 90 to 95% of these tend to be the classic typical neural-based meningiomas. Now all of you might remember that you have seen meningiomas as small as 2 to 3 millimeters in size but with a florid brain signal abnormality or attenuation change in significant mass effect associated with it and people must have seen 10 centimeter size meningiomas with absolutely no brain changes or absolutely clear subjects and brain. So what is the relation to this? Why do some meningiomas do that? Basically what happens is there is toxins released by this and the closer and more adherent to the meningioma to the brain pattern kaima the worse the reaction. So the size of the neoplasm has absolutely no relation with the abnormal signal intensity but it has direct relation to the receptability. The ones that we see with significant brain changes, significant attenuation or signal abnormality within the surrounding brain or significant associated mass effect with that is basically because of the adherence of the meningioma and release of toxins directly into the brain pattern kaima and the surgeon will have difficulty resecting that and post-op examination you will see that there is portions of the brain which ended up getting resected along with the meningioma and typically the patient has subjects and reds restricted effusion because of ischemia in the subjects and brain pattern kaima whereas these huge meningiomas with no brain changes they just come off without any difficulty by the surgeon and they are completely resected without any secondary brain changes. So that signal abnormality has direct relation to the receptability of the mass lesion so this is what we have to keep in mind. So this was an example CT example of an extraxial lesion intensely enhancing on contrast administration this was a post-contrast scan so extraxial lesion with this kind of enhancement undisproven otherwise it is going to be a meningioma. Now meningioma may be maybe entirely calcified partially calcified centrally calcified punctately calcified they can follow any form of calcification this was a meningioma which was densely calcified lobulated in appearance this is a CT as well an MR appearance where there is susceptibility or signal loss on T1 sequence where minimal associated mass effect is identified and we can see the hypostosis associated with the subjects and bone. Now this being an extraxial tumor frequently what we'll see is a CSF cleft that separates it so there'll be a client this would be best seen if you do a thin slice T2 sequence what you will see is a line of CSF intensity CSF fluid completely lining the meningioma separating the brain panorama with buckling of the gray matter gray white matter on the underlying brain. So that would be what would be described as a CSF cleft sign in a meningioma classically associated with convexity meningiomas. On diffusion sequences this will be associated with restricted diffusion just like how round blue cell tumors so this was an T2 and T1 post-contrast sequence which shows iso-intense to gray matter signal intensity extraxial mass lesion with buckling of subjects and brain pattern comment we can on this one we can see CSF cleft as well as those T2 hyper intensity which we are seeing along the lateral and posterior aspect in the frontal lobe there that is the secondary brain changes so some sort of edema so this would have some difficulty in receptability again not significant but there would be some because there is associated brain changes and on contrast administration there is intense enhancement of this mass lesion with associated neural tail again this is going to be a meningioma. One of the things that you have to keep in mind when you see a neural based enhancing mass is metastatic disease neural based metastasis and typically the prostate cancer metastasis can frequently fool us very very frequently it can give an identical appearance of meningioma stay stable for a long period of time and suddenly starts growing then you should think of either a malignant conversion of the meningioma malignant meningioma or a prostate cancer metastasis that has started progressing but they can behave in a very very similar fashion where they are dormant for a long period of time and suddenly start growing so always think if you see a meningioma changing characteristic and the patient is a male patient think of a metastatic prostate cancer so when do you suspect that the meningioma is a malignant meningioma when you see rapid growth or there is a brain or bone invasion or it suddenly starts changing characteristic but like I mentioned with this always think of prostate cancer metastasis also and sometimes what happens is when the meningioma is located in the supracellar region which is a very very common location for the meningioma it becomes very difficult to differentiate whether that that is a pituitary macriadenoma or it is a meningioma and treatment for this there is some variability and the surgeons insist on asking us what is this is this a meningioma or is this a pituitary macriadenoma and there are some ways where we can differentiate now think of meningioma as a round-blossel tumor we said that this is a tight tumor this has density to it this has strength to it so what would it do when it is situated in that it will have when it starts encasing vessels it will actually narrow the vessels whereas macriadenoma pituitary macriadenoma is a very very soft pliable tumor which both of these will encase vessels but pituitary macriadenoma would not decrease the caliber of the vessel meningioma would actually decrease the caliber of the vessel and the second study that can be done is a nuclear medicine study where this takes up meningioma takes up octotide so an octotide scan the meningioma will be positive whereas a pituitary macriadenoma would be negative so these are the classic features remember round-blossel tumors lymphoma meningioma primitive neural tumors and germinomas all will have the same characteristics densely packed tumors hyperdensal CT isointense to slightly hyper intense on t1 t2 intensely enhancing tumors with a diffusion so this is another one that I talked to you about that the meningiomas can be from many multiple location we saw those multiple examples of it along the convexity this is arising from meningial cells inside the ventricular lining this is a typical classic appearance of a meningioma within the ventricular lining isointense to gray matter signal intensity restricted diffusion with a true restriction it's seen on adc as dark and intense enhancement on contrast administration this is an intraventricular meningioma so moving on from that since we are on the long the meningial lining let's talk about enhancement along the left of meningioma so what how do you know there is patchy meningial dural versus left of meningial enhancement so dural lining as we talk about it hubs the bone it is along goes along the fox so a patch meningial dural enhancement will be along the bone it will not dip in into the brain parent comma whereas the pl lining or left of meningial lining lines the brain parent comma is the pl lining it dips along the cell side it does not touch the bone where it will touch the bone in the concept of that it is along the surface of the gyri also so that way yes it will be touching the bone but actually every single cell side will be lined by the pl lining and in left of meningial enhancement that is what is we'll see is enhancement so here there's a pre and post contrast administrative CT scan so here you can see that there is enhancement going inside deep inside the cell side dipping in so yes there is enhancement along the surface because the pl lines along the surface also but the fact that it is dipping in this is going to be a left of meningial enhancement now when we see left of meningial enhancement immediately we should think of a differential what can it be infection yes it can be that but the classic differential would be sarcoid lymphoma leukemia granulomatous infections like tuberculosis or metastatic disease which is left to meningial carcinomatosis which is from breast and lung classically these are the things that we see when we see left of meningial lining and the classic test to be done is csf encyclopedia and we will know exactly what it is now when you see abnormal signal on that enhancement on the along the lining you know there is a depth of meningial disease how do we figure it out when there is no contrast administer supposing the patient got an mr of the brain without contrast what we have to see is on flare sequences so on flare sequences when you see the hyper intensity within the csf spaces as we are seeing over here two different patients on the first one there is along the white pre central and central sulcus and compare it to the opposite side where we clearly see csf sign the other side we don't see that so an artifactual appearance can be seen when there is edema in this area but if there is no edema there's no mass effect then think of something sitting within the csf spaces on the second one there is diffuse abnormal signal intensity throughout within all the csf spaces so just like you have a differential of when you see alveolar opacities that alveoli can be filled up with fluid protein cell pass those are the things exactly the same way you should have when you see abnormal signal intensity on flare sequences within the brain the first thing that you should make sure is was the patient sedated if the patient was on supplemental oxygen or he was sedated during anesthesia hen he was given oxygen free oxygen radical hyper oxygenation can do that so that is an itrogenic thing that has no relation to pathology and this is very very frequently seen in pediatric patients who are getting mr scans under sedation remember anesthesia if it is not the case then you have to think of pathology it can be blood from seborrhecinoid hemorrhage it can be pus from infection it can be recent gadolinium injection or multiple doses of gadolinium within the past 24 to 48 hours or it can be cellular debris which can be tumor cells or leptomeningal carcinometasis or infection or something growing within the csf spaces so that is your standard differential when you see something within the csf spaces you see this you bring the patient back either for csf evaluation clinically or you bring the patient back for post contrast to confirm that this will be some leptomeningal disease and when you do give contrast this is what it does there is enhancement dipping in inside the sulci there is enhancement along the surface of the brain panchama this was a patient of tuberculosis he was this is granulometous disease but fungal infection would do the same thing leptomeningal carcinometasis would do the same thing so this is confirming that the patient has leptomeningal disease again this is not what is going to kill the patient immediately look at the patient he's got hydrocephalus see those temporal wounds massively dilated see that aqueduct of sulvious massively dilated that is what you have to hold the patient back and call the clinician whether he needs to go to the ER or he needs to go to the clinic to the to see the clinician this patient should not go home with that kind of medical system always look at those what used to be called at look at the corner of the films here we have to look at all the associated findings don't get bogged down that you always see a positive finding then that is very very common with even the most experienced radiologists that we get bogged down when we see one positive finding and tend to ignore all the other positive findings so anyway this is a case of leptomeningal carcinometasis so when we see meningeal or leptomingeal or patchy meningeal enhancement what do we do how do we differentiate? Dural enhancement this is going to be lining the bone it will hub the calvarium it will not dip into the sulci differential for this would be infection intracranial hypotension multiple lumbar punctures recent lumbar puncture or dural based metastasis how do we call whether the dural is enhancing when you see more than three consecutive slices of enhancement on a coronal sequence we call it abnormal dural enhancement if you see it on one or maybe two it may be a vessel or partial volumin but if you see on three or more consecutive slices then it is abnormal dural enhancement we should take that as abnormality besides this of course sarcoid lymphoma leukemia is always something that we can throw in the differential that is associated with dural enhancement also leptomeningal enhancement the classic appearances it dips into the sulci verifying enhancement lines all the pl lining differential for this again would be sarcoid lymphoma leukemia but you have to think of leptomeningal disease we talked about all the differential of those leptomeningal disease we just went through including leptomeningal carcinometasis that would be the differential for that is how you differentiate between meningeal enhancement lastly we will quickly go through with the metastasis just think about this that all metastasis behave like their primary tumor so if a primary tumor is a tumor that scansifies then the metastasis will have a tendency of cancerification so you see a classified metastasis multiple lesions when do you think of metastasis when you see multiple lesions of course think of it that the most common solitary brain mass in an elderly patient or an adult patient is going to be metastasis but we think of metastasis when we see multiple lesions now here is a case of multiple calcifications within the brain parenchyma with associated mass effect if there was no mass effect this could have been old granulomatous infections even if there is a mass effect this can still be a granulomatous infection it could be still be cystic surfaces but in an older patient think about metastasis again calcified metastasis exceedingly there the tendency should be to go in favor of granulomatous disease or neurosis surfaces or a dying cyst which should all give this kind of appearance with some cysts having calcifications but calcified metastasis is a possibility that classic metastasis associated with calcification would be from gut tumors like musinocercinoma or originally bone producing neoplasms like osteosarcoma controsarcomas a hemorrhagic metastasis if the primary tumor is hypervascular metastasis would tend to be hemorrhagic in nature so think about the primary hypervascular tumors it would be renal cell carcinoma melanoma thyroid carcinoma choreocarcinoma these all would give classically hemorrhagic metastasis but even though lung and breast in itself do not typically cause hemorrhagic metastasis they're so common that between the two of them they outnumber overwhelmingly the classically hemorrhagic metastasis so if you see a case of hemorrhagic metastasis chances are it's going to be lung and breast even though the typical metastasis of which bleed are from renal cell carcinoma melanoma thyroid choreocarcinoma so those would be the differential for a hemorrhagic metastasis think of few that bleed on its own now this is a case of typical metastasis where you have central necrosis peripheral enhancement multiple lesions but on diffusion sequence what you are seeing is kind of an unusual appearance you see restricted diffusion this broadens your differential you have to think about a micro abscess an abscess a septic emboli keeping in mind that small hemorrhagic metastasis do cause restricted diffusion now this was a case of a small hemorrhagic metastasis that was causing restricted diffusion but when you see a restricted diffusion with peripheral enhancement your first thing something that is going to be rapidly killing the patient rapidly deteriorating would be a septic emboli endocarditis abscess those are the things you want to rule out once you approve those out then you think of a hemorrhagic metastasis or a metastatic disease so this was these are two these are this was a case of hemorrhagic metastasis so again last what i want you to take home from all my lectures is all neoplasms masses hemmass effects think of what is going to kill the patient immediately herniation hydrocephalus these are the things you have to watch out in all neoplasms once you recognize a mass the patient has enough time to be treated for that but if a patient has associated obstructive hydrocephalus herniation subfolds in trans-tonutrient herniation the patient does not have more than 24 hours he can die potentially in 24 hours yes it's not necessary that he's going to die from the herniation but that is what kills the patient very very quickly so that is what you have to keep in mind whenever you are looking at it then depending on your practice i've told this again and again and again if you are in a neuro oncology center you have to give a more detailed correct approach to what the neoplasm is you have to give a relatively potential cell line of what the tumor is arising you have to unfollow up examination think of the genetic underlying mutations and then you have to talk about that and whether there is recurrent residual tumor or radiation across post-treatment change if you are in a diagnostic neuro radiology what you your most important thing is to recognize what the kind of tumor is you have to keep in mind that this is a neoplasm it is what associated with masses it is associated with secondary changes like hydrocephalus or herniation those are the things you have to and you have you have to keep in mind if you are a general radiologist it is important for you to recognize that differentiating between acute versus a chronic condition things like infection versus neoplasm these are the things you should be able to differentiate and then you should be able to refer it to correct appropriate person and make sure that a benign condition doesn't get operated and a malignant condition doesn't go home I hope my lecture was of help to you in furthering your knowledge of brain neoplasms I am glad I've got this opportunity to speak to you and thank you