Okay, so here we are. Quick review, because we don’t have ... · Okay, so here we are. Quick...

MODULE ONE TRANSCRIPT – CEREbRAL CORTEx | COPyRIghT © 2016 FUNCTIONAL NEUROLOgy SEMINARS LP | PAgE 1

FUNCTIONAL NEUROLOGY ANATOMY AND CENTRAL NEUROLOGICAL PATHWAYS (MODULE ONE)

Transcript – Brain Clinical Concepts of the Cerebral Cortex

Presentation by Dr. Brandon Brock

Okay, so here we are. Quick review, because we don’t have to get into too big of a hurry here. And again, some of the repetitiveness I think is important. We’ve looked at “Where in the world is the problem?” Can you start to identify, “Hey, it looks like there’s a problem here, or a problem there, or in multiple areas.”

So let me just break this down for you again. Is it in one Brodmann area? Or one portion of one hemisphere? Or the whole hemisphere? Or are multiple areas starting to neurodegenerate? Or is it in other structures like the basal ganglia, which we’ll talk about tomorrow. Or the cerebellum, which we’ll talk about tomorrow. Is the vestibular system starting to become involved, which we’ll talk about later on.

So the rest of the day is going to be involved with this thing called the cortex. And we decided to do this. First, give you the big concept. Why are you here? What is different than other components of medicine? What does it mean to have plasticity? What does it mean to be able to change a brain? What are your limitations? What are your capacities?

And then as we get that big picture, you know there’s a smaller picture called the cell. Is the cell stable? Is it becoming plastic? Is it becoming immunoexcitotoxic? Is it starting to die? Is there inflammation?

And all of those metabolic things we’ll get to as we go through the program, so I’m giving you that promise so that you don’t have anxiety. And now we’re going to bloom out to the area called the cortex and start saying, “Hey look, here’s some generalities about the human cortex.”

Now, we’re going to do it in an hour and a half. Good luck, right? What I want you to understand is this: I don’t care if you understand every single thing about the cortex, because the cortex will be sprinkled in multiple other modules. When we start talking about treatment, and we start talking about doing this and doing that and, you know, we sat down and very methodically put it together. But we want to start with the outer noodley thing called the cortex, and I want you just to be able to kind of put your hand on your own head and say, “If I was going to drill a hole here, this is what would be going on right underneath it.” Okay?


So to kind of get you to appreciate your… this is the beginning of your journey. So today we’ll talk about cortical function, then Dr. Kharrazian will come behind me and talk about what happens when those areas start to screw up. What do they look like? And then at the end of the day we’ll talk about human language. Because language is a very good way to give you a representation of the whole thing. And it will change you. Whenever you start to see some of the language stuff.

So involved in a lot of this… now one of the things whenever I was learning neurology that bothered me to death is, nobody ever gave me any terms or definitions. I don’t want to bore you. I’m going to give you some terms and some definitions, but I’ll try to put clinical meaning around them, so that at least it’s not just me reading off a slide, which we just don’t want to do very much, okay? But it’s something that we have to be able to do because at the very beginning, you’ve got to learn to speak a language, and that language is the language of neurology. And you have to know what some of these words mean so that as we go on, and I just sort of nonchalantly use that word, I don’t have to go back and continuously redefine it. We have quite a bit of that in language, and we have some of that in cortex. Okay?

So as we get going, this is the most amazing structure that probably has ever existed that we know of. Up to a hundred billion neurons, maybe a few more or less, depending on who you are. We really have this giant frontal lobe up here that does everything, like give us executive function, make us plan our day, make us be motivated, make us be able to prioritize things so that we can do this before that, so that we can become executive. And when I mean executive, I’m not talking about being a CEO, I’m just talking about life.

Life requires a certain level of executivism. And one of the things you’ll find is when you start to lose cortical function, the executivism of life starts to wear people down. They can no longer multitask, they can no longer keep up, and it really does stress them out to the point to where their stress hormones may go up. And let me just say something about stress hormones and brain. They kind of kill brain, in particular the hippocampus. And the hippocampus is deep; it’s that little thing that gives the short-term memory. But one of the first things that starts to go with stress and hippocampal damage, before the frontal lobe goes away and before Alzheimer’s goes away, is depression.

So we have a big journey. I have to be able to talk to you about, “How does this thing develop from the embryological perspective, and what does that mean?” And then I have to go through this and say, “This is what each region is, and kind of what it does, and these are some things that you’ll see whenever you look at the function.” Dr. Kharrazian will come back and say, “This is what the dysfunction looks like.” So all the way through this, we’re going in tandem back and forth.

And then I’ve got to make sure that you understand the anterior from the posterior, the left from the right, the middle versus the outside, and the up from the down. Make sense? And then I’ll teach you little swirl-ing patterns, like language. It’s just a little swirl right here. There’s the motor centers, there’s the sensory centers, and there’s sensory pathways and then motor pathways, and then there’s auditory integration and visual integration. And I’ll just show you – hey – there’s five terms you need to know. If you know the five terms, the five conditions, it will take you five minutes. Got to put it together somehow, right?

Okay. So this is that cortex. You see a beautiful temporal lobe out here, and this posterior occipital region for vision, and this right here gives us auditory function, and it all integrates right here into this parietal lobe, and then we go up here in the frontal lobe, and then here’s the cerebellum that sort of helps orchestrate the


whole thing and organize it and plan it and put things in sequential order. And I’ll pull apart the cerebellum for you tomorrow, and start showing you how to clinically look at it and what it means.

So the goal of the weekend is for you to be able to walk away and just do the one box that Dr. Kharrazian said, and that is, “Do I know anything about where the problem is? Can I know start to talk to somebody and say, ‘Man, your orbitofrontal system is bad’?” I’ll show you what that looks like. There’s a few of us that are here – mine’s probably not the best either; I don’t know. So every now and then there’s a little impulsive. Okay.

So we’ve go to… Here’s some of the key concepts. We have to know embryology, okay? And not from the perspective of “here’s the telencephalon,” but I want to show you how the diencephalon and the mesencephalon fire the telencephalon, and how the outpouching of the pons, which is myelencephalon fire into the pons and how they all integrate together. So the way they bloom out shows us the order, and then that order tells us how we can treat things.

Now, let me go back and just tell you this. If I have somebody with a frontal lobe lesion, and they can’t handle frontal lobe activation, I may go to an embryological derivative and say, “I can activate that area,” because I know it is hard-wired and connects to that area, and it’s more of a subtle approach. Okay?

So we don’t always directly bust down the door that we need to go to. Sometimes we go through the back door, and do some things to kind of creep in on that condition and make it better.

We’re going to know the anatomy. I don’t care if you know every gyri and sulci. If you want to learn it, knock yourself out. And that’s probably what you’re going to do is knock yourself out! But, you know, we’re not going to get quite… But I want you to understand regions, and I’ll give you some Brodmann regions and say, “Hey, 3, 1, and 2 means this; 5 and 7 means this.” But I really care this: what’s going on in that area, and can you recognize it if it’s a pathology versus writing “Brodmann area number such and such”? Because you really can’t do that in your notes anyway, because you don’t know. You’re not doing an EEG, you don’t have 24 spikes or leads. You don’t… you’re just saying, “It looks like your parietal lobes aren’t so good because of these tests.”

And I’m going to show you some simple tests. And then I’m going to go home later on and make videos on how to do each one of those tests, so that you can go back and replay them over and over and over and know how to do it. Because some of you don’t have a lot of clinical neurology examination skill, and that’s not saying anything negative, it’s just saying that we know there’s gaps we have to fill. We can’t ask you to evaluate these things if you don’t know the tests to evaluate them. And the best way to do it is to have a bank where you can go back and watch it. Fair enough? Okay.

So, left and right. You’ll find out that some people have hemisphericity. Meaning one whole hemisphere seems to not be as functional as the other. Now, it’s not as common as you would think. A lot of times this is spread out. There’s a little bit of the right, there’s a little bit of the left, there’s a little bit of this, that, and the other. Sometimes one hemisphere will really just outshine the other and further suppress it. So if one’s really dominant it may kind of suppress the other, and then you may see clinical symptoms because of this one, or clinical symptoms because of this one. Alright?


Well, what’s the difference in the front versus the back of the brain? Hey, is it sensory or is it motor? Left versus right? Is it creative versus intellect? Upper versus lower? Is it leg, arm, auditory? Everything in the middle: emotional, limbic. Everything outer: more executive, higher function.

So I’m going to start giving you some generalities so that we can kind of creep our way in from the generali-ties and get more specific, and then once we get more specific, I’m going to give you some examples of, “Hey, person walks in with this, do you know what it is?” Or, “What do you suspect?” And, “By the way, does it show up on MRI?” You don’t always have a tumor, a meningioma pressing on something. A lot of times it’s just a group of cells that don’t fire and don’t summate, or are physiologically dysfunctional, so you see a brain that is not orchestrated or in harmony. That can happen from underlying metabolic disease, it can happen from trauma, it can happen because you’re genetically not what you should be. The vast majority of people, if you ask them, they’ll sit down and say, “Yeah, I have a little cognitive complaint, and I wish I was better at this. I wish I was better at that. I wish I was better at names. I wish I was better at faces. I wish I was better at math.”

And I also want to say this: We’re not here to, like, diagnose personality and say, “Man, you can take somebody with this personality disorder and completely change it.” What we’re trying to do is say this: “There’s been a big change in cortical function, and based upon that change, can you identify it?” Later on we’ll teach you how to treat it, and we’ll teach you how to monitor it, and we’ll teach you how to do this: multiple things to really get specific on localizing it.

So all these things. Know the regions. I gotta know… you have to know the layers, and then I have to go into neurochemistry just a little bit. Neurochemistry is like one of my favorite topics, because if neurochemistry is not balanced, or not correct, meaning the level of neurotransmitter or the level of post-synaptic receptors, and then the capacity of the recycling mechanisms – if they’re all off, there’s going to be a problem. There’s going to be symptoms. Okay?

We can do an easy experiment. I could just give somebody a high dose of psychiatric medication that didn’t need it, and just watch them change. You know? If they have a problem and you give them that medication, and they do better, then hey! it was therapeutic. But if somebody takes it and they’re tripping out, that’s called acid. As I look around…

So this is kind of the [?skip in playback 12:18]. There’s embryology, there’s neurotransmitters, there’s anatomy, there’s cortical function, and then there’s layers. I just need you to get a grasp, just a simple grasp on each one.

Now here’s the disclaimer: I’m going to be basic and go through it. Every now and then you’ll see me jump through and say something that sounds kind of crazy, but I’m doing it for people who have already been through the program, and I’m going to give them a little advanced piece. Don’t let that short-circuit your brain if you haven’t been through the course yet. I just need to warn you, okay? Maybe I should just say, “Earmuffs.”

So, reflex. Now before we get going, I have to do this, because I got a report back from an orthopedist the other day, and this gentleman said, “The patient has hyperreflexia. This is obviously a lower motor neuron lesion.” Okay, now how many of you think that’s correct? The patient had hyperreflexia in the knees, and


they had nerve root damage is what they said. That scares me, because obviously lower motor neuron lesions… they start to make your reflexes sluggish, and they’re not there.

Think about this: It’s a two-lane street. Sensory stuff coming in, activating a ventral horn cell, and then the motor – the other lane is the motor stuff coming out, okay? The brain comes down and actually inhibits that, that ventral horn cell. So when there’s damage to the descending pathways, it’s like taking your foot off the brake, and your threshold comes up. So when you activate the sensory pathways, the motor pathways just instantly go. And it creates – it’s not quite that simple; I’m giving you a simple version – you get hyper-reflexive findings. Now when the lower motor stuff is damaged, or the peripheral nerve is damaged – ventral horn cell out – the street’s just blown up. So the information can’t get in or it can’t come out, so whatever you tap, it doesn’t respond. Is that simple enough? Does everybody get that?

So we’re going to have to go through that. Now I made this chart for you, so feel free to use it. It’s real simple. I told you, we have to know if it’s central or if it’s peripheral, and the reason why I’m giving this to you with the lobes of the brain is because this: the cortex orchestrates this. We’re going to have a whole section over reflexes, primitive reflexes, and how to use reflexes in therapy. But what I need you to understand is, at certain ages you have reflexes. When you develop a cortex, they get suppressed. If you don’t develop those reflexes, that’s bad. If you don’t suppress those reflexes, it’s bad. If your brain gets so bad that it can’t inhibit them any more, and they come back, those are bad.

So when we look at this, upper motor findings make something spastic. You’ll see something like this: flat hand – go ahead – thumb in, fingers like this, arm rotates like that, pull it up. This is a cortical fist. That is a cortical fist. We’ll have striatal hands, cortical fists, we’ll have claw deformities… we will look like we’re doing gang signs up here pretty soon. We’re going to create the neural… we’re in California. We can make a gang, can’t we?

So, by the way, if you’re in a gang, that’s nothing against you. I’m pretty sure Dr. Comey’s a Crip already, so… somebody.

So we’ve got spasticity. Now if you think spasticity can create a gait change… having to circumduct that leg because it’s so stiff. That’s markedly different than the gal I just showed you, which had so much flaccid findings, because cells wouldn’t summate and our biggest pathways were damaged, and she was just like this. She could not… she would tell her leg to move; it just wouldn’t. Okay?

So when somebody comes in and they’re weak, and they’re spastic, and they start to get a little bit of muscle loss – not because it’s denervating; denervating means this: a nerve has been damaged and it de-nervates. So it does this: the axons are actually doing this: “Hey, we’re just going to completely come out of the fascicle and we’re not even going to tell you what to do any more.” So the muscle’s sitting there going, “We only replicate protein when we’re activated.” You don’t make a whole lot of new muscle cells. The only way you get bigger is when the ones you have hypertrophy. So when you start losing them, that’s bad. That’s why these lower motor neuron findings, with active denervation you need to do something quickly.

But when somebody has upper motor findings and they’re spastic, and they’re hyper reflexive – you tap a knee and it goes out and it sticks – or they have clonus, or you stroke the bottom of the foot… I’m going to


just make a video for all of you. It’s just this: Here’s the five upper motor findings that you need to know. It’ll be five minutes long. It’s simple. You can watch it on lunch break, okay?

So when you stroke the bottom of the foot, you may see a Babinski. It’s just a plantar reflex if you do it. If it’s positive, it’s called Babinski. And so the toe comes up. You always watch for the initial movement. If it goes down and then comes up, negative. If it flares up and you have an exaggerated withdrawal response, that’s positive, okay?

So in this, we have upper motor findings of spasticity. That can cause gait changes, cause range-of-motion loss. If I have gait changes, that can change my posture and center of pressure, and then it can create all kinds of plastic adaptation. Think about it. Is my brain going to change over time if my arm is stuck in a flexed position? What’s going to happen to the extensors over time? They’re going to become de-activated, and that’s going to change the other limb, and that’s going to change the legs, and that’s going to perpetuate my circumduction gait.

So one of the things we need to do, with a lot of our stroke patients, is get them to where they can have limb movement to where all of the muscle groups are activated so they don’t get that plasticity of aberrancy at the level of the cord and the level of the brain, okay? Man, they can get weak and disused. But the EMG is normal. The only thing on the EMG is, they can’t activate well. There’s decreased activation.

So, lower motor findings, there’s no reflexes. They’re week. It’s denervated. They’re getting atrophy. It’s flaccid. What you start to see is… the best way to check is to feel. And when you start to feel, one’s boggy and then the skin is saggy, and then you feel one side is different than the other. I feel for atrophy before I see it, because some people that have some adiposity – being polite – some of them have a little adiposity, they’re muscles can really atrophy underneath the fat, and you don’t even see it until you feel it. And in the hands – I’ve got one video just on hand evaluation – where you can feel and hook the hypothenar versus the thenar, and then look for rutting, and then look for your little mound here, and there’s ways you can evaluate the hand that’s really easy.

But the biggest thing is, if the brain is involved, do we have upper motor findings? And these upper motor findings are usually involving corticospinal tracks or pathways. Most people that get spastic, like they’ve had a spinal cord injury, they’ll go flaccid, but then within two to three hours those ventral horn cells – because they’re not controlled – what do you think the resting membrane potential does over time? It starts to come up, so what do they do? They get spastic.

Here’s the other reflexes. I’m not going to really go into them, because we have a whole section on brain stem. I’m going to break the brain stem down for you. It’s a scary place, and to try to do that and the cortex together is ridiculous. But remember that we have brainstem reflexes that can all be monitored and used therapeutically. And we have vestibular reflexes that can be monitored and used therapeutically. And then we have pupils that can be looked at, and we have pediatric reflexes that need to be looked at, and we have cortical reflexes. This is a beautiful flow chart of how it’s all going to eventually come together for you. I want you to be able to just put your finger anywhere and work to any box, okay?


So I’m sort of giving this to you as a visionary diagram, and I like to do that to people, because people sometimes – they want to know where they’re at. They want to know the story, but they also want to know where we’re going. So that’s why you have this.

So let’s talk about some embryology real quick. I could care less if you’re an embryologist. If you are, cool. But I want you to understand a little bit about how this system hooks together, okay?

Can it have anything to do with you as a clinician? Well, let me just say this: I’ve got a spinal cord – and this is just basic anatomy – I come through the frenum magnum, what’s next? The medulla, then I go up to the pons, and at the pons is where this beautiful thing called the cerebellum just sort of outpouches. And the pons is an embryological outpouch… the cerebellum is an outpouching of that pons. And in the pons, we’ve got 12, 11, 10, and 9 in the medulla, and then we have 8, 7, 6, 5, and some parts of 4. They’re kind of spread out. It’s not that simple. But we have the middle ones right there, the vestibular nuclei. Some vital center nuclei. All these things that the cerebellum can come in and control. The things that live in the pons are the things that need control, because they deal with detail fine-motor function. Swallowing, talking, heart rate, breathing, vestibular function.

The cerebellum is this: the master calibrator of a detail-oriented task. And then it tells the brain about it. It says, “Hey brain, this is what I did.” And the brain says, “Hey cool. We’ll do it different next time, because you said it wasn’t right this time.” And the cerebellum says, “Absolutely.”

So the cerebellum says things like this: “Look man, you’ve got to make these motor programs go in this order at this speed, and it’s got to start and stop and start and stop in order to make things accurate. So when I go from here to here, it’s billions of starts and stops, but they happen so quickly that it’s smooth.” If it breaks down, you see this as it gets more intentioned. Okay? I’m glad I didn’t poke my own eye. I’ve been practicing.

So what I’m telling you is, the cerebellum is that guy that says this: “Let’s do it better and different next time. Hey cortex, this is what we’re doing.” The basal ganglia looks down and says, “Oh, we actually gotta do something? Let’s let the cortex come to threshold and do it.” And then the cortex is just where it all lives. It’s just hanging out there. But it doesn’t just spontaneously go. It has to have a finger that pushes the play button, and that’s the basal ganglia. And then when it does go, it has to be done efficiently, and in an organized fashion, and that’s the cerebellum. And it goes up to these motor strips, and these supplementary premotor strips, and it tells them: “This is how we’re going to package it together and make it nice and beautiful.”

So it’s an orchestrated thing between thought, movement, coordination, sensory stuff giving us cues, and what we see giving us cues, and what we hear giving us cues. Does that make sense? Let’s do it again.

What I think and what I’m planning and what I’m feeling. Goes right back just a little bit to motor execution. Motor execution is times with cerebellum. Cognition is times with cerebellum. You go back behind the central sulcus where the parietal lobes are, and that’s information coming up from limbs, and it says, “Hey look, brain, this is what’s going on in real time. Let me tell you about it.” And then you go back a little bit further and it says, “Here’s some information about the details of the objects that… your surroundings.


In other words, as we go back a little bit, it says this: “This is what your surroundings are like. This is the depth, this is the distance. There’s different components where the parietal lobes and the occipital lobes talk to each other. Pretty soon I’m going to start giving you conditions and names of things that deal with these areas.

So the story is: thought, motor, sensory, sensory integration, visual integration, hearing, hearing integration, into all of it right here. Don’t hurt this area. Lots of people do: head injuries, highly vestibular. The brain is not square like a brick, it’s round. So when you hit, it squishes, rotates, and it’s rotating on a pole that has vestibular nuclei in it. So we get vestibular complaints, we get contracoup, we get an area that’s damaged, and then we get another area on the other side that’s damaged, and then we get secondary neuronal pools that get damaged because the primary neuronal pools, they get damaged.

So with embryology, we just know this: that we have neural crest cells, and we have this primitive streak. This thing zips up, makes our spinal cord. When it doesn’t zip up, we get things like spina bifida, and it usually doesn’t zip up at the ends. Okay? Down low we can have spina bifida, we can have a meningomyelocele, we can have different portions of it actually popping out, so actually part of the cord or the nerve roots are actually coming through the spina bifida. A lot of people are just missing pieces of the posterior arch, or the elements of the vertebral segments. It’s not a big deal really, but you may see just an incomplete arch. It happens in the low back and the top.

Now if the whole thing doesn’t develop at the top, you get anencephaly. Have we had an outbreak of anencephaly lately? Or microcephaly? Yeah, where? Brazil. What are they correlating it with? A virus. Or could it be a larvicide? Or could it be something else? I don’t know. Conspiracy theorists all over the world would talk. Bottom line is this: there’s been an outbreak of small brains or brains that aren’t developing because you have to have good DNA and developmental and progenitor cell differentiation so that this works the right way.

So basically it’s this: Let me make it simple. The telencephalon turns into the lobes of the brain. The diencephalic region turns into the thalamus and some of the subcortical stuff. Well, the mesencephalon turns into the mesencephalon. That’s your midbrain. Think flexor. Think sympathetic. Think cranial nerves 3 and 4. Just giving you some ideas. The met- and myelencephalon – this is pons and medulla. Here’s your fourth ventricle, and then your cerebellum is over here. The fourth ventricle is an area of CSF flow. Then we go down through the frenum magnum, and this is just some of the developmental stuff you kind of need to know. Look, eyes pop out here, here’s your cortex, this down here is your outpouching, your aqueduct is here, all the way down to the fourth ventricle.

So within each region is layers. Now, I think it’s kind of important to actually look at this. And this shows that within each portion of our cortex, some of these are thicker than others. Now I’ll give you a really clear reason as to why I’m just giving you some minutiae on this here in just a second.

Here is a cell type. Glutamate activates it. Here’s another cell type. Glutamate activates it. Do you see how it’s sharing layers? Okay, here’s the striatum and brainstem. Glutamate. [Screen goes dark] I hit the bad button! There’s a button here that, if you hit it, it explodes. So.


Now, let me ask you a question. Do we have any problems where glutamate may be in excess? Now, first of all we have to have glutamate to make the system summate. But some people, when you have, like, citric acid cycle, and different metabolic cycles, they create glutamate, and glutamate turns to GABA. Why would GABA need to be hanging out with glutamate? Yeah – just say this: “Look, glutamate, you gotta chill out, man. Like, calm down. Here’s some GABA.” Well, there’s an enzyme, GAD, that actually creates the capacity to go from glutamate to GABA, and some people have antibodies against that, so they can’t slow glutamate down. Some people have too much food in their diet that has a similar molecular structure that’s an excitotoxins.

So what I’m telling you is this: If you have cells in these layers that are already fragile and close to threshold, based upon the story I told you earlier, and then you start putting more glutamate in the system, or don’t have enough counteractive GABA, or they become excitotoxic, areas of the brain can spontaneously depolarize. Dr. Kharrazian’s going to talk to you about that later.

It’s not just as simple as saying, “Hey, it’s one part of the brain.” It’s also knowing this: There is one neurotransmitter that is all over this thing, and it’s called glutamate. Okay? So as we go, we realize here’s a cell. And here’s glutamate activating it, here’s GABA saying, “Hey, slow down.”

Now, which drugs are GABA-ergic? Does it matter? See, this is a big question. Do benzodiazepines do anything to them? Yeah. Do Z drugs do anything to them? What’s a Z drug? Sleep. What’s the difference in one type versus the other? There’s one sleep drug that just works on the brain stem. There’s one that works on the cortex. These layers. When you give the medication for a long period of time, it remodels the receptors and the membranes, and so the drug alters who you are. I need you to think about that.

So if somebody comes into the clinic on these medications, you need to be able to think, “Oh, you’re on a benzo. That means this.” Or, “Hey look, you’ve got pancreatic problems and it looks like you’re getting diabetes and there’s other things going on. I wonder what your GAD 65 antibodies look like,” because there’s a correlation between anxiety, low GABA, not converting the right way, and the production because they’re in both areas.

So we’ll start giving you clusters of symptoms, and you see all these different GAB… these little interneurons are GABA-ergic. So this just kind of tells you there’s pyramidal cells, and these guys project to other areas, and then there’s stellate cells. And stellate cells are the guys where the GABA in there sitting there going, “Hey, cool it.”

So there is a balance between the pyramidal cells and the stellate cells, and the stellate cells are always the guys that control the output of an area, while these layers are sort of doing this: sending connections to each other and connections up and down. So one Brodmann area will have function, but then it will go up to another area and spread to another Brodmann area, so that when you think about doing something, this Brodmann area’s linked to this one, linked to this one, linked to this one. And through the basal ganglia, they all come to threshold at once.

And when we retrain people to function differently if one of these is screwed up, we’re getting other regions to train together and to summate differently for the same function. So we’re retraining the brain to do something differently for a purpose that it lost. Okay? A little bit deeper.


Oh man, these are just the layers. It’s really easy. It’s either molecular is the outer, then we’ve got granular, pyramidal, granular, pyramidal. I think you guys can remember that, right?

Now, I put some of this in there because for those of you that will take board exams later on and do different things, these are really big test questions, and I want you to kind of understand these.

The molecular layer, the outer, it gets dendrites. These are part of a projection from a cell, and they go into the deeper layers. So the outer layer goes down deeper and it starts to spread out and communicate with the layers below it. Now remember, it’s doing all of this with neurotransmitters. Hold on to that thought.

Now in layer II, what happens is, the stellate cells are grabbing these axons that are going to the deeper layers, and it’s saying this: “Look, start or stop.” So as they’re going down, they’re like this: bink bonk, bink bonk, bink bonk. So they’re making them start or stop based upon GABA. People that take a lot of benzodiazepines, they lose that capacity, so they have to have more and more and more drug. Okay? I don’t want to really say any drug names. I’m just saying drug class. Alright? I guess I can say generic. Like alprazolam. Okay?

Now, you’ve got to understand, these medications are used for anxiety. They’re used for hyperkinetic over-firing systems that can’t shut down. “My mind is constantly running. I can’t get it to slow down. I’m having anxiety. I’m having fear.” It’s just an area that’s firing. There’s no inhibitory system. So alcohol stops it. Marijuana stops it. Benzodiazepines stop it. So what do people do? They jump, jump, jump, jump, jump from drug to drug, to slow down a system that won’t stop firing.

Now I tell you this because people are going to come in, you’re going to look at their drug history, you’re going to look at their symptoms, and you’re going to say, “This is a hyperkinetic pathology. This thing is firing all over the place. It can’t slow down. Why?” Not what. You see, the drug is taking care of the what. It is not fixing the why. Do they have hyperthyroidism? Do they have an insulin problem so all of their neurotransmit-ters are off? Do they have antibodies? There’s lots of stuff we’re going to go through that says, “Hey, these layers aren’t doing what they’re supposed to be doing, and neither are the neurotransmitters – why?”

Okay. So we go down here. Now these pyramidal cells down a little bit lower, where they project to the ipsilateral cortical areas via association fibers. So it’s up here at the top, it comes down, it’s regulated, it goes down a little bit further, and then right there it just goes to the same cortex.

We go down a little bit further, and now there’s more stellate cells. But now they’re being interacted on from the thalamus. And we go down a little bit further, and now we’ve got the basal ganglia, and it goes all the way down to the spinal cord. So it’s really in an order, and it’s at the top, cognition, goes down, controls it, goes down a little bit further, and it spreads out, it goes down a little bit further and it’s the limbic nuclei that relay up and down, and you go down a little bit further and it’s how the basal ganglia feeds into it, and it does it all with neurotransmitters. Dopamine, serotonin, GABA, glutamate.

All of these guys, acetylcholine, they’re all part of the story of – you’re a cell. You have what’s called a central integrated state, meaning can you fire or not, and how do you fire, and who do you talk to. All of these neurotransmitters gathered around it, and all of the information from the other cells that summate on you make your central integrated state. And if your central integrated state is like yours and like yours,


you all tell the same story, and there’s no confusion. And you fire up and down through the layers, and everything is inhibited appropriately, and you don’t have cortical disorganization from a layer perspective. Making sense? Okay.

So, look at these neurotransmitters. So here’s that cell again, and glutamate drives it, so glutamate is the spark plug. If you’ve got too many spark plugs, you’ve got a lot of sparks. Here’s the other areas. Look, they come up and they give glutamate also. All of this together gives you the net positive charge, which is part of your central integrated state. The cell is like, “I’m ready to go, man! I am ready to go!” However, there’s serotonin, there’s norepinephrine, there’s dopamine. And by the way, serotonin might come up and inhibit it and modulate it. It depends on which receptor type it is. There’s like five to seven different receptor types. I’ll even take it as far as to say this: The older-school SSRIs shotgunned all the receptors, now the newer-school ones just pick out one receptor type. It’s nice to know the difference between something like trazadone and Prozac. It will change what you see. Okay?

Ah, here’s histamines. Boy, do they do a lot. And there’s acetylcholine. And they come from other areas. And then there’s the thalamus. It comes up and it has it’s play. So now here’s the deal. Sometimes one area might be dysfunctional because of another cortical area. Or, because the lower brain stem is not making enough neurotransmitter or turning over the monoamines to neurotransmitter, like as in the brainstem. Or, the neurotransmitters might be deficient because of another metabolic condition like what insulin does to it. Or the thalamus is dysregulated because the basal ganglia has screwed it up. That can all make the cortex not work the right way.

So when I start talking to you about the cortex, you need to start thinking to yourself, “Has that area been damaged? Is there another area that’s not firing into it the right way? Is it neurotransmitter imbalance?” If it’s neurotransmitter imbalance, is it because a genetic problem with the recycling mechanism? Is it because there’s another metabolic pathway that’s not allowing that to be created? Is it a deficiency or malabsorp-tion? Or is it inflammation blocking it? What is it? Some of the literature shows that anti-inflammatories work as good if not better than antidepressant medications. Interesting.

And then, looking at the thalamus and the basal ganglia.

So listen: We’ve got a whole lot of stuff about each one of these and how to look at them and how to assess them, and then how to say, “Look, do I need to deal with this from a nutritional perspective, or even a medication perspective?” Where does functional neurology fit into it? That’s the biggest question that we’re going to be going through.

So take a good look at this. This is just one example of hundreds that I’m going to give you. Glutamate activates a brain cell. Artificial sweeteners, MSG, hydrolyzed processed foods may make this a lot higher than GABA. And now we have GAD antibodies. So glutamate doesn’t convert to GABA very well, so now glutamate’s beating GABA, and this guy is activating everything, and this guy’s inhibiting nothing. What do you think the person’s going to crave? They’re going to crave something that’s going to upregulate GABA, like carbs. Or benzos. Or alcohol. But you give them methamphetamines, they do terrible. Don’t give anybody methamphetamines, okay? I mean, you know, street methamphetamines, that is. Okay.


And then you look at these other neurotransmitters, and they all go to the brain cell and say, “Hey, this is the story you’re going to tell based upon, you know, what’s going on.

So now let’s kind of look at the really, the big thing, the anatomy. So we already know the layers, we already know there’s neurotransmitters, we already know there’s things that can impact neurotransmitters. But now what does each area do? And this is really where you kind of got to start getting the meat and potatoes of the lecture. It really means everything for us.

So, real simple, easy squeezey. Do you see this red area? That’s… blood from the middle cerebral artery goes there. So everybody watch close. Ready? Vertebral [raises right hand], vertebral [raises left hand], basilar [puts hands together]. Got it? Vertebral artery, vertebral artery, basilar, posterior circulation [moves hands behind head]. Carotid [raises right hand], carotid [raises left hand], comes up [puts hands beside head], middle circulation [raises hands over head]. Up here in the circle, you go forward, anterior circulation [puts hands in front of forehead and passes them over top of head]. The anterior circulation gives you a Mohawk. The middle gives you the classic – like – male pattern balding spot. The posterior circulation is all back here: brainstem and cerebellum. Real simple.

Anterior circulation, middle circulation, posterior circulation, it’s all connected together by the circle of Willis. It’s not typically used unless there’s a problem in one area, and then it starts to now do this: we’ve got a way to go other directions. Okay? I am going to make a nice little video, five minutes, to know the three areas, and there’s three branches off the three main branches. Simple. Three minutes. Three, three, three. Okay?

But right now, just look. This is the anterior cerebral artery, this is the middle, this is the posterior, and it’s going to matter because I might say, “Hey, there’s an arm affected more than a leg.” Or, “There’s a visual deficit versus an expressive aphasia.” It’s going to matter that you kind of understand, because if somebody comes in with sudden rapid onset of symptoms, you immediately start thinking what? Dementia. Rapid onset dementia. No. That’s called delirium, and it does happen, like from an elderly with infectious disease and stuff like that. You start thinking stroke. And then when you start thinking stroke, by the end of this program, you will know every little vessel and the difference between one versus the other.

It’s not that hard. It’s more than just this: “I can’t walk.” It’s going to be, “Can you walk and talk and think?” Or, “Can you not walk, talk, and think?” Or, “Is it arm more than leg?” Or, “Is all my motor stuff preserved but now I can’t determine objects versus shapes?” There’s a lot of different strokes. I want you to be able to rip through them very fast, from the cortex all the way down through the brainstem. I know today is not the day, but that’s coming. I’m going to make it easy as it gets, promise you. Okay?

Here’s the big frontal lobe. We’re the only ones with it. And then this is the parietal lobe. So think about this: motor function. Now, is thought really a motor function? It kind of is; there’s just no output to my arms or legs. So watch this. This entire thing develops because this fires to it and this fires to it. Without it, your frontal lobe’s kind of in trouble. All motor systems are driven by sensory input. I want you to understand that right now. That’s why receptor-based therapy works. That’s why exercise has been proven time and time and time again to make the brain better and to make people think better and to have higher cognitive function.


So when you deafferentate somebody, meaning you take away sensory stimulation, the system starts to go down. When you afferentate it, with auditory stimulation, visual stimulation, manipulation, exercise, movement, whatever – we’ll teach you how to do them in specific orders for different regions. Is that fair enough? Okay.

So this guy drives this. This temporal lobe is kind of like the most unusual thing ever. It’s out there. It gives you all kinds of cool stuff like, “Do you think you’re God or not?” I used to do some work at Rusk State Hospital, and I got all the people together that thought they were the Devil, and I was like, “One of y’all is wrong.” You know, “There’s six of you standing here. Who’s wrong?” And they were like, “I’m the Devil.” “No, I’m the Devil.” I’m like, “Come on man, there’s only one Devil. Which one of you is not the Devil and is the Devil?” In other words, “Who really is the Devil and who has a bad temporal lobe? That’s what I’m trying to find out right now.”

So then we have this occipital lobe back here, which is mainly vision. This is hearing, this is touch, this is thought and movement. Let’s make it simple. Thought and movement, touch, hearing and emotion, vision, coordination, output and input of pathways that integrate that says this: All the stuff coming down and all the stuff coming up, it either runs through a reticular system that integrates it, or it goes by a nuclei that gives you vital function like, “Hey, you gotta be able to breathe.” So everything should activate those nuclei so they don’t transneurally degenerate and you quit breathing. Is that cool?

That’s why they’re there. They’re right here. And as everything passes down and passes up and says, “Hey, here’s a little bit of activation.” “Hey, here’s a little bit of activation.” “Hey, here’s a little bit of control.” “Hey, here’s what this means.” And so they stay alive, because they’re massively, massively integrated. But they will change, and we will teach you how to measure them and say, “Is that area fatiguing or not?” So I’m giving you, again, something down the road. I will teach you how to do a baroreceptor response, and does it summate and fatigue rapidly? You will learn to measure spirometry and breathing to say, “Hey, these respiratory centers are not so good.” You’ll be able to talk about swallowing and fatigability, and people, like when they start eating, all of a sudden they get choked a lot.

So there’s all kinds of cool things that we’re going to teach you about vital center function as a window of brain output, okay? But I just want you to see, just from a simple picture you can see it. So here’s how it works: The frontal lobe is creativity, decisions, muscle control, and thought. Here’s the dividing line: the central sulcus. You do behind that and now you’ve got parietal lobe, and it’s touch and spatial awareness. And then you go back a little bit further, and we have the occipital lobe and it’s vision. Now, do you think that your vision needs to tie in to your spatial awareness, You certainly want to know where you’re at when you’re touching something. Need I say any more?

And then right here, the temporal lobes are this: sounds and the memory of what happened. So I hear it, I turn and look at it, I know how far away it is, and I decide based upon my frontal lobe, do I want to go over there and even deal with it. If my limbic system is greater than my frontal inhibitory systems, then I go over there and beat it up without thinking about it. That’s called impulsiveness. And what you’ll see after a head injury is, a lot of people become this: promiscuous, explosive, and angry, because they don’t have those inhibitory centers from higher cortical function coming down to the limbic centers, and the limbic centers just want to do this: breed, fight, eat, and remember things that it doesn’t need to mess with.


That’s your amygdala. It will remember a face, like, “Whoa, hey, you tried to eat me last time I saw you.” Okay? So it kind of works in a circle. It all comes into this area, and then it spreads out, and then if it’s vision it comes into this area and spreads out, and if it’s hearing it comes into this area and spreads out, and it all goes up into the frontal lobe, and the frontal lobe says this: “I give a crap. Or not.” If it doesn’t, the person’s like this. They get “facies.” You ever seen one? They’re sitting there with their lips apart, and they’re drooling, and they’re like “ehh ehh” and you’re like, “Are you drunk?” “No.” And you’re like, “That’s not a good frontal lobe.” And then you start having them do tests that will teach you, with fingers, and they’re like super slow, and their creativity is gone, and you can just look at them and say, “They are apraxic.” They have no output.

We just had a girl that came in from Eastern Europe, and she was completely frozen. She ended up not having any dopamine driving the frontal system to actually make it go. Okay?

Anyway, so this is it, man. This prefrontal cortex. It gives us executive function and it allows us to pay atten-tion. You see these people with attention-deficit problems, and they’re frontal a lot of times, right? Now we’ll talk about right versus left, and if it’s orbitofrontal versus dorsolateral. I’ll break down each region and each lobe. Right now I’m just kind of giving you the general perspective. Concentration, emotions, impulses, are you obsessed, are you compulsive, like look at this. Are you a gambler? Do you have to flip the light switch on? Do you constantly whistle at women? Are you very unhappy? Can you not take care of your tests? Do you not pay attention to your spouse? And can you not keep a job? Anybody know anybody like that?

Okay. Are you suicidal? Now, I’m going to show you which of these are left and right brain, and which parts of the brain they belong to. But when somebody comes in and they’re, like, suicidal, and they’ve lost their job, and they’re getting obsessive, and they’re worrying a lot, and they have a lot of pain, and they’re very negative, and they have motor problems, and they’re compulsive, can you not start looking at them and saying, “I think your frontal lobes kind of aren’t so great.”

It’s not this simple. There’s other subcortical structures that may be firing too high or too low, which is making the frontal lobe not fire the right way. Like, I’ll give you a good example. You might get D1 or D2 antibodies, and it allows the basal ganglia to not fire, so your cortex doesn’t summate. But let’s keep it simple right now. Okay? That’s called PANS.

Now, we can go get a little bit deeper, to the nucleus accumbens. The nucleus accumbens is the part of the brain that fires activation. So it’s part of the basal ganglia, and it’s the twin brother of the amygdala. But it’s the nice guy, not the bad guy. So the nucleus accumbens fires to activate the brain and everything is cool. Like, pleasure and interest and libido. But if you don’t have good nucleus accumbens function, you will seek a reward. Like addiction.

Now let me tell you something. Everybody follow me here. This is a nugget. Earmuffs. So here’s the thing: If somebody in their brainstem doesn’t have good dopamine production – dopamine is the reward guy. It goes up to the basal ganglia, and it hits the nucleus accumbens, and that’s in the neostriatum. And it fires through to the thalamus, and allows the thalamus to activate the cortex for like, “Hey! This is awesome!” You take things like methamphetamines, they massively throw out dopamine. It goes and hits the nucleus accumbens and it goes, “Woo hoo!” And then it fires to the basal ganglia and it activates the cortex, and it says, “Life is awesome.” You get that?


So the nucleus accumbens is the subcortical stimulator of awesomeness. When you don’t have it… your libido is part awesomeness. Okay? Your reward is part awesomeness. Your motivation. A motivated, sexually interested, very happy, not hallucinating individual usually does okay. Alright? And it all fires right up to the frontal lobe, and the frontal lobe says, “Cool. Alright. Let’s not overdo it. Alright. It’s okay to do it that much. Okay.” And so what it does is, the subcortical structures start to sync in with the higher cortical structures, and they interdigitate and talk to each other, and make things right. Make sense?

This is a little deeper than maybe what you thought… I’m going to make it simple for you. Dr. Kharrazian and I made questionnaires for each region. Is that a diagnostic tool? No. It’s not a standardized and validated tool. It’s just simply something for you to look at and say, “Whoo! All their frontal lobe stuff looks terrible.” Because I don’t expect you to memorize every single thing. Like, paperwork is good. Don’t be that person that says, “Alls I need is a blank piece o’ paper.” Just be careful. That’s all I’m saying. Those people don’t typically do so well. Okay? They miss a bunch.

So this right here, right next to the nucleus accumbens, notice how this part of your basal ganglia makes you have motor function. And notice how these are all what? Cognitive motor functions. Your basal ganglia makes you move, and it also makes your limbic system go, and it also makes everything go. Not just motor function.

Now I’ll just let you know: If anybody wants to know… this is right out of Stephen Stahl’s book on psycho-pharmacology. He made this… I mean, with permission, okay? So pain is back here in the thalamus, and lots of other things. And then motor function is coordinated in the cerebellum.

Now here’s the interesting thing: In the brainstem, you have raphe nuclei that turn over monoamines, and turn them into serotonin. So serotonin goes up to the cortex, and it interdigitates in those layers and organizes output. But it also comes down, and Dr. Kharrazian will talk about pain later. It comes down and it does this: “Hey, pain-projecting nuclei, turn off.” So I want you to understand something. When somebody is depressed, and they have chronic pain, there is one area that there is a common factor. That’s called the brainstem. Ooooh.

Are you starting to see how you can now learn things to localize where it is?

So you’re like this: “Wait a minute. You’ve got pain all over your body.” “Yes.” “And it hurts everywhere.” “Yes.” “And you’re depressed.” “Yes.” “And you’re not sleeping well.” “Yes.” This sounds a lot like a condition called fibromyalgia. And now they have medications, and what do they upregulate? Synthetic opiates, serotonin, and norepinephrine. All the things that come down, descending, and inhibit pain projectors. And all the stuff that goes up and activates the cortex to inhibit the suffering of pain. I’m not going to name the medication, but it’s widely used.

Why isn’t anybody activating those nuclei? Why isn’t anybody stopping the inflammation that actually makes the turnover? Why isn’t anybody activating the vestibular system to drive into that area? Why is medicine so stuck on the what and not looking at the why? Because you’re going to have a neurotransmitter questionnaire, and a lobe questionnaire, and a metabolic questionnaire, and you’re going to get to look at all these together and say, “Holy cow, there’s an insulin issue creating a neurotransmitter issue, and this


part of the brain is bad, and I can see it based up on my intake, and I know it based upon my observations.” Bam. Do you see where we’re going?

It is so much fun, you will never want to do anything for the rest of your life different. You start giving them to everybody to fill out. You’re like, “Hey, just fill this out.” You’re going to go on a date. “Can you fill this out first please? I really need you to fill these out.” So Datis and I are coming out with a date kit. It’s like, “I need to know if you have these antibodies, these tests, could you please fill these forms out? I need to send these to somebody for analysis.” And they’re like, “Hnuh? My wife passed. Way to go.”

I actually… I failed. So…

So now we come down to the hypothalamus, and we are going to talk to you a bunch about endocrine dysfunction, because guess what? If your estrogen is low, and you just went through menopause, you can become demented within three to four weeks. I’ve seen it. You know the average age of the onset of female dementia is in my facility in Dallas, Texas? Fifty-one. Fifty-one. Girl walks in, has no adrenal f unction so there’s no backup after menopause. Estrogen goes pflpfl. And now it’s like the Star Trek Enterprise without its force field on. And the Klingons are just blasting it: brr pffow pffow, and it just… you just degenerate. That’s just one piece of the story.

I can’t wait ‘til we get beyond this beginning stuff and really get into neurodegeneration, and I’ll watch all of you grow into like this person that can really have a conversation like, “Look at this! Look at that!” You’re going to start seeing patients from a whole different perspective. And it’s really cool – there are people that I’ve worked with for ten, twelve years, and they’re better than anybody I’ve ever seen at this. I promise you, you will learn it, okay? I know it seems scary right now.

You go down here a little bit further, and now we have amygdala and hippocampus, and these guys are together. Why do you think… I told you, the amygdala is like where all the bad stuff happens, like scary fear, dinosaur going to eat me, those kind of things. Why do you think it’s right near the hippocampus that gives me short-term memory? Because what’s going to kill you? You’d better remember.

But what we also found was this: geographical location is also in that area. So when grandma says, “You know, I took like five right turns, and missed that turn,” and you’re like, “Grandma, you’ve been driving here for like sixty years! You got like a little lost or made an extra turn?” She’s like, “Yeah, I don’t know what happened.” You’re like, “Hippocampus.” The cortisol decimates it. It has to have serotonin. It’s very fragile. When it starts to go, you get short-term memory loss, but you can remember what happened in the flood of, you know, 1948. Okay?

So really cool things that we’ve been talking about, and it’s fear and panic, and listen, when the amygdala heats up, you’re going to have some problems, okay?

So anyway, when you go through this – I’m going to sit here because people can’t see the laser streaming, and I apologize for that. I’m still in the process of becoming a streaming star.

These are just some basic areas of function. Okay? So look at this. Remember what I told you just a second ago? How sensory comes up and it goes up and drives motor function, and motor function is the window


of our life. Everything that has motor output we will teach you to monitor. So we’ll have a whole list, and you’ll go, “Check check check check check check check,” and then you’ll be able to say, “This goes there, this goes there.” And if they all triangulate into one place, fantastic. If they’re all over the place, it’s multiple areas. If they fatigue rapidly, then you’ll go back to the chart that Dr. Kharrazian told you. And it’s very easy just to layer them. Okay? And we’ll have workshops.

So look – this is just kind of a picture that just shows you what’s what. Now this is a midline cut on the bottom, right here. This is a midline cut. And then on the top, this is obviously a lateral cut. Alright, perfect. Now if you’re really really, really, really wanting to learn everything, here’s your Brodmann areas. Now let me tell you about a few of them.

Here’s areas 3, 1, and 2. Information from fascial release, information from mechanoreceptors, and then 2, information from muscle spindles. They all fire into areas 5 and 7, and 5 and 7 give us this: What does all that information mean on my hand or weight or environment? So when you draw on somebody’s hand, can they tell you what it is? Like a six? Or when you put something in their hand, they’re like, “Yeah, that’s a reflex hammer.”

So listen. If somebody has a peripheral nerve lesion, they’ll lose sensation. But if somebody has intact sensation, but they can’t tell you what detailed organization is, that’s in their cortex.

So I’ll give you a good example. “Can you feel this?” “Yep.” “Can you feel this?” “Yep.” “Can you feel this?” “Yep.” “What number is this?” “I have no idea.” That’s more posterior parietal integration. And then you do something like get a tuning fork, and you just sit there and you hold it and activate it, and activate it, and activate it, and then you go back and you redraw and they’re like, “Oh, that’s a six. That’s a seven. What’d you just do?” You just activated the parietal lobe; now the parietal lobe said, “Hey, let’s work, and let’s integrate information.” And now the person has a better understanding of their environment.

So crude stuff, 3, 1, and 2, like, “Can I feel pain, temperature, light touch?” And then it all goes back and those things are the basis for firing into the higher parietal centers that say this: “Do I know the weight of something? Can I tell you what it means when you draw? Can I visualize it?” A lot of people… now let me ask you this. If you have diabetes, and a polyneuropathy, and you don’t have good sensory input, could your visualization of those things diminish? Yeah, because if you don’t have any sensory input driving it, you lose it.

So as we do this, again, these are just putting numbers with regions you’ve already seen, and here’s the frontal lobes. Now the reason why this is yellow and this is pink – these are higher executive centers, these are lower limbic centers, and these are motor centers. So look: primary motor, supplementary and premotor, dorsolateral, orbitofrontal, medial frontal. They all do something different. I have a nice slide that shows you all of them. So just hang tight.

You come back here, you have association areas, then you have vision, then you have temporal lobe. These guys right here are emotional reg… There’s a little key right here. See this little orange? These are emotional regulators. When you lose the orbitofrontal region you become impulsive. You’ve seen the kids… How many of you have seen ADD kids that are impulsive? Hello, orbitofrontal system. I walked into the room one day – I used to do pediatrics – and there was a kid. We had like a ten-foot shelf. He was standing up on


the shelf like a trophy. I’m like, “Hey, can you please get your kid down?” She’s like, “You get him down.” He was like making bird noises and stuff. I was like, “Whoa. That’s interesting.”

Here’s your cingulate system. 24 highly, highly deals with motivation.

So anyway, these are just some of the areas that do certain things.

So this is really a better picture. This is your money slide, the one that I would go home and study as far as function, okay? You’ve got Brodmann area number 1 back here… or not Brodmann area number 1, but visual area 1. This gives you the ability to see, recognize, and have perception. Now, that information goes up into the temporal lobes and parietal lobe and gives you more information about shapes and colors and stuff like that. So when we give you eye exercise stuff, we’ll give you different shapes, colors, backgrounds to mean different parts of the brain, okay?

2 – you can see area 2 right here on the temporal horn. It’s short-term memory and emotional control. This is one of the areas where schizophrenia lives. Alright? Number 3. This right here is your motor strip. It just does what it’s told. It executes motor function. It’s not higher-order cognition. As you go up here, into area number 13, 12, and 4, this says, “I think I want to move,” and this says, “This is how we’re going to package it,” and 3 executes it.

So you think of things like stuttering, and having disjointed movement, and stuff like that… Some of these motor programs are not packaged well in the supplementary and premotor areas, so by the time they get to the motor strip, they don’t get executed well. Okay?

Now, the left part of the brain moves the right side; the right side moves the left. Does everybody get that? Okay.

So anyway, we’ve got our sensory strip right here – I’m sorry, our motor strip right here, we’ve got a 3, we’ve got more motor function right here. And these are just the Brodmann areas – or not Broadman areas, but they’re numbered areas on this particular slide, and what they do is, they just show you what’s going on.

So we will use olfaction as therapy, but it’s deep. We will use hearing for therapy, if it’s out here. We’ll use a whole lot of things as far as speech is concerned. I’ll talk about that this afternoon. We’ll do short-term and long-term memory exercises. We’ll do sight and visual exercises and different things with shapes, colors, and so forth. And then we’ll do higher mental exercises, which are frontal. Concentration, planning, judgment – all these things we have a whole list of frontal exercises that we’ll do.

But how many of you understand now that your judgment, thought, attention, planning, and executive function is now frontal lobe? Okay. If you get that, then you’re with us.

So now this is just something you need to realize, and that is, this is your superior versus inferior portion of the lecture. So up on the top is, you know, shoulders, wrists, hand – it goes all the way down to my eye, face, lips, jaw, tongue, all the way down out here lower. And then this is your left versus right brain. This is raw. This is not the whole story, okay? I gave you a very detailed diagram in your package.


But it’s really interesting. When you see people get together, like sometimes you see a left-brain person get with a right-brain person and they complement each other. But what happens if two left-brain people get together and have a super left-brained child? Is there a possibility they could become autistic? I don’t know. Interesting. So, doctorate advisor – student. These people on left brain are highly analytical, logical, good language, good reason, math, and science, but they may not get the joke. Just saying, okay?

Right brain intuition, very artsy, 3D-creative, can see things, you know, like – well, you know, like decorating your house, “let’s put a plant there,” different things like that, okay? So when you look at this stuff it’s… Once you’ve been around people long enough, you’ll be able to say, “Wow man, their right brain is probably not as good as it should be.” Or, “Their left brain is really terrible. They can’t… But their right brain is so good that they have a great life so they don’t even care.” Okay?

This is a great slide. Check this out. This is the right brain. And so over here, vision. Look at the very back. It just gives you this. Angles and lines, and then you go a little bit further and it gives you distance, motion, and shape, and then you come down a little bit further and it gives you object recognition. I have developed a series of exercises that hits all of those layers differently. so we can give you that, if it tests poor as we go down the road.

On the right side: body 3D awareness. Now let me ask you something. Body 3D awareness? There’s actually some literature that shows that when you start looking at this part of your brain, if it’s not right it actually causes dysmorphic syndromes. How you see yourself. “Man, I’m way too fat.” “You weight eighty-eight pounds!” In other words, perception is everything. Don’t bypass the fact those are neurological phenomena.

So when you see these things, you’re like, “Man, right brain!” And the ability to, like, see objects and understand their angulation and things like that – there’s tests that we can do.

Over here, right just a little bit lower at the beginning of the temporal lobe is harmony and pitch, and then you go down here and it’s music memory. I used to have a family member – removed – and this individual had a right brain that was amazing. He remembered every song. He remembered every movie. But he had temporal-lobe epilepsy. So his right brain was firing all the time, really high, but the rest of his brain was completely not capable. Like he’s not a high-functioning individual, unless you’re talking about movies from the ’90s, then he knows everything. Okay? Some people, after they have seizures and stuff like that, start having problems with this.

Now as we go up here, we have: how do you do it, how do you imagine things, create things, and then as you go down in this orbitofrontal region, it’s the ability to say no, or inhibit. So: what not to do, right and wrong, mannerisms, and conscience.

Here’s the other side, the left side. This is spelling, reading, the sounds of language. Language, language, language, language, language. Language is all over the left brain, especially in most people who are right-handed. So listen. When I talk about language later, it’s going to be: Most of your language is left brain, but the ability to have intonation of your speech is right. It’s called the prosodic variation. And you guys have all seen the highly intellectual college professors, they’re like, “We’re going to study math 101….” You’re like, “Please, right brain, can you just come to the room please?” It becomes difficult.


So anyway, this is a different kind of math. Geometry versus algebra and stuff like that. They’re on different sides of the brain. Some people do really good in geometry; they do terrible on algebra, okay?

Back here the occipital lobe is about the same, but really spelling and matching and finding words. And then here’s the deal: faces and names. Over here, just facial memory. Now, some people have awesome facial recognition and feature recognition, but they can’t put a name with the face. Great differential diagnostic indicator of right versus left temporal lobes. Okay, I like to throw some little things out there that we’re going to be talking about later as we talk about ways to, you know, differentially work through this.

So this is just a little paper that I like to throw in every now and then, and that says this: Physical exercise actually creates neurotrophic stimulators, brain-derived neurotrophic factors. It helps with blood flow. It helps with neuronal tissue, and it helps with cognition, and it helps prevent age-related stress.

This is just showing you this: Movement activates NMDA receptors, which activates a gene response, which makes plasticity, which makes cells connect, which makes your volume loss not go down as fast, and you do better. Ta-da! Everybody get a treadmill, right?

Okay. So here we go. This right here is everything about your frontal lobes. So I thought to myself, “Man, it’s like, why make seven hundred slides about this whenever we can just do one? Let’s make it simple. My frontal eye fields deal with eye movements right now, and it’s called a saccade. It’s an all-or-none movement that makes my eyes go from one target to another.

We’ve got my premotor area, and it’s divided up, and it gives me the ability to learn and get new motor commands, and it’s highly communicative with the contralateral cerebellum. So is the supplementary motor area over here.

Now here’s Broca’s area. I’m going to talk about this a little bit later. It gives us the ability to have the motor component of speech. The motor component of speech.

Now there’s Exner’s area, which gives us the ability to write.

Orbitfrontal. Social behavior, judgment, avoiding distraction. A lot of people that don’t have orbitofrontal components are in prison. They couldn’t help but steal that car, or beat that person up, or take your bag, or whatever.

If you go down here to the medial frontal area, it deals with speech, gait, and continence. It’s the anterior cerebral artery; it’s right here in the front. If all of a sudden you have somebody that becomes, like, very out of it, they urinate on themselves, and they don’t talk well, and their legs don’t work good, you need to start thinking about an anterior cerebral artery stroke. They happen. Leg more involved than arm, anterior circulation. Arm and leg together, probably internal capsule. I’ll give you all the different patterns of stroke later on.

Here’s the big one: dorsolateral prefrontal cortex. We’re the only ones that really have this. It gives us working memory, recalling events, numbers, and reading, and it really helps us organize things, okay? I’ll talk about what all these lesions mean and the names.


So your frontal lobe allows you to plan, motivate, have attention, reward, memory, impulse control. Do you think that you can start to ask patients questions about this and just quickly see how they’re doing? “Hey, how’s work? How’s your family? Can you keep up with your life? Are you organizing things the right way? Can you pay attention? Hey, pay attention to me when I’m talking to you.” I mean, you see what I’m talking about, okay?

And really, I kind of spelled out for you what everything does in the notes. I kind of spelled everything out for you. So you’ll be able to look at it and say, “Hey, Broca’s is speech, prefrontal is what he said it is,” and then we’ve got the primary and supplementary motor. So let’s just run through it real quick.

Okay, right here. Primary motor. Supplementary and premotor. Dorsolateral prefrontal, orbitofrontal. Let’s do it again. Orbitofrontal, dorsolateral prefrontal, supplementary and premotor, motor strip, medial wall. Right down here, and then underneath that is the cingulate system, and it’s the anterior cingulate system. Motivation into wanting to do things.

Women, you’ve got us beat. You’ve got a huge anterior cingulate system, and it does all kind of cool things. Like if a baby cries, it says, “I’ve got to get up and go take care of the baby.” Males, they don’t have a big one, so guess what they do? They eat babies. So… don’t be a male lion, alright? They’re sitting there like, “My cingulate system’s not ready for this!”

So look at this. The frontal lobes, they shape our attitudes, they give us organization, they give us self-regulation, and they give us self-awareness. Of all things in life a person should strive to have the best frontal lobe. They get the best job, best girls, best health, most fun. That’s my quote.

No, but really, it gives you everything that makes you a high-functioning human, okay? So it deals with restraint and initiative and order. Restraint, down here; initiative, deep; and then order right up here.

So let’s do it again. Real simple. Restraint, down here, okay? And then we have initiative which is out here and you go deep into the anterior cingulate, and then we have order, which is all of it put together. And it all goes together and says, “Hey look, I gotta do this before I do this, because if I don’t, then this is going to happen. So I’ll execute this and then I’ll execute that, and I have to do it by this time, because if I don’t then that person’s going to get mad.”

You start seeing that’s like everybody’s day. The person that loses their frontal lobe, they do this: they go on disability. They can’t keep up with life. I can’t pick up my kids and work at the same time. I can’t cook… In other words, they start losing their frontal lobes. So that’s why you have to look at some patients and say, “You know what? Your life is exceeding the ability of your frontal lobe to do it. That’s causing stress, and that stress is making you degenerate faster.”

So they may be apathetic, they may be abulic – that means just totally out of it. They may perseverate, meaning they say things over and over and over. How many of you’ve seen a kid that doesn’t have a very good frontal lobe, and they come in and they just constantly want to stick their finger in the light socket? You’re like, “Hey man, don’t stick your finger in the light socket,” and they go “Tssst.” “Don’t stick your finger in the light socket.” “Tssst.” They perseverate over things. And a lot of people do that. Some people


will get a song stuck in their head and it just lasts forever. Sort of like, I’ve had a BeeGees song in my head since the 1970s. I’m like, “Oh my God, man!”

Okay. So here’s just some terms for you. Perseveration means inappropriate repetition of word, apathetic and persistent mutism. Confabulators are people that say stuff that don’t make any sense. A lot of times you see this in strokes, okay? So I’ll talk about those a little bit later on. But here’s the questions: “Hey, Suzie-Q, can you not listen? Are you distracted? Are you having poor motor planning? Are you not motivated? Are you, you know, difficulty waiting your turn? Does your thing do that again? Are you, you know, impulsive?” These are all questions. “Can you not sustain attention in routine situations?”

So you go through all these things and you just realize, some of these things mean frontal lobe, some of them don’t. Like, you could be in a brain fog and just have blood sugar issues. It doesn’t necessarily mean your frontal lobes are gone. So you have to realize, these questions are not completely exclusive or inclusive. They’re just ideas.

Man, these people may be inappropriately jocular. We all have that one friend. He’s inappropriately jocular, and confabulates, and can’t talk real well, but he’s fun to be around. And he’s probably incontinent about 11:30 every night.

So here’s the left brain, detail versus big picture. Appreciate the routine versus novelty. And then frontal lobe testing. We’ll teach you how to do this. It’s a dual task. “Can you walk? Swing your arms? Say things at certain times?” We’re going to teach you to do tests like this, tests like this, and grade them. So I have a whole section on… how do you grade and evaluate a frontal-lobe lesion? Okay? I’ll teach you how to grade freezes and hesitations, and you’ll be able to say, “Wow, that person’s frontal lobe,” and then you can grade their face, whether they’re just empty or blank. And then you can start putting that together and say, “Wow, this frontal lobe does not look well.” Assuming there’s nothing else affecting their hand, like, you know, a broken wrist.

So depression versus mania, expressive aphasias, all these things are all frontal lobes.

Now to the parietal lobes. Nice and simple. The parietal lobes are this: “Can you perceive sensation and touch? Can you make a big multimodal picture?” Now here’s what I did. I took all of the dominant versus non-dominant stuff and put it together for you. So dominant versus non-dominant is this: So, if you go over here, and in your non-dominant hemisphere, opposite of language, typically, the patient really has a disability but they don’t care. They’re like, “Uh. I don’t care.” They don’t dress the other side of their body. They can’t find where they’re at, but they’re pretty cognitive. And really, they can’t copy a picture or manipulate objects into a pattern. All of that stuff is a representation of your environment. It’s parietal lobe.

You go over here to the other side, and now they become very damaged with math problems, and they can’t write, but they can read. It’s called alexia without agraphia. So weird. They can’t… You go over here and some of these people… If you go further back by the corpus callosum, it’ll change. But sometimes they can read but they can’t write. Sometimes if you go a little bit further back, it’ll switch. Can’t read. There’s a nice document in the literature of a neurosurgeon who, all of a sudden was doing surgery, and just couldn’t read, couldn’t talk, and couldn’t do certain things, but understood and knew everything he was doing. Weird things happen in the parietal lobes.


But basically what happens is, you just don’t understand your environment. You can have altered pain and temperature, and really, no matter what’s being sent to you, you just don’t package it into the right kind of deal. So a couple of tests: graphesthesia is a real easy one. So I just have them hold their hand out and just draw, like, a number or a letter, and they have to tell me what it is. And you do all your sensory tests, which we’ll teach you later. And then you can do stuff like put weight of an object, barognosis; drawing is the graphesthesia; and then, you know, putting things in their hand like a cell phone, and they don’t know what it is. You know, it’s like, “That’s a cell phone.” Everybody should really kind of be able to feel it and know what it is. Everybody’s held an iPhone long enough to pretty much know.

So with parietal lobe, it’s this. Man, they can’t integrate sensory information. And that’s a bad deal.

And here is the terms. And this is just a summary for you of all of it. So, anosognosia, which is, you know, you don’t… that’s the disability but you’re unaware. Dressing apraxia… these are all the things I just taught you, and they were in the chart. And then over here on the other side, that’s all the acalculias, and alexias and aphasias. They can’t talk right, they can’t read right, they can’t do math right. And these people really fail significantly in an academic environment. A lot of times on their left side.

Bilaterally, you can get what’s called a Balint’s syndrome, where the person’s just fixated on a target and they don’t move. And that’s something you obviously don’t want to see.

So look: nice little chart, and what it does is, it gives you right versus left parietal lobe. Here’s the cool thing: The right side of your brain contains a map for both sides. The left side is only for the right. This is concerned with stimulation outside of the body, concerned with more stimulation arising from the viscera. Anybody ever heard of, like, abdominal migraines? Hm. What’s going on in the right parietal lobe? Interesting thought pattern.

Environmental sounds, noise, and awareness, self-awareness, which is body image. Body image.

Cool. So here’s your nice little tests, and this is showing graphesthesia, sharp versus dull, and these people have dyscalculia, dyslexia’s in the left brain, apraxia, and then these are all the things that kind of happen in left versus right brain lesions. But really what I want you to just realize is, again, this is where all sensory stuff is integrated and gives you the ability to sort of perceive your environment and know your environment, walk through your environment, calculate distances in your environment, and know who you are in your environment.

Temporal lobes. So this is really the last thing, because the, you know, back in the posterior occipital region, it’s vision. There you go. Pretty tough.

The whole reason why I got into neurology is, I had an occipital concussion and lost vision for about three hours. That sucked. It came back, but during that time period you’re like, “This is it man, this is the big one.” You know, I was a stunt man for a while, and I fell and hit my head on some concrete, and my vision just went like this: fssshhh. And miraculously it came back within about three hours, thank God. But I know exactly where the visual centers are. I hit them and they went away. So…


The temporal lobes… Really, let’s make it simple. The temporal lobes are highly emotional and highly, highly, highly auditory. Hearing. So, vision… just watch this. Vision, hearing, feeling, experiencing and doing. Do it again: seeing, hearing, feeling and perceiving, experiencing and doing. Alright?

In the middle: emotion. On the outside: more executive. Like language versus being ticked off and saying certain things. Okay? Your temporal lobe gives you the ability to say, “I’m not going to say the four-letter word, I’m just going to chill and just say, ‘Excuse me, can you just relax, or pass the Grey Poupon,’ or something like that. Instead of, ‘Gimme that…!’ ”

Okay. So as we go through this, when you pull all these, you pull this down, you’ve got this thing called the insular cortex, and that is where a lot of the visceral stuff lives. Visceral stuff: pain and suffering and fetishes live in the insular cortex. Pretty interesting deal there.

So anyway, as we go through this a little bit further, this is just more stuff, really speech and sound, and all this stuff travels through the left temporal lobe. I’m going to show you that a little bit later on. You know, I’ll show you language whereas… Here’s the things I’m just going to kind of give you a preview of, and then we’re almost done here with lobes, and I’ll wrap it up pretty quick, because we’ve got lunch here in just a few minutes.

“Are you fluent in your speech? Can you basically do the same thing? Can you mimic somebody? Can you have repetitive speech?” So fluency, repetition, you know, paraphasias, which I’ll teach you what those are, and then, “Is there meaning or not to what you’re saying?” And, “Can you name things or not name things? Do you have emotion in your speech or not have emotion in your speech?” You should be able to quickly say, “Is your speech problem left or right side? Anterior, posterior, brainstem, or cerebellum?” So I’ll show you that.

Anyway, these are just all temporal lobe things right now, and I’m going to go over mainly most of it is speech. So the last thing here is, I just wanted to kind of go over what memory is, because I’ll be talking about different types of memory.

And with memory, your working memory, which is the ability to actively hold information in the mind that you need to do to complete tasks. That’s your parietal and frontal lobes. Okay?

Now declarative memory is, you’ve got to be able to consciously recall it, such as facts and events. And these are people that are really good at Jeopardy and stuff like that. That’s your medial temporal lobe. So we’ll have, whenever we start teaching you the evaluation portion, we’ll give you memory questions and you can say, “Wait a minute, is this frontal parietal memory, or is this like the temporal lobe?”

And then procedural memory is, like, “How did I get there? How did I do it?” Can you repeat certain steps in sequential order? You know, that’s cerebellum. And short-term memory is your hippocampus.

So you can do a battery of quick memory things that will say, “Is it working, declarative, procedural, or short-term?”


So just to kind of summarize: vision, sensation, hearing and memory – certain types of memory – and language, and then up here, executive function.

Declarative memory back here, right here is your working memory, and then your declarative memory is here, and then your short-term memory is deep, right next to your amygdala. What does your amygdala do? Fear. Scared. Respond quickly. You have to know it just like that. Now you sleep and other things happen, and information goes from the short-term systems and it projects out to the cortical systems.

So we’re going to teach you how to treat these areas from multiple angles. And they’ve got some nice little things like yoga changes brain, mindfulness changes the brain, and when your brain goes downhill, it can change your autonomous nervous system, it can change things like intestinal function, barrier function. This is all coming down the road. This is one of Dr. Kharrazian’s really nice slides.

So just to summarize: My cortex is that outer layer, that outer noodley shell. It has layers in it, and within that layers it has cells that function locally, project to other areas, and then project to the other hemisphere through the corpus callosum. There’s neurotransmitters that activate it – that’s glutamate. There’s those that inhibit it – that’s GABA. And there’s those that modulate it – serotonin, acetylcholine, dopamine, histamine, and so forth. We’ll talk about how you kind of pick out all of those.

And then each area of the brain has those layers, and each part of your brain does one specific thing, but it always hooks to another area for complex function. What makes that area go is the basal ganglia saying “start” or “stop.” Okay? What coordinates a lot of the function is the cerebellum. And this is vision, and this is hearing, and this is sensation, and this is executive function and motor control and planning.

This is your literal brain, this is your creative brain. This is your IQ. This is your geometric structures. So I gave you one intake form that goes through all of it. Not too hard. I want you just to be able to sit down tonight and get the basic gist of what each lobe is. Because as we go and we add, here’s the deal. I want to be able to say, the person comes in, I want to write a one-sentence description. The person comes in, and is impulsive, doesn’t have any motivation, and then go and put several other things, and you go, “Boom! I know exactly where that is.” And then we can start talking about other things that might cause that, what else might be going on, and then start talking about treatment strategies, and that will be a big, big deal. But the biggest step is now that you just get the basic lobes. And if you get that, there’ll be more lobes spread out as we go.

So right now you have that basic organization chart which says, “Where are you?” And right now you know, “Okay, I’m in the cortex. And am I in the front or the back? Inside, outside? Up or down? Temporal, parietal, frontal, or occipital?” If you got that, you can go eat lunch.

We’re done.

FunctionalNeurologySeminars.com Courses.FunctionalNeurologySeminars.com

https://functionalneurologyseminars.com

http://courses.functionalneurologyseminars.com

Date post:	18-Apr-2018
Category:	Documents
Upload:	dangdiep
View:	217 times
Download:	4 times

Okay, so here we are. Quick review, because we don’t have ... · Okay, so here we are. Quick...

Documents