FUNCTIONAL NEUROLOGY ANATOMY AND CENTRAL … · And I’ll be honest with you: that’s the area...

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

FUNCTIONAL NEUROLOGY ANATOMY AND CENTRAL NEUROLOGICAL PATHWAYS (MODULE ONE)

Transcript – Introduction to Functional Neurology Concepts and Anatomy

Presentation by Dr. Datis Kharrazian

First of all, again, thank you for being here. Just so you get the schedule; know what’s going on: We have about close to 400 people streaming, and we have close to ten universities streaming with student clubs. So we have medical schools, chiropractic schools, naturopathic schools, all streaming. So today is probably going to go out to several hundred people. So we want to stay on time, and this is a big deal for all of us.

Now, we want you guys to be really, really good at this. We really want you to own this Functional Neurology concept. So the key thing you have to understand understand is, there is going to be some things that are at times a little frustrating, but you just have to go through it. The biggest mistake people have is that many times they don’t know the thought process. They learn something in class, and they go and try it with every single person. Like they learn saccades, and they think saccades apply to everyone.

Now, in this group, we have a spectrum of new people that are coming in from the functional medicine community, and then a spectrum of people that are coming in from a neurology rehab perspective. And our goal is to kind of merge those two concepts together, so that we can have a very thorough approach to managing cases, whether it’s a child developmental disorder, or someone who’s had brain trauma, or a neurodegenerative disease, or someone who’s just losing their memory and their function.

So the goal for us is really to teach you the thought process. We want to teach you neuroanatomy this weekend, but in a clinical thought process. It’s not what you – it’s not really related to treatment, meaning you don’t want to jump at the treatment until you know where the site of involvement is, and how to clinically think through it. The only difference between an experienced clinician besides seeing things, and a new practitioner, is their thought process. So we’re going to go through a clinical decision-making tree, how we cover all the steps, and if you stick to the thought process, then you can do a very thorough workup.

So if you guys look at your notes, you guys have the PDFs as one file, but then you have each of the topics as individual files. In those individual files, when you go on your site, and then you go on the site and look at it, you’ll have concept papers. The concept papers are Word document, PDF document, but written out in paragraph form, so all the key principles that you need to learn are in there. So I would strongly


suggest making sure you guys read those key concept papers after the seminar, and really review each of the sections themselves.

Now, what I want to go over first is: how do these metabolic and neurological factors integrate? Every component of a neurological disease has both. There’s things that impact neuron endurance, there’s things that impact neurotransmission, there’s things that impact plasticity potential, and there’s pathways you have to activate. What we don’t want to do is be the practitioner that goes, “All neurodegenerative diseases are heavy metals, you’ve got to do chelation, it’s all mercury.” We don’t want to do that. And we don’t want to just to rehab and not look into these metabolic factors as well.

So one of the things we’re also going to do in this presentation is go over a decision-making tree, and then we’re going to go over the concepts of fatigue, and how you decide how much therapy you would do, when do you choose metabolic approaches versus neurological approaches? That’s a key thing. That’s an area a lot of people have frustration with, difficulty with. Do you do them both simultaneously? Again, we’ll go through a decision-making tree and teach you guys how that applies. And then we’ll go over metabolic factors that can potentially impact your rehab.

So let’s start by making this very clinical, by going over a clinical case example. So let’s say you hear a patient come in the office – this is their chief complaint. Patient complains of dizziness and disorientation whenever they go upstairs. The symptoms started after mild head trauma. So the first thing that we want to really make sure that you guys understand is how to initially diagnose where in the brain the involvement is just from a couple chief complaints. If you don’t know where it is, you have no chance of rehabbing it, you have no chance of supporting it, you understand?

So we want to look for is key concepts, key words in their history, and the goal of this seminar is: by the end of it, you should be able to hear any chief complaint, and you should know exactly what area of the brain’s involved. Once you know that, that’s going to change everything to you when you do and exam, because you certain areas you need to focus into, you need to consider pre-synaptic pools, vasculature, all those things that are involved.

So let’s take this for example. If a person has dizziness and disorientation, then you have to know that those are common symptoms of the vestibular-cerebellar system, right? So if that’s their chief complaint, you initially go, “There’s a vestibular-cerebellar mechanism involved here.”

The way we evaluate patients is, we want to be able to localize the region before we even pick up a penlight, a reflex hammer, anything. So from the history, you should immediately know the regions involved. That’s the first thing. And I’ll be honest with you: that’s the area most people who practice functional neurology are not good at. They go jump into the exam, hoping their exam will do something, and then they go into the typical treatments they do for everyone, and they don’t really dissect the specific areas. The more symptoms you hear from the person from the history, the more you can dissect their anatomical pathways.

Our goal this weekend isn’t to teach you neuroanatomy from a textbook model, it’s to teach you how to think in a clinical, neuroanatomical way. Now, we also want you to think in a metabolic way. Are there any metabolic factors here? This person had mild head trauma. Mild head trauma has an inflammatory cascade that takes place, and research shows the blood-brain barrier breaks down, the gut barrier breaks


down, there’s an inflammatory cascade in the brain, there’s even systemic inflammation, there’s immune suppression…. We’re going to go into this in great detail in a separate module.

So right off the bat we go, “Wow, this person tells us they… first sentence, patient complains of dizziness and disorientation whenever they go upstairs, the symptoms started after mild head trauma, we know we need a lot of things in play.” We know we probably have an inflammatory consequence in the brain, we know all the consequences that take place from head trauma, we have to address those issues. We know that there’s probably a vestibular-cerebellar issue. So just from the first sentence, we already have a therapeutic approach.

Does that make sense? That’s what we want to make sure you understand: the thought process as we get into the clinical decision-making tree.

Here’s another case example. Thirty-five-year-old female has blurriness of vision, weakness in her right leg, symptoms of numbness in her face and arm. So how do you evaluate this patient? Well, we start with listening to the chief complaint, and trying to identify the regions that are involved. So where is this lesion? Where is the site of lesion for this case example? So: blurriness of vision, we have some issues either with muscles that constrict or dilate the pupils, maybe the optic tracks are involved. She has weakness in her right leg, so that lets us know that her left motor strip and homuncular fascia in the areas of the superior right motor cortex are involved, and then she has numbness in her face, so we know her somatosensory cortex is involved as well. So these are multiple sites of involvement.

With this type of history, what do you think the mechanism could be? It’s probably not an isolated area. So this is characteristic of multiple sclerosis, demyelinating event. So we’re thinking, “Wow, this could be autoimmune mechanism.” So if it’s an autoimmune mechanism, and there is myelinating immune reactivity and reactions that are taking place in this nervous system, we may not want to jump into therapy until we kind of calm the inflammatory cascade. Or we may want to do both. It just depends on a case-by-case basis. But right off the bat, just from a simple one-sentence issue, we know we probably have neuro-autoimmunity, and we probably have multiple sites of lesion. Right off the bat.

So then we go, “Is this autoimmunity?” We do a followup testing, we see if it’s there, and then we dissect the autoimmunity. Is it Th1? Th2? Th3? Th17? Th2? Th16? Are these factors involved? How do we identify them? How do we go through them?

We’re going to teach you how to do all those things. But we just want to, in this session, teach you how to go through the thinking process. You should be able to hear any sentence and immediately go to metabolic and neurological factors.

So here’s another case example. A nine-year-old child is having developmental delays with language, and difficulty focusing. So how do you evaluate this patient? Well, from that , we should immediately think of neurological sites.

If you don’t know your anatomy, you can’t play this game. It’s that simple. This is not “you learn a treatment and then just do it for everyone.” This is “you fine-tune your diagnostic skills and see what’s involved, and then you go to those regions in your exam, and you look at metabolic factors.”


So developmental delays with language. So what part of the brain is involved? The language centers of the brain, which are where? They’re in the dominant hemisphere. Usually left, in ninety-seven, ninety-nine percent of people. Now, we can then – if he has difficulty focusing – where does focusing take place? Focus and concentration is in the frontal lobe. So right away, just from that one sentence, we know we have prob-ably a left-sided developmental delay, involving language centers and the frontal cortex. That is important.

Now the question is, why would a nine-year-old have that? Well, there’s things that are impacting this person’s brain development, and that’s where you have to look at all the metabolic factors that could be involved. Is it inflammatory? Is it autoimmune? Is it poor circulation? Is it that he has a sedentary lifestyle? All those factors come into play, and then that’s how we evaluate our case.

Now, if you had ten more sentences, you could even dissect this further. So one of the things that we want to make sure that you guys know how to do is, once you hear a patient history, you should be able to sit down and just isolate local… localize the areas involved, just from the history, and then localize metabolic factors that can be involved.

Then the next question is, how do you merge those two? Where do you start? And how do you go from there? Does that make sense? Okay.

Now, one of the things that I want to make sure that we can go over is this clinical decision-making process in functional neurology, in our model of how we do it, and how we’re going to teach in this program. So if you guys notice, the first thing we hear is the patient’s chief complaints. So we went over one or two sentences, and just from one or two sentences, you can immediately identify and localize the area, and look at metabolic factors. Everyone understand? Okay.

So once we identify the chief complaint from their history, we can localize the region, just like we did in those case examples. Now what we’re going to teach in Module Two is how to localize the region involved with a general survey. The general surveys: Are they on time? How is their handwriting when they fill out the office forms? What’s their head position? What’s their eye position? How’s their speech? How’s there movement? How’s their gait? So before you actually do your exam, just by observing the patient you should be able to also localize regions of the brain. We’re going to go into that in great detail next module.

In this module, we really want you guys to understand the thought process, and we also want you to understand how to localize regions with a history. We have extensive paperwork and notes for you to cover all of it, and you can replay this back as many times as you need. You have everything you need to take that first step and become a master of this. If you’re going through this program, and you want it to follow through how we’re teaching it, between now and the next session you should be able to read any history and localize the region just from that. That’s your goal if you’re learning functional neurology. That’s what you should be able to do. You read all the notes, and you go through it, you will be able to do that, and you should be able to do that hopefully by the end of Sunday, as we go through these different regions.

Now, once you localize a region – and this is just giving you guys the big picture of how we actually apply this stuff clinically so you can see the big picture first and then we can focus in this weekend on just localizing the regions from the history. Once you localize the region, then you ask… for getting the clinical decisions we ask, “Well, what kind of exercises can we use to activate that area?” Maybe we have a left language


center issue and a frontal cortex issue with that child. So what kind of things can we do to activate those centers? Do we give him math? Do we give him eye movements? Do we give him physical exercises? Do we give him some motor-sensory stimulation? Those are all the things that we want to consider that directly activate that area.

Sometimes, clinically, we go, “We don’t want to directly impact that area because it’s too fatigued and it’s too compromised from having symptoms,” and we do that, so we might want to activate something that’s pre-synaptic to it; something that fires into it. So if their frontal cortex is involved, maybe we do cerebellar therapy, because it fires into the cortex. Does that make sense? There’s reasons why you have to do one versus the other. There’s times where people can’t handle direct activation, so you have to go into pre-synaptic pools that fire into the regions involved, so you can develop some connectivity.

Also, once we find the region that’s involved, there’s times where we have to consider just using vasculature. So if their frontal lobe is involved on the left side, we may go, “oh, that’s the medial cerebral artery branch.” We may want to do activity in other areas of the brain that don’t fatigue the person or make the person crash, that shunt blood through the medial cerebral artery. So we’re going to go through the vasculature in detail. You guys will all be able to draw out all the pathways, all the circulation and everything, out, and know when you would apply therapies to shunt blood flow to certain regions. Does that make sense?

So our goals are: we hear the history, we localize the region, we make a general survey, we get ideas of what’s going on with them, we do our exam – which helps us understand things more – we go, “How do we activate that area? Can we activate the area directly? Do we activate that area with pre-synaptic pools that fire into it? Do we activate common areas of the brain that use common vasculature to get blood flow and shunting in that area to help that brain and area heal?” For example, maybe someone has a symptom of severe brain trauma, and you can’t activate any of the areas that are involved because they immediately crash and they can’t handle the stimulation, but you can do therapies that activate collateral blood flow to that area, so you can help them recover and get the nutrients and oxygen they need from the blood flow there. Does that make sense?

So those types of things help us develop pieces specific for brain exercises, and then the most important step of this is that we want to figure out how much can they do? Because you can’t just go, “This is left frontal and these are left-frontal exercises, let’s do those.” That is a very sloppy, inefficient way to practice functional neurology. You have to go through your steps in this decision-making tree, and really thing through it, and we’ll teach you guys how to do that so then you don’t have a patient that crashes on you when you try to do therapy. It’s very specific, and then you can observe your outcomes and see how you go.

Now at the same time we’re localizing the neurological region, we want to localize the neurochemical pathways involved. So every pathway has a neurotransmitter response. Is it a GABA pathway? Is it an acetylcholine pathway? Is it a catecholamine pathway? Is it a dopamine pathway? We know there’s things we’re going to do nutritionally that can impact those. We know that there’s drugs and pharmacology that they may be on that could impact those pathways, so maybe it might be appropriate for them to take. So that’s another part of – as we identify the region of the brain and their symptoms – what are the metabolic factors?


The other thing that we do is, we go down here and we look at fuel issues. Do they have oxygen? Do they have glucose? Do they have hormones? Do they have all the metabolites they need to make the neuron function? And then we can do lab tests, we can do followups, we do a complete physical exam. You guys can’t just do a neurological exam. You have to do eyes, ears, throat, heart, lung, abdomen. You have to be a complete doctor. You can’t do a focused, limited neurological exam and do something, because that’s plain and simple sloppy work. It’s not philosophical. It’s just sloppy practice in general. You do your complete workup, you do your labs, your history, and then you decide if you need to do metabolic interventions, drug intervention, or whatever you think is appropriate for that patient at that time. Does that make sense? Okay.

So what we hope that you guys learn as you go through this is this whole thought process I’m going through. If you can go through this thought process clinically and be efficient with it, you’re going to have really secure outcomes, you’re not going to miss things, you’re going to identify all the factors involved. And this is how people think that do this functional neurology model very, very well. Does that make sense? Okay.

Now what tends to happen is, when you don’t have the clinical decision-making tree, you kind of just do what you’re good at. So if you know about methylation, and checking for gene defects, you’re going to look at everyone from a methylation perspective. And they need methyl donors. And they have a SNP. If you think it’s all toxicology, then you’re going to look at every patient from that model, and then you’re not really going through a clinical thought process evaluating everything. Does that make sense? Okay.

So we want to make sure you go through each of these single steps, piece by piece. Again, our focus this module will be on localizing region with their history, and next time the focus will be on localizing the region from just looking at a patient move, walk, talk. And that’s fun once you learn that, because you can go to the mall or look at your friends in class, whatever, and then assert to know what’s wrong with them! And then you can talk to your buddy, who’s also learning it, and then you guys can yell at us for sure: left cerebellar, look at that hypotonia, look at that guy’s walk, he’s swaying that way, look, there’s an arm swaying… that all helps. So that’s the key goal. Between now and next time, we can just have you listen to the patient for a few sentences, watch them. You should immediately know what area of the brain’s involved. Does that make sense? Okay.

Now the other key issue is this. When do you do metabolic factors? When do you do neurological factors? When do you do both? So this is where, once you’ve gone through and you’ve observed the patient through general survey, you’ve done their history, then you do your exam. And then your examination is going to tell you a lot about their endurance. So here’s the key concept: It’s not that high to localize regions of the brain involved from a workup. That’s not difficult to do. You guys will all learn how to do it by the end of this weekend.

What’s going to be hard clinically is, how much endurance do they have? How much can you treat them? How much activation can they get? Because the common theme that happens when people learn how to rehabilitate the brain is, they fatigue the brain. The brain crashes. They overdo it. And then the person ends up getting worse than before. Does that make sense? So if you, for example, had torn your biceps, how do you get your bicep strength back? You’d have to gently lift some weights. You do it too aggressively, you’re going to reinjure yourself. It’s the same thing when you look at brain development issues, brain injuries, neurodegenerative issues. You have to figure out what your endurance is. And this is where metabolic factors really come into play.


So this is another clinical thought process flow chart that we use. So you’re going to do a neurological exam at this point. So you’ve done a general history, you know enough to localize the region, you’ve done your general survey, and then let’s say you do an exam. Whether it’s a Rhomberg test, or some kind of eye movement, or deep tendon reflex, you do the examination findings, and what you’ll see: is it normal, or is it abnormal? That’s the first question you’re asking. So let’s say you check finger-to-nose. Is it normal, or it is abnormal? Easy, right? If it’s normal, then you’re going to… what we want to do is, we want to repeat the test to evaluate for endurance. Now, you would only… you wouldn’t do this for every single neurological test, but you would definitely do it in regions you know there is a problem from their history during their general survey. Does that make sense?

So if you think I have… if I come in and I tell you I have all these symptoms that are associated with the cerebellum, you’re going to evaluate my finger-to-nose looking for what? You’re going to be looking for maybe a little termination tremor at the end. So I do the first one, and it’s perfect. Do-to-do. You’re going, “Hey, you’ve got some sort of cerebellar issues – let’s see what happens. I want you to do that a few more times.” And if they do it, all of a sudden you start to see this [demonstrates tremor]; as they keep doing it, you start to see this [demonstrates more pronounced tremor]; and as they keep doing it, they continue to make it get worse. Does that make sense? Or, you might have someone that has a problem, and as they repeat it, they just start to get smooth. Those things clinically matter.

You’d have to observe how they change to getting better or worse, and you’d do repeat testing in areas of the brain you know are involved from your history and from your general survey. So if we have someone who’s got some kind of examination findings like finger-to-nose, and it’s normal, we want a repeat test to have them do it more than once, and if they still have no change, they’re still fine, it’s still normal, we go, “Those pathways are intact – we’re not worried about them.” But if they, with repeat testing, they start to have abnormal findings, so now as they repeat-test, they start to have some tremors show up, then we go, “Hey, those pools of neurons are not healthy.” And then we may do exercise and therapy there with a thoughtfulness of how many reps, how often they would do it, because we know they would fatigue. Does that make sense?

So here’s a little simple concept for brain rehab: Whatever they can’t do is their therapy. I mean, we’re going to be much more advanced than that, but just – when you’re first starting – they can’t balance on the left foot? You can give them balance on the left foot. They can’t touch their nose? Have them touch their nose. They can’t do supination-pronation because they’re all over the place? Have them focus on doing it. That’s 101 rehab. You guys can all do that without any advanced training, right?

Now the key thing is this. If, let’s say, someone does supination-pronation and you think they have a cerebellar issue, and then they start to… over time you really start to see it, but for the first five seconds it’s good, and then it starts to give out, how long would you do a therapy for? Well, you do it for under the time it takes to fatigue, and then you would eventually have them do it longer and then longer. But you wouldn’t go, “Well, if they got to five seconds, do that for a minute straight.” Because you would make them crash. Does that make sense?

So do you guys realize, do you understand how critical it is, to identify the involved region of the brain before you even do your exam? Because it’s going to tell you what areas you need to examine further with repeat testing to check for endurance and the factors that are there. Does that make sense? Okay.


So those are all examples on this flow chart of what you do when you see examination findings that are normal, and then you push it to see what happens. But what if someone has abnormal examination find-ings? So they touch their nose, and they have a little bit of termination tremor, but they do it again and now it’s perfect. So this is the scenario here. They have abnormal examination findings, they improve with repeat testing. So it was abnormal once, then you do it again, you go, “Hey, look at this! They have a tremor!” and then they do it again and they don’t any more. So that normalized. That is clinically significant to you. So what that means is, that’s probably not the primary area. That’s probably a network that’s involved, but they were able to compensate right away. It’s probably not the area you really want to focus your time rehabbing or reactivating or doing things for; that there’s other things in that mechanism that could be involved.

And what if they were like this [demonstrates big tremor], and they repeat test, and they start to get better? Well then you know that you can rehabilitate them without so much metabolic concerns, because with some people, for example, their balance is really off, but as they practice and do it repeatedly, they get better and better and better. What that tells you is, those neurons are involved, but there’s a lot of good endurance there. They’re metabolically fit, so you can be pretty aggressive with their neuro-rehab protocol. Does that make sense to you? Okay.

Now, there will be times when someone has abnormal findings, and the examination findings get worse with repeat testing, that tells you “Whoa, you’ve got to be very careful doing any kind of brain rehab.” So if you’re doing finger-to-nose, then they start to go from big tremor to big… their limbs are totally involved, and now they start to get titubations when they keep doing it, you probably don’t want to jump into a lot of rehab, because you’re going to make them crash. Because just doing this exercise a few times is making it worse and worse, that’s when we go, “Man, we really need to address the metabolic needs. We’ve got to see what’s going on.” Do they have an inflammatory issue? Is there severe degeneration? Is there an autoimmune process there? Because those people, if you try to treat them and rehab them, you’re going to definitely make them crash. They’re going to get worse under your care.

Now, another possibility is, they develop a different symptom. So they do finger-to-nose, and they go, “Oh, this is straining my eyes. Now I’ve got a headache.” That tells you that that activation fired into post-synaptic pools, so you have a neuronal pool firing into a post-synaptic pool, and those pools weren’t healthy enough so they had an outcome. And where their symptoms are helps you localize what’s involved.

So here’s an example: I do finger-to-nose, as I do it I get a headache and my eyes are strained. That’s totally different than if I do finger-to-nose and now I feel nauseous. Then if I do finger-to-nose and now all of a sudden I start spinning to the right – those are all telling you different pathways involved. Those are the things you need to be able to clinically do as a practitioner of functional neurology that does it well. You guys understand? Okay.

So those are the key flow charts we’re going to be teaching throughout the course, but now you guys see the big picture. You guys understand the big picture of how these things work? This is helping us decide: Maybe we need to do metabolic stuff first; maybe we need to do brain rehab, we’re not too worried about the metabolic stuff.” We always want to address it but maybe it’s not the key thing; we can be aggressive with therapy. Or maybe we do a combination of both, based on what you see from their exam findings.


So just to review one more time: You hear the patient’s chief complaints. From their chief complaints, you localize the region of their history. From your general survey, their posture, their head tone, their speech, their movement, their tone, you also localize the region. You do the exam, and then you figure out areas that are involved. And then once you do your examination, the areas you think are involved, you would consider repeat testing in those involved regions to see if they’re getting better or worse to determine if you do metabolic stuff more initially, or you do neurological stuff without worrying about fatigue issues. That’s the initial key thought process we really want you guys to understand. Everybody good? Okay.

So what separates an average clinician from an advanced clinician is their skill set at understanding and managing neuron fatigue rates. Because it is not hard to identify and localize areas of the brain involved. It’s very easy once you understand the concepts. What makes a practitioner really do a phenomenal job with a patient is understanding how far they can push him, what factors are getting in the way for them to develop plasticity, and how to integrate those two things together. And this is what Dr. Brock and I saw as a huge weakness in how functional neurology is being taught. There was a localized exam, very simple, and no addressing of these metabolic factors or fatigue issues, and that helps impact your patient’s case.

Now, one of the things that we always talk about is the basic needs of a neuron. So, neurons have to have oxygen, neurons have to have glucose, and neurons need activation and stimulation, and inflammatory mechanisms uncoupled the mitochondria , and that impacts a neuron’s ATP. Basic concept. So when you’re looking at if someone has metabolic issues, endurance issues, they’re fatiguing as you do more and more exam findings, they’re getting worse and worse with your repeat testing, the place we always start is, does the neuron have what it needs? We don’t go into, all of a sudden they need methylation support or all of a sudden they need this single vitamin. We go, “Do they have oxygen going to their brain? Do they have glucose steady supply in the brain? Is there an inflammatory process in the way, or is there some kind of disuse or lack of activation degenerative process taking place?” Those are the key things.

Now, when neurons get glucose, oxygen, stimulation, and the mitochondria are healthy, neurons make ATP. When neurons make ATP, then they have a resting membrane potential that’s far away from threshold at a healthy level. If it’s too close to threshold, if neurons are too close to threshold, then trivial types of stimulation can excite them and make them fire. So those people you’ve noticed, that if they get around gasoline fumes, all of a sudden they get a headache, well, their olfactory five is going to be close to threshold. Some people, as they go outside, as soon as sunlight hits them, they notice discomfort and have a headache. Their visual pathways are too close to threshold. If someone also has ringing in the ear and tinnitus, their neuron pathways are too close to threshold. When neurons are too close to threshold, and they don’t have enough ATP, that’s what’s happening with people as their getting worse as you do exam findings. Does that make sense?

So if someone’s doing finger-to-nose, and they keep getting worse, then we’re dealing with: something is impacting those pools of neurons. Maybe there’s lack of oxygen because they have anemia and poor circulation. Maybe they’re dysglycemic. Maybe those pathways just have disuse and atrophy from lack of activity. Maybe there’s an inflammatory process going on. Those things lead to less endurance.

If there’s less endurance in the neurons, what happens as you do repeat testing? They’re fatigued! And then neurons are close to threshold because here’s how this works: When neurons have ATP, neurons can provide fuel to the sodium-potassium pump. So when you activate a neuron, you get an influx of sodium


that comes in, and that brings that neuron’s resting membrane potential close to threshold. Now, you’d have to push that sodium out – that requires ATP.

So if you have a neuron that doesn’t have enough glucose, oxygen, stimulation to make ATP, they can’t push that sodium out, and they don’t have enough ATP, so they quickly fire, and react, and they can fatigue really quickly.

So let’s say my auditory cortex is close to threshold. Now auditory cortex… so let’s say, for example, I’ll give you a scenario. First person has otosclerosis. They have lack of sound conduction fire into their auditory pathways. They have it, let’s say, on both sides to some degree, and they’ve had lack of activation for a long period of time. They’re also diabetic, and they’re a smoker. And now they’re anemic. Their chief complaint is tinnitus. What does that tell you? Tinnitus is temporal lobe, close ring spontaneously firing on its own, those neurons are close to threshold. You put a tuning fork next to them, they surprisingly move around and it bothers them and it starts to give them a headache. What does that tell you about the fitness of those pools? They’re not healthy. They react adversely.

Now, would you do auditory rehab with that person? No, you might have to go back and go, “We need to make sure you get some oxygen to your brain, control your diabetes,” and once they get a little more integrity, so you can put a tuning fork next to their ear without them wigging out on it and reacting adversely to it, then you can start to do some auditory temporal lobe types of stimulation. Does that make sense?

Or, you can go around and do different types of things, but that’s just the concept.

So that’s one of the things that we try to do in this model: is to really understand that those basic concepts apply.

Now, this is the diagram that you have, and it goes into when you’re actually seeing people have lack of endurance, those mitochondria and those neurons are impaired. That’s a degenerative process. So let me give you an example. Have everyone stand on their left foot, and in this room, some people will first of all be shaking right away, which means there’s a problem there. But at some point, if people stand long enough, there’s going to be a point at which people fatigue. Does that make sense? So, like, some person will be here in like a minute, and they’re still fine, and other people are like shaking crazy, and they’re all over the place. That’s telling you their mitochondrial integrity of those neurological pathways. And let’s say we’re talking about posterior column cerebellar pathways. What happens if the minute they do it, after four seconds they cramp and they fatigue? That tells you those areas of their brain are degenerative. The mitochondria in those areas of the brain are not healthy.

Now when you activate neurons, you actually cause mitochondrial biogenesis. You develop mitochondria. It’s very fascinating. Now the goal of everything we want to do is, when we see a brain that’s impaired or a brain that’s injured is, we want to have neurons branch into each other. So one of the things you’ll see here is, you’ll see a neuron, and there’s a healthy neuron and there’s an unhealthy neuron, and through activation, neurons branch into other neurons. Now this neuron is unhealthy so nothing’s happening on the right, but this neuron is healthy, and as it gets stimulated, it can now connect to another neuron. Function can come back. That’s the plasticity.


Now, there is no supplement in the world that can make neurons branch into each other. Just like there’s no supplement that can make you have more muscles. Right? You can’t just take a vitamin and your biceps get bigger. You can’t just take a supplement and your neurons branch. You have to have activation. And that’s a limitation of trying to work with brain-related issues only doing nutrition, because you’re not making things connect. That’s why we have to do therapies. But at the same time, if the mitochondria in that neuron’s not healthy, it doesn’t have healthy sodium-potassium potentials, it doesn’t have fuel, it doesn’t have growth factors like brain-derived neurotrophic factor, and thyroid hormones, and glucose, it can’t branch either. So that’s why we’re always trying to look for both factors clinically, and approach it so as we do things we can get their brain to become healthier and have connectivity.

So I want to go through this flowchart with you, and I want to show you guys a case. So here’s a case, and he’s going to go through a bunch of tests, but you’re going to see we’re going to do these tests repeatedly, over and over again. So here’s what you’re going to see. If you see an exam finding, does it get better with repeat testing, or does it get worse? You understand? We’re going to practice the flowchart.

Now, I’ll just give you some history. Patient, traumatic brain injury, and I’m going to tell you the injury was to the left cerebellum.

[video of patient] August 27, Matthias Springstrom. Go ahead and move your hands back and forth as fast as you can: fast, fast, fast, fast, fast, fast, fast, fast, fast, fast, fast, fast, fast. Keep going, keep going, keep going.

You see the left side? What’s happening as he does it is he getting bigger movements or smaller?

Okay, and bring your elbows in, do the same thing. Elbows in like this. There you go. And as fast as you can, fast as you can. Okay. And then go ahead and put palms, flat palm, fast as you can, fast as you can.

As he keeps doing it, see how it gets even worse there as he just repeats it.

And then go ahead and “play the piano” as fast as you can. Okay, that’s good. And just relax.

Now watch what happens here as he does it. It gets slower and… right here he cramps.

And then what we’re going to do is, we’re going to have you… Matthias, I’m going to have you stand back a little farther. Close… Okay, go ahead and close your eyes.

So this is just the Rhomberg’s, not seeing much there. Now there are a lot of things you can pick up right away: relocation to the left…

And then go ahead and put one foot in front of the other, and then… open your eyes first… go ahead and put one foot in front of the other, and stay in that position with your eyes open. And then eyes closed.

What you guys will see as he keeps doing this, instead of just falling someplace, his whole body starts to get involved.

Okay, switch feet the other way, with your eyes open first. Eyes open.


As you’re repeating, he’s getting worse and worse and worse. Do you want to do aggressive left cerebellar therapy with him? Now, you could still do it, but you’d have to do it before he fatigued, so it would only give you a very short period of, like, “do this for two seconds.” Or three seconds. And then you were gone. This is the person that, their inflammatory cascade from the traumatic brain injury was a factor in their case. Does that make sense?

So we look at this case, and maybe be very aggressive with how we rehab them initially. We know the area involved, we know things we could do, but we may want to try to get the metabolic factors involved. So that’s what you guys saw in this scenario, a person that had abnormal findings, and with repeat testing they kept getting worse. So those are unstable neurons, so you have to really consider any metabolic factors.

Now, his history shows he had traumatic brain injury. There’s a whole cascade of metabolic things that take place after that. The key concept being: they get severe neural inflammation. So you would go back to your model and go, “What’s going on? Is it an inflammatory model uncoupling mitochondria? Does he have blood sugar issues? Does he have anemia?” Well, in his case, he had an inflammatory model. An inflammatory response uncouples mitochondria so he can’t produce enough ATP. It’s going to be very, very hard to develop plasticity and really rehabilitate someone if that’s not addressed.

Now, I’m going to show you guys a couple more examples so you can practice with these flowcharts.

We’re going to look at pupils, and what you guys are going to see are pupils showing up here, and we have infrared cameras on them, and then what’s happening is, they’re looking at a blank white wall, and I’m turning the light on and off. You guys will hear a click: that’s the light turning on, light going off. And what should happen when you turn the lights off, the pupil should what? Dilate. And the lights come on, they should constrict. Now both neuronal pools, left and right, are being stimulated at the exact same time, because looking at a blank wall, the light in the room is going off and on. So there’s not one side being stimulated more than the other. So if one neuronal pool is more compromised, you would see fatigue and non-response in this first. That make sense? On that side.

So the practice for this one: see if you see anything with this. So as you can see… see the constrict? And then you can see some dilation. Now you see all that blinking? That’s diagnostic to you. See how his eyes are really teary? That’s diagnostic to you. The thing is, for the most part, those are pretty normal. You guys can watch this in replay again in the videos, because you’ll have streaming replay. But if you play those again, they constrict, they dilate, they constrict, they dilate, one side isn’t worse than the other. Seems pretty good. But you do notice excessive blinking, the eyes are watering, right? So those are classical histamine type reactions. So we know that’s a factor in their case.

Now watch this one here. Now right away, do you see one pupil larger than the other? This one here on the left. So watch this one. Turn the volume up if we can. [clicking sounds] What you guys will see is, this one tends to start to let go sooner than the other. So we know that left side is more compromised than the other.

You guys, if you’re new, you’re going to have to watch these a thousand times. There’s just going to be some flight time you’re going to have to get. Just like a boxer going in the ring, and they can punch a bag all the time, but you have to be in the ring. You have to just look at these over and over again. The good thing is, when Dr. Brock and I got together, it’s like, “We have to give people a replay video.” That’s why


you’ll be able to watch these videos over and over again, and the cases, until you start to see it. We have two thousand of these for you during this course.

Now you can look at this one. Now you guys can hear the clicking? What should happen with the pupils? There’s a click. You guys see any change in that thing? No. There’s no change happening. Is that diagnostic? Yes! There’s no pupil response! So sometimes things are just pathology. There’s no fatiguing issues, because you see the pathology right in front of you. It’s right there. Because this isn’t optic neuritis. This is the MS-type pattern. This is inflammation in the optic nerve. It’s a non-responsive pupil. So white-matter lesions all throughout the brain. Do you want to go and do therapy? No. You want to go in there and try to deal with the neuro-autoimmune process, because the brain’s being chewed up. You’ve got to address those issues.

Now, you could address it for many factors. This is a paper we recently published. We found that plant aquaporins… so if this person has neuromyelitis optica, or neuroinflammatory response, if they require aquaporin receptors, we found certain foods can cause antibody reproduction there, that also have aquaporin proteins in them. Spinach, corn, tomato. We’re going to really get into cross-reactivity, neuro-autoimmunity in this module. We’re going to teach you guys all the latest research and some of the stuff we’ve been publishing ourselves. So, very interesting stuff.

Now I want to show you a couple more cases of just optokinetics, and then fatigue, and just have you guys practice this concept. So if you guys aren’t familiar with how this works, one of the things that you can do in a neurological exam is, you can take a red-and-white strip, and then move it across someone’s visual field, and you’ll see their eyes rapidly move. This is called an optokinetic reflex. It’s what you do like when you’re in a train and you’re looking outside the window, and looking at images, and your brain’s constantly trying to readjust to where the new visual field is, right?

So you’re going to see these eye movements go back and forth like this, as they look at this image. What you want to see is what happens over time. Are they efficient all the way through? Do they all of a sudden crash? Do they deviate? Does something take place?

So here we can see… the triangles show that this person actually has pretty healthy pursuits, and saccades – these quick eye movements – so when you look at this person, you’ll see that as they go through it, they’re not really fatiguing. The pupil size is healthy, you don’t see any ptosis develop, you see no deviation in the eyes. They’re doing this for ten seconds, and they’re pretty intact. So this is a normal finding. You guys understand?

Now, clinically, let’s talk about a few things. Did you observe fatigue? No, we didn’t observe fatigue. What if you saw fatigue on a repeat testing? What if you go, “I know that this pathway’s involved from their history; I’m going to do that two more times”? And as you did it again, now you see after five seconds they start to not be able to do it. After three seconds they’re not going to be able to do it. That tells you you could probably rehab them, but you would be careful how many reps you do for how long. Do you guys understand that?

Now, what if they did it and it looks fine on the exam, but they go, “I’m spinning. I’m spinning to the right”? What happened in that scenario? That’s a scenario where they had new symptoms develop with testing, or even repeat testing. That tells you those neurons are very unstable. In the middle of the examination


finding, looking at the fact that they have those symptoms is telling you that they have some problems with it, right? Or if they had right-sided headaches? Then you know that type of activation fired vascular pools that are now causing abnormal tone. What if they got nauseous? Then you know projections from the cerebellar stem are firing into the pontine vagal areas abnormally. So they’re all important to you. When you see a person have symptoms after an exam, you should immediately ask what are they, because they’ll tell you the pathways involved.

Now, look at another one here. Now take a look at this one. You guys will see, with the image, after five seconds they stop. So look for that. You see a little bit of ptosis on the left. So they’re moving, things are cool, five seconds starts to hit, they stop their optokinetic movement even though they’re being stimulated, they start to get that ptosis on the left, their eyes start to dilate. This person had a five-second window. So do you guys see fatigue? Yes. After five seconds. Do you rehab this person or do metabolic support? I don’t know. From that one finding, if you did rehab, we definitely don’t want to go past five seconds. Right? Or maybe do you do metabolic stuff first, because that’s the key to your history, and now they can do it for ten seconds, or twenty seconds, and now you start doing some serious brain rehab.

So those are the type of questions we ask. When their response is less after five seconds, what if they only had two seconds on repeat testing, and they have nausea, and they crash? Well they’re definitely people you don’t want to rehab right away. Does that make sense?

So trying to merge where metabolic fits in to neurological rehab, once we identify and localize the region, we test those areas a little more repetitively, we figure out what the neuronal pools are, and if they immediately start to get worse and worse and crash, we know that metabolic components are a critical thing, versus the neurological component. And then if they fatigue, we go back to our concepts: do they have glucose, do they have oxygen, do they have stimulation? We look at all those factors, we address those, and then we see if their endurance and their things on repetitive testing makes a difference.

Take a look at this one. This is optokinetic to the left and right. So one way, and looks decent. And the other way. Then actually what’s happening is, they’re closing their eyes because their brain’s getting tired. You guys will notice that after they do one, they have to close their eyes. So they can do the movements, but do you see brain fatigue? Now the thing is, this person, as soon as she did that, optokinetic left by right, she noticed the symptoms of dizziness right away, with stimulation to the right. Does that help you? The fact that only when you went to the right, she had dizziness? That just told you the involved region. If you see she felt like she’s moving along the table, lasted for several minutes, promoted left-sided headaches, and symptoms of hypothermia and clammy hands. You know we’re getting an autonomic effect as well. So this may be a person where you go, “Hm, is there a metabolic factor involved? They’re fatiguing – what’s involved with this? This is a cerebellar case.” And you guys, this is a person that had cerebellar antibodies, that had an autoimmune response to their cerebellum. And I want you to take a look at this. I want to you look at the data of this test. This is 2006. We were doing this stuff ten years ago. We just never had a place to teach it. So here we are!

Now, we’re going to share with you what we’ve been doing and have been frustrated about not being able to share with everyone is, these factors are critical, and they happen. A large population of celiac disease, gluten-sensitive people, have cerebellar autoimmunity. If you don’t address that, that can be a factor.


So let’s move on. So in those types of scenarios, we look at the factors that are involved, and we go through it. So those are the key concepts that I hope you understand. So let’s review this really quickly, and then doctor Brock is going to go over a case with you.

You listen to their history. Whether they have focus issues, concentration issues, their speech is involved, they can’t read as well any more, they can’t remember directions any more, whether they have tinnitus, whether they feel numbness on their face, is going to tell you the region of their brain involved, if you know your neuroanatomy. We’re going to go the opposite way this weekend, and go, “Here is all the different regions of the brain, here are the symptoms.” And then you have to memorize and know that. And then we’re going to add that in with the general survey, and you watch them talk, you see their movement issues, their gait, their posture, their eye movement, their tone. Then you even localize the region further. Now you know the regions that are involved, then you evaluate those regions, and if you think the region’s involved, you do repeat testing and see if they get better, if they get worse. And that lets you know if you need to do more metabolic stuff initially, or more neurological stuff initially, or both together. Does that make sense?

I guarantee you, most people doing functional neurology don’t do that. They just go, “I know how to do this therapy! Here you go! It’s this! It’s left brain! Right cerebellum! Do this for a while and see how you do! Oh, you crashed? Sorry!” We don’t want to do that. We want to go through our thought process and know where those things are immediately after the exam. Dr. Brock is going to go into a case for you, and we’ll go from there.

Okay. Thank you.

Presentation by Dr. Brandon Brock

So, landmark time. The first time ever that someone has really put that on paper. I’ve been doing functional neurology now since – I don’t even know if I should say – early 90s. And it was one of those things where what I always noticed is, the functional neurologist would end up doing great work, but then there would be a metabolic factor that would kick in, and it would change the pathways, and the findings would change, so then the therapy would change. And the neurologist would say, “Oh God, it changed, let’s do this.” And then the metabolic stuff would change again, and they would change their therapy. And it turned into a giant tail-chasing session. Does everybody understand?

So we kind of started thinking, “Man, maybe there’s more to this than meets the eye! Maybe there’s just this metabolic stuff!” And all of a sudden I’m like, hanging out at the bar, and I meet this guy named Datis. And we started drawing things out on napkins, and then I meet another person. And then I started drawing… What we find it, everybody has their own problems, right? So the nutrition world, they’re like “Well, we can’t get the gut to change,” because what they don’t realize is, they can’t get brain-vagal output to function the right way. And then we have some of the people in medicine, they can’t get some of the things to work because it’s just a shotgun neurochemical approach that doesn’t really work on brain-specific regions.

So we started thinking, “Hey, wait a minute. Maybe, just maybe, somewhere all of this stuff comes together.” And what we really created is a functional integrative neurology approach. Scare words. I’m not trying to change the path of anything, but I just want you to know that integrating this is cool. Now what we just did was a really good example of just saying this: “When do you go where?” And the art of functional


neurology is determining the rate at which you do functional neurological services, and where. And do you do metabolic work before, and then do neurological care? Or do you do it while you do neurological care? Or do you do it after, to keep your neurological care standardized? Or standard and functional and doesn’t digress back down into being pathological again?

We spent the last two years working on that. Some people were like this: “You need to work on your nitric oxides before you go onto therapy, because you need some vasodilation so you can get some blood to your brain, so you can do more than five seconds of care.” And now they go to thirty seconds, or forty seconds. And so they build up tolerance.

The next couple of years, or however long we’re going to be doing this, is going to teach you the art of blending what you do in with functional neurology. And when you do functional neurology, how do you integrate? And if you integrate, how do you do a little bit of each one to make it get it all… become an orchestrated, beautiful piece of work that makes them their most functional? And then somebody else sometime down the road will do it even better, and they’ll teach it. But right now, this is where we’re at.

So let me put it in context real quick. We have this girl, she comes in, and she can’t walk. She has lost the ability to use her right side. She did not have a stroke, and it happened after an upper respiratory tract infection.

Now, I just gave you a sentence that Dr. Kharrazian told you about, and I want you to think about the flow charts. You can not ignore the fact this started after a possible infectious disease. You can’t do that. If you do, you’re deleting evidence, and you’re going down a pathway of dissonance, which means this: You’re trying to stuff everything you do just in the box that you utilize. Does that make sense?

You have to say this: “Man, maybe I need to learn a little something about inflammation, and infectious disease, and can infectious disease do anything to the brain, and if we do something to the brain, can it change leg function?”

Now, I’m going to make it a little bit more complicated. I’m going to give you another layer. If they come in with a leg that doesn’t work, you have to be able to say, Rule Number One – and this is Rule Number One in functional neurology – “Is the lesion central, or peripheral, or both?” And with that rule comes this: people can have more than one problem. They can have both of them at the same time.

So when this girl comes in, she’s been to fifteen different doctors. She lives in England. And she came in, and she’s a beautiful girl, has her whole life ahead of her, has been accepted into college, but she can’t get around. So let’s just watch.

She has weakness in the right leg, started for no reason, according to her. She had a steroid shot. She had an infection. She got a steroid shot.

Now, I don’t want to get into all of the immunology right now, but we will. And I will discuss drugs, because there are people here that utilize medications. But steroids have a profound impact on your immune system. And if you have certain infectious diseases, and you immunosuppress somebody, or alter their immune system, you can now have the expression of inflammation, or expression of replication, or the load


of that organism which can create more inflammation, and can damage neurological tissue. It can make those systems not fire right. Or, there can be mimicry, so it can start to attack certain tissues, and you get neuro-autoimmunity. We don’t know, but the bottom line is this: this is the facts. This is what she’s telling us.

So she went and got this shot, and so we have to say this: “Where’s the site of the lesion? Is it in her left brain or right brain? Is it here left leg or right leg? If the leg is involved, is it in a dermatome nerve root? Is it the whole leg, but just from here [gestures to waist] down? Like with a lower thoracic cord lesion, or a transverse myelitis? Or is it the leg and the arm? Or is it the leg, arm, and face?”

So now this is where the localization game kind of starts – and I like to play a little game called the localiza-tion game. Every morning we do a little warmup. And the bottom line is this: Is it neuromuscular junction? Is it primary muscle disease? I’ve got this all broken down into a chart for you. Is it peripheral nerve? Is it plexus? Is it one nerve, or many nerves? If it’s many nerves, is it the myelin or the axon? And then we go all the way up through the brain. I made a nice little chart for you. In your diagrams, it is the Longitudinal Level of the Lesion chart. And so you can review that chart without me having to get into it implicitly. Next module, when we start saying, “Hey, here’s a patient, tell me the regions that you think might be involved,” it’ll really come into play. But right now, we’re just giving you, “Okay, these are what the regions mean.” Next module it’ll be “How do you look at them from a clinical perspective?” and then we’re going to start getting more microscopic and saying, “Let’s talk about just this one area in the big picture.” Does everybody see how it’s really going to actually be in order?”

So I have to say, “Is there any metabolic factors? Is there any neurological factors?” Where do you start? This is no different than what Dr. Kharrazian just said. I’m just taking it a little bit further. And you always have to put yourself in the patient’s shoes. She’s young, she wants to be a mother, she wants to be married, she wants to finish school, she doesn’t want to live disabled. Are you starting to feel what I’m saying? You all – many of you – have seen these patients. Of course you want to do something for them.

So, is it upper or lower motor neuron lesion? You’ve got to learn this one principle. Upper means it’s spinal cord up to brain. Lower motor means it’s nerve root out. Ventral horn cell disease will give you a mixed bag of things, and I’ll of course go through that, but I know many of you don’t know neurology well, and some of you are like, “Oh my God, he’s talking about upper and lower motor neuron lesions!” Well, yes I am. Because many people who think they know really don’t. And by the way, this girl’s coming in with a right-leg weakness. Every single doctor had called it a lower motor neuron lesion. Every doctor. And she ended up in our clinic no better.

So, is this metabolic, anatomic, or both? We’ve been talking about that. Is it a combination of two? What’s the problematic loops that might be involved? So we’re going to start talking to you today about things like this. Inflammation, which will cause damage to one area, which can perpetuate more inflammation. So there’s about a hundred and fifty of these vicious loops that we’re going to go through, and we’re really loop breakers when it comes to metabolic function.

So, do you know how to work through it? Go back to the charts that Dr. Kharrazian and I have put together. Now those charts were made out of basically this: a lot of just discussion. What do people need? How do people really start this stuff? It’s very difficult for to teach somebody to walk into a room and say, “Go: do functional neurology.” That’s why it’s been hard to teach, that’s why it’s been difficult to bring people into


it. But I think we’re actually starting to capture the essence of being able to say, “This is actually how you start this stuff.” Okay? And this is it. This is the same chart, but I’m just going to say this: I need you to look at this patient and start to say, “Where could the problem be?” Okay? Where could the problem be? And then once we say, “Where could the problem or problems be?” I’m going to start working through the process of differential diagnosis.

Now, I’m not going to talk about treatment today. Because as soon as I do that, it blows everybody out of the water, and everybody starts going, “Oh my God, that session was great, and then all of a sudden it ended crazy and I can’t keep up with what he’s saying.” But what I want to do is, I want to take the… do you know some basic regions? And by the way, we’re just starting out with some examples. We’re going to do the whole weekend. We’re going to discuss these regions, okay? So if you’re like, “Hey man, he’s been talking about regions, we didn’t even discuss them yet,” just hang on. These are just examples.

But I need you to be able to look and say, “I think this may be involved, or I think that might be involved.” So when you walk into a patient room, I want a little three-dimensional thing to pop up and then all of a sudden it looks like this: brrrr, these are all the areas that could be involved with this patient. Is it contralateral cortex? Did they have a stroke? Is it the corticospinal pathway that’s damaged? Did the spinal cord get damaged? Did a nerve root get damaged? Did multiple nerve roots get damaged? Do they have a neuromuscular junction disease? I will teach you how to work through each one in a song and a dance that I made in three minutes.

Now, I will also tell you this: I’ve got somebody that I’m cueing, and every time that I cue them, I need to make a short clinical gym video that everybody can get, so that you can watch that part, and it can be a little bit more in detail. Okay? We are going to the nth degree to make sure that you can say, “I actually understand neuromuscular junction disease versus ventral horn cell disease.”

And don’t say it won’t walk in. The other day – or not the other day, nine months ago – I had a guy walk in. It looked like he had popcorn everywhere, all over his shirt. His shirt was like tk tk tk tk tk. And it was in his face, it was in his neck and his hands were starting to atrophy. And I looked at him, and like a little tear just rolled down my face, because I was like, “This guy’s going to be dead in a year.” Me and my wife went and visited him last week. He can’t talk. He’s on a respirator. He has no muscle tone, and he can only speak with his eyes on a computer pad. He has ALS.

Now, the reason why I’m telling you that is because after you do functional neurology for a while… he had been to seven different doctors, the VA, and then within three seconds I knew, I was like, “That guy’s going to be dead in a year.” That does not make me special. It just means that what we’re going to teach you will give you the capacity to localize a lot of these lesions, and make a difference. Because knowing… do you know that just him knowing allowed him to get his affairs in order, and his family not go bankrupt? I’ll just tell you that right now.

So, cases are used as an example to explain academic principles. We have about two thousand cases that we’re going to be going through, so don’t worry.

This patient wanted to fly from England and come stand on stage for you, and I was like… I’ll just play the video. I’m like, “You’re welcome to come if you want, but I’ll have to call Bud and make sure it’s okay!”


So we have a long way to go, and I want you all to understand one more thing, and I’m kind of soapboxing a little bit, but you know, there’s really kind of a few types of people that get into neurology. There’s those that get into it and they’re like, “I hate this, it’s way too hard,” and they quit. And there’s those that get into it and they become maniacal and they go way off and they love it, and it’s everything they want. And there’s the people that are in the middle, which is were a lot of them are, and they’re like, “Ah, I just don’t know if I can do it. I think I can do it.” When I started out, I was in the middle. I’ve got to be honest with you.

We’re trying to take those middle people and make them really feel like they can do this in a way that’s not so crazy. Okay? So, we’re going to observe, diagnose, integrate, treat, determine efficacy. That’s what we’re going to end up doing as we go.

So Dr. Kharrazian’s telling you this: Can you observe? Can you see? Can you localize? Can you combine therapies? Can you integrate? Do you know enough when you walk in the room to say, “I think it’s this, that, or the other”? Okay?

Well, this right here takes down all your motor weakness patterns. So, I’m not going to go through it in super-duper detail, but I just want to show you that if you actually look at this, there’s global weakness. Global. Is it neuromuscular junction? Do they get weaker as they activate? Like with Lambert-Eaton in the body, or with myasthenia gravis in the face? Global. Neuromuscular junction. Autoimmune to that system, to different post-synaptic pool, or post-synaptic receptors. Is it a metabolic disorder? Do they have small-vessel disease, so they give out? Is their autonomic system completely incapable of tolerating shunting stuff where it’s supposed to go?

If you go over here, you have to be able to say, “Alright, it’s just hand weakness only.” Well, it could be cervi-cal root disease, it could be a plexus lesion. Ventral horn cell disease starts out in the hands first; primary muscle disease starts out in the proximal muscles first. Please catch that. Someone comes in, they’ve got atrophy in their hands, and so they’ve got this: Ready? They’ve got lower motor findings in their upper extremities. And I’ll talk to you more about upper and lower, but lower motor findings are like this: muscle atrophy, nerve damage, fasciculations, everything’s kind of shrinking and shriveling up, reflexes are gone. So they’ve got lower motor findings in their upper extremities, and upper motor findings in their legs. So their legs are getting tight and spastic and hyper-reflexive, and their hands are going bye-bye, and they have a tremor, but it’s not a tremor across a joint, it’s a tremor over the muscle. That’s called a fasciculation.

Now, let me stop real quick.

Here’s a muscle. The muscle’s now broken into a smaller group called a fascicle. And that fascicle is broken into smaller groups which are called fibrils. Fibrils show you fibrillations. When a whole fascicle fires off you see the fasciculations, and when ventral horn cells start to die, they spontaneously fire. Go back to the chart. They’re undergoing oxidative stress, they’re reaching threshold, they have changes in superoxide dismutase, they have free radical damage. Their sodium-potassium equilibrium potential changes, it shifts the threshold, and poof, it fires, and all of a sudden you see tk tk. You’re like, “Wait a minute, that was like a tremor,” but it wasn’t across a joint. It was over a muscle. That’s the muscle firing in the belly, and it’s not actually causing an oscillation of the whole limb. Okay?


So, just some observation stuff. So if you follow this over here, and now you have to say, “Is it central nervous system disorder? Are they hyper-reflexive? Are they rigid with basal ganglia? Are they spastic with corticospinal damage?”

Then you go over here, and you have to say, “Look – it could be cervical root, but maybe it’s up here [gestures to shoulder], not down here [gestures to upper arm].” So if it’s lower in the plexus, or lower in the cervical root, you’ve got to look at the hand. If it’s higher, you’ve got to look at the shoulders. And I’m telling you this because it goes in context with the next case. Alright? It could be an orthopedic injury, it could be primary muscle disease. Primary muscle disease starts up here [gestures to upper arm]. Facioscapulohumeral dystrophy. Limb girdle dystrophies. Muscular dystrophies. X-linked dystrophies. Polymyositis. Statin-induced muscle disease. Starts here [gestures to upper legs].

We’ll show you all the tests that you can do that look for toxicological imbalance, or they can’t biotransform those drugs, and also where they’re getting symptoms because they have a biotransformation error. That’s one of my favorite things to do.

So, we skipped through this. Now, I just want you to tell me what you see here. First of all – well, don’t tell me, because we’re on video, but just think to yourself for a second – look at that hand right up here [gesturing to slide], right there. And then here it is right here. This is the guy just at rest. So his hand’s like this [demonstrates hand with fingers hanging down]. Now, this is a guy that – they have these giant metallic cauldrons where they pour things in and make these big casts, and it’s about as big as this section of the room. He fell in it, and bling, bling, was just bouncing around all over the place, and ended up breaking his arm. And he broke his arm right on the humerus, and he broke it right back here [gestures to back of upper arm]. There’s this little thing called the radial nerve, and it adheres to the spiral groove. So when he broke his arm, it sheared the nerve. So now he has a wrist drop.

Lower or upper motor neuron lesion? Lower – good! Very good. Now, just watch.

Let’s see. Just open the hand up.

Does he have flexion? Okay. If it’s a C7 root lesion, you’ll lose both. And I’m starting to show you now differential tidbits. I love the differential game. He can go open flexion… Watch carefully now. Look at that thumb.

Open your fingers up. Open them. “When I try to open, this one’s going to go.”

Okay, beautiful. Now here’s him trying to extend his hand.

Let me have you lift that up. [patient groaning]

And that’s good. So which one’s better? Flexion or extension? So here’s how it works. You lose these fingers first [drops middle and ring finger], these fingers second [drops index and pinky finger], thumb comes in third, and then you can’t do this [demonstrates inability to extend fingers]. I will show you the three levels of the three big nerves in three minutes off the three parts of the plexus. You will know it in one hour. Not today, but you will. I’ve got a trick and a song and a dance for everything. I have to learn it that way.


I’m giving you a good example of a lower motor neuron lesion. This dude’s toast! This is one of those guys where I have to say this: “I don’t know if this nerve is going to grow back. Let me do an EMG on you.” Now, I’m not trying to teach you EMG today, but let me just show you something. A nerve at rest should not fire. If a nerve is being denervated, it fires spontaneously, so that you can keep the protein replicating so the muscle doesn’t die. What an ingenious mechanism! Is that cool or not? Tell me if you see any spontaneous potentials.

“No, that was…”

Tell me if you see any spontaneous potentials. [EMG display on video] Who sees spontaneous potentials? That’s me moving the needle around. Now right… here. Now watch this one. Any spontaneous potentials? Now, these are individual fibrils denervating. So you get sharp waves and fibs. As long as you have that, the muscle’s going to continue to atrophy and die. This guy, based upon this, is not going to recover.

So now I can say, “You’re going to have a lot of muscle atrophy. This is probably going to be permanent.” The nerve has been ablated, and they’re already getting atrophy, and so now we can start to say, “Hey, you’ve got some problems here.” You can’t always give a good prognosis, okay?

So these are just some examples. So you notice the muscle tone is gone, you notice the movement is damaged, you know that’s lower motor. We’re going to teach you how to read EMGs, not do EMGs. And then you can say to yourself, “This looks like a lower motor neuron lesion,” or, “This is a lower lesion. It’s in the nerve. It’s not in the spinal cord.”

Now, based upon plasticity, could this end up changing the central nervous system? Yeah. If you affect what a peripheral nerve does, you’ll affect the entire… everything in the first, second, third order pathways.

Here’s our girl.

I just gave you that other stuff to kind of show you what a lower motor neuron lesion looks like, and kind of divided it up into categories. Now that little slide I showed you, with all those different things. I have a whole day on that, down the road. So don’t stress out about it and go “Boy, you went through that quick!” You’re right, I did. But I’m just sort of quantifying what I did.

Now here she is. This was a few months after her event. Okay, after her event. Now, what do you notice right out of the gate? She has to have crutches, and she has to have assistance. Now that’s bad. You want somebody to be able to ambulate. If people can’t ambulate, they can’t activate their brain. If people can’t ambulate, they can’t take care of themselves. They lose autonomy. If you lose autonomy, there’s going to be a problem. So let’s just watch this.

Here’s her walking. She can’t lift her foot up. She has a foot drop. She has internal rotation, and she has a breakdown in hip mechanics, and she has a breakdown in spine mechanics. But she can use her arm. She has no idea where her right leg is. Now, what nerve root does that? The hip and the foot? Inversion and eversion? See, it would be very easy to look at that and say, “Ah, it’s an L5 nerve root lesion, and they’ve got a foot drop.” But she also has hip mechanical issues, because it’s weak. She’s also got proprioceptive loss. She also can’t feel the limb. She also doesn’t know where it is. And we did an EMG on her, and it was normal.


So I would have to ask myself, “Central or peripheral?” Central. And we were the only people that said, “You know what? Thank God it doesn’t look like you have a polyneuropathy.” I mean, if it was an axonopathy, or an autoimmune disease, or something like that, then we’d be stuck chasing that down, and that’s very difficult.

When I looked at this, I got extremely happy. I said, “You know what? You’re going to walk again.” Like, I actually said it. I go, “Your peripheral nerves are intact. You had an inflammatory event. We’ll work on that, don’t worry about it.” I’ll show you some of the labs in a minute. I said, “This is going to get better, because I think we can change your brain.”

Listen. Everybody just hear me. We didn’t invent the understanding of plasticity. We just get everybody’s research and integrate it. There’s tons of research being done on plasticity. It’s called the Hebbian process. And we know that you can activate a brain. If everything is metabolically good, you can activate a brain to make it better. And for those areas that can’t quite tolerate it, sometimes you can go to another area and activate it to feed into that area. That’s a whole other second layer that we’ll get to.

So now, this is her with an AFO. That means it keeps her foot from going pffft and dropping down. Now the reason why we get concerned about this is because if you’re walking, and your foot is dragging, you have a greater chance of falling and then having another injury. So we don’t want those kinds of things to happen, obviously.

But this is her. She has not been to see us yet. This is her, pretty much right when she got the AFO. She still can’t do that hip follow-through. She has no hip flexors, and no hip stability.

Now, pause real quick. I know many of you are like, “I’m a naturopath. I don’t do anything with biome-chanics.” You do now. Neurology is biomechanics. Biomechanics is neurology. By the way, chiropractic is neurology. You can’t separate it. Those bones, those ligaments… and even if you decompress the nerve, bone off nerve, they’re still nerves. But what we find is, when you activate the brain, the brain has descend-ing regulatory factors over movement and curves. Those little subluxations are small-movement disorders.

So here we go, “I don’t want this to be the rest of my life, do you?” So if this person comes in, what’s your goal? Don’t say “cure” please. Don’t say “miracle.” “Miraculous!” Don’t say that. Set realistic goals. “Hey, I want to get you to walk with one crutch.” “Hey, I want you to not look disabled.” “Hey, I want you to be able to be functional.” And so when you start talking to a patient, if their expectations meet your idea of what you can do, you’ve got a patient. If they’re not, you need to send them down the road.

Dr. Brock and Dr. Kharrazian practice-building tip number one, okay?

Because you may have somebody that’s probably not that sick, but if you can’t… they’ll come and say, “I want to be like I was when I was fourteen.” I’m like, “Well, I do too. Kind of. In some ways. Not every way.”

So here she goes. You can see that she can’t… she has no hip… she has no step-through and push-off. You guys, that is bad, okay? That’s not good.


This is just another video of her before she came in. Same old thing. This is her doing therapy with, like, a family member. They’re just trying to get her to move. And I applaud them. Amazing. They just re-did stuff over and over and over.

So, how many of you observe weakness there? So many of you at home, you observe weakness, right? What about spasticity? Did the leg look stuck, like a stroke patient, where it’s like this [demonstrates stiffness] and she’s like this, and she’s having to circumduct herself around like this. So when you look at this, you wouldn’t say, “The whole body’s affected, I wonder if it was a stroke?”

This is the thing: with stroke, the pathways become damaged. So if I’m trying to build a house, and I blow the highway up, and I can’t get materials there, it’s going to be hard to build a house. The pathways are still there. What happens is, the pools that are actually function just can’t cut it. So here’s the deal: Does she have an inflammatory event? Yeah. Are there viruses that live in the central nervous system? Yes. Can it go from the upper respiratory tract to the brain very quickly? Yes. You’ve got Parsonage-Turner Syndrome, you’ve got vestibular neuronitises, you’ve got transverse myelitis. They go all over the place. Can they pick on one part of the brain versus the other?

Let me ask you this: Which side of the brain would that right leg would you think would be affected on her as far as motor cortex? The contralateral side, okay? So for her, if it’s right-sided leg, it could be the left brain. Now, is it down… This is where I was going to let Cedermark draw on my head, but he wanted to use a permanent Sharpie, so I have to watch out. Is it down here [gestures near ear] or up here [gestures to top of head]? Yeah, the leg is here [gestures to top of head].

So I’m going to teach you how to learn the brain, left from right, anterior to posterior, superior to inferior, outside to inside. That’s all you need to know. We’ll teach you that in just a few hours.

Now, it’s up here [gestures to top of head] and in the frontal lobe. Which one’s more involved with the leg? The dorsal, lateral, prefrontal, or the orbital frontal? Orbital frontal. So you’ve got to check for impulsivity. She has no impulsivity, and she has no signs of orbital frontal lesion. So we rule that out, and we just say, “strip.” And then we say, “What is the vasculature that goes to it?” It’s the anterior cerebral artery. It does the Mohawk. The middle cerebral artery goes out here [gestures to side of head]. So if it was a stroke, it would be anterior cerebral artery, but she doesn’t have any other frontal signs, so it wasn’t a stroke.

So we have to look at this and say she had inflammation. She probably had asymmetry before it began, and the whole thing wound down, and now you can see her asymmetry even worse. And maybe the inflammation damaged some of the peripheral nerves. We don’t know. But the EMG was perfectly normal.

So that’s the part of the central nervous system that might be involved. I don’t think the corticospinal tract is involved, because it would be spastic. I don’t think the cerebellum would be involved, because it would be hypotonic. She’s not hypotonic. This looks like the contralateral cortex got damaged, and it was just in a localized area, and it didn’t go away to the frontal lobe, and it didn’t go back to the occipital lobe, and it probably impacted a little bit of the parietal lobe, because she doesn’t have any spatial awareness, and that’s what the parietal lobe does.


So it’s just like this: Here’s what I want you to be able to do. Zzzzzzt! [makes circular motion on head] You could drill a hole right where the problem is. Right there. Take about three fingers, put it right there [puts fingers over contralateral cortex]. Her lesion is right up here. She had lost her stereognosis, barognosis, and graphesthesia. She had no idea where her leg was. That’s why she walks like this.

Now, why would the flexors be better than the extensors? There is greater representation of flexors and extensors, so she has more flexor control left than extensor control, so she has a hard time with all of her extensor mechanisms. She can’t bring her leg back. She can’t lift her foot up. The only thing she can do is lift this a little bit, and pull this back a little bit [gesturing to hip area], which is the only saving grace that she has as she moves.

Alright. Does this look like neuromuscular junction problems? No, it’s not global. See how you’re already figuring it out? Does it look like myopathy, primary muscle disease? No, that starts proximally in the hips and the shoulders. It’s not that. Does it look like it’s one peripheral nerve? No.

But do you know what happened to her? She went and got a facet injection with a steroid. Now, I don’t know which doctor linked this to a facet problem. Strange. I’m going to just say, strange. She got a facet injection. Facet injections are done with lidocaine, or Marcaine, which is to numb, but they put steroids in it. Do you understand? Steroids are immune modulators. This is her second round of steroids. She had an upper respiratory tract infection, then she had a facet problem. So now we have another immune-dysmodulatory event that is putting her in a situation where she could become compromised if there is an underlying metabolic issue.

So I know the whole time there’s a metabolic issue. I know there’s probably infectious diseases. And by the way, we know them. We mapped them out. We tested for them. Don’t worry about that right now. I want you to just observe: central or peripheral? Because this will be one of those cases that will drag you into the world of peripheral nervous system.

So, you’re no longer a functional anything. Now you’re a clinician. That’s pretty much the way it goes. This is where the dissonance stops. You can’t just say, “I’m going to make it all fit in my world, and it doesn’t belong in another world,” and I think you heard Dr. Kharrazian say that. You truly have to do what I call cross training. So we’re going to cross-train you. That’s what the whole program is.

This is where the emotions of the patient begin. This is where what you know matters. That’s why we’re teaching it to you in this fashion. And this is where you have to know what’s going on, because if you don’t, you’re not going to help this patient. You won’t get lucky. That’s the thing. If you don’t know, you won’t get lucky.

So we’re going to start to treat the whys, not the whats. No, medicine does very good at treating the whats. “I have depression, so I’m going to take an antidepressant.” But they don’t look at the fact that insulin problems are allowing serotonin to be changed, and as a results of serotonin levels going down because of the insulin issue, now you’re depressed. That’s a why. We’re going to take you back to the whys.

So just kind of watch her a little bit here. She’s at the clinic now. So she’s starting to learn – we’re just doing this to show you – look how unstable her core is. She’s falling everywhere. She can’t even go down on her


leg. Like she’s having a really tough time. I’m going to show you even more videos of her later on in the summary portion of our day.

We’re just showing you, she’s struggling. She doesn’t know where she’s at. She has to use the therapist there. That’s Caleb. She has to use him. It’s really not her best day. She’s having a really rough time.

Okay. You do not need this, but I’m going to show you what’s going on. She has vestibular dysfunction, visual dysfunction, and somatosensory dysfunction, creating her imbalance. Her center of pressure is way, way, way back, and overall she is completely unstable. Now just watch.

When you just have peripheral nerve disease, a lot of times you just lose the somatosensory column. That means this: You’re ataxic, or you can’t balance, right? Because you don’t have any input from your feet. We see it in diabetics all the time. Some people will have visual problems because they have optic neuritis, or neuromyelitis optica, or MS, and so they can’t see where they’re going, so they’re unstable. And then some people have vestibular problems, like a head injury, o now their vestibular system’s not integrating, so they don’t know where they’re at that well.

She has all of them. This is a cortical problem. Her somatosensory stuff is not integrating, and her vestibular stuff is not integrating, her visual stuff is not integrating. She has no idea where she’s at with any of the systems. So we have to rehab all of them.

Sometimes you will lose one of these, and you have to strengthen the others, if one is completely destroyed. And then sometimes if it’s not completely destroyed, you just activate that one and the patient gets stable.

Now this was done with an expensive machine. You don’t need it, but I’m just kind of showing you this as an example. And when we looked at this, I was like, “This is not a peripheral nerve lesion.” And then we went back and we started doing cortical testing, left versus right, and her left brain much weaker than her right brain.

Now I put in your little handouts my intake form for lobes of the brain, left versus right brain, and stuff like that. I gave it to you now so next module, when we get going, you’ll be able to sort of understand what it is, because in the cortex portion, we’re going to go through it pretty well.

So this is her pre. Now I’ve got post everything. That’s the cool part about our videos.

So, that test just said this: “Not only can you not walk, you’re not stable. And not only that…” Now, this is like you’re looking down at the top of the person’s head. So this is to her left, this is to her right. This entire part of her world doesn’t exist [gestures to right of diagram]. She almost has a hemineglect. But her language is intact.

Now let me tell you something. With left-brain lesions that are global, in a right-handed person the vast majority of them lose language. And I’m going to go through language later today. She has not lost language. So when you look at this, you have to say, “This is here because she doesn’t have good leg function.” It’s not because her brain is completely toasted.


So you look at this, and you’re like, “It’s still localized to here, it’s not spread to here.” Thank goodness. If it had spread to the frontal lobe, she’d be flat. Or impulsive. But she’s not, she’s extremely smart. If it had gone to the back, she would have all kinds of difficulties with, you know, probable language: interpretation, maybe forgetting words, maybe understanding faces and features and things like that. She would have changes.

So this is her pre limit of stability. This is her after one week of treatment. Now, this is not to be cool. Do you see everything’s green now, in the somatosensory, visual, and vestibular system? And do you see how her center of pressure at least came forward, and now she’s just going over to her dominant leg? That’s because we took one of her crutches away.

So when you look at this, you’re like, “Wow!” Her composite score still needs work, but every system is now starting to fire. We started to increase neurological function, because we said this: “Is this peripheral or central?” We decided it was central. “Can these neurons take therapy, or not take therapy?” We decided they could take therapy. And then we decided, “Hey, what’s the weakest group? Extensors or flexors?” The extensors were terrible. We did a four-to-one ratio of extensor therapy to flexor therapy, and we did a gait protocol on her. Which we’ll teach you all that later.

But the big thing I want you to get right now is this: We decided to treat her brain for a leg, versus give her a shot in the back for a problem that – I mean, facets don’t even really relate to every nerve in your leg, okay? So that’s pretty cool.

And now here’s her limits of stability. They still look terrible, but I want you to realize something. Right here there was nothing to the right. That thing you see squiggly over to the right was just a perturbation. Now she’s starting to at least aim for the front and back corner boxes. That means she can do this. She can now put a little bit of weight on her heel, which means she can now dorsiflex, and she can now start to go forward, and she can now plantar flex, to counteract those things.

The very first things we wanted to do on her was just say, “Can you dorsi- and plantar flex, so that you can actually maintain your balance around your ankle?” So we had an ankle strategy, and we moved up to a hip strategy to help give this stability in her brain know where it is. So I’m like, “Cool, we’re doing it.”

So this test is going to be able to demonstrate, “Hey look, we made a difference.”

So the big question number one is: central or peripheral?” And if it’s central, can you find the area? And if you can find the area, as we go through this, can you develop the art to stimulate that area to make it metabolically stable, to make it be able to get plasticity, and then to be able to collateralize so that she knows where that leg is and can move it. Is everybody following the basic gist of that?

That is a totally radically different way of thinking than mainstream medicine. And that’s okay. Because a lot of people haven’t been exposed to “What is a functional system? We thought the nervous system was hardwired.” Well, part of it is, but part of it changes. And a lot of people thought, “Well, okay, I’m a functional neurologist. I just do functional neurology. I don’t know what a nutrient would do to that.”


I’m going to show you another patient later on in the language section where I basically had to put a feeding tube in him just to get his brain to be able to be activated before I did any neurological care. He was only swallowing one out of every eight bites. Try that at lunch. Spit out seven, swallow one. For like three months. He was dying.

So when we do this, it’s finding the region, finding fatigability, can you access the ability to make it better, and then can you intertwine the different modalities that you know and that are going to learn to make a difference. That’s what we did with her.

We did do some stuff with her immune system. We did do some stuff with different portions of her metabolic function, which we’ll go over later. But all of this matters, because it’s going to change your rehab.

Here’s her visual system. I’ll just play this. Tell me just… it’s this simple. I’m not going to go deep into this. Can you see anything strange? She’s just tracking up and down. These are supposed to be smooth. How many of you notice the saccadic intrusions, or the lack of pursuit? It’s going tk tk tk tk tk tk tk. As your body becomes efficient in one plane, it will lose efficiency in another plane, and you’ll see it translate into the eyes.

Now, I’m going to be very careful how far I go into this, because this will short-circuit everybody’s brain. You can see posture and mechanics and movement in ocular efficiency. Do they have down-gaze efficiency? Do they have up-gaze efficiency? Can they not go up because they’re perceiving themselves in another plane? I have so many videos of this to show you, and what it means, and I have the patients’ video before and after. So just hang on.

But what I want you to know is, that wasn’t a smooth vertical pursuit. There was torsion in that. That was skipping all over the place. And that translates into this: her posture. Did you know that when one gets better, so does the other? You can’t walk if you can’t fixate very well and move your eyes well, and move your eyes and head together.

I’m just giving this as something to where it says, “Can you start to see this?” and then “Can you start to integrate it?” And by the way, who in the world would link a leg to an eye? Where’s that pathway? There’s a lot of neurons in between a leg and an eyeball. But she got a facet injection. Okay? So really, that’s the bizarreness of it. When you start, you know, pulling apart the case, and you start looking at it for what it is, you’re like, “Wow, there’s a metabolic thing! Wow, there’s an immunological thing! Wow, there’s a sequence of events! Man, that whole leg doesn’t work!”

This is not a neuromuscular junction disease. This is not a primary muscle disease. Her brain looks like it’s involved, but her nerves are intact. She has good muscle tone. She’s not spastic. Her eyes show that she has an equilibrium problem. You saw her center of pressure – it’s way back here. Eyes down here. She can’t look up efficiently. You’re like, “Man, as soon as I get her center of pressure of better, she’s going to be able to look up better, and be able to do things in that plane better.” It’s called performance enhancement.

So what I’m trying to show you right now is the fact that this nervous system links. And it is contiguous. And there is a guy named Cajal, way back in the early 1900s: he said this: The nervous system is contiguous


and changes. We didn’t invent this. It got invented over a century ago. Thank God it’s there. You’d never be able to learn how to be a professional bowler – because I know everybody wants to learn that.

Here’s another one. Just kind of take a look. Okay, first of all, it’s difficult sometimes to see pupillary sym-metry if there’s light seeping in. It has to be a perfect environment. But right now, do you just see a change in pupils? Let’s just say there is, that this is perfectly accurate. Yeah, you do see that. Now, this happens to be on her left side. Hm. We’ll teach you a little bit about what pupillary size and hemisphericity means later.

These are bump-bump – did you see it? Pretty good there. Dunt, dunt, dunt, in-gaze there. Dunt… Now, how many of you are seeing just the failures in smooth pursuit? Okay. That’s all I care about right now. Those are in the horizontal pontine centers. The vertical ones are in the mesencephalic centers. The mesencephalic centers deal with reflexogenic gait; the pontine centers deal with horizontal vestibular integration. All those pathways descend down to the ventral horn cell to give you stability.

Now, you can hit the replay button on that a lot. We’re going to teach you what all of that means: these reticular pathways, from the vestibular system, from the vestibular nuclei, from velocity storage, from superior integrators and inferior integrators, into dynamic vestibular posture, and what they mean.

This girl’s developing also a vestibular lesion, and the inability to have core stability, because your vestibular system gives you core stability. So she’s losing it. You can’t walk without it.

So as we get going, you get the fork in the road. Now what? Do I just treat an infection? Do I just do immunological therapy on her? Do I just refer her out? Do I just say, “You’re a lost cause”? I just said, “Hey, what do you want?” Her name’s Jody. I said, “Hey Jody, what do you want?” And Jody said, “I want to walk again.” I said, “Well, why?” She goes, “Because I want to go back to school.” I said, “Well, why?” She goes, “Because I want to graduate and have a life.” I said, “Perfect.”

She has no bowel or bladder problems. It’s not a cauda equina. She’s not spastic. She didn’t have a stroke. She had three different viruses, and had a bunch of immunomodulating drugs. And she switched from IGG to IGM, and she started replicating those things, and started having some significant problems. Just going to throw that out there as some background stuff. That had to be modulated a little bit.

So that fork in the road, we’ve got to down both ways. So there were some metabolic issues, and there were some things we knew existed, and we had to address those. And really, here’s what we had. There was some possible thyroid stuff. Her gut was killing her. She was acidic. Her immune system was destroyed. She was inflamed. And she had some blood sugar imbalance. And by the way, her red blood cells didn’t look all that great.

Now, do you think any of that could contribute to brain changes? Let’s say it had absolutely nothing to do with the event. Could it have something… could it have potentially something to do with your capacity to rehabilitate somebody? If somebody has anemia, good luck. If somebody has blood sugar dysregulation, have a good time. If somebody’s thyroid is completely – you know – dysfunctional, good luck with that metabolic fatigue.


What I’m telling you is, all those things deal with that one slide Dr. Kharrazian showed you which is this: Can you make energy? Do you have good ATP? And can you have good mitochondrial function? So that when you activate that brain it actually creates plasticity like that one slide showed you.

So now I’m looking at, I’m going, “Okay doc, you’re great at saying this is where it is, and I think I know what to do, but do you have the substrate to make it happen?” That’s why we’re here today. Do you have the substrate? Meaning this: is it so inflamed it doesn’t matter what we do? We’re not going to be able to make plasticity that’s greater than the inflammation that’s causing damage? Is the basal metabolic rate and the thyroid function capable of giving us enough energy and function to make this happen?

There are so many patients that come in with thyroid problems that have brain fog, or head pain, or neuro-logical symptoms. So let me just through this out, just as a suggestion. You might want to start learning to look at a few labs. Because we did do some internal statistics, and seventy-five percent of our neurological patients have something clinically relevant on them. That’s a pretty high percentage. That means that three out of four patients, if you don’t do some labs, you’re going to miss something clinically relevant. That’s called praying. Pray. Pray for me, while you pray for your patient.

I’m just saying, there’s some things that we want to look at. We know that she has gastric inflammation. She has immune insufficiency. Not so much fatty liver disease. A little bit of hypochlorhydria. These are all some things that we went through and addressed.

And when I say, “Name ten things that might impact the nervous system,” for you at home, I want you to start thinking about, “What are ten metabolic factors that might actually impact the nervous system?” Oxidative stress, inflammation, thyroid dysfunction, gut dysfunction… in other words, we’re going to cover all of them. We have to, because if we don’t, then you’re really not going to be able to be an efficient functional neurologist, and I think I’m just kind of beating a dead horse. You heard Dr. Kharrazian already talking about that.

This was before we even saw her. These are labs that she brought with us. One of the things that we noticed right here is that after her event, her CRP went up and her homocysteine was already high. So guys, listen: she had small vessel problems, nitric oxide problems. She was not getting oxygen to the areas she was supposed to get. Her MCV was going up, so she was getting macrocytic anemic, and she was getting inflamed because she had some viruses. Wham-o! She got a shot, boom! they go up, inflammation goes everywhere, brain changes, and leg is gone. Just like that. Boom.

That is the difference in a total health care paradigm. You understand? That is a different healthcare paradigm. That’s why this is exciting. Every day that I do this, I get to unravel a mystery – a true mystery. Not just say, “Hey, let’s do a facet injection,” which, by the way, I’ve got patients that do great with facet injections. There’s nothing wrong with that, if it’s a facet problem. But if you’re the guy that does facet injections, I guess everybody has a facet problem.

Here she is, after her first three days of treatment. We decided to make her walk backwards first, what the hell.

She couldn’t even walk forward.


Okay, relax. And, go.

Here she is later on in the week. Now, notice she has one crutch, not two. So first of all, which one looks a little bit better in public eye? I mean, there is vanity involved in everything, correct? One crutch that’s smooth is a lot better than two crutches and dragging it around. It’s called getting from one place to another without really breaking apart.

Now relax.

Now watch this.

Okay. Day one.

Okay, central nervous system, not peripheral.

Okay, stay there.

Leave her facets alone, please. Now to be honest with you, if you load the facets differently, she had back pain. She had back pain. That’s why she had a facet injection. But she also has biomechanical aberrancy. The biomechanics on this kind of case can break down to the point where the knee degenerates, the ankle degenerates, the other leg degenerates. Because it’s not normal biomechanics.

Here she is again a little bit later, and I just love it.

Turn around.

Now watch her turn around. Two-step turnaround.

Go.

She even saw the person in there in her field of vision and didn’t run her over.

“Sorry.”

I’m going to show you some videos of her later on walking without a crutch.

So let’s go back to the patient again, as we wind down. We’ve got about fifteen minutes before our break, so hang in there. Put yourself in her shoes. “I can’t walk anymore. I can’t get up and make a sandwich. I can’t get up and go to the bathroom.” You know, life starts to change. Now you have to be dependent on people, and just hope to God they help you out, or hire people. Maybe you don’t have the money. The amount of expenditure that goes into this skyrockets. When you lose the ability to ambulate or you can only use one side, it will develop brain hemisphericity and dominance. Her left leg works. She’ll get a very, very massive right brain, it will inhibit her left brain, and it will change her IQ, it will change certain types of perception, and it can even change language and her affect.


I don’t want that. I want this side to move so the hemispheres stay stable. I want her blood sugar to be normal so she gets fuel. I want her thyroid to be perfect. I want her to have good TSH, good T4, good T4-to-T3 conversion, all the receptor sites are not saturated and they’re working good, I want all that to be perfect. All these viruses and everything, I want her immune system to be high enough so where she can actually keep the viral load down so inflammation doesn’t go crazy within her brain, cause glial cells to get primed, and that starts to destroy, globally, the entire brain. I don’t want that to happen. I’m going to show you that in just a second.

So, has it improved? She improved. And I’ll tell you why she improved. Because we found the area, we found what worked, we determined if there was a metabolic factor, we determined her fatigability, we gave her… I’ve got videos of her later on where she couldn’t move her toes and now she can lift her toes and do this. Huge! Now she could just do this, now she can do the whole anterior tibialis, and now she can stand on a box and squat all the way down and stand all the way up, and squat all the way down and stand all the way up.

So we got her hip mechanics better, her ankle mechanics better, her toe mechanics better so she can grip into the ground, and now her knee is not completely unstable. She’ll blow out her medial compartment, and she’ll start to get bucket-handle tears in her menisci. That’s not cool. So we know it’s not polyneuropathy; it would have affected the other leg. We know it’s not primary muscle disease; it would have been proximal. We know it’s not neuromuscular junction; it would have been global. Are you starting to see the differential game? Is it important to know if this is central or peripheral? Is it important to know where the problem is? I think so.

So when we do this kind of stuff, do you think she had this? This is at rest. That is not a motor unit. That is called active denervation. It happens from peripheral nerve damage. Now, when I did the EMG on her, she did not have that. Does that make me happy or sad? Well, it makes me happy unless they’ve had a catastrophic stroke and they’re in a coma. Then I might be like, “Wow, I wish just had one nerve denervat-ing.” She was totally conscious. She had good muscle tone in her leg. And I didn’t see denervation. I started saying, “Yes! This is brain! And bam! the brain is not too damaged! And when I start activating it, it makes changes.” So I could see that this was a perfect functional neurology patient.

Okay. Here’s another patient. Now, this is them when they contract their muscles. It should be just a single bi- or triphasic wave form. Is that bi- or triphasic? Let me show you what happened. This person denervated out of one neighborhood of muscle fibers, and then because this nerve was damaged, this nerve said, “I’ll take over for you. I’ll just grow into that neighborhood.” So it pulled two neighborhoods together, and now you hear it like this: dub dub dub dub dub dub dub dub dub dub, and it’s in a polyphasic motor unit.

So if I look at her and I say, “Hey, you’ve got polyphasic motor units. You were denervating, now you’ve reinnervated. But when you reinnervate that way, now the muscles don’t move as separately, so you have to rehab their coordination.

I’m just showing you a few things that we’re going to be jumping through as we go through this.

“Hi, my name’s Jody. I’m twenty-five, and I’m from England.“

I don’t know – do we have…


“Three-and-a-half years ago I had a chest infection which left me with severe back pain, a loss of sensation and movement in my right leg.”

Okay, so she had upper respiratory tract infection which left her leg screwed up.

“At the time I lost sensation in my leg I was hospitalized for eight days.”

So she lost sensation first. Anterior brain or posterior brain? More posterior. So it started out in the parietal sulcus. I’ll show you later on when we do lobes. It started back here, and all the sensory stuff projects to the motor stuff. So you can’t have any motor function without sensory input. So some of the ascending sensory pathways got damaged, which changed her motor output.

“Here I had a series of tests carried out which showed nothing. I was then discharged with a diagnosis of stress.”

She was diagnosed with stress. Now hey, could stress screw things up? It could make the hippocampus get screwed up, it can make the immune system get screwed up, it usually just means we don’t know what the heck this is.

“Three months later I was still having severe back pain…”

A few months later she was still having a lot of back pain.

“… I was only able to walk with the assistance of two crutches.”

Couldn’t walk; had to have two crutches.

“Due to my back pain, I had a lumbar facet injection…”

Okay, let me give you the – “lumbar facet” – it’s a lumbar facet injection. Okay? Which, again, she had an upper respiratory tract infection, and now she’s getting medications that do not modulate the immune system. It has the potential to modulate it; it also has the potential to make it go the other way that you don’t want it to go. These are corticosteroids. We can name them all off. I’m going to try to not name drugs on here, but I can just tell you: in the corticosteroid category, they do massive things to the immune system. That’s why they’re anti-inflammatories. Inflammation is an immune response. Okay?

You would think that would be great in a person that might have something like this. But it didn’t, because her underlying problem was not that. Whooh! Wow. Now listen: I’m going to make you think about medications whether you prescribe them or not. It doesn’t matter to me. I’m not going to teach you to be a prescriber; I’m going to teach you to think about this: When that person takes that SSRI, and now all of a sudden all their dopamine pathways are different, how did that affect them?

You are going to learn that, but you’re not going to learn how to write out “such-and-such medication, take it this many times, number thirty, blah blah blah.” I don’t care if you can do that. But what I want you to be able to do, because everybody walks in with a giant list of medications, and you’re like, “You have four medications that all deal with dopamine. No wonder why you’re hyperkinetic.”


That matters.

Or, “You don’t have any vestibular function, and you’re on three narcotics. It turns your velocity storage mechanism off. No wonder why you fall.” Everybody got it? Okay.

So let’s go a little bit further.

[unintelligible]

Volume? Okay. We’re not going to start over. But it’s just her telling her story that I’ve already told you. And that is: upper respiratory tract infection, got that problem, got a facet injection, got worse, told she had stress, went to a bunch of doctors, nobody helped her. She showed up at our clinic, and we said this: “Your problem is here, and here’s the things that are surrounding it.” Her thyroid was optimized, her blood sugar was optimized, her immune system was optimized, while we were activating and controlling her brain, and activating just that one region that needed to be stabilized, and now we have a patient back, to the point where she wanted to fly down and say, “Thanks.”

Now, just real quick before our break: You guys have seen this chart. And we know this: that when you change nerves, your brain changes. So there’s some literature here that I’ve put in here just to show you that plasticity does exist from activation.

I just want to tell you this one story real quick. This is the story of good things, like you can’t… how you’ve got to have stimulation, you’ve got to… you know, you can’t have oxidative stress, you can’t have lack of activity. Just real quick, let me tell you what happens in the process of immunoexcitotoxicity. Let’s do it quickly.

I’m a cell, and I’ve got receptors on me, okay? And on me is these things called NMDA receptors: N-methyl-D-aspartate receptors. And so whenever there’s a stimulation from a receptor, that information comes in, and it activates an ampa receptor which is surrounding… so I’ve got like a posse around me, okay? And they’re all called ampa receptors. They carry the action potential to the next cell and to the next cell. But at the same time, the ampa receptors activate the NMDA receptor, and then it fires a gene response which makes protein replicate, which makes more receptors and more connectivity and more synaptic plasticity. Does everybody see how important that is? That’s why you heard Dr. Kharrazian say that when we don’t move, we don’t get the plasticity. Nutrition can’t always do it.

Now they’ve tried to show that some drugs create synaptic connectivity, but here’s what they found: They don’t create long-term potentiation. That means that when you take the drug away, it goes right back, unless you exercise on top of it. Then it stays. Some cool studies on SSRIs and frontal lobe function, where, when you gave the SSRI, the plasticity developed, and then when you exercised and got off the medication it stayed. If you didn’t, it kind of digressed.

Movement and activation is what activates those NMDA receptors to make a gene response to make me, as a cell, talk to you, as a cell. It’s cool. However, when you get inflamed, those NMDA receptors can get ticked off. They’re covered by a magnesium plug, and calcium’s out there floating around. And when calcium comes in, it activates the gene response. It makes the mitochondria happy, it does an uncouple, cytochrome C doesn’t spill out, and everything’s good. You don’t get superoxide anions and oxidative stress.


If you get inflamed, you get excessive calcium influx, and everything goes backwards. Now you don’t make protein. Now the mitochondria dies. And now what happens is, the ATP pumps that push sodium out and potassium back in after there’s been a discharge – it doesn’t happen. So the sodium builds up within the cell, so the threshold goes tk tk tk tk and it creeps closer and closer and closer to threshold. Just like on that far right portion.

So with a low component of energy, here’s what happens. The resting membrane potential goes closer to threshold, and now you’re more prone for seizure. Now you’re more prone for chronic discharge of a cell group, like pain. Or migraine.

And by the way, they fatigue easier. In the olden days, we called this transneural degeneration. A lot of you guys are from the TND era. This is TND. Oh by the way, why don’t you heap some artificial sweeteners on top of that? They hook right on those NMDA receptors. Or put a little MSG on that. This is the basis of all of our neurodegenerative patients. They’ve got glial activation. They’re inflamed. All those inflamma-tory cytokines destroy cells and sensitive these receptors. And then the foods you eat upregulate these excitotoxins, and they attach on there. So these cells fire, they don’t have the capacity to deal with it, and so they start to metabolically fail. And we have a whole section on neurodegeneration, and I will teach you how to go through all the dementias, all the different neurodegenerative illnesses, and the mechanisms to help prevent them.

Right now, clinically, our average Alzheimer’s score is a fifteen on an MMSE, and it scores from zero to thirty. The average amount of improvement is to a twenty-five. If we don’t give them nutrition, and we don’t give them exercises, and they don’t come in periodically, it goes back down to a fifteen. Now we have a group of people, after six months they’re still at twenty-five. It’s an integrated approach. We can’t let these cells die; we have to stop excitotoxicity.

So what’s good for the goose is bad for the gander. In other words, the thing that creates plasticity, the activation, if you get Alzheimer’s stage six, and you start activating those cells, they just die faster, okay?

So, when you look at this, this is an animated slide. So glutamate can create excitotoxicity. When one cell busts, all the glutamate spills out, then it activates the surrounding cells. That’s why the seizure gets more efficient and grows. Dr. Kharrazian will talk about that later.

We can have resting membrane potential that goes up. So now the cell fires easier. You can have free radical damage, which can cause DNA damaging, which can cause duplications and deletions, and now when you replicate those, you have an epigenetic response where now you’re no longer the same human.

Man, you can decrease energy and mitochondrial failure, inflammation can create microglial activation – that’s these… we’ll talk about all the different glial cells and what they do, but if they’re too activated and turned on, they can make the cell kind of start to die off a little bit, and damage a bunch of surrounding other things.

Listen: whenever you lose ATP production, and you have ADP and P, the P will go and phosphorylate the bilipid membranes, and it breaks. And it will go right up to the NMDA receptor and open it up, and calcium goes bbbbbb, and goes flooding in. There’s a great paper – I didn’t include it – it’s the calcium buffering


system intracellularly, and it describes all these mechanisms beautifully, so it’s not me that’s coming up with this.

By the way, guys, we’ve got a break in two minutes.

Well, the cell can blow up and die. That can damage the surrounding tissue, cause secondary plastic changes in the cells around it. You can have seizure disorder, metabolic failure. Like when you – go back to our original slide. Do they have failure with repetitive activity? If you do one activity, is it very brisk and does it fire very quickly and then go down? Like with the pupils? Is it so damaged that it doesn’t fire at all?

What I eventually want you to learn how to do is say, “Okay, this is where the lesion’s at,” and now be able to go, “and I envision what a cell looks like and what’s going on metabolically within the cells in that region,” and that will help you with your metabolic journey.

So you have two visualizations: where is it, and then what are the cells doing in that area? And if the cells are not capable of tolerating stimulation, fix them. If you can’t fix them, be honest with the patient. And when you go through and you look at this slide and you rehearse it, if this goes on, you lose cortical volume and integrity, and you end up being a research project in an NFL study called chronic traumatic encephalopathy. I’ve had so many head injuries, so much glial priming, so much inflammation, so much cell destruction, so much volume loss, that I now have neurodegenerative disease.

So, one minute to summarize this morning.

You need to think about where things are occurring. And you’re going to go through a journey of learning how to do that. You do not know how to do it yet, so relax. You have to realize that more that one area can be involved. That can be a metabolic thing, or a degenerative thing, or an infectious disease thing, or a systemic illness thing. You need to learn that maybe the central nervous system and maybe the peripheral nervous system might be involved, so how do you jump in from one to the other?

And when we start looking at this, and we say, “Man, is there a metabolic factor?” when does the metabolic factors need to be initiated or integrated? And then once you start to learn to do all these things, and you just see the big picture – because right now we’re just trying to describe the paradigm to you – but when you get the paradigm and then you start to learn all the little things, and you start to develop the art of putting it all together, you will make really difficult patients very, very happy.

And with that, we now have a break, right at time.

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FUNCTIONAL NEUROLOGY ANATOMY AND CENTRAL … · And I’ll be honest with you: that’s the area...

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