper intensity. So one may feel that this is a normal chemical spondylo diskitis which one would get in the postoperative period and that is not the case there is an in addition lot of soft tissue and obsessed formation in the epidural space and even the marrow edema is much more hyper intense on T1 and hyper on T2 weighted images. So when you have these imaging findings and when you combine that with the abnormal lab parameters your diagnosis of postoperative infective spondylo diskitis is made. This is another case here there is reduction in the height of the disk space as expected but look at this particular disk space it is enlarged it is looking heterogeneous and on contrast imaging one can see a peripheral diskal enhancement as seen in disk obsessed. So this was indeed a disk obsessed and it had to be surgically drained. This is another case normally we can see little bit of diskal hyper intensity and contrast enhancement in the posterior portion of the disk because that is the portion which has been handled by the surgeon. But look at this particular image the anterior portion of the disk is showing abnormal enhancement indicating that there is postoperative diskitis. So postoperative infections the incidence is variable 0.7 to 15% MIS has got a much lesser incidence of about 0.4% that it is a very serious complication because it leads to long standing and sometimes permanent morbidity. It probably occurs because of direct interoperative contamination of the organisms or because of pre or perioperative infection somewhere else in the body or because of compromised immune status and the organisms which are blamed are staff epidermides, staff aureus and gram-negative organisms like enterococci and pseudomonas. So before we give diagnosis of infection on MR one has to make sure that there was a clinical suspicion of infection there should be a pathological evidence in the form of abnormal lab parameters and when we see a large abscess or soft tissue in the epidural space like this or when we see anterior portion of the disk showing enhancement and when the enhancement is so intense or when you see abnormal patterns of contrast enhancement like this or when you see restricted diffusion then one can give a diagnosis of infections otherwise one has to think twice before labeling something as infective spondylo diskitis. Let's go into another clinical scenario. This was a two years post-operative patient presented with pain and radical apathy in both lower limbs. This is T2 and this is T1 axial. So what is the abnormality? Now this is the normal disposition of the nerve roots of caryconia within the fecal sac but look at this disposition the nerve roots are clumped together and after giving contrast there is abnormal contrast enhancement. So we are dealing with arachnoditis. So this is not arachnoditis this is chronic sterile arachnoditis the incidence of which is about 6 to 16 percent. The literature describes three patterns of arachnoditis. The first pattern we have already seen that is scattered group of matted and clumped nerve roots the second pattern is that of an empty fecal sac where the nerve roots get plastered along the walls of the fecal sac and the central portion of the fecal sac remains empty. So that is called as an empty fecal sac sign and the third pattern all the nerve roots would come together forming a large a soft tissue mass which is also called as a pseudo mass sign or a pseudo chord sign. The changes of arachnoditis can be focal or diffuse. Contrast enhancement of the o-line meninges and nerve roots may or may not be present and if you land up performing a CT myography for this patient you would see a large filling defects within the contrast filled CSF column. The factors which are responsible for development of arachnoditis are the surgical procedure itself the presence of intratural blood following surgery and treated perioperative spinal infection. Now coming to another clinical scenario this was a 41 year old lady who was normal for about a period of one year but after that she started developing pain in the distribution of the right S2 root and what I have shown you is the post contrast even facts that actual image. So what do we see here there is no fecal sac indentation the fecal sac is looking otherwise very fine but there is one thing which is abnormal look at the rest of the nerve roots and look at this nerve root and this is another case there was pain in the distribution of the right S1 root again one year post operative and look at the appearance of the right S1 root which is enlarged and looking edematous and hyper intense on T2 weighted images. So in both these examples not all the nerve roots were abnormal so you cannot call this as arachnoditis there is only single nerve root which is abnormal it is referred to as radicalitis which is basically because of abnormal inflammation and thickening of an isolated nerve root and this brings us to the concept of blur nerve barrier. So the way we have blur brain barrier so similarly within the spinal canal we have blurred nerve barrier because of which the nerve roots of quadra equina do not show contrast enhancement under normal circumstances but when the nerve roots are because of are severely compressed because of a large disc herniation or there is too much of interoperative handling then the patients can develop radicalitis and there will be enhancement along the isolated nerve roots. A caveat here should be noted that in the first 6 to 8 months after the surgery sometimes you can see enhancement along the nerve roots despite the patient being asymptomatic. So if you see the contrast enhancement in first 6 to 8 months after the surgery one has to be little careful if you see contrast enhancement along the nerve roots after 8 months then we can give a diagnosis of radicalitis very safely. Coming to various post-operative collections out of which pseudo meningosyl stands tall they constitute about less than 2% of all post-operative collections they occur because of inadvertent interoperative dural tear or because of persistent opening in the dura after the surgery. Now as the name suggests it is not a true arachnoid lined sac and it is lined by surrounding reactive fibrosis so therefore it is called as a pseudo meningosyl. Most of the times it is asymptomatic but it can cause mass effect because of their size. It is important to differentiate the pseudo meningosyl from other types of collections because aspirations of these can lead to meningitis and because of continuous CSF leak patients can develop what is known as spontaneous intracranial hypotension and then one may have to image MR brain for such patients. So that is an example of a large pseudo meningosyl which is showing communication with the parent CSF tickle sac. These collections can go as high up to the skin and then they become very very susceptible for secondary infection or cutaneous fissure formation. Now how to differentiate these various types of collections like pseudo meningosyl, hematoma, steroid collections and abscesses. So when you see T1 hyper intensity like this within the collection or when you see blooming on GRE images then probably we are dealing with a hematoma. When you see a very clear cut communication with the parent CSF sac and our dual tube then we are dealing with a pseudo meningosyl. If you see a very thick irregular contrast enhancement along the periphery of the collection and apart from that when you see restricted diffusion then you are dealing with an infected collection or an abscess formation. I thank Darshan for providing this particular image and when you don't see any specific imaging feature then probably you are just dealing with a sterile post-operative collection. Sometimes the collections are not in the epidural sac, they are within the thecal sac or within the dual tube and they can displace the nerve roots anteriorly and these are called as intradural but extra arachnod collection and the sign which has been described in this particular image is the rising root sign. I thank Dr. Rajesh Bhochu for allowing me to use his image in this presentation and despite all these guidelines one can go wrong so this was a 15 day post-operative patient and he started worsening two weeks after the surgery because there was so much of metallic hardware I did not use GRE but the collection was looking pretty much blackish on T1 and brightish on T1 so I called this as a sterile collection but at the time of the surgical evaluation this turned out to be a subacute hematoma. Now post-operatively patients can present back with evidence of spinal canal stenosis which can occur in the central spinal canal or in the foramen or along the lateral recess. So foramenal stenosis and root compressions can occur because of loss of the disc height and that can narrow the neural foramen. Lateral recess stenosis generally occurs because of inadequate resection of the medial margin of the facet but the central spinal canal stenosis typically occurs one level above or one level below the fused spinal segments and that is because of the altered patterns of load sharing. So this is a susceptibility artifact of the metallic screws and this segment of the operator's spine is absolutely fine but now there is a new disc bulge at L2-3 level which has started compressing on the thickest side. These are two side-by-side examples of clover's fusion. This is a successful clover's fusion this is an artifact and this is not a screw but look at this particular image the fusion is nice but now there is a new disc bulge just one level above the fused segment which has now started compressing on the spinal cord. Similarly the patients can present back to us with segmental spinal instability and that basically indicates a failed operative fusion they can have either anterior list thesis or a retro list thesis it typically occurs because of excessive resection of the posterior elements because of multi-level laminate tummy. The fixators can undergo fracture, there can be fracture of the facets, there can be an infection with loosening of the fixators and in elderly individuals they can present back to us with trauma or repeated falls and that can lead to disruption of the metallic prosthesis. So in this example one can see that there is a break once again in the posterior elements and there is list thesis with compromise of the neural foramen and compression of the nerve root. Now we come to a very important topic of how to distinguish between recurrent disc herniation and epidural fibrosis and why that is so important because if there is a recurrent disc herniation generally the patients are given an option of repeated, repeats surgery in cases of epidural fibrosis the surgeon is little bit more careful because a re-surgery in the setting of fibrosis can incite fibrosis more and the patients can land up with worsening of symptoms. So these are just certain salient points which help us in distinguishing between recurrent disc herniation and epidural fibrosis the herniation of the disc generally looks blackish on T2-acted images as against fibrosis which looks slightly hyper intense or bright on T2-acted images When you give contrast the disc herniation shows peripheral enhancement and the central portion does not show any contrast enhancement as against that the fibrosis shows a diffuse intense enhancement now a point to be remembered over here is that this imaging needs to be completed within first 2 to 5 minutes after contrast administration because 10 to 15 minutes after the contrast has been given there would be centripetal dissipation of the contrast from periphery towards the centre of the disc material if you land up imaging these patients may be 10 or 15 minutes after the contrast has been given the disc herniation and fibrosis will look the same disc herniations will show mass effect fibrosis generally does not show any mass effect it tends to encase the nerve root not to displace the nerve root disc herniations can occur at anywhere within the spinal canal but fibrosis typically occurs only at the site of the surgery on cross sectional imaging disc herniation is either anterior or entrelateral or lateral to the thickal sap but epidural fibrosis can be posterior lateral as well as anterior to the thickal sap so this is a classic example of recurrent disc herniation you do not need to give contrast when you get such images so that is a large T2 hyper intense lesion which is showing continuation with the parent disc so this is a large disc herniation but you need contrast study when you see such findings so there is a soft tissue in the epidural space so after giving contrast one can make out that there is peripheral enhancement so this is definitely a disc herniation and not epidural fibrosis as against that look at this particular image there is a lot of ISO intense soft tissue intense contrast enhancement and there is encasement of the nerve roots and no distortion of the thickal sap so this is classical case of epidural fibrosis in the post-operative period so this is just a speed to speed comparison epidural fibrosis is intense enhancement disc herniation is peripheral enhancement there is some mass effect in disc herniation no mass effect encasement of the nerve roots so this is how one can distinguish between these two conditions with the advent of endoscopic spinal surgeries and minimally invasive surgeries one can encounter incomplete removal of the disc herniation or residual disc herniation so this was a pre-operative image with superior as well as inferior migration of the disc herniation and in the post-operative period one can make out that the superior portion has been removed nicely but the inferior portion was left behind so this is an example of a residual disc herniation and multiple causes can be present in the same patient so in this particular example one can see segmental instability there is empty thickal sac sign that is arachniditis and there is a lot of fibrosis also gossipibioma or textileoma refer to formation of granuloma or a foreign body granuloma because of a retained gauze piece I do not have an image to show it to you all so interested people can look to these articles where they are nicely demonstrated examples of textileoma or gossipibiomas now coming to imaging of instrumentation MR is not the modality for imaging of instrumentation instrumentation is basically imaged by X-rays and CTs but on MR one has to deal with the instrumentation and one has to minimize those artifacts obviously titanium is far better as compared to stainless steel because stainless steel produces artifacts like this and one just does not know what one is imaging as compared to that when titanium is put even with so much of metallic hardware one can obtain reasonably good information regarding what is happening within the central portion of the spinal canal and then there are certain ways so as to minimize the artifacts on MR so there are various protocols like metal artifact reduction protocols which are indigenously provided by the vendors apart from that one can try swapping the phase encoding and frequency encoding direction of imaging so as to minimize the artifact when should you stir instead of frequency selective fat saturation FAC is preferred over AC larger field of view increase the TR, increase the redoubt bandwidth, increase the number of excitations, use a smaller Voxel size and if possible try to image the patient on a 1.5 tesla instead of a 3 tesla in certain selected cases so as to minimize the artifacts these are the two main metallic implants which we commonly encounter in spinal surgeries and these are particular screws and these are the intervertebral disc cages so particular screws are supposed to be seen midline between the two cortices of the pedicle and they are supposed to be parallel on surgical images to the vertebral implants and there are the two types of intervertebral disc cages where the posterior portion is just about 2 millimeters anterior to the posterior margin of the vertebral body any position apart from this should be viewed with suspicion so in this case one can see there was infection, there was electrolysis surrounding the pedicular screw and if you try and perform MR imaging this patient will see lot of contrast enhancement because of surrounding postoperative infection with loosening of the instruments occasionally the pedicular screws can break the anterior cortex and can pose a thread to the retroperitone vascular structures in this example this was an immediate postoperative radiograph with a nicely placed intervertebral disc cage but which then displaced got posteriorly displaced in the late postoperative period and started impinging on the traversing nerve root and even the screw got medially displaced and that also started impinging on the traversing nerve root the screws can undergo fracture over a period of time and that needs to be assessed and now this is going to be my last case after that I will conclude my presentation this patient presented to us in the year 2012 and there was an aragnoid cyst in the dorsal lumbar region which was responsible for the patient's symptoms and this is one of the parasurgical image of the same patient the patient underwent excision of the aragnoid cyst and was absolutely fine for few years after the surgery till he presented back to us in 2019 now look at the surgical side there is no evidence of any residual or recurrent aragnoid cyst there is nothing which is alarming in the lower dorsal spine apart from little bit of the biosis which is expected but the site of pain is somewhere caused because of something else look at this particular d7 vertebral body lesion so there is a sort of polka dot appearance surrounding soft tissue which has started impinging on the thickle sac and it is now touching in the core so I just went back to the previous images in 2012 and this is what I found so there was a hemangioma in d7 vertebral body to begin with it was normal over a period of time and was actually responsible for new symptoms so this is something which one needs to remember that recurrence of symptoms can be because of an entirely new pathology which is totally unrelated to the pre-existing treated pathology so with that I conclude and I thank all of you for the patient listening thank you thanks Vardhan if you can just