Hello, my name is Aarti Sarwan and in the next few minutes, I will be discussing the neuroimaging primer, basically covering a little more advanced neuroimaging than we just covered. No relevant disclosures in relation to this talk, but one big disclosure is it is a pretty big topic to cover in the limited time we have today. So I have provided a significant amount of case studies, which are abnormal pathology in the end of this presentation. Please go through these individual images and concepts at your own pace. These will not be covered in the limited time that we have today. We'll go over the cerebrovascular anatomy. We will review the basic principles of interpretation of CT angiogram, CT perfusion, CT peripheral angiogram, and review the basic classical pathology. And then we will go over some MRI imaging and interpretation for use in cerebrovascular disease. All of us should be familiar with the cerebrovascular anatomy in the neck, as well as the intracranial circulation, the aortic arch anatomy with the external carotid and internal carotid in the neck, the vertebral in the back of the head, and the circle of Willis intracranially. Please make sure you're familiar with the major branches for the posterior circulation, anterior spinal pica and ica, which have major stroke syndromes attached to them. And on the basilar side, scar, superior cerebellar artery, and the pontine artery. In the circle of Willis itself, the branches of the anterior cerebellar artery, middle cerebellar artery, internal carotid artery, especially in the neck, the ophthalmic, is a key one to know, and the posterior cerebellar artery itself. In the neck, please be familiar with the segments of the carotid. Typically, ICA does not have branches in the neck. All the branches of the ICA arise intracranially. And be aware of the cervical, the petrosegment, the other segment of key importance is the cavernous segment, the C4 segment, and then the ophthalmic segment, which gives rise to the ophthalmic artery, and largely the communicative segment, which gives the MCA and the ACA. The vessels intracranially are also named by the segments in proximity to the midline. So middle cerebellar artery is labeled as M1 as the first branch out of the ICA. Then when it branches further, the two branches are called M2, and then further distally M3, M4, based on the degree of branches. Similar numbering with A1 as the proximal ACA, and after the A-com origin, it's called the A2. And the P-com distinguishes the P1 and the P2. Typically, large vessel occlusion can be seen on the CT angio. Here you're looking at a CT angio-axial image. Starting from the posterior circulation, I'm pointing towards the basilar, you can start seeing the MCA on either side, and grossly, you can see some asymmetry in the distal part of the MCA, and in this particular case, the M2 junction, because this is the M1, and that's the M2. Such large vessel occlusions can also be seen sometimes on the CT non-contrast. So this is a CT angio, where we've actually given contrast, and the contrast is filling the blood vessels, and showing you this asymmetry of the M2. This, on the other hand, is a non-contrast head CT, that is showing you a thrombosed MCA, called the hyperdense MCA sign, and the corresponding infarcted area. The corresponding CT angio in this particular case shows the MCA on the opposite side, filling nicely with the contrast, but there is a MCA cut-off, where you can see the thrombus here. This is your PCAS. We also look for a little distal filling of these vessels. You can see here, the distal filling is less compared to the opposite side, so this seems like a more distal infarct in addition to the proximal MCA cut-off that we see here. You can also see this in the posterior circulation, so this is a CT angio of the posterior circulation that we're focusing on. The non-contrast CT on the right side is the hyperdense basilar version, and on this side we just saw the basilar cut-off, and on the CT angio reformatted images you can see the cut-off very nicely here. This would be your common carotid, giving rise to the thrombus in the internal carotid going up here, and you can distinguish the other vessel, this is your external carotid because it has lots of branches, and that's your thrombus going into the ICA. ICA does not have any branches in the neck. These are lateral views of CT angio of the neck. CT perfusion is obviously the latest imaging paradigm that has changed the acute interventional therapy in ischemic stroke and rests on the idea that we can measure cerebral blood flow by giving a contrast bolus. The contrast bolus goes through the heart to reach the brain arterial circulation, then the contrast goes to the capillaries and then gets fleshed out by the veins. And if we take pictures at a certain time of the cardiac cycle, we can use this to measure cerebral perfusion. Normal perfusion is 60-100 milliliters per gram per minute, and anything below that would be hyperperfusion. Now the degree of hyperperfusion depends upon the ischemic threshold. Initially drop in blood flow is called oligemia, where the patient stays asymptomatic but can become symptomatic in times of stress or increased demand for blood. If the hyperperfusion falls below the ischemic threshold, then the brain starts becoming symptomatic or ischemic. An initial part of ischemia is where the brain is still salvageable, which is called penumbra, where it's taking longer for the blood to get there. So it takes more than six seconds for the blood to get to the, say, the NCA. But if that continues, the penumbra, the delayed perfusion continues, brain will die and that would be the infarct and the blood flow will be interrupted. Less than 30 ml sustainable is the limit that we talk about and our job is to find the penumbra and find the right patients for thrombectomy. There are multiple protocols for CT angio and CTP. Typically both are done together, but in some certain circumstances you may only do perfusion depending on patient's contrast risk, but that is becoming more and more of a rarity. Please familiarize yourself with your institutional CTP protocol and I've put in some resources for you to read on this topic. Traditionally we used to do CT perfusion with CT angio where we'll talk about the MTT. MT is the mean transit time and you can see the scale here 0 to 15. Red means it's taking 15 seconds, blue means it's taking barely any time. And you can see the left MCA territory here kind of in the red zone, which is way more than six seconds. This is the average time for the blood to transit through the volume of the brain. So this tells you that the hose going to the garden is clogged or it's taking longer for the water to get there. The actual time we measure for arrival of the bolus, that's called Tmax. Although in the past these terms would be used synonymously, it is extremely important to distinguish these terms now because of some automated CT perfusion software terminology that we will discuss in a few slides. The cerebral blood flow is the compromised irrigation channel on the grass, means dry grass that is at the risk of dry grass that is kind of ischemic now and this will be a core infarct if it does not get affected by reperfusion therapies. Now this is the traditional CTP where enhanced MTT shows at risk corresponding to the decreased blood flow and cerebral blood volume would be the volume of the blood flow that is now completely dead and unsalvageable grass. This was traditional CTP. This would be classical salvageable penumbra where on this side you have blood flow that is compromised so it's towards the lower side. MTT is pretty high so high MTT low blood flow but intact blood volume. This would be typical penumbra but no infarct and this classical would be increased MTT decreased blood flow and decreased blood volume and this would be an infarct. So you would not take this patient for a thrombectomy while this patient would be suitable thrombectomy candidate. Most likely your institute has now transitioned to an automated CT perfusion software which are quite a few available no conflicts of interest here. In this particular case machine learning algorithms are used to basically look at the patient's CT perfusion maps and two of those labs are used to create an automated calculation of the patient's Tmax and the cerebral blood flow and remember here Tmax and cerebral blood flow and we'll talk about that. It is important to know how this is derived. Typically they will put an arterial density region of interest to kind of that would be the standard against which the arterial blood is measured. This would be typically on the ACA but sometimes can be on the MCA like in this case and then on sagittal sinus they will put the venous density of interest basically to see how much time did it take for the contrast to get to this arterial region of interest versus this venous region of interest and they will map this over time to make sure that this is a good image acquired by a good contrast bolus and this would have a sharp upstroke sharp downstroke will come back to the baseline and venous obviously will be delayed compared to the arterial and on the Hounsfield units this typically would be way more than 100 units. So this is the arterial output function and this is the venous output function and this is a good graph. They will also give you some graphs that will show you the technical limitations that went into getting an image. In this particular case the patient does not have any motion along any axis so this is a great image. The arterial region of interest was put in at the ACA, the sagittal sinus had the venous region of interest, the input functions look great, rapid upstroke less than 100 and more than 100 Hounsfield units so this looks great compared to this particular contrast bolus which was affected to some extent by motion at this part and then you have to decide whether the overall picture is affected by this or not. So these attenuation curves are extremely important to look at especially if you have a major perfusion deficit and this will be your satisfactory attenuation curve compared to this curve which is way less than 100 Hounsfield units and slow upstroke there's a pretty broad peak and these are not quite coming back to baseline and this may be due to low contrast bolus, low injection rate, contrasts are infiltrated or patients have very low cardiac output or there's a significant proximal arterial stenosis. So these are the caveats to know that help you in technical interpretation of abnormal images. The algorithm itself will give you initial maps from again two slabs, the typical maps are computed by two slabs, this is only one slab and they will give you cerebral blood flow and they will only give you blood flow less than 30% of the volume which is defined as the unsalvageable brain which typically corresponds to the DWI restriction that you will see on the MRI. Then it will also give you t max more than six seconds, what part of the brain is requiring more than six seconds for the contrast bolus to arrive there and that will define your penumbra or the mismatch and then they'll give you the mismatch volume which is typically the penumbra minus the infarcted core and that mismatch volume this part is what decides whether you want to salvage this brain and this patient qualifies for thrombectomy or not. They will also give you the mismatch ratio which rather than the difference there could be a ratio and typical patients that are candidates for thrombectomy will have a ratio of the hypoperfused to ischemic core of more than 1.8, in this case it's 2.4 and ischemic core volume of t max more than six seconds of less than 70 ml. For both CTP whether you do it by regular radiology means or automated software, please understand the concept of looking at the attenuation curves and how the contrast bolus timing can be affected by poor cardiac output, bilateral carotid stenosis, significantly irregular heart rate and atrial fibrillation, a significant proximal arterial stenosis especially on the right side like the inominate or some bad subclavian stenosis which can affect especially if the IV access is only available on that side and then poor placement of arterial and venous density regions of interest. Also remember CT perfusion maps will not display an infarct. Typically the Hounsfield units that are generated by an infarct have such low cerebral blood flow that to allow adequate interpretation these are removed. So infarct signals are removed from a CT perfusion so even if there's a gross evidence of encephalomalacia infarct it will not show on a CTP. Then comes cerebral angiogram. Now cerebral angiogram typically is kind of an x-ray of a patient that is undergoing a contrast bolus. This is a cerebral angiogram of the neck in which we are doing a lateral view and AP view. There are quite a few available but these are the two classical ones that we look at. In the neck external carotid artery has lots of branches which will be great for you to familiarize with. Internal carotid artery does not have branches in the neck. Intracranially this is a carotid injection where we're looking at the carotid and then the carotid gives rise to your MCA. This is your M1 segment and then it divides into the M2 segments so this is your anteroposterior view where we're looking at the ACA going towards the midline, A2 going upwards in the sagittal line and then MCA is going towards the sylvian fissure in towards the lateral part of the brain and then these are the distal branches. So this is anteroposterior you can kind of see the eyes here and you can see kind of the eyebrows here. Different branches can be identified here as well and obviously be aware of the segments. So this is AP view anteroposterior view of the carotid injection. We also do lateral view of the carotid injection. In this particular case we're looking from the side and this would be your carotid. MCA is typically coming at you so this would be your MCA and you typically will not see this like a spaghetti or a noodle. It will be coming at you and then this is your ACA going up. Different branches can be identified here as well. This would be another lateral view of internal carotid artery and this you can see the ACA very nicely here and all the branches of the ACA especially the pericallosal one kind of follows the corpus callosum curvature and then here you can see the PCA and the MCA is obviously coming out at you. It's nice to know kind of the branches on the anatomy. So this is your ACA, this is your MCA coming at you and this is your PCA going backwards. The vertebral injections given from the back also have the same views, the AP view and the lateral view. One of the AP views is called the Town's view and many times there will be oblique views as well. The best way to do this, get to know the anatomy is to keep looking at the views as the case coming along but here we'll be only discussing the AP and the lateral view. In this particular case you can see both the vertebral arteries, the basilar and the PCAs here and they're filling up the cerebellum and in this case the lateral view is the vertebral arteries, the PCAs and they're filling up the cerebellum and you can see individual arteries, the pica coming out from the vertebral, the ICA, SCAR and the PCAs as well. It's also important to pay attention to the posterior communicating arteries here since that can be an important source for collateral circulation in the case of a stroke. Cervical again it's important to know intracranially especially the different segments of the internal carotid artery and you must have heard these terminologies multiple times. So no branches in the neck, this is the cervical part, then the petrous and the lacerum part, it goes to the bony canal, the cavernous part goes to the cavernous sinus, then your clenoid part followed by the ophthalmic part which gives rise to the ophthalmic artery, another common source for collateral circulation followed by the communicating part that gives rise to the PCOM and to the caroidal and then breaks down into the ACA and the MCA. C1, C2, C3 and then your M1 and A1 segments on each side. This is your frontal view and this is your lateral view. You can see the ophthalmic artery branching out from the ophthalmic part and then you can see the internal caroidal artery here. This classification of C1 to C7 segments is called the Cincinnati classification or the Bouthillier nomenclature. Please familiarize yourself if your cerebrovascular group is using a different nomenclature which are prevalent and there are quite a few of them but this is the one that is most commonly reported. The intracranial segments themselves and the branches are also a learning point. In this particular case, you can kind of see the lenticular striate arteries and the recurrent artery of Hubner. You're looking at the anterior-posterior view ACA, this is your MCA and then this is your anterior-posterior view of the vertebral injection, the caroidal injection here, vertebral injection here. So V1, V2, V3 segments. V2, V3 would be extracranial, V4 is typically intracranial and then your pica coming out, your ica, your basilar and then your scar followed by the PCAs. This would be a good example of a ICA aneurysm with the caroidal injection and you can see this big aneurysm that has now been also seen on the anterior-posterior view. This is your MCA, this is your ACA, so your ICA is giving rise to this aneurysm that's also visible on the MRI here, pretty big over and you can see the artifacts from possibly another intervention done here in the test. This is what a dissection and associated thrombus would typically look like. On an angiogram, you can kind of see the vertebrae towards the back and you can kind of figure out the anterior-posterior based on the bony landmarks, that's the best way to look at it and then here you can see the teeth but typically when you're doing the injection, just by looking at the image sometimes can be difficult but once you're familiar with the AP view and the lateral view and figure out whether this is a caroidal injection or the vertebral injection, basic anatomy can help you correlate what you're looking at. So this particular case the contrast is interrupted, there is thrombus, dissection flap may or may not be typically visible, sometimes has to be inferred from the location and the nature of the thrombus itself. Compared to this particular image where you have right ICA injection, seems like an anterior-posterior view here and you can see the secular aneurysm coming out of the ACOM, this is your carotid, this is your MCA going to the other side and your ACA coming here and ACOM has an aneurysm and this is the same view after clipping of the aneurysm, so you can see the carotid in this particular case, the ACA you have no aneurysm here and then your distal ACA or A2 segment and this is your MCA segment. This is a common example of a sphere stenosis of carotid bifurcation and right ICA origin, this is a neck view for lateral view for the carotid injection and you can see how the luminal stenosis is pretty sphere and in this particular case they're also doing the oblique views. Another view of a patient with intervention that was done in which you can see how in which you can see how the pathology is really interrupting the flow here and then after stenting the patient has restoration of the flow and you can check perfusion by doing carotid and intracranial segment view as well. Moving on to MRI, we all are familiar with the advantages of MRI over CT scan, it's important to know components of the body that are not safe for exposure to a magnetic field, there is a standard source for looking up these things called MRI safety and your radiology department will have typical protocols. More and more pacemakers and intracranial devices are becoming MRI conditional which can be used in settings of low MRI like 1.5 Tesla, 3 Tesla versus stronger MRIs, so it's important to be aware of. MRI basically the physics depends on a magnetic field that is given to the brain in both the longitudinal axis and the transverse axis and the movement of the protons in the brain is kind of assessed typically they are haphazard all over the place but once you give them protons they all get aligned either parallel to the magnetic field or perpendicular to the magnetic field and then when you stop giving them the magnetic field the time it takes for the protons to come back to the baseline both in the longitudinal field and the transverse fields is called t1 and t2 and two different times are measured the repetition time and the echo time if both the times are really short this gives a very good black and white picture of the anatomy of the brain and that's called a t1 view and if both repetition times are long this gives you a really good picture of the kind of physiology of the brain whether there is pathology or not and that's called t2 images. I almost equate it to where you're trying to herd people into a line dance and how long does it take for people to kind of get aligned and there's a good resource site here for you to look at if you need more if you're more interested in learning the physics of MRI. This is a very oversimplistic view how I can explain it to MRI naive people. The t2 image again this is a very kind of learning way of describing MRI it is not the most scientific way but from a pathology perspective water is white on t2 images and fat is black so when I say white and black this is white again the MRI kosher terms are intensity hyper intense hypo intense iso intense but this is a very big overview of how to kind of look at pathology in the MRI. So water is white this is your CSF and gray matter which is the neurons has more water compared to the dendrites and the white matter which has the myelin sheath so it has more fat. So gray matter is water white matter is fat CSF is water so water is white fat is black water is white typically infarct which is basically brain converting into a mush of water tumors and demyelination which is not enough fat so demyelination is not enough myelin so the black signal is gone so lack of black equates white so water is white on t2 if you remember that much anything that's white on t2 is too much water or not enough fat bone air and flowing blood will be dark on everything remember that now t1's opposite water is black fat is white so in this particular case water would be black so in this gray matter is darker compared to the white matter and the white matter you can see corpus callosum is pretty white so and this is good for anatomy and again the gray matter would be darker than the white matter and the white matter looks more white that's t1 so t1 fat is white t2 water is white t1 gray matter is darker because water is darker t2 water is white so gray matter is lighter but fat is black so the white matter here is a little bit darker you can see a white lesion on a t2 image water is white so csf is white that's the typically first thing i look at so if csf is white that's a t2 image most likely and i see a t2 lesion here that doesn't belong here so it is too much water which is a spinal infarct or not enough fat that would be a demyelinating lesion again there are more nuances to mri images and different sequences it's a very oversimplistic view now flare is where water in brain can be due to edema or or because of csf we take t2 images so water is still white but we remove csf specific signals we don't remove the water signal we remove the csf signal so here water is white gray matter is whiter and here we took away the csf signal so csf becomes black but the gray matter continues to be lighter than the white matter so water is still white but csf is black what do you use it for if a signal is white on t2 and stays white on flare that basically means that csf signal was not contributed for by csf and demyelinating lesions can sometimes do that and we also use this to distinguish between lacunar spaces the virtuorobin spaces and edema or infarct this is another view of a picture where water is white so this is t2 gray matter is whiter so lighter compared to the white matter so this is a t2 image and you can see the edema too much water or not enough fat and in this particular case we took away the csf signal so the gray matter continues to be lighter so that's why it's a flare image and the vasogenic edema has stayed so flare and t2 hyper intense or water is white but flare csf is black DWI ADC images are specific sequences where we do a diffusion weighted image and then apparent diffusion coefficient to look for the brownian motion and the inherent entropy of normal brain to distinguish cytotoxic edema if there is cytotoxic edema remember i didn't use the word infarct if there is cytotoxic edema cell death less than seven days old the lesion would be white on DWI and the corresponding part will be black on ADC white on DWI black on ADC by seven days the ADC signal will match the DWI and then eventually will disappear and you need to be aware that any bright signal on t2 can cause both white ADC and DWI to be white as well that's called t2 shine through but otherwise cytotoxic edema less than seven days old will be white on DWI black on ADC and depending on the pathology the distribution will decide what the etiology is in this particular case you see a diffusion restriction throughout the cortical gray matter and the basal ganglia gray matter and this is a classical case of global anoxic injury causing cytotoxic edema from anoxic brain injury compared to an ischemic stroke which is causing a DWI whiteness here in the pons and you will look for corresponding ADC maps and if they're black this is less than seven days old. MRI is also great for posterior fossa um please spend some time to get yourself accustomed to the posterior fossa anatomy your midbrain looks like a mickey mouse or a koala beard these are the ears and this is the mouth pons looks like a molar tooth and then in the lower pons the fourth ventricle looks like the molar tooth and medulla looks like a inverted butterfly on the sagittal section midbrain pons medulla fourth ventricle your cerebellum and tentorium be aware of the cisterns the subarachnoid space and the convexity the lateral ventricles third ventricle connected by the foramen of munro the cerebral aqueduct followed by the fourth ventricle and the pre-medullary pre-pontine and the interpeduncular cisterns the quadrigeminal cistern and this is this would be your interpeduncular cisterns between the two peduncles your ambient cistern and then your quadrigeminal cistern. SWI GRE or T2 star is a specific MRI sequence that helps you figure out appearance of blood. This does not help you age it both blood bone and calcium will appear dark on these particular images and the amount of blood that you see will typically be much a kind of voluminous compared to what you will see on a typical ct scan or corresponding t2 t1 images so this blooming artifact please be aware of that but old cerebral microbleeds and fresh blood both will cause susceptibility weighted image on MRI and this is a common sequence we use for diagnosing amyloid angiopathy to look for the number of microbleeds. You can age ICH with MRI as well my personal big picture way of looking at MRI for aging bleed is just kind of thinking about the news so this is your t2 image how do i know that water is white the first thing i look at is water is white and the gray matter is lighter so that's t2 compared to water is black and the gray matter here you can see is darker so that's t1 this is t2 if it is dark on t1 and bright on t2 it's fresh blood 8 to 12 hours so dark on t1 bright on t2 fresh blood if both are dark yesterday's news if both are bright last month's news so these are the things that we sometimes use just to kind of make sure that the patient's pathology is known whether they're re-bleeding again and again and it only applies to intracranial blood there are other acronyms and formulas people use most commonly it be itty bitty baby doo doo i can't remember it for some reason but it's put here it was supposedly created by Dr. Smarni Topalos who's a famous neuroradiologist who teaches a lot of good neuroradiology sources that you can familiarize yourself with you can use contrast as well just like you use it with ct scan it's a different contrast iodine based contrast is used for ct scans but gadolinium is used for mri and the contrast these are actually safer even from the perspective of nephrogenic systemic fibrosis familiarize yourself with ring enhancing lesions and the differential diagnosis normal contrast enhancing t1 images typically what you do with a contrast but you can do t2 as well in certain circumstances and meningeal enhancement is another good pathology to get familiar with time of flight images are basically kind of ct angio version of mri called mra and very commonly used in pediatric stroke where we don't use ct angio as much and time of life does not need contrast it basically depends upon fast flow and flow related enhancement and reformatted images can give you the imaging of the intracranial circulation it is not good for distal circulation so m3 m4 levels are a little less visible on time of flight the higher power mris are making it better but in general mras are restricted to proximal circulation abnormalities when time of flight is used so i've put in some case studies here for you to do it on your own time i've tried to be as descriptive in what these pathologies are and i hope you enjoy learning neuroimaging thank you

neuroimaging

CT angiogram

CT perfusion

MRI imaging

cerebrovascular disease

cerebral angiography

DWI