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MODULE FOUR TRANSCRIPT: CEREbRAL VASCULATURE REVIEw | COPyRIghT © 2016 FUNCTIONAL NEUROLOgy SEMINARS LP | PAgE 1

PeriPheral Vestibular and Cerebellum disorders with aPPliCations (module Four)

transcript – General Cerebral Vasculature review and Vascular syndromes of the Vestibular system

Presentation by dr. datis Kharrazian

Okay, we’re going to get into general cerebral vasculature blood flow, and we’re going to transition to the vestibular system. So, one of the things I just want you guys to know is, you’ve been learning through the process. I think at this point, everyone’s learned the basic regions of the brain, their functions of deficit, their functions of spontaneous activity. You guys know seizures, you guys know the exam findings, you guys have forms to explain all the symptoms. So for the most part, you have all the major forms, but there is a major deficit in what we’ve shared with you that we don’t want to let it continue any longer. We need to make sure you guys know the vasculature. So we’re going to review just general cerebral vasculature, and then what I’m going to do is, I’m going to end that with how cerebral vasculature involvement takes place with dizziness and vertigo, the syndromes that can cause dizziness and vertigo, whether it’s vestibular migraine, whether it’s stroke, whether it’s vertebral basilar insufficiency. Whatever those key things are as it relates to these concepts. And then what’s going to happen is, Dr. Brock will then start teaching everyone diff-di, and for the most part, the first day, we’re really going to go over the basic physiology concepts, differential diagnosis, applications, and then tomorrow, we start with treatments. So we’re going to go into nutritional, neurochemical applications for all the vestibular diseases, and then we’re going to go into actual repositioning and therapeutic strategies for the vestibular system. Okay? But you have to know what you’re treating, and you have to know what things you treat and what things you refer out, what things are emergencies, and so forth.

So, this is the overview for this module. We’re going to cover each of these major topics as we go through. So, right now we’re going to go into general cerebral vasculature and vascular syndromes of the vestibular system.

Now, once we get with this… through this, we’ll go into how all these pathways integrate, and then Dr. Brock will go into integration, and that will really, I think lead… Hopefully you guys will leave here with a very good understanding of vestibular basic physiology and integration and so forth.

These are the different types of vestibular conditions. So when you look at someone who’s got a peripheral vestibular disease, is it inflammatory? Is it vascular? Is it structural? Is it endolymphatic hydrop? Is it


vestibular receptor site damage? Or is it essential lesion or integration disorder, which we’ll focus mostly next module on.

So, the goal of this module is for you guys to have someone come in that has, let’s say, dizziness or vertigo, and then you’re going to go through each of these diff-dis. Is it that the vestibular system’s inflamed? Is there lack of blood supply going there? Is there a rupture, you know, an open window or round window? Do they have otosclerosis? Is there a compressive tumor? Is it a dislodged crystal? These are the key things that all have characteristic patterns. Do they have Ménière’s disease? Do they have this hydrop? Do they have some kind of drugs? Medications cause ototoxicity. So if you know this flow chart, you should be able to – like I said – someone comes in with dizziness, just smile, because you can easily go through it. Okay?

Now, what I’m going to focus in will be the vascular parts of this at the end, but I want to review the vascular syndromes first. Now, for the most part, one of the key things with vascular insults, when you look at patients that come in with dizziness, the key thing that strongly suggests to you that there’s a vascular component to their dizziness, is there’s a rapid onset or acute symptoms. That’s a very characteristic pattern of infection to the vestibular system, or some time of vascular compromise. Okay? So immediate onset of dizziness, just came out of nowhere, it’s severe, it’s sudden, you immediately start to think: Is it inflammatory? Or is it vascular? Okay?

To be honest, most people that have an acute immediate onset of symptoms are generally just going to go to the ER, and get help. They’re not going to, like, walk into, let’s say, an alternative health care provider, or a rehabilitation center. They’re going to go, “There’s something seriously wrong,” they’re scared, and they’re going to go in. However, you may be with a patient, or the patient trusts you and nobody else, and they come in and they have an acute onset of symptoms, so… but for the most part, when people… if you had immediate dizziness and vertigo, and all of these sudden onset symptoms, you would probably end up, you know, calling for help and things like that. But the key feature of these pathways is that they’re acute onset.

So what I want to really go over… I have about four parts to this presentation that will take us into lunch. I want to review the cerebrovascular circulation, I want to show you some tools we made for you, so it can really help you learn this very efficiently, and then I want you guys to understand how using cerebrovascular collateral shunting can support brain therapy. So if you have an area of the brain that’s injured, you may not activate that area of the brain directly with stimulus, but you may activate another region that shares the same vascular supply, to shunt blood there, because they’re too unstable. Okay? Or, there’s reasons sometimes when you do some kind of stimulus to the patient that doesn’t involve that part of the brain, but it changes that function, because you’re actually activating similar blood supply. Okay? It’s not… Activation is not all about activating a specific region, but it’s also shunting blood there, okay?

And then you want to understand cerebrovascular pathology, so we’ll talk about these: Whether it’s TIA, or stroke, or vestibular migraine, or vertebrobasilar insufficiency. They all have characteristic patterns. I want to make sure you guys are familiar with those. And then we’ll focus at the very end on, as we transition more specifically into this vestibular module, the vascular insults that cause vertigo and dizziness. Okay? Because whether we’re focused on peripheral or central, you’ve got to know what the red flags are. You’ve got to make sure you know when someone is coming in and they have a stroke, versus some type of vestibular peripheral disorder, right? You just have to know that. So we have to cover this as a key part of


your diagnostic skill, so you don’t miss something that could really impact someone’s life in a negative way, and you have any medical legal issues, and things of that nature. Getting the patient where they need to go.

So, one of the key things, to start with, with cerebrovasculature is just this circle of Willis. I’m sure you guys all remember studying this, right? Just take a second right now. Grab a piece of paper, and let’s just go through this really quickly, okay? There’s some things you’re just going to have to memorize, or you’ll never be good at this. Okay? This is one of them. This diagram right here is something that you should be able to just do from memory. It’s going to save you a lot of time as you learn all the… To try to learn vasculature without knowing this would make this very, very difficult, okay?

So, when you look at the vasculature, they refer to brain vasculature, cerebral vasculature… There’s the anterior circulation and posterior circulation. So here you see the internal… You see the internal carotid artery that comes in, becomes the middle cerebral artery that’s part of the anterior circulation. And then you have the vertebral arteries that then combine and form the basilar artery, which is your posterior circulation.

So, let’s start here. You have two vertebral arteries that come together. So, if you guys can take a piece of paper and then draw one side, and then draw the other side coming in, and you have the two vertebral arteries forming the basilar artery. So they’re coming in through the front of the spinal cord, and they go through – right? – the cervical spine, and the foramen – cervical foramen – they go all the way through, they get up to the medullary areas. Right around the pons they form together, become the basilar artery. Right? So they’re right in front of the brain stem. And the key thing that I want you to really make sure you understand is, we’re not so concerned about the anterior spinal artery, but we’re – in this module – but we see this first branch before it becomes the basilar artery? This is the posterior inferior cerebellar artery. This is a common area for stroke, and this is a common area for dizziness and vertigo. So you just want to understand where this is. This is the artery that supplies the cerebellum. When you have vertebrobasilar insufficiency, and you have compromise in the vertebral arteries, or you have plaquing in these arteries, there’s less blood flow into the split, the division, the posterior inferior cerebellar artery. PICA. Right? It’s called PICA syndrome, or Wallenberg syndrome, or lateral medullary syndrome. This is all involved with that. So again, know that the vertebral artery is from the basilar, but the branch before they form the basilar is the posterior inferior cerebellar artery.

Now, the basilar artery gets formed, and then you have a branch off it, and this is the anterior inferior cerebellar artery. This is important to us because any compromise of the anterior cerebral artery can also cause dizziness and vertigo. This would be a lateral pontine syndrome. Okay?

Then you have the basilar… you have these pontine divisions of the basilar artery, and then these are going to then… the basilar artery’s going to then form again into two separate divisions called the posterior cerebral artery, but before it becomes the posterior cerebral artery, you have the superior cerebellar artery.

[9.31]

So basically, you have three major blood supplies to the cerebellum and to pathways from the cerebellum to the brainstem: the posterior inferior cerebellar artery, the anterior inferior cerebellar artery, and the superior cerebellar artery. Which means that if someone has a vascular compromise that causes dizziness,


and other brainstem symptoms, you’re thinking of one of these three arteries, most common one being the posterior inferior cerebellar artery. Okay? So, here’s another way to look at it. If someone has a vascular compromise, and they have dizziness as one part of their component, and nausea and vertigo and nystagmus, if it’s a vascular component, you’re looking at blood supply to the cerebellum, which is posterior inferior cerebellar, anterior inferior cerebellar, and superior cerebellar artery. Those are the three main arteries. Okay?

Now, when you look at the blood supply… so we’re going to focus on those again at the end, and I’m going to show you those syndromes and how they all bridge… I just want to give you the big picture first, as a review.

So the posterior cerebral arteries… So the basilar artery then divides to left and right posterior cerebral artery, and for the basic concept, the posterior cerebral arteries, they give vascularization of blood supply to the posterior areas of the brain, the midbrain, the top part of the brainstem, and the thalamus. Right? Just know the generalizations: Posterior cerebral artery is going to give vascularization and blood supply to the posterior regions of the brain, the top part of the brainstem, the midbrain, and the thalamus. Okay? Because, you guys, if you try to just… If you get overwhelmed trying to memorize every single little branch and their name, you’re wasting time. Just know the basic concepts, okay?

Now, the posterior cerebral arteries then basically attach to the internal carotid artery where you have the middle cerebral artery. So here you see the internal carotid artery. Obviously it’s coming in, in the front, and then that turns into the middle cerebral artery, and then the middle cerebral artery gives blood supply to the frontal parietal cortical areas. Right? There’s an inferior and [superior] division, some of it temporal, and the outer part of the front of the brain is mostly middle cerebral artery. And then you have the middle cerebral artery that then branch… Then you have branches off the middle cerebral artery, the anterior cerebral artery, and the communicating branches of them. And then the anterior cerebral artery’s going to give blood supply to a Mohawk distribution midline, parasagittal. Okay?

So, really, really, simple. Posterior cerebral artery, posterior division – okay? – of the brain, top of the brainstem, the midbrain, and the thalamus. The middle cerebral artery is going to be your frontal, parietal, even some parts of your temporal areas, but the anterior division of the brain and bits of the cortical area of the brain, and the middle cerebral artery has deep branches which vascularize the internal capsule. The internal capsule is a very common area for stroke. So a lot of pure motor strip hemipareses, pure sensory type patterns, are in the internal capsule, which is supplied by deep branches of the middle cerebral artery. Okay? And then you have the anterior cerebral artery, which is the Mohawk distribution in the front.

So, look at some pictures. You can see how they work. So, here they are when you look at them on a brain specimen. Two vertebral arteries coming together; there’s the basilar artery. There’s your posterior inferior cerebellar artery. You can see that it’s giving vascular supply to the cerebellum. And then you can see the brainstem here. This comes off, and then you have divisions to the cerebellum, the anterior and inferior cerebellar. And then before the basilar artery divides again, you have the superior cerebellar arteries. So those are the three vascular supplies to the cerebellum. And then you can see the posterior division here, coming in. But as you see the posterior communicating artery combined with the internal carotid artery, and becoming the middle cerebral artery, the middle cerebral artery comes into deep areas inside the brain, fires… gets blood flow to the internal capsule – there’s the basal ganglia – and then the anterior portion of the brain. And then the anterior cerebral arteries come in, and they go midline, in the middle of the brain.


So if you ever take a brain specimen, and it’s like… and you pull it open like that, the blood supply you see there, that’s all anterior cerebral artery. Okay?

So, here’s another illustration. But I want you to see something. You see the temporal lobe here? I want you to see, if you look at the middle cerebral artery, you see the temporal lobe? When they cut it off, you can see that the middle cerebral artery branches out to the cortex, but then these inner branches here, these lenticular striatal arteries, go into the internal capsule, the common area for stroke, especially lacunar strokes. Okay?

So, here’s a picture of the middle cerebral artery. You can see that you have superior divisions, inferior divisions, and all the areas of the frontal lobe, the parietal lobe, some areas of the temporal lobe are all supplied by the middle cerebral artery. And you know, you can go down and memorize all these different names, but I just want you to understand the concepts. Now, we have an entire module just on vascular syndromes and the vasculature, but we have to make sure, as we’re getting you guys to where we want to take you, you guys at this point know the vasculature and the basic concepts. It’s going to help you as you divine rehab protocols and all the other various things that we’re going to get into clinically.

Now, here’s the posterior cerebral artery. So, here’s what’s been cut out. The basilar artery and the brainstem have been cut out. The pons… This is the midbrain, so this is the basilar artery, then forming two divisions, and then you can see the posterior cerebral artery gives blood supply to the midbrain. You guys all see that, right in there? And then it gives all the blood supply to the posterior divisions of the brain, occipital lobe, the caudal areas of the temporal lobe.

And then here’s the anterior cerebral artery. This is all midline. So your Mohawk vasculature. Okay?

Here’s another picture. You guys can see, again, how it looks in the brain. So I just want you to see these images so you can get these oriented with yourself, okay?

So… and here you guys see a really good illustration of cerebellar vasculature. You see the vertebral artery coming up to form the basilar. Here we see the posterior inferior cerebellar artery coming off here. Here we see the anterior inferior cerebellar artery. And then here you guys, up here, can see the superior cerebellar artery. Okay? These are vascular syndromes. And here’s another illustration of the cerebellum pattern.

So let’s recap one more time. Vertebral arteries. They come in. Before they form at the basilar artery, there’s a branch: posterior inferior cerebellar. Then they become the basilar artery, right? Basilar artery has a first division: anterior inferior cerebellar artery. Goes all the way up, you have pontine branches. Before it divides, there’s another branch called the superior cerebellar artery. Then the posterior cerebral artery – right? – develops, and you have communication to the internal capsule, and the middle cerebral artery branches off… I’m sorry, to the internal carotid artery. Then the middle cerebral artery branches off to the internal carotid artery, then there’s a branch anterior, the anterior communicating artery, to the anterior cerebral arteries, and then you have that vasculature. Okay?

Posterior cerebral artery: midbrain, thalamus, posterior brain circulation. Middle cerebral artery: anterior brain circulation, and the internal capsule, right? Middle cerebral artery. Anterior cerebral artery is going to be the Mohawk distribution throughout. Easy. Okay? Which one causes… Which branches cause dizziness


and vertigo and nystagmus? Posterior inferior cerebellar, anterior inferior cerebellar, or superior cerebellar? Okay? Which one would cause a stroke pattern only in the feet? Anterior Cerebral Artery, because the Mohawk. Remember the somatosensory cortex? What would spare the feet but cause loss in face and arm? Middle cerebral artery. Because remember that homunculus distribution?

So the minute you, you know, you see someone’s impairments, if you know your vasculature, you can go, “Oh, that’s the blood supply,” right? So, what we did intentionally is, we gave you the brain compilation charts very first, and then made sure you guys knew all the regions and all the sections and knew all the functions, and now we’re going to overlap the circulation and the vasculature over it, so now these strokes and terms are really easy to learn, because you already know the functions. You’ve just got to know the general concepts of these blood supplies are to… that they go to. Okay.

Here’s some other, just, illustrations so you can see the picture and really get this in your visual memory. Middle cerebral artery you see in red, and then you can see the anterior cerebral artery and Mohawk distribution, and then posterior cerebral artery, the posterior regions of the brain. Okay? If you look at the specimen here, this thing, this vasculature on the outer area, this whole area here is the middle cerebral artery, and then parasagittal anterior cerebral artery. Okay.

So as you guys know, up to this point, we gave you this brain region localization form, and we gave you this brain compilation form. Okay? So, what we’ve added to your intake forms, this module, just a basic vasculature atlas, Okay? This are just some really beautiful diagrams that summarize the vasculature and blood flow to the brain. Make sure you guys know them, right? Whenever we give you a form or compilation form, that means you need to memorize it, if you’re trying to go where we want you to go.

[19.59]

So, you know, Dr. Brock and I have a vision of really taking people to a very competent and clinical level. So when there’s something that we feel you just have to memorize, we’ll put together forms, and give it to a chart, and say, “You just need to memorize and know this,” okay? So you need to know your atlas that we gave you, and so you know all these things. Now, you don’t have to actually know every single name and branch, but to be quite honest, it’s not hard. You can spend a few minutes and memorize and then draw them out. It will help you.

So here you are. You can see that parasagittal, the intracerebral artery view, and then you can see the posterior division there. Now, this is a great part of this illustration chart, because it shows you, when you cut the brain – not looking at it from the outer, but the deep structures – here’s the anterior cerebral artery, here’s the middle cerebral artery, and the posterior communicating artery comes in, supplies the posterior regions of the brain – the thalamus and the midbrain – and then you have the anterior choroidal artery, which is a branch of the IC, and impacts some of the internal capsule findings. But for the most part, most of the projections to the internal capsule that you guys see here are from the lenticulostriatal arteries, these little branches here, from the middle cerebral artery. These little tiny blood vessels are very prone to have little lacunar infarcts – boom! – and then people have pure motor hemipareses, or pure sensory, or a combination of both, depending on what part of the internal capsule that a person has compromised. Okay? So those are the divisions there.


Now, if you have those visually in your head, that’s how people read cerebral angiographs. So you can have someone get a study, and you can cure it. Like, you can see the vertebral arteries from in the basilar, you can see the posterior communicating artery, right? See some of the anterior cerebral circulation. It’s just exactly like the images. So know your vasculature, know how they work, and that’s part of the learning step that we need you to do as we move you along into the goal that we have to teach you.

Now, this is one of the charts we gave you from the very first module, which was the clinical decision-making tree. And one of the things that we know, and we’ve gone over is, we say, know your patient’s history, and from the patient’s history, you should be able to come up with regions of the brain that are involved. And we made the brain region localization form to help you immediately identify the chief complaints, so you can localize the history.

Then we went into initial survey, and we went over: hey, what’s their posture like, what’s their facial tone like, what’s their gait like ¬ – before you really get into a really deep examination – how’s their speech, how’s their language. That also helps you localize the region, right? Then once you localize the region, we talked about clinical applications. But here’s the thing that I want to focus in on now. One of the things on this flowchart is, identify regions with common vasculature to activate collateral regions using the same arterial branches.

So you guys, you may have someone who’s so compromised that you can’t activate that region specifically, but you get blood flow there. Okay? You can, by doing similar pathway projections. So, here’s what I mean like this. So let’s say someone had injury to this region of their brain. Okay? What blood supply is this? This is middle cerebral artery. So if you’re looking at this region of the brain, and you’re looking at this somatosensory strip, could you do motor activity? Could you do motor… If they had sensory paresthesias in their right arm, could you just give them a motor activity and coordination to activate that without totally stimulating that area of the brain? Right? You may even get away with doing some, like, frontal lobe executive functions, and then have shunting of blood to the middle cerebral artery, and then see some change in their exam findings.

So, I think sometimes people get confused. They’re like, “Hey, why did I have a person, like, think about something, and it changed their sensory perception? Why did I have someone, like, focus on counting backwards or timelining, and all of a sudden their spasticity changed?” Because as you activate regions of the brain, you get shunting there. So when you look at some of these vascular PET scan studies, and they see blood flow go to certain regions, as soon as you use an activity… Like, if I did this, like I’m doing this right now, if there was an imaging study looking at my vasculature shunting, my entire middle cerebral artery would be activated. So I’m getting vasculature to my entire left side of my brain. So I might see other collateral local areas change because of that. So that’s important to know as you’re working up patients, testing things that change their function.

But if you don’t know your vasculature, everything becomes a mystery. “It’s strange why that happened!” It’s not strange. You just didn’t know your vasculature. So knowing your vasculature helps you figure out other areas.


So for example… let’s go back here. So if we wanted to have some activation here to the somatosensory cortex, you could use branches of the middle cerebral artery and try different various types of functions to see if it would make any difference there.

Here’s another one. So this is the speech area; left side of the brain. So if you had impairment there… First of all, what artery supplies this? Middle cerebral artery, left middle cerebral artery. Okay? So, if you have a person where you… Listen, they try to do language and speech; the minute they do it, they get fatigued, they get tired, they’re frustrated. What happens if you… What if you go a little bit higher up and start to activate the frontal eye fields? So the language centers aren’t working so well, so you have them do right saccades. Right saccades activate the left frontal eye field, and now you do what? You shunt blood flow there. So now their speech changes.

So this is something you should understand. Sometimes when you do exam findings, and other things change, even though it’s not supposed to be for that function, since you’re getting shunting of blood flow to that nearby tissue, you can change their activity. So if someone damaged, let’s say, their speech areas of their brain, and you went in there and started to do frontal eye field activity with saccades, you’re going to nourish that area of the brain with blood flow and circulation, and impact outcomes. Okay?

So, once you know your vascularization really well, exam findings changing from various types of activities all of a sudden become very clear. Okay?

What if you guys had injury to this area? So, what vascular supply area is this? Anterior cerebral artery. Okay? So, what else could you do here? You could do sensory motor to feet, you can do any type of things that activate the somatosensory distribution to feet, to make some kind of shunting or blood flow to that region, right? So, we know, like, for example, a lot of kids that – this is also where the micturition center area of the brain is; some people get a stroke here, they usually end up, you know, urinating – so kids that have bed-wetting, enuresis all the time, they have lack of frontal activity in their midline. And what are they also? They’re toe-walkers. So what if you do motor-coordinating activities with their feet? What are you getting blood flow to? You’re getting blood flow to the anterior cerebral artery, and the same distribution and shunting of the micturition center. Okay?

So, vasculature is important to learn and figure out other types of therapies.

Okay. So I hope this makes you understand why we have this area of the flow chart. Because once we find the region – we localize the region – our clinical workup is, we identify exercises to activate the involved region – right? – usually specific to the area that’s involved, or we may do things presynaptic, or we may impact vasculature and blood flow to that area.

So if I have something going on with spasticity on my left… on my right arm – right? – I know my right motor strip is involved. I can maybe activate that region by doing movements and seeing if that changes my arm spasticity, right? I can activate presynaptic areas. I might activate my right cerebellum to activate this area presynaptically, or I might do other types of things like visualizing my hand in movement to fire my parietal somatosensory areas to shunt flow to my MCA to see if that changes my spasticity.


So, once you identify a region, you can either activate that area, you can either do presynaptic projections to it, or you can do vascularization. How would you know which one you would do? You would try some things and see if your exam findings change or not change. And the things that change in a positive ways will be the therapies that you do. Okay? So any time you’re trying to do brain rehab, you try to either activate the region, activate projections that are presynaptic to it, or activate areas that have collateral shunting of blood flow. Okay?

So, let’s move on here. So, you have now the brain region localization form, you have your brain compilation forms, you have your cerebral vasculature atlas, and we made together for you a stroke complication chart. And I’m going to update this as we go through. All these charts and things we’re going to keep adding to, making you more efficient as time goes on, but we don’t want to give it all to you at once and have you get depressed, okay? But we just want to give you each of these and the key concepts and pieces to really help you. So, you guys, here they are. Just remember, you’ve got to memorize this. This is a chart, if it were made, were given to you, which means you’ve got to memorize it. You memorize it, this all becomes easy. Okay. And a lot of times people go, “Hey, I don’t know where to start. I’m trying to learn functional neurology; I don’t know where to start.” Start with all the charts, the inflow charts, and forms we give you. Memorize that. Don’t waste your time with other stuff yet. Memorize that and that gives you a strong foundation to understand all of the other material. Okay?

[30.03]

So, here we have – if you guys look at the way these MCA distributions and the middle cerebral artery strokes take place, you have superior divisions and you have inferior divisions, and then you have the deep areas, which are in the lenticulostriatal areas, which impact the internal capsule, and then same with these stem. Stem is right where it branches off the internal carotid artery. So if it branches right off the internal carotid artery, you have more findings than if it was just the end part of the artery, right? So as you get closer to the source of the internal cerebral… to the internal carotid artery, you have more damage and so forth.

So, if you have a left middle cerebral artery damage, what area of… and you… obviously you’re going to impact motor areas of the face and arm, but you wouldn’t have any leg pattern… leg manifestation. So if someone had spastic upper motor neuron patterns, and it included their face and their arm but not their leg, you would think it’s MCA. Okay? What if it just involved the leg? ACA. What if all three of them – face, arm, leg – then it’s not MCA or ACA, it’s probably in the internal capsule. Because all these different branches of the arteries of all these projections of these pathways from the somatosensory strips eventually come together into a little area of the brain called the internal capsule. So when you see… So, think of it this way. If you just see leg spasticity, upper motor neuron signs and it’s stroke, you think it’s what? Anterior cerebral artery. If it’s just face and arm, middle cerebral artery. If it’s face, arm, and leg, you’re probably looking at internal capsule. Makes it very easy, right?

So you have here areas that are… This is a left, left, left, left. This whole page is left. So what part of the area is involved with left? Hemineglect, or language? Language. So as people get more of the inferior divisions involved of it, specifically, they start to get the receptive aphasias, and they get more of the somatosensory parietal symptoms, and paresthesias involved with the parietal somatosensory strip. Okay? But does it include the leg? No. Doesn’t include the leg. Just includes the face and arm, but not the left. Then as you go deep, you get the lenticulostriatal areas. So these right pure motor hemiparesis means face, arm, leg.


It’s all three. Okay? And then you get to the stem branches, which can then cause gaze preferences, and the frontal eye field changes, and the whole cascade of things.

But just understand the concept. If you have… If you’re impacting the left side, for the most part you’re going to have language issues. If you have middle cerebral artery involvement on the right side, you have more of a hemineglect type of pattern. As you have injury to the blood vessels closest to the stem of it, you have more symptoms. As you branch out, the artery branches out, you have less symptoms, because of less tissues that are involved. Okay?

And now you see the right MCA, and same thing. You have superior divisions, inferior divisions. Would you expect to see language issues with the right MCA? No. But you would expect to see hemineglect patterns. Okay? And you would expect to see weakness on the opposite side. So with the MCA, once again, face and arm weakness are the key issues here. And then you see more of the hemineglect patterns as it hits the parietal lobe, and then as you get into the deep areas, you have your pure motor stroke patterns, and then you get into the ACA, left, and that right ACA. These involve the leg without the face and arm. And then you get the posterior cerebral artery, which then causes your visual losses, your hemianopias. Right? And things of that nature.

So, you can learn those really quickly just by memorizing this chart. Okay?

Now, the next page of this chart, the third page of this chart, or fourth page of this chart, starts to go into the brainstem syndromes. And you guys, the brain cortical areas are really easy to remember. When you get to the brainstem, it gets a little bit more complicated. Okay? But to make it easy, here’s what I’m suggesting that you do. Before you start memorizing the brainstem sections, read this paper. Okay? By Dr. Gates. The rule of four of brainstem. If you read this, it all becomes easier. Everything for the brainstem and vascular syndromes become easier, because it talks about how the brainstem is oriented.

So here’s how this works: You have midline, or lateral. So the blood supply to the brainstem either impacts the midline division or the lateral divisions. Okay? Now, in midline structures, you have – what do you put in here? – MN, motor neurons. Those are for the cranial nerves, right? And then you’re looking at cranial nerves 3, 4, 6, and 12. And then there’s the medial longitudinal fasciculus. The medial longitudinal fasciculus is the pathway that makes your eyes have conjugated activities, so when you move one to the left, the one to the right follows at the same speed, and you have conjugate movement between them. People that have lesions, like MS, which is a common area that impacts medial longitudinal fasciculus, their eyes don’t have conjugate movement. Okay?

The medial lemniscus, which is your dorsal column projections – right? – so, posterior column vibration sense, proprioception coming in from dorsal columns, and then you have your motor pathways, like your corticospinal. So if you see someone that has a midline vascular syndrome, you’d expect to see the cranial nerve involved, specific to the regions, so with 3 and 4, in the midbrain – right? – 6 in the pons, and 12 in the medulla. Very easy, right? Here’s the other thing. The midline structures of the brainstem are all divisible by twelve: 3, 4, 6, and 12. It’s the rule of four. Okay? Four cranial nerves – 3, 4, 6, 12 – all divisible by twelve, all midline. So cranial nerves midline, with medial longitudinal fasciculus, with medial column, dorsal column, and then the motor pathways, corticospinal.


So with medial brainstem stroke syndromes, you can have contralateral facial weakness that involves the pons and midbrain; contralateral hemiparesis, arms and leg; contralateral loss of vibration sense; and depending on if it’s in the midbrain, pons, or medulla, you’d have those cranial nerve symptoms on the same side. And that’s one of the features of brainstem syndromes. You get ipsi- and contra-. Any time you see ipsi- and contra- exam findings for a stroke, you know it’s got to be in the brainstem. Okay? If it’s in the cortex, or in the internal capsule, it’s going to be on one side. But if you see brainstem cranial nerve involvement, and contralateral symptoms whether it’s spinothalamic loss, or it’s motor loss, you know you have a brainstem syndrome pattern. Okay?

Now, with the lateral ones, here you have SC, SV, and the SC stands for spinocerebellar. This is important for us for this module, because where do you think posterior inferior cerebellar artery strokes take place? They take place in the lateral medullary area. Okay? Anterior inferior cerebellar arteries, superior cerebellar arteries, they all impact areas of projection to the cerebellum or the lateral pontine areas. So the lateral medullar area is the posterior inferior cerebellar artery; the lateral pontine areas, the anterior cerebral artery, and the superior cerebellar artery really impact projections from the cerebellum to other areas, and you get exact symptoms of either one. Okay? But the key thing is, with lateral brainstem syndromes, you have spinocerebellar; you have cranial nerve 5 trigeminal sensory nuclei, so you get sensory loss in the face; you get sympathetic fibers that are involved so you get your Horner’s syndromes; and then you get your spinothalamic projections here. So when you look at lateral brainstem syndromes, you get ipsilateral Horner’s, ipsilateral sensory alteration of pain, contralateral loss of temperature, and then cranial nerves 9, 10, or 11 vagal loss of pharyngeal spinal accessory, or facial, or trigeminal involved, depending if it’s in the pons or medulla.

So, save yourself a lot of headaches, save yourself a lot of frustration. Try to go through an read the paper we have by Dr. Gates, understand the rule of four, and then once you understand the rule of four, you can go right in there and then go back and then look at your midbrain, vascular syndromes. And guess what? They all get really easy. But if you try to memorize them first, it’s a nightmare. Okay? And again, if you understand the concepts and the general rules, it’s very easy to understand everything else. If you just try to purely memorize, it becomes very difficult.

So my suggestion to you is: Read that paper and then learn the brainstem. And now, over the summer, or between now and the next session, these are the four things you just need to memorize. And if you haven’t memorized these other ones yet, honestly, you’re wasting your time. You’re becoming inefficient as a learner. You should have all these just memorized without question. Someone could pull out anything from these charts, and you should know it. Okay?

So, let’s get into mechanisms of cerebrovascular insults.

[39.40]

Before I go there, let me just recap one thing. At this point, you guys know… You’re going to… You know the concept of shunting, right? You guys know your vasculature; some of you, you’ll have to recall and think about how much you need to go back and memorize, and then you get it down. And then once you get it down, it becomes… Everything else becomes easier; things make more sense. Because as you memorize this… When people learn functional neurology, when they first start, it’s like this huge mass of everything,


and you go, “Oh my God, when am I going to know it all?” But as you learn key concepts and principles, it just gets smaller and smaller and smaller. Right? So hopefully if you guys memorize your brain compilation form, everything – whoossht – got smaller and easier to learn. As you learn your vasculature – whoossht – everything gets smaller to learn. And then you go, “Wow, neurology’s really easy.” Okay? And then everything else applies.

When people don’t know their basics and fundamentals, they don’t know how to interpret an exam finding, they don’t know what to do next, they get confused, they see an exam finding and they freak out. So just make sure you have a good foundation.

Now, let’s talk about things that actually can happen to the vascular system. So you guys remember… You guys know your pathways, you guys know the distribution. But let’s talk about what can happen.

So, you can have different types of stroke. You can have the hemorrhagic stroke. with the hemorrhagic stroke, the artery just ruptures. Most people don’t survive a hemorrhagic stroke. Okay? You can an ischemic stroke, where either an emboli or a thrombus blocks vascular circulation. So an emboli would mean, like, a piece of plaquing breaks off, and then causes stroke into a smaller blood vessel. A thrombus is something like bone debris, or an air bubble, or some kind of cholesterol plaque breaks off and then goes into the vascular system, and then ends up in the smaller blood vessel. The smaller blood vessels are either in the heart or in the brain. So when people get thrombolytic events, they usually end up with small particles ending up in the small blood vessels of the heart, causing stroke, or small blood vessels of the brain… causing heart attack or in the brain causing stroke. Okay?

Then you have lacunar insult, which is a small-diameter infarct, usually by an occlusion penetrating a branch of a larger artery. Then you can have transient ischemic attacks, which is an episode of neurological… the deficit in ischemia, but it’s under twenty-four hours, and there isn’t significant damage but there is potentially some damage. And then you have microvascular disease, where the entire blood vessels of the brain are ruptured. And then you have migraine. Okay?

So, once you’ve memorized the vasculature and you feel really comfortable with it, you want to understand the concepts of each one of these diseases, so it helps you understand clinical applications and diagnoses. So, here’s a plaque, here’s a clot; it breaks off. There’s your emboli, or thrombus, and you get compromise. Two types of stroke: a hemorrhagic stroke, the blood vessel ruptures; embolic stroke, you get an emboli that blocks function.

I’m going to show you guys a video that really does a really good illustration, animation, of different types of strokes, okay? Just a couple minutes, so Ben, if you’re ready for some audio…

There are two types of stroke: hemorrhagic and ischemic. A hemorrhagic stroke occurs when a blood vessel in the brain bursts, due to high blood pressure, atherosclerosis, or a congenital malformation. A burst vessel causes bleeding into the brain and decreased blood flow in the damaged vessel. Blood buildup increases pressure in the brain, damaging nerve cells, and collapsing smaller vessels. The second type of stroke is ischemic stroke, which occurs when blood flow through a vessel is blocked. There are three categories of ischemic stroke: thrombotic, thromboembolic, and embolic. A thrombotic stroke occurs


when flow in a blood vessel in the brain is obstructed by arteriosclerosis. A thromboembolic stroke occurs when a clot breaks off from an arteriosclerotic plaque, and lodges in the downstream vessel, blocking blood flow. An embolic stroke occurs when a clot travels to the brain from elsewhere in the body. Patients with atrial fibrillation, or who have suffered a heart attack, are at high risk of embolic stroke. This is because slow, irregular, or interrupted blood flow has a tendency to clot. Sometimes an individual will experience a transient ischemic attack – TIA – which is temporary, and improves before cells die. A TIA is a precursor to a thrombotic stroke, or short-term embolus.

Okay. So, here’s a scenario with the person having a TIA. So what makes it… How do you know if it’s a TIA? Well, you don’t know initially, because they have symptoms of a stroke, but then either… So the theory is, they do… There’s a spasm of the artery, or there was an occlusion and the occlusion dissolved and broke away. Okay? So that’s the theory. When this starts to happen, they’re going to have a stroke. When people start to have TIAs, there’s a very high probability they’re going to have a stroke, okay? Now, I would also suggest, for your learning the vascular system, I wrote up pretty detailed key concepts for all the major mechanisms in vasculature and strokes in your material. So read over the key concepts, read over the Gates paper, memorize your charts, and then you’ll really start to… This vascular part of the brain becomes very easy to learn. Okay?

So, let’s see this example here. Now, first of all, do you see her face? Do you see a difference? See a facial paresis on the left side? Right? So, the question is, which arteries could be involved that can cause a facial paresis? Could the anterior cerebral artery be involved? No, because the anterior cerebral artery doesn’t distribute to that area. It’s going to be a leg. So right away you know it’s going to be what? Middle cerebral artery, or it’s going to be the middle cerebral artery and the impact could be either in the MCA branches, or involving the what? Motor areas. Or it could be in the internal capsule where you would have arm or leg. But you don’t see arm or leg in this one. So here you go.

[…unintelligible…]

Volume?

... and sensation’s happening again. Smile, is that smile? It’s all tingly on the left side. On the left side. The doctor said breathe in, breathe out, if I’m having distress, and I’m trying. I don’t know why this is happening to me. It happened this morning again. And when I left the hospital Monday night about twelve thirty in the morning. So now I’m taking a picture for an example of what happens. It’s six forty-three. My hand is hard to lift up…

So arm’s involved

… and to touch something, touch my nose.

Okay. So, her face and arm are involved. She didn’t say anything about leg. What branch? MCA branch, right? Left or right side? Right side. Okay. Now, she videotaped this because when she went and told her doctors she was having symptoms of weakness and pins and tingling on her face and these sensory symptoms, they just said it’s stress. So she had to videotape it, and she’s showing she has a TIA. So, this


has happened before, so she’s having these episodes of TIAs. What’s going to happen next? She’s going to have a stroke. So when you start to see TIA issues, you really want to get in there and figure out clinically what you can do to reduce this risk. We’re going to talk about treatment applications and all those as well.

Let me show you another case. Ben, we have videos for a few of these. Okay. So this is a person who gets hemiballistic after diabetic lacunar stroke.

My sugar was way, way high. First it’s a long period of time with this. On Monday afternoon I just started gradually kind of losing control of my right side of my body. And Tuesday, of course, it was worse. And Tuesday, Wednesday, and today are all about the same.

So again, this is a thalamic stroke, branch of what artery? Smaller branch of what supplies the thalamus? Posterior circulation, right? Posterior cerebral. But just… Again, you should be able to look at a finding, and if you know your anatomy we just went over, it becomes very easy to determine what things are there, okay?

So, this is a paper that you guys have in your notes. But just the key thing is, there’s lacunar strokes are very, very common, and they impact the basal ganglia, they impact the thalamus, the corona radiate, and here you can see an illustration here where it impacts the basal ganglia. So all your major fibers go through the internal capsule. And here’s an illustration; you have just a little small occlusion that impacts that pattern. Okay.

So, let me show you a case of basilar migraine. You guys may have seen this before.

[unintelligible] Well, a very, very heavy… ah, heavy… vertation tonight. We had a very, very barrison, but let’s go ahead, terris tasing but a havvin pet.

Right? She’s lost the ability to produce words. She basically had a basilar migraine. So what does… What’s the blood flow for the basilar artery? Basilar artery supplies the entire pons. Right? So when that starts to get into spasm, and starts to constrict, you lose all blood supply to pathways that project for autonomics, for speech, motor pathways, and it looks like it’s a stroke, but there’s no hemiparesis, no loss; it’s just this type of deficit.

[50.10]

Now, the other thing that you want to know, especially when you get into diagnosing vestibular disorders: People sometimes have migraines, and migraines can be anywhere, but for vestibular migraines, the major-ity of them have auras or prodrome patterns before. Okay? So, let me show you an illustration of visual aura. So if someone had a visual aura, and then they got really dizzy, you’d probably think they had a vestibular migraine. They may or may not have a headache. Most vestibular migraines don’t have headaches. They especially don’t have headaches along with their dizziness. They’ll have a prodrome and an aura in many cases, and then they’ll have dizziness. Okay?

So, this is an illustration of what a person going through a visual aura will have. You guys can start to see some deficit in the visual system. So, what they would be experiencing. Now you see it gets bigger and bigger. See the color changes.


So, this is a key concept. Visual aura… You see any aura or prodrome patterns, you know you’re thinking of migraines. You see visual auras before someone gets dizziness and episodes, you’re thinking you probably have a patient who’s suffering from vestibular migraine. Okay?

And then one of the things that you also want to know that can take place with this vascular system is, it’s this microvascular disease. You see all these little black spots? Those are ruptures. Those are ruptures of blood vessels. And people that have chronic hypertension start to get these little tiny strokes all over their brain. So, you know, they get a little stroke and they get spasticity in their limb; they get another stroke, they get dysarthria; they get another little vascular stroke, they can’t feel some things. Then they heal, they go away, and they get another one. They’re constantly having these little mini strokes that happen all the time.

I had a patient recently, and she had microvascular disease, and one of the first things you think about is hypertension. But I ran her homocysteine, and if you guys know, homocysteine should be… we like it below 7 from a functional preventive number. Most labs have a range of 15. Her homocysteine was in the 50s. I’ve never seen homocysteine in the 50s before. But the thing is, she’s had microvascular disease for the past three years, had multiple strokes and seen multiple experts, and no one checked her homocysteine levels, right? So this was very frustrating, because it can damage blood vessels and so forth.

Now here you can see, you know, all of it again. All these different lesions all throughout the brain. So you can have little ruptures of the small arteries; that’s microvascular stroke. You could have hemorrhagic stroke, you could have an ischemic stroke, you could have a spasm, transient ischemic stroke, or an occlusion that dissolves, or you could have another spasm that causes migraines. So, those are all the different pathologies. And where they occur, the symptoms they have, lets you know what those pathways are.

So the question is, what do you do? What are the risk factors that start to cause blood vessels to get injured. Right? So, there’s things that happens to blood vessels that then cause stroke, vascular compromise, and what I want to go over right now is really things that injure the vascular system. So migraine’s just in a dif-ferent category. Because migraines, it’s its own world. We have to talk about that when we do a section on vascular. Because with migraines, peptides, growth factors, hormones, autonomic function, inflammatory changes, can all impact migraines. And sometimes there are multivariable things, and they’re complex. But what I want to focus right now on, I want to talk about risk factors, is what actually causes damage and injury to the blood vessel, right?

So remember the blood vessel, the inner lining of the blood vessels, the tunica intima, which has been reclassified as an endocrine gland, because it produces growth factors and peptides and nitric oxide. So what happens is, things injure and insult this artery. So here’s all the major risk factors that injure the artery.

High blood pressure. So how does high blood pressure impact the arteries? Why does it damage the arter-ies? Well, the pressure hits against the tunica intima. As it hits it against the tunica intima, it’s like waves hitting a shoreline. They start to injure those cells. They start to injure those cells. Those cells get injured, and then calcium deposits start to patch it up, and you start to get this occlusion pattern happening over time. So hypertension is a major risk for all these vascular syndromes.

Cigarette smoking; it… a very inflammatory response to blood vessels. It just destroys and shreds blood vessels. Alcohol intake, and then heart disease. Atrial fibrillation is… promotes people that have more of


a dislodge, because as their heart rate changes, they can have plaque break off, and this becomes a risk. Diabetes creates inflammatory cascades in the blood vessels that destroy it completely. And then blood cholesterol is another factor. And most of the research – you know, it’s controversial with cholesterol – but let me just tell you this: If you have inflammation with high cholesterol and especially with lipoproteins that are more damaging, it is a risk factor. Okay? And then sedentary lifestyle, and then obesity. Those are all involved.

There’s this guideline – and I didn’t include in your notes; it’s free to download, but I didn’t include it in your notes because it’s half the size of your notes. But I know some of you guys are printing this, so if I gave this to you, people would be upset because they’re printing up so many pages. But this is an entire review of the literature, by the leading experts, of all the risk factors for stroke. It’s all summarized in this beautiful document, okay? You can google the name of this, and then download the document and all the research there for all the major factors for stroke, and the studies are all summarized there for you. Okay? So if you have an interest in that, you can check it out.

Now, when people have a TIA, or people have a past history of stroke… So here’s the other thing. If someone has a stroke and they survive, what do you think is going to happen next? They’re going to have another stroke. So once people start to get into the point where they’re getting emboli, and plaque’s breaking off, and they’re having these cardiovascular events, they’re prone to have these things continue. So I want to spend a few minutes here talking about the vicious cycle of things that we see. Okay?

Now, the most common… One of the things you should always do in your office is, look at blood pressure. And you guys, if blood pressure is high, here’s what you need to know: The blood vessels re being damaged. Just the increased pressure to those arteries is going to damage their blood vessels. The higher it is, the more injury they have. Okay?

Now, we know that the most common cause of cardiovascular disease is what’s called cardiometabolic syndrome. So this is diabetes or pre-diabetes, and those patterns. So when you guys see someone who has neurological symptoms, whether it’s TIAs or you can start to see vascular deficits. Now, when we do brain dissections, a lot of times when you look at the brain, you’ll see certain areas of the brain just completely atrophy. So sometimes you’ll look at a brain specimen and you’ll just see the distribution of the MCA atrophy. So you see increased gyri and sulci, but it’s just in that area. And if you go and feel the artery, and cut the artery up to that distribution, you just see that artery’s just mush. It’s just not healthy compared to the other side.

Sometimes people start to get plaquing in certain area of the vascular tree, for whatever – no one knows why – and then they’ll start to have degenerative changes in that area of their brain. So you can also see, if someone has got, like, degenerative changes, they’re impacting their frontal and parietal on their right side, there’s a possibility that they’re getting less blood flow and delivery to those branches that are going into those areas too. Okay?

Now, the key thing that I want to show you here is, these are the different mechanisms that take place. Obesity, insulin resistance, and blood pressure changes, hypertension, and then clotting factors. So with cardiometabolic syndrome, you’re basically looking at someone who’s pre-diabetic, or is diabetic. The main thing you’ll know from them from an initial survey is, they’re overweight. So someone comes in, they’re


overweight, they have hypertension, you pretty much know you’re probably dealing with cardiometabolic syndrome. Right?

Now, there’s guidelines, if you look at their waist-to-hip ratio, and you look at their glucose levels, and look at their blood pressure, but it’s very easy to diagnose cardiometabolic syndrome. On lab work, they’ll have high glucose, high triglycerides, high LDL, high total cholesterol, low HDL. But at a mechanistic point of view is, these inflammatory react… these pattern shifts actually cause increased fibrinogen, which is prone to clotting and developing embolic strokes. They get high blood pressure, which damages the blood vessels, and they get insulin that causes inflammation. So when you have inflammatory reactions from insulin that activates something called the rage inflammatory cascade that destroys blood vessels, in combination with blood pressure destroying those blood vessels, in combination with fibrinogen levels going up, which takes place with them, they’re basically developing a recipe for stroke. Okay? Then they end up with fatty liver and so forth.

So, these are just some of the lab markers – you guys that are doing blood work – that you’ll see with people that have cardiometabolic syndrome. And on a routine blood test, you’ll always have glucose and lipid panels, for the most part. You can always look at things like HbA1c, which is a better marker.

[1:00.01]

Now, HbA1c is glycosylated hemoglobin. And it’s not just an average of blood sugar for six to eight weeks, okay? So remember, you’ll have people that have normal fasting glucoses that sometimes, just from the inflammation, have high HbA1c. They’re getting high amounts of oxidation, which is a major risk factor for their blood vessel health You guys see how HbA1c… You know, you have to load them up on anti-inflammatories, antioxidants, and if you’ve already managed their blood sugar, and it’s under control, you’re dealing with an inflammatory free radical process. As you get that under control, you’ll see tat HbA1c drop. Okay? Don’t think… Please don’t think all HbA1c elevations mean you need to improve their insulin resistance and support that pathway. A lot of these are related to oxidative stress and inflammation.

So, when people have cardiometabolic syndrome, it clues to you that they’re having significant inflamma-tion of their arteries. If you look at their blood work, you can look at their ferritin. Ferritin is a marker for iron storage, but it’s also an acute phase reactant. When people are inflamed, they have very high ferratin levels. If you guys see very high ferratin levels, HbA1c, and high blood pressure, guys, that’s the recipe for stroke. Okay? And then, as people develop metabolic syndrome, some get fatty livers, their uric acid levels go up, they may get… renal impairment gets more progressed. But then you can see increase in platelets, increase in fibrinogen, and so forth.

So, let me give you an example. Someone comes in to your office, and say they have a transient ischemic attack, and they had some neurological symptoms. Just like that lady, that video I showed you. Let’s say she becomes your patient. “My doctors didn’t believe me; they thought it was always stress. I did this video. They still think it’s stress-based. I’m tired. Can you help me?” So she goes over the symptoms, and she tells you, “Hey, my face gets tingly and numb and feels off, and I can’t move my arm and I can’t move my face.” Okay? And it’s on the left side. So now you know, as a clinician, what? It’s left MCA. And it goes away in a few hours. And several episodes have happened, and it’s in the same pattern. So now you have something happening in the MCA artery, whether it’s a spasm or some plaquing breaking off, or something.


Now, you look at her labs. Let’s say you see high glucose; she’s pre-diabetic. You look at her blood pressure; it’s high. Okay? What would you do from a neurological therapeutic perspective, and what would you do from a laboratory perspective? What followup tests would you do, and what kind of nutritional intervention would you do? How would you mix it all together? So let’s talk about that for a second, okay?

So let’s say you look at her blood work, and she’s a little bit overweight, and she has some insulin resistance patterns, but you look at her HbA1c, and remember that should be below 6.5, so her HbA1c is 7.9, which is pretty high. Okay? But her fasting glucose isn’t in a diabetic range yet. And then the other marker you look at, you look at her blood work, you see her ferratin and CRP are very high, and you look at her platelets; they look normal. But you order a fibrinogen, and her fibrinogen levels are off the chart, which is the clotting proteins impacting blood vessels. Right? So now you go, “You have fibrinogen elevation’s high, you have HbA1c, you have hypertension, and you have an insulin resistance pattern. Do you want to ignore those?” Please don’t be the neuro wizard that’s going to go, “Oh, I’m going to do some brain stimulation and do a party trick, and everything’s cool, and diet and nutrition don’t really matter; that’s all crazy.” Don’t do that. This is a person you have to help, okay?

Now, if she’s not a full-blown diabetic, what are you going to do in the conventional medical model? Not much, unless they see… Some doctors, some really sharp physicians will go, “Hey, you have TIAs ,” and might immediately put them on blood thinners, immediately control their blood pressure. Right? But it’s really common to not have that happen too. So you can then go in there and then try to control her insulin-related patterns.

For me, in my practice, with patterns like that, I’d probably put them on a fast right away. I’d put them on fasting for, like, two to three days, and then… because I want to get everything down as quickly as possible. So if I can have them go into a fast for three days, you know, where they have water or… one of the things we do, we have them make, like, limeade or some people call it Master Cleanse: just water and some lemon juice and a little bit of maple syrup. Just have that, and drink that every fifteen to twenty minutes for, like, three to four days, just so they don’t totally pass out. You’ll see all your numbers drop within the end of three days. You see blood pressure go down, you see HbA1c levels drop, you see fibrinogen drop. HbA1c not as much – a little bit of slight – but you see definitely things like ferratin, CRP drop, fibrinogen markers change. It’s pretty cool. Okay? And I would have them do that, and then repeated stages of that, like three days, take a break for a while, do another three days, do another three days, until that acute stage of that pattern gets under control. And I’d be putting her on high amounts of antioxidants and anti-inflammatories to block her blood vessels destruction, help with that. And then I want to see that HbA1c start to go down, I want to see her swelling and inflammation throughout her body go down, and that’s how I’m kind of going to managing that pattern. Okay?

Now, she has an MCA issue. Do you want to activate it or not? If you activate it, and there’s already some vascular insults there, you may promote it, especially if she has no brain deficit. You understand? So this becomes a clinical call which you want to do. For me, I would handle that metabolically, completely, for a while, and just see what happens to all those symptoms, and then when she’s stable, I would look for any deficits and any branches of the MCA – frontal, somatosensory, right motor strip – if there’s any deficits there, and then slowly do some activity. But in very acute stages, I wouldn’t want to go in there and increase shunting of blood and blood flow to an area where the vasculature could be compromised. Okay?


And then this is just a diagram that shows these different cascades that take place. Now, for metabolic syndrome, you know… One of the things you know is we have this inflammatory cascade, we get hormone shifts, we get intestinal permeability. Those are all involved.

Now, I want to move into things that… vascular problems that can include dizziness and vertigo, as we transition into this peripheral vestibular system. So let me just kind of give you a big picture snapshot of where we’re going. What we’ve done this morning is, we’ve kind of reviewed over the basic concepts from past modules, and then started to translate into the vestibular system. What I’ve done for this section is, I wanted to go over the vasculature and teach you the vasculature, show you the mechanisms. But now I want to transition it into vestibular vascular insult patterns. Okay? Things that can cause dizziness, things that can cause vertigo.

So, the vascular syndromes that can cause dizziness and vertigo involve, first of all, these arteries, which are which ones? Posterior inferior cerebellar – right? – anterior inferior cerebellar, and superior cerebellar artery. So that’s it. So if you’re thinking of… If a vascular pattern is causing dizziness, these arteries have to be involved. Now, you could have a basilar migraine cause it too, because the basilar artery can spasm and increase blood flow to these distributions. Okay? So, let’s go through each of these.

Let’s talk about vestibular migraine first. The key thing with vestibular migraine is a prodrome or aura before the onset, in most cases of dizziness and vertigo. Now, when you look at the stats on this, only ten percent of people have this for a few seconds. The most common… Thirty percent of people have vestibular migraines, and the vestibular symptoms last for several minutes. Thirty percent have them last for several hours, and thirty percent have them last for several days. It can be up to two weeks. So someone can have vestibular migraine and then have dizziness that won’t fit any pattern that we’re going to teach you – it’s going to be it’s own all-over-the-place type of pattern – because for most of these, the basilar artery is basically what’s involved. It’s constricting abnormally, it’s spasming, and that impacts blood flow to these divisions into the cerebellum. Or it could even be the vertebral artery that’s compromised or spasming. But some division of blood supply to the cerebellum is having these spastic types of activity that’s then causing migraine. Okay?

So, it’s not the stroke pattern. What’s the stroke pattern? Acute, abrupt, severe symptoms, nystagmus, severe vertigo, panic, brainstem symptoms. This is just they have some aura, prodrome, visual aura is the most common thing, and then they have dizziness and vertigo that lasts for some period of time.

There’s a great paper that you guys have in your notes that really goes into the basic concepts of diagnosis with vestibular migraines. But I want to show you a history of a patient that suffers from it. So Ben, can we have volume here?

So, when I first came in for assistance with my migraines, I was falling all over and was having migraines…

This is not my patient

… every day, twenty-four seven. I was sensitive to light. I had very much trouble reading, and I wasn’t able to walk in a straight line, and had very much trouble concentrating on whether it be the person in front of me or on an idea. I was treated with physical therapy


and medication, and now I can see clearly, I can read fine print, I can walk in a straight line. I was in a wheelchair, but now I can walk freely by myself. I can exercise completely, and things are much better.

[1:10.29]

So, this was a hist… This was not my patient. This is a history of a patient suffering from vestibular migraine. But I just want you to get an idea of the severity of it. So, once that basilar artery goes into spasm, or branches that go into the cerebral artery go into migraine in a spastic pattern… I mean, people are disabled. Okay? And dizziness is one part of it. It’s completely different than benign positional vertigo that lasts a few seconds. It’s completely different than an infection like vestibular neuritis. So, the key thing is that they can last for a long period of time, and there’s all these diverse symptoms that take place.

I’m personally, you know, always like to do things naturally, but if it’s a vestibular migraine, I mean, the medications for it work really well, and you can go ahead and do all your rehab and do all the functional medicine stuff afterward, but they need treatment. So it’s really important to get them wherever they need to, to get the best change.

So, we talked about vestibular migraine. So you guys understand the concept. Now, Dr. Brock’s going to go over the diff-di with all these different syndromes for you. I just want to give you guys a review of the vasculature as we get into differential diagnosis.

Now, the two main stroke patterns that are involved with dizziness and vertigo is your lateral medullary syndrome and your lateral pontine. Why lateral? Because your spinocerebellar projections and vascular supply to them is in the lateral parts of the brainstem, not in the midline. Okay? Your lateral medullary syndrome is your posterior inferior cerebellar artery, and your lateral pontine syndrome is your anterior inferior cerebellar artery. Superior cerebellar… I’m sorry, superior cerebellar arteries are not commonly involved, but they can be, and they mask both of them. Okay? But the most common one would be the lateral medullary syndrome off the… the branch off the vestibular arteries.

So remember, the rule of four. If you guys look at the rule of four, here’s your lateral brainstem patterns. This is your lateral medullary pattern. So when you look at your PICA syndrome, the blood supply from your posterior inferior cerebellar artery goes to the cerebellum, but it also vascularizes the lateral medulla. Okay? And this is why, in addition to getting nystagmus and vestibular symptoms, you hit the spinocerebellar pathways, and get the ipsilateral ataxias and dysdiadochokinesias. You hit the spinothalamic 5, so you get the facial tingling, numbness, paresthesia; you get a sympathetic involvements, so you get a Horner’s syndrome – right? Horner’s syndrome – you get ptosis, and the pupils are… The sympathetic pathways are involved so they can’t dilate, so it’s constriction with the ptosis, and then anhidrosis so they have less sweating on that side. If the spinothalamic projections, so you have contralateral, pain and temperature loss, so it becomes a pattern. Ipsilateral, Horner’s; contralateral, alterations of pain and temperature. And then you get cerebellar ataxias on that side. They get nystagmus, they get vertigo. So if someone all of a sudden has new onset of dizziness and vertigo, and you see nystagmus, and they have facial pain and paresthesia on their ipsilateral side, and they have contralateral spinothalamic loss of pain and temperature, it’s not the vestibular apparatus. It’s a stroke. It’s a lateral medullary syndrome. Right? And these are… These need


to go to the ER, because most of these are ischemic, and if they can dissolve that emboli right away, you have some protection there.

So, this is the breakdown of symptoms of lateral medullary syndrome, and these are all the structures that are there. So, loss of… sensory loss, face, pain and temperature; facial pain; ataxias, arm and leg on the same side; gait ataxia; nystagmus; nausea, vomiting; vertigo; hoarseness and dysphagia, because why? These are cranial nerves 9 and 10 that are in the lateral part of the brainstem. It’s not 3, 6, or 12, which divides by twelve; they’re 9 and 10. So these are on the lateral side, when we look at the rule of four. and then hemisensory pain and temperature, hiccups. Those are all signs of that.

So, you can go through your forms and we have them all broken down for you as the Wallenberg, posterior inferior cerebellar artery syndrome, and those diagrams, and then this one here. Marie-Foix syndrome is involved with… It’s basically anterior cerebral artery, or basilar artery division.

So, here’s a distribution of blood vessels, and if you take a look here, this is the inferior cerebellar artery stroke, following vertebral artery dissection. So the vertebral artery dissected, and you got a little bit of emboli into the vasculature, and you guys see that? Right there? On the right. Okay? So this is stroke, and if it is involving the posterior inferior cerebellar artery, and it’s on the right, what kind of symptoms would you have? You’d have right-sided what? You would have right-sided cerebellar symptoms, ataxias and so forth. You would have a Horner’s syndrome, you have contralateral spinothalamic loss, you have facial pain that’s involved. So those are all the things that are involved with the lateral Wallenberg syndrome. And lateral pontine ones are very similar to that. You guys take a look here. It’s the combination of contralateral symptoms involving the rule of four. But with the pontine ones, you don’t get the dysarthria, you don’t get the 9 and 10 involved. Okay?

Now, look at the labyrinth artery syndrome. You guys, look at the blood supply here. Right off the anterior inferior cerebellar artery, there’s the internal… you guys see this internal auditory area right here? This blood supply? This is what gives blood supply to the saccule and to the utricle. So sometimes when you have a migraine spasm here, or an occlusion here, you can cause all types of vestibular-type syndromes, which include hearing loss. So you get hearing loss, and dizziness, and it’s abrupt, immediate onset, and it doesn’t involve other brainstem areas, it’s just hearing loss and tinnitus and vestibular disease, you may have a labyrinthine artery syndrome. Okay?

Then you have your vertebrobasilar insufficiency, which you can see here. This is an MRA, it’s the angio-graph. Here’s the vertebral artery. It’s supposed to become the basilar artery, and then lack of blood flow, as you guys can see there. Okay? And with the vertebral basilar insufficiencies, those are the symptoms. You guys are all familiar with them. Double vision, nausea, vomiting, slurred speech. It looks just like the stroke patterns, just don’t have that clear, always, brainstem patterns. And you can change these with position. So a lot of people get vertebral artery basilar insufficiency, and strokes related to that, when they are stuck in a position to extend their head backward.

You know what the most common cause of some of these stroke patterns are? It’s people going to their hair stylist. Not people getting adjustments. So they go and get shampooed, they strain an artery that’s already injured, they stretch it, and then they get it dislodged, and then they get the stroke pattern. So most hair salons have to carry these insurances, medical insurance plans, for people that have these vertebral artery


dissections as they get their hair shampooed, and then end up with PICA syndrome or lateral Wallenberg syndrome. Okay?

So, just remember: Go through your notes, make sure you guys know the branches – okay? – for this course, this module, related to dizziness and vertigo. Make sure you guys understand that the vertebral artery branches have the PICA, posterior inferior cerebellar artery, the anterior inferior cerebellar artery, the superior cerebellar artery; the posterior inferior cerebellar artery, the lateral medullary syndrome being the most common one. And then you can go in there and look at each of these different conditions, okay?

So, let me summarize the key points here. First of all, let’s go through this.

Vestibular migraine: how does it present? Aura, prodrome before vertigo attack, vertigo attack can go away, then they can have a headache, or they may not have a headache at all, but it’s usually the prodrome, aura type pattern before they get their dizziness.

Lateral medullary syndrome: what do you have? You have acute, abrupt onset, vertigo, nausea, nystagmus, facial pain, spinothalamic loss, Horner’s syndrome. That’s a whole cascade of brainstem patterns. Lateral pontine is the same thing; you just don’t have the dysphasia, the dysarthria, because there’s an impact, 9 and 10, that’s higher up in the pons. Okay?

And then if you have a labyrinthine artery syndrome, what do you get? You don’t get as much of the brainstem involvement, but you get hearing loss, you get dizziness, okay? And then as you get into superior cerebellar arteries – we’re going to talk about that – but they cause the same thing: acute, abrupt nystag-mus, vertigo, cerebellar symptoms. And then you have vertebral basilar insufficiency, which causes diplopia, vertigo, but positional changes tend to make it the biggest influence, and vertebral basilar insufficiencies take place usually because there’s arteries… those arteries are already calcified and plaqued, and if those vertebral arteries are calcified and plaqued, and you extend… you stretch that area, they get less blood flow to the brain and they can have some symptoms, but that means there at major risk for what? They’re at major risk for a lateral medullary stroke, because the vertebral arteries, they get further occluded, or branch off, and emboli can go into the posterior inferior cerebellar artery, which you’re worried about. Okay?

[1:20.21]

Now in summary, this is what we’ve gone over so far. We’ve gone over the general cerebral vasculature and vascular syndromes. So once again, memorize these four documents. Okay? Just own them. And once you own them, you’ll be very surprised at how much you know. Okay? Then from there, one of the key concepts that we just went over is, you can – once you know your vasculature – you can design protocols and therapies to activate regions of the brain by using the same blood vessels to nourish that area as well. So we gave you several examples of that. And also realize that sometimes we need to do challenges to a patient’s brain by doing different stimuli of thought cognitive processes, or balance exercise, or eye move-ments. You may see change in areas, not because you directly activate it neurologically through presynaptic pathways, but you activate it shunting blood flow to that area. So if you know your vasculature, that can make a difference for that as well.


And as you get into mechanisms of cerebral vascular insults, you have the hemorrhagic strokes, which most people don’t survive with; your ischemic strokes; your lacunar strokes; your TIAs; your microvascular disease; and your migraines.

Now, let’s talk about stroke patterns as a review. If I just have spasticity, upper motor neuron symptoms in my face and arm, which artery? MCA. If it’s just my leg, it’s what? ACA. If it’s all three, then you’ll probably think of a lacunar stroke impacting the internal capsule. MCA branch, lenticulostriatal branch. So that immediately just saves you so much time, because you can visibly see someone and go, “Is their leg involved? Are they in the spastic posture? Is their face involved?” Then you can immediately go down to the arteries, right?

Another key feature that you need to… by vascular syndromes. If you see ipsi- and contralateral, if you see cranial nerve findings and contralateral sensory motor loss, you know right away that it’s what? It’s a brainstem syndrome. Okay? Because all the cortical regions are always on the contra. All the brainstem regions have ipsilateral cranial nerve involvement with contralateral motor sensory losses. Okay?

Now, the key difference with a TIA is, it looks just like a stroke, but it doesn’t last. But once they have a TIA, they’re prone for a stroke. So you want to go on there and look at factors. Most common things would be metabolic syndrome, cardiometabolic syndrome. High insulin, high glucose, high blood pressure, obesity, inflammation, high homocysteine. Those are factors that you want to look in there. And then microvascular disease is little small little infarcts people have all the time. Most common cause is hypertension, and then over time, destruction of the blood vessels. So it’s… most of these vascular syndromes, whether its stroke or transient ischemic attack or microvascular disease, it’s inflammation destruction of the arteries, in combination with high blood pressure. Okay? That’s usually the culprit. And then you have migraines, which could be a whole list of mechanisms.

And then we went into the vascular syndromes that can cause dizziness. So one more time: Vestibular migraine. Symptoms? Aura, prodrome before dizziness, vertigo. May not have headaches involved, but sometimes they do. But usually the vertigo and the headaches don’t want to accompany each other. Lateral medullary, lateral pontine, you have immediate onset of symptoms, you have brainstem involvement, right? Dysarthria, dysphasia, facial pain, Horner’s syndromes. Right? And then labyrinthine artery syndrome, you don’t have all the brainstem involvements, but you have loss of hearing, you have vertigo, dizziness. Superior cerebellar artery can be any diverse cerebellar symptom, hard to tell. And the vertebrobasilar insufficiency stage of it is when you stretch the artery. You can know people extend their head, they can feel those.

Now, there’s two symptoms, there’s two patterns that people develop symptoms when they extend and rotate their head. BPPV, and vertebrobasilar insufficiency. So what’s going to help you distinguish one versus the other? One could be, if the they have nystagmus, see what direction their nystagmus is. Because if it’s upbeat torsional, then you know it’s BPPV, because it’s the [?] canal, which pushes their eyes in that specific direction. If it doesn’t push them in that direction, and at the same time their speech goes and you have brainstem symptoms, in addition to some mixed nystagmus all over the place, then you know that it’s more a vascular pattern. Okay? So those are things to consider as you do your diff-di.


So where we’re at right now as we go into… We’ve gone over this general cerebral vasculature and vascular syndromes, and then we went into the vestibular system. Okay.

Now, let me put this together for you in the context of what we’ve done and where we’re going, okay? We had to go through and review all the vasculature for you, so you can go over the brain region localization form. So know those forms, and then memorize that atlas I gave you, and if you have that atlas you can clearly see the different patterns. The brainstem is a bit difficult, because there’s so many structures in a very small region, but just know this: cranial 3 and 4, if you see any involvement, it has to be in the midbrain. If you see 5, 6, 7, 8, it has to be pons. If you see 9, 10, 11, 12, has to be in the medulla. So if you know your cranial nerve findings, then you pretty much know if you see any vascular compromise it’s going to be in which area of the brainstem. Then you can use the rule of four. The rule of four midline, you have what? You have your cranial nerve motor, 3, 6, 4, and 12… right, I’m sorry: 3, 4, 6, and 12; 3, 4, 6, and 12 that are midline by the rule of four. They’re all divisible by twelve. Medial longitudinal fasciculus, which allows you to have conjugate eye movements; medial lemniscus, which is your dorsal column projection pathways – right? – for your balance and position sense; and you get your motor neurons, which is your corticospinal tract.

So if you have cranial nerve 3 and 4 loss, and you have spasticity in one side; if you have… Let’s say you have an eye that’s deviated out, you have a ptosis, and you have spasticity in one side, you guys know that the lesion is where? Midline. And since you see cranial nerve 3 involved, midline midbrain, because cranial nerve 3 is in midbrain. Okay?

So, go through the rules of four, know which… Review all your cranial nerves, and once you know the cranial nerve, and you see ipsilateral cranial nerves and contralateral motor symptoms, those are all you midline brainstem strokes. And then when you go into the lateral parts of the brainstem strokes, that’s when you get your ataxias, your Horner’s syndromes, your facial pain, and your contralateral spinothalamic loss; pain and temperature loss on the opposite side. Okay? So if you see facial pain, pain and temperature loss here and facial pain, and then spinothalamic pain and temperature loss here and paresthesia on the opposite site, right away, since it’s on the face and on the opposite side, you know that it’s brainstem, and it’s going to be involved… All the cranial nerves are ipsilateral to where the vascular lesion is. So that would be a lateral brainstem stroke. Okay?

Now, whenever you see these patterns, whether it’s migraine or vasculature, I’m just going to go out and say this: There’s always a nutritional dietary metabolic component. Injury to the vascular system should always recur at some point for you to do a nutritional metabolic vascular component. The key lab markers you always want to do, when anyone has TIA, stroke, as a summary is, you want to make sure you look at homocysteine for methylation defects; CRP for inflammation; ferritin, which is sometimes even better than CRP to find acute inflammatory reactions; fibrinogen as a factor to look at clotting; and then just look at your overall lipid panel, and just see what’s happening with them. Usually when people start to have chronic insulin surges, the chronic insulin surges, the insulin, will shift their glucose metabolism so their triglycerides will be equal or higher than their cholesterol. Whenever you see that, you know you probably have the metabolic syndrome pattern. Those are accompanied by hypertension.

So hopefully, you guys understand the vasculature of all the major regions of the brain – right? – as a review, vertebral arteries come in basilar artery, and then you have your… as far as your cortex goes, posterior


cerebral artery. What is the posterior cerebral artery give vascularization to? Posterior region of the brain, the midbrain, and the thalamus. Post… That’s all posterior cerebral artery. Middle cerebral artery: What’s the vasculature? The vasculature is the anterior parts of the brain, your frontal parietal areas, and then the deep branches, or the stem branches go into the lenticulostriatal, which is the internal capsule. And the anterior cerebral artery is your Mohawk, where your leg and limbic areas for behavioral and patterns and your micturition centers are. Right? Go to the anterior cerebral artery, you have presentation in the leg, you have personality changes because it hits their cingulate, and you have urination because it hits their urinary micturition centers. Those are common patterns there.

So those are the cortex patterns, and then you have your cerebellar branches: PICA, AICA, and SCA. Right? Posterior inferior cerebellar, anterior inferior cerebellar, and superior cerebellar. That’s the vasculature; those are the mechanisms. Go through those, and this vasculature thing can become really easy. Read the key concepts, memorize the charts, go over your compilations.

Okay, that’s it for now. We’re going to take a break for lunch, so you guys, see you guys after lunch.

[1:30.40]

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