Brain Tumours (Part 2 of 4)

Welcome back to Songs for FRCR. Back with the much anticipated Brain Tumors Part 2. If you have not heard Brain Tumors Part 1 from 2 weeks ago, please go and listen to that first. In Brain Tumors Part 1, we covered groups 1 to 4 and today we will do groups 5 to 7. The Tumor groups we are doing today are Intraventricular Tumors, CP Angle Lesions and a miscellaneous group of things that I have thrown together. Before we make a start, we would just like to take a moment and say thank you to everyone who has shown their appreciation through email, through Twitter, voice messages. It really does motivate us to create more. We have had messages of appreciation from the UK, from Portugal, from Nigeria, the States everywhere. Soon, we are going to start reading out some of your emails and playing the voice messages. Do keep them coming in. We have had a few requests for Disney songs and shockingly there are no Disney songs about cancer, brain tumours or illness in general. But of course we are here to help you so we have been thinking laterally and we have come up with a song that is in some way related to brain, the visual cortex and sight. So buckle up, here we go, Brain Tumors Part 2. [Music] We are going to start with Intra Ventricular Tumors and there are five I am going to talk about. These are the only five you really need to know. They are Central Neurosythoma, Intra Ventricular Meninjiuma, Horroyd Plexus Papaloma, Saga and Sub Appendemoma. We are going to start with Central Neurosythoma. How are you going to spot a Central Neurosythoma in an exam? That is what you want to know and I am going to tell you. A Central Neurosythoma will be a young adult. 70% occur between the ages of 20 and 40. This young adult, between 20 and 40, will present with a slow history a few months of a headache. When you image this 20 to 40 year old who has had a headache for a few months, you will find a heterogeneous, lobulated mass attached to the septum per lucidum. It will have multiple cystic areas giving it a bubbly appearance. It is often calcified and the pattern of calcification is usually punctate and if it is big then hemorrhages quite common. It is a low grade tumour, it is a who grade two tumour and prognosis is excellent. Let us just recap that. Central Neurosythoma, a 20 to 40 year old presenting with a few months of a headache. You image them and you will find a lobulated heterogeneous mass attached to the septum per lucidum. It will have multiple cystic areas giving it a bubbly appearance, punctate calcification and if it is a large Neurosythoma it will have hemorrhage. That is it for Central Neurosythoma. Let us move on to intraventricular meningioma. Whereas Central Neurosythoma affected younger adults, an intraventricular meningioma classically affects females in their 40s. The question will talk about a middle aged female with a solid mass in the tri-gone of the lateral ventricle. If you hear that it is an intraventricular meningioma. 80% of these are in the tri-gone of the lateral ventricle. Like with all meningiomers they are hypercellular and homogenously enhancing. Compared to regular meningiomers, the intraventricular ones are more likely to be calcified. 50% of them will be calcified. So an intraventricular meningioma will be a middle aged female in her 40s with a solid hypercellular homogenously enhancing calcified mass in the tri-gone of the lateral ventricle. Let us quickly recap. I make no apology for the repetition. It is the only way to learn. We are doing intraventricular tumors. I said we are going to talk about five different tumors. Central Neurosythoma intraventricular meningioma, coroid plexus papaloma, SAGA and sub-appendimoma. So now we have done central neuropythoma and intraventricular meningioma. We will move on to the third of the five in this group, coroid plexus papaloma. A coroid plexus papaloma is the most common rangeum in babies under the age of one. In babies you will find it in the atrium of the lateral ventricle. If you have it in adults you will find it within the fourth ventricle. It can occur in other places like the third ventricle but by far the most common are atrium of lateral ventricle for kids and fourth ventricle for adults. What features make a coroid plexus papaloma recognizable in an exam? Let me tell you. What you will see is a lobulated heterogenous mass. It is sometimes described as a cauliflower-like mass. A mass will be hyperintense on T2 and enhance avidly. It is a solid vascular tumor and the enhancement is described as being very vivid, front-like enhancement. So I have said a lobulated heterogenous mass which is T2 hyperintense and avidly enhancing with vivid, front-like enhancement. 25% have speckled calcification, 80% of people will have hydrocarefulis. That is both because there is CSF overproduction and there is also decreased resorption. Coroid plexus papaloma does have some associations. The first is acardicindrome, AICADI and also Von Hippellindau. If it occurs in the setting of Von Hippellindau, you may well also see an associated hemangioblastoma. Hemangioblastoma we talked about in group 4. Now coroid plexus papaloma is a hougrade one lesion but it does have a malignant counterpart, the coroid plexus carcinoma. It is usually very difficult to distinguish the papaloma from the carcinoma on imaging. One clue would be a papaloma usually enhances homogeneously. If you see heterogenous enhancement then consider carcinoma. So let's go over coroid plexus papaloma again. It's the most common brain tumor in children age less than one year. I've said in kids you'll most likely find it in the atrium of the lateral ventricle, in adults within the fourth ventricle. You will see a lobulated heterogenous cauliflower-like mass. It's a solid vascular tumor which will be T2 hyperintense and avidly enhancing with vivid, frond-like enhancement. A quarter will have speckled calcification. 80% of vast majority will have hydrocephalus. Cards are acardi syndrome and von Hippell-Lindau in which case you'll often see an associated himandia blastema. That's three down two to go. If you notice the demographics have been very different for the three tumors I've talked about. Central and Neurocyteoma was young adults 20 to 40. Intraventricular men in Geoma were 40-year-old females, middle-aged females. and the coroid plexus papilloma is babies under the age of one. Let's move on now to SEGA. SEGA SEGA is sub-appendimal giant cell astro-cytoma. This is almost exclusive to patients with tuberous sclerosis. These occur in young people under the age of 20. What we think happens is patients with tuberous sclerosis develop sub-appendimal nodules within the ventricular wall. Over time, these sub-appendimal nodules become a SEGA. What you'll see on imaging therefore is an enhancing mass in the lateral ventricle somewhere near the framerate of Monroe. It's usually a bigger than a centimeter, and it can be calcified. If you do see this, if you see an enhancing mass in the lateral ventricle, near the framerate of Monroe, which is calcified and bigger than a centimeter in a patient with tuberous sclerosis, that's practically pathodomic. SEGA will enhance, usually enhanced, avidly, but enhancements will not differentiate between a simple sub-appendimal nodule of tuberous sclerosis and then the formation of a SEGA, because the nodules also enhance. So to recap SEGA sub-appendimal giant cell astrocytoma, this is almost exclusively in tuberous sclerosis patients. They are aged under 20, and enhancing mass is what you'll see, avidly enhancing within the lateral ventricle near the framerate of Monroe. It may be calcified, usually bigger than a centimeter. If you see this appearance, if you see an enhancing mass near the framerate of Monroe, within the lateral ventricle, and it's calcified, bigger than a centimeter, look for other signs of tuberous sclerosis. That's it for SEGA. Final one in this group is sub-appendimoma. The name sounds like it might be related to appendimoma, or it might be related to SEGA. It's not in fact related to either of them, it's got nothing to do with either of them. A sub-appendimoma is a tumor of the appendimals cells that line the ventricles. First of all, it is non-inhanceing. It's a non-inhanceing low grade tumor, and often is only found incidentally. The patient will be middle aged or older. Where will the sub-appendimoma occur? It will either occur inferiorly in the fourth ventricle, or at the framerate of Monroe within lateral ventricle. Let me say that again. Sub-appendimoma is a non-inhanceing low grade tumor, which is often incidental finding, middle aged, older adults. I've said it's commonly found inferiorly in the fourth ventricle, also called the fourth ventricle Obex OBEX, and also found within the lateral ventricle near the framerate of Monroe. If you were listening, your member, Sega, is also found in lateral ventricle near the framerate of Monroe. So how can you tell them apart? First of all, I've said twice now, sub-appendimoma is non-inhanceing. Sega is usually avidly enhancing. That's the first way to tell them apart. Secondly, I did say Sega is usually bigger than a centimetre. Sub-appendimoma is usually small. It's usually less than a centimetre at the worst 1-2 centimetres. So if you don't have the clue of tuberous chlorosis, the two main ways you'll differentiate Sega from sub-appendimoma is enhancement, Sega enhances sub-appendimoma does not, and size. Sega is usually bigger more than a centimetre. Sub-appendimoma is usually less than a centimetre at most 1-2 centimetres. So that's it. That's all five intra-ventricular tumors. Let me quickly recap and then we'll move on. The five tumors I talked about were central neurosidomer, intraventricular and meningiomer, coroid plexus papaloma, Sega and sub-appendimoma. Central neurosidomer, first of all, this was the tumor that occurs in 20 to 40-year-olds. It's a lobulated, heterogeneous mass attached to the septum polysidium. It will contain multiple cystic areas giving it a bubbly appearance. It will have punctate calcification and if large, may contain hemorrhage. Intraventricular meningiomer was in middle-aged females. 80% are in the trigon of the lateral ventricle. It's a solid mass like any meningiomer anywhere else. Hypercellular, homogenously enhancing and more likely to be calcified compared to other meningiomers, 50%. Coroid plexus papaloma, the most common tumor in a child under the age of one. In children, you will find it in the atrium of lateral ventricle, in adults within the fourth ventricle. This is a lobulated heterogeneous cauliflower-like mass lesion, which is T2 hyperintense and avidly enhancing. The enhancement pattern is described as an avid frond-like enhancement pattern. Quarter of them will have speckled calcification. The majority have hydrocephalus and it's associated with acardic syndrome and Ron Hippell-Lindale. Coroid plexus papaloma is avidly enhancing. If the enhancement pattern is heterogenous, this raises suspicion of a coroid plexus carcinoma, although it's not easy to distinguish the two on imaging. Saga is exclusive to patients with tuberous sclerosis. What you'll see is an enhancing mass in the lateral ventricle near the framin of Monroe, usually bigger than a centimetre and may be calcified. Finally, sub-apendomoma, a non-enhancing low grade lesion often found incidentally in adults and older patients. Usually, inferiorly within the fourth ventricle, or in lateral ventricle near the framin of Monroe. It's usually small less than a centimetre and does not enhance. I repeat, does not enhance. And it's warm and real and bright in the world to somehow shift it. Fall at once, everything looks different now that I see you. We now move on to group six of our seven brain tumor groups. Group six are tumors of the cerebellipontine angle. What is the cerebellipontine angle? Well, the clue is in the name. It's the space between the pons and the cerebellum. And what hangs out at the cerebellipontine angle that we might be interested in? A few things hang out there. Crenul nerve's five, seven, and eight. And acre, the anterior inferior cerebellar artery. Most CP angle lesions are extra-axial. And let's go through five of them. The five are shwanoma, meningioma, arachnoid cyst, aneurysms, and epidermoid cyst. We're going to start with shwanomas, and particularly we're talking about vestibule shwanomas, or acoustic neuromas, as we often call them. How will an acoustic neuroma present? Classically it's with non-pulsatial tinnitus and sensory neural hearing loss in an adult. Let's talk about the pathology of acoustic neuromus, first of all. These are benign, they're who grade one tumors. The vast majority over 90% arise from the inferior division of the vestibular nerve. And they're said to arise at the transition point between glial and shwan cells. That's called the Obersteiner redlic zone. So I'll say that again, the Obersteiner redlic zone is the transition point in a nerve, where the glial cells are replaced by shwan cells. And that's where vestibular shwanomas are said to arise. If they occur bilaterally, that is strongly suggestive of neurofibromatosis too. so you have an adult with sensory needs. your hearing loss plus binus non-pulsatile tinnitus. When you image them, what you will see classically is a solid mass that causes widening of the porous acousticus. The porous acousticus is simply the inner or the medial opening of the internal acoustic canal and that's where the facial nerve, the vestibular cochlear nerve and the labyrinthine artery pass through. So let's say that again, acoustic neuromers are solid masses that cause widening of the porous acousticus, the medial portion of the internal acoustic canal. These lesions are avidly enhancing and if they become particularly large then cystic change is common. Memorrhage is also quite common but the one thing you won't see is calcification. You can spot acoustic neuromers separate from the nerve fibers and they'll usually display and displace the nerve fibers rather than engulf them. Finally, acoustic tronomers are often described as having an eye-screen cone appearance. The eye-screen bit is the CP angle lesion and the cone is the intracanelicular component. Let's quickly regroup and recap tronomers before I move on. Tronomers comprise almost 90% of CP angle lesions. The vast majority arise from cranial nerve 8 and are termed acoustic neuromers. These are T2 hyperintense, avidly enhancing lesions. They're solid nodule masses that will cause widening of the porous acousticus. If they get particularly big then cystic degeneration is very common so they appear head fodgenous. I've said it a million times but I'll say it again, they are very avidly enhancing and do not calcify. That's acoustic neuromers, the most common CP angle lesion. The second most common lesion of the CP angle are meningiomers. How are we going to tell a meningioma from an acoustic neuroma? There are a few ways, a meningioma will have duoral enhancement. You'll also see a broad duol base and bony hyperostosis. 20% will calcify. Remember, schwanomas do not calcify. And finally, CP angle meningiomers will not enlarge the porous acousticus, so lots of ways to separate meningioma from acoustic neuroma. They'll be quickly recap. We're currently on group 6 of our 7 brain tumor groups. This is the CP angle lesions. The first one we talked about was a schwanoma, most often arising from the crignol nerve 8. The way to tell a schwanoma, it will be solid, nodylla, avidly enhancing mass, often head fodgenous with cystic degeneration if it's large. It will cause widening of the porous acousticus and it will not calcify. The next most common is a meningioma. And the way to tell this apart from a schwanoma, well there are a few ways, you will see dual enhancement, a broad duol base, bony hyperostosis and in 20% calcification. A meningioma will also not enlarge the porous acousticus. Now, as you know, because I've repeated it a million times, schwanoma comprises the vast majority of CP angle lesions. So all you really need to know for group 6 is how to differentiate a schwanoma from everything else in the group. We've just talked about how to differentiate it from meningioma. I'm now going to move on to epidermoid cyst. So how do we tell an epidermoid cyst apart from a schwanoma? That's very easy. First and foremost, an epidermoid cyst will not have any enhancing component and we know schwanoma is avidly enhancing. An epidermoid cyst will also not widen the internal or the trigonel and schwanoma will. On MRI, on T1 and T2 rated imaging, an epidermoid cyst will follow water signal. However, it won't suppress on flare and it will have restricted diffusion. Then we recap that again. epidermoid cyst versus schwanoma. Epidermoid cyst will not have any enhancing components. It will not widen the internal or the trigonel. It follows water signal on T1 and T2 rated MRI. It will not suppress on flare, however, and will show restricted diffusion. That's an epidermoid cyst. Another cyst you can get at the CP angle is an arachnoid cyst. This should be very easy because an arachnoid cyst will just follow CSF signal on every sequence, including flare so it will suppress on flare. It's also not going to have any restricted diffusion. Finally, aneurysms can occur at the CP angle and there are four main vessels really. Peaker, the posterior inferior cerebellar artery, Aker, the anterior inferior cerebellar artery, and the vertebral and bazzle arteries. Aneurysm is obviously going to be well defined. It's going to be avidly enhancing and will have flow voids on MR or pulsation artefact. A CTA or an MRA will diagnose that. So that's it. A very quick recap of cerebellar pontein lesions. These are all usually extra accel and I've mentioned a few. Schwanoma being by far the most common up to 90%. A Schwanoma usually arises from the vestibular cochlear nerve when you'll nerve eight. You will see a T2 hyperintense avidly enhancing solid mass causing widening of the porous acousticus. If it's bilateral then very strongly associated with neurofibromatosis two. If it's particularly large then cystic degeneration is common but you will not get calcification. Compare this to a meningeoma which can also occur at the CP angle. These will have a broad dual base and dual enhancement like with all meningeomas. They will also cause bony hypostosis and 20% will calcify. They will not enlarge the porous acousticus. An epidermoid cyst was next which follows water signal on T1 and T2 weighted MRI imaging. It does not suppress on flare however and will show restricted diffusion. I then mentioned an arachnoid cyst which just simply follows water on every MRI sequence. It does not show restricted diffusion. And finally aneurysms usually of pica, acar, the vertebral and basilar arteries. They are easily identifiable with CTA or an MRA. Now I've said that CP angle tumors are usually extra accel and they are. A few intra accel lesions can spread into the CP angle. These are usually the posterior phosphatumas that we've already talked about. Gliomas, appendimomas, appendimomas remember the toothpaste tumor from Group 2. These can squeeze out from the framinor of lishka into the cerebellar pontine angle. Also other posterior phosphatumas like hemangia blastoma and medeloblastoma can also spread into the cerebellar pontine angle. So tumors arising within cerebellar pontine angle are usually extra accel but other intra accel tumors can spread into that area. That's it for CP angle lesions. We have one final group and then we're done. [Music] We now move on to Group 7 of 7, the miscellaneous group that I threw together. The three things I'm really. to mention in this group are lymphoma, menendiuma, which I've already alluded to many times, and metastases. Third, start with primary CNS lymphoma. This is usually a B cell lymphoma, where lots of immature blast cells form aggregated lymphoid tissue around the cerebral blood vessels in a periventricular pattern. This periventricular pattern is a key feature of CNS lymphoma. There are two other key features, the first of which is high cellularity. The high cellularity is what gives rise to its hyper-attennuating appearance on CT, and the low T2 signal and restricted diffusion. The third key feature is lymphoma is classically known to melt away very quickly with chemo radiation treatment, but tends to recur aggressively. So primary CNS lymphoma occurs in a periventricular pattern. It has high cellularity, which gives it a hyper-attennuating CT appearance, low T2 signal on MR, and restricted diffusion. It also responds quickly to chemo radiation, but does recur very aggressively. Now the appearance of lymphoma depends on whether the patient is immunocompromised or immunocompetent. We'll start with the immunocompetent patients. In this case, what you'll see is an enhancing periventricular mass, which crosses the corpus colosum to involve both cerebral hemispheres. These common locations are the frontal lobes and the basal ganglia. I have already mentioned this in group one, but the differential diagnosis for tumor that crosses the corpus colosum is lymphoma, glioblastoma, multiformy, GBM, and demyelination. So an immunocompetent patient with a primary CNS lymphoma will have enhancing periventricular mass that crosses the corpus colosum. They will enhance homogenously because there is no necrosis. In contrast to this, an immunocompromised patient will not have homogenous enhancement of their lymphoma. Lymphoma in an immunocompromised patient will have ring enhancement because they'll be central in the process. So what you'll see is periventricular ring enhancement, predominantly within the basal ganglia. Now, something you absolutely have to memorize is the main differential for necrotic primary CNS lymphoma and the main differential is toxoplasmosis. So an immunocompromised patient with ring enhancing lesions, your two biggest differentials are lymphoma and toxoplasmosis. There are four main ways to reliably tell the two apart. The first way is easy. You just give some toxoplasmosis treatment. If it responds, that's what it was. The second way is using thalium. Lymphoma is thalium avid. It will uptake volume. Thirdly, you can do a PET scan. Lymphoma is also PET avid. It will uptake. And finally, perfusion scanning. The lymphoma will show increased cerebral blood volume CBV. I'm going to say that again because it's really important that you memorize this. The main differentials for ring enhancing lesions in an immunocompromised patient are lymphoma and toxoplasmosis. The way to tell them apart are as follows. Lymphoma will be thalium avid. It will also be PET avid. It will not be PET avid. And will not have increased perfusion. So primary CNS lymphoma, quick recap, the key features are as follows. It is in a very ventricular location. It is particularly highly cellular, which will mean it will be hyperattentuating on CT, low signal on T2 MRI and show restricted diffusion. That's true for anything that's highly cellular. Features also, it will melt away with treatment, but tends to recur very aggressively. Appearance depends on whether the patient is immunocompromised or immunocompetent. With the immunocompetent, you'll get an enhancing periventricular mass, a homogeneously enhancing mass with no necrotic areas, which will cross the corpus callosum. Predominantly within the frontal lobes and the basal ganglia. In an immunocompromised patient, you'll see a periventricular ring enhancing mass, predominantly within the basal ganglia. The main differential in this case will be toxoplasmosis. The way is to tell toxoplasmosis apart, first of all you can give some toxoplasmosis treatment. The other ways are phallium scanning on which lymphoma will be avid. Pet scanning, again lymphoma is avid and perfusion scanning, again lymphoma shows increased cerebral blood volume. The next miscellaneous lesion is meningiomas. I've talked about them quite a lot in other groups, but meningiomas generally are benign lesions of older adults. You will find multiple meningiomas in neurofibromatosis 2 and also post-radiotherapy treatments. They're usually higher attenuation than the surrounding brain perinchyma and 25% of them will calcify. 25% calcifying is a general number if you remember what I've said previously. If they are intraventricular meningiomas, they are more likely to calcify 50%. And if they are a CP angle tumours, around 20% will calcify. Now while you spot a meningioma, they have a broad-based dual attachment, that's key, and a dual tail. The dual tail is formed by vasoactive substances released by them in meningioma. It's not tumour. I'm not going to dwell on meningioma because it's so common many of you will know this anyway. So meningioma, benign lesion, older adults, multiple meningiomas in neurofibromatosis 2 and post-radiation treatment, they are hyper attenuating calcified in 25%, they will have a broad-based dual attachment and a dual tail. And finally, metastases. We all know what mets look like. We've seen them on CT heads. Metastases most commonly come from the lung, breast and melanoma. Most spread hematogenously and therefore occur at the grey-white metadjunction where the calibre of these small arterioles changes. Mets are fairly straightforward, but I have to give them a passing mention. So that's it. That is brain tumours part 2. We have covered intraventricular tumours. We've covered CP angolisions and a bunch of miscellaneous things. I'm going to do a quick recap of everything and then we're done. [Music] Right, final quick recap. We're going to hate me but you're going to remember it. Intraventricular tumours first of all, we talked about central neuropsychoma, intraventricular meningioma, choroplexus papaloma, seiga and sub-apendimoma. Central neuropsychoma was between 20 to 40 years of age, a low-grade young adult tumour, a populated heterogeneous mass attached to the septum polucidum with a multiple cystic or bubbly appearance. Punk date calcification was a common feature and if they were big, then hemorrhage was common. We then talked about intraventricular meningiomas, middle-aged, 40-year-old females with a solid [BLANK_AUDIO] mass in the trigon of the lateral ventricle. 50% calcified. Corrid plexus papilloma, most common tumour in babies under the age of 1. It was a lobulated, hetrogenous, cauliflower-like mass lesion, T2 hyperintense, avidly, foreign-like enhancing. 25% had speckled calcification and almost all had hydrocephalus, associated with a cardicintrome and von Hippel Lindau. Sega is exclusive to tuberous sclerosis, an enhancing mass in the lateral ventricle near the framer of Monro. The Penda moma is a non-enhancing mass, often in the fourth ventricle or within the lateral ventricle near the framer of Monro. As I've said, it did not enhance and is often smaller than a Sega measuring under 2 cm. We moved on to CP angle lesions, lesions between the ponds and the cerebellum, the vast majority of which are schwanomas. Schwanomas remember are solid masses, intensely enhancing high T2 signal, which cause widening of the porous acousticus. If they are big, then cystic degeneration is common, but they do not calcify. We must be able to differentiate schwanomas from other lesions of the CP angle. So comparing them with meningiomas, meningiomas will cause dual enhancement, they will have a broad, dual base like with all meningiomas, they often cause bony hyperostosis, 20% will calcify and they will not enlarge the porous acousticus. Comparing a schwanoma with an epidermoid cyst, an epidermoid cyst will follow water signal on T1 and T2 weighted images. However, unlike water, it will not suppress on flair and will show restricted diffusion. Comparing it with an arachnoid cyst, an arachnoid cyst is easy, it just follows CSF on everything. Aneurysms are common at the CP angle of the pica, acre, vertebral and bazzle arteries. This should not be difficult to differentiate a CTA or MRA will give you the answer. And finally other lesions in the cerebellum can spread into the cerebellum on tine angle. These will be things like appendimoma which will squeeze through the famine of luscia, hemangia blastoma and medillo blastoma. Finally we did the miscellaneous tumours, primary CNS lymphoma which looks different whether you are immunocomptent or immunocompromised. Essentially this is a periventricular highly acetylillal lesion. If you are immunocomptent, it will show as an enhancing periventricular mass with no necrosis. In immunocompromised patients, it will show as a ring enhancing mass because of central necrosis. The main differential for which is toxoplasmosis. Finally we did meningiomas and metastases. This recap was obviously not comprehensive just a summary of the main points I've talked about. So that's it, that's Brain Tumours Part 2. Thank you so much for listening, we really hope you enjoyed that episode and learned something. We did Brain Tumours Part 1 a fortnight ago. The following weekend we gave you a break and did something else, testicular tumours. And this weekend we've come back to Brain Tumours that was intentionally done. We don't want to bombard you with too much information on the same topic because it will just cause things to be jumbled in your mind. So you have plenty of time for Brain Tumours Part 1 to sink in and become part of your long-term memory. We'll be doing the same thing again, so next weekend we'll bring you a topic unrelated to Brain Tumours and come back to Brain Tumours Part 3 in two weeks time. Brain Tumours Part 3 will be SupraCellar and Pineal Mass Lesions. You asked for Disney Music and we delivered, music today was from the movie Tangled, quite possibly the most underrated Disney movie of all time. If you haven't seen it, go and watch it, it's brilliant. If you liked what you heard, spread the word, drop us an email, drop us a tweet or a voice message, we love hearing from you. Don't forget to enter our competition. The details are on the competition time podcast episode. The best entry so far has only scored 3 out of 5, that's awful. Also the current top entry is not even from a radiologist, so you guys are really letting the specialty down. Have a great week guys, we'll see you next weekend. Bye.