Crash Course in Reading Neurological Imaging

Welcome back everyone. This is Dr. Rybinnik. Imaging is part of our daily professional life in neurology. So, let's give you a crash course in reading it. This video is rated MS for medical students due to basic concepts, clear language, and case-based examples. Medical student participation is advised. Our objectives for this talk are to introduce a case that will act as the glue keeping the sections together, to introduce an approach to reading imaging, to review major anatomical landmarks so you can find your way around the scans, to assess the degree of symmetry or asymmetry to allow you to spot abnormalities, to review the causes of hyperdensity and hypodensity on CT, And since we're on the topic of hypodensity, we will introduce the concept of cytotoxic and vasogenic edema. Edema will transition nicely into a discussion of the causes of hyper-and hypo-intensity on various MRI sequences. We will conclude with a review of patterns and locations of enhancement. And summarize. Let's start with a case. It just got real. You are asked to see the following patient. This is a 73-year-old previously healthy woman with weeks of memory difficulties, 10 days of increasing lethargy, 3 days of urinary incontinence, and now mild left-sided weakness and rigidity. Head CT was already conveniently done for you by the emergency department team. Radiology resident is passed out. Your neurology resident is writing a stroke code. So, it's up to you to diagnose this patient. First things first. It's the clinical history and not imaging that will lead you to the final diagnosis. Imaging can at best help you with a reasonable differential. So, whenever facing the unknown, it's useful to have an approach. First step is to identify the scan, the imaging sequence, and the slice. Then, look for symmetry. or, more appropriately, asymmetry. Next, we need to identify the lesion causing the asymmetry and its density and intensity, decide if contrast enhancement pattern may be useful, and locate the lesion in the extra-axial compartments outside the brain or intra-axial compartments in the brain parenchyma. Put all this data in a blender, puree it, and you get the delicious smoothie that is the final differential diagnosis. Yum! First up, landmark review. And for our landmarks, we'll use the head CT. Head CT without contrast is the most common imaging modality that we get. Contrast can be added to look for breakdown of blood-brain barrier, for example with neoplastic or infectious lesions, but that's better seen on MRI. CT can be used to obtain vascular imaging by rapidly tracking a bolus of contrast into the brain. This is called the CT angiogram. By the way, the difference between the CT with contrast and a CT angiogram is essentially the timing of the scan with respect to the contrast injection. CT angiograms are really powered to identify vessels, not brain parenchyma. And finally, CT-based perfusion can be used to estimate brain blood flow. But for the purpose of this talk, the only sequence we will focus on is the plain old non-contrast head CT. Here's a typical normal head CT. Axial slice with a cut through the orbits. You can even make out the lenses inside the eyeballs. By convention, the patient is lying in front of you on a table, feet first, like in the anatomy lab or the operating room. So the nose is pointing up, patient's left is on your right, and the back of the head is on the bottom of the slide. In this image, we're looking a bit higher in the brain. The slice is taken through the upper frontal and parietal lobes. How do I know that? Well, the slide is labeled. A better method is to locate the central sulcus. It makes a curve that looks like the Greek letter omega. Anything anterior to that sulcus is the frontal lobe, and posterior is the parietal lobe. Fun fact, the omega-looking bump in the precentral gyrus is also called the hand knob. This is where the motor control of the hand resides. Since we're on the topic of anatomical localization, we probably should quickly introduce the T1 sequence of the MRI. T1 is called the anatomical sequence because it shows white matter as white and gray matter as gray, as they would look in gross pathology. Can you still identify the omega sign? Yep, here it is on the scan. And if you need extra help, netter to the rescue. Scanning lower down, now we're at the level of the basal ganglia. Lateral ventricle is in the middle. Head of caudate is next to the frontal horn of the lateral ventricle. Thalami are separated by the third ventricle. Head of caudate and thalamus are separated from the lentiform nucleus by the internal capsule. More laterally, you will find the insular cortex covered by the anterior temporal lobe. Now, can you identify those structures on a T1 image? Head of caudate, thalamus, internal capsule, lentiform nucleus, insula, and anterior temporal lobe. Here's an illustration. Moving right along. This is a slice through the sylveon fissure. Incidentally, the orbits on eyeballs are back. What lives in a sylveon fissure? Yeah, the middle cerebral artery. Here it is, isodense to the brain parenchyma. It's generally very difficult to distinguish from the nearby brain. But, when you can make it out because it's brighter, that's when you know things are bad. More on that later. Here's the sylveon fissure on T1. As you can see on the localizing image in the upper left corner, T1 and CT slices are not necessarily at the same angle. So, on this T1, you can actually make out the Mickey Mouse looking midbrain. And once again, the Netter illustration. Speaking of the midbrain, here is the CT, axial cut, at the level of the midbrain. The midbrain is central here. with the CSF-filled basal cistern right behind it. The medial temporal lobe, or uncus, is lateral to the midbrain. Uncus as in uncle herniation. The uncus may herniate onto the midbrain, so needless to say, it's important to be able to locate it. More on that in the coma talk. Next. temporal horn of the lateral ventricle. Normally, as in this example, it's slit-like. If it becomes dilated, it's one of the earlier signs of hydrocephalus. Moving lower down, now we are at the mid-pontine level. Here's the pons with its brachys pontus, arms of the pons or cerebellar peduncles. It's as if the pons is reaching out to the cerebellum for a hug. While the pons and the cerebellum are hugging, the structure in the middle of the hug that's feeling all the love is the fourth ventricle. The place where Brachys Pontus meets the cerebellum is called the... wait for it... cerebellopontine angle. Later in the talk, we'll take a look at some mass lesions in this area. And here's what the pons looks like on T1. Where's the fourth ventricle? Getting hugged right in the middle. And here's the illustration. Now this slice is even more caudal, or lower. Here's the medulla with the fourth ventricle adjacent to the cerebellum. Look at how much better the resolution of MR is, especially in the posterior fossa. Here's the illustration of the same thing. And finally, the foramen magnum with the cervical spinal cord bathed in CSF. So now that you're an expert, let's make things a little more challenging. Can you identify the major landmarks on our patient's head CT? Pause the video now. First, let's identify the ventricles. frontal horn of the lateral ventricle, occipital horn of the lateral ventricle, and the third ventricle. Now you should be able to locate the basal ganglia structures. Caudate head, thalamus, separated from the lentiform nucleus by the internal capsule, then more laterally, the insula, covered by the anterior temporal lobe. Well done, Grasshopper! Progress to the next level. Let's talk about symmetry. Here is a non-contrast head CT, axial slice, through the basal ganglia. This image should haunt you in your nightmares by now. Let's locate the midline by drawing a straight line from the foc cerebri to the confluence of venous sinuses, right through the septum pellucidum in the middle of the lateral ventricle. There is no asymmetry here, and the midline is where it needs to be. Now, what about the slice through the pons? Also symmetric. By the way, whenever you see overlapping slices during this talk, both slices come from the same study and the same patient. What about in this picture? Is there asymmetry? Absolutely! Once you spot asymmetry, look for the lesion causing it. It has to be on the patient's right side, since the shift is towards the left. And here it is. A concave subacute subdural hematoma. What about this image? Again, there is significant mass effect and midline shift. But this time, the lesion is a massive acute right middle cerebral artery stroke. Don't worry about how I figured out what these lesions are. That's for the next section. Who's up for another challenge? Let's analyze a posterior fossa slice. Who says there is a lesion on the patient's right? The patient's left? No lesion? Let me highlight the pons, the fourth ventricle, and the cerebellum. Does that help? Yes, there's definitely a midline shift. Now, what's causing the mass effect? There's a mass at the right cerebellopontine angle. You see how difficult it is to pick up on CT? This happens to be a vestibular schwannoma. And finally, not all asymmetry is just about the midline shift. Does this image look symmetric to you? No. There are two subcortical hypodensities that are present on the patient's right side, but not on the left. This happens to be a patient with toxoplasmosis. Again, don't worry about how I knew that. All shall be revealed in its own good time. Let's return to our case once again. Is our patient's scan symmetric or asymmetric? Asymmetric. Now look for a lesion causing the asymmetry. And here it is. Now that you have an understanding of the basic approach to the head CT, it's time to talk about density. Step into the light, young padawan. Hyperdensities on CT are easy to spot and by design, which makes them an excellent diagnostic tool. Bright signal on CT is caused by mineralized structures such as calcium-rich bone and chronic calcified lesions. But also, head CT is wonderful at detecting acute blood with a sensitivity of above 90%. But before we get bloody, I want to remind you that not all hyperdensities are abnormal. Here is a non-contrast head CT, axial cut through the sylvian fissure. Calcified pineal, calcified choroid plexus, and bone are some examples of normal hyperdensities. What about this image? There are multiple calcified lesions in the left hemisphere and a small one in the right thalamus. I'm about to ruin your appetite. This is a calcified scolex of the tapeworm tinea soleum. You probably know this disease by another name, neurosystosarcosis. It's a common cause of seizures worldwide. On this image, the lesion is bright, but less dense and less bright than calcium and bone. This basal ganglia hyperdensity is an acute hemorrhage with some interventricular extension. Where is the hyperdensity on this scan? It looks like all the sulci were outlined by chalk. There is diffuse hyperdensity in the subarachnoid space, which is extra-axial, outside of the brain parenchyma. This is a great example of diffuse subarachnoid hemorrhage, with some intraventricular extension of blood. Once again, identify the midline shift, then look for the lesion causing it. There's an extra-axial, lens-shaped hyperdensity, respecting the suture lines. You can actually adjust the contrast setting on the CT to bone window. This will help you to identify bony abnormalities, like fractures, and landmarks, like sutures. At this point, it's probably painfully obvious that this is an example of epidural hemorrhage. If the last image was an example of an epidural, this is a subdural. Identify a midline shift, look for a lesion causing the shift, and identify the lesion location. We know this lesion is located in the subdural space, because it's concave and crossing suture lines, and therefore extra-axial. So, this game should be getting pretty boring by now. Time for another challenge. Pause the video and identify abnormal hyperdensities on these two scans from two different patients. The image on the left shows a serpentine hyperdensity outside of the brain in the sylvanian fissure. What lives in the sylvanian fissure? That's right, middle cerebral artery. The image on the right also shows a hyperdensity, but this time it's between the cerebral peduncles, in the interpronunculus cistern. This is the top of the basilar artery. You know that all acutely clotted blood looks hyperdense or bright on CT. So these dense vessel signs represent acute clots. Pretty important information to have when treating a patient with suspected acute ischemic stroke. to the dark side and learn to use the dark side of the force. The dark side is more challenging to grasp, but holds great power for those who can wield it. Fluid is less dense and appears dark on CT, so hypodensities usually reflect chronic lesions, cysts, or cerebral edema. Let's look at some examples. First up, chronic damage. This hypodensity is very well defined, wedge-shaped, same density as the CSF, and conforms to a vascular territory. The brain on the patient's right side looks shrunken, and the frontal horn of the lateral ventricle is expanded as a result. The proper name for this loss of brain tissue is encephalomalacia. So, you probably guessed by now that this is an example of a chronic right MCA stroke. Where is the encephalomalacia on this image? You're right. It's bifrontal. More so on the left, but the right is abnormal too. This does not conform to a vascular distribution. Bilateral frontal lobes are a common site of trauma, so this is an example of chronic traumatic brain injury. Now, how is this hypodensity different? Is it involving the brain parenchyma? Is it encephalomalacia? It looks well-defined, but also smooth, unlike the previous examples. The location of this lesion is extra-axial, with similar density to CSF, because it's a CSF-filled structure. This is an example of a frontotemporal arachnoid cyst, which is fairly benign, but may become large enough to exert mass effect and cause seizures. Get ready for your next challenge. Is there a hypodensity? If so, which side? Feel the dark side of the force calling to you. Difficult, isn't it? There's a large, faintly hypodense lesion within the right MCA territory. You may remember that acutely ischemic neurons swell. but that edema takes several hours to show up on the head CT. Let's just say 6-8 hours on average. So, it's very challenging to detect edema related to acute ischemic stroke on a head CT in the first 6 hours after symptom onset. In fact, most early head CTs in acute stroke patients are normal. This scan was actually done 8 hours after symptom onset. Here's another example. What's unique about the abnormality on this scan? Hopefully, you noticed the finger-like subcortical hypodensities. Looks like a giant hand gripping a small ball. Well, that ball is a brain metastasis. And the hypodense hand is another type of cerebral edema. So, you can see how the hypodensity on the CT can only take us so far. Time to introduce the MRI. Data, data, data, I cannot make bricks without clay. As the famous fictional detective Sherlock Holmes would say. It's worth noting that when placing a standard order for a non-contrast MRI of the brain, you typically get the following four-course meal. T1-weighted imaging for appetizer. Your main course will be a T2-weighted imaging with a side of T2 derivative called fluid attenuated inversion recovery, or FLIR. Arguably the most filling and useful sequences. The cheese and fruit plate would be diffusion-weighted imaging and its evil twin, the apparent diffusion coefficient, which are essentially designed to diagnose energy failure and ischemia. And for dessert, we have the gradient-recalled echo sequence. or GRE to detect hemorrhages. If you want to finish your meal with a cup of delicious coffee, may I suggest T1 with gadolinium contrast, but this must be ordered separately and you have to pay extra. MRI can also image vasculature, which requires an order for MR angiogram. Finally, there are numerous specialized sequences including fat suppression, perfusion, spectroscopy, tractography, etc. There are more fancy MRI sequences than Ben & Jerry's ice cream flavors. MR angiogram and special sequences are outside of the scope of this talk. You can't digest everything in one meal. So, take a normal head CT, zoom in, and adjust contrast. You can plainly make out two different tissue densities. The lighter, or less dense, is the gray matter. And the darker is the subcortical white matter. The junction where the two meet is called… wait for it… the gray-white junction. Now let's bring in the T2. Fluid is bright on T2. So identifying fluid-filled cell bodies of the cortical gray matter and distinguishing them from the darker subcortical white matter and the subcortical gray matter is much easier. What is actually happening on a cellular level in all of those crevices? I know, I know, you're allergic to basic science, but stay with me. Have you ever heard of the neurovascular unit? This unit consists of astrocyte foot processes wrapped around capillary endothelial cells, which are connected by tight junctions. Brain parenchyma filled with neurons is outside, and blood is inside the capillary lumen. You may call it a barrier between blood and brain. Despite that, the blood-brain barrier remains essentially intact early on. This is called cytotoxic, or cell body, edema, because it's toxic to the cells. Here is a patient with acute right middle cerebral artery stroke. Edema is everywhere. Gray matter, white matter. The cortical ribbon is completely lost. And the loss of this gray-white junction is a clue that we're dealing with cytotoxic edema of ischemia. T2-weighted imaging is much better at highlighting that fluid. Get it? Highlighting because it's bright? No? Alright. The edema is bright, but CSF is also bright. So, interpretation of this image is somewhat hampered by the CSF-filled sulci. Here's an idea. What if we subtract the CSF signal? Introducing... FLARE It's unmistakably related to T2, since grey matter is lighter than white matter, and fluid appears bright, with one important exception. The bright signal from CSF has been subtracted. And now, you can quickly identify the abnormality from across the room. Now, imagine that instead of energy failure, the integrity of the neurovascular unit is compromised. The tight junctions become leaky, allowing the plasma to escape into the interstitial space. This type of edema is called vasogenic, as in poor vessel integrity. This happens with neoplasms and cerebral abscesses, which secrete substances that increase blood-brain permeability, brain trauma, which can cause mechanical disruption, and even very high blood pressure that can overwhelm the neurovascular unit's ability to regulate fluid flow across the capillary endothelium. In this example, a brain metastasis caused these finger-like projections of vasogenic edema, which is much better seen on T2-weighted imaging. The edema essentially stops at the grey-white junction and does not affect the grey matter. The cortical ribbon is preserved. And you can make out the angry heterogeneous mass in the middle. And of course you can see the full extent of the edema better on flare. So one more time. Vasogenic edema because of failing neurovascular unit integrity, which can be caused by tumors, abscesses, trauma and severe hypertension. And cytotoxic edema. or cell-body edema caused by energy failure and ischemia. Got it? Look at the hypodensities on CT. How much more inferior they are to FLIR and T2. T2 and FLIR are superior by design. And just when you thought the dark side was winning, the light strikes back. With CT, it's all about density. With MRI, it's all about intensity. Bright signal is easiest to see, so we've been tackling edema first. If MRI were a book, the first chapter would be called, look on the bright side, it's swollen. So, we discussed non-contrast head CT, T1, T2, and flare. But when it comes to cytotoxic edema caused by ischemia, T2 and flare kind of behave like CT. It takes hours for a lesion to build up enough cerebral edema to show a bright signal. Diffusion-weighted imaging is designed to detect ischemia earlier, within the first 30 minutes from onset. A parent diffusion coefficient is DWI's evil twin. It's the anti-DWI. Ischemia will cause bright signal on DWI and dark signal on ADC. Well, all of this seems overly complicated. You're telling me that we need another sequence of MRI to be confirmed by yet another sequence of MRI? Unfortunately, yeah. And here's why. DWI is related to T2 and FLARE. So whatever's bright on DWI will also be bright on those sequences. Or it's probably more accurate to say that whatever's bright on T2 and FLARE will also be bright on DWI. This phenomenon is called T2 shine-through. T2 flare abnormalities shine through to the DWI. Now, look at the ADC. Is this an example of an acute stroke? No. ADC is bright, not dark, like in the last example. This is T2 shine-through. Bottom line, always check DWI against ADC to confirm acute ischemia. Our brightness motif continues. Here's another T21 flare pair of sequences from the same study. What kind of edema is this? Vasogenic or cytotoxic? Finger-like projections? Gray matter unaffected? Has to be vasogenic. This is an example of a brain abscess in right parietal lobe. Incidentally, Abscess-forming organisms usually spread through the bloodstream from a primary site. And of course, more of these emboli will end up in the vascular territory of the artery that supplies the majority of the hemisphere. So, it's not surprising that the most common locations for abscesses are in the frontal and parietal lobes, in the distribution of the middle cerebral artery. Again, we're really focusing on the bright signal here. From these sequences alone, you cannot unequivocally distinguish an abscess from another mass. You need other sequences of the MRI, but more on that later. Ah, speaking of masses. What's the most common neoplasm in the brain? That's right. Metastasis. What is the type of edema pictured on this T2 image? Right again. These are finger-like projections of vasogenic edema. And you can make out the small, well-defined round masses that are isointense to the brain parenchyma. Let's bring back our illustration of the cortical ribbon. Have you noticed that these metastatic lesions are near the gray-white junction? Nearly 80% of the mets are. That's because, like bacteria, metastases generally spread through the bloodstream. And arterioles at the gray-white junction are just small enough to trap traveling neoplastic cells. Lung and breast cancer metastases are the most common. This example happens to be lung cancer. But again, the imaging is never that specific. Tissue biopsy is generally necessary to confirm the tumor type. Now, say one of those metastases moves into the posterior fossa, exerting tremendous mass effect on the fourth ventricle. What is the abnormality on this flare sequence? Notice the symmetric smooth hyperintensity that is paraventricular. Under pressure, CSF is being pushed out of the ventricle across its walls into the brain parenchyma. So, this trans-appendymal flow of CSF is seen in obstructive hydrocephalus. Lateral ventricles are also certainly dilated. In this case, the hydrocephalus was caused by a posterior fossa mass, conducting the fourth ventricle, below the level of the slice. Let's move on to the next example of flare hyperintensity. This is a sagittal image, just lateral of midline, with the patient looking to your left. How would you describe the abnormalities? You probably said that these are avoid periventricular hyper-intense lesions. These are Dawson's fingers in patients with multiple sclerosis. And on the axial flare image, You can see them as well. Ovoid lesions. Now, that's a strangely specific appearance. Do you know why that happens? Well, there are so-called central veins running perpendicular to the ventricles. This is one of those fancy MRI sequences that we're not going to cover. In MS, immune cells exit these veins and penetrate the brain parenchyma here, causing this ovoid-appearing inflammation. How is this image different? Is this another example of a patient with multiple sclerosis? The hyperintensities are still paraventricular and subcortical, but they are more confluent, not ovoid. Also, the salsae are quite deep and prominent because of significant brain atrophy. Confluent subcortical lesions with brain atrophy in a patient with vascular risk factors are likely caused by small vessel ischemic disease. Judging by how ugly this image looks, you would probably expect this patient to have vascular dementia. Small vessel ischemic changes are so common that I'm showing them to you twice. Now that we discussed bright signals on T2 and flare, let's quickly mention bright signals on T1. Generally, bright signal on T1 is caused by paramagnetic substances like iron, copper, melanin, calcium, fat, protein-rich lesions, and subacute bleed. Here's an example of metastatic melanoma in the right eyeball. It's showing up as a T1 hyperintensity. And note that the orbital fat is also bright on T1. That's normal. How about this example? The bright signal in the basal ganglia corresponds to pathological copper accumulation. This is Wilson's disease, an autosomal recessive disorder where gene mutations causes impaired trafficking of copper in and through the hepatocytes, so it deposits in many organs and tissues, including the brain. And one more example. This well-circumscribed T1 hyperintensity corresponds to a mass at the foramen of Monroe, which is protein-rich. This mass is called a colloid cyst. Its claim to infamy is that it can act like a ball valve occluding the foramen of Monroe and causing hydrocephalus. This can happen so acutely and so severely that it can kill. Blood in the brain doesn't quite play by the rules, and its intensity on T1 and T2 actually evolves over time. In the first several days, the hematoma containing deoxyhemoglobin looks isointense on T1 and darkens on T2. Beyond three days from bleed onset, both T1 and T2 signals brighten as deoxyhemoglobin is converted to methemoglobin. Ultimately, deoxyhemoglobin is a very important hormone that is used to treat the brain's immune system. The side of hemorrhage is essentially replaced by a CSF-filled slit-like hole, which looks dark on T1 and bright on T2, as all fluid does. It sort of looks as if the brain has been stabbed, and there's usually a rim of hypo-intense signal on T2 representing the rim of hemocytarin, which is like a fingerprint left by the chronic hemorrhage. So, what's the stage of this hematoma? Right. It's late subacute stage, about 3-14 days. Both T1 and T2 are bright. Whew, that was a long section, but it had to be. MRI is really designed to highlight lesions, so most abnormalities will be hyper-intense. So, a brief summary. T2 and flare brightness will help you diagnose ischemic stroke, DWI is also indispensable for stroke, vasogenic edema due to metastatic disease, brain abscess, trans-ependymal flow due to hydrocephalus, inflammatory lesions like the ovoid lesions of multiple sclerosis, small vessel ischemic changes, and subacute hematoma. T1 brightness will help you diagnose metal deposition, like copper in Wilson's disease, other paramagnetic substances like melanin in this ocular melanoma, fatty lesions, which we didn't really cover, protein-rich substances like a colloid cyst, and subacute hematoma. I for one dislike mnemonics, because eventually all I remember is the words, not what they stand for, but if you need one, here it is. Shine and shimmer. Shine for T2, and shimmer for T1. stroke and subacute hematoma, hydrocephalus, ischemic and inflammatory lesions, neoplasms, and edema. Shimmer stands for subacute hematoma, iron, metals, melanoma, and rich in protein. Let's switch gears and talk about hypo-intense lesions. Lesions or structures that appear dark on T2 are essentially the same ones that appear bright on T1. Well, that was easy. We are once again talking about protein-rich masses, paramagnetic substances like iron, copper, melanin, and calcium. Flowing blood inside of blood vessels does not get imaged on T2 and also appears dark. And hematomas make their own rules. So acute hematoma looks dark on T2. Hey, no! Get out of here, Kylo Ren! The light side of the force rules MRI. That protein-rich colloid cyst we just saw as bright on T1 appears dark on T2. Flowing blood is not imaged, so it creates dark signals called flow voids on T2. These are T2 slices from the same study. Pause the video now and identify all the flow voids on these images. Time for a Circle of Willis review. Internal carotids, MCAs, PCOMs, and PCAs. But there's just one more. The confluence of venous sinuses. What's wrong with this T2 image? Maybe an illustration will help. There's a flow void corresponding to the ICA on the patient's left. Where's the flow void on the right? Absent! The right carotid is occluded. I'm giving you this next example because this radiological sign has a really cool name. This disease is called panthothenate kinase-associated neurodegeneration. Panthothenate is vitamin B5. Please don't memorize it. It's rare. Essentially, it's an autosomal recessive disorder where a mutation disrupts energy and lipid metabolism and can lead to accumulation of iron or copper in the brain. Remember Wilson's disease? Was that lesion bright or dark on T1? Bright. And T2 is opposite of T1. So the dark signal on T2 in this image is iron accumulation. The bright signal is gliosis, which corresponds to the iron damaged basal ganglia. This sign is called the eye of the tiger. And finally, acute hematoma. On this T2 image, this basal ganglia hematoma appears dark, surrounded by a small rim of bright edema. Is this vasogenic or cytotoxic edema? I'll leave that to you to look up. We talked all about dark signals on T2, but T1 is generally only useful as a baseline against which to compare hyperintensities on T2 and other sequences. Hypointensities on T1 are chronic lesions and fluid. And chronic lesions are filled with fluid, so it makes perfect sense. T1 in this respect behaves a bit like CT. For example, you can use T1 to see chronic lesions in multiple sclerosis. These are known as black holes. Incidentally, the number of black holes correlates with disability. Quick recap. T2 hyperintensities are caused by protein-rich lesions, like the colloid cyst, flow voids corresponding to normal circle of Willis vessels and venous sinuses, deposition of paramagnetic substances, like iron in this example, and acute hematoma. When it comes to hypo-intensity on T1, it behaves like the non-contrast HET-CT, showing fluid-filled lesions as dark. And if you need a mnemonic, how about FAB-PIC? Fabulous picture. Flowing or acute blood, protein, iron and other paramagnetic substances, and chronic lesions on T1. One more time, let's do it together. What is hyper-intense on T2? Cytotoxic edema of stroke, vasogenic edema of tumors and abscesses, trans-appendable flow of hydrocephalus, subacute bleed, and inflammatory lesions of disorders like MS. Fluid that is bright on T2 appears dark on T1. So, edema and chronic lesions are hypo-intense. What is hypo-intense on T2? Paramagnetic substances, protein-rich lesions, flowing blood, and acute bleed. What is hyper-intense on T1? Baromagnetic substances, protein-rich lesions, fat, and subacute bleed. Oh, do not. There is no try. Now, let's get back to our patient. Brief reminder, the non-contrast HET-CT showed a large confluent white matter hypodensity and a small hyperdensity. Let's proceed with T1. What's dark on T1? Edema. So, T1 did not provide any more useful information than CT, so we generally skip it. Next up, T2 and flare. You can obviously see the huge hyper-intensity on T2, and even more so on flare. Considering that we spend a huge chunk of the talk identifying edema, which edema is this? These are finger-like projections of subcortical vasogenic edema, which spares the cortex. Do you see any other abnormalities? There is one more mystery left to solve. That little hypo-intensity in the right frontal lobe. I keep forgetting what is usually dark on T2? Pertinacious lesion, flow voids, paramagnetic substances like iron, and acute blood. Aha! So this is a lesion with tremendous amount of vasogenic edema and small acute hemorrhagic focus. but we're still missing one crucial piece of information to help us crack this case. And without further ado, we enter the final stage of our journey together, the patterns and locations of enhancement. Return to the light you must! Start with a normal T1 sequence. Now add gadolinium contrast. Gadolinium is a ferromagnetic substance that, when injected intravenously, shows up as a bright signal on T1. So you can see arteries, like MCA and PCA, and veins, like the left transverse venous sinus. Also, fat, which is bright on T1, has been subtracted on this contrast image to avoid confusing it with contrast. You can barely make out the orbits here, which are typically fat-filled. Let's bring in some other, more rostral slices from the same study, and fill them with contrast. Again, you can see the serpentine vessels traveling in the sulci. and deep draining vein and superior sagittal sinus. Bottom line, seeing contrast outside the brain in the sulci may be normal, but since gadolinium does not cross the blood-brain barrier, you should never see enhancement in the brain parenchyma or the meninges when the neurovascular units are intact. So let's talk about what happens when the blood-brain barrier is not intact. Here are some common patterns of enhancement. Dural tail, leptomeningeal, and periventricular are extraaxial. Outside the brain, ring, subcortical nodular, and mural nodule are intraaxial in the brain parenchyma. There are certainly more types of enhancements than this, but this is a nice sampling. First up, the focal dural enhancement. Here is an example of an enhancing dural mass. How am I so confident stating that this is a dural mass? Well, two things. First, there is a dark room of CSF that separates the mass from the brain parenchyma. This so-called CSF cleft tells us that the mass is extra-axial. And second, there is this dural tail. This is a meningioma, the most common extra-axial neoplasm. Meningiomas are usually benign, but can grow large, cause vasogenic edema, and invade venous sinuses. By the way, dural tail mainly represents reactive changes to the meningioma, and not necessarily neoplastic involvement. Also, dural tail is definitely a distinguishing feature, but unfortunately it's not unique to meningiomas. Dural mets can have dural tails too, but you will likely have other signs of metastatic disease, like weight loss, multiple lesions, so on and so forth. Most meningiomas are supertentorial. But how about this example? CSF cleft? Check. Smooth homogeneously enhancing dural mass? Check. Dural tail? Check. This is another meningioma, but this time at the cerebellopontine angle. Now what about this lesion? How is this different? CSF cleft is present, so it's an extraaxial mass. It's located at the cerebellopontine angle and causes mass effect on the pons and 4th ventricle. Enhancement seems more heterogeneous than the meningioma on the left. There is a tail of sorts, but actually it's more of a head than a tail, since the tumor extends from the internal acoustic canal. This is an example of vestibular schwannoma. And that internal acoustic canal involvement is what helps us diagnose it. Now, let's talk about leptomeningeal enhancement. Normal sulci are fluid-filled and appear dark on T1. So what's abnormal? There's leptomeningeal enhancement all over. And in a patient with fever and nuclear rigidity, you would be seriously concerned about bacterial meningitis. Well, of course you're concerned. You ordered this MRI of the brain with and without contrast, right? Not all leptomeningeal enhancement is so obvious. In fact, most of it is quite subtle. Can you spot the areas of enhancement on these two slices from the same study? There's some serpentine leptomeningeal enhancement, but also enhancement around the pons and the medulla. This is an example of basilar meningitis caused by tuberculosis. Meningitis is actually the most common presentation of TB and CNS. Since basilar meninges are involved, cranial nerves which are covered by those meninges are often dysfunctional as well. We're talking about cranial nerve 6, 7 for example. And one more thing, CSF flow is often obstructed, causing hydrocephalus. This is yet another example of leptomeningeal invasion and enhancement, but this time by metastasis. You've seen example of solid mass metastases at the gray-white junction. That's the more common location. Here, the tumor cells travel to the meninges. Leptomeningeal carcinomatosis, or carcinomatous meningitis, is a rare complication of advanced cancer, usually breast or lung, just like any metastasis. Notice the enhancement around the pons and the cerebellar folia, especially on the sagittal slice. I want to stress the fact how similar these three examples of LEPTOMENINGEAL ENHANCEMENT appear on imaging. It's not the imaging. but the history and CSF sampling that will help you differentiate between bacterial meningitis, tuberculous meningitis, and carcinomatous meningitis. Since we're talking about metastasis, we might as well jump ahead and look at some examples of subcortical nodular enhancement. You've seen this patient's T2 imaging before, when we discussed vasogenic edema. Call out the lesions. multiple well-circumscribed enhancing mass lesions at the grey-white junction, surrounded by vasogenic edema, which appears dark on T1. With the appropriate history, this scan is the definition of metastatic disease. What's abnormal here? Once again, subcortical, well-circumscribed enhancing nodule. And on this slice? and on this coronal slice, with patient looking at you and patients left on your right. So, what are these? Metastases? I don't see any edema. These look suspiciously ovoid and paraventricular. These are acute multiple sclerosis lesions. Next up, a medical student favorite, ring enhancement. Ring enhancement generally implies a lesion with a necrotic center. And your first example is a brain abscess. Smooth ring enhancing capsule. Necrotic center. Finger-like projections of subcortical visogenic edema that is hypo-intense on T1. What about this lesion? Another abscess? You should know by now not to fall for that trick. It's a ring enhancing lesion, I give you that, but the ring enhancement is irregular. and there's involvement of the corpus callosum. This is a high-grade invasive glioma, otherwise known as glioblastoma multiforme. Now, these are hand-picked cases, but often the distinction is less obvious. If only there were another MRI sequence to help! Enter DWI and its evil twin, the ADC. The lesion is bright on DWI and dark on ADC. True restriction of diffusion, and not a T2 shine-through. Remember that we talked about DWI in the setting of stroke and energy failure. Brain abscess is another situation where DWI has high sensitivity and specificity. Moving right along. Multiple ring-enhancing lesions with predilection for basal ganglia. What if I told you that this patient has HIV? This is toxoplasmosis. And you will often be asked to differentiate from another very similar lesion that occurs in this patient population. CNS lymphoma. Can you spot the difference? There is a large, solitary, ring-enhancing mass of lymphoma, as opposed to numerous small ring-enhancing lesions of toxoplasmosis. The lymphoma dyslesion is in the basal ganglia in this case, but it doesn't have to be. And in general, it's much more difficult to distinguish the two pathologies. This is where another pattern of enhancement can help. Another enhancement. Lymphoma has predilection for the paraventricular region and sub-appendimal spread, appendima being the wall of the ventricle. Look at this neoplasm coating the ventricles. Toxoplasmosis does not affect the ventricles. This is lymphoma. And the final enhancement pattern that we will discuss is the mural nodule, mainly because it's so bizarre. Imagine that this is a 14-year-old boy who slowly developed truncal ataxia to the left side, especially noticeable while playing sports. His MRI with gadolinium showed this lesion. It has a cystic component, fluid is hypointense on T1, and an enhancing mural nodule. You can also see that on the sagittal cut with the patient looking to the left side of the slide. This is an example of pyelocytic astrocytoma, the most common infratentorial neoplasm in the pediatric age group less than 20 years of age. This astrocytoma is generally benign, but enhancement unfortunately suggests higher grade of tumor. Remember the following enhancement patterns. Dural, meningioma and schwannoma. Leptomeningeal, bacterial, tuberculous, and carcinomatous meningitis. subcortical nodular, metastases, acute MS lesions, ring enhancing, abscess, toxoplasmosis, and lymphoma, which affects the ventricles causing paraventricular enhancement, and mural nodule enhancement generally caused by pyelocytic estrocytoma. And if you really need a mnemonic, try this one. MR lights the damage very nicely. M for mural nodule, R for ring, L for leptomeningeal, D for dural tail, V for paraventricular, and N for nodular subcortical. Now for the last time, let's get back to our case. Remember our lesion had tremendous amount of vasogenic edema, and small acute hemorrhagic focus. And this is the contrast-enhanced T1 sequence. What is the pattern of enhancement? This is ring enhancement, although it's irregular and has some satellite lesions. This lesion crosses the corpus callosum. At this point, the cat's out of the bag. This is a high-grade glioma. I'm sorry to end on such a somber note, but I needed this case to glue together multiple MRI sequences. But on the bright side, we're done with this talk and we're going to move on to a really quick summary. After obtaining clinical history, we typically start with a head CT, identify the slice and landmarks. Basal ganglia is a good place to start. Look for asymmetry. and the lesion-causing asymmetry. On CT, calcified structures and acute blood are bright, and chronic lesions and edema, or anything fluid-filled, is dark. Next, brain MRI without contrast. Remember that you typically get T1, T2, FLARE, DWI, ADC, and GRE as a bundle when you order a non-contrast MRI. An active lesion in the brain is usually identifiable by the edema it causes. So, we should look at flare first, since hyperintensity identifies edema. Vasogenic edema is the result of failing neurovascular unit integrity, which can be caused by tumors, abscesses, trauma, and even severe hypertension. And cytotoxic, or cell-body edema is caused by energy failure and ischemia. In general, bright signal on T2 may be caused by edema like strokes, tumors, abscesses, hydrocephalus, inflammatory pathology such as multiple sclerosis lesion, and subacute hematoma. Dark signal on T2 may be caused by paramagnetic substances such as iron, copper, melanin, Protein-rich lesions, flow voids of normal circle of Willis vessels and venous sinuses, and acute bleed within 3 days from onset. Next, if you're suspecting a pathology that will break the blood-brain barrier, like inflammation, infection, neoplasm, order an MRI with and without contrast. And remember your patterns of enhancement. Dural, like meningioma or schwannoma. Leptomeningeal, like bacterial, fungal, and carcinomatous meningitis. paraventricular, ring in the case of lesions with necrotic core like abscesses, toxoplasmosis, and lymphoma, subcortical nodular like metastasis to the gray-white junction or paraventricular multiple sclerosis lesions, and mural nodule such as in the case of pilocytic estrocytoma. T1 without contrast is generally less useful for diagnosis, with a few exceptions. but can serve as a baseline template to which all other sequences can be compared. Bright signal on T1 typically suggests paramagnetic substances, like iron, copper in Wilson's disease, melanin and melanoma, protein-rich lesions, like colloid cyst, fat, and subacute bleeding 3-14 days from onset. Dark signal on T1 basically corresponds to chronic lesions, which are filled with fluid. DWI-ADC pair is extremely important for detection of early brain ischemia as well as brain abscesses. True restriction of diffusion, or energy failure, is when a bright lesion on DWI looks dark on ADC. In patients where we're concerned about stroke, we may even review the sequence first, right after the CT and before flare. Finally, remember that blood on MRI plays by its own rules. Acute blood becomes dark on T2 within the first 3 days and slowly brightens on T1. Beyond 3 days, methemoglobin creates a bright signal on T1 and T2. And that is all. Thank you for joining me. You should feel incredibly exhausted, but hopefully wiser. Go forth and read imaging studies. Compare your impression with a radiologist's report. That's how you learn. Practice makes perfect. Until next time, bye! I can show you the world, shining, shimmering, splendid. Tell me, princess, now when did you last let your heart decide? I can open your eyes.

Medical student participation is advised. Our objectives for this talk are to introduce a case that will act as the glue keeping the sections together, to introduce an approach to reading imaging, to review major anatomical landmarks so you can find your way around the scans, to assess the degree of symmetry or asymmetry to allow you to spot abnormalities, to review the causes of hyperdensity and hypodensity on CT, And since we're on the topic of hypodensity, we will introduce the concept of cytotoxic and vasogenic edema. Edema will transition nicely into a discussion of the causes of hyper-and hypo-intensity on various MRI sequences. We will conclude with a review of patterns and locations of enhancement.

And summarize. Let's start with a case. It just got real. You are asked to see the following patient.

This is a 73-year-old previously healthy woman with weeks of memory difficulties, 10 days of increasing lethargy, 3 days of urinary incontinence, and now mild left-sided weakness and rigidity. Head CT was already conveniently done for you by the emergency department team. Radiology resident is passed out. Your neurology resident is writing a stroke code. So, it's up to you to diagnose this patient.

First things first. It's the clinical history and not imaging that will lead you to the final diagnosis. Imaging can at best help you with a reasonable differential. So, whenever facing the unknown, it's useful to have an approach. First step is to identify the scan, the imaging sequence, and the slice.

Then, look for symmetry. or, more appropriately, asymmetry. Next, we need to identify the lesion causing the asymmetry and its density and intensity, decide if contrast enhancement pattern may be useful, and locate the lesion in the extra-axial compartments outside the brain or intra-axial compartments in the brain parenchyma. Put all this data in a blender, puree it, and you get the delicious smoothie that is the final differential diagnosis.

Yum! First up, landmark review. And for our landmarks, we'll use the head CT. Head CT without contrast is the most common imaging modality that we get. Contrast can be added to look for breakdown of blood-brain barrier, for example with neoplastic or infectious lesions, but that's better seen on MRI. CT can be used to obtain vascular imaging by rapidly tracking a bolus of contrast into the brain.

This is called the CT angiogram. By the way, the difference between the CT with contrast and a CT angiogram is essentially the timing of the scan with respect to the contrast injection. CT angiograms are really powered to identify vessels, not brain parenchyma. And finally, CT-based perfusion can be used to estimate brain blood flow. But for the purpose of this talk, the only sequence we will focus on is the plain old non-contrast head CT.

Here's a typical normal head CT. Axial slice with a cut through the orbits. You can even make out the lenses inside the eyeballs.

By convention, the patient is lying in front of you on a table, feet first, like in the anatomy lab or the operating room. So the nose is pointing up, patient's left is on your right, and the back of the head is on the bottom of the slide. In this image, we're looking a bit higher in the brain. The slice is taken through the upper frontal and parietal lobes. How do I know that?

Well, the slide is labeled. A better method is to locate the central sulcus. It makes a curve that looks like the Greek letter omega.

Anything anterior to that sulcus is the frontal lobe, and posterior is the parietal lobe. Fun fact, the omega-looking bump in the precentral gyrus is also called the hand knob. This is where the motor control of the hand resides.

Since we're on the topic of anatomical localization, we probably should quickly introduce the T1 sequence of the MRI. T1 is called the anatomical sequence because it shows white matter as white and gray matter as gray, as they would look in gross pathology. Can you still identify the omega sign?

Yep, here it is on the scan. And if you need extra help, netter to the rescue. Scanning lower down, now we're at the level of the basal ganglia. Lateral ventricle is in the middle. Head of caudate is next to the frontal horn of the lateral ventricle.

Thalami are separated by the third ventricle. Head of caudate and thalamus are separated from the lentiform nucleus by the internal capsule. More laterally, you will find the insular cortex covered by the anterior temporal lobe. Now, can you identify those structures on a T1 image?

Head of caudate, thalamus, internal capsule, lentiform nucleus, insula, and anterior temporal lobe. Here's an illustration. Moving right along. This is a slice through the sylveon fissure.

Incidentally, the orbits on eyeballs are back. What lives in a sylveon fissure? Yeah, the middle cerebral artery.

Here it is, isodense to the brain parenchyma. It's generally very difficult to distinguish from the nearby brain. But, when you can make it out because it's brighter, that's when you know things are bad.

More on that later. Here's the sylveon fissure on T1. As you can see on the localizing image in the upper left corner, T1 and CT slices are not necessarily at the same angle. So, on this T1, you can actually make out the Mickey Mouse looking midbrain.

And once again, the Netter illustration. Speaking of the midbrain, here is the CT, axial cut, at the level of the midbrain. The midbrain is central here.

with the CSF-filled basal cistern right behind it. The medial temporal lobe, or uncus, is lateral to the midbrain. Uncus as in uncle herniation.

The uncus may herniate onto the midbrain, so needless to say, it's important to be able to locate it. More on that in the coma talk. Next.

temporal horn of the lateral ventricle. Normally, as in this example, it's slit-like. If it becomes dilated, it's one of the earlier signs of hydrocephalus. Moving lower down, now we are at the mid-pontine level. Here's the pons with its brachys pontus, arms of the pons or cerebellar peduncles.

It's as if the pons is reaching out to the cerebellum for a hug. While the pons and the cerebellum are hugging, the structure in the middle of the hug that's feeling all the love is the fourth ventricle. The place where Brachys Pontus meets the cerebellum is called the...

wait for it... cerebellopontine angle. Later in the talk, we'll take a look at some mass lesions in this area.

And here's what the pons looks like on T1. Where's the fourth ventricle? Getting hugged right in the middle. And here's the illustration.

Now this slice is even more caudal, or lower. Here's the medulla with the fourth ventricle adjacent to the cerebellum. Look at how much better the resolution of MR is, especially in the posterior fossa. Here's the illustration of the same thing. And finally, the foramen magnum with the cervical spinal cord bathed in CSF.

So now that you're an expert, let's make things a little more challenging. Can you identify the major landmarks on our patient's head CT? Pause the video now.

First, let's identify the ventricles. frontal horn of the lateral ventricle, occipital horn of the lateral ventricle, and the third ventricle. Now you should be able to locate the basal ganglia structures.

Caudate head, thalamus, separated from the lentiform nucleus by the internal capsule, then more laterally, the insula, covered by the anterior temporal lobe. Well done, Grasshopper! Progress to the next level. Let's talk about symmetry.

Here is a non-contrast head CT, axial slice, through the basal ganglia. This image should haunt you in your nightmares by now. Let's locate the midline by drawing a straight line from the foc cerebri to the confluence of venous sinuses, right through the septum pellucidum in the middle of the lateral ventricle.

There is no asymmetry here, and the midline is where it needs to be. Now, what about the slice through the pons? Also symmetric. By the way, whenever you see overlapping slices during this talk, both slices come from the same study and the same patient.

What about in this picture? Is there asymmetry? Absolutely!

Once you spot asymmetry, look for the lesion causing it. It has to be on the patient's right side, since the shift is towards the left. And here it is. A concave subacute subdural hematoma.

What about this image? Again, there is significant mass effect and midline shift. But this time, the lesion is a massive acute right middle cerebral artery stroke. Don't worry about how I figured out what these lesions are. That's for the next section.

Who's up for another challenge? Let's analyze a posterior fossa slice. Who says there is a lesion on the patient's right?

The patient's left? No lesion? Let me highlight the pons, the fourth ventricle, and the cerebellum. Does that help?

Yes, there's definitely a midline shift. Now, what's causing the mass effect? There's a mass at the right cerebellopontine angle. You see how difficult it is to pick up on CT? This happens to be a vestibular schwannoma.

And finally, not all asymmetry is just about the midline shift. Does this image look symmetric to you? No. There are two subcortical hypodensities that are present on the patient's right side, but not on the left.

This happens to be a patient with toxoplasmosis. Again, don't worry about how I knew that. All shall be revealed in its own good time. Let's return to our case once again. Is our patient's scan symmetric or asymmetric?

Asymmetric. Now look for a lesion causing the asymmetry. And here it is.

Now that you have an understanding of the basic approach to the head CT, it's time to talk about density. Step into the light, young padawan. Hyperdensities on CT are easy to spot and by design, which makes them an excellent diagnostic tool.

Bright signal on CT is caused by mineralized structures such as calcium-rich bone and chronic calcified lesions. But also, head CT is wonderful at detecting acute blood with a sensitivity of above 90%. But before we get bloody, I want to remind you that not all hyperdensities are abnormal. Here is a non-contrast head CT, axial cut through the sylvian fissure. Calcified pineal, calcified choroid plexus, and bone are some examples of normal hyperdensities.

What about this image? There are multiple calcified lesions in the left hemisphere and a small one in the right thalamus. I'm about to ruin your appetite.

This is a calcified scolex of the tapeworm tinea soleum. You probably know this disease by another name, neurosystosarcosis. It's a common cause of seizures worldwide. On this image, the lesion is bright, but less dense and less bright than calcium and bone. This basal ganglia hyperdensity is an acute hemorrhage with some interventricular extension.

Where is the hyperdensity on this scan? It looks like all the sulci were outlined by chalk. There is diffuse hyperdensity in the subarachnoid space, which is extra-axial, outside of the brain parenchyma.

This is a great example of diffuse subarachnoid hemorrhage, with some intraventricular extension of blood. Once again, identify the midline shift, then look for the lesion causing it. There's an extra-axial, lens-shaped hyperdensity, respecting the suture lines. You can actually adjust the contrast setting on the CT to bone window.

This will help you to identify bony abnormalities, like fractures, and landmarks, like sutures. At this point, it's probably painfully obvious that this is an example of epidural hemorrhage. If the last image was an example of an epidural, this is a subdural. Identify a midline shift, look for a lesion causing the shift, and identify the lesion location.

We know this lesion is located in the subdural space, because it's concave and crossing suture lines, and therefore extra-axial. So, this game should be getting pretty boring by now. Time for another challenge.

Pause the video and identify abnormal hyperdensities on these two scans from two different patients. The image on the left shows a serpentine hyperdensity outside of the brain in the sylvanian fissure. What lives in the sylvanian fissure? That's right, middle cerebral artery. The image on the right also shows a hyperdensity, but this time it's between the cerebral peduncles, in the interpronunculus cistern.

This is the top of the basilar artery. You know that all acutely clotted blood looks hyperdense or bright on CT. So these dense vessel signs represent acute clots. Pretty important information to have when treating a patient with suspected acute ischemic stroke.

to the dark side and learn to use the dark side of the force. The dark side is more challenging to grasp, but holds great power for those who can wield it. Fluid is less dense and appears dark on CT, so hypodensities usually reflect chronic lesions, cysts, or cerebral edema. Let's look at some examples.

First up, chronic damage. This hypodensity is very well defined, wedge-shaped, same density as the CSF, and conforms to a vascular territory. The brain on the patient's right side looks shrunken, and the frontal horn of the lateral ventricle is expanded as a result.

The proper name for this loss of brain tissue is encephalomalacia. So, you probably guessed by now that this is an example of a chronic right MCA stroke. Where is the encephalomalacia on this image?

You're right. It's bifrontal. More so on the left, but the right is abnormal too.

This does not conform to a vascular distribution. Bilateral frontal lobes are a common site of trauma, so this is an example of chronic traumatic brain injury. Now, how is this hypodensity different?

Is it involving the brain parenchyma? Is it encephalomalacia? It looks well-defined, but also smooth, unlike the previous examples. The location of this lesion is extra-axial, with similar density to CSF, because it's a CSF-filled structure. This is an example of a frontotemporal arachnoid cyst, which is fairly benign, but may become large enough to exert mass effect and cause seizures.

Get ready for your next challenge. Is there a hypodensity? If so, which side?

Feel the dark side of the force calling to you. Difficult, isn't it? There's a large, faintly hypodense lesion within the right MCA territory. You may remember that acutely ischemic neurons swell.

but that edema takes several hours to show up on the head CT. Let's just say 6-8 hours on average. So, it's very challenging to detect edema related to acute ischemic stroke on a head CT in the first 6 hours after symptom onset.

In fact, most early head CTs in acute stroke patients are normal. This scan was actually done 8 hours after symptom onset. Here's another example.

What's unique about the abnormality on this scan? Hopefully, you noticed the finger-like subcortical hypodensities. Looks like a giant hand gripping a small ball. Well, that ball is a brain metastasis. And the hypodense hand is another type of cerebral edema.

So, you can see how the hypodensity on the CT can only take us so far. Time to introduce the MRI. Data, data, data, I cannot make bricks without clay. As the famous fictional detective Sherlock Holmes would say. It's worth noting that when placing a standard order for a non-contrast MRI of the brain, you typically get the following four-course meal.

T1-weighted imaging for appetizer. Your main course will be a T2-weighted imaging with a side of T2 derivative called fluid attenuated inversion recovery, or FLIR. Arguably the most filling and useful sequences.

The cheese and fruit plate would be diffusion-weighted imaging and its evil twin, the apparent diffusion coefficient, which are essentially designed to diagnose energy failure and ischemia. And for dessert, we have the gradient-recalled echo sequence. or GRE to detect hemorrhages.

If you want to finish your meal with a cup of delicious coffee, may I suggest T1 with gadolinium contrast, but this must be ordered separately and you have to pay extra. MRI can also image vasculature, which requires an order for MR angiogram. Finally, there are numerous specialized sequences including fat suppression, perfusion, spectroscopy, tractography, etc.

There are more fancy MRI sequences than Ben & Jerry's ice cream flavors. MR angiogram and special sequences are outside of the scope of this talk. You can't digest everything in one meal. So, take a normal head CT, zoom in, and adjust contrast. You can plainly make out two different tissue densities.

The lighter, or less dense, is the gray matter. And the darker is the subcortical white matter. The junction where the two meet is called… wait for it… the gray-white junction. Now let's bring in the T2.

Fluid is bright on T2. So identifying fluid-filled cell bodies of the cortical gray matter and distinguishing them from the darker subcortical white matter and the subcortical gray matter is much easier. What is actually happening on a cellular level in all of those crevices? I know, I know, you're allergic to basic science, but stay with me. Have you ever heard of the neurovascular unit?

This unit consists of astrocyte foot processes wrapped around capillary endothelial cells, which are connected by tight junctions. Brain parenchyma filled with neurons is outside, and blood is inside the capillary lumen. You may call it a barrier between blood and brain.

Despite that, the blood-brain barrier remains essentially intact early on. This is called cytotoxic, or cell body, edema, because it's toxic to the cells. Here is a patient with acute right middle cerebral artery stroke. Edema is everywhere. Gray matter, white matter.

The cortical ribbon is completely lost. And the loss of this gray-white junction is a clue that we're dealing with cytotoxic edema of ischemia. T2-weighted imaging is much better at highlighting that fluid.

Get it? Highlighting because it's bright? No?

Alright. The edema is bright, but CSF is also bright. So, interpretation of this image is somewhat hampered by the CSF-filled sulci.

Here's an idea. What if we subtract the CSF signal? Introducing...

FLARE It's unmistakably related to T2, since grey matter is lighter than white matter, and fluid appears bright, with one important exception. The bright signal from CSF has been subtracted. And now, you can quickly identify the abnormality from across the room. Now, imagine that instead of energy failure, the integrity of the neurovascular unit is compromised.

The tight junctions become leaky, allowing the plasma to escape into the interstitial space. This type of edema is called vasogenic, as in poor vessel integrity. This happens with neoplasms and cerebral abscesses, which secrete substances that increase blood-brain permeability, brain trauma, which can cause mechanical disruption, and even very high blood pressure that can overwhelm the neurovascular unit's ability to regulate fluid flow across the capillary endothelium.

In this example, a brain metastasis caused these finger-like projections of vasogenic edema, which is much better seen on T2-weighted imaging. The edema essentially stops at the grey-white junction and does not affect the grey matter. The cortical ribbon is preserved. And you can make out the angry heterogeneous mass in the middle. And of course you can see the full extent of the edema better on flare.

So one more time. Vasogenic edema because of failing neurovascular unit integrity, which can be caused by tumors, abscesses, trauma and severe hypertension. And cytotoxic edema. or cell-body edema caused by energy failure and ischemia. Got it?

Look at the hypodensities on CT. How much more inferior they are to FLIR and T2. T2 and FLIR are superior by design.

And just when you thought the dark side was winning, the light strikes back. With CT, it's all about density. With MRI, it's all about intensity. Bright signal is easiest to see, so we've been tackling edema first.

If MRI were a book, the first chapter would be called, look on the bright side, it's swollen. So, we discussed non-contrast head CT, T1, T2, and flare. But when it comes to cytotoxic edema caused by ischemia, T2 and flare kind of behave like CT. It takes hours for a lesion to build up enough cerebral edema to show a bright signal.

Diffusion-weighted imaging is designed to detect ischemia earlier, within the first 30 minutes from onset. A parent diffusion coefficient is DWI's evil twin. It's the anti-DWI.

Ischemia will cause bright signal on DWI and dark signal on ADC. Well, all of this seems overly complicated. You're telling me that we need another sequence of MRI to be confirmed by yet another sequence of MRI?

Unfortunately, yeah. And here's why. DWI is related to T2 and FLARE.

So whatever's bright on DWI will also be bright on those sequences. Or it's probably more accurate to say that whatever's bright on T2 and FLARE will also be bright on DWI. This phenomenon is called T2 shine-through.

T2 flare abnormalities shine through to the DWI. Now, look at the ADC. Is this an example of an acute stroke? No.

ADC is bright, not dark, like in the last example. This is T2 shine-through. Bottom line, always check DWI against ADC to confirm acute ischemia.

Our brightness motif continues. Here's another T21 flare pair of sequences from the same study. What kind of edema is this?

Vasogenic or cytotoxic? Finger-like projections? Gray matter unaffected?

Has to be vasogenic. This is an example of a brain abscess in right parietal lobe. Incidentally, Abscess-forming organisms usually spread through the bloodstream from a primary site.

And of course, more of these emboli will end up in the vascular territory of the artery that supplies the majority of the hemisphere. So, it's not surprising that the most common locations for abscesses are in the frontal and parietal lobes, in the distribution of the middle cerebral artery. Again, we're really focusing on the bright signal here.

From these sequences alone, you cannot unequivocally distinguish an abscess from another mass. You need other sequences of the MRI, but more on that later. Ah, speaking of masses. What's the most common neoplasm in the brain?

That's right. Metastasis. What is the type of edema pictured on this T2 image? Right again.

These are finger-like projections of vasogenic edema. And you can make out the small, well-defined round masses that are isointense to the brain parenchyma. Let's bring back our illustration of the cortical ribbon. Have you noticed that these metastatic lesions are near the gray-white junction?

Nearly 80% of the mets are. That's because, like bacteria, metastases generally spread through the bloodstream. And arterioles at the gray-white junction are just small enough to trap traveling neoplastic cells. Lung and breast cancer metastases are the most common. This example happens to be lung cancer.

But again, the imaging is never that specific. Tissue biopsy is generally necessary to confirm the tumor type. Now, say one of those metastases moves into the posterior fossa, exerting tremendous mass effect on the fourth ventricle. What is the abnormality on this flare sequence? Notice the symmetric smooth hyperintensity that is paraventricular.

Under pressure, CSF is being pushed out of the ventricle across its walls into the brain parenchyma. So, this trans-appendymal flow of CSF is seen in obstructive hydrocephalus. Lateral ventricles are also certainly dilated.

In this case, the hydrocephalus was caused by a posterior fossa mass, conducting the fourth ventricle, below the level of the slice. Let's move on to the next example of flare hyperintensity. This is a sagittal image, just lateral of midline, with the patient looking to your left. How would you describe the abnormalities?

You probably said that these are avoid periventricular hyper-intense lesions. These are Dawson's fingers in patients with multiple sclerosis. And on the axial flare image, You can see them as well.

Ovoid lesions. Now, that's a strangely specific appearance. Do you know why that happens?

Well, there are so-called central veins running perpendicular to the ventricles. This is one of those fancy MRI sequences that we're not going to cover. In MS, immune cells exit these veins and penetrate the brain parenchyma here, causing this ovoid-appearing inflammation. How is this image different? Is this another example of a patient with multiple sclerosis?

The hyperintensities are still paraventricular and subcortical, but they are more confluent, not ovoid. Also, the salsae are quite deep and prominent because of significant brain atrophy. Confluent subcortical lesions with brain atrophy in a patient with vascular risk factors are likely caused by small vessel ischemic disease.

Judging by how ugly this image looks, you would probably expect this patient to have vascular dementia. Small vessel ischemic changes are so common that I'm showing them to you twice. Now that we discussed bright signals on T2 and flare, let's quickly mention bright signals on T1. Generally, bright signal on T1 is caused by paramagnetic substances like iron, copper, melanin, calcium, fat, protein-rich lesions, and subacute bleed. Here's an example of metastatic melanoma in the right eyeball.

It's showing up as a T1 hyperintensity. And note that the orbital fat is also bright on T1. That's normal.

How about this example? The bright signal in the basal ganglia corresponds to pathological copper accumulation. This is Wilson's disease, an autosomal recessive disorder where gene mutations causes impaired trafficking of copper in and through the hepatocytes, so it deposits in many organs and tissues, including the brain. And one more example. This well-circumscribed T1 hyperintensity corresponds to a mass at the foramen of Monroe, which is protein-rich.

This mass is called a colloid cyst. Its claim to infamy is that it can act like a ball valve occluding the foramen of Monroe and causing hydrocephalus. This can happen so acutely and so severely that it can kill.

Blood in the brain doesn't quite play by the rules, and its intensity on T1 and T2 actually evolves over time. In the first several days, the hematoma containing deoxyhemoglobin looks isointense on T1 and darkens on T2. Beyond three days from bleed onset, both T1 and T2 signals brighten as deoxyhemoglobin is converted to methemoglobin. Ultimately, deoxyhemoglobin is a very important hormone that is used to treat the brain's immune system. The side of hemorrhage is essentially replaced by a CSF-filled slit-like hole, which looks dark on T1 and bright on T2, as all fluid does.

It sort of looks as if the brain has been stabbed, and there's usually a rim of hypo-intense signal on T2 representing the rim of hemocytarin, which is like a fingerprint left by the chronic hemorrhage. So, what's the stage of this hematoma? Right. It's late subacute stage, about 3-14 days.

Both T1 and T2 are bright. Whew, that was a long section, but it had to be. MRI is really designed to highlight lesions, so most abnormalities will be hyper-intense. So, a brief summary. T2 and flare brightness will help you diagnose ischemic stroke, DWI is also indispensable for stroke, vasogenic edema due to metastatic disease, brain abscess, trans-ependymal flow due to hydrocephalus, inflammatory lesions like the ovoid lesions of multiple sclerosis, small vessel ischemic changes, and subacute hematoma.

T1 brightness will help you diagnose metal deposition, like copper in Wilson's disease, other paramagnetic substances like melanin in this ocular melanoma, fatty lesions, which we didn't really cover, protein-rich substances like a colloid cyst, and subacute hematoma. I for one dislike mnemonics, because eventually all I remember is the words, not what they stand for, but if you need one, here it is. Shine and shimmer.

Shine for T2, and shimmer for T1. stroke and subacute hematoma, hydrocephalus, ischemic and inflammatory lesions, neoplasms, and edema. Shimmer stands for subacute hematoma, iron, metals, melanoma, and rich in protein. Let's switch gears and talk about hypo-intense lesions. Lesions or structures that appear dark on T2 are essentially the same ones that appear bright on T1.

Well, that was easy. We are once again talking about protein-rich masses, paramagnetic substances like iron, copper, melanin, and calcium. Flowing blood inside of blood vessels does not get imaged on T2 and also appears dark. And hematomas make their own rules. So acute hematoma looks dark on T2.

Hey, no! Get out of here, Kylo Ren! The light side of the force rules MRI. That protein-rich colloid cyst we just saw as bright on T1 appears dark on T2. Flowing blood is not imaged, so it creates dark signals called flow voids on T2.

These are T2 slices from the same study. Pause the video now and identify all the flow voids on these images. Time for a Circle of Willis review. Internal carotids, MCAs, PCOMs, and PCAs.

But there's just one more. The confluence of venous sinuses. What's wrong with this T2 image?

Maybe an illustration will help. There's a flow void corresponding to the ICA on the patient's left. Where's the flow void on the right?

Absent! The right carotid is occluded. I'm giving you this next example because this radiological sign has a really cool name.

This disease is called panthothenate kinase-associated neurodegeneration. Panthothenate is vitamin B5. Please don't memorize it. It's rare. Essentially, it's an autosomal recessive disorder where a mutation disrupts energy and lipid metabolism and can lead to accumulation of iron or copper in the brain.

Remember Wilson's disease? Was that lesion bright or dark on T1? Bright.

And T2 is opposite of T1. So the dark signal on T2 in this image is iron accumulation. The bright signal is gliosis, which corresponds to the iron damaged basal ganglia. This sign is called the eye of the tiger.

And finally, acute hematoma. On this T2 image, this basal ganglia hematoma appears dark, surrounded by a small rim of bright edema. Is this vasogenic or cytotoxic edema?

I'll leave that to you to look up. We talked all about dark signals on T2, but T1 is generally only useful as a baseline against which to compare hyperintensities on T2 and other sequences. Hypointensities on T1 are chronic lesions and fluid. And chronic lesions are filled with fluid, so it makes perfect sense. T1 in this respect behaves a bit like CT.

For example, you can use T1 to see chronic lesions in multiple sclerosis. These are known as black holes. Incidentally, the number of black holes correlates with disability. Quick recap. T2 hyperintensities are caused by protein-rich lesions, like the colloid cyst, flow voids corresponding to normal circle of Willis vessels and venous sinuses, deposition of paramagnetic substances, like iron in this example, and acute hematoma.

When it comes to hypo-intensity on T1, it behaves like the non-contrast HET-CT, showing fluid-filled lesions as dark. And if you need a mnemonic, how about FAB-PIC? Fabulous picture.

Flowing or acute blood, protein, iron and other paramagnetic substances, and chronic lesions on T1. One more time, let's do it together. What is hyper-intense on T2? Cytotoxic edema of stroke, vasogenic edema of tumors and abscesses, trans-appendable flow of hydrocephalus, subacute bleed, and inflammatory lesions of disorders like MS. Fluid that is bright on T2 appears dark on T1.

So, edema and chronic lesions are hypo-intense. What is hypo-intense on T2? Paramagnetic substances, protein-rich lesions, flowing blood, and acute bleed. What is hyper-intense on T1?

Baromagnetic substances, protein-rich lesions, fat, and subacute bleed. Oh, do not. There is no try. Now, let's get back to our patient. Brief reminder, the non-contrast HET-CT showed a large confluent white matter hypodensity and a small hyperdensity.

Let's proceed with T1. What's dark on T1? Edema.

So, T1 did not provide any more useful information than CT, so we generally skip it. Next up, T2 and flare. You can obviously see the huge hyper-intensity on T2, and even more so on flare.

Considering that we spend a huge chunk of the talk identifying edema, which edema is this? These are finger-like projections of subcortical vasogenic edema, which spares the cortex. Do you see any other abnormalities?

There is one more mystery left to solve. That little hypo-intensity in the right frontal lobe. I keep forgetting what is usually dark on T2? Pertinacious lesion, flow voids, paramagnetic substances like iron, and acute blood. Aha!

So this is a lesion with tremendous amount of vasogenic edema and small acute hemorrhagic focus. but we're still missing one crucial piece of information to help us crack this case. And without further ado, we enter the final stage of our journey together, the patterns and locations of enhancement.

Return to the light you must! Start with a normal T1 sequence. Now add gadolinium contrast. Gadolinium is a ferromagnetic substance that, when injected intravenously, shows up as a bright signal on T1.

So you can see arteries, like MCA and PCA, and veins, like the left transverse venous sinus. Also, fat, which is bright on T1, has been subtracted on this contrast image to avoid confusing it with contrast. You can barely make out the orbits here, which are typically fat-filled.

Let's bring in some other, more rostral slices from the same study, and fill them with contrast. Again, you can see the serpentine vessels traveling in the sulci. and deep draining vein and superior sagittal sinus. Bottom line, seeing contrast outside the brain in the sulci may be normal, but since gadolinium does not cross the blood-brain barrier, you should never see enhancement in the brain parenchyma or the meninges when the neurovascular units are intact. So let's talk about what happens when the blood-brain barrier is not intact.

Here are some common patterns of enhancement. Dural tail, leptomeningeal, and periventricular are extraaxial. Outside the brain, ring, subcortical nodular, and mural nodule are intraaxial in the brain parenchyma. There are certainly more types of enhancements than this, but this is a nice sampling. First up, the focal dural enhancement.

Here is an example of an enhancing dural mass. How am I so confident stating that this is a dural mass? Well, two things. First, there is a dark room of CSF that separates the mass from the brain parenchyma. This so-called CSF cleft tells us that the mass is extra-axial.

And second, there is this dural tail. This is a meningioma, the most common extra-axial neoplasm. Meningiomas are usually benign, but can grow large, cause vasogenic edema, and invade venous sinuses. By the way, dural tail mainly represents reactive changes to the meningioma, and not necessarily neoplastic involvement. Also, dural tail is definitely a distinguishing feature, but unfortunately it's not unique to meningiomas.

Dural mets can have dural tails too, but you will likely have other signs of metastatic disease, like weight loss, multiple lesions, so on and so forth. Most meningiomas are supertentorial. But how about this example? CSF cleft? Check.

Smooth homogeneously enhancing dural mass? Check. Dural tail?

Check. This is another meningioma, but this time at the cerebellopontine angle. Now what about this lesion? How is this different? CSF cleft is present, so it's an extraaxial mass.

It's located at the cerebellopontine angle and causes mass effect on the pons and 4th ventricle. Enhancement seems more heterogeneous than the meningioma on the left. There is a tail of sorts, but actually it's more of a head than a tail, since the tumor extends from the internal acoustic canal.

This is an example of vestibular schwannoma. And that internal acoustic canal involvement is what helps us diagnose it. Now, let's talk about leptomeningeal enhancement. Normal sulci are fluid-filled and appear dark on T1. So what's abnormal?

There's leptomeningeal enhancement all over. And in a patient with fever and nuclear rigidity, you would be seriously concerned about bacterial meningitis. Well, of course you're concerned. You ordered this MRI of the brain with and without contrast, right? Not all leptomeningeal enhancement is so obvious.

In fact, most of it is quite subtle. Can you spot the areas of enhancement on these two slices from the same study? There's some serpentine leptomeningeal enhancement, but also enhancement around the pons and the medulla. This is an example of basilar meningitis caused by tuberculosis. Meningitis is actually the most common presentation of TB and CNS.

Since basilar meninges are involved, cranial nerves which are covered by those meninges are often dysfunctional as well. We're talking about cranial nerve 6, 7 for example. And one more thing, CSF flow is often obstructed, causing hydrocephalus. This is yet another example of leptomeningeal invasion and enhancement, but this time by metastasis.

You've seen example of solid mass metastases at the gray-white junction. That's the more common location. Here, the tumor cells travel to the meninges. Leptomeningeal carcinomatosis, or carcinomatous meningitis, is a rare complication of advanced cancer, usually breast or lung, just like any metastasis. Notice the enhancement around the pons and the cerebellar folia, especially on the sagittal slice.

I want to stress the fact how similar these three examples of LEPTOMENINGEAL ENHANCEMENT appear on imaging. It's not the imaging. but the history and CSF sampling that will help you differentiate between bacterial meningitis, tuberculous meningitis, and carcinomatous meningitis. Since we're talking about metastasis, we might as well jump ahead and look at some examples of subcortical nodular enhancement.

You've seen this patient's T2 imaging before, when we discussed vasogenic edema. Call out the lesions. multiple well-circumscribed enhancing mass lesions at the grey-white junction, surrounded by vasogenic edema, which appears dark on T1.

With the appropriate history, this scan is the definition of metastatic disease. What's abnormal here? Once again, subcortical, well-circumscribed enhancing nodule. And on this slice? and on this coronal slice, with patient looking at you and patients left on your right.

So, what are these? Metastases? I don't see any edema. These look suspiciously ovoid and paraventricular.

These are acute multiple sclerosis lesions. Next up, a medical student favorite, ring enhancement. Ring enhancement generally implies a lesion with a necrotic center.

And your first example is a brain abscess. Smooth ring enhancing capsule. Necrotic center.

Finger-like projections of subcortical visogenic edema that is hypo-intense on T1. What about this lesion? Another abscess?

You should know by now not to fall for that trick. It's a ring enhancing lesion, I give you that, but the ring enhancement is irregular. and there's involvement of the corpus callosum. This is a high-grade invasive glioma, otherwise known as glioblastoma multiforme. Now, these are hand-picked cases, but often the distinction is less obvious.

If only there were another MRI sequence to help! Enter DWI and its evil twin, the ADC. The lesion is bright on DWI and dark on ADC.

True restriction of diffusion, and not a T2 shine-through. Remember that we talked about DWI in the setting of stroke and energy failure. Brain abscess is another situation where DWI has high sensitivity and specificity.

Moving right along. Multiple ring-enhancing lesions with predilection for basal ganglia. What if I told you that this patient has HIV? This is toxoplasmosis. And you will often be asked to differentiate from another very similar lesion that occurs in this patient population.

CNS lymphoma. Can you spot the difference? There is a large, solitary, ring-enhancing mass of lymphoma, as opposed to numerous small ring-enhancing lesions of toxoplasmosis. The lymphoma dyslesion is in the basal ganglia in this case, but it doesn't have to be. And in general, it's much more difficult to distinguish the two pathologies.

This is where another pattern of enhancement can help. Another enhancement. Lymphoma has predilection for the paraventricular region and sub-appendimal spread, appendima being the wall of the ventricle.

Look at this neoplasm coating the ventricles. Toxoplasmosis does not affect the ventricles. This is lymphoma.

And the final enhancement pattern that we will discuss is the mural nodule, mainly because it's so bizarre. Imagine that this is a 14-year-old boy who slowly developed truncal ataxia to the left side, especially noticeable while playing sports. His MRI with gadolinium showed this lesion. It has a cystic component, fluid is hypointense on T1, and an enhancing mural nodule.

You can also see that on the sagittal cut with the patient looking to the left side of the slide. This is an example of pyelocytic astrocytoma, the most common infratentorial neoplasm in the pediatric age group less than 20 years of age. This astrocytoma is generally benign, but enhancement unfortunately suggests higher grade of tumor.

Remember the following enhancement patterns. Dural, meningioma and schwannoma. Leptomeningeal, bacterial, tuberculous, and carcinomatous meningitis.

subcortical nodular, metastases, acute MS lesions, ring enhancing, abscess, toxoplasmosis, and lymphoma, which affects the ventricles causing paraventricular enhancement, and mural nodule enhancement generally caused by pyelocytic estrocytoma. And if you really need a mnemonic, try this one. MR lights the damage very nicely. M for mural nodule, R for ring, L for leptomeningeal, D for dural tail, V for paraventricular, and N for nodular subcortical. Now for the last time, let's get back to our case.

Remember our lesion had tremendous amount of vasogenic edema, and small acute hemorrhagic focus. And this is the contrast-enhanced T1 sequence. What is the pattern of enhancement?

This is ring enhancement, although it's irregular and has some satellite lesions. This lesion crosses the corpus callosum. At this point, the cat's out of the bag.

This is a high-grade glioma. I'm sorry to end on such a somber note, but I needed this case to glue together multiple MRI sequences. But on the bright side, we're done with this talk and we're going to move on to a really quick summary. After obtaining clinical history, we typically start with a head CT, identify the slice and landmarks. Basal ganglia is a good place to start.

Look for asymmetry. and the lesion-causing asymmetry. On CT, calcified structures and acute blood are bright, and chronic lesions and edema, or anything fluid-filled, is dark.

Next, brain MRI without contrast. Remember that you typically get T1, T2, FLARE, DWI, ADC, and GRE as a bundle when you order a non-contrast MRI. An active lesion in the brain is usually identifiable by the edema it causes.

So, we should look at flare first, since hyperintensity identifies edema. Vasogenic edema is the result of failing neurovascular unit integrity, which can be caused by tumors, abscesses, trauma, and even severe hypertension. And cytotoxic, or cell-body edema is caused by energy failure and ischemia. In general, bright signal on T2 may be caused by edema like strokes, tumors, abscesses, hydrocephalus, inflammatory pathology such as multiple sclerosis lesion, and subacute hematoma. Dark signal on T2 may be caused by paramagnetic substances such as iron, copper, melanin, Protein-rich lesions, flow voids of normal circle of Willis vessels and venous sinuses, and acute bleed within 3 days from onset.

Next, if you're suspecting a pathology that will break the blood-brain barrier, like inflammation, infection, neoplasm, order an MRI with and without contrast. And remember your patterns of enhancement. Dural, like meningioma or schwannoma.

Leptomeningeal, like bacterial, fungal, and carcinomatous meningitis. paraventricular, ring in the case of lesions with necrotic core like abscesses, toxoplasmosis, and lymphoma, subcortical nodular like metastasis to the gray-white junction or paraventricular multiple sclerosis lesions, and mural nodule such as in the case of pilocytic estrocytoma. T1 without contrast is generally less useful for diagnosis, with a few exceptions. but can serve as a baseline template to which all other sequences can be compared.

Bright signal on T1 typically suggests paramagnetic substances, like iron, copper in Wilson's disease, melanin and melanoma, protein-rich lesions, like colloid cyst, fat, and subacute bleeding 3-14 days from onset. Dark signal on T1 basically corresponds to chronic lesions, which are filled with fluid. DWI-ADC pair is extremely important for detection of early brain ischemia as well as brain abscesses.

True restriction of diffusion, or energy failure, is when a bright lesion on DWI looks dark on ADC. In patients where we're concerned about stroke, we may even review the sequence first, right after the CT and before flare. Finally, remember that blood on MRI plays by its own rules. Acute blood becomes dark on T2 within the first 3 days and slowly brightens on T1. Beyond 3 days, methemoglobin creates a bright signal on T1 and T2.

And that is all. Thank you for joining me. You should feel incredibly exhausted, but hopefully wiser. Go forth and read imaging studies. Compare your impression with a radiologist's report.

That's how you learn. Practice makes perfect. Until next time, bye! I can show you the world, shining, shimmering, splendid.

Tell me, princess, now when did you last let your heart decide? I can open your eyes.

Transcript for:Crash Course in Reading Neurological Imaging

Transcript for:
Crash Course in Reading Neurological Imaging