We'll get started. My name is Samadha Tripathi. I'm a consultation and liaison psychiatrist. I'm at the University of Arkansas in Little Rock. As a CL psychiatrist, reviewing images or coming across cases with overlap with neurology is something that we see very, very commonly. And I, myself, personally struggle a lot in trying to figure out, hey, which sequence am I looking at? What exactly am I looking at? What structure is this? It seems like everything that we learned in medical school just vanishes by the time you start practicing. So this was something that I thought would be helpful during my learning. So, and that is something that we are trying to implement with our residents and our medical students as well. So this is a pilot. All feedback is welcome. So on the panel, we have a radiologist, Dr. Sharma. He is a neuroradiologist over at the University of Arkansas as well. And then my colleague, Peyton Lee, who's also a CL psychiatrist and is on our consult service with me. So we'll break down the presentation into three parts. I'll do a very quick overview of the basic neuroanatomy. This is probably something that you guys know. For the sake of time, I don't think we'll have time to go into the vascular distribution and how the blood supply works, but Dr. Sharma will be touching upon that briefly. The second part is gonna be an overview of the basics of neuroimaging. When do you order a CT scan? What does a CT scan look like? What does an MRI look like? The basics of the different sequences. And then in the third part with Dr. Lee, we will try and apply what we have learned. So we'll have an interactive poll-based question session, and we'll show you the code on how to log into the poll, hoping that it works. Otherwise, we'll just do dibs and have people yell out the answers. And we'll go over five or six cases going over different aspects of what we have learned. So with that, all of you are familiar, the brain's divided into two main cerebral hemispheres and connected by the corpus callosum. Each hemisphere is divided into four lobes by different, you know, sulci and fissures. The lobes have a significant overlap in the functions, but it would be helpful for us to know about one or two key features of each lobe that might be relevant to us as we are seeing patients on the floors, or, you know, we are seeing patients even in the outpatient clinic who might be presenting with symptoms, neuropsychiatric symptoms. So first and foremost is the frontal lobe. So this is the central gyrus. There are primarily three main things to remember about. This is the pre-central gyrus, and this is the motor cortex. So the motor cortex is responsible for signaling about movements. This is which will be controlling how our gross motor functions happen. Then there is the Broca's area, which is the language center for express language. So this is how we produce speech and writing. So if somebody has, say for instance, a stroke or a lesion in the Broca's area, one might present with Broca's aphasia. So in Broca's aphasia, the person is able to understand speech, but they're really struggling with production of speech. So there might be difficulty with formulating words. Even writing can get affected. So these people might struggle with writing in between lines as well. But they're able to comprehend speech pretty well. They're able to write as well. And we'll come on to the other type of aphasia when we hit upon the temporal lobe. Then the olfactory bulb, as you can see here, is stuck right underneath the frontal lobe. Then the other major function of the frontal lobe is what we talk about is executive function. So planning, sequencing. And in the frontal lobe, right in front of the frontal lobe is the prefrontal cortex. The prefrontal cortex is really important as we learn about it in a few more slides. It is what associates through the association fibers to our limbic system, which is our emotional brain. So the prefrontal cortex is responsible for everything that gives us the filter. The reason why I'm standing here supposedly calm and composed is because my prefrontal cortex is functioning a little bit and I'm not disinhibited. So it's controlling your impulses, regulating emotions. It is also how we flex our responses, empathy, morality. All this is what is coming from our emotional brain. And as you'll see, it is connected through association fibers to our limbic system, which are more deeper structures. The next is the parietal lobe, separated by the precentral gyrus and the lateral fissure, which is extending to the back. So primarily in the parietal lobe is the sensory strip, which forms the sensory cortex in the postcentral gyrus. This is what is responsible for pain, touch, temperature. Then another important thing about the parietal lobe is it basically controls our visual and spatial processing. So how we perceive things in the environment, putting things together, like if there is a car, piecing together different parts of the car and having a full picture of that. The important thing for us to remember is what happens if there's a dominant or a non-dominant parietal lobe injury. So as you all know, most, in 92% of the people, the left side of the brain is the dominant part of the brain. So in a non-dominant parietal lobe injury, the patient can have what we call hemineglect and also anoswagnosia, that they don't know that they have a neurological or psychiatric issue going on. If there is an injury to the dominant lobe, or usually left lobe, and the parietal lobe is involved, the patient can have agnosia, that they might have a stimulus or a sensation, either visual or tactile or sound, which is present, but they won't be able to interpret that. So for example, the most common board question is Gerstmann syndrome. So the patient can have acalculia, agraphia, and also finger agnosia, that they can see the fingers, but they're not able to identify it, and also have right-left confusion. Then the next is the occipital lobe, which is responsible for visual processing. And then this is the temporal lobe. In the temporal lobe, again, three main things to remember. This is the Wernicke's area, which is responsible for comprehending speech and language. And as you can see, this is also extending a little bit into the parietal lobe. So if there's an injury to the Wernicke's area, since this is responsible for comprehension of speech and language, the person doesn't understand what they're saying, so they're still able to produce words, sentences, they might even come up with new words, but they might come across as just rambling statements. So sometimes these patients can be labeled as disorganized or even psychotic. So it's really important to remember that there's a sudden change in mental status or the speech patterns are changing. This is something that we should be thinking about. Then the other area, sorry, the temporal lobe is also the seat of the primary auditory cortex. And then it's also the seat of memory. As you'll see in subsequent slides, the amygdala and the hippocampus are all folded deep into the temporal lobe, which also form a part of our limbic system. So the temporal lobe is also the area which is responsible for memory. And like I said, there's a significant overlap. This is an extreme oversimplification to explain things. So I don't want people to leave with the thought that all memory is in the temporal lobe, but some of the deeper structures are here. This is just an overview of what we spoke about. So as you can see, if there is a stroke in the frontal lobe or if there's a lesion in the frontal lobe, depending on what part is involved, the person can have apathy, lack of emotion, disinhibition, amotivation as well, a parietal lobe, as we had discussed, depending on the dominant or a non-dominant lobe lesion. And then as we go on to the other structures, we'll talk a little bit about the midbrain and the thalamus as well. This is just a representation of the human body on the cerebral cortex, the humunculus. As you can see, the area which is involved with the face, the mouth, the lips, and the hands, this occupies a pretty large portion on the cerebral cortex. So that just tells you how precise instructions are needed to carry out speech, to carry out fine motor movements, given how much representation is responsible for these areas on the cerebral cortex. So another thing to be familiar with is, to be familiar with, pertinent to us as psychiatrists, is the, are the deeper structures. Sorry, I keep losing my cursor. So as you can see, this is the thalamus. This forms our relay station. Every information that is coming into the cerebral cortex or going out of the cerebral cortex usually goes through the thalamus. Right underneath that is the hypothalamus. And this is actually the meeting point between the nervous system and the endocrine system. It's also where emotions are converted into physical responses. And this is also the seat for controlling satiety, hunger, thirst, as well, and our breathing movements. So, if somebody, if somebody, you know, feels a strong emotion, like anxiety or rage for whatever reason, because of a thought or an external stimulus, then the hypothalamus basically sends signals. Once the hypothalamus receives that signal from the cerebral cortex, then the hypothalamus, through the autonomic nervous system, is cuing us to produce either hormones or secretions which will then lead to, like, increased heart rate or shallow breathing. So these are the physical responses that happen with emotions, which are actually being controlled by the hypothalamus. Then, of course, the hypothalamus is connected to the pituitary through the pituitary stalk. And the hypothalamus, as you all know, is sending out release hormones to the pituitary, which is in turn releasing hormones for growth, maturation of muscle, sexual development. Then we have the brainstem, which is the midbrain pons and the medulla. And this is the midbrain pons and the medulla. This is what is responsible for sending signals to and from the brain to the rest of the body. So our breathing, heart rate, movements. As you know, the medulla has the pyramidal tracks which cross over here. So controlling the opposite side of our body, the motor functions are happening here. And this is also really deeply concentrated with all the cranial nerve nuclei passing through as well. This is just an overview of what I just discussed. And then lastly, a brief overview of the limbic system. As we had spoken, the limbic system forms what we call our emotional brain. The term comes from the Latin word limbus, border or hem. Essentially, this is not functioning in isolation. The limbic system is getting input from the rest of the cerebral cortex through association fibers from the prefrontal cortex. And the various, the four most important structures to remember is the cingulate gyrus, the amygdala, the hippocampus, and the thalamus. So the amygdala is the seat for emotional responses, motivation, hippocampus and the amygdala are also controlling memory. So our limbic system is primarily responsible for our basic drives. So fear, fight, flight, fornication, and also our emotions. It is also the seat for learning and memory. So one thing that you'll commonly see in a patient who's got severe alcohol use disorder or with prolonged use has damage to the hippocampus or the mammillary body, their memory can really get affected. And the other thing to remember is what I'd said, like the amygdala and the hippocampus, as they're like deeply into the temporal structures, this is also close to the olfactory bulb, which was there. So remember how our patients who might have seizures, they can have auras where they can smell things or have olfactory hallucinations. And it's fascinating and complex how the amygdala, which is also getting input from the olfactory bulb. So if a seizure is triggered and this area is involved, if they're getting input from the olfactory bulb, the patient can also have auras or have olfactory hallucinations. And as you know, in a patient who might be struggling with limbic encephalitis, they can have seizures, involvement of the temporal lobe. They can also have neuropsychiatric symptoms, psychosis, memory issues, difficulty retaining information, difficulty processing information. With that, I'm gonna hand it over to Dr. Sharma to start giving you guys an overview of the neuroimaging. Good morning, everyone. I'm Shobhit Sharma. I'm a neuroradiologist at the University of Arkansas. And I will be talking to you about the basics of CT and MR imaging. And hopefully by the end of this presentation, everyone will feel comfortable looking at imaging in your cases that you see on a daily basis. So the imaging that we typically see for any neurological disorder, any psychiatric disorder, any person who gets imaging is broadly classified as structural imaging, which is what I'll be talking about mostly. So you get CTs and MRIs. You have functional imaging as well, which utilizes some markers, indirect markers, to look at the function of different parts of the brain. SPECT-CT, which is single photon emission computer tomography and PET imaging, these utilize radioactive tracers and they have an established role in the diagnosis of dementias. Functional MRI, although is predominantly in the research realm, but there are promising results in different disorders on functional MRI, as well as on biochemical imaging in the form of MR spectroscopy, which also has promising results in different disorders such as schizophrenia. I'll be focusing mostly on the structural imaging today. So when we talk about CT, the mechanism is there is an X-ray tube which projects a beam of photons which pass through the head, and they're absorbed by detectors which are on the other side of the patient. And the images which are produced, they're based on the density of tissue those photons pass through. So depending on whether you're passing through soft tissue, bone, hemorrhage, calcification, metal, different things look different on CT. And we'll take a look at how things look on CT. There's ionizing radiations which are involved. It's great for acute hemorrhages, calcifications, strokes, bony anatomy. CT is fast acquisition, so if someone is unstable, a CT can be done in seconds, whereas an MRI would take 30 minutes at least to get something meaningful. So it's really fast, readily available, cheap, and has fewer contraindications. So it's the workhorse of imaging. MRI utilizes the small magnetic fields which protons have around them. So our body is made of protons in each and every cell because water contains protons. And when we place a patient inside a magnet, those protons align along with the magnetic field of that huge magnet. And we can tweak, manipulate the magnetic spins of those protons using different RF pulses and produce meaningful results which translate as images. There's no radiation involved, so it's very safe for using kids, pregnant patients, even for fetuses. There is a very high soft tissue resolution, so you can look at smaller structures with crisp resolution. It's slower, it is expensive, may not be as readily available as CTs, so there's some limitation there. A lot of people experience claustrophobia in the magnet board because there's very small room over there. A lot of people with old metallic devices such as implantable defibrillators, they cannot be put in a magnet because they're contraindicated. But most of the newer devices, newer clips and newer leads and wires that people get these days, they are compatible with MRIs. So how do things look on a CT? So we measure density of different tissues in Hounsfield units, and the Hounsfield units range from negative 1,000, which is air, which is the lightest material that you can have in your body, to metal, which would be in the several thousands. And everything in between would be between the negative 1,000 and plus 1,000 range. For water, it's labeled as zero Hounsfield units. So on this image, which is a post-op HCT of a patient with MCA aneurysmal clipping, you can see almost all the densities that we see on a CT. So this hyperdensity right structure that you see just deep to the skull is hemorrhage. You've got air, which is not unusual in a post-op brain. So air is very light, and the Hounsfield unit would be in the negative 1,000 range. There is water in the ventricles, which you see over here, which would be Hounsfield units of zero. Subcutaneous tissue has fat, so that would be in the minus 100 range. The calvarium, bony calvarium, is bone, so that would be in the 1,000 range. And here you can see that there is an aneurysmal clip which is also producing streak artifacts. That's metal, so the density of this would be highest amongst everything that we're seeing here, so that would be in the thousands. And gray matter and white matter that you see over here, they're kind of similar in density, gray matter being denser, and white matter is slightly less dense as compared to gray matter. So those are all the densities that we see on a HCT. And this is an overview of, this is another chart which shows you all those densities and how they vary between different shades of black, white, and gray. You can see bone is intensely white, air is intensely dark, and gray and white matter are different shades of gray. Moving on to CT anatomy. So when we acquire CTs, they're acquired in an axial fashion. We start from the skull base, go to the skull vertex. And right at the base, this is at the level of the foramen magnum, which is this circle on the right. This is where the brainstem comes out of the skull base and continues as the cervical spinal cord. This is where the middle oblongata continues as the cervical cord. As we move up, this slice on your left is at the level of the internal auditory canals. We don't see the internal auditory canals because this is a brain window that we're looking at. If I showed you a bone window, we would appreciate the bony detail a bit more. So here is where the internal auditory canals would be. What we're seeing are the cerebellum, the pons, and a little bit of the temporal lobes. As we move higher, we see more of the cerebellum, pons, and the temporal lobes. And the second image on the right is at the level of the scella, which is somewhere over here. Again, cella is a structure which houses the pituitary gland. We see it much better on sagittal and coronals. So brain window, there are different windows with which we can look at a head CT. So a brain window is something which we can manipulate on our workstations, and it'll show us differences between gray matter and white matter to great advantage, whereas it will minimize any other structure which is outside of those structures. So bone and anything outside of the calvarium, you will not be able to appreciate the detail in those structures. You'll see the detail in gray matter and white matter, which we are looking for, but once we are done looking at the brain, we want to look at stuff outside, sinuses, calvarium, there are fractures, foramina that pass through the skull base. For those, we need the bone window, which will minimize all the information that's there in the gray matter, white matter, and just accentuate bony information so you can appreciate bony detail a lot. And I have a slide at the end where I'll show you a bone window and you can appreciate those things. This slide is at the level of the supracellar system, which is a CSF-filled space just above the cella or the pituitary gland. It's a star-shaped space, and you can appreciate the cerebellum posteriorly, the pons in front of it. You see more of the temporal lobes on either side. This is the basal forebrain that we are seeing in front. And as we move higher up, we see different cisternal spaces like the quadrigeminal cistern over here. We're starting to see the basal ganglia on either side, which are paired structures, and we'll see more on the subsequent image. So here, we can see the internal capsule and the basal ganglia. The internal capsule is denoted by these two lines. So this is the anterior limb of the internal capsule. That's the genu, posterior limb. And it's present between the basal ganglia. So on its lateral aspect is the putamen and the globus pallidus. Medial to it is the head of the caudate nucleus. Posteriorly, you have the thalamus. And these are paired structures, so the contralateral side is over here. So symmetry is our friend when we look at imaging. Anything that makes things asymmetrical alerts us, and we can identify the problem. As we go further up, we're basically seeing the white matter tracts, which come down from the cerebral cortex, which is called the corona radiata, so which is all this white matter on either side of the ventricular system. So these are the lateral ventricles. And finally, at the very top, this is at the level of the motor cortex or the sensory motor cortex. And we'll take a look at this on MRI, where we can appreciate the differences, the anatomy a lot better. For every HCT that we acquire, we usually get sagittal and coronal reconstruction. So sagittal is when we're looking from the side. And so this is the front of the patient. This is the back of the patient. This is the top, and this is the bottom. You can see that the cerebellum, brainstem, they're posteriorly located in the posterior fossa. You can see a lot of midline structures here, corpus callosum being an important one over here. This is the pituitary gland over here. This is the coronal reconstruction, so you're looking from front to back over here. And you can appreciate this ventricles. And these are the temporal lobes, the parietal lobes on either side. This is the bone window. And you can see how you can appreciate the fine detail of all the bony structures, the sinuses, the foramina in the skull base on this image much better, whereas you can hardly see anything that's inside the brain parenchyma. So this is something we can manipulate on our workstations to accentuate the details of bones. All right, moving on to MRI. And this is, the next couple of slides are important. We can look at the different MR sequences that we obtain. So on the left is a T1-weighted image. The second one is a T2-weighted image, and the third one is a flare. So I remember T1 simply as gray matter is gray, white matter is white, and CSF is black. You can see that gray matter on this is a medium shade of gray, whereas white is much lighter gray. As compared to a T2-weighted image, where the most important thing is CSF is bright. So all the bright structures that you see are containing CSF. So in the middle you have the ventricular system, and outside everything that has brightness in it are sulci filled with CSF. A flare sequence is also a T2 sequence, but here we've subtracted the signal from CSF. So you can see that while the gray pattern of the gray matter and white matter are same as this image, the white of the CSF has been subtracted out, and this helps us identify a lot of disease processes which happen right next to the ventricles. When you don't have the distraction of the CSF, those things just stand out. So a very useful sequence for almost anything that we look at. So that's flare. And then we look at a diffusion sequence, and this is an ADC map which comes along with the diffusion sequence. As you can see, these are slightly blurry, not as detailed as compared to the T1, T2 flare sequences that we looked at. The diffusion imaging is acquired very quickly. So this sequence can be obtained in 30 seconds, and that's of great utility to us because we can image a patient in 30 seconds and get a lot of information within those 30 seconds. So strokes will be seen very easily, hemorrhages. If for any reason a person cannot continue the scan, we at least have a diffusion-weighted sequence which can give us a direction as to whether there is something abnormal or not. And on the right is a gradient sequence. This helps us identify hemorrhages which just show up as huge black blobs of blooming circles when there is a hemorrhage within the brain parenchyma. So it's really sensitive to picking up hemorrhage. And this is another chart showing different appearances of different structures on T1 and T2-weighted sequences. You can see that air and bone and calcification appear intensely black on both T1 and T2. And once we see something like that, we would want to look at the CT to see what that correlates to. So if we know that we're looking at the sinuses, then we understand it's going to be dark. But if we see something dark in the brain, we want to see a CT to compare and see what exactly we're looking at. Hemorrhage, depending on what phase of hemorrhage, acute, subacute, or chronic it is, will have different appearances on T1 and T2. All right, now looking at MR anatomy, this is a sagittal slice through the mid part of the brain. And this is an important slice since we can see a lot of midline structures here. So you can see the midbrain up top, the pons, the medulla. And as the medulla continues on, you see the upper cervical spinal cord. Here's the cerebellum behind. This is the corpus callosum, which connects the two cerebral hemispheres. This is the pituitary in front. So you can see on this magnified image, all these structures can be seen to great clarity. Here's the mammillary body, which is appreciated on sagittal quite well. So that's the mammillary body. This is the pituitary gland. Just like CT, MRIs are acquired in an axial fashion. They can be acquired in a sagittal or coronal as well, but normally we look at it on axial. So same thing, this is the level of the foramen magnum where you can see the upper cervical spinal cord. As we go up, we see great detail in the cerebellar hemispheres, the pons. Going further up, you can see the amount of clarity and high resolution that an MR provides when compared to a CT. So this is at the level of the cerebellopontine angle. So the angle between the cerebellum and the pons is called the CP angle, which is all this area and houses a lot of nerves, vessels. A lot of pathologies happen here. So for example, you can see the seventh and eighth nerve complex entering the internal auditory canals at this level. If we move a slice up, you can see the trigeminal nerve going forward towards the Meckel's cave, cavernous sinus, and skull base foramina exiting from the pons over here. Moving further up, you see a large part of the temporal lobes bilaterally. You see posteriorly, we have the occipital lobes. This is the very top of the cerebellum that we're just catching on this image, and this is the midbrain. So we're going from bottom to up. Further up, you can see more of the temporal lobes. This is the basal forebrain. So we're starting to see some of the frontal lobe. The image on the right is the level of the cerebral peduncles, where the brainstem is connected to the cerebellum. So that's called the cerebral peduncles, which is this area. Here you can appreciate a large sulcal space, which is the sylveon fissure. Sylveon fissure is important because here you can see what is called as the frontal operculum. A temporal operculum, which are just a lid-like structures, and they're kind of folded in, and there is a gray matter area, which is housed deep to those folded parts of the brain, which is called the insula. So the insula on the right side, the insula on the left side. This is the level of the basal ganglia, and you can see the pitamen over here. The globus pallidus is just deep to the pitamen, and you can see it better on this image. The head of the caudate nucleus is in front. The internal capsule passes between the basal ganglia. These are the paired thalamus. All these structures are paired, so the same thing is seen on the contralateral side. As we go towards the top, we see some important sulci, which delineate the different parts of the brain. So these are the parieto-occipital sulci, which separate the parietal lobe in front from the occipital lobe behind. These sulci are seen much better on a sagittal image, where they are seen as a straight line. But the one which is quite important is the central sulcus over here. It looks like the Greek letter omega, which is one of the commonest signs of how we identify the central sulcus. And what the central sulcus denotes is the frontal lobe from the parietal lobe. So you can separate the two, and this is broadly known as the sensory motor cortex because the motor cortex is right in front of it. The sensory cortex is right behind it. So if someone has a specific stroke, specific weakness, arm weakness, leg weakness, we know to check this area to look for an abnormality over there. Briefly, we'll go look at brain anatomy on T2-weighted imaging. So as you saw on T1-weighted sequences, the gray matter appears very well on T1, and it's great for identifying anatomy. T2 is great for identifying pathology. So although you see the gray matter and white matter on T2 as well, it's better for looking at pathology. And the other thing is all the CSF-filled structures are bright. So whatever you see which is bright is a CSF space. So like the supracellar cistern here, the interpeduncular cistern between the midbrain. As we go further up, you see the lateral ventricles. This slit-like third ventricle in the midline. And up top as we go, this is towards the end of the lateral ventricles. And everything outside of it are sulcal spaces which contain CSF. This is coronal images of the brain through, coronal images at the level of the splenium of the corpus callosum which is the posterior part as you can see on this inset over here. Posterior part of the splenium of the corpus callosum which is here. A lot of anatomy can be identified on coronal imaging. So as we move forward, we see more and more of the cerebellum. You see the temporal lobes over here. You see the parietal lobes up top. And as we come further towards the front of the brain on coronal imaging, you identify these paired structures. These are the hippocampi on either side. This is normal anatomy of the hippocampus. You can see that there are layers to it. It's kind of a folded structure, symmetric on either side. So a coronal T2 is great for identifying abnormalities with the hippocampus. Just like we saw on the axial, the sylvean fissure can be seen on coronal which separates the temporal lobe from the parietal lobe up top. Further in front, you can see the optic chiasm which is where the optic nerves meet before they decussate again as optic tracts. And the very anterior part of the temporal lobe, the medial temporal lobe is the amygdala. So amygdala and hippocampus, important structures. When we have specific indications, we obtain scans in the coronal plane and look at those structures in detail. Very briefly, coronal T1 images through the brain. Same anatomy, the only difference being we can identify the anatomy a lot better on coronal imaging. Okay, moving on to vascular territory. So vascular territory is different parts of the brain are supplied by different vessels and they are sharply demarcated areas. So as you can see in red is the lateral part of the cerebral hemisphere which is a large part of the brain and it's largely supplied by the MCA. So MCA supplies a big portion of the brain. In front, close to the midline, what you see in blue is supplied by the ACA, the anterior cerebral artery. And posteriorly, close to the midline, what you see is the supply from the posterior cerebral artery. So the occipital lobes, the thalami, they get supplied from the PCA. The thalami actually have a dual supply. Caudate nucleus gets supplied from the ACA, large part of the cerebral hemisphere gets supplied from the MCA. So this is my last slide and we'll move on to cases after this. So for image analysis, what do we look at? We look at the normal anatomy of the brain. Is everything there? Is there anything missing? Is there anything new? If there is anything new, is it a lesion? Then we visualize the lesion, see if it's in an important part of the brain which can cause dysfunction, loss of function. We locate whether the lesion is intraaxial or extraaxial, which means whether it's in the brain parenchyma or outside of it. So is it coming from the dura, the calvarium, the sinuses, or is it primarily from the brain parenchyma? If there are multiple lesions, is it localized to one part of the brain or is it a diffused process? Is there a vascular territory involved? Is there edema associated with the lesion? Edema can be of two kinds. Cytotoxic edema, which is when there is cell death, as in an ischemic stroke, where both gray matter and white matter are edematous. Most other lesions, metastases, hemorrhages, abscesses, they produce vasogenic edema, which is edema of the brain which is reacting to the presence of the lesion within it. And once we have localized the lesion, we look at the imaging characteristics on CT. So does it have calcification, hemorrhage, fluid, fat, air, what is it made of? And CT helps us identify all those densities a lot better and we can characterize it either on CT or obtain an MRI to look at it better. We get contrast on most scans and the kind of contrast enhancement also helps us identify whether we're looking at a tumor or an abscess or anything else. Then we can also obtain specialized sequences which help us characterize a lesion. CT or MR angiography to look at the vascular pattern of the brain, perfusion-weighted imaging to look at whether a lesion has increased perfusion or not. That helps us understand whether this is a tumor or something else. So that's about it for me and we will move on to cases by Dr. Lee. Okay, so I'm Dr. Lee. I'm one of the CL psychiatrists also at the University of Arkansas. So what we will be doing now is applying some of the things that we've learned in some cases. And so we'll be testing our knowledge on imaging and then diagnosis and all that. So these are some cases that may be pretty common as a CL psychiatrist. We'll be using Poll Everywhere and I'll give that information when we get to the actual questions. But if that doesn't work, we'll just do how we do with our residents and medical students and make it maybe raising hands or going and answering like that. So let's start for the first case. So we have a 56-year-old female with a history of schizophrenia and lung adenocarcinoma who presents to the emergency department with a one-week history of jerky movements of their left upper extremity and left-sided weakness. Two weeks prior to presentation, the patient saw their psychiatrist and were changed from olanzapine to haloperidol. So in the workup for this, they got this head imaging. And so our first question is, what side of the brain is this lesion on? So I'll go back to that one more time. What side of the brain is this lesion on? So, if you, going on there. So you can go to polev.com slash Peytonlee528. Let's see if this works. All right, we got that 100% correct. So that is on the right side of the brain. Very good, all right. So then the next question, what brain area is affected in the MRI? Yeah, and again, that's right here. So what brain area is affected there? All right. So we've got 68% say the primary motor cortex, 16% say the posterior parietal cortex, and 12% say the primary somatosensory cortex. So taking a look at that, does anyone feel comfortable saying why they chose an answer or why they didn't choose other ones? Say that again? Yeah. Uh-huh. ?? Right, so you're saying being mindful of the sulcus. Yeah, so the correct answer is the primary motor cortex in this case, and we will have Dr. Sharma explain. Yes, that's exactly right. So that was what I had shown you earlier, the omega sign of the central sulcus, which separates the motor area from the parietal lobe. So with the history of arm weakness, we are already suspecting something in the motor cortex. You can see, it can be a little difficult to see when you have a lesion there, but what you're looking at is a lesion in the motor cortex, and hence the presentation. So then the last question for this, what type of lesion is this? Metastatic cancer, abscess, vascular malformation, or ischemic stroke? All right, so we've got 72% of people saying this is metastatic cancer, and 28% saying this is an abscess. So let's take a look at this again. So the correct answer is this is metastatic cancer to the right primary motor cortex. Dr. Sharma, do you want to talk about that a bit? So both are great thoughts, because what you see is a ring-enhancing lesion, and you see a lot of vasogenic edema around it. The history of this case kind of takes you to one diagnosis than the other, as well as the fact that for me to show you an abscess, I would show you a diffusion-weighted sequence which shows restriction within that lesion, which is specific for abscesses, because they contain pus. Pus restricts on diffusion-weighted imaging. So that is something that we utilize. Also, the thick, irregular enhancement that we see is more, points more towards tumors, so primary or metastatic tumors. Abscesses tend to develop a capsule around them, and the capsule is very uniform. It's a thin-lined, uniform, rim-enhancing lesion. But both are great thoughts. This person, of course, had a history of malignancy, and this was a metastatic lesion. What's the contrast between the two? The contrast, it will outline which areas, if it's a lesion, is it an enhancing lesion or not? So there are lesions which can be non-enhancing. There are a lot of brain tumors which don't enhance, which kind of points us towards the grade of the lesion. So a non-enhancing lesion means it's not as aggressive for certain diagnoses. So for primary brain neoplasm, that's an important factor for us to say that, okay, this is probably a lesion which is less aggressive. It also outlines where the lesion exactly is, because on a non-contrast image, we see a lot of abnormality. Whereas when we give contrast, it localizes to one point and be like, okay, this is the abnormality, this is the lesion, everything you see all around it is edema or secondary effects from the lesion. It also tells us, is there one lesion, two, three? How many are there? Does it have a satellite lesion? Because if someone wants to go in and treat, resect, radiate, they need to know if they're dealing with one, two, or multiple lesions. So contrast helps us with a lot of things. Any other questions before we go to the next case? All right. Oh, yeah. Yeah. Okay, so as I've shown, this is the central sulcus. Like I said, when you have a lesion there, it's hard to identify the normal anatomy. So on the contralateral side, this would be the central sulcus. And this would be the motor cortex. So when you see, this is sitting right on the central sulcus, more so towards the motor area, and that's why the patient had the presentation of motor weakness. It also helps, going back to the last slide that Dr. Sharma had, where he spoke about like, what are you looking at? So just comparing it with the other part of the brain, which appears normal, you can see the central sulcus better there, so if you compare those two, it's helpful to understand that way. But on the affected side, it can be difficult to have that differentiation. All right, so case number two. So in case two, a 45-year-old male is brought to the emergency department by his wife due to a three-day history of altered mental status. On the interview, the patient was confused, they had a flat affect, and they were very apathetic. The wife stated that he had been a very social, outgoing person. She became concerned when he seemed lost at home in one of the days before. On physical exam, he had mild left-sided weakness, though he denied that he was having any weakness at all. So, starting there, what other history would you want to obtain? So in this part, you just type in other history. It'll pop up, and people can vote for it. Vote for it. It's past medical, medical substance use. All right. Just a smiley face. OK. So like we sometimes get seeing patients in the emergency department, we want all this history and maybe not able to get every single thing. So I'll get you what we were able to get. So past medical history, this patient has a history of hypertension, hyperlipidemia, type 2 diabetes, alcohol use disorder, and depression. As far as specifically past psychiatric history, they've had depression since they're 22 years old. That's been well controlled on sertraline. They have a history of two previous suicide attempts and three psychiatric hospitalizations, but those have been quite some time. They have a family history of a father with vascular dementia, a brother with alcohol use disorder, and a cousin with schizophrenia. And as far as a social history, he lives with his wife and two teenage sons. He works as a bank teller. He drinks between 6 to 12 beers daily, and he smokes two packs per day. We also obtained lab work as we do in the emergency department and basically everything was normal. Normal CBC, BMP, liver, your UA, drug screen, and thyroid studies. And since it's a neuroradiology lecture, we got head imaging. And it showed us this. So our next question is, what imaging modality is shown on the left? And I will go back to that. So this right here. What image modality is shown right there? All right, so 100% correct, that is a CT, awesome. So going here, that is a CT. Does anyone wish to guess what is seen on the right? That's correct. I heard diffusion somewhere, DWI. So it's a diffusion-weighted sequence. All right, so then looking at this. Okay, so on the left, you can see it's a CT, calvarium is dense, it's bright. CSF is dark, but then you can also confuse it with other MR sequences. The most important thing for CT is calvarium is dense, calcified. For diffusion, so if you look at diffusion, at times it looks very similar to a flare sequence, but as you can see, it does not have the great definition, resolution that a flare or a conventional sequence does. You almost do not see anything of the calvarium. If you see, you're identifying only the brain parenchyma. The T1, T2 flare, almost every other sequence shows you the skin, the calvarium, whereas the diffusion sequence only shows you the brain and it's not great in resolution. And it's great for picking up what we're showing here, which we'll discuss in the next slide. All right, so then what is the most likely diagnosis? All right, so we've got 80% of people saying this is a stroke in the right MCA territory. 12% saying this is a right subdural hematoma. And then 8% saying this is a right subarachnoid hemorrhage. And so this is a right MCA stroke. Yeah, so on the CT what you're seeing is the classic pattern of loss of gray-white differentiation. So as you can see, there is blurring that happens between the deep gray nuclei, which is especially if you can see the caudate nucleus, it has lost definition and is blurred with the surrounding white matter. The overlying cortex is also blurring out, so that's a typical finding of an ischemic stroke. On diffusion imaging, ischemic strokes restrict, so they show up as bright on diffusion-rated MRI. And so what you're seeing are those corresponding areas showing up as bright. So there's predominant restriction in the MCA territory, in the frontal lobe, the insula, the deep gray nuclei. There's a caveat on this image. This is not only an MCA, but also an ACA territory stroke. As you can see up front, there is a sliver of restricted diffusion right off of the midline, which is in the cingulate gyrus, which is supplied by the ACA. And this person actually had an occlusion at the ICA terminus, so basically occluding both the MCAs and, both the MCA and the ACA on the right side. So that's a stroke. Any questions before we go to the next? All right. So case three, we have a 55-year-old female with renal cell carcinoma with a status post resection. And they presented to the emergency department with a one-month history of bizarre and uncharacteristic behaviors per the daughter. One month earlier, the patient suddenly left her home to stay with a friend without explanation, and she did that for 10 days. When she returned, all she would do is lay in bed and rarely get up. She, at various points, had left the bathtub running overnight, causing it to overflow. The family had to hide the plug of the bathtub. The daughter reports that the patient seemed more tired than usual, and has had some episodes of shaking of all four extremities, but no frank seizure episodes. They went to their primary care doctor the week before, who was concerned for an infection causing this altered motor status, and they were started on an antibiotic with no change in behaviors. In the emergency department, vitals, physical exam, and lab work were all relatively normal. And we got this imaging. So our first question is, what type of MRI sequence is this? And we'll go back to that. Go back to the image, yeah. All right, so 84% of people said this was Flare, about 8% saying T2, 4% T1, and 4% DWI. So yes, this is Flare imaging. Do you wanna talk about how we know this is Flare? Yes, so that's correct, this is Flare, and as we had discussed earlier, T2, Flare is a T2-weighted sequence minus the CSF. So what you don't see in the ventricles is bright CSF. The gray matter and white matter appear exactly like they do on a T2 sequence, so this is a Flare sequence, and everything else is the abnormality and its secondary effects, which we will discuss. So this is our imaging. The next question is, what is the finding that is represented by the arrow? So specifically, this area of white. Go back to the image as well. All right, 100% edema, that's correct. Yes, so we do see vasogenic edema in this case. If you look at the extent of edema, you can see that there is sparing of the cortex outside of that edema, so it basically involves the white matter, which is what vasogenic edema does, and I think we have one more question on this, and then we can talk about this pathology in detail. All right, so the last question, what is the most likely diagnosis? All right, so 84% said this is a glioblastoma. That is correct. Yeah, so this is a glioblastoma. The appearance, the location itself is a giveaway. The only other lesion which looks like this and can present like this would be a lymphoma but would have different imaging characteristics. But as you can see, this lesion is a large, heterogeneously enhancing lesion involving the right frontal lobe and it crosses the midline along the corpus callosum to the contralateral side. There's a lot of midline shift. To the left, there is extensive vasogenic edema on both sides and there's mass effect on the ventricular system as well, so this is a GBM. On the left, you see the post-contrast image and on the right is the flare. And the other options that we had were the abscess stroke. The abscess stroke, again, for stroke, what you would see would be restricted diffusion on a diffusion-weighted sequence, loss of gray-white differentiation on a CT, so those would be the imaging findings that someone would show you for a stroke. For an abscess, again, restricted diffusion within a well-encapsulated lesion would be the typical imaging finding that we look for for an abscess. And as you can see, this is a very large lesion and compared to the size of the lesion, the edema isn't as significant as you compare to the first case where the lesion was small and the vasogenic edema around it was several times. So primary tumors tend to have a little bit of vasogenic edema around them. Metastatic lesions tend to have edema out of proportion to their size, so even a tiny one-centimeter lesion, which is a metastatic lesion, can have several centimeters of edema around it. So that's another thing that helps us identify whether we're looking at a primary brain neoplasm or not. At times, it's difficult to distinguish and then we just have to say it's a neoplastic process, could be a primary or a secondary, then we look for other things. Any questions before the next case? Yeah? Just talking about the sentence versus where it would be. Yeah, so in this person, we had, let's go back to this. So change of behaviors, right? Changes in their personality. So that's kind of more consistent with this being in our frontal lobe. Really, outside of these behavioral changes, we weren't really seeing much else, right? There was these episodes of shaking, which, kind of hard to characterize that. Not seizure, it's not on the motor strip. And really, all else, like vital signs, physical exam, all else was normal. So really, just with these personality changes, most consistent with it being in the frontal lobe. I think I saw another question. I was just wondering if you had some symptoms like numb, tired, and, and, anyone who sees, which kind of, okay. Yeah, so the edema that you see over here is all this over here. On flare, you can see this is what, this is where the lesion is, and around it is vasogenic edema. So that's edema in the white matter. So if I go back to my, to the first case, which, or the second case, which was a stroke, what you see over here is cytotoxic edema. Cytotoxic edema is cell death because of ischemic, ischemia, loss of blood supply. And if you see, there is, it extends all the way out to the gray matter. So that's one difference which I highlighted between cytotoxic versus vasogenic edema. So this example highlights cytotoxic edema, which helps us identify this case because it extends all the way to cortex, and that's what strokes do. There's cell death of gray matter, white matter, so the cytotoxic edema extends all the way out to the cortex. As compared to a tumor where the edema is basically the brain responding to the presence of the lesion, trying to limit it, getting irritated by it, and, you know, showing signs of inflammation. So that's edema, vasogenic edema that we see here. All right. So in case four, we have a 65-year-old male with type 1 diabetes, hypertension, heart failure, alcohol use disorder, and depression who's admitted for a two-day history of shortness of breath due to heart failure exacerbation. On day two, they started to exhibit signs and symptoms of alcohol withdrawal, which resolved after treatment with diazepam taper. Psychiatry was consulted on day five due to altered mental status. And on interview, the patient was noted to be oriented to self only, frequently fell asleep during the questioning, and failed bedside attention testing. Physical exam showed a frail-appearing man with minimal lower extremity edema, lungs clear to auscultation bilaterally, non-tendered, non-distended abdomen, and bilateral horizontal nystagmus. So what workup would you like to obtain? Okay. Let's see. There we go. Great, we've got imaging. Okay. All right, I guess it locked us out. But I see a lot of good thoughts on here, so definitely a lot for imaging, labs, thiamine levels, LFTs, ammonia. So good, let's go through that. So, on their CBC, they were noted to have an elevated MVC, about 105. Otherwise, everything else was in normal limits. The basic metabolic panel, again, roughly normal. Sodium was 132. Kranin's looking fine. Everything else there is pretty good. LFTs, they had a mildly elevated AST, depending on what your institution uses. Their T-billy, maybe mildly elevated. Their urinalysis was normal. Their drug scheme was positive for cannabis only. Chest X-ray was normal. HIV was normal. RPR, negative. TSH, T4, T3 were normal. And then vitamins, we got a folate and B12, which were normal. And a thiamine, we ordered, but that is pending, as those generally take a few days. So we got imaging. And it's here. And our first question is, what affected brain structure is shown by that arrow? I'll go back to that right here. So what brain structure is this that's affected on this imaging? All right. Yeah, so 96% of you got this correct. This is the mammillary bodies. So you can see that there. And we'll spend more time talking about some of the other findings that we can see on this. So then our next question, what's the most likely diagnosis? Yeah, so 100% of us got this right. This is Wernicke encephalopathy. And so let's go to the imaging, because there's quite a bit more to it than just the mammillary bodies, which, as we know, aren't always seen in every imaging for Wernicke encephalopathy. And everybody knows this is, what sequence this is, right? What sequence are we looking at? That's a flare sequence. So this, both slices, both thoraxes are flare slices, and these are characteristic findings of Wernicke's encephalopathy. So what you're seeing over here on this slide is the dorsomedial thalamus on the right and the left. They're showing symmetrically high signal. So remember, the T2 sequence would have bright CSF right next to it. It would have been quite challenging to identify this brightness against the brightness of CSF. That's why flare is extremely useful for something like this. So those are paired signal abnormalities in bilateral dorsomedial thalami. And on the first image, you're catching the mammillary bodies in front of the midbrain over here, which are hyper-intense. They do not light up like this on flare. And the other area which is abnormal is this periaqueductal gray matter in the midbrain. So this tiny dot over here, that's the aqueduct of silvius, goes through the midbrain. So the parenchyma right around it is also hyper-intense over here. So these are the typical findings of Wernicke's encephalopathy. Someone had also mentioned the hippocampus, which we are catching a bit of on this. Over here, you're just seeing the anterior part of the head and anterior body of the hippocampus, maybe a little bit on the contralateral side, but they're not hyper-intense. I would ideally show you a coronal image for that or a better axial plane where you can see the hippocampus in entirety. All right, any questions before we go to case five? Yeah? In the end, I think we wouldn't do a scan here because the clinical presentation is so obvious, but what's the benefit of the scan in this case? So as far as the benefit of the scan, in this case, we're probably just scanning because we're trying to work up an altered mental status. As far as for Wernicke's encephalopathy, a scan is not necessary to make that diagnosis. And so, again, this is just a finding that you may see, but you don't always have findings on the brain in Wernicke encephalopathy, so the absence of these findings does not rule out that diagnosis. So this would have been obtained just in kind of the standard workup for a patient with an altered mental status and some neurologic findings. Yeah, and oftentimes, the history isn't as conclusive as we saw in this case. Oftentimes, the history is kind of leading you to a diagnosis and you don't have it for sure. And a lot of times, we have come across those cases where all you have is altered mental status. You cannot assess the patient for other stuff. You don't have more history that the patient can provide you. So the imaging is obtained mostly in those cases where we chance upon the diagnosis. A lot of times, it's not only a person with the alcohol use disorder, but a lot of patients on chemotherapy, they can have Wernicke's encephalopathy as a complication of their treatment and it's an incidental finding in those patients. So there are times when physicians are not suspecting this diagnosis, we chance upon it and we call them, hey, your patient has Wernicke's, start thiamine infusion. And as a CL psychiatrist, I also teach my residents a lot about non-alcoholic Wernicke's, so high metabolic states. It's an acute illness that can happen. So your patients who have a high metabolic state, cancers, or who've been NPO for maybe like a week or so for certain procedures, it can rapidly precipitate in a compromised individual. Sometimes patients can present with this. This case, we sort of set it up so that it's easier for people to work their way through. But as you mentioned, they might present with a very characteristic history and in the ER, the patients do get loaded with thiamine and glucose any time they're presenting with altered mental status. But this would be something that we would think about if you're seeing somebody, say on med surge floors, ENT floors, at least in our hospital are notorious for patients having altered mental status on day three, four, post-op, either from withdrawals or now we're seeing some acute insult happening. All right, and then to our final case. So this is a 61-year-old female with generalized anxiety disorder and multiple myeloma on chemotherapy who presents to the hospital for altered mental status and seizures, which by day two of hospital admission has progressed to status epilepticus. Per the husband, two weeks prior to the hospital, patient began to experience severe anxiety. And over the course of the next week became concerned that there were cameras planted in their ceiling. Her medications include paroxetine and cyclophosphamide. And initial lab work shows anemia and hyponatremia. So for this first question, what are some of the thoughts on an initial differential? Just first diagnosis that you may be thinking of. So, a lot of delirium, encephalopathy, metastases, perineoplastic, I think I saw PRESS, medications, electrolyte disorders, potential metastases. All really good thoughts. Okay, yeah. So what we'll do is skip now to the imaging, since we've got this right here. So as part of the workup, this patient got all sorts of tests, all that, and then we're skipping right to the imaging. Our first question is, what affected brain area is shown by the arrow? All right, so 92% of you said hippocampus and 4% each for basal ganglia and thalamus. And this is the hippocampus. Dr. Sharma, do you want to talk about that a little? So again, the sequences that we see are an axial flare and a coronal flare. They appear slightly different because even on the same scanner, things can appear slightly different on how they're acquired. This one is actually a fat-suppressed flare, so the signal from all the calvarium has been suppressed, whereas this one still has fat in the subcutaneous tissue. So there are several sequences on the same scanner which can look slightly different. Both of them are the same thing, they're flared. The hippocampus is an obliquely oriented structure. If you look at my face, it'll kind of downward and forward. That's the orientation. So there is no great plane, an axial or a straight coronal or a sagittal. You can only acquire the hippocampus in a plane which is angulated for the hippocampus, so that as you go from forward to backward, you see it in an orthogonal plane and you can follow it head, body, tail, all the way through. So that's why the one on the right is tailored along the plane of the hippocampus, so you can identify the hippocampi on coronal plane. On axial, you'll catch part of the hippocampus, mesial, temporal lobe over here, which are showing the abnormality. So you can see there is asymmetry between the two. This one is hyper intense, and that's why it's abnormal. Actually the basal ganglia, we don't see them very well on either. This one is too low for the basal ganglia. And on this one, we're a bit more anterior, so we're not catching the basal ganglia on either of those. Same goes for the thalamus. The thalamus is again a more posterior structure. So on coronal, if we were a couple of slices back, we may have seen the thalamus. So then next we've got kind of a two-part question. So the first, what test can confirm the diagnosis? All right, so we've got a good range of responses, and then let's just skip to the next, which, what is the most likely diagnosis? All right. So the actual answer to this one is this is anti-GABA receptor autoimmune encephalitis. And if you want to talk about some of the findings that you may see there versus in like a CNS for multiple myeloma. Usually in multiple myeloma, the CNS involvement, the most common thing that we're going to see is like punched out lesions in the calvary. Yeah. So calvarian marrow involvement, multiple myeloma is a marrow disorder. So you see involvement of the marrow, which is in the calvarium. So you would see lesions in the calvarium. At times when they present, there are breakthrough lesions. So they will break out from the calvarium and extend out outwards. So someone may present with a scalp lesion, which is a huge extramedullary disease is the term that we use for that, or the lesion may project inwards into the brain parenchyma. So in those cases, it would be an extra axial lesion. It would be outside of the brain parenchyma, something coming from the outside pressing on the brain. So it will be a lesion directly involving the calvarium and then going either in or out. Same, it involves the skull base a lot. So myeloma involvement of the clivus is pretty common, expansile marrow involvement of the clivus. And from there on, you could either have a big lesion going in towards the brain or elsewhere. Here what you're seeing is a primary process involving the hippocampus, hippocampus as well as the anterior mesial temporal lobe, which is the region of the amygdala on the right side. So temporal lobe, hippocampus involvement is characteristic. And when we see something like this, the differentials that I think of are postictal state, a post someone who's had a status epilepticus can have findings like this. And when you have the correct history and you follow the patient over the next few days, these findings improve. So repeated MRI in that case, say one week later, would show improvement of these findings and clinically you would see improvement. The other thing I would think of is herpes encephalitis, common area of involvement in the brain, mesial temporal lobes, herpes encephalitis. The third thing that I would think of is an ischemic stroke involving the hippocampus. Uncommon, but it happens. So a PCA territory stroke, because hippocampus is supplied by the PCA, can stroke the hippocampus and you can see something like this. But in this patient, the history and workup kind of take you towards an autoimmune encephalitis, which is the other top differential for this finding. Autoimmune encephalitis involves the mesial temporal lobes, the hippocampi, the insular cortex over here, the cingulate gyrus, which you see over here. So if you look at the coronal, if I draw a circle all around here, these are the areas which are involved in the limbic encephalitis or autoimmune encephalitis. Hippocampus, mesial temporal lobes, insula, cingulate gyrus. So you would see signal abnormalities in those areas and your autoimmune antibody panel will reveal the exact diagnosis. That is it for our cases. Any further questions? What would a hemorrhagic stroke look like? So CT is great for hemorrhagic strokes. So hypertensive hemorrhages that you see commonly in the basal ganglia or the cerebellum, CT will show that as a big, hyper-dense, bright blob in the region of the basal ganglia. So that's a hemorrhagic stroke. Lesions that can have hemorrhage in them, renal cell carcinoma metastasis, thyroid cancer metastasis are hypervascular. They can hemorrhage and present as a hemorrhage. And when we scan the patient, the first thing that we see is a big blob of hemorrhage, hyper-density on a CT. On further workup with an MR, post-contrast MR, we can see what the underlying cause is, vascular malformation, metastasis, or is it plain old hypertensive hemorrhage. So CT is the way to go for that. Yeah? Can you speak to patients who have MRI contraindications and what mid-tumor dialogues you would choose based on what you're looking for? So the most common MR contraindication that we come across is somebody with a pacemaker that is not compatible with the scanner. A lot of newer pacemakers, clips, coils, catheters, wires, they're all either safe or MR conditional, which means we can tweak our parameters so that we can make it safe for the patient to be scanned. A lot of, for those patients, then we're left with an option of CT. So we would have to go with a CT. If we cannot place them in a magnet, it would be very unsafe to place such a patient in a magnet. So we usually go with a CT and see how much information we can get. It would be slightly limited, but we'll know at least something. The other thing that patients have contraindications to is gadolinium contrast, or patients who cannot get gadolinium, such as patients with poor renal function, pregnant patients, they cannot be given gadolinium. So for them, we can always get routine non-contrast MRIs, which provide us enough information, even without the use of contrast, that we can arrive at a diagnosis in most of the cases. Thanks so much for the walkthrough. For working up delirium versus dementia, elder patients, we often have a CT head already, even on MRI. Would you say a CT head suffices to get just a gross sense of generalized atrophy, or it's just too unreliable? So a CT head, I would, for a dementia, it would be a baseline workup for dementia. It will show us atrophy. Now, atrophy is so common, anyone above the age of 50 gradually will show some degree of atrophy or the other, unless we see a pattern of atrophy or something which is out of proportion for patient's age. So a 30-year-old or a 40-year-old with a lot of atrophy raises alarm. Unless we see something like that, it would be hard to say for sure if we have nailed down a diagnosis for dementia. The way to go after getting a head CT when you see something like that and you're suspecting a dementia is nuclear medicine imaging, SPECT, PET-CT, which will show you how much metabolism the brain pancama has. Has it lost metabolism in a particular area of the brain? Does it point towards Alzheimer's, frontotemporal dementia, Lewy body dementia, others? So nuclear medicine really comes in over there with the answers. These are also sometimes not easily available or cost prohibitive on an inpatient setting. We've had to pull strings to get SPECT for making the diagnosis of frontotemporal dementia in one of our challenging cases. Usually what we tend to do is talk to our colleagues in neuroradiology, focus a lot on the history, and also look for other things in addition to atrophy, like vascular changes or risk factors. It is still a clinical diagnosis. Relying heavily on imaging for the subtle and the mild cases is not very helpful. Thank you. I think we have time for one last question. Thank you so much for this talk. I was just wondering if we wanted the radiologist to be able to comment more on the hippocampi. Is there a way we should write the order? Yeah. So when we get an order for a brain MRI, someone protocols the order so that the correct imaging can be performed for that patient. So every MRI is not the same. If we have the history of, say, seizures, movement disorders, epilepsy, we know that this needs to be tailored to that patient so that we can image the hippocampi mesial temporal lobes better. And in that case, we would get what we call a seizure protocol brain MRI, where we would get a dedicated coronal flare along the plane of the hippocampus to look at abnormalities over there. So neurologists, epileptologists who deal with these cases on a daily basis, they know to order this and ask for specific imaging when they're placing that order. You can always call and say, hey, this is what I'm suspecting. You guys protocol your scan accordingly. I think the other helpful thing is we're all in such a hurry of getting through the EMR checkboxes, the little box that is there. It always helps when we're putting a requisition in. If we provide like a Reader's Digest version of the history, that can really help the radiologist who's reading the scan sometimes ask for certain sequences. So just putting in AMS is not super helpful. If that's all we have, that's fine. But if there's anything which is pertinent, it always helps them, because then it can help them tailor the sequences accordingly and protocol it as well. Yes, we can do that. Thank you.

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