hello my name is Fender Ghazer I am a neurologist working against university hospital in Belgium and welcome to this video on imaging of brain arteriovenenous malf forations This presentation is part of a series of presentations on the topic of imaging of brain vascular mal formations What a radiologist must know Normally it was my intention to just make one presentation but it got way out of hand So it's going to be a couple of presentation on each of these kind of mal forations separately And I'm going to start with uh one of the most important ones But first what kind of vascular mal forations are there in the brain so there are f five main types I believe every radiologist should know You have your developmental venous anomaly You have capillary tankasia You have the cerebral cavernous malf for also known as the cavernoma We have the arteriovenenous mal foration And finally we have the arteriovenenous fistula Now if this topic is new to you this might be a bit daunting This might be a bit much all these terms But to keep it easy we can group these in two categories We have the so-called I'm going to remove the video screen because it's a bit in the way We have the so-called slow flow malf forations and we have the high flow malf forations And how can you tell them apart well the high flow malf forations have the term arterio in them even arteriovenenous And this already points out to the fact that these mal forations are characterized by the presence of an arteriovenenous shunt So to um uh depict it simply so high flow malf forations or mal forations characterized by high flow high pressure flow So there's a lot of pressure inside these malf forations while low flow malf forsations are characterized by low pressure flow So to understand these malf formations it's good to take the normal anatomy of the vascular bed as a starting point and the normal vascular anatomy is quite simple So we have arteries and arteries supply oxygenrich blood to various tissues Then we have veins and veins carry oxygen poor blood back to the lungs where they will receive oxygen And then we have the capillary bed And the capillary bed is a fine microscopic vascular bed in which the gas exchange takes place So that's the place where nutrients and oxygen are delivered to the tissue and waste and uh carbon dioxide is taken up and um brought to the pulmonary system Now when it comes to the various vascular mal forations we have lowflow vascular malf forations or mal forations that involve a structure of the capillary bed or a venus structure while the high flow malf forations are characterized by the presence of a direct shunt So a direct connection between the arterial system and the venus system without a capillary bed in between And the capillary bed is normally responsible for the fact that we lose a lot of pressure between an artery and a vein So if you remove the capillary bed what we get is a high pressure situation in which blood carrying um a high arterial pressure is pumped directly in the Venus system and the Venus system normally doesn't take that well So okay that's a nice starting point So let's now try to look at the various subtypes of vascular malf forations So we have the high flow vascular malf forations Two subtypes arteriovenenous mal foration and the arteriovenenous fistula What's the difference well to put it quite simply an arteriovenenous malf for and well all cases a congenital malf for it is characterized by the presence of a so-called nidus So we don't have a capillary bed instead we have an abnormal conglomerate or a tangle of displastic vessels and these displastic vessels while this is not a capillary bed this is a direct shunt from the arterial to the venus system and the fistula while fistulas are mostly acquired lesions and then we have no nidis but just one or in some cases two or multiple direct connection ctions between an artery and a vein As simple as that So the mal for we have a nidis this conglomerate uh of vessels and these are congenital and the fistula is an acquired lesion with one or multiple direct connections but without a nitis When it comes to the lowflow vascular malf forations these can have some exotic sounding names but are not that difficult So we have the capillary tilangiasia This involves the capillaries and this it's a mal for in which the capillaries are uh dilated and there is interspersed brain paranca Then we have the cerebral cavernous malf for also low flow and in that we have a cluster of caverns venus caverns filled with slow flowing blood but there is no interspersed brain parennema and finally we have the so-called developmental venus anomaly which is actually not really a mal foration as the name implies it's a congenital developmental anomaly and the venus drenage of the brain I will talk about these malf forations in more detail in a future presentation which is already finished by the way but I'm going to start for this presentation with the arteriovenenous malf for let's just summarize the basics here before we jump into it So what are the high flow malf forations characterized by a direct connection between arteries and veins they have no capillary bed high pressure and as a consequence a high hemorrhage risk and in the lowflow malf forations we have no shunt These are uh malf formations characterized by abnormalities at the level of the capillaries of the veins or the veins The blood flows slowly pressure is low and as a consequence these malfformations have no or a low hemorrhage risk Okay of all these I'm going to start with arteriovenenous malf forations because well there's an hemorrhage risk there which makes them very important They are lesions you don't want to miss They are lesions you have to look for when dealing with a spontaneous a patient with a spontaneous cerebral hemorrhage Now to understand them and I've actually already talked about this Let's compare it with a normal capillary bed Well there's an arteriovenenous malf for a mal foration without a capillary bed and this nidus this conglomerate of abnormal vessels providing a direct arteriovenenous shunt It's congenital and also mostly sporadic So there is one genetic association and that is the Render Weber uh now the Randu Weber oller syndrome also known as hereditary um hemorrhagic uh tangiactasia uh which is a syndrome in which patients typically have tangiactas uh on the mucosa of the lips the tongue uh and so forth but also arteriovenous malf forations and various visceral organs and most cases in the lungs But these patients can also have them in the brain But I said that's a minority the majority of patients with brain arteriovenenous malf formations and the majority these are sporadic Now why are they important because as said there's a high hemorrhage risk Arterio venous malf forations are the most common cause of spontaneous brain hemorrhage in children and they account for about almost 50% of spontaneous cerebral hemorrhages in this group and less than 18 year olds and even in somewhat older patients somewhat the young adult group let's call them less than 40 let's say less than 40 this is still a very common cause of hemorrhage accounting for up to 33% of spontaneous cerebral hemorrhages in this age group So it says here less than 18 this is a typo should be less than 40 So when less than 40 um and people under 40 with a spontaneous hemorrhage and about a third the cause as an arterial vice malf for these are lesions you don't want to miss Patients can present with a brain hemorrhage but they can also present with an incidental AVM Now if a patient has an incidental AVM that hasn't bled what is the hemorrhage risk there are actually there's actually data on that and that is let's say uh in this patient with this tiny AVM over here that is about 2 to 4% per year it's higher in an AVM that has in the past bled and uh AVMs that have ruptured in the past the hemorrhage risk varies between 6% to 15% per year and it's higher in the first years after the hemorrhage Now you could say in a patient with an uh an incidentally discovered AVM that hasn't bled well 2 to 4% that isn't that high Yeah but it's 2 to 4% per year So what's the lifetime hemorrhage risk suppose this is a 40year-old patient There's a formula for that And if you want to know what all these letters means uh all these letters mean just uh freeze the screen now make a print screen and you can read it in detail I'm not going to read it out loud But if we use that formula in a 40-year-old with an incidentally discovered unruptured AVM the lifetime hemorrhage risk is 70% You don't want to have those odds Those are pretty big odds So and there are possibilities for treatment elective treatment in incidentally discovered AVMs I'm not going to talk about that because it's a topic on its own But needless to say as a diagnostic radiologist you don't want to miss an incidental AVM Okay and this presentation is going to focus on what they look like on imaging So you won't miss them So these are the various ways in which an AVM can present clinically as said a hemorrhage hemorrhage is the presentation uh clinical presentation in about 50% of cases of AVM So that's a lot and that's also the most traumatic presentation and about 25% of patients the clinical presentation which leads to the discovery of the AVM or seizures and because diagnostic imaging is performed more and more and more for a variety of reasons The number of completely incidentally discovered AVMs is rising In the old days that used to be a pretty low group but now the most recent publications already report incidentally discovered AVMs and about 10% to in some studies even up to 20% of AVM cases So that is definitely increasing So okay we want to be able to recognize them How do we do that well we can look at AVMs on several imaging modalities We can use CT and CT angography We can use MRI with MR angography or the gold standard digital substraction angography To recognize an AVM on any of these modalities it's good to have a good knowledge on the basic architecture of the AVM And what is that well I'm going to repeat myself but it's something I just tend to do a lot despite my young age They consist of central hallmark denidis and dinitis is something we can if it's large enough easily recognize on imaging studies So that is what we're going to focus on And this nidus is supplied with blood by feeding arteries and blood is carried away into the venus system by draining veins And we can recognize all these components of the AVM on all the imaging modalities I've shown you on the previous slide But let's start with digital substraction and geography and why I'm pretty sure that the majority of people watching this video probably don't do angographies or it's not their core business or their core work rather Um I've done them in the past but I'm a diagnostic neurologist so I no longer do angographies myself but I know how to read them a little bit probably not as good as an interventional radiologist but nevertheless they are the gold standard for evaluating these AVMs Why is that because they allow us to look at the changes and the blood flow to the AVM and NDAVM on different times uh different points in time So they have an excellent temporal resolution and also a spatial resolution that is way superior to CT and MRI allowing us to even discover very small AVMs So okay we have this dynamic visualization and information just as an example this is the profile view of an AVM Uh if we go through these images in time so time is passing by we see more and more of the AVM We can see blood entering the AVM We can see the nidus of the AVM appear and then we see the blood leaving again through the venus system Let's analyze these images now in a bit more detail We start this is a profile view by injecting by injecting contrast in the internal corroted artery And we see that the internal corroted artery has appeared as well as the uh anterior cerebral artery and the middle cerebral artery But we don't see the uh AVM just yet So if you have a bit of experience with reading angographies or doing angographies well people with experience might say well the anterior uh anterior cerebral artery looks a bit thick It looks a bit hypertrophic And this branch this media branch does so too And what is this blush over here people with less experience like myself just wait less than a second and then this happens Now we see opacification and a slightly later phase but still the arterial phase of the nidus So we see the nidus appearing this conglomerate of vessels constituting the core of the AVM And now we see that those hypertrophic vessels are actually the feeding arteries We see that feeding arteries are supplied by the anterior cerebral artery but also by the middle cerebral artery So you can have feed multiple feeding arteries and they can come from different main branches They can also come from both pile branches so superficial branches or they can come from deep perforating arteries In this case they are supplied by pile arteries So feeding arteries are often hypertrophic They are often uh larger than uh the contrateral arteries that don't have to supply an AVM And why is that well an AVM as a direct AV shunt So they there's a lot of blood going there and leaving immediately without going to the high resistance system called the capillary bed which would normally decrease the pressure in the vascular system uh also important is to scrutinize the feeding arteries for anorisms But more about anorisms on feeding arteries later Let's examine the next phase Well next phase we're still in the arteral phase but slightly later And now we see something new happening We still see the nidis We still see feeding arteries but we also see the appearance of a cortical vein That shouldn't be We're still in the arterial vase We even see that this cortical vein drains into the superior sagittal sinus And we see some contrast opacification of the superior sagittal sinus This is an early draining vein Veins shouldn't be visible yet If they are this is proof of an arteriovenenous shunt And well this is an AVM So of course this is an AV shunt And if we wait just a little bit later and look at the images we see that the blood is starting to leave the arteries entering the capillary system and we see progressive opacification of the superior sagittal sinus uh without any visualization of any of the other dural sinuses uh because this carries away the blood from the arteriovenenous malf information It's very important to evaluate the venus drainage of an AVM In this case this uh AVM has what we call superficial Venus drainage There is drench of the AVM by way of superficial cortical veins and these can also include some of the larger ones like the trolar vein or the lab vein into the superior sagittal sinus But other structures that would be allowed would be the transverse sinus and sigmoid sinus So this is superficial venous drainage and that's basically a good thing if you have an AVM because it's associated with a lower hemorrhage risk If you have deep venous drainage which is drainage into a deep vein which then drains into uh parts of the internal cerebral veins or the gallant vein or the straight sinus Deep venous drainage is associated with a higher hemorrhage risk So this patient only has superficial venus drainage venus drainage rather which is a good thing Didn't have signs of deep venous drainage Okay let's examine the frontal view of the same patient This is the arterial face and we clearly see the nidis and we also see that there are multiple feeding arteries supplied by the anterior and middle cerebral arteries but there are no anorisms to be seen on the feeding arteries And here we see the Venus face with with a clear visualization of uh draining cortical veins that enter or give their blood to the superior sagittal sinus And we see the blood even already in the right transverse sinus and the sigmoid sinus So this is pure superficial venus drainage Okay All fine and dandy But the majority of you are probably just like myself diagnostic radiologists who have to examine MRI studies or CT studies or in whom that's their core work Uh but luckily we can visualize the things I've just shown you on DSA also on MRI and CT It's not as great That is to say you don't have the temporal aspect For instance here we see a time of flight angography and we can't selectively visualize for instance the right internal coroted artery All arteries containing fast flowing blood will be visualized on an emmer angioraphy So we don't have that We don't have temporal information and the spatial resolution is great but not as good as from a DSA But okay we can work with that and we can translate everything we see on DS DSA into things we see on CTA or MRI Uh for instance over here we see the Nidus we see feeding arteries and we see a superficial draining vein going towards the superior sagittal sinus and we can recognize all these things on the time of flight angography as well Over here we have the large nidis Here we have the feeding arteries which are hypertrophic which is something you can clearly see if you compare these thick uh arteries with the normal arteries on the contraateral side And then here we have the um enlarged cortical vein which is already visible Uh which is a bit strange because normally you shouldn't see veins on a time offlight angography because on a time offlight angography you see only T1 uh you see only hyperintense signal in uh structures containing fast flowing blood So the fact that we can see this vein means that it contains fast flowing blood and is a sign of an AV shunt Okay let's now focus on the Nidus What does a Nidus look like on basically any imaging modality this is a CT angography This is the Nidus of an AVM This is the two- weighted image And on the two weighted images flow is black So a nidis a conglomerate of vessels containing fast flowing blood will be black This is a T1 weighted image with gatalinium and these vessels contain blood So these will opacify if you administer gatalinium And finally we have a time of flight angography And as explained just about yet on the time offlight angography we can visualize structures containing fast flowing blood So arterial structures without having to administer catalinium So it's a good way to visualize AVMs or other arterial pathological entities without having to give catalinium Okay If we zoom in a little bit what does the Nidus look like on whatever modality you are using to visualize to the AVM as a back of worms so that's a good way to remember it or to recogni to recognize it Look for the back of worms on your imaging study on a CT image And well some of these patients will present at the ER with for instance a firsttime seizure It can be a bit more difficult to recognize an AVM Why because AVM so this is an AVM patient got a CT angography And here we see a very large draining vein surrounded by anis Because the draining vein was so large we saw it on the unenhanced CT as well but it can be difficult So if an AVM hasn't bled they can be difficult to detect because while AVMs don't really have MARS effect they just replace brain parentheses of Mars effect and the density is often is parallel to that of the blood pool So it's slightly more dense than your cerebral cortex Sometimes calcifications can be present and that can sometimes make it a bit more easier to visualize them Here's another example of a patient with an incidentally discovered while incidentally patient presenting with seizures at the ER And if you look carefully on the unenhanced on this unenhanced CT you might say that the cortex looks a bit abnormal in the left frontal lobe And we even if we look a bit closer see some areas that are more dense What is that is it blood doesn't really look like blood It isn't dense enough to be calcium Once again this was an AVM These are vascular structures and the increased density is because they are filled with blood and this has a slightly higher density Just look at the superior sagittal sinus for instance On CT angography we can clearly see the nidis but not just the nidus If we really try to discover all components of the AVM we can recognize these thickened arteries which probably reflect feeding arteries coming from the anterior cineable artery and we can detect these cortical veins that are also enlarged probably reflecting superficial draining veins Final example of a patient with an AVM detected on an unenhanced CT of the brain The AVM is once again difficult to see We see that the cortex looks a bit abnormal over here or there's an abnormal density over here But it's probably wouldn't have been easy to pick this AVM up because it is an AVM Look at this back of herbs over here if it weren't for these calcifications So longstanding arteriovenous malf forations can contain distrophic calcifications probably due to tissue damage as a consequence of chronic hemodynamic stress or maybe old micro hemorrhages or trombosis or infuctions or whatever doesn't really matter how you get them the thing is AVMs can contain them or be associated with them and they can help you detecting an AVM or suggesting an AVM Now what about a patient presenting with a spontaneous hemorrhage in some cases you can even see the AVM on your unenhanced CT images So here we see a large loberer uh hemorrhage and the left frontal lobe But we see that the cortex looks quite abnormal the cortex overlying the hematoma And over here we see once again it's even looks like a bag of worms on your unenhanced CT these structures located in the cortical region with a density that is slightly higher than cortex uh reflecting the density of the blood pool So this was an AVM patient shouldn't have uh should have got a CT angography but instead got an MRI and we see the back of worms of the AVM nitis on this MRI image This is a T1 weighted image with gatalinium This is another example of a patient presenting with a lo entroparenimal hematoma A lober hematoma is a hematoma located along or in the vicinity of the surface of the brain and per definition it's very unlikely that these are going to be hypertensive he him hematomas This patient received a CT angography and we see over here this conglomerate of vascular structures uh laterally of the hematoma This was the nitis of a small arteriovenenous malf for final case This is a 21-year-old male patient who was brought to the ER Uh originally the patient had headache but suddenly he deteriorated quickly and went into a coma and the patient had a cerebellar hematoma And on CT angography the hematoma can be seen here as this area devoid of vascular structures but posteriorly of it we see what what looks like a bag of verms reflecting the nidus of an AVM we see arteries running towards the AVM coming from both the posterior cerebral artery and the posterior inferior cerebellar artery and we even see an enlarged draining vein over here So all components of the AVM are present Now in a patient with a clinical question or clinical radiological question and a patient presenting with a spontaneous cerebral hemorrhage when should you suspect an arteriovenous malf foration and when should you do a CT angography it all boils down to age in children defined as people under 18 there's a very high probability as said they are responsible for about a half of spontaneous cereal hemorrhages and young adults the probability is still medium to high causing about one/ird of cerebral hematoma spontaneous hemorrhages Now in middle-aged adults the probability starts to decrease but if you see a hematoma especially in a patient without hypertension and in a hematoma that has a lower location definitely do it to rule it out And in old patients the probability is actually low Now now we're dealing with a situation in which the patient if a patient has a spontaneous bleed it's either going to be hypertensive or cerebral amaloid angio angopathy The chance that this patient has an AVM is less than 1% But not zero So to keep it easy so we see that the probability decreases with increasing age But just to keep it easy I just tell my residents just do a CTA and every spontaneous intra cerebral hemorrhage I'm not going to tell you what to do It's what I do because what can you do wrong and a patient with a spontaneous feal hemorrhage The patient is in a bad shape Your job as a radiologist is not just give the diagnosis of the hematoma but also try to find out the cause of the hematoma And in your older patients radiation exposure the dangers of administering uh iodine contrast are all very relative compared to the fact that a patient has a brain hemorrhage So just give it in everyone That's the easiest thing Okay let's move on from MRI to CT No from CT to MRI Once again the concept is quite simple An AVM looks like a bag of worms at least the Nidus So here we have a Nidus on TT and on T2- weighted images visible as a tangle of flow voids and here we see the AVM Nidus on a time of flight angio angography So basically same uh looks the same but now the signal is not hypo intense but is hyper intense because it's another sequence but it's at the end a bag of worms This can be very small So we remember this case This patient received an MRI because of seizures And if you look at the two- weighted images we see this cluster of flow voids located in the occipital lobe cortex or in the temporal occipital transition transition area And patients with epilepsy don't automatically receive a time offlight angography in our center they don't automatically receive catalinium So these tiny AVMs can be missed if you're not watching your examination carefully So in this patient of course when we saw this we wanted to confirm we already realized well this is going to be an AVM but we need to confirm it and we did that by uh doing a time offlight angography So we didn't have to give calinium to the patient We do the time of flight and we see the well it doesn't really look like a bag of worms but we see that these vascular structures or T1 hyper intense which means that they are filled with fast flowing blood So this is an AV shunt This is an AV malfformation because this is a Nidus and I don't know why I'm going back and forth on these slides but okay let's move on So okay the nidis is not difficult to recognize and we should also evaluate feeding arteries and draining veins which is also not that difficult So we can't really pinpoint each and every arterial feeder on uh MRI and CT studies like you can do on digital substraction angography but I don't think anyone is having any doubts as to the feeding artery of this arteriovenis malfformation over here quite clearly it is the right posterior cerebral artery So this is the nidos and the right posterior cerebral artery looks a lot thicker compared to the left one So it's hypertrophic as it has to feed this malf for over here And this is the same patient Let's now look at the draining veins Can we say something interesting about that we definitely can If we magnify this a bit This is a enlarged vein but it's not a superficial vein It's not a cortical vein No it's a deep vein So this is a patient with deep venous drainage This goes to the internal cerebral vein and from the internal cerebral vein into the gallon vein and the straight sinus So as said deep venous drainage is associated with an increased hemorrhage risk So this is something we don't like to see in arteriovenous malf forations There are other things we should scrutinize on our MRI or CT studies Here we have the bag of worms So this is the nidus of the AVM But look at this This flow voids looks a bit bigger right compared to the other ones Let's look at the time of flight study On the time of flight angography we see the nidis over here We see a feeding artery This is once again the right posterior cable artery But we also see two arterial anorisms These are located in the nitis and these are associated with an increased hemorrhage risk We even see a stain over here This could be a hemorrhage because um time of flight angography uh can also depict spontaneous T1 hyperintense lesions but it isn't It was not a hemorrhage This was a Venus anorism And the high signal is because it is filled with fast flowing blood Let's talk about anorisms in um arteriovenis malf formations This is the digital subtraction angography in the same patient This is the profile view Uh and we see over here the arteriovenenous malfformation and this is the intra nidal anorism one of the two we saw on the MRI images on the previous slide Arterial anorisms are reported in about 16% of brain AVMs So that's not very frequent but it's not rare either So it's something you have to look for because they are associated with an increased hemorrhage risk And well there are a lot of studies on the subject and as usual they tend to one study says this and the other one says that but often quoted and cited as the following that if you have an anorism uh in the vicinity or on a feeding artery or endonitis of an AVM your hemorrhage risk increases and it increases from 2 to 4% per year to 7 to 10% per year So that's not insignificant This is the Venus anorism The same patient as previously We're now looking at the Venus phase of the digit digital substraction angography So here we have the Venus anorism And can I say something interesting about that well not much They are not true anorisms because often they don't contain all layers of uh the vein and a true anorism contains all layers of uh the blood vessel uh they are rather kind of stretching with damage to the vessel layers but you know that's more academic they are out pouchings focal out pouchings of a draining vein let's call them venus anorisms and uh because we can't see the different uh vessel wall layers on imaging studies can be now are they associated with increased hemorrhage risk it's clear for me or I didn't really find found a lot of hard figures So a lot of studies that say yeah there is some increase Um I think it's better to just see them as a red flag if you see them uh in a brain AVM because they definitely point to a situation with increased Venus pressure especially in the location of the Venus anorism and unstable flow dynamics So it just points to a very unstable situation So I would see it as a red flag This is a patient with a lower hemorrhage and we did of course a CTA and there is the nidis of the AVM And if you look a bit more closely to the nidis of the AVM and the hemorrhage we also see an anorism Oh that wasn't my intention An anorism located over here It's located next to the hemorrhage So it's probably the cause of the hemorrhage This is the second example of an anorism I'm showing you and it's not located in the Nidus This is the digital subtraction angography of the same patient as previously and we see that the anerism is located in front of the Nidus This is what we call a distal flow related anorism The anerism is located on a small distal feeder near the nidis but not inside the nidus for comparison because we have three types of AVM associated anorisms For comparison let's look again at the intra nidal anorism located over here which is located inside the nidis And a last type and I haven't shown you an example yet is of a proximal flow related anorism So that's an anorism that's located on a main feeder but at a far away distance from the nidus So it's located on one of the major feeding arteries And the hemorrhage risk increases but it's most increased in anorisms that are closest to the nidis So especially those two the distal flow related and the intronidal anorisms or anorisms you should be careful with Okay I've talked a lot about hemorrhage risk factors So this is not science Well it's kind of science but you know how medicine is It's a bunch of statistics that are incorrectly interpreted and then we draw certain conclusions that are wrong Anyways what do we know about risk factors in brain AVMs because you have a lot not every AVM is different Can we draw some general conclusions on the likelihood that this particular AVM is going to hemorrhage and that one isn't it's difficult No one can predict the future But there are some things that return and uh if there is deep Venice drainage any kind So this patient can also have superficial venous drainage but if he also has deep venous drainage there's an increased hemorrhage risk If the AVM is located in a deep structure like talamus basil ganglia or infotenatorally like in the brain stem those are associated with an increased hemorrhage risk Anerism that are located superficially So low no AVMs that are located superficially So lower AVMs have a lower hemorrhage risk Now this may sound strange but a small Nidus size Smaller AVMs tend to rupture more frequently than do large AVMs And what could be an explanation for that well it might have to do with the fact that smaller AVMs are probably associated with an increased intraidal pressure The bigger your Nidus is the more pressure can be diverted along the various components of the Nidus If you only have a small Nidus well let's say there's a an increase in pressure it can't really be diverted as much So that probably explains why smaller AVMs tend to rupture more or easier Now this one we discussed and it's visible over here The presence of an intraidal or a distal flow related anorism and also proximal flow related but as you saw the closer to the nidis the higher the hemorrhage risk And finally the presence of a stenosis or some kind of obstruction on one of the draining veins or part of the Venus drainage system Now if you look at all these factors what do they all or mostly have in common the fact that these are situations that are often associated with increased venus pressure So if there is deep venous drainage there are often less draining veins sometimes even only one they are often uh they often have to take a longer course and are more torturous which increases the pressure in the venus system uh the small nides I explained intronidal anorisms well those are just uh weak points that are more prone to rupture and if you have a venus obstruction or stenosis that will also increase venus pressure So okay these are all hemorrhage risk factors So for diagnostic radiologist we don't have to make the decision on are we going to treat this and how are we going to treat this but these are all things we can keep in mind when evaluating an AVM on an imaging study to mention in our report and I'm going to at the end give a summary of everything I think is important to mention in your report First let's look at another example This is a patient with a deep hematoma in the region of the right basil ganglia And what do we see if you look at the CT angography we see a very small nidis over here Yes that was a nidis And here we see a draining vein This was the basil rosental vein So this kind of proves what I have said earlier This was a very small AVM definitely less than 3 cm and it has a deep venous drainage So two risk factors and this uh AVM has split Of course that doesn't prove anything They're just anecdotically So this is here the hematoma as you can see This is the feeding artery which is a perforating artery and perforating arteries well those are more difficult to treat surgically for instance because they are located inside the brain parenma So here we have it and there we have the very small nidus So remember small is dangerous when it comes to AVMs Okay I'm almost finished The last thing I would like to talk about is the Spetszler Martin scale Why it's old It has been introduced in the 80s if I'm not mistaken So it's like 40 years old already Just as old as I am Uh well I'm a bit older than that but never mind So it's old uh but still it's uh being used a lot even now with all we know because it's an easy way to communicate about AVMs So what is the Spzler Martin scale it's a scale that was developed in the 80s not to give an estimation of the hemorrhage risk of an AVM but to give an estimation of the surgical risk So Evan AVM had a low grade on the Spzler Martin grade It would be considered a low risk AVM and then surgery would be the preferred way to treat it If it had a high score on the Spler Martin grade well then an alternative option had to be sought and surgery was not advocated What are the components of the Spzler Martin scale there are there are three You have the size of the Nidus You have the location of the AVM and more specifically is the AVM located in an eloquent part of the brain What does that mean eloquent means it's a part of the brain where even minor damage can lead to severe neurological symptoms For instance the pre-entral gyus or the primary motor cortex That would be an eloquent brain area the language areas the primary visual cortex the internal capsule because that's where the tractorus uh the cortical spinal tract runs into the brain stem and the talamus and hypothalamus just to mention the most important ones but you get the idea that's an eloquent brain territory and the final criterium venus drenage Now when it comes to neid the size there are three types is the is the AVM smaller or the nid smaller than 3 cm is it between 3 and six or is it bigger than 6 cm and depending on it you give a score from 1 to three When it comes to the location if it is located in a non- eloquent brain area so an area that's not important functionally it gets score zero If it's located in let's say the primary visual cortex it gets score one And when it comes to the venus drainage if it's superficial only score zero and any deep dage gets score one Let's practice by using this case We see anidis and it is a nidis of 4 cm I'm just making it up It was smaller but it was 4 cm for me So we give it score two It's located in the talamus which is an eloquent brain area So it gets score one and there is deep Venice drainage You can't really see it but that was the case so just believe me Final score four Now Spetszel Martin score one and two are considered low surgical risk Score three is considered moderate surgical risk and score four and five are considered major surgical risk So this is considered a high surgical risk and in this patient surgery will not be advocated and an alternative option will be sought So treating AVMs is as said a topic on its own because I do not do interventional neuroraiology I am not the right person to talk about that Just know that you have the options of surgery interventional radiology and radio surgery and sometimes in combination with one another It's difficult because there are a lot of things to take into account and each technique has its advantages and its disadvantages The most difficult decision is as always what to do with the patient with an AVM that hasn't bled because nobody can predict the future and nobody can say if it's going to bleed and if it's worth taking the risk So it's a matter of statistics Okay let's summarize what are my key points Arterial mal arteriovenenous malf forations or congenital mal forations They probably arise due to failure of formation of the capillary bed We recognize them as anitis of abnormal vessels with direct AV shunting and they are mostly sporadic and rarely genetic and the only known genetic association is with randu weber osteo disease The clinical presentation is a hemorrhage in about half of cases seizures in a quarter and they are increasingly being found incidentally on imaging studies The hemorrhage risk is about 2 to 4% per year but there's a lot of variability over there I forgot to mention it but when we talked about the various risk factors to a hemorrhage uh if you have let's say a patient with an AVM located superficially and only superficial venus drainage the annual hemorrhage risk can decrease to less than 1% per year But if you have a small AVM located in let's say the brain stem with only deep Venice drainage your annual hemorrhage risk can increase to up to 30% So all these factors will change the annual hemorrhage risk So this is just true for like the entire group of unruptured AVMS but there are a lot of uh variabilities So treatment difficult endovvascular surgery radiotherapy must be decided on an individual basis And now more important what should you report as a radiologist the location of the AVM more specifically is the AVM located superficially lower in the cortical or cortical subcortical region Is it a deep AVM an infratoral AVM and is it located in an eloquent or a non-eloquent area of the brain look at anis and measure it because the size is important Larger AVMs have a worse score on the specular Martin grade because there is a higher surgical risk but smaller AVMs have a higher hemorrhage risk Look at your arterial feeders and report if the uh anorism is supplied by pile arteries or perforating arteries That's not always easy to say on uh CTA or MRI and easier on digital substraction and geography which is the gold standard and look for the presence of anorisms Look at the Venus drainage pattern Is it deep or superficial and do you have arguments for a Venus stenosis or obstruction also this is easier on digital subtraction angography And I didn't show any examples but do you see signs of previous hemorrhage also not unimportant because that means that the AVM has ruptured in the past And as said AVMs that have a history of hemorrhage have a higher risk to a hemorrhage again Okay that concludes my presentation on imaging of brain arteriovenous malf formations If you have any questions comments or feedback you can send me an email And this is going to be the first in a couple of presentations on vascular malf forations of the brain Thank you very much for watching