identifying the most common neurodegenerative diseases and ... · so, we always start with the...

MODULE tHREE tRANSCRIPt: FN CONCEPtS AND REVIEW | COPyRIgHt © 2016 FUNCtIONAL NEUROLOgy SEMINARS LP | PAgE 1

IdentIfyIng the Most CoMMon neurodegeneratIve dIseases and ClInICal applICatIons (Module three)

transcript – functional neurology Concepts and review

presentation by drs. datis Kharrazian and Brandon Brock

dr. Kharrazian

Okay, everyone. Thank you for coming to Module Three. We have a lot of information to go through. This is really one of those modules where we really integrate nutrition, pharmacology, examination, brain rehab all together. And the reality of things: many people have nerve degenerative issues, and I think the question that usually doesn’t get asked in the field of brain rehab is: Why does someone have signs of early degeneration? So what we want to do is, when you see someone that has any type of memory deficit, or signs of dementia, early signs of Parkinsonism, the question is: What’s the mechanism, and then how do you get there, and what are the clinical things you can do to improve their brain function right away, and what are the things you can do to prevent it and slow down the progression of it.

So, you know, last night we did a workshop. Even with a healthy population, we could see neurodegenera-tion signs all throughout the room. So as people start to hit their thirties and forties, that’ll mean you’re going to see signs of neurodegeneration in different regions of the brain. Now, we’re going to distinguish whether what’s disease and what’s not disease, and what are the applications you would do. And for the most part, what we decided to do when we organized this neurodegeneration course is to really go into the most common things you’re going to see. So, the most common things you’re going to see is Parkinsonisms and its variants, and dementias and its variants, and cerebellar degeneration. Some of the rare forms of genetic degenerative diseases, like Huntington’s and things like that, it’s not so critical that we really go over. I can tell you, I’ve never see a Huntington’s patient come into my office. It’s just not something that you see routinely. But you will definitely see Parkinson’s and dementia and cerebellar things in your office. So, with limitations of time, we’re going to focus our material into what you’ll see ninety-eight percent, ninety-nine percent of the time related to neurodegenerative diseases, okay?

Now, outside of neurodegenerative diseases, there’s neurodegeneration that takes place. So some people actually have neurodegeneration in certain regions of their brain. Maybe they damaged their brain when they were young, and then those things have caught up with them. Maybe they didn’t develop plasticity in some areas of their brain, and as they get inflammation throughout their lives, certain areas of the brain


are starting to degenerate. They don’t necessarily have a neurodegenerative disease, but they have areas of neurodegeneration in certain regions of their brain, right? So there’s that distinction that you really want to make. You really want to be careful not to freak people out and tell them they have dementia when you don’t have all the facts. You really don’t want to freak out and tell people they have Parkinson’s or if you don’t have the facts. You should know what they are; you should know what signs to look for. So we’re going to go through all that with you this weekend.

Now, as we go through the course material, we have some fundamental concepts. The biggest thing for us as educators is not to give you information, but it’s to do a clinical thought process. How do you think through a case? And this is where I think most people will have difficulty with when they’re new to the field of functional neurology.

So, we always start with the patient’s chief complaint. Now, one of the things that we’ve done to help everyone with just narrowing this down is, use the brain region localization form. Right? Now, the brain region localization form is going to help you, but then it may not correlate with the chief complaint. They come in to your office…

My microphone’s going in… over here… might manage…

We need to, you know, look at the patient’s chief complaint, and then see if they have things like depression as their chief complaint. If they have depression, you can have any area of their brain involved. You can have someone that comes in, has an anxiety disorder, but when you actually work them up, they have a vestibular imbalance firing into their autonomic centers. You can have someone coming in and their chief complaint is chronic constipation, and they have early Parkinsonisms. Right? So what’s important to do is, the patients that come in are never really going to tell you that their chief complaint is a specific region of the brain, but what you’ll start to see is, chief complaints, as you do your workup neurologically, many times have a neurogenic or neurological component to them. Most common things like fatigue… A lot of fatigues are actually brain-based. And one of the ways you tell if it’s brain based is, they… When they use their brain, that’s when they get tired. On days they’re off and resting, they’re okay. So you see lots of early neurodegeneration literally being brain fatigue.

So, one of the most common complaints that people go to health care practitioners for is fatigue, pain, fatiguing… Three most common: fatigue, pain, and depression. So fatigue, pain, and depression are all early symptoms of neurodegeneration too. So when someone comes into your office and says they’re tired all the time, you have to look, you know, think about this and go, “Is this a brain component to this?” And again, the biggest clue is that when they use their brain, that’s when they really fatigue. So the days they’re at work, the days they’re driving, that’s when they’re really exhausted.

So, I recently had a patient, and she had chronic fatigue, and then I talked to her, and she goes, “Well, the days I really have chronic fatigue is when I’m at…” – she has two homes – “…when I’m at my home by the beach.” And they live by the beach and they have a three-story unit, because, you know, things by the beach are close together, you don’t expand out, you go vertical. But she goes up and down all day; she gets tired. But if she’s… She’s working out and doing exercise at home, at her home in Arizona where there’s only one story, she doesn’t have any problems. So when you see someone in their environment, you go, maybe there’s something in their house, maybe it’s chemicals, maybe it’s toxic mold; maybe it’s all these things,


but it wasn’t; it was just going up and down the stairs. So what she had, she had vestibular and cerebellar degeneration, and early stages of it, and she walks in with an essential tremor handing out form… handing me the forms, and it was like, “Okay, this is pretty clear.”

So when you look at the neurodegenerative model, people are not going to come in to your office ever telling you that they have symptoms of neurodegenerative disease. As a matter of fact, if they come in to your office telling you they need help for Parkinson’s or dementia, let me be honest with you: It’s almost too late to have interventions we do really make that much of a difference. So if you’re waiting for that diagnosis to be told to you in a chief complaint, you’ve pretty much missed your window. Because by the time the conventional health care model finds that diagnosis, it’s already too late. Okay? So you have to be able to catch [break in recording].

The other thing you really want to think about is their depression. Another chief complain people have as their brain starts to degenerate is, they start to get depression. Because as areas of the brain lose activity to areas of the frontal cortex, to the limbic system, many people then complain about depression. So you go through your workup and data.

Chronic pain is also another one. You guys remember the pathways we talked about? Pain, as the pain pathways, as you look at pain inhibition in pathways, a healthy cortex fires to the periaqueductal gray, to these descending inhibition pathways. So when people get neurodegeneration, they get chronic pain syndromes. So when you have someone come in to your office and their chief complaints are their fatigue, they’re depressed, and then they can’t handle stimuli, and then they start telling you that everything’s bothering them, and they can’t even drive any more, you’re pretty much looking at a patient that has neurodegeneration. Okay?

Now, whether that neurodegeneration is a neurodegenerative disease, or it’s just brain general degenera-tion that’s happening, it what you have to determine. So there’s a difference between mechanisms of, let’s say, Parkinson’s, and someone who’s got global degeneration of their brain, or someone who’s got dementia. This is protein misfolding, and progressive things that are predictable.

So, when you look at this model, you look at the patient’s chief complaints, the key thing is, you’re not going to have patients come in with early neurodegeneration, tell you they have a neurodegeneration disease. You know, Parkinson’s patients come in, they’re going to have gut motility issues and chronic gut issues and constipation; you’re going to have Parkinson’s patients come in and have stiff shoulders; you’re going to have people come in with vestibular diseases and cerebellar diseases telling you they have spinal instability, and their back hurts, and they can’t stand for long periods of time; you’re going to have people with cerebellar disease tell you they have vertigo; you’re going to have people with dementia tell you they have depression and they can’t remember things and focus. That’s how it’s going to come into your office. Okay?

So you really want to have that radar for looking at those symptoms. If you catch them in those early stages, they actually could have a chance to really have some nice outcomes in their case. When you have someone comes in, and says, “Hey, my mom has dementia, what can you do?” you should probably be thinking, “Well, if it’s at the point where everyone knows, they’re probably very progressed.” So the prognosis is not as good. Right? Or, “My husband has Parkinson’s for five years.” That’s a whole different scenario. Those


are much, much more difficult to do much for, versus you found them in their early stages of stiffness and then you find out they have Parkinsonian pattern, you can do much more impactful things with them. Okay?

So we start with the history. Patient’s chief complaints, we localize the region – you can use your brain region localization form to then help you localize the region – and then you look at their posture, head position, joint angulations, the initial survey. So what we did in Module Two is, we really wanted to go over the initial survey. So they come in: Are they slow? Do they forget things? How’s their personality? So if you can joke around with them, and they’re funny, and you guys have interactions, that tells you the frontal lobe is really healthy. If they’re kind of dull and don’t really understand what you’re saying, and aren’t really social with you, and interacting with you, you know that their frontal lobe could be compromised, right? If they come in and they’re moving very slow, you may consider a Parkinsonian pattern. They have a wide-stance gait, you know that they may have a cerebellar issue, right? So you just take a look and generally see what’s going on.

So the minute you see someone, you look at their face. Do they have a facial symmetry? Do they have ptosis? Do they have a dilated pupil? Do they have head angulation? Right? How’s their hair? How’s their skin? Are they wearing things that are inappropriate for a degree of temperature change in your office? Are they all bundled up? Right? Or is it freezing and raining outside and they’re wearing shorts and t-shirt and they’re sweating in your office? Those things really make a difference.

How’s their gait? Do they have arm swing? What’s their balance as they walk? What’s their head position when they walk? Do they look at the ground when they walk? Those are all clues to you of what’s going with them.

How’s their speech? Can they find words? Do you notice that their speech becomes compromised as their brain gets tired? Right? Those are all the things that you want to think about in your initial survey.

So, you know, we know that the minute you just talk to someone and see someone walk a little bit, you have a pretty good idea of what’s going on with the status of their brain, before you get to the examination.

So then we get to localizing the region, and then at that point we start to think about which exercises to do. We’re going to get into rehabilitation in this session, for each region of the brain, and some things you can do for each region, so that should really help make that make more sense. And then we’re going to consider the neurochemical component.

All neurodegenerative diseases have a neurometabolic chemical component. Actually all brain-related disorders do. But all neurometabolic, you know, all neurodegenerative diseases have a neurometabolic chemical component to it. And we’ll go over some of the key ones and the mechanisms that take place with protein misfolding and protein aggregation disorders, and apophagy, and all those things that are important to us.

Now, once we’ve gone through and we’ve localized the region, the next question we ask – and this is really, really critical when it comes to neurodegeneration – how aggressively do you do brain rehabilitation? Because people that have neurodegeneration, you can actually make them much worse if you give them exercises beyond their brain’s capacity. So one of the things that’s really critical is, once we identify the region – and usually you can identify the region from your brain region localization forms, from your initial


survey of what’s going on, you have a pretty good idea, then you do a few tests in your office, you get an idea what findings they have – then we do repeat testing to see, do they get worse? Does their movements break down, and when they’re doing rapid alternating or repeated movements, do they crash? Do they start to get dizziness when they’re standing in Romberg’s position? How long can they stand there before they break down? Does their ataxia get worse as they keep repeating it? And if it gets worse, you know that they’re falling apart.

So, we’re going to go through case examples, and really go through this flow chart with you, because the most important thing for us right now is this: You guys know this clinical decision-making thought process flow chart, and you know this. If you know these two charts, and then you have your brain region localization form, and you know all those symptoms, then you should know all those symptoms, so if you don’t have one, you can still identify areas of the brain with your history, and then if you look at the brain compilation forms we have for you, and you have those forms together, you’re know really having the foundational skills you need to identify and do applications for brain-related disorders. Okay?

So what I want to do is, I want to go over some cases. And the key thing with these cases is just to kind of build up upon skills for the initial survey, and just to have you be clinical with what you see.

So, what’s your initial survey of this gentleman right here? First of all, is he young or old? He’s old. So if he’s old, he’s older, then you suspect there’s a possibility they may have neurodegenerative disease, just by the fact that they’re older. Because one thing is sure: as we age, we all have loss of neurons to some degree, and any time someone comes in to your office and they’re elderly, you always have to diff-di and kind of figure out what’s their state of degeneration, and where are they, just by age alone; by nothing other than age, okay?

Now, when you look at him, do you see a difference in their facial tone? Okay? So, does one side… You see a facial paresis on one side. Does one side have a weakness compared to the other side? Is one side drooping more than the other side? So take a look at this side, and then compare it to that side. Okay? And take a look here, at the mouth. And sometimes when you see the asymmetry, it’s really hard to know which side is involved, so the easiest way to do it is, ask the question, “Which side looks like the patient’s older?” Right? That they’re aging more. Compare that side to that side. Okay? Let’s do that again. Okay? That side? Right side? His right side compared to his left side. So when you do it that way, it becomes much easier to see it, right? So with his right side, he looks pretty… He looks much more vibrant and awake than this side. He looks really more tired and fatigued and so forth. Do you guys see the difference with that? That side compared to that side? Okay. So this is more of a left facial paresis, and then obviously we have to look at his eyelids, and his eyes, and see if it’s the top of the face or the lower part of the face.

So, one of the things you really want to do when you look at neurodegeneration right away is, do that initial survey. When you do that initial survey, you want to be in there… to go in there, and really look at their facial features. Now, when you look at the facial features, many times you’ll see their facial paresis show up with you.

Now, when you look at facial paresis, here’s the key thing: The facial muscles have bilateral innervation in the top part of the forehead and their eyes, for closing their eyes, but the lower part of their face is contralateral innervation. Okay? So here’s an illustration here. So when you look at the purple – this is the top region,


upper region, of the facial muscles – you have bilateral innervation to both of this; when you look at the facial nuclei, there’s a dorsal and ventral portion of the nuclei. The dorsal portion has bilateral innervation to the nuclei, to the top part of the face, and the ability to close the eyes. This is really important, because if you can’t close your eyelids, what happens to your eye? You can dry your eye, you can actually lose your eye, because of not having the ability to close and to keep it moist and fluid. So this is really critical that we have this, So we have a bilateral innervation to the upper part of the face, so it doesn’t really tell you much, and if you see that involved with lower face, then you know that you have a facial nerve. But when you look at the lower two-thirds of the face, or lower one-third of the face, you can see this projection that’s in blue; it goes from the contralateral cortex to the nuclei, and then to one side.

So a facial paresis can tell you a lot, if you look at the lower parts of it, about what’s going on with someone’s brain and their degree of brain health, with the degree of motor-associated neurodegeneration. Does that make sense to everybody? Okay. So if you see a facial paresis on the right side, which motor cortex would you think would be involved? The contralateral one, right?

So here’s also an illustration you can see of this, and let me go back to this. The only time you would have, like… If something injures the facial nerve, like an infection, or a Bell’s palsy, you would have the entire upper and lower parts of the face involved. When you’re looking at neurodegenerative changes associated with the motor cortex, you’re going to see just the lower division that’s involved, right? Okay. So, here’s an illustration here. So, here’s one where you see the drooping of the face, but their eyelid and forehead are okay. That’s a central one. And this this is a peripheral one. I mean, you guys all see people with asymmetries of their face all the time. So right away, when you do an initial survey, that should give you some clues of which areas of the brain may have some early signs of impairment, versus others. Right? I mean, facial symmetry is one of the easiest things to see the minute you talk to anyone or start speaking to someone.

So, you can see that this person has a little bit of facial asymmetry. Right? And we know that the facial asymmetry is in such a way where his left side has more of a sagging effect than his right side, so which part of his brain do you think could be potentially showing signs of early neurodegeneration more? His left or his right? His right. Because you’re seeing that left-sided facial paresis. Okay?

Now, I want you to take a look here, and… okay… See the videos here. Not getting the videos to play, Brandon. Can you help me? Can you guys see that? Okay.

…using his left hand. Later in the tape you’ll see it’s actually his right leg and his right hand, not…

So he’s got a left facial paresis. You guys all see that? Okay. Now, let’s say he has Parkinsonian types of history. Which side would of his hand would you see involved first? Left or right? It’s his right brain that’s involved, because you’re seeing the left side… you’d expect his left hand to be involved, right? So before we even look at his hands, we know from his face that you’re probably looking at a right-sided brain issue. Degenerative change. And then you can see, if we go back to his hand here, you can see some of those changes there.

…using his left hand. Later in the tape you’ll see it’s actually his right leg and his right hand, not so his chin. It persists through most different positions of rest. This is a fascicle resting tremor of a patient with Parkinson’s


disease in the fairly early stages. His movements on the right side are quite brisk. When he tries the same on the left side, he finds it much more difficult in the hand movement.

Okay, now you guys have to understand that Parkinsonism is a global brain systemic neurodegenerative change, but it’s going to show up on one side first, right? So it’s not to say that it’s just a hemispheristic issue, but his entire brain’s involved, but usually you’ll see signs in one side first, in the early stages. So if you see a facial paresis, and someone starts to have a little bit of resting tremor and stiffness on one side, you would start to think, “Hey, what’s going on with their basal ganglia indirect pathway? Am I seeing all these signs of neurodegeneration?” Tremor is actually one of the late stages of Parkinsonism. Right? So if you see tremor, you already know they’re pretty progressed.

Now, what would you expect to see with his gait? Well, he might have… it depends how progressed he is. He might have a shuffling gait. What would you expect to see with his arm swing? It would be less. And which side would probably be less? Probably his left. And then you might see shuffling gait, you might see some festination, so let’s just see how his gait looks here.

Yeah. When he’s walking, his left hand is not swinging, but you see it is shaking. And even though we talk of patients having a resting tremor, this does very often persist into walking.

You guys see that all the time, right? Airports, everywhere.

He’s turning without difficulty, and his walking is otherwise normal.

So the key thing is, if you guys saw a person with arm swing like that, that’s just… it’s rigid. Now, with people that have more of a cortical issue, you might see a little angulation there, but it’s just rigid and to the side like that, you see a facial paresis. You should already be clinically, in your initial survey, going, “Hey, what’s going on with the brain? There’s something happening with that whole motor integration area.” Right now, if you saw there was stiffness, and you guys saw a tremor, then you would know this is the basal ganglia, and you would question, do they really have an early neurodegenerative disease? Do they have some type of Parkinsonism? And we use the word Parkinsonisms because when the basal ganglia direct pathway’s involved, it could be a whole list of other degenerative diseases. One’s Parkinson’s disease, one’s the supra-nuclear palsy, one’s multiple system atrophy, another one’s cortical basal degeneration. Dr. Brock is going to go through and break those down for you. But the key thing is to first look at that and go, “Hey, there’s something that’s degenerative with my initial survey.” Right? So we’re just trying to merge the initial survey with you into neurodegeneration this morning, to make you have the clinical eye to look for these things.

So, you know that when you see these types of patterns that the basal direct pathway’s involved. If you can go through and review your basic ganglia notes, cortex fires to the striatum, the striatum has inhibition to inhibition to get this inhibition, which then causes motor… which causes this amplitude to the ventral anterior ventrolateral nuclei of the thalamus, and you get that movement that takes place, okay?

Now, could this person that you just saw with the facial paresis come in, and lack of arm swing, and their chief complaint to you is that they have a frozen shoulder? Now, let’s say they don’t have tremor yet? They come in to you and say, “I just have a frozen shoulder. I’ve been doing therapy for it. I get muscle treatments. It helps.” If they get muscle treatments and stretching, they’re doing what? They’re getting muscle spindle


Golgi tendon stretches. What part of their brain are they going to fire into? Their ipsilateral cerebellum, their contralateral cortex, which is therapeutic, and gets blood flow to those areas, so now they may notice, “Hey, it feels better.” But it doesn’t last. Right? So they’re the person who’s constantly getting treated for something that… It seems effective, but it’s not really treating the underlying condition of it.

Could he come in with a tight psoas problem, and just say, “I just have a tight psoas, and that’s the only thing that’s going on”? Absolutely. Can he just come in with no motivation, no drive, depression, and his wife forced him in there and you actually see facial paresis and lack of arm swing, and you’re actually dealing with maybe a probably early neurodegenerative disease? Right? So that’s what you want to be able to clinically do as you look at your initial surveys, is to pick up on these things really quickly, which I think everyone’s getting really good at.

So with this patient that you just saw – and let’s assume just for the sake of being a better diagnostician that the person doesn’t have a tremor yet, so you just saw lack of arm swing, you saw the facial paresis, and what other examination findings would you expect to see? So let’s say you stretched his arm. So what would you expect to see with stretching his arms? Just passively, you’d probably expect to feel rigidity, right? The kind of person you go, “Hey, relax, relax!” “I am relaxed!” And it’s still really tight. You go, “No, no, no, relax. Let go.” And like, “It is.” This side’s maybe smoother than this side, right? And so you would expect to see maybe that. You might see change in his voice. He might have hypophonia, not be able to project as well. He may not swallow as well, so he’s always complaining of having excess saliva, because you start to lose your ability to swallow as well as you get older, right? And you start to have these. Many Parkinson’s patients have chronic pain syndromes, because they start to impact their pain regulation pathways, so they may have chronic pain disorders and chronic frozen shoulder, or a chronic injury that keeps… Now it’s worse and worse, so they’re seeking help for pain.

And then the question to ask is, let’s say it’s Parkinsonism, what’s causing it? If it actually is Parkinsonism, what’s going on? Please don’t be this person. You guys know what this person is? Please don’t be this person. “It’s heavy metals!” “It’s mercury!” Don’t be that person. “It’s methylation!” “It’s a COMT!” Don’t be… Don’t do that. Okay? Do not go to the treatment mechanism unless you know the cellular mechanism first. So what’s a cellular mechanism? If it truly is a Parkinsonism pattern, it’s a protein misfolding disorder. What causes a protein misfolding disorder? What things cause proteins to misfold? It could be a whole list of stuff. And then once proteins misfold, how do you get rid of that protein? So with Parkinson’s you get alpha-synuclein, alpha-synuclein builds up, you get Lewy bodies, and these Lewy bodies start to infiltrate and aggregate all throughout the body and the brain, and you start to get degenerative changes. If you get protein aggregation like Lewy bodies, you can ask the question: what’s causing people to have more and more misfolding, and then what mechanisms can help degrade these proteins? And then you start to think clinically from cellular back up, instead of thinking every neurodegenerative disease has to be heavy metals, because you tested them and they have high mercury like everyone else in the population. Or you check them for a COMT SNP, which one out of three people have. Right? So you want this to be diagnostic in your perspective. So, we’re going to go through and teach you all the cellular mechanisms, so you can then take a step back and kind of see the bigger picture.

And then the question is, you know, what kind of treatment options would you consider? Well, you’re going to look for all the misfolding type of mechanisms that can take place from a metabolic, nutritional, inflam-matory model, see which of those you can identify and support. And then you want to go in there and try to


support their brain, and do some therapy to see if you can get his cortex to improve, because maybe if it’s frozen shoulder, and chronic pain as you get their basal ganglia more efficient and their stiffness and rigidity changes, they may have better function for a while, right? And then start to do exercises and regenerative things, like to slow down degeneration. So burst activity and exercise, when people have Parkinsonism early signs, they can go and do sprints, if they can go out there and play tennis, and do explosive activity which causes huge dopamine surges, it’s very protective for them. So you want to ask them, “What’s your… What are you doing for exercise? Well, I really want you to do some more burst types of activity and do some more. Definitely the most important therapeutic thing for your brain would actually be physical exercise.” And let’s say an eye movement, or, you know, some kind of fine-tune functional neurology exercise.

Now, what would be the prognosis with a patient like this? Yeah, the prognosis is going to be poor, if it’s Parkinsonism. It’s an uncurable – make sure you guys understand this – it’s an uncurable progressive disease. Despite everything you will do. Don’t be the naïve practitioner. Don’t be, “I caught this, I’m going to really… I’m going to reverse this and it’s going to be cured.” You’re setting yourself up for a failure model, and you’re going to really impact your patient’s psychology. You can absolutely change all the findings clinically, for a while. You have a patient like that, you start treating their brain and doing rehab, their tremors can go away, their arm swing can come… can normalize, their tone can improve. But guess what happens over time? All your findings disappear because it progresses. Okay? So you have to understand what environment you’re getting into when you’re dealing with Park… When you’re dealing with any type of neurodegenerative disease.

Now, a neurodegenerative disease is different than neurodegeneration in part of a person’s brain that isn’t associated with protein misfolding and things of that nature. Now, if you have a person that doesn’t have Parkinsonisms patterns, but they had a brain injury and they impacted their frontal lobe and now their basal ganglia direct pathway’s not efficient, and it’s been some time, you might see some degenerative change, and develop plasticity connectivity, and their prognosis is really, really good. Then you have someone who actually has Parkinson’s disease, which you have a cellular protein misfolding disorder, and if you think that you’re going to have the same effect with someone who doesn’t have that mechanism, you’re going to really be depressed, you’re going to be shocked, and your patient’s going to be upset, and you’re going to have a problem with that.

So, we typically find there’s a lot of practitioners don’t understand neurodegenerative diseases. They think once they see some clinical skills change that they’ve cured it. Don’t be that naïve. So understand that when you’re looking at Parkinsonisms, dementia, tau protein buildups, Lewy bodies, alpha-synuclein buildups, that you’re dealing with something that is uncurable. No one in the world has found a cure. You guys understand that? And if someone did, they’d win the Nobel prize in medicine. Don’t confuse improving brain integration and function and symptom change as a cure, because you haven’t. Those neurons that are dead are still dead. All you’ve done is make their existing neurons healthier and they’re connecting into each other more, and they’re more efficient, and as time goes on you expect those findings to change. If you didn’t do that, you’d go, “Oh, I changed your symptoms. Now you’re back again. What happened?” “Oh, I think you’ve got another toxic load of mercury. What did you do?” You know what I mean? Don’t do that. So those are the things that you really want to understand.

Okay. Take a look at this person, your initial survey. Whoops. Start with facial tone. Do you see a difference in facial tone from one side to the other? Let’s just start with… Do you see facial asymmetry? Okay, everyone


sees facial asymmetry? Okay. Now, do you see that in the top part of his face or the lower part of his face? Is his forehead and eye muscles pretty much, like, equal? Yes. How about the lower portion of this face? Well, this tone… Well, these areas here look pretty symmetrical, but when you go down here you see a difference in tone, right? You see muscle tone here, and you see a lack of muscle tone there. You guys see that? So you’re seeing a left-sided lower facial paresis. It’ll help if we do this. So which side does he look tired, more fatigued, aged older? This side? Or this side? He looks more worn out and tired on his left side compared to his right side, okay? So it’s really easy and really critical, right away you just start looking at someone’s facial muscles, and trying to see what you see with that. Okay? So, this side compared to that side. And then you have the general tone.

So right away, when you see that, you know that there’s some asymmetry happening, and the question is, well, first of all he’s older, so what you should be thinking: What degree of neurodegeneration does he have, just because age is a factor. Secondly, you go, “Is there anything I see obviously?” Wow, you see some facial asymmetry. And the facial asymmetry is on the left side, so if anything is less efficient with him, it’s going to be his right areas of his brain. That make sense?

Now, if you go in there and just do passive range of motion, and you do passive range of motion and this side is the left side, so it’s with facial paresis is tighter and has more tone than this side, then you might think there’s something going on with their corticospinal frontal motor strip. They have rigidity and tightness, you’re, “Hey, is this an early basal ganglia Parkinson pattern?” Right? Those would all give you some clues of what’s potentially happening with them. Or there’s nothing obvious there, so it’s maybe not as progressed, you don’t see that clinical finding there.

Now, did you guys look at his platysma muscles? Do you see his platysma muscles? Let me… Take a look here. Do you see a difference in tone? See how that left side doesn’t have as much tone? So now you’re going, “Wow, there’s some muscle tone changes taking place, not only with his face, but with his platysma muscles, so now you’re going, “Wow, that could be a degenerative change that’s happening in with his motor areas.” Right? Just from your initial survey, you should be able to tell that.

So what region of the brain may be compromised from initial survey? So right away, we know that this is a motor pathway, that there’s some things going on with their corticospinal projections into his facial nuclei, to his upper cervical motor areas, to his platysma muscles. So we already know that there’s some right brain related issues.

Would you expect any changes in his handwriting? Well, question is he left- or right-handed? If he’s right-handed, and he’s got left corticospinal frontal, let’s say degeneration, and it’s isolated only to that, would you expect to see any changes in handwriting? Well, probably not, because if he’s right… If he’s left-handed, maybe, but if he’s right-handed, maybe not. Right?

Would you expect to see any… What examination findings would you expect to find? So now you’re going to go in and go, “Hey, is this… I’m seeing some degenerative changes with the corticospinal pathway, but that corticospinal pathway can overlap with how it fires into the striatum. Do they have early Parkinson’s pattern? Is this just a frontal degenerative issue? Do they have previous head trauma? Am I seeing degenera-tive changes from some type of insult over time that’s caught up with them?” But you would think about that, and you would go, “Hey, how is your deep tendon reflexes on the left? What’s their tone like on the


left? How do they… How is their arm swing when they walk?” So the minute you see them, you’re going, “Okay. Deep, deep, deep, deep, deep. Those are the things I need to check out.” And you already have an area where you’re looking into. It’s critical that you know where you’re going to go into, because you’re going to do repeat testing and check the integrity of it.

But this is why we really focused on the initial survey last time, because let me be honest with you: Most practitioners in initial surveys suck. And they spend… They communicate with the initial survey trying to be social, and that’s how they think their initial communication is, and then they go, “Oh, I’m in exam mode, let me go through my exam. What’s on my form?” But all the key things you will… you need to identify what’s going on with their brain is all in front of you. A lot of it is front of you when you see them. Of course you’ll have to do the exam.

So, let’s go into another case. And I just want you to listen to this person’s speech, so let’s make sure the volume’s okay.

“Take this test please. First, stand, [?]. Sit up. Now hold your hand [?]. Now. Close your eyes. Lift a foot off the ground, and balance on the foot. Now I’m going to count out loud. One, two, three, four, five, six, seven, eight, nine, ten, eleven.”

Okay. So her speech is obviously involved. Right? You guys all… So as we go into the initial survey. So there’s different types of speech imbalances, right? We have things like echolalia, where they repeat themselves. Palilalia where they just mumble and blutter… just mumbleness comes out, right? Arpiolia where you have the… just random… tic kind of disorder. You have dysprosody, where their dialect and their speech sounds different as if they’re speaking a different language, aprosody where they just have no emotions in their voice. Right? You have spastic dysphonia, where they’re speaking like this; they’re shouting things like that. You have hypophonia, where they sound like they’re whispering. But that’s not any of those. And then you have staccato speech, where la-la-la-la-la breaking down, but it isn’t that, but it’s close to that. This is a what? This is a cerebellar ataxic dysarthria. So just like when movements aren’t as smooth, her voice is not as smooth.

So we made an ancillary video for speech, and I put examples of all the different speeches for you in the ancillary videos. If you go watch that over and over again, you’ll be able to tell the difference between flaccid paralysis versus spastic dysphonia and hypophonia, and it initially helps your initial survey. So right away, if you hear someone’s speech, you can think of it as, they sound kind of drunk. Someone’s speech sounds almost like they’re drunk and just not smooth. You start to think, “What’s going on with their cerebellum?” Okay? You can have patients in your examination come in and they’re fine, and as you go through exam and start talking to them, start doing their history, they start to sound a little drunk, which immediately tells you that they have ataxic speech, and you probably have some type of cerebellar type of involvement. Okay?

Let’s look at case number four here. Okay, right away, initial survey. Do you see any asymmetries? Do you see any asymmetries with the eyes? Do you see any asymmetries with their face, right?

So let’s start with the eyes. Do you see any vertical deviation of the… of this person’s eyes? Yes. Okay. So right away, one is… there’s a vertical deviation. And usually the weak eye is the one that’s sitting there, and then the eye that’s compensating is the one that’s moving all over the place. So event though it looks


like typically that the eye that’s deviated is the one involved, usually it’s the compensatory ones. We’ll talk about cover/uncover tests as we go into different modules. We’ll show you how to uncover and figure it out, each of these different types of eye muscle weaknesses and so forth.

Now, do you see changes in the facial tone? Is it symmetrical? No. Is there one side that looks that it’s drooping, that the person looks older and more tired with? So let’s do what we’ve been doing to help. Okay? Look at his fatigue level, his fatigue appearance, and his age compared to that side. Left side versus right. So if you look at his right side, that looks like he’s focused, he’s more attentive, he’s there. And then if you look at his… if he looks at… if you look at his left side, you can see that it looks a little bit more fatigued. Right? You guys see that? His right side, his left side. So this is the left facial type of pattern, okay?

Now, I want you to take a look at his speech. So right away, what’s the first thing you just know right now? What you know right now is, this left side, on the lower two areas, is different than the right, and it’s got a skew deviation. And what? He’s older, so you start to think, “Does he have any neurodegeneration? And do I see any signs of it?” So right away, you go, “I see some patterns of asymmetry, and his facial tone, in the lower area…” because his upper areas are not too bad, even though you see some sagging of the eyes, his forehead is okay, but it’s more of this lower facial paresis. And if you weren’t sure, you just have him wrinkle his forehead and close his eyes and see if those were intact. So you can always do followups. But this is a lower facial paresis on the left side, so you would think that the right motor areas were involved. Does that make sense? Now, you then diff-di. Is it corticospinal? Is it cerebellar? I mean, is it frontal? And then go through those types of patterns that way.

Okay. So let’s look at his speech, and this can help you. Now, if his speech… If he has no emotions in his speech, so can… So, let’s talk about this. If we think that he’s got a right-sided issue, what are some speech language areas that we see involved with the right side? So, you could have aprosody, which means he doesn’t have any emotions in his speech. He’s just kind of monotone and so forth. And if that’s the case, then you know you’re dealing with some right temporal related degenerative changes. Now, could he have brain injury, and he’s got actually spasticity in one side? If he has spasticity in one side, what kind of speech would you expect to see? He would have a spastic dysphonia. Rrrr-eeee, you know, that we see people with examples that are trying to get voice out, their vocal cords are spasming, and they’re rrrrrr, shouting like that, right? Now, could he have… If his right side’s involved, would you expect his things like Broca’s, or fluent, dysfluent? Not necessarily, because those are more with the dominant hemisphere, but the right side could have things like aprosody, where they have no emotion to their speech, right? Or, this could be a person that’s got early Parkinsonian pattern, so you expect to see whispering or hypophonia and those types of patterns, right?

So you do your initial survey, you hear him talk, and boom! You’re putting some things together, and you’re starting to triangulate where the brain’s involved, and if they have a neurodegenerative disease. Everybody with me? Great. So let’s watch… Get some volume?

How would you characterize your voice? How would you describe it? “Very low volume.” Okay. And it that bothering you? Or does it bother other people? “It bothers my wife because she doesn’t…” Because she has to ask you to repeat? “Exactly.” Okay. And when that happens, is there anything you can do to improve your voice? “Well, I try to speak louder, but the next time I say something, I forget and…” Alright. So it doesn’t always last from moment to moment, huh? “Yes.” Alright, so…


So that’s a hypophonia. You see hypophonia with facial paresis, you start to think, “Okay, does this person have a Parkinsonian early pattern? So you can watch him walk. What you want to see with his gait: Does he have an arm swing? Does he have rigidity? Does he complain of rigidity? Does he have any type of rest tremor? Does he have any gut motility issues? Does he have any constipation? Is his olfaction in place? We’re going to go over all some of the early findings with these tests, but right away you should have this initial appearance, clinical appearance, of this could be a neurodegenerative disease. We know it’s starting to involve the right side of the brain; now you see hypophonia along with facial paresis, you know that there’s something happening to their brain.

So, as you guys know, patients you see in your office over forty, you should just ask the question: What degree of neurodegeneration do they have? It’s that simple. You shouldn’t use a small drill to go, “Now I know how to… what to do with people that come in that have dementia,” because if you did, they’re already too late. You want to be able to find everyone’s degree of neurodegeneration. And, you guys, we did workshop yesterday; we found it everywhere, right? With healthy people. So these are real scenarios.

Now, let’s move on to case number five. So, we’re going to do another speech here, with volume.

Take a look at this guy’s speech. Here’s the questions you want to ask. “Do you have hypophonia,” which would be basal ganglia direct pathway. “Do you have echolalia, palilalia?” which is basal ganglia indirect. “Do you have aprosody?” no emotions to the voice, which is more of the non-dominant right, right? “Do you have changes in your dialect, where it sounds like you’re speaking a different language?” which is involved with the connections of motor… of your language centers on the left side, right? Dysprosody versus aprosody. Aprosody is the right side, no… very little passion in the voice. Dysprosody is disconnection. “Do you have ataxic speech? Staccato speech?” Cerebellar. “Do you have spastic speech?” Those are all the things you want to think about, right? Or, “Do you have ataxic speech?” like, sounds like someone’s drunk.

“As you can see by the second steps boxed [?], you can see their bare feet walking. Those are not mine. You can tell by the first foot is [?]. Those are my wife’s. She was standing up to do this because I would kill myself trying to video…”

Okay. So, was… first of all, a question. Did he sound like he could be drunk? So right away, your first impres-sion, is this cerebellar, which would be more of an ataxic speech? Was there… There’s some changes, there’s not many fluctuations of his voice. Did you see him struggling to produce words? Like, he was trying to really make… He wasn’t really struggling to produce words, just the words are produced more efficient. So people that have, like, a motor Broca’s aphasia, they… are… trying… to… make… a… word. I’ll show you some examples of it. That’s not what you’re seeing here. You’re just seeing it’s just not smooth. So just like you see dysdiadokokinesia with movement, you see the same thing happening with his voice. So this is a cerebellar pattern of speech. Right? It’s like an ataxic speech that you see. It’s not hypophonia, it’s not aplastic paralysis, it’s not spastic. So this is a clue that there is some cerebellar type patterns.

Okay, let’s move on to this next one. So let’s look at her speech here. So remember, you have, when you look at speech, usually you’re looking at speech areas on the left side of the brain. The left side of the brain, you have your fluent and non-fluent speech patterns. So if they can’t understand what’s going on, what you’re telling them, then you’re suspecting that it’s this whole Wernicke’s area, right? And the temporal regions. They have a hard time producing the words, you know it’s frontal. And if they have a hard time repeating,


then you know it’s the transcortical information between back and the other, right? Those are the issues associated with different speech patterns.

Volume here?

The producer asked us to count to ten. Remember that? “Yes.” Can you do that again? “Why? One, two, three, four, five, seven, n.. boing, two, gabrice, April, go… I can’t no.” That’s good. Let me get you started.

Okay. So could she speak fluently? She could speak, right? She had no problem speaking. Could she understand directions? She could understand directions. She was doing the history and communicating. But when asked specifically to repeat a task, the communication wasn’t there. So she could understand, she could speak, but to do them both in sequence, being told directly to do something and then repeat it, was a problem. So that’s, you know, is usually arcuate fasciculus type of patterns. Okay? So there’s a saying: If the patient is frustrated doing their history, you think of Broca’s. If the doctor is frustrated, because they’re just trying to talk to them and they can’t understand, then you’re thinking more of a sensory, right? Or posterior type of speech disorder, where the Wernicke’s areas are involved. That association auditory cortex. Okay?

But with her, she can understand and she can speak, but when you have her repeat, she has a problem with it. That’s the transcortical, right? And you can have global aphasias where it’s both. So just make sure you guys know your speech patterns, your initial surveys. They become really critical as you look at all types of things.

Take a look at this one.

Fine, how are you? “I’m happy. Are you pretty? You look good.” What are you doing today? “We stayed with the water over here at the moment and talked with the people at the dam, over there. They’re diving for them at the moment. They’ll stay at the moment. They have water over there for him, with luck, for him.” So we’re on a cruise and we’re about to… “We’ll start right here, and we’ll shake their hands right there.” And what were we just doing with the iPad? “At the moment, I don’t see a darn thing.” With the iPad that we were doing. Like, here? “I changed for me, and changed hands for me. I was happy. I would talk with Anna sometimes. We’re out with them, other people are working with Anna then. I’m very happy with them. This girl was very good.”

Okay. What did you see? Could he produce words? Okay, so that’s fluent. But questions were being asked, and he was going all over the place. He doesn’t really understand the questions, right? So if you’re taking history on this person, would you be frustrated? Or would the patient be frustrated? He’s not frustrated. He’s totally happy. He’s thinking everything’s cool. He’s speaking. He doesn’t know there’s anything wrong, and if you asked him, he wouldn’t know. But what you’re asking him and what he’s saying is different. So that’s more of the fluent aphasia. He’s fluent, he can speak, but he just can’t process what you’re asking him, right? So then you would think about that posterior language areas involved versus the anterior Broca’s. Okay?

Alright, let’s do case number eight. Now let’s go over this one here.


Hello, what day is it? “I don’t know.” You don’t know? “No. I want to know.” When Dee is coming? “That. That.” Wave to Dee.” Say hi, Dee. “That.” Wave to Dee. “That. That. Oh no.”

Is he there? Does he understand the questions? Yes. He understands the questions, the questions the person is asking, he can understand them, comprehend them. He has difficulty producing the words. It’s not ataxic, right? This is a Broca’s type of lesion. So the speech center anterior type of lesion. This person had a stroke. So it was non-fluent, because he just wasn’t fluent. He has had difficulty with how his words and language are coming out.

So those are the patterns that you want to be able to tell. So you guys, just looking at someone’s face, and then you just look at their speech, and you look at their gait, and then look at their eye position, then look at their pupil, then you look at their personality, you have a general idea of what’s going on with the health of their brain, right? That’s the whole concept of initial survey. So what we want to do is take this initial survey we taught you guys last time, and then start merging and then blending into neurodegeneration, okay? And then we also talked about metabolic initial surveys, because there’s a lot of metabolic factors that have an impact with this.

So, let’s go into, say, cases nine through twelve. If you guys saw this on your office forms, what would you immediately think in your initial thought process; your clinical workup? What’s happening with the lines as a person writes? They’re getting smaller. And what’s happening with the writing? “Today’s a sunny day…” Take a look at, for example, the Y here, compared to the Y here. It’s getting smaller. So this is micrographia. So, if you had any kind of office form and they’re filling this out, you had micrographia, you immediately start to think what? What’s going on with their basal ganglia direct pathway? Doesn’t have to be Parkinson’s disease, but it could be a Parkinsonism, and then you have to diff-di it, which we’ll teach you how to do that. But you start to think, “What’s going on with the basal ganglia indirect pathway?” Parkinson’s definitely one of the things you’d expect to see.

Now, what could be some possible chief complaints the patient come in with? Could they come in with a complaint of depression, chief complaint? Yes. Could they come in with a complaint of writer’s cramp? Could they come in with a complaint of frozen shoulder, or chronically tight psoas? Could they come in with a complaint of lack of motivation and drive, which is completely dopaminergic? Yes. Could they come in with chronic constipation issues? Yes. Or chronic gut issues no one’s been able to help? Those are all possible, so that initial handwriting immediately starts to let you through a cascade of events.

So then you watch them walk. Do you see rigidity? Do you see spasticity? Do you see shuffling gait? Right? You do your examination and you look for stiffness and rigidity signs, look for postural reflex signs, you look for defects in eye movements. But you already have a major clue of where to go, just from your initial findings, which makes you then be able to do repeat testing and look for endurance levels, and then get to the bottom of it.

Let’s do another one. What do you guys see with the handwriting here? First of all, is it small or large? Is it totally messy? Is it angled and skewed? Do the letters down… Do this look bigger than the ones up here? A little bit? So take a look, for example, of an A here, A here, compared to an A here? Compared to an A here? They’re starting to get a little bigger, right? So, macrographia. When their cerebellar gets fatigued, as they continue to write, it’s harder for them to make smaller, so they can… to write better. It’s not to say


you can diagnose cerebellar disease from this, but you would start to suspect it, because you’re seeing large handwriting. But the biggest clue to you isn’t that it’s large; the biggest clue to you is that you start to see potential increase in size as they continue to write. Okay?

And then what about this one here? “This is my handwriting; This is my handwriting.” They repeated it. So first thing is, do you see handwriting get smaller from the first to the second? That’s your micrographia. So you immediately start to think what? Basal ganglia direct, and from a neurodegenerative model you’ll be thinking, “Do they have a Parkinsonian type of pattern?” Next thing you see is, you see a skew, right? You see it’s going up to the right. So what kind of head tilt would you suspect they may have? Probably one to the left. It’s going up to the right. And if they have one to the left, that means they may have a weakness of a muscle, maybe superior oblique on the same side, inferior rectus on the other side, or they could have cerebellar integration issues, or compensating, trying to activate the vestibular system through tilting their head to that side. Those are things you would have to figure out from the examination. Okay?

And then how about this? What region of the brain is involved with this case example? Well, do you see micrographia? Do you see the handwriting getting smaller? Not really. Do you see macrographia, where it’s kind of getting bigger and it’s big? No. Do you really see a consistent skew to one side? Like up to the right or up to the left? Not really. It’s just what? Sloppy. It’s just sloppy, doesn’t… So you’re going, “What’s going on with their corticospinal motor integration, fine motor activity? And the question to ask is this: “Has your handwriting gotten worse in the past few years?” Now, if they say, “No, my handwriting’s been consistently bad. I haven’t noticed any difference,” you’re not as concerned. If they tell you, “My handwrit-ing has really gotten bad over the years,” that’s telling you that they have a neurodegenerative model, potentially. Neurodegenerative mechanism. You guys understand that? The key thing isn’t that they have bad handwriting, because some people just have bad handwriting. The key thing is that they’re actually getting worse over time. Okay?

Now, if they tell you that their handwriting has rapidly declined in the past six months, that tells you that their neurodegeneration is going fast. If they tell you that it’s happened over the past couple years, then you know that’s some degree of information to you about how fast that the degenerative process is taking place with them. So it’s important to always ask, when I see sloppy handwriting, if they’ve noticed a difference, and then what period of time. Okay?

Let’s go to a couple last few examples.

So now let’s say you’ve identified a person. They have some type of neurodegenerative disease, and let’s say it’s either a dementia, or Parkinsonism, or you just see some time of corticospinal degeneration from past injury and disuse; whatever the case may be. Okay? So then you have to ask the question: why, and what are the factors that are causing it? And this is really where you have to jump into what’s going on metabolically with them; what’s going on chemically with them, nutritionally with them, right?

So, what would this tell you with the patient? Well, you see white nail beds, so you’re thinking of circulation. Can circulation impact neurodegeneration? Absolutely. So you check their capillary refill time, right? You check their temperature from distal to proximal, and just see if there’s any temperature change, which is related to… associated with circulation. We want to make sure you check to see if they have any pulmonary or respiratory issues. You want to listen to the lung and the heart very well, make sure there’s no diseases


there of any kind. You want to look at labs, make sure they don’t have any types of anemias or things that can impact the red blood cells. Those are all the things that would impact the paleness.

Now you have lined nails, and lined nails are classically associated with protein deficiencies, but people today don’t have protein deficiencies; people have protein malabsorption syndromes that you see. So pro-tein malabsorptions are very real, and they take place if people have small intestinal bacterial overgrowth. That definitely causes malabsorption syndromes. People have intestinal permeability; they get malabsorp-tion syndromes. People that have hypochlorhydria, people that are taking antacid medications, they have protein malabsorption syndromes. So now you’re seeing this person’s not getting protein, just by looking at his nails, and this person has poor circulation. So you have some immediate metabolic factors that are impacting their brain. And that’s going to be a key thing as you look into brain rehab, with the potential for the progression of their neurodegenerative disease. Does that make sense?

When you… Here’s the interesting thing: When you get really… When you really start to sharpen up your clinical skills, you’ll have a patient, and if you… let’s say you get a referral from a practitioner, and then you start working up the patient together. What they usually find is, everything was right in front of them. “Oh, you’re right! Their arm wasn’t moving!” “Oh, you’re right! That left part of their face was drooping!” “Oh, you’re right! That pupil is totally dilated!” “Oh my God, his handwriting is terrible!” “Oh yeah, those nail beds are super white!” “Oh yeah, their hands are freezing!” “Oh yeah, there’s lines over their nails!” “Well, I did check him for heavy metals, and they had high aluminum.” Yeah, and that could be part of it. The point is, all this other stuff is right in front of you, and those things have to be addressed. So you want to see if they have a malabsorption syndrome. Did their nails… Their nails should change in a couple months if you start to have those factors improve. Then as their nail beds change and they’re not as pale, as their circulation changes their hands and fingers won’t be as cold. Those all will let you know if you’re addressing some of the factors that can cause neurodegenerative changes.

What if you had a patient that has memory issues, can’t remember, can’t focus, can’t concentrate, and you see this metabolically? What are you guys seeing? Some obesity, some hair thinning, right? And maybe some insulin resistance. Her diabetes… Could that impact Alzheimer’s and dementia? Right? So please don’t be the person that goes, “I’m going to give you matching brain game skills, and I just want you to…” Those are all important, but if you have an underlying mechanism you’re not addressing, you’re not going to have much success, and you want to treat the underlying issue first.

And then here we have what? What do you guys see here? Fungal nail growth. You’re going to see this in a lot of your neurodegenerative elderly population, because their circulation mechanisms become impaired. And if it’s not pulmonary disease, it’s not cardiovascular disease, it’s just basically circulation. And you’ve got to look at strategies to improve their circulation. Number one thing is for them to get some exercise in. The more intense the exercise is, the better effect it has on the circulation, because it impacts more endothelial nitric oxide synthase. You can do nutritional things to improve circulation: Vinpocetine, ginkgo, to just try to get some circulation and blood flow there, right? Because you may have someone who’s got vascular dementia, or someone who’s got lack of blood flow to the brain, really promoting their neurodegenerative process first, and if you’re seeing these, these are concerns that they may have. Remember, when the blood flow doesn’t get to the distal toenails, then you don’t have natural killer cells and T-cells get to the issues, so that you create an opportunistic environment for fungal overgrowth to take place. Okay.


So the key concept is, we always go back to this chart. Once we find that someone has a neurodegenera-tive disease, we look at factors that impact mitochondrial function: their body composition, their nails, their general appearance, their neck, their eyes, their skin, their hair. So you should be able to pick up neurodegenerative changes by implementing all the stuff that we talked about in the initial survey.

And then the goal is, as we get into this neurodegenerative module, this same flow chart applies. You look at their chief complaint. Remember this: From the patient’s history, they’re not going to tell you what their chief complaints are, so you’re going to see depression, frozen shoulder, chronic pain, constipation, lack of motivation, lack of drive… Those are all things you typically see in the history. You’ll probably see some memory issues, some focus and concentration issues. You use your questionnaire form, you then use your compilation forms, you do your exam, now you’re starting to measure the degree of neurodegeneration someone has. Okay?

And then we’re going to go into the… identifying neuron fatigue mechanisms, and then we’ll get into case number sixteen. So Dr. Brock is going to take it over for the next hour. He’s going to show you a whole nother case and teach you these principles and blend this all together for you.

dr. Brock

A couple things first. Hands-on workshop was really good. For those that came, thank you very much.

What I’m going to do right now is, take the review of concepts, and then take it into a preview of the concepts that are going to be coming through this module. And I know that everybody online is loving the leopard print right now, so I do hear you. So.

Anyway, so look. What we’re going to do now is, I’m going to go through a case. We’re going to go slow, and I’m going to take each little piece of what we’ve been doing, I’m going to comment on some labs, I’m going to comment on some neuro findings, I’m going to show you some video, real patient. Okay? I tried to, in this initial section, give you somebody that’s real, so that you can see it and say, “You know what? Does this really exist? Is there really anybody doing anything about it?”

The things that Dr. Kharrazian just said that kind of strike me is, with neurodegenerative disease, it is imperative that you watch your patients, catch these things early, and then say to yourself, “What can I do to keep this from progressing as fast as it may progress?” Sometimes we have Parkinson’s patients that come in, and my only goal is to get them functional enough to where their medication now works better. Or they can actually get up, go to the bathroom, and take care of themselves. So the goals become different. It’s not a “let me cure you and do some sort of magic trick.” What it is, is “Let me increase your function enough to where you can live your life better; to where your family can now live their life and be happier, because you’re happier, and you can maybe perceive your grandchildren, or maybe you can get around and, you know, make a sandwich. I don’t know. Whatever the case may be.

But we’re.. the world of medicine is losing the game of treating neurodegeneration. I just want to say that. That’s why this class, to me, is so important. I think the medical system is probably not happy with how well they have not progressed in the world of treating neurodegeneration. But when you look at it from the model that I’m going to show you, and that is a compilation of multiple things: all the comorbidities, all the environmental things, all the neurological things, and you start putting it together into one picture,


and then you see the person improve – not cured, not healed, but improved – you can say, “That’s cool.” So I need you to get, and I need you to understand what it is that we’re trying to teach you, and that is, make somebody’s journey from A to Z better. Okay?

So, we’re going to be reviewing the regions of the brain. And last night in the workshop we… This is really important, because we started seeing some people who had deficits in various regions. And when you can identify the regions, you can treat the regions, or you can do things to stimulate those regions and the patient does better. So we have to keep reviewing that. Every module we will do it. This module we made some really good forms that are starting to tie in not just the examination, not just the history, not just the intake, but now it’s going to start adding in some of the treatment factors, and every time we do a course, we will add more stuff to that. So it’s going to be a growing body of information.

I’m going to start giving you what I call layers of treatment. So do you just treat everything at once? Or, when do you kind of look at somebody and say, “Maybe I should do this before that,” and start giving you some rational thinking behind that, because that really is the art of what it is that we do.

Help you start to see severity. What you will also find is this: The better at this that you get, the more severe the patients will be. So you have to be extremely cautious about what you promise, and the things that you know that you can fix, you have to be extremely sure of yourself. But let me just say this: The reward for helping somebody that can’t even tell time any more, and they forgot the names of all of their children, and all of a sudden some of that starts coming back, and they can do it for a little while longer… that reward is greater than probably anything that you will experience in your health care career. Alright? Maybe.

Start to see the forms at use. So I’m going to bring these forms and say, “Look, this is how they got filled out. This is what the patient did.”

And then most of all, my favorite thing, is learn to differentially diagnose these neurodegenerative illnesses. Is it a true Alzheimer’s disease? Is it frontotemporal demise, or dementia? Is it Lewy body disease? Is it Parkinson’s disease? Is it multiple systems atrophy? I’m just going to give you little key things to go through that will teach you how to just jump through them pretty quickly, so that you can say, “You know what? This looks more like frontotemporal demise than it does Alzheimer’s disease. Does it matter? Yes. On a cellular level it might be different, and if on a cellular level it’s different, your nutritional component might be different, and the medication may be different.

Now, the other thing we did this module is this: I just said, we have to talk about pharmacology some. Not to make you a prescriber, but to make you understand that when somebody comes in on seven medications, why did somebody put them on those meds? What are they? And if one works, what does that tell you about the patient’s physiology? That’s why I want to teach it to you. Now, some of you may be prescribers, so this may be invaluable for you in the way you practice. I’m fine with that, okay?

We’re going to start to see some physical exam components. Again, the hands-on workshops are the best place to go, because you get to see it, do it, watch it. I mean, again, last night we saw some pathology that I really one hundred percent did not expect to see. It’s, I mean, hey. If you’re a student, you probably have neurodegeneration, right? Or maybe you don’t. I don’t know.


We’ll start to see the treatment components this module, and I’ll show you how we stack it, how we build it. And the case that I’m going to give to you in just a second, I’m going to show you what it looks like leading up, and then at the end of the module, I’m going to show you the same case, but the other end of it, and what we did for treatment.

So as we’re going through the weekend, I want you to start thinking. Keep this person in the back of your mind and say, “I wonder what they have? I wonder what’s going on? I wonder what I would do?” And then as I show you applications, start saying to yourself, “What would I do?” Now I’m taking you to that place that says this, “What would I…” Finally, we’re here: “What would I do to make this patient better?” And I want you to do that throughout the whole thing, and then I’m going to show you the final results, and what exactly we did.

Now, I want to make something very clear. There may be multiple ways to activate this person’s brain, and still get good results, and it not be exactly like mine. Can everybody just breathe a sigh of relief? It’s not like there’s one person on the planet and that’s the only person that could do it, because there’s lots of people getting others better with functional neurology, or with principles of integrative neurology.

So really, this is where we’re at. You guys have seen these forms over and over. And here’s our patient history. Okay, this is a lovely patient. Lovely family. Great referral. This is the kind of patient – to put it in perspective – that you really, really, really want to help out, because she’s such a young, vibrant triathlon, goer, she does everything; very, very active, and all of a sudden, her life changes. She starts getting dementia. Within a year. Within a year. So she’s got short-term memory loss, and recall for facts, figures, names, and places. So I immediately want you to start thinking about this: Where in the brain is that on the intake forms? Okay? You have to start thinking that.

Now, is there any way that you could take those weaknesses and loop them into therapeutic applications? Possibly. And I’m going to show you how we layered them and use some vestibular therapy with some cognitive therapy with some visualization therapy, to try to get some integrity back into what she has left. But you’re going to be surprised when you see the things that are blocking that, here, in just a second.

She has some language issues. She’s fluent, she has comprehension, she has repetition, but she can’t find some of the words that she wants. So it almost appears… it’s getting so bad. So it started out as, like, “I can’t… can’t think of the name of that thing right there.” But now it’s getting to the point where it almost looks like she has an aphasia, because she can’t find so many words that it almost looks receptive, or it almost looks like she has a lack of comprehension, or it almost looks like she has a lack of fluency. So you can start to see it and go like this: spread, from the inferior parietal region and the frontal region. And now you’re like, “Oh my God, she’s got a neurodegenerative disease that’s starting to spread.” Okay?

So, she’s been under some stress. Now, let me just tell you something real quick. You’ve got a hippocampus. And if you take cortisol… so, I’m going to start giving you some metabolic principles that I need you to understand. You go to that metabolic intake form, you go through the area that’s the hippocampus, it’s short-term memory stuff. And one of the very first signs of hippocampal damage is just depression. But the one area that decimates it is cortisol. Cortisol fluctuation, cortisol inadequacy, cortisol too much. It’s not good for the hippocampus, and neither is inflammation. And neither is a lack of estrogen. And neither is abnormal insulin. And neither is abnormal glucose. So what I’m telling you is this: I have to spare this


person’s hippocampus, allegedly, if that’s the area that looks like it’s going bye-bye. I have to take it, and now make to where that’s going to slow down, and then enhance whatever function is left. Because if I don’t, it’s going to continue to degenerate. And I’ll tell you about these conditions that are these neurodegenerative, possibly dementia-types of issues, and falling under the broad category of dementia. Once they get to a certain point, if you activate the brain too fast, with very little neuro-metabolic support, they just degenerate faster, because you exceed their metabolic rate very quickly.

So, we keep going. She’s in her late forties. Actually, I’m sorry, she’s in her late fifties. About fifty-five. So that was a goof-up on my part. She feels as if her brain endurance is just low, like “I just don’t have any… I’m tired. I can’t cook. I can’t go to the supermarket. I drive down the street, I start to get lost. When I get mentally tasked, or I don’t sleep enough, I don’t remember things.” And her husband is sitting there, and he’s explaining these things to me, and she’s just like, “Yeah.” She’s agreeing with me. And as she’s talking to me, she’s starting to fatigue out and then can’t answer questions very well.

So she has it, then she doesn’t. And so you look at it, and it makes your heart kind of bleed a little bit, because you see such an amazing woman, and an amazing man, and they have this family that’s really awesome, and you’re seeing it to… the whole family unit is deteriorating right in front of your face. Now, the reason why I’m telling you things like that is because I need you to get the emotions behind the treatment. Because if you don’t, this is just another exercise in going through a case, alright?

Now, here’s where she’s at. You remember these things? Let’s take our time. Now, one of the things she’s having is difficulty with restraint and some impulses and desires. Now, what that means is this: She’s starting to have some repetitive thoughts in her mind, so she’s starting to perseverate a little bit. Back of the brain or the front of the brain? Yeah, front. Look, it’s right here. See it under the dorsolateral and orbitofrontal? Now, if somebody starts to perseverate, and then become impulsive, and then act out on that, you see a dorsolateral down to the orbitofrontal region, and those areas inhibit your limbic system. And so you just become one of those people that just does whatever they want, and they don’t think about the consequences, and then the consequences usually are not… can sometimes be not so good.

Look at this: Difficulty making and planning decisions. And there’s also, up there, difficulty planning and organization is bad too. This tells you the following: They don’t have enough short-term memory to put sequential things in order to execute them. So that is a… not a good sign. So the frontal lobe is really kind of starting to not look like a beautiful place right now.

We come down: Difficulty getting a sound or melody or thought out of the mind. That’s perseveration. That’s kind of what I was talking about. And we go all the way down, and then you see things right in this area, where it looks like there’s some mental fatigue. And then difficulty with analytical thought. So when you go through this, you’re like, “Man, difficulty with analytical thought, and then there’s difficulty with numbers and skills, and there’s problems with appreciating art and music.” What you’re starting to see is left- and right-brain dysfunction. It’s not that it’s just one side or the other.

The other thing that has really started to happen is, it can only be one hemisphere. Neurodegeneration and neurodegenerative disease may start in one hemisphere first, but then it may climb over to the other, and they start to look more and more symmetrically pathological as the disease progresses. So somebody’s


underlying hemisphericity, so to speak, where it’s like their right brain is just not so good, but their left brain’s amazing, and then you bring the whole brain down, one side becomes very symptomatic.

So you can look at these and score it, and say, “Okay, look. They’ve got problems on the left, they’ve got problems on the right, but the right-side stuff is really going downhill quick.” So now you may say this: They’ve got some neurodegeneration in the anterior half of their brain. The right side or the left side may be doing worse, and that tells you kind of where they started. Does that make sense? You’re starting to see it now, not just from “Hey, this lobe works or that lobe works,” but where did it start? How did it progress? How bad has it progressed? Which areas are worse than the others? As we start going through this, you’re going to see that the temporal system and the parietal system is not near as affected as the frontal system. Welcome to the world of Alzheimer’s disease. Okay? Just… You’ll understand whenever I start telling you things about the frontal lobe and the temporal lobe. Or all of it globally, and dysautonomia with, like, multiple systems atrophy. Or they’re sitting there and they can’t remember things, and now they’re shuffling and they have a movement disorder, with, like, a supranuclear palsy or Lewy body dementias. All of these things are going to play into effect. That’s why these forms, it’s very important that you get the concept of using them. A lot of people don’t get it yet, because they’re not using it. But when you start using it, and then you compare it to the physical exam forms, and then you do your therapy and they go back and they fill these out again, and they’re getting better, then you can say to yourself, “I’m seeing improvement, tangibly.” Okay?

So we go down here, and again, difficulty with analytical thought, difficulty with creativity, imagination, and intuition. So I have a left-sided problem that is at a 5, and a right-sided function that is at a 5. So now I start thinking: “Okay. This person is degenerating. It’s both halves of the brain. It’s starting to become symmetric, and I’m becoming scared.” And here’s why I’m a little bit worried: Her husband’s worried. She’s happy as can be. She knows there’s a problem, but she’s still pretty happy. Okay?

We go over here to the other side, and look at this. The supplemental motor areas are all normal. Broca’s is all normal. She doesn’t have fluency issues. She doesn’t have repetition issues. She has word-finding issues. So it’s starting down here low, it’s coming up to the very, very front, and it hasn’t come back and hit the motor strips yet, but it’s up here right in the poles. So now you can… Here’s what I want you to learn to do. How many of you are starting to learn to draw, in your own mind, a three-dimensional brain of the patient’s brain? I know that sounds a little crazy, but what I want you to start doing is visualizing: What does this person’s brain look like? And I’m sitting there, and I can… I’m visualizing the gyri and the sulci changing, and the frontal lobe, and everything in the front starting to crumple up, and getting more separated, and losing volume and mass. And by the way, I have imaging that will correlate with the brain index intake form in your physical exam. So it’s important for me, right now, to ask you to start writing down what you see. Because it’s going to be important to test your skills.

Okay, so we come over here, and the parietal somatosensory area’s looking good. Broca’s speech is looking good. The posterior part of the frontal lobe is looking good. But the frontal part of the frontal lobe is not looking so great. The… what we would call executive function, now the hippocampus, is very deep. It’s short-term. It’s related to the amygdala, and it’s related to other things, so it’s not so much in the frontal lobe, but the circuitry from there goes right to the frontal system, so short-term memory ends up turning into executive function, and it starts turning into linear order of your day. Another sign of this is depression, procrastination, can’t get things done, you can’t empathize with people, you start losing relationships, and


things start falling apart with these frontal neurodegenerative conditions. And then people become flat, they become misinterpreted on their emotions, they become slower, and then I’ll show you, it’s like this: Did it veer into Parkinson’s? Did it veer into a dementia? Is there a dementia related with a movement disorder? Is their cerebellum starting to fall apart? By the end of the weekend I just want you to be able to say, “I know exactly where it is in the brain.” And, “Here’s some stuff we can do for their neurochemical function.” And, “Here’s some exercises that we can start out with.” Those forms will continue to expand. Okay.

So the cortex is involved, including the frontal lobe, and we know it’s progressing both left and right.

Oops, went the wrong way.

Okay, so here’s the parietal system. Everything looks good. Now we go over here to the hippocampus. Now, did I already show you the frontal system? Yeah. It didn’t look terrible, but it didn’t look good. Now look at the hippocampus. If you look at this area, that I just highlighted, right here, bang. It’s 5, all the way down. The patient is having memory less efficient. Memory loss that impacts their life. Confusion about dates. They can’t remember events. They misplace things. They have difficulty with memory of locations, addresses. All the way down, difficulty remembering words. You guys can read this. The hippocampus is going, going, gone. The frontal lobe is starting to now follow. The back of the brain is doing pretty good. So now you can see this: Development. Are you seeing the progression now, on the intake? It’s not just an intake any more, like is it there, is it not? Now it’s, “Whoa, that’s really bad, and now this is starting to become really bad.” And as it gets worse, you’ll see gait changes, you’ll see instability, and you’ll see parietal changes, and then you’ll see that they don’t know where they’re at in person, place, and time. They’ll get calculation stuff, they’ll lose facts and figures. It’ll start to move back this way, and then it’ll stop. And then part of the brain will just crumple on the front, but they’ll still be able to see, maybe have some depth perception. Who knows what they’ll keep. Are you following that important concept?

Okay, so what part of the temporal lobe is progressing? Did it possible lead to the changes in the frontal lobe? Well, the deep portion of the temporal lobe, hippocampus, is the one thing that’s involved. So now you have to ask the question: Why? I mean, now some of the newest literature shows this: that when one gene flips on, it flips on four or five other genes, and certain things start to happen in combination with Alzheimer dementia or certain types of dementia. Blood sugar dysregulation happens, vascular changes, lipid changes. So you have to start to say to yourself, “Wow, is this a complex, or is this just something that’s by itself and you’re just unlucky and your brain’s starting to fall apart because the environment is not so good any more?” It’s just not that simple.

So let’s just keep going through this a little bit.

Okay, so here’s the cerebellum. How does it look? So now you look at this, and you’re like, “Man, is this a cerebellar issue?” Well, she walked in perfectly non-ataxic. When she talks, she has no dysarthria. When she moves her fingers, she has no termination tremor, or essential tremor, and no kinetic pathology with posturing and stuff like that. You look at it, and you’re like, “Wow man, the cerebellum looks pretty darn good.” And you go through it, everything looks good, everything looks good.

Down here on the bottom, you have a little bit of autonomic issues going on. Possibly. Now look: There’s some anxiety. Why is there anxiety? Maybe she’s a little nervous with the fact that her brain is deteriorating.


And when your frontal lobe starts to deteriorate, you can’t inhibit some of these limbic pathways that may start to produce anxiety, insomnia, and dread. So it’s not that it’s just a high-firing sympathetic system. It might be the sheer fact that the cortex can’t control deep limbic emotions. This happens. As people get, like, Alzheimer’s disease, and they progress, they sometimes become violent, alright?

Not easily startled. That’s good. Difficulty relaxing. Again, these things down here are just related to… there’s now some autonomic changes, and there’s some cognitive changes with an intact limbic system, and the patient has realization that they’re actually having problems. I would have a little bit of anxiety too, and probably so would you. But we see this: sleep problems, anxiety problems.

So now we’re looking at this person. Let’s build it out. Bilateral brain; hippocampus, which is deep; temporal, hippocampus is massively related; frontal system is starting to go. That is what I want you to understand as an Alzheimer presentation. We’ll talk about tau, we’ll talk about amyloid, we’ll talk about oligomers. You will be able to go from the neurochemical to the physical exam findings to the progressions to the treatments to the expectations. That’s the order we’re trying to give it to you in this weekend. I love the forms, because it just quantifies: “Hey man, this is how this is progressing; this is what it is; it’s jumping out and screaming at me before I even do any physical exam.”

No seizures. No peripheral nerve disease. Now, is it possible to have seizures at the same time? What if you’re that unfortunate a person that has epilepsy and neurodegeneration? It’s possible. What if you’re that unfortunate a person that has diabetes, a peripheral polyneuropathy, and that is perpetuating your Alzheimer’s disease? Very possible. I didn’t want to overcomplicate that this module, and I want to tell you, she doesn’t have those findings. Deal?

This right here is her gait. She’s not falling yet. She’s pretty stable. Now, we’ll say this: statically, statically, standing here, she’s stable. But when she moves, or leans, and we check some of her limits of stability, she’s not so great. But she doesn’t perceive that yet. I’ll show you what that test looks like here in just a second.

Okay. Now, I’m going to freeze for a second, and tell you where we’re at so far. We looked at an intake form, and we simply said this: What does the terrain and the environment of this person’s brain look like based upon their perception or their family’s perception? Because some of this was hard for her to fill out. So her husband helped her. Now, you’ve got to also look at him and say, “Does he have a lesion?” So, is there the capacity to even fill these things out? That’s why you always have to take these with a grain of salt. They’re not diagnostic. We just simply use them as a tool to maybe help us get in the ballpark. Deal? Please don’t go off and say, “Their standardized intake forms have alluded to…” They’re not standardized. They’re just directional.

So I start looking at this, and the patient comes in, and they’ve got all these things that look like dementia. So first of all, dementia. They’re losing function for memory, and the capacity to do life. What kind is it? Which areas of the brain are there? This module takes the regional index index form, and then starts putting it into progressive patterns, so that you can watch it degenerate and say, “That degenerative pattern is related to this disease.” And then you can say, “This disease is related to this neurochemical issue. And here are some phytochemicals or some nutrients that help with that cellular process.” By the way, the cellular process is different in some diseases than the other. So it’s actually important that you identify the disease.


Because you don’t want to deal with one process when you actually have another. Just kind of trying to show you the forms.

Now, right here: IgM positivity Epstein-Barr. So with IgG positivity, there’s IgM positivity. You have to start thinking this: What if there’s inflammation from infection. In other words, why? What are some of the things perpetuating this? I like to ask sometimes: is there an infectious disease present? Because a lot of people don’t. They just assume: “There’s no infectious disease present. They don’t have a fever.” That doesn’t always mean anything. Okay? So I sometimes like to say: is there an infectious disease that might need to be dealt with so that there’s not an inflammatory process, and the inflammatory process that’s crossing the blood-brain barrier is constantly telling the hippocampus this: “Die!” That’s not cool, if I’m trying to rehabilitate neurological tissue. Does everybody understand the simple concept? If there’s something destroying tissue, please stop that process if you can. You have to get that at this point in time. Okay.

Now, her glucose, February twenty-third, was at 94. This is perfectly fasting. Now it’s gone up to 105. Okay, is there diabetes in this patient? Now yeah, I’m going to start talking about some metabolic stuff. It’s time. It’s not really considered diabetes until it’s really fasting over 128. So it’s 105. But is it normal? No. Is it becoming?

Remember, labs are this: It’s a hundred-meter dash. Whenever something gets way over the lab absolute range, you’ve crossed the finish line. Everybody knows the race is over; you can see it; it’s right there in front of you. But if you catch something on the twenty-yard line, the thirty-yard line, or the forty-yard line, there’s something you can do about it to stop it so that it is not one of the many factors that’s going around and beating up the hippocampus, stopping your beautiful work as a functional neurological practitioner. Okay? Some of you this resonates with better than others because of what you do. Some of you are, like, uncomfortable with this, because, “I don’t run labs,” or, “I don’t know any of this stuff.” That’s fine, man. Just relax and learn.

So when you look at this, the hemoglobin A1C is at 5.6. Not crazy, but maybe it’s starting to climb up a little bit, and what we have to say is this: This hasn’t been around very long. We know it hasn’t, because back, you know, a year ago, her blood sugar looked pretty good. A year later it’s starting to climb up a little bit. The A1C is not popping a little bit above the optimum range, but it’s still not high enough – like, it’s 6.4 – to become diabetic. So you have to look at this patient and say, “You’re trending toward blood sugar problems, and you’re trending towards diabetes. We need to trend you away from that so that we can protect your brain from becoming pathological.” I’m going to show you some papers about what insulin and blood sugar does to deteriorate the brain. Or degenerate it.

We come down here, and now we have sodium and potassium. Potassium is not exactly what I would call stellar. It’s not outside of the – if you look at this right here – it’s not outside of the actual lab range, but it’s not exactly what I would call optimal. Now, sometimes with stress, the sodium and the potassium ratios will start to skew or strange. Sometimes with renal disease it’ll start to skew or change. But remember how I told you that cortisol will decimate the hippocampus? When I started seeing some of these ratios that are abnormal, I may go back and do a cortisol test, or an adrenal stress index, and say, “Is there any stress going on that is now going to beat up the hippocampus?”


So now you have to picture this: The hippocampus is the center of the fight, and there’s eight people trying to beat the hippocampus up. I’ve already found blood sugar as one. I’ve already found maybe some electrolyte changes. As we go down a little bit further, we see this right here: We see, look: the anion gap went from 14 to 21. The person’s now becoming functionally acidic, and nothing works well, for the most part, in an acidic environment, that you want, if it means net improvement in brain function. I will tell you this: When sodium and your anion gap and potassium are not correct, your brain doesn’t fire appropriately. Because what makes all of those electrical synapses fire? Appropriate electrolyte balance, sodium activity, sodium conductance, potassium conductance, pH. All of these things are very important. So now I look at this; I’m like, “Man, the anion gap isn’t that great. CO2 isn’t that great. Potassium and sodium are fluctuating out of balance.” And you’ve got to go through and say, “Mm. The kidneys look like they might have been a little bit stressed, but not too bad. Kidney function got a little bit better. GFR’s still over – at 77 is pretty good.

So now you’re starting to put together this thing of, “Can I even get a brain to fire?” because there’s enough electrolytes, and because the pH is good enough, and is the blood sugar balance out the right way, or are they hyper- or hypoglycemic, which is going to screw everything up? So I’m starting to show you the integrated approach to this case.

So, could blood sugar or insulin impact the areas you just looked at on the intake forms? That’s the question you have to ask. Now, the resounding answer, based upon the literature, is one hundred percent “yes.” So as a neurological practitioner, or somebody that’s trying to increase brain function, why in the world would you not look? It’s a simple lab. As a matter of fact, it’s called a routine lab. Meaning, on just a yearly, you know, physical. People get it routinely. And all of a sudden you start saying, “Wait a minute. This person’s blood sugar, like, became, in a year, unstable. They’re not diabetic, but they’re on the thirty-yard line. I think I want to do something.”

This is nutritionally and dietarily correctable at this point. In fact, most practitioners in the medical world will say this. And I can say this because I’m in the medical world. “We’re not going to medicate you for this right now. We’re just going to sit back and watch. And while you’re sitting back and watching, you know what happens? Her hippocampus just goes pfft, pfft. A little bit down each time, and you can just watch it go downhill. And what Dr. Kharrazian said a minute ago is a hundred percent true: The more cells you lose, the less luck you have at fixing it. Or, sorry, helping it.

So let’s keep going.

Could adrenal function, electrolytes, anion gap, along with acidity, impact this patient? Yeah. Are we going to go through a lot of these lab things in the future? Yes. Am I giving you a preview, like I said? Yep.

Ah. Well, look at this: ferratin of 100. Now, that’s definitely not low. Ferratin is stored iron. But you have to start looking at ferratin as: is it trending upwards? Like an acute-phase reactant? So in other words, I may have an infection, and does infection lead to inflammation? And if I have an acute-phase reactant that looks like inflammation, can that perpetuate the damage that I’m looking at on my intake form?

And then you go down, and look at this. Look at all of the lipids. You see this? The triglycerides are off, the HDL’s not right. The HDL’s up a little bit. So you start looking at this, and you start going, “Wait a minute. If my lipids aren’t right, and I’ve got an acute-phase reactant, and I’ve got inflammation, and I’ve got stress


hormones, and I’ve got other things going on, maybe there’s some small vessel disease developing, in association with the stress hormones, and association with the blood sugar problems.” It’s all equaling this, ladies and gentlemen. There’s not enough fuel for delivery, and there’s too much inflammation for cells to sustain health. And the person is now starting to become unwound. And if you don’t catch it early, you’re going to catch it later when the person doesn’t even know where they’re at, and they then have to be, like, put in a short-term or long-term care facility. You following? Okay.

We come down here: Homocysteine is at 10.3, vitamin D’s at 37. So look: Homocysteine above 10 is really something that needs to be dealt with. Now, some lab companies will tell you 15 is the absolute upper limit; some will tell you 7 is the absolute upper limit. But they are starting to trend down the absolute upper limit. We know that if it’s above 10, this is not so great. So now look: The person has high homocysteine. It’s like a ninja running through the blood vessels and slicing walls in the endothelial lining.

Then you’ve got all this cholesterol that’s impacting itself into the wall lining. And then you’ve got these inflammatory markers that are causing these things to turn into foam cells. You’re sitting there going, “Wait a minute. Are they getting small vessel disease on top of this?” This is a very important issue for you, because they may need something to de-inflame them, and they may need something to control their homocysteine, because homocysteine also creates inflammation, cellular damage, and there’s some literature that shows that it goes straight to the brain and just creates… it wreaks havoc. A1C and homocysteine are not friends to a brain that is trying to not degenerate. I want you to understand that. Like, I literally would say this: Everybody that has a neurodegenerative disease, you need to check those values. And an acute-phase reactant is this: Let me translate it for you. It’s like a marker that shows that maybe there’s an inflammatory process going on.

Macrophages just love iron, so when there’s some sort of process where you need macrophages, sometimes your need for consumption of certain types of elements go up. So, what does iron and cholesterol have to do with this case? Told you: Maybe it’s not depletion; maybe it’s showing inflammation. Why is homocysteine so important? Maybe it’s showing small vessel disease. Homocysteine, lowering by certain types of B vitamins, slows the rate of accelerated brain atrophy and mild cognitive impairment.

Now listen to this: An RCT study – that means it probably has a higher grade criteria and quality. So I thought to myself, “You know what? I don’t want to just say this. Let’s throw some papers up every now and then.” We gave you over a hundred and fifty references in your notes. Wow. So I’m like this: “We’ve got to get homocysteine down. Whatever the case, however we have to do it.” Now, we could sit here and talk about homocysteine all weekend long. That’s not the goal. The goal is just to get you to realize this: Homocysteine can be a problem with the brain. So let’s talk about it.

So we go a little bit further. White blood cells are up. What is going on with the person’s size of their red blood cells? Right here. I like looking at MCV. The cells are getting bigger. Homocysteine’s going up. When you start seeing things like that, you have to say, “Are they really absorbing B vitamins? Do they have gastritis? Do they have low stomach acid? Do they have intrinsic factor antibodies? Is there a pernicious anemia going on or developing?” Because if that’s the case, guys, and you can’t get B vitamins in the system, the brain’s going to deteriorate even faster on top of the homocysteine dysregulation.


So I’m showing you all these things. I’m like, “Wow.” I’m leading this up to Sunday afternoon, showing you all the problems, and then Sunday I’ll show you all the things we did to fix some of these lab findings.

Okay. So infection, anemia, inflammation. All of these things that are starting to pop up, we have to make something out of them, even if there’s just early signs. Even if they’re just early signs. Because here’s some literature that says this: Depletion of oxygen can change cognitive function. Depletion of glucose, or changes in glucose, can change cognitive function. All of the inability to make energy can have consequences. And look at this: potassium, sodium, calcium – all my electrolytes – can create cognitive dysfunction. So now you start going through the literature, and you’re like, “Why in the world would I not look at it, if the literature says that I need to?” And let’s put it all together into one package, and not just become an expert at one thing, but if it’s an eight-headed beast, let’s cut off all heads. Because if we don’t, then I’m going to activate a brain. And I hope that my activation is greater than the deterioration that’s caused by the other comorbidities. Alright.

These are just some of the raw labs. But look down here. That’s, again, 105. This, now, the reason why I showed you this, without looking at some of the functional values, this is what it looks like to the standard doctor. “Looks pretty good!” “That’s not so great; we’re just going to watch it.” Know what you just missed? The entire race until you get to the finish line. That is my point right now. I don’t diagnose people off func-tional values, but I look at a trend based upon functional values. I diagnose what’s going on when they’ve crossed the absolute lab limits. So I don’t want you to misinterpret what I’m telling you. I wanted to show you this because when we broke down the data and looked at it very carefully, it shows that there’s some trends that are not cool. When you look at just the regular labs, you’re like, “It’s not so bad. That MCV at 95, even though it’s way, way, way away from 79, it’s almost a 97, it doesn’t mean anything until it gets to 97.1. It’s completely harmless.” But what that’s really saying is, it’s getting close to being a problem. You should pay attention.

Well, we know that there’s metabolic syndrome developing. We know there’s some insulin resistance. The C-peptide is high on this patient. We know they’re in acidosis. We know they probably have some atherosclerosis occurring. We know that there’s an anemia where the cells are getting bigger. They don’t have the B vitamins that they need. Do you see any possible trends in this case that need to be corrected for optimal function? You want optimal function so that when you activate that brain, it says, “Yes, I can be summated, I can synaptically connect, I can make brain-derived neurotrophic factors, and I can actually create plasticity, and we can see a difference.” If you don’t correct those things, it says, “I can’t do what you’re me to do with stimulation.” Here’s why: All of the things that you never looked at on your labs.

We have a couple of years of this. To learn labs, and to say: okay, we’re going to break it down real slow, and here’s an anemia. And then break it down real slow and say: here’s a blood sugar issue. And then break it down real slow and say: here’s a thyroid issue. Right now, I need you to understand: I’m giving you a preview of what it’s going to take to go into the world of neurodegenerative diseases. Dr. Kharrazian reviewed what we have looked at. I am previewing where we’re going. Okay.

Well, let’s just… Now we can look at the trends: 99, 104, 105 for blood sugar; A1C went from 5.5 to 5.6; C-peptide went from 1.80… it’s functionally up but it’s not up real high. It’s not up around 4, it’s not up around 5. By the way, I don’t expect you to know all these norms. I’m just talking through this right now. Down here, not so bad here. Right here the person was at 17, now they’re at 21. They’re becoming more


and more and more functionally acidic. Here’s what we found in some of the research at our facility: The people with the most acidic anion gaps healed the slowest with head injury. That’s what the data’s starting to show.

Look at this down here. We’re starting to see ferratin change. What’s getting worse in this case? Everything that I don’t want to get worse. Hmm, look at this up here. Lipids are not getting any better. Lipids do matter, especially in the right environment. That thyroid, I’m not too worried about that right there. 1.23 is actually… I’m okay with that. We come over here; the white blood cells are up. Red blood cells are up. Not bleeding. The person is starting to trend towards a macrocytic presentation with high homocysteine, and they’re getting older, their brain is going down, their vagal output isn’t that good. That is high tide for hypochlorhydria, meaning you just don’t absorb what you need. You have to have B vitamins, ladies and gentlemen, to have a good brain. You have to. You have to, have to, have to. If you can’t get them in, you have to figure out a way to get them in somehow. This is a real patient. And they’re like, “I need answers.” You’re like, “Let’s look. Let’s find them.”

You go down here. Lymphocytes are low, neutrophils are up, but the white blood cells are normal. This is probably not bacterial infection. This is probably just signs of inflammation.

Okay, now look. This is called a mini mental status evaluation or examination. I want you to understand something. This is not the best scale for Alzheimer’s disease, or dementia. This is just a simple thing that says this: How intact is your mental status? And I can get the same person to do it. It’s reproducible, and it’s usable. You can go online, you can get rights for the forms, you can do it the right way. I need you to look at something. Look at what she scored. A sixteen out of thirty on day one. Guys, this is straight up hippocampus frontal systems. I mean, it really is. And some temporal. Look at all of the zeros out of two that she’s getting up here. She didn’t know what county we were in. She didn’t know what day of the week it was. She didn’t know what month it was, or the season. She missed the month the first time she did it. Those are… That’s not good. Last but not least, look at the handwriting. Look at the ability to look at geometric shapes and reproduce them. Zero.

Now, this right here, out of a scale from, you know, zero to seven, or one to seven, this person is starting to become right around the three, four, to five mark. They’re right in the middle. Once they scoot past that, it becomes… They’re at the brink of me saying this: “I don’t know what I can do for you.” Right now, they’re in a situation where I’m like this: “I think I can do some stuff to help you.” So I’m learning my limitations. That’s hard to teach, because everybody’s limitations are a little bit different, depending on what you learn. I will promise you one thing: You will never regret getting good enough at this to be able to say, “You know what? I can help this person,” or, “I can’t help that person,” and, “The people that I do help, it makes a dramatic difference in their life.” It’s worth sticking around and doing it, and learning it, and getting that good. I will promise you, it is the one thing that makes you want to get up in the morning and go do your job. Okay?

This is halfway through treatment right here. Twenty-five out of thirty. Now, how did I treat her? I treated her metabol… I’m not telling you how I treated her yet. But I’m going to tell you: I addressed every one of those labs, with nutrition. I can’t give you that until Dr. Kharrazian does his part. I treated all of those brain regions with functional neurology. I can’t tell you that until I go through my part, on the neuro rehab. But when I go through it, you’re going to start saying, “Aha, I would have done this.” Or, “Bam! I would have


added that.” That’s what I need you… I need you to keep that context all weekend long, as we’re doing this, okay?

So, as you go back up here, look. Starting to score some ones out of twos instead of all zeros. Now, we did it the same time of the day, with all the same things in her body. I mean, I’m not going to do this at midnight, after she’s been going all day. It’s not fair. So we did it the same time every day, repeatedly, under the same factors and the same conditions, so that we have less external forces creating fatigability, where there’s no way we can have reproducibility. Does that make sense?

Now, here’ s her final exit. We got her up to a twenty-seven. Some of you, at the end of the day, might not even score a twenty-seven. I’m joking. You probably would. But look Can she draw the shapes now? Better. What’s interesting is, she drew it on the other side. She hit ones on at least every single question. That means that every part of the brain that we hit, improved. It’s pretty cool. You can take this and break it down, and correlate it to your regional intake… your brain index intake form, and you can just correlate this test with all those findings, and go, “I need to hit that area, that area, and that area with my treatment.” And when I show you how we start stacking the treatment, we will activate one area, and we’ll combine it with another treatment from another area, and then another area, and then bring all those together at the same time, and it makes all those regions light up together. That’s where it gets fun. I’ve got to be honest with you.

So, you look at this person, and you’re like… Look, this is not “do you feel better or not,” this is “you performed better on a test that’s been standardized and made to use in a clinic.” It’s hard to fake this, unless you just duff it. And believe me, people with dementia, they are… in the early signs of it, they’re embarrassed about it anyway, so they’re… trust me, nobody duffs these tests usually. They try their hardest, because they don’t want to look sick. The person doubled their score.

Now, let me ask you a question. Let’s say I activated this brain, and I did nothing metabolically on this patient, and they go home. What do you think is going to happen? Well, I can tell you what’s going to happen, because we’ve done it. They go just like this. Rrrrrwww. But when we help them out metaboli-cally, and they do exercises at home, and they come in the clinic, and they get two-hour sessions every couple of weeks, we now have some people up to six months that have not degenerated or gone downhill any more. They’ve stayed at the same score. Alzheimer’s disease alone, by the year 2022, 2025, will cost more to treat than what the entire United States is taking in in taxes. Potentially. And there’s not a lot of good stuff out there, really treating it. What I’m telling you is, I think a functional practitioner has a huge place in the treatment of somebody that has a neurodegenerative illness, so that it stops or slows down the degeneration, so they’re functional for a longer period of time. If this woman becomes dysfunctional, completely disabled, in her fifties, she might live to where she’s eighty. That’s thirty years of taking care of her where she cannot contribute to society, but society has to take care of her. Do you see the monetary… That’s decimating on the economy. It’s not just health care costs, it’s a lack of productivity cost. It’s worth it to learn it.

Okay, look at this. Now, I just want to tell you something real quick. These vertical eye movements right here, I’m going to show you what a lot of these tracings mean, but I’m just giving you some… a little bit of a preview. This green line represents the target just moving up and down and up and down. And one of the very areas to go in early degeneration is the midbrain and the ability to move the eyes up and down. The


mesencephalon projects to the frontal lobe to keep it alive. Look at this. She has lost that ability completely. Completely. But she can stand still. She’s not falling over yet, thank God. The top is when she came in. So this is doing this: limits of stability, leaning over, and hitting certain boxes. The top is when she came in, the bottom is when she left. So she did improve in limits of stability a little bit, and got a little bit better. I just wanted you to see that.

Now, here’s a video of her. So I’m like, “Look, I like videos, because I want to see how you’re doing.” This is her two weeks after care, and doing what she does. Now I want you to understand something real quick. She hasn’t driven, she couldn’t tell time, she was losing words, and was starting to forget the names of people around her. I need you to understand that. I want to recap that real quick. Okay? The reason why I show videos like this is because this is a real person, a real patient. It’s not fabricated. This is after the fact, not before the fact where I did some cool little trick and all of a sudden function increased for a few minutes and then it goes away. This is her – actually more than two weeks; this is a month since she left. Everybody catch that? Okay. Do we have volume? Uh-oh.

What’s your name? “Laura Slater.” Well, Laura, what are you doing right now? “I’m going down the road.” Yeah, well, you’re driving all right. Now, keep it between the margins. We went to Cerebrum Health Center back in February for two weeks. How do you feel since you got back? “Great. Really.” Okay, what’s the difference? What do you think? Are you more confident? “I think so.” How’s your speech. Is it better than it was? “My speech is better.” Okay. Do you like your husband better now than you did then? “Not really.” Ooh, I’ll ask that. I’ll have to scratch that one. “I was liking it.” Okay. Let’s see. How about the people there? How did they treat you?

Okay, who cares how the people treated her? Look, what I want you to understand is this: She was joking, she could respond, she could make eye contact, and she was driving. Now, I can understand, and I can relate to this a little bit. We’ve got just a few more minutes to discuss this. I’ve got a teenager that’s learning how to drive. Every time I get in the car, I’m like, “This could be my last trip. Could be it.” I mean, he gave her back the keys. You understand what that means? “I can remember my way back to the grocery store, I can go get some things, and have some autonomy.” In other words, it’s called dignity. When you give somebody back function, you give them back their dignity. When you give them back their dignity, you have just changed their life a little bit. And even if it’s for a year or two, that’s one-seventieth or –sixtieth of their life. It’s invaluable.

So, we know that the part of the brain is the frontal system, because of a damaged hippocampal system, and the patient is trending towards dysglycemia, and dyslipidemia, and acidity, and bad, bad, bad red blood cell function, because of B vitamin and homocysteine changes. And maybe there’s an infection that we need to deal with at some point in time. Did you see how I kind of gave you a metabolic blueprint? None of that is really difficult to find. I’m going to show you a video of this person Sunday, where the whole thing is testimonialed. And we’re like the eighth doctor that they’ve been to, and they were angry because nobody sat down and said this. They all said this, “Yeah, you have dementia.” In other words, “You’ve crossed the finish line. Congratulations. Now see you later.” How does that make you different, to be able to say that? Everybody can say that. We’re not trying to be naïve and foolish by saying we’re going to cure you. We’re just like this: “Hey, you know what? Maybe we should try to enhance your function a little bit, okay?” If you become a slow runner, everybody can say, “Man, you’re a slow runner.” Why doesn’t somebody try to make you a little faster? If it’s bothering you?


So you guys know which areas of the brain that you’re not too worried about: back. You know you’re worried about the front. You know you’re worried about left and right. This is not a hemisphericity, this is global degeneration. There’s a genetic component to this mixed with a lot of other comorbidities. A comorbidity means this: it’s something else you have going on at the same time as your condition. Do you think this type of patient needs care by a functional provider? That’s the ultimate question. Do you have any business? And I’m not asking an association right now, I’m asking you as a provider. Of course you do. Please, if I ever get like this, take me to one of you, before I forget where the hell I’m at, which is probably not too far away. But what I’m saying is this: I don’t want to just be told, yeah, I’m sick. I want somebody to say, “Yes, you’re sick, now let’s do something.”

I need you to look at this. This is her MRI. She has advanced Alzheimer’s disease. Cingulate system cortices frontal, hypometabolism in the left superolateral temporal region. So this right here goes through. It’s in your notes. It shows every area that’s starting to break down a little bit. They labeled her as having advanced Alzheimer’s disease with asymmetric left frontal and contiguous left… even back to the occipital region is actually involved. A Lewy body variant of Alzeimer’s disease may be present. I’ll go through the differences later on, and show you this. But what I want you to understand is this: She was structurally there. You see the video of her driving? That video does not match this imaging any more.

So, just to summarize here: We know the lobe, we know which pathway’s involved. Not too much there. We know the midbrain has to be activated. I’m going to show you that when we start going through treat-ments. And we know that there’s cellular fatigue. We have to go through that, and we’ll show you that this weekend. We know that the brain is just dying; it’s becoming excitotoxic probably. And we know that there may be a little bit of autonomics involved, but some of that might just be anxiety, because there’s no frontal system. And we know that the motor system is not that involved yet, but there’s a little bit, and the language is involved, and it’s not a comprehensive issue; it’s not an expressive issue; it’s a word-finding issue. And then right here, this is that… Look, this is that giant frontal chart that scares everybody to death. But it’s real simple just to say this: Prefrontal, anterior cingulate, dorsolateral, more involved than anything else. And there’s all the things. She’s starting to get short-term memory loss in the hippocampus. Working memory is not as bad. Declarative memory is getting a little bit worse. There’s no procedural memory.

This is going to now lead us into what Dr. Kharrazian is going to start talking about in a little bit, and that is this: What are the early signs? What are the cellular mechanisms? And then I’m going to go into: What is the differential diagnosis? How do I take all that and put it together and show you how to say, “Is it one versus the other?” And look: She had a peripheral infection. She had all this inflammation going on. She had all the things that were making progressive cognitive dysfunction, and as we go through this, she was sliding downhill, and she’s going to become sick with Alzheimer’s disease.

Hyperinsulinemia, blood sugar, mitochondria dysfunction, all of these things that we’re getting ready to talk about. Look at this: insulin over here binds with some of the amyloid plaques, and it doesn’t allow them to degrade, and you get Alzheimer’s disease. So if you have type 2 diabetes that’s insulin resistant, it screws it up. Or, if you have type 2 diabetes where there’s insulin deficiency, it screws it up. Either one. Blood sugar has to be perfect.

So, this is just sort of a preview of what’s going to be happening as we go through this. The one big thing she had that I didn’t tell you is this: She went through menopause; her estrogen sank to nothing, and she


became demented within a month. Estrogen is extremely, extremely, extremely, extremely neuroprotective. Well, hey. We corrected it. Testosterone reduced neural secretion of Alzheimer beta-amyloid peptides.

So on Sunday we’re going to review the case again. And between now and then I want you to think about this wonderful lady, and I want you to think about what you are going to do. I’m going to go through the medications. We’re going to go through the neurological treatments. We’re going to go through the cellular mechanisms. We’re going to take you through it, and it’s part of your learning process.

Buckle up; it’s going to be a fun, fun journey. Do we have a break? Thirty-minute break. We’ll be back.

FunctionalNeurologySeminars.com Courses.FunctionalNeurologySeminars.com

https://functionalneurologyseminars.com

http://courses.functionalneurologyseminars.com

identifying the most common neurodegenerative diseases and ... · so, we always start with the...

Documents