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MODULE tHREE tRANSCRIPt: IDENtIFYING EARLY NEURODEGENERAtION | © 2016 FUNCtIONAL NEUROLOGY SEMINARS LP | PAGE 1

IdentIfyIng the Most CoMMon neurodegeneratIve dIseases and ClInICal applICatIons (Module three) transcript – Identifying early neurodegeneration

presentation by dr. datis Kharrazian

Okay, so we’re going to get into identifying early neurodegeneration. Now, in the previous section, we talked about facial paresis, and one of the things that some people have commented on is that there’s… what about soft pyramidal signs. Soft pyramidal signs are really an area where there’s a lot of confusion. So there’s people that have made this claim that the cortex fires to the pontine medullar area, inhibits anterior muscles above T6 and posterior below T6. That information is all wrong. That information is completely inaccurate, okay? The reason people have stroke-related patterns is because they’re usually in flexor tone most of the time, or sensor tone, and when they actually lost corticospinal integration to the anterior horn, there is where they have the greater motor units, and [?] cause those flexion patterns in their arms, and extension patterns. It’s nothing to do with the pontine medullary anterior spinal, pontine medullary above T6 – below T6 models. And the reason you see signs on the opposite side is because of cross-cord reflexes.

So there’s a whole list of things we’re going to actually start putting out and listing, where there’s a lot of misguided information, and this is why, when we present material to you in our courses, we have lots of references and the materials are all there for you. Okay? And we have a great collection of papers for this module, for all these various pathways, and we have a great selection of papers in your notes for identifying early neurodegeneration.

So, just to expand about what we were going through this morning, and to kind of give you the big picture of where we’re at, these are the topics we have organized this weekend. So, today, day one, our critical goal is to make sure you guys know how to assess neurodegenerative diseases. So we’re going to go into identifying early neurodegeneration, particularly in three divisions. Is it a cognitive memory dementia pattern? Is it a Parkinsonian movement, slowness degenerative pattern? Or is it a cerebellar pattern? And then there’s some variations between, but those are the major ones. And then Dr. Brock is going to go on, and he’s going to go into the differential diagnosis. What kind of dementia is it? What kind of Parkinsonism is it? What’s involved with the cerebellar disease? What kind of cerebellar disease is it? And then at the end of the day, I’m going to go into the cellular mechanisms. What are tau proteins? What are Lewy bodies?


Right? What’s this concept of autophagy? What’s this concept of protein misfolding? What are protein aggregate disorders? How do they work? What are mechanisms of how we have neuroprotection?

So by the end of today, you should be able to have a really good idea of identifying the concepts with neurodegenerative diseases. And then tomorrow, we’re going to go into nutritional principles. So we’re going to go, “Hey, here’s all the cellular mechanisms of neurodegeneration; here’s all the research; and here’s how you apply each of these things clinically, from a single nutrient model to a functional system… functional medicine system biology model, how they all integrate. And there’s some strategies you can use, and Dr. Brock is going to go into rehab for every single region of the brain involved with neurodegeneration, and talk about thinks you can do to activate those areas. And then we’re going to go into pharmacology, and then you can understand which drugs have an impact, and which ones do, which ones really don’t. We’ll review those with you. Which ones can cause changes in your examination findings, and then trying to see the big picture of how it all relates together.

And then we’ll end with case… we’ll show you case videos and do it throughout the course, but we’ll show you some reviews of putting all these concepts together on Sunday. But that’s the process. So today, if you can just focus on just identifying it, understanding it, and then tomorrow we’ll really focus on treatment. Okay?

Now, the key thing is to identify neurodegenerative diseases, is what we’re going to start with, and there’s key principles that I want to really go through with you. First of all, you want to make sure you understand the clinical difference between general neurodegeneration and neurodegenerative disease. So all of us are going to have, over time, some areas of our brain that are going to have some degree of neurodegeneration. And usually it’ll be the areas of our brain that have less plasticity. So if you grew up in your life, and you had some areas where you just… or some areas of your function in which you were deficient in… Maybe you were discoordinated when you were a kid, and you kind of grew out of it; maybe you were really bad with numbers and math, and kind of grew out of it, or then you kind of avoided it. The areas of your life that you haven’t developed as much plasticity in your brain are the areas that are going to first show up as you get older and neurodegenerated. So if someone had, like, a tic disorder when they were a kid, as they grow up, as the brain degenerates, they may have some of those things come back. If someone was really uncoordinated and had bad movements and sloppy coordination, as they degenerate and have systemic brain inflammation, those are the areas that are more likely going to present first.

So those are kind of neurodegenerative changes, but they’re not neurodegenerative diseases. And the reason why it’s so important is because if it’s neurodegenerative changes, your prognosis and your ability to change it is much different than if it’s a neurodegenerative disease. Because with a neurodegenerative disease, you have a cellular mechanism of protein misfolding and protein aggregation and accumulation that is progressive and uncurable, and it changes the entire spectrum of what you’re looking at. So you have to understand that there’s those two clinical differences. And I think a lot of people that get into functional neurology exams, they really don’t. And this is something we really want to make sure you’re clear with.

We want to then go into… What I want to go into next, is understand the common clinical presentations of both neurodegenerative changes and neurodegenerative diseases. How do they present? So you know how to pick them up.


And then I want to go into the earliest symptoms of Parkinsonism, and dementia, and cerebellar disease, and then we’re going to go into the earliest symptoms for each brain region. We have some nice forms for you.

I’ll just have this backup in case… Thank you. Alright.

So, in the first module, we talked about the difference between the pathological lesion and a functional lesion. So let me be honest with you. Here’s what’s going to happen: You’re going to identify people that have early brain degenerative changes, and they’re going to go see a neurologist, and they’re going to be told that they’re fine. Because there’s a standard of… It should be normal for you to become more unbal-anced, lose your memory, lose your cognition, lose your focus and concentration, as you get older, but there’s no more clear understanding of timeline what that is. So if you don’t really understand neurology, which most people don’t, and if you’re only trained to look at end-stage disease, what you’ll see is, when people walk into the conventional model, even though they’re having neurodegenerative changes in symptoms, they usually will come out with normal exam findings, and that’s a problem. Because that’s really the only opportunity they have to really make some diet and lifestyle changes, do some brain exercises, to change those findings.

There will be clear examination findings. People will have ataxia. People will have lack of arm swing. People will have hyporeflexia. People will have abnormal eye movements. The examination findings are all there, but there’s not enough degree of symptoms to promote it, so they can be dismissed. So someone can say, “My memory and focus and concentration have completely declined, I can’t remember anything. If I read something, I can’t follow through with it.” And they go, “Well, let’s have you follow and draw a clock test, and do a mini mental status exam. Oh, you’re fine.” They know they’re not, and then every year they get worse and worse. Well, they just lost the opportunity to help this patient get some direction, potentially to impact their progressive dementia that may be taking place, right? And you’ve got to understand that in a conventional health care model today, the way it works for Parkinson’s, unless you have tremor, you’re probably not going to get diagnosed. Which is the end-stage pattern of Parkinsonism. So there’s going to be this level of reality you need to understand is, there’s going to be a little bit of disconnect of neurodegenerative diseases, and early neurodegeneration, and communication between a preventative model and a disease end-stage model. Okay?

Just be cool with it, and you know it’s there, and then you work with them. You let your patient know, like, “You really don’t have clear Parkinsonian pattern, but you have all the early signs,” “Here’s what all the early signs are, here’s what they are, we want to monitor them,” “You have all the symptoms of early dementia,” “Here’s the American Alzheimer’s Disease Association scale; you’re right on it here,” “Here’s the American Parkinson’s Association Early Symptoms, here’s what they are, you have them.” And then you’ll see that they’ll still be frustrated because they may have some time to get really diagnosed. Okay?

Now, your opportunity to help them in our model, in functional neurology model, you do things to improve their brain function, do rehabilitation through plasticity, through nutrition, through diet, through lifestyle, even pharmacology if necessary; whatever the factors are, to improve function of their brain. If neurodegenerative diseases happen we can identify them early. Okay?


So what you see here is, we talked about the difference between a pathological versus a functional, let’s say, lesion, or a functional impairment of some kind is, for the most part, pathology there’s abnormal electrodiagnostic imaging findings. So you do an MRI, and go, “Oh yeah, you actually have volume change. It really shows some atrophy.” Or, you have someone who’s got impairments, and then they do some testing, and everything’s off in the examinations and symptoms and history, but their MRIs could be normal. So in the early stages, you’re going to have people that have clear history findings of brain degeneration, clear examination findings of brain degeneration, but they may not have imaging findings yet, right? Or elec-trodiagnostic studies yet. And that’s your opportunity to really have the biggest impact. As they progress, those things happen. You can monitor them, and work with them, but just be aware of that.

So, we get functional versus pathological. So if you have normal neuroimaging, early diagnostic studies, you could have early neurodegenerative changes, or you could have integration disorder, our focus is on early neurodegeneration. Now, one key thing again: Neurodegeneration versus neurodegenerative disease. Neurodegeneration is loss of neurons or loss of connectivity in generalized or specific regions of the brain. Those have good prognosis. Neurodegenerative disease, there’s buildups of things like tau proteins, you’ve got amyloid plaque, alpha-synuclein Lewy bodies, leads to progressive changes in the brain. So as soon as you identify any loss or deficit in a person, your next question to really think about is, do they have a neurodegenerative disease?

The three main neurodegenerative diseases you have to own – okay? – by the end of today is, your dementias, your Parkinsonian patterns, and your cerebellar patterns. If you have those down, you’ll cover the majority of neurodegenerative diseases you’ll see in a real clinical setting.

So, take a look at this image. Do you see any type of neurodegeneration here? So you can look at a healthy brain, you can see that the gyri and sulci are tight, but then you can see atrophy in spaces between the grooves. That’s a degenerative change. And it’s systemic, it’s going through the whole thing, and that’s a neurodegenerative type of disease. With things like Alzheimer’s, you actually have the brain atrophy; things like Parkinson’s, you actually start to have clear degenerative changes that are also predictable over time with people that have the disease process. But then you have people that don’t fit those patterns. Right? So, you look at their brain specimen like this, what do you see here? You see degenerative change, right? But what about here? No. So this is the selective degeneration in one area of the brain. It’s not this global degenerative disease. So there’s people that have degenerative changes, and there’s people that have degenerative diseases. Okay? And you need to know which category you’re dealing with.

And same with this one here. This portion of the back is okay, this frontal area is a little bit compromised. So you can have specific areas of neurodegeneration. You see this cerebellum, you can see part of the cerebellum has some neurodegenerative changes. So that’s important to you.

Now, the reason, again, why it’s important to you if they have neurodegenerative disease is, first of all, your prognosis with them is going to completely change. The way you talk to them, the realistic expectations you have for them, the way you teach them how to follow their progression, is important, because it does become somewhat predictable. If someone actually has a Parkinson’s disease, you’re going to know how they’re potentially going to progress, because of the nature of the disease. If someone has Alzheimer’s dementia-type patterns, you probably know how they’re going to progress. If someone doesn’t have those changes, but has an area of the brain that’s just impaired from disuse or trauma or inflammatory changes


over time, that’s a different scenario. The prognosis is not as bad. So you want to make sure you’re clear with those types of findings.

Now, it’s really important for us to teach you how to get to there very quickly, so we made some teaching tools for you. So, in Module Two, we really wanted you to have this brain region localization form. The goal of the first two modules was for you to know your neuroanatomy, listen to the history, as soon as you’re done with the history be able to know where… what region of the brain is involved. So, for this module, we went in there and we put a form together where we went over the function, a picture of the region of the brain, the brain region localization form symptoms, and then exam findings, and then applications. So what I’m going to do is, I’m going to show you all the early signs of… clinical signs of Parkinsonisms, dementia, and cerebellar disease first, and then I’m going to show you region by region where the examination findings are. So I’m going to go through each region of the brain with you, and go over the examination findings that you might see, and then Dr. Brock, on Sunday, is going to go through and add this in with the applications.

We have to give you some internal notes you can hold on to and know you can count on and review, and that’s where it all is, because it helps you in the learning process. If the information’s scattered all over the place, it just makes you very inefficient. So we want you to have very efficient learning, so we have these forms, we have these things for you to do, and these two forms you have to memorize. You just have to know them cold. Know these two forms cold, know your clinical decision-making tree forward… clinical decision tree flow chart perfect, and know your flow chart of identifying neuron fatigue. If you know those two flow charts, and you have these forms down, and you just know the material very well, you have the structure to start playing this game.

Now, with subsequent modules, then we’ll go into the peripheral vestibular, or cerebellar, or basal ganglia. We will go to very, very deep levels of evaluation, analysis, treatment, but you’ve got to have the general structure first. Okay?

So, as we get into neurodegenerative diseases, let’s start with that. Because these are the ones that have the worst prognosis, these are the ones you’re going to see in your office, especially as people become elderly. And let’s start with the three main types.

So you have the dementias, the Parkinsonisms, and the cerebellar degenerations. One of the key things with these is that whether someone gets Parkinson’s or dementia or cerebellar degeneration, there tends to be some impact on the overall frequency of firing of the brain, and impact in areas like the frontal system. So they usually come in, many times, with generic symptoms of things like we talked about earlier: fatigue, depression, difficulty concentrating, poor brain endurance, focus, attention, working memory.

Your earliest sign of neurodegeneration is actually brain endurance issues. They just can’t do things as long. They can’t stand as long. What if they tell you that? They come in and go, “Hey, I can’t stand as long as I used to. I used to be able to work and just stand all day; now I can’t. Now my entire back goes into spasm and I just be unstable. I just have to sit down.” What are of their brain could be degenerating? That’s probably their cerebellum, spinocerebellar projections, vestibulospinal tract. That’s what they’re telling you, right? They’re not going to tell you they have cerebellar disease; they might tell you they have vertigo, or essential tremor. They’re just telling you they lost some endurance in that key brain pathway. Or if someone tells you that, “You know, my memory used to be fantastic; I could recall things, I would read something, know


it right away; now I’m having a hard time at work, have to write all these things down, I have to make all these little tricks I use to try to be efficient in my job.” They’re basically telling you their memory recall is inefficient. Or they can say even things like, “I’m okay the first part of the day, but the second part of the day I can’t remember anything. That’s a brain endurance issue. So you’re going to see with many pools of neurons, if they start to degenerate, they’re going to… you’re going to see endurance issues first. Okay?

With someone who’s got something like a Parkinsonian pattern, they just may notice their mind is slower. Their movement is slower, as the day goes on. They’re not as efficient. Their motility changes by the end of the day. You know. Those are key things. So be very conscious of the fact that endurance is one of the earliest presentations. Fatigue is a very common presentation. Depression is. And then go through your workup and try to identify any of these areas of the brain that are involved.

So, let’s talk about Parkinsonism. So, Parkinsonism generally means that the basal ganglia direct pathway is not working. You can have brain trauma-induced Parkinsonism that’s not neurodegenerative. So there’s a flow chart we made you in Module One, where it goes into Parkinsonism, and kind of talks about the different types, primary and secondary. The ones we’re concerned about in this module is Parkinsonism direct pathways involved, and we’re looking for a neurodegenerative disease process, meaning a protein buildup aggregation disorder in the brain.

Now, I know one of the things we said earlier is that the fact that we see a patient come in, and the initial survey, if they’re older, you want to really assess what the degree of their brain function health is, because just age alone is a factor in neurodegeneration. You need to make sure you remember that fact that ten percent of cases of Parkinsonism are young-onset, ages twenty to forty. So you could have a twenty-five-year-old or thirty-year-old come in, and actually have Parkinson’s disease. Okay? So don’t underestimate that. And then fifty percent of them develop dystonias and postural [stiffness], and tremor is less common. With the young-onset Parkinson’s, the most common thing with them is going to be rigidity and stiffness. So they’ll complain of a leg or an arm becoming really rigid or stiff, and then if you test them, they’ll be slower in that limb. You’ll see the hypokinesia. That’s your earliest sign, especially with young-onset. Okay?

And then the other key thing is, once you get past the age of sixty, ninety percent of people will start showing some signs of Parkinsonism. Once you get past age sixty, there’s a majority of people that start to show signs of dementia. I mean it’s… I’m sorry, once you get past this age, these rates go up. That’s not what I meant to say. What I meant to say is, as people get older, you have a higher rate of Parkinson’s dementia, but when you’re looking at Parkinsonisms, most of those cases are sixty years and older. So the fact they’re sixty and older, they have Parkinson’s, that’s the more common thing, but you see them in younger people.

There are some studies that show that as you get older, every decade of life, the prevalence of dementia is increased dramatically, and the same goes with Parkinson’s. This is a really good video clip, with volume that we need to make sure is okay here. From the World Parkinson Congress, giving you a perspective of what starts to happen the early stages of Parkinson’s.

What do you guys see? Tremor. And that could be a patient’s intake form. The other thing you might see in early Parkinson’s is micrographia. They’re trying to do toe tapping, and it usually starts on one side, so they’ll be slower; the hypokinetic movement on one side, whether it’s the hand or the feet. They’re losing dexterity. One of the things they start complaining about is it’s hard to button their shirt, do fine-motor


activity. Or, they might have writer’s cramp. Their swallowing gets impacted. They might feel like they have excess saliva in their mouth, because they’re not reflexively swallowing it. Most of them will start to notice that they’re not blinking as much. They’ll have… people might tell them they’re staring at them. You might see some of those blephera constrictions. And as they progress, they might start having some tremor as they do some activity. Tremor’s not the earliest symptom. Okay?

So all the things we talked about in the initial survey, all the things in the brain region localization form, they all become critical things for us to evaluate when we look at them.

Now, this is a chart that you have. And this is one that you need to make sure you own. Okay? So the earliest signs and symptoms of Parkinson’s, all the way to where you see Parkinson’s disease. So just to understand the landscape of health care, most physicians, most neurologists, are going to wait for a person to get to this stage: resting tremor, rigidity, even dementia, expressionless face, before they make that call. It’s too late for you to have the best impact with them. You need to catch it up here. Early signs. Loss of smell… and if you lose smell, what else do you… you also lose what? Taste and appetite.

Gastrointestinal constipation. But when you have cons… When you lose your gut motility, what else happens to your gut? So when you don’t move your food, what happens to your food? It ferments. So when it fer-ments, you get dysbiosis. You get yeast growth syndromes. You also lose the ability to make enzymes, right? So you get dysbiosis. Then you literally… and they might go online and have these digestive complaints, and go, “Oh my gosh, I have yeast overgrowth syndrome. I have dysbiosis.” And they walk in and see a health care professional, and they go, “Yeah, I have… You do have dysbiosis. You do have yeast overgrowth syndrome,” and they’re trying to treat their gastrointestinal disorder, and no one’s making a difference for them. Your chronic gastrointestinal patients, if they come into your office, chief complaint chronic GI, no one’s helped; whether they call it SIBO, or leaky gut, or dysbiosis, or yeast overgrowth syndrome, if you see them walk in, and they’re walking slow, and reduced arm swing, you see an expressionless face, you should completely change your approach. Because they really could have this protein buildup aggregate disorder causing their impairment in their gut motility, their contraction of muscles, controlling bowels, releasing enzymes becomes a key concern.

So a lot of your chronic Parkinson’s patients are going to come in; most of them are going to tell you that they’ve lost their sense of smell, but they might tell you they don’t enjoy going out to restaurants any more, or eating any more. A common thing to ask Parkinson’s patients : “When was the last time you had a great meal?” They can’t tell you. We’re talking early, before they even know they have it. They can’t taste it. There are certain senses they just don’t appreciate.

Then you might see the slowness of movements. That should be very obvious to you, especially if you have them do repeated testing, as we see that slowness pattern. And then depression would be another key symptom they complain with. And then postural instability. So as people develop Parkinsonian patterns, they have this characteristic pattern where they are moving forward, because they have a postural instabil-ity where they don’t have… They basically feel like they’re falling back, so they tend to reflexively move forward. Even in the ones that have these stooped postures, there’s nothing wrong with their spine. And it may start initially with an anterior head carriage, and then it starts to be their trunk, and they’ll come in with slowness. But their chief complaint is chronic GI issues. So you want to catch that.


Sleep disorder’s another common one. They don’t get into healthy REM sleep. Another key feature of early Parkinson’s is, they have sporadic myoclonic jerks and their limbs fling, so they’re… if they’re married, their partner won’t sleep with them any more. They’ll sleep in a different bed, because they’re getting whacked in the middle of the night all the time. So without having good sleep, their partners aren’t feeling safe around them, because they’re having excessive jerking movements in the middle of the night. Those are all clues to your early Parkinson’s patterns. Because at this stage, they may not have any visible, really clear visible signs of tremor to most people, but when you watch them, and you’re very critical of looking at them, you’ll find some early signs. Okay?

As they start to progress, their dexterity becomes impacted, so they may get writing cramps, they may get the micrographia, they might get some changes in their writing, their voice may become softer. And again, their voice becomes softer as you do the history with them, and as time goes on, you can see their intensity of their voice just soften up on you, which will happen early changes, because it’s an endurance issue initially. You see all this stuff as they get tired, okay? And then postural instability where again you see that posturing forward over type of response that continues to get worse.

Then eventually they get into tremor. So what you have to really want to… What you really want to be able to do is, you want to get in here and know how to identify these early symptoms. That’s your key thing. Okay? So let me give you some examples.

Patient comes in, and they tell you that they’re not sleeping well, they’re having a hard time sleeping, it’s… and they just have… they’re, “I’m having violent dreams, and I’m, like, all over the place so my wife won’t sleep with me any more.” And you see they have… they’re staring at you through the whole exam, and their movements are a little bit slow. That should be a person you should be concerned about early Parkinsonism pattern. You shouldn’t go in there and call them Parkinson’s disease; you shouldn’t give them the diagnosis of Parkinson’s disease, but you should be considering that that possibility may exist.

Another person can come in, and like I said earlier, they may have chronic gut issues, and they have slow-ness, and they have a little bit of expressionless face, and that’s about it. But not one’s been ever able to make a difference for their gut. And you listen to their gut sounds, their motility’s impaired, they don’t have a good vagal response. You do repeated testing, maybe it’s fine, and then it just starts to slow down. But it’s really early, so you see endurance signs first. So those are the patterns you really want to be looking for.

Okay. Now, a lot of times, you’ll just be able to tell things from gait. So I think a lot of people that were at the workshop could definitely see gait imbalances very well, after really spending some time focusing on it. So let’s go through some of these gait patterns. Just see if you can… See what you’re noticing. First of all, what’s his posture like? He’s stooped. So right away, that’s a red flag for you. Now, there could be something going on with their spine, but remember, with Parkinson’s patients, in their brain, their perceived center of pressure is to the point where they feel like they’re falling back, so they tend to reflexively move forward. So the fact you see someone stooped right away, you’re starting to diff-di: Do they have any of the findings for a Parkinsonian pattern? Okay?

Now, go ahead and watch. Do you see a reduced arm swing? You guys see the reduced arm swing on the right? And some tremor? Do you guys see this person, how she’s moving, shuffling like that? See how her…


she’s… face is a little expressionless, her hands aren’t moving? See how she’s shuffling or titubating around the side? Look at this person: no arm swings at all.

Watch those over and over and over again. A lot of these cases, if you watch them over and over again, you start to develop plasticity in areas of you brain where you can recognize these things. So, a lot of these are subtle. And if we go to the lobby, or if we go to the airport, you can see this stuff all over the place. Do not dismiss it. Know that that’s a potential mechanism, but also at the same time, don’t see that and go, “They have Parkinson’s disease,” because you don’t know that. All you know is they have inefficiency in their basal ganglia indirect pathway, which is Parkinsonian, and that could be a Parkinson disease pattern.

Okay, I have… we have great papers, full papers for you guys in your notes. These are open access papers that are just phenomenal. If you get a chance to read them, it really will show you what’s published in the research. But this is… a great one that was published in Current Opinion in Neurology. So here’s the key points: So first of all, the premotor and non-motor features of Parkinson’s disease are the ones you’ll see first. So decreased sense of smell, depression, night-time sleep disturbances, mood, and gastrointestinal problem symptoms are really the premotor phase of Parkinson’s, and really manifest years before the classical motor systems. Okay? Now, you’ll find the early Parkinson’s motor symptoms right away as well, but those are the ones you really want to make sure that you look at.

This is another great paper in Nature Reviews Neurology. And they go through the different stages, the Braak stages 1, 2, all the way up to 6. So in stages 1 and 2, what you’ll see first is that the olfactory bulb is involved, digestion and vagal activity’s involved, and then as they go into stage 3 and 4, you have sleep and motor disturbances involved, you start to get some motor symptoms. And then in stage 5 and 6, that’s when you get the obvious presentations of Parkinson’s, and you may start to have some cognitive issues and dementias, and a progression to those stages. You want to try to identify these in the stages 1, 2, 3, to really have the best clinical outcome, okay? And they’re all over the place. They’re very, very common to see.

Now, let’s focus on the olfactory bulb and smell. There’s some really good research with this. So, olfactory dysfunction is an early pre-clinical sign of Parkinson’s disease, and this is the paper they did. They were looking at diagnostic value of impairments in olfaction in Parkinson’s disease, and then what they found was, “our findings indicate that testing odor identification can be a supportive diagnostic tool for Parkinson’s disease. The application of only three odors performed will in [discriminating] Parkinson patients from controls, which can facilitate a wider application.”

So, they wanted to know whether certain odor or scents you should definitely be checking for, if someone may have Parkinson’s disease, and what they found was, peppermint, coffee, and anise were the single most diagnostic tests, smells, that you can check for. Okay? “…the best sensitivity contrast between healthy controls and Parkinson’s disease were coffee, peppermint, and anise.” So, if you have vials in your office, you definitely want those three. And you can reference this paper. It’s published. And these are the ones that will show up first. Okay. So, not all smells are the same. So if you just happen to have lavender oil, because it’s cool, and that’s just what’s easy for you, you need to step it up and get, like, the ones that are very specific for disease process. Okay?

Now, what they also found, when they were looking at smell with Parkinson’s, is the ones that had olfactory dysfunction – and the more severe it was – they could now predict that those that had greater loss of smell,


compared to other people, were the ones that are most likely to get dementia, even in a three-year period. So not only is smell one of the early signs of Parkinson’s – loss of smell, because these protein aggregation disorders impact the olfactory bulb, initially – but that as they look at their smell, they can have some issues.

Now, there’s different ways you can measure tests… you can measure smell. There’s the standardized method called the odor sensitivity test, and I have the forms and how to do this in your paperwork in your notes. And this is a standardized test, and you can order these test kits, like, for their samples, like sniff sticks. You can order them, and they come with sheets patients can fill out, that can be done very quickly, from any neurological supplier. So if you want to have a standardized way of doing it, instead of just three random scents, you can do this, and there’s some good studies on this published on it.

So, when they did this odor sensitivity test with sniff sticks, here’s what they found: For the most part – let me just show you the imaging – Parkinson’s disease patients with severe hyposmia compared to Parkinson’s disease… I’m sorry, without severe hyposmia, lack of smell… Those that had significant lack of smell, they could immediately see when they scan them, the ones that had more significant lack of smell had more dementia-related changes in the brain. So that smell itself wasn’t just an early indication of Parkinson’s, but the more severe the loss of smell is, the more… most likely changes they have in their brain related to degenerative dement… changes associated with dementia.

And then they followed them up, and you can see the followup of patients that had… didn’t have… the ones that had significant smell decreases had much more degeneration than those that didn’t have the significant smell. So you can actually have a scale of different scents in your office, and if they’re getting worse, they’re going to have problems with these types of standardized smell tests. And the worse these become, the more likely that they’re going to have cognitive dementia-type patterns from their Parkinson’s disease. So smell can be a very good tool to help you identify this by the early signs, especially things like peppermint and coffee, and then you can do standardized tests and look at smell, and see if they’re progressing more. There’s some correlation between their smell and degenerative changes that take place in their brain.

So, some other researchers went in there and started to look at what’s actually happening in the brain. And this is another way you can measure tests… smell in your office, the smell identification test. It’s out of the University of Pennsylvania. There’s these little booklets you can purchase from them, and it’s a scratch-and-sniff. You have a patient, they smell something, and then they mark off what scent they think it is. And then you can take your booklet; they have a little key, you put it over the key and you can see how many they missed. And they get a very good and clear standardized way to measure their smell.

These tools can also be used to provide evidence for the fact that you actually have categorized what degree of smell loss they have, with a testing method that has multiple publications and literature with it, and it can be used as a tool.

So in this study, they used this form of smell testing, and they measured hippocampal acetylcholinesterase activity, and they found as their smell became more impaired, their hippocampal acetylcholine function associated with memory and recall became more impaired as well. It’s another correlation between those two.


So the key thing is this: When you’re looking at someone and you start to see that they have slowness and hyperkinesia, and you start checking their sense of smell, you should probably screen with things like anise, peppermint, coffee – those are the ones that are the most sensitive – first. And then it would be a good idea to do some of these standardized tests. Like the little booklet, where you measure smell, they’re not cheap. You’re going to have to purchase those and, you know, depending on how many you buy, you could end up spending ten dollars for one of those. Or, you know, more, depending on where you’re sourcing them from. But… and you know, you can even have the patient pay for the tests, for the booklet. But the point is that you want to screen, and then you want to be more detailed. You don’t want to run all those… And even the smell test with twelve things with the Scantron, that takes a lot of time. So you might want to have the screen-through test with things like peppermint, anise, and coffee, then if that’s off, you can go to the more standardized testing, and then see where they are, and then use that as a tool to measure their function.

So, there’s direct evidence of olfaction, and early diagnosis of Parkinson’s patterns. Now, you have to combine that with you see bradykinesia, you see slowness, you see postural instability, right? And these are all before you may even see tremor. Okay. So that’s the pathway associated with smell.

Now, let’s move down to stages 1 and 2, with early Parkinson’s disease, and talk about their pre-motor vagus digestive types of patterns. This was a very interesting study that was published, that looked at vagotomy and subsequent risk of Parkinson’s disease. So let me explain to you why. What we know is that Parkinson’s disease impacts the olfactory bulb first, and then the gut. Those are the initial areas that it impacts. And there’s alpha-synuclein Lewy bodies. In animal research, when they take alpha-synuclein and inject it into mice, those neurons dies. So alpha-synuclein is neurotoxic. Okay? So alpha-synuclein is part of normal neuron structure – we’ll talk about this later this afternoon on molecular structures – but when it starts to break off and misfold, it becomes a neurotoxic substance. So in early Parkinson’s, there’s a lot of alpha-synuclein that’s in the gut. Researchers are finding that this alpha-synuclein that’s in the gut actually migrates up the vagus nerve, and then starts to infiltrate the brain. And this is where a lot of people are starting to head as researchers, and going, “Maybe Parkinson’s disease starts in the gut, to some degree.” And maybe this inflammatory cascade of causing misfolding proteins – because when proteins misfold, they start to make alpha-synuclein – it’s from an oxidative stress, inflammatory insult. So there’s now this whole area of research thinking, “Is this really an inflammatory gut issue that’s progressing into the brain?” So when this study was done, they kind of, as already suspected… this study was very interesting. So what they did was, it was a Danish study, they looked at subjects for a twenty-year period. Those that had a whole vagotomy for whatever reason, that had the vagus nerve completely severed, and those that had partial injury to their vagus nerve, and these findings say that research suggests that “having an intact vagus nerve increases the risk of developing Parkinson’s disease. The finding is in accord with the primary pathological process being initiated in the gastrointestinal mucosa, which then uses the vagus as a major entry point into the brain.”

And here they are. They looked at their stats. Here’s the… Here what you see is a comparative… For those that had partial… their vagus nerve was still intact, the rates of Parkinson’s was the same in the population. For those that had their vagus nerve severed, you can see that – here is the normal population – it was actually protective. They didn’t develop the same incidence of Parkinson’s disease. This was over a twenty-year period, in a database. Danish database. Really interesting, right? So it makes you think: How much of some of these inflammatory degenerative diseases – because these are for sure inflammatory – has some


component that’s more than, you know, heavy metals in the brain? How much of it really takes a system biology approach? So we’ll talk about some of those things.

Now, constipation is a common problem in Parkinson’s disease, occurring in about fifty to sixty percent of patients, and may occur even before the motor symptoms appear. So constipation should be a red flag for you, that someone may have a neurodegenerative disease. But then what do you need to combine that with? Do you see a masked face? Do you see lack of blinking? Do they feel like they have saliva build up in their mouth? Are they slower? Do they have a stiff shoulder? Do they have, you know, frozen shoulder? Is their gait different? Do they have hypokinesia? You start seeing those patterns, you have a whole different gastrointestinal case. Now, do you need to manage it as a gastrointestinal issue? Yes, because it’s inflamma-tory, and it can promote the alpha-synuclein misfolding theoretically, because it creates an inflammatory oxidative stress model, which we know is the mechanism in this. But you also now have a different take on what you need to do to improve their digestive function.

Now, one of the things we always do in a functional neurology model is, we listen to bowel activity. So taking your stethoscope, listen to the abdomen. Do you hear bowels contracting activity? And you just have to listen to a bunch of guts to know what a normal-sounding gut sounds like. So what you’ll see is, you’ll just see these sounds just reduce. They’re not as… The contraction’s not as intense, they’re not as frequent. It’s when you start to hear that just slow down, you can barely hear it, it’s kind of a whisper contraction, and then they have constipation, motility issues. Then you check their palate; you have them say “ahhh” and the palate doesn’t move much, or their gag reflexes are abnormal. You start to think that this whole vagus loop integration may be off. Right? So that’s kind of a brain-gut, but it’s also a gut-brain potential inflammatory response. We have people gargle with that to activate that vagus nerve; we have people take tongue blades and push on the back of their tongue to get that vagal response, try to help raise plasticity there. But it’s a common issue.

Now, here’s one related to sleep. “Sleep disturbances, which include sleep fragmentation, daytime somnolence, sleep-disordered breathing, restless leg syndrome, nightmares, and rapid eye movements, sleep behavior disorders, are estimated to occur in sixty to ninety-eight percent of patients with Parkinson’s disease.

So let’s go back. We have a clinical decision-making flow chart in functional neurology. The first thing is chief complaint. So, let’s talk about what the chief complaints would be with someone who’s got Parkinson’s. Stiff shoulder, right? Stiff muscles, stiff psoas, stiff shoulder, no one’s been able to help, frozen shoulder, major common ones. Chronic gut issues, chronic constipation, nothing’s been able to help, there’s another major chief complaint. Sleep disorders, there’s another major chief complaint. Usually patients don’t tell you that they ‘ve lost their sense of smell. That’s something you have to check for. Okay? Fatigue, depression, could be any version of these, but it’s also one of their early findings that you see with Parkinsonian patterns.

Now, here’s what’s going to happen. You’re going to find some of your patients have some of these findings. And when you do that, it’s nice to give them paperwork from national organizations that make them aware of it, instead of their weird alternative practitioner that found something that no one else agrees with, right? So there’s a great booklet from the National Parkinson’s Foundation that goes, “Here’s all your early symptoms,” and you have these in your note package and papers. But download these in your office – you have the link to them – for your patients, and then go through and see what these things are.


So, soft or low voice, that’s a hypophonia. In early stages, it only happens when they’re tired. They don’t just have – boom! – hypophonia. They’ll have hypophonia like that whispering, typically with brain degeneration from an endurance perspective. The day goes on, they start to lose their voice, or they start to whisper. Okay?

Dizziness or fainting. So these Lewy bodies, that these protein aggregations take place, they actually build up in brainstem autonomic centers first, like the locus ceruleus, and they do get orthostatic hypotension. It has nothing to do with adrenal gland disorder. They’re actually getting protein buildups and aggregation disorders in locus ceruleus, which is involved with catecholamine release. That starts to degenerate, so they, as they transposition, they get this orthostatic hypertension, because of the degenerative process.

They get the masked face because the earliest part of the masked face isn’t that they look like this individual, it’s that they just don’t blink much. If you are doing a patient history, and you feel like your patient’s just staring – assuming it’s not hyper – that could be one other earliest presentations of the masked face. So they have… they just… they’re just not blinking. You feel like your patient’s staring at you, which kind of makes you feel uncomfortable. Have you ever been, like… and you’re intense. Okay, red flag. So that’s what you may see with some of these things.

And then stooping, hunching over, just the head first, and then the body. Those are some early signs. And then tremor could be one of them. Loss of smells. You know, coffee, peppermint, anise are the most early and the most sensitive associated with smells.

Stiffness, trouble sleeping, small handwriting, and then constipation. So you could have a patient come in with constipation, and just give them this brochure from the National Parkinson’s Foundation, and go, “Hey, you have this, and here’s all these other things. This is what we’re starting to think about your case. This is maybe why you haven’t been able to fix your digestive issues with this cleanse that you’ve done ten times. It’s maybe why you have chronic yeast issues, because you’re not getting motility to make this happen. This is a bigger issue. So let’s understand what we’re dealing with so we can have the best strategic approach to manage you.” Okay. So these tools become very helpful.

Now, in the brain compilation forms we have, I’m curious how you’re going to take it up if you follow the structure we’re teaching you. They’re going to come into your office, they’re going to fill out the brain region localization form, and they’re going to let you know if they have slowness in movements, stiffness in their muscles, that goes away during movement. That’s characteristic. Basal ganglia direct pathway. They’re stiff, but when they move it loosens up. And you can actually do this with them: You can see their rigidity, and as you move it around, it starts to let go. Okay? Cramping of hands when writing, stooped posture when walking, voices become softer, facial expressions change leading to people frequently asking if you are upset or angry. So if you use the form, you’re already screening for symptoms involved with basal ganglia, which is some of the early symptoms you have with Parkinson’s.

Then you go into the examination findings. So we’ve talked about a lot… about a lot of these, but they’re all in a form for you. Because we have to make sure that, as we take a group of people that are learning functional neurology, we just get them to be trained to see one area of the brain, know all the symptoms, know all the exam findings, know all the ways to activate it. Right? That’s the ultimate base structure you need to have to be good at that.


So, do they have the masked face? Do they have reduced blinking? Do they have hypophonia? Do they have aprosody of speech? Do they have any kind of tremor? Do they have camptocormia, where they’re moving forward? Do they have lack of arm swing? Do they have glabellar tap reflex? That’s when you tap; after a few taps you stop blinking. When you do pull tests – we’ll go over some of these in exam findings – when you pull someone, then you see if they can stabilize themselves with three steps. Do they have micrographia? Do they have smell loss, especially with what? Peppermint, coffee, anise. So you can start going through each of these examination findings, and then start to see if that basal ganglia direct pathway’s involved. And then Dr. Brock will go into some applications for each one of these, and we’ll go into nutritional strategies first.

So, know your flow charts, know your basal ganglia direct pathway, make sure you understand this diagram here, and those are the ways to identify early Parkinson’s. Okay?

Now, let’s move into early dementias. Okay.

So when you look at dementias, the key thing is, they just can’t recall, their memory’s impaired, and they have difficult with the activities of daily living. Now, when you look at the scale of all the things that cause dementia, there are things that are degenerating. The medial temporal lobe first, the memory recall, visual-spatial processing area of the brain, and seventy to eighty percent of those people have dementias, which means they have amyloid plaques, or tau protein tangles. That’s important to you because those are progressive, uncurable conditions. Now, even though it’s progressive uncurable doesn’t mean you can’t change their brain integration to make their function improve, but when Dr. Brock showed you that case of dementia, that MRI… those MRI findings were there, but there was a dramatic change in that patient’s function, because Dr. Brock was able to probably reconnect some of those neurons, through their therapy, change the chemical environment of that brain, and so even the person had less… even had the same volume loss on MRI, those connectivity, the function and integration was improved. Right? But that tau protein process continues on, so you know that those things still have potential to come back as time goes on.

Now, the second most common types of dementia are vascular dementias: the multiple silent infarcts, post stroke; hypertension is one of the key factors here. Hypertension, diabetes, is the major cause of vascular dementias. There’s a very characteristic pattern of little lacunas all throughout the brain, when you see those. And then you have dementia with Lewy bodies, and all these different variations of Parkinsonisms that can lead into dementias. Those are going to start with movement: hypokinesia, bradykinesia, stiffness diseases first, then go on to the mind. And then you have things like autoimmunity, or infections, and other… hypothyroidism, alcohol abuse, that can eventually lead to dementia.

But for the most part, you’re most concerned about Alzheimer’s disease. Why? It’s the most common, and it’s progressive and uncurable. But you can still get in there and try to do some things to improve function and slow it down.

So, let me tell you where the rest of the health model is. They’re waiting for late stages. The late-stage symptoms are: They can’t communicate, they can’t recognize people, places, or objects, they may not be able to walk, they can’t smile, they have difficulty swallowing, and they start to have some seizures. And these people have really poor outcomes. But the key thing is, they just start… don’t recognize their family members, they can’t recall events, family members start to see that they can’t function on their own very


well. That’s a huge thing. But family members know that a patient can’t function on their own, like going to the grocery store, going shopping, and doing things. That’s a red flag for dementia. Okay? But what you want to do is, you want to be able to pick up on the early symptoms, not the late, okay? Early symptoms. They forget recently learned information. They forget date and events. Some of you may already have some of that. Okay? Challenges in planning and problem-solving. So it could be checkbooks, could be recipes, difficulty completing familiar tasks at home or at work, confusion with time and place. They have visual spatial issues, they have difficulty with directions, they can’t judge distances, they can’t remember where they put their keys, where they put their phone, poor judgment.

So, take a look at this chart, and just be familiar with it. But it’s symptoms many people start to have as they get older, but guess what those symptoms are? They’re degenerative changes happening in the medial temporal lobe. It’s not just age, it’s age then causes degenerative changes in that area of the brain. If you’re having them, or your patient’s having them, or family member’s having them, here’s what this means: You have some impairment in that area of your brain. If it’s getting worse each year, it’s progressing. You have a progressive dementia starting. It could be in the very early stages, but that’s what it is. The brain itself is not working well.

Now, they found another test, related to smell, specifically peanut butter, for Alzheimer’s. And smell becomes another great tool that you can use in your office. So besides having peppermint, and coffee, and anise, you need to have peanut butter. And there’s a way to do this peanut butter test, that I have instructions for you in your PowerPoint slide and in your notes, how you actually do it. But let me know you a video clip they did on it. So let’s make sure the volume’s okay on this.

Some people like creamy, while others prefer crunchy. Whatever you like, a new study shows peanut butter may be useful for more than just making a tasty sandwich or a snack.

We’ll go ahead and start. I’m going to test your ability to detect an odor.

Researchers at the University of Florida say peanut butter may help diagnose Alzeimer’s disease.

Just tell me as soon as you’re able to detect an odor. “I smell it.”

Study participants with mild cognitive impairment, Alzheimer’s disease, and other forms of dementia, were asked to close their eyes and with one nostril at a time, to detect an odor. Researchers then used a small container of peanut butter to measure the distance from each nostril that a person could detect an odor. The study shows, people with Alzheimer’s disease have a harder time detecting odors from their left nostril when compared to their right nostril.

All of the Alzheimer’s patients had a left tendency… a left nostril impairment, and their right nostril was normal at early detection, which is about twenty centimeters for an older person. And so their right nostril was right at twenty centimeters on average, but their left nostril was about ten centimeters on average, where they were able to detect odors. There was a big asymmetry there.

People with Alzheimer’s disease can lose their ability to smell before memory problems start to happen. Detecting Alzheimer’s early can help doctors prescribe drugs that may slow down the effects of the disease.


If we can catch it at that earlier stage, we can start treating it more aggressively at that earlier stage, and you prevent a lot of the progression.

Researchers say this peanut butter test is a much faster and cheaper way to help doctors confirm the diag-nosis of the brain deteriorating disease than current methods. At the University of Florida, I’m Chris Dole.

Okay, and then we have the paper for you in your notes. You guys can read the full paper and so forth. So really powerful, like, testing you can do in your office. So as you apply some information from this weekend, make sure you have your peppermint, your coffee, your anise, little vials. Make sure you have a little tub of peanut butter and a ruler. If someone comes in and you start to see on the brain region localization form that they’re having focus, concentration, memory issues, go ahead and take the ruler out, so the peanut butter test, follow the steps, see if they follow these guidelines. And probably most won’t, and they still have some early dementia, but if you see it, it’s a red flag. This is just… if you see this test come up, this would be someone you definitely want to consider sending out for some imaging, just to see what the volume size of their brain is, whereas just because someone comes in and has dementia or memory cognition issues and recall issues, you wouldn’t send out for an MRI right away, right? But if they start to fail the peanut butter test, it’s probably a good idea to really start, if they haven’t had it done, measure it, and see what’s going on with it, okay?

So, adding just a few little specific types of scents in your office, in your examination, can be very useful to identify early neurodegenerative diseases.

Now, if you find that someone has all the early symptoms of dementia – and a lot of this is subjective; they’re telling you they can’t remember words, they can’t – you’re not going to see many examination findings with the medial temporal lobe involved. Do you guys understand? Because if the medial temporal lobe is involved, you’re not going to see many changes in gait. You’re not going to see many changes in deep tendon reflexes. You’re not going to see many changes with motor eye movements. You’re not going to see many changes with sensory. So you’re going to have to pick up on lots of early dementia patterns from your forms, that look at screen for those symptoms, and then doing something like a peanut butter test, and maybe doing some imaging to help you.

Now, once you find that they have those symptoms, you want to refer to the Alzheimer’s Association’s seven stages, and get an idea of where they’re at, okay? And get an idea of where you’re at. Where a lot of people will usually start to have symptoms of, and start complaining to you that their memory’s impaired, is stage three. So in stage three, individuals have trouble remembering names of individuals of new people, they forget material that they just read, and experiences increasing trouble with planning or organizing.

Now, a lot of people hear this and go, “Oh my God, I have it.” And guess what? You might. So it is true. And here’s the thing you want to look for: Is he getting worse over time? Because you… Everyone at this point in their career is past… usually past the age of thirty – I know we have some students that are exceptions – but you can get dementia early. And then as you start getting older, these symptoms really start to become more obvious. And you can definitely see this in family and friends, and people that you’re around all the time.

Now, stage four is when you really start to see some serious clinical signs. They forget about events, they have this dyscalculia, counting backwards with sevens – like, start at a hundred, counting back by sevens


becomes a major problem with them – the difficulty planning and paying, managing. This is where, like, their spouse has to make sure that they handle the checkbook. This is where someone has to make sure they call them so they can be on time and they remember the event. When that starts to happen, they’re starting to enter stage four. And this can have its, you know, greater progression as well, and then as it gets into stage five and six and seven, that becomes where they start to get diagnosed in a conventional model more, but you’ve lost that window to make the biggest change. Okay?

So, recall and memory impairments are really big deals. The area of the brain that’s involved is the medial temporal lobe area first. It’s also your visual, spatial orientation area. So the other things they have difficulty with is the sense of directions. So recall, planning, remembering, things like, just like grocery lists. Like, they write down a grocery list before they go, that’s a bad sign. And sometimes it’s good to do that just so you don’t forget something, but if they have to do that, or it just can’t get done, there’s always going to be something wrong, that’s a problem. Okay?

Now, in the tools we have given you, we have a section on the brain region localization form that screens for medial temporal lobe symptoms, which then is translated to: it screens for the early symptoms of dementia. If you guys see individuals have the medial temporal lobe section of the brain region localization form filled out with areas of impairment, you should definitely be looking at a peanut butter test. You should definitely be asking questions about how bad it is, and most importantly, have they noticed if it’s gotten worse, and then what time period have they noticed it getting worse. You want to see how fast this is going. Because you’re going to be pretty much picking up on early dementia.

Now, dementia is scary. So you have to be very, very careful with how you use that. “Oh yeah, you have dementia. See you next week.” Do not do that. Okay? “You’re starting to show memory impairments. This is the first area of the brain that’s involved. It’s not clear this early if you will have that disease, or you go there, but this is where it starts, so let’s take strategies to improve your function here. Let’s take your brain health very, very seriously, because this is your window of time. This is your opportunity to make the differences here. You’ll be able to tell yourself if your memory and recall and visual spatial orientation are getting better. But please do not think that’s normal, please don’t think that… It’s not normal, it’s just common. Please don’t think that’s normal, and please don’t think it’s just associated with age. It’s actually a loss of function in that area of your brain, and we need to make sure we can change that.”

So, we’ll talk about nutritional things that we can do with them. And then you can do some things in the exam. You can have them do memory recall, so you give people, like, three items that they have to remember, like, “Remember pencil, umbrella, pickle,” or something like that. And then you do a history, and then you have them recall it to you. Or you give them a few numbers, and then you go through history and you have them focus on other things and have them try to recall those numbers for you. So you can do word recall, number recall, and see if that is a problem with them. You can do mental status exam. There are some examination forms, like Sage – you have them in your notes – and a mini-cog test, clock-drawing test. You can also look at – that’s in your notes – there’s some standardized ways people look at memory and recall. Okay? And then you can go into the applications.

So, let’s just, like, take a step back and just reflect on what we’ve gone over so far. There are two differ-ent types of neurodegenerative patterns. One is isolated neurodegeneration in the brain, for whatever reasons: chronic, cumulative, inflammatory, disuse, lack of plasticity over time that starts to show loss of


function. And then there’s actual neurodegenerative disease. The thing that you’ve most worried about is neurodegenerative disease, because it’s progressive uncurable. So when you see someone has Parkinson’s, realize that when they come in with stiff shoulder, depression, voice that gets softer throughout the end of the day – right? – constipation, chronic GI symptoms, that’s their chief complaints. Dementia, for the most part, people just tell you: “My memory sucks. I can’t remember anything. It’s really terrible. It’s impacting my life, my work.” Those are pretty clear.

Now, if you use the brain region localization form, you’re going to screen for basal ganglia symptoms, and you’re going to screen for the medial temporal lobe early dementia symptoms. The best followup tests you can do, when you see those, is olfactory testing. So then you have your peppermint, your coffee, your anise. You test those, go in there and check the peanut better test, and then do your normal evaluation, and then you start to kind of get an idea of what’s going on with any patterns of early neurodegeneration. Everybody good?

Let’s move on to cerebellar degeneration. Okay. So, when you look at cerebellar degeneration, worsening balance, car sickness, sea sickness, nausea looking at things in motion, are a common thing. Now, remem-ber that the cerebellum is involved both with integrating muscle movement, but it also integrates your vestibulo-ocular reflex. And when people have vestibulocerebellar issues, if they’re on windy roads, and they’re getting all this vestibular input, and their eyes are tracking, the body’s trying to figure out where they are in space, and if their cerebellum isn’t that healthy, it can’t dampen its output to the Purkinje inhibition system, and it projects into the vagal nuclei, because the cerebellar projections to the brachium pontis, firing to the area acoustica, where you have vagal activity, and you get this neuron that gets close to threshold and it fires, and people many times get nausea with movement, right? Or motion. But they may tell you, “I had motion sickness as a kid, and now it’s back, but I’ve always had it, so it’s no big deal, right?” No, they probably had a cerebellum that didn’t fully develop and have plasticity. They had a developmental delay; they kind of got over it as they got older, but not in very great development there, and now they’re degenerating, what’s showing up again? The areas of the brain that didn’t have plasticity weight. So please do not assume that they tell you that they’ve had car sickness or sea sickness, that it’s a personality thing, that it’s a family trait. It’s not. It’s a lack of integration in cerebellar vestibular pathways.

So, you want to see if they have a wide-stance gait, if they have positive Romberg’s, they have a termination tremor, they have dysdiadochokinesia. Those are the signs you see with cerebellar related disorders. Okay.

Now, we’re going to get into this more as we move on, but the question to ask is, “Why?” Why does someone have a vascular dementia? Well, we know that they can have actual dementia, for example, because they have diabetes, or they have hypertension. Why would someone have Alzheimer’s? Well, they have mechanisms that promote protein misfolding, things like diabetes, things like oxidative stress. Cerebellar degeneration, we know lots of things can cause it, but we’re seeing a huge rate of cerebellar degeneration because of food proteins, and this is gluten. This is the whole gluten ataxia. The rates of gluten sensitivity have gone up. We’re seeing a lot of people that are now showing early signs of cerebellar degeneration, even in their twenties. So we’re looking at twenty-year-olds, thirty-year-olds, and their cerebellum is just completely degenerated away. It’s actually more of a neuro-immune component. I’m kind of classifying a neurodegenerative disease, but it… Technically it’s a neuro-immune disorder that’s causing a neurodegenerative pattern.


Anyone in your family, anyone that walks into your office, first of all that tells you they have gluten sensitivity, you need to immediately screen their cerebellum. Anyone in their… walks into your office, says they have a family history disease, your really need to immediately screen their cerebellum. Anyone that comes into your office and says they have hypothyroidism, you need to definitely screen their cerebellum, because hypothyroid people are ninety percent or higher have Hashimoto’s, and the majority of Hashimoto’s people have celiac disease; for sure gluten sensitivity. Okay? So if you hear hypothyroidism, Hashimoto’s, history of celiac disease, gluten sensitivity, you need to start looking for cerebellar dysfunction. Okay?

Now, gluten is an issue because gluten proteins can bind and cross-react with the cerebellum. If you look at the amino acid sequence of gluten, and the amino acid sequence of cerebellar tissue, you see how EVPL are identical, and it’s close to similar sequence? That’s called molecular mimicry. So antibodies against the cerebellum can actually attach to cerebellar tissue, and then that causes T-cells to destroy them. So this is a cross-reactive food protein model. Okay? We have a paper right now in submission where we checked a hundred and twenty foods, and we found other foods besides gluten that can cross-react to cerebellum. So hopefully we’ll get that finalized and published and put on Facebook, okay?

Now, this is what it looks like in the lab. Here you guys can see different wells, and on these wells there’s different proteins attached to them. So in this well here, you have a gliadin peptide, purified gliadin protein. Here’s crude gliadin, not purified. Here’s cerebellar. So these wells here have gliadin peptide, crude gliadin, cerebellar protein, myelin basic protein, egg protein, soy. So that’s on the well. That’s the protein that’s been binded to the well. Then they take blood, which has antibodies in it. So if they have blood that has cerebellar antibodies, and it mixes with cerebellar protein, what should you see, if you see a reaction? That’s a control. That’s the antigen antibody binding. But look what happens here; look what happens here: gliadin with gliadin reacts; you see cerebellar reaction. You could even see cerebellar antibodies mixed with egg protein. This is what actually prompted us to do a study, because people can have egg protein food sensitivity, and get exposed to eggs, and then have high antibodies, and those antibodies have a molecular mimicry potential to cause neuroinflammation of the cerebellum. So we’re learning that sometimes food protein reactivity is a major cause, and this is why we’re seeing a high degree of early neurodegenerative changes in cerebellar disease patients. Okay? So that’s one of the ones you’ll see early for.

This is a study we published in Nutrients a few years ago. We looked at wheat and milk antibodies. We took four hundred patients and subjects, and we tested them for milk and wheat protein antibodies, and we found roughly – we thought it would be more – there was only about twelve percent of the population had high amounts of gluten or milk protein antibodies. And then what we did, which was actually more than what they say, because they say gluten sensitivity is only in about three percent of the population, and celiac disease is less than one percent. So our study showed it was, like, really much higher. And then what we did is, those that had antibodies to milk and wheat, we wanted to check to see which of them had cerebellar antibodies or myelin, and it was approximately fifty percent. So if they made antibodies to milk or wheat, fifty percent of them had antibodies to myelin or cerebellar tissue. The ones that reacted to milk protein, we found a very high association with myelin antibodies, and the ones that had cerebellar… that had gluten antibodies, had a very high association with gluten-cerebellum associations. So anyway, so you have that full paper, I also put included in your notes.

So, the studies are also showing that we’re seeing some of these gluten-related ataxias. This was a great paper because in this MRI, this study, we’re in fifteen months. You guys see the white-matter lesions in here?


And then fifteen months later, they have this progressive response. So, we know that a lot of accelerated cerebellar degeneration is taking place, because of neuro-immuno-inflammatory models, and it’s impacting young people. This is why we have zero tolerance for people that think gluten is nonsense, because… Let me just say it this way. Let me just be frank. If you think gluten sensitivity is nonsense, you’re just an idiot. That’s just what it comes down to. Number one: You’re an idiot. Number two: You don’t know how to read the literature. Number three: You’re blinded by your own bias. And number four: You’re dangerous. Okay? So, if someone has antibodies to gluten, and we have all the evidence now, and you say that’s okay, that patient progresses, I’ll be the first one that goes to court and testifies against you. As well as other researchers and people, okay? It is a real issue, and many people have problems with it, so just be aware of that, okay?

Now, if you guys see those histories, then you want to go in there and check these things out.

Now, what the literature is showing is this: If a patient has… and this is important for you guys to know, so you pick these things up early. If a patient has idiopathic sporadic ataxia – which means this: you have them walk in a straight line, heel-toe, and they fall all over the place; they have ataxia. So you have them close their eyes, walk. They can’t really get more than three steps, that’s a positive test for ataxia. And if it’s idiopathic and sporadic, what that means is this: Some days it’s better, and some days it’s worse, and there is no head trauma, there’s no obvious disease; they just don’t know where it’s coming from. It’s idiopathic. Which is what you’ll see most of the time with people. They say that you need to rule out gluten sensitivity, because you know what accounts for it. Papers show it’s as high as sixty to seventy percent of people that have sporadic idiopathic ataxia, have gluten ataxia, okay?

So if you see someone coming in… Let me put it to you a different way, so you can identify these things early. Someone comes into your office, says, “I have hypothyroid for five years, and I… you know, recently I found out I was gluten sensitive. I went off it and I feel a lot better.” What’s the area of the brain you definitely want to check? Cerebellum. So you go through, you check to see if they have termination tremor, you check to see if they have dysdiadochokinesia, you check their Romberg’s out, you have them walk in a straight line, see if they have ataxia. They have ataxia, and you see dysmetric movements, and kinetic tremors, and you see dysdiadochokinesia, you’re looking at a degenerative cerebellum. And you guys, they may be twenty years old. They may be thirty. So these degenerative diseases can happen pretty quickly.

Be aware of the studies that have been published. This one’s published in Brain. Seventy-nine… Thirteen percent of the people that have cerebellar ataxia have GI symptoms. Only thirteen percent of people that have gluten causing their brain inflammatory condition actually have GI symptoms. So most of them won’t notice that gluten changes their gut function; it just changes their brain focus, their concentration, their brain inflammation. So you don’t start… don’t associate it with celiac disease pattern. We also know that there’s GAD antibodies involved with many of them, so many type 1 diabetics end up with cerebellar degeneration early.

And this is an interesting paper. What they found is, TPO antibodies actually bind to astrocytes in the cerebellum. So the antibodies against the thyroid can actually bind not just to the thyroid gland, but to the cerebellar tissue. And if they attach, then T-cells destroy them. That’s why, in your history, when you hear someone tell you they have a thyroid disorder, you want to really look at their cerebellum findings, and see if they have any early cerebellar degenerative changes.


There’s a paper that I published - it’s in your notes – “Neuroendocrine-Immunology Mechanisms of Subtle Cerebellum Impairment.” I gave you a list of the most common things involved, with some references to the literature. That’s something you might want to check out.

Now, the way we’ve worked this out in the model is this. We have a brain region localization form that you guys all have, right? So you have basal ganglia direct, early Parkinson’s; medial temporal for dementia; and then we have all these symptoms on the brain region localization form for the cerebellum. And we broke down the cerebellum to cerebrocerebellum, vestibulocerebellum, and spino-. Any of them can be involved with degenerative changes. Some may show up first, with these or the others. So you can screen for your symptoms on your brain region localization form, and then you can go into all three different cerebellar patterns, and then you can get in there and look at the examination findings.

So let’s just go over the examination findings right away. If someone has early cerebellar degenerative disease, okay? Let’s start with their history. What are they going to… What are going to be some possible chief complaints? Well, I can tell you, they may have car sickness, they may have sea sickness, they may have uncontrollable nausea, they may come in with dizziness, disorientation, vertigo. They may tell you that they get really fatigued at the end of the day. At the end of the day doing what? Activities that stress out their balance and movement. So you might want to then look at their history: “What makes you tired?” Find out what’s… days where they’re actually having to watch things, move things, or have balance challenges move against them; those are days when they’re really worse. Right? Those are things that you might pick up in the history. You fill out the form, you clearly will see symptoms of cerebellar degeneration on the form, then you go to your exam. First thing you do is, you watch them walk. What you see with their gait; if they have cerebellar issues, they lose their stability, their feet will spread out past their shoulders, so they have a wide-stance gait. Or as they’re falling, they may cross their foot like a scissor every now and then; alternating scissor here and there to control their stability. They may sway to one side when you watch them walk. You might see hypotonia, because their arms are flailing all over the place. Because people who get cerebellar disease, they’re… they get increased movements, so the hypotonia, wide-stance… I’m exaggerating, of course. You guys can see those. You can do finger-to-nose. At the very end of movement, you can see termination tremor. As they get worse… In the early stages you’ll see it at the very end of movement; you won’t see it at the beginning of movement. You’ll see dysdiadochokinesia so if they move their hands one side, it doesn’t coordinate as fast, turning muscles off, as the other side.

Those are your key findings. If you guys see those, and they come in with a history of, let’s say, hypothyroid and autoimmunity, do you think you’re going to fix this patient just by doing vestibular brain rehab, core exercises? No. Because they have an ongoing process. So, let’s say, here’s an example. They have gluten antibodies through the roof, they’re still eating it. They have TPO antibodies through the roof. Those are all potential target sites for the cerebellum. You see cerebellar degeneration; they’re fairly young. Now, you go in the exam finding, and let’s say you do some cerebellar types of stimulation. What would you expect to see with their exam findings? They change. There’s a little magic trick; a party trick. Changes. What happens over time? You haven’t addressed the underlying issue, so they continue to progress. Now, you still need to see that change in your office to know what kind of therapy to give them, but you have to know clinically; you have to go and treat the underlying mechanisms that are there. Okay?

Now, for Parkinsonisms and dementias, we have to kind of work our way into it for you, because we’ve got to teach you the cellular mechanisms of how proteins and alpha-synuclein buildups and Lewy bodies


and neurofibrillary tangles, and then talk to you about how we approach that. But for cerebellum, we’re not seeing those degenerative disorders really being… most of them not really being protein aggregation disorders, but more of neuroinflammatory neuro-immune. So when you see cerebellar disease, you’re going to hand… and direct yourself into more of an autoimmune neuroinflammatory model. Okay? When you see things like Parkinsonism, and dementias, we’re going to be involved with other types of things. So you can look at those, and then identify each of these main symptoms.

So, let’s recap and put this together. First thing you’re going to do is, when a patient walks into your office, is try to assess if they have any neurodegeneration. Okay? You’re going to look at their age. The older they are, the numbers are, the facts are, the greater likelihood they’ll have some degree of neurodegenerative change. So the minute you see that they’re an elderly patient, you have to suspect they have some neu-rodegeneration. But don’t let that throw you off, because young-onset Parkinson’s happens in twenty- to forty-year-olds in ten percent of cases. Many cerebellar degenerative changes happen with young people not elderly, because it’s a neuroinflammatory component. Okay? So, you get that first initial impression.

Now, one you get the first initial impression with them, you’re just going to just see how they function. Look at their facial paresis, look at initial tone, look at how they walk, look at their slowness, look at their speech, see how they’re communicating with you, see if their frontal cortex is intact, and then you can simply just go into your brain region localization forms.

So, what areas of that form are critical for you? The basal ganglia direct, for Parkinsonism, early Parkinsonisms; the medial temporal lobe for early dementias; and the cerebellar areas for the cerebellar degeneration. Now, these may not be degenerative, but we’re just focusing on the neurodegenerative theme, because that’s our goal this weekend. Now, you guys are all with me, right? So you screen for those things.

If you guys see early Parkinsonism patterns in your metabolic… in your brain region localization form, what are you going to be looking for in their handwriting? Let’s recap. You’re going to be looking for tremor, or micrographia. What are you going to be looking for in their speech? Hypophonia, right? And especially in early stages, hypophonia that starts to show up as they get tired. Remember, there’s a brain endurance component to it. Now, what are you going to be looking for in their face? You’re going to see if they have a masked face, which is progressed. A masked face basically means their facial muscles are rigid. Just like their arms get rigid, their facial muscles get rigid, so their tone goes… tone becomes impaired, they become hypokinetic in their face. That’s what causes the masked face. Okay?

Now, before you see masked face, you’re going to see loss of blinking, so you’re going to see the staring and lack of blinking. And then as it progresses, you may see the masked face. You just might see a facial paresis in one side, which makes you go, “Hey, this could be their side of their brain involved.” Maybe you see Parkinson-type patterns there. Okay?

So you’ve looked for the handwriting, looked at their speech, looked at their face; you’re trying to determine if they have any Parkinson’s. You’re looking for, in your history, do they have constipation, do they have stiff shoulders, do they have stiffness. Does their stiffness change when they move, which is a diagnostic sign with their muscles? Do they have chronic yeast or GI problems? Those are all starting to be the pattern for early Parkinson’s. Okay? Everybody there? As you go into your exam, you’re going to see them walk.


What are you looking for in their gait? You’re looking for lack of arm swing. And lack of arm swing that’s not spastic, but lack of arm swing where it’s kind of stuck to one side. If it gets more progressed, the MCPs turn in, kind of coalesced striatal hand, and then they’re walking like that, versus walking spastically. Now, you could see that, but more than likely you just see rigidity when they’re walking, okay? You might see that they’re just walking slow. Right? You might see, if it gets more progressed, what does it turn into? The head bent forward, and they start to shuffle, their arms are going that way.

So you want to see what degree of progression they have, but your initial observations are the shuffling, is there head-forward posture, do they have lack of arm movement? And then you get into your exam. One of the best things to do is smell. So pull out peppermint, anise, and coffee. Check those, see if they’re impaired. Now, they’re not going to be impaired with most people, but if they’re impaired, you’ve got a problem. If they’re impaired, then you want to do your followup testing with some of those standardized tests, and see… monitor them over time, because their smell is directly related to their progression, and even can be predictive of their dementia that can develop. Okay?

Now, as you go through the exam, one of the best things to do is just check rapid movement, and see if they’re slow. And with Parkinsonism, it’s going to start on one side first, so usually start with one side presents, and then it moves, and it becomes bilateral. Okay? So see if you see that hypokinetic movement. Do it with their hands, and then do it with their feet. So you have them tap as fast as they can, okay? And then if they’re going really slower on one side, and this side’s slower, you might have a pattern of presenta-tion of Parkinsonianism. You’ll see the head posture that adds to it, okay?

Now, you want to listen to their gut, their abdomen – especially if they have the constipation issues – see if they’re involved, and you want to passively feel for their range of motion and tone. If you feel a really lead-pipe rigid tone, like they can’t let go and relax, that can be associated with that. But sometimes if you just shake around and move it, it gets fluid, which is another common sign that you see with basal ganglia direct pathway. And then you want to see if they have tremor, but tremor can be last-stage.

That’s how you look for early Parkinson’s pattern… Parkinsonism pattern.

Now, what Dr. Brock is going to do is, then he’s going to go, “Hey, you have early Parkinson’s pattern, but is it supranuclear palsy? Is it multiple system atrophy? Is it corticobasal degeneration? Because the prognosis of these things all change, and there are different types. You’re getting more specific with the disease. But right now, I just want you to look for the whole concept of just Parkinsonism. Okay?

So, let’s recap dementias. With dementias, they’re actually going to come in and tell you that they have memory issues, and memory impairments. As a matter of fact, it could be one of their major chief com-plaints, because it’s scary. Now, you have to then assess where they are. Usually, if someone drives them to the office, and someone’s helping with the daily activities of life, and no one trusts them with checkbooks and planning and organizing, it’s probably heading into stage four of the scale of one to seven. If they can function on their own, but still have noticeable impairments, they’re probably in stage three. So those are the early signs of where they could be at. On your brain region localization form, you’re going to see a whole list of symptoms associated with the medial temporal lobe, and then you can have… in the office, you can find several words: “I want you to remember five words,” do your history, and see if they recall back to you. Give them, like, a phone number, see if they can recall it back to you. Write those down, so


you can say… because sometimes patients will say, “No, that’s not the words you asked. That’s not what it was.” It’s nice to show them the sheet. “No, you don’t remember the phone number right.” “Okay, here it is.” We use the same one for everyone. And then that also helps because sometimes it’s very scary for them, and they become very defensive. And if you feel that, you have to make sure you chill out and make it a safe place for them, because it is scary, okay?

Now, that’s the dementias. Cerebellar, here’s the key thing: Cerebellar, you’ve got to think of young people as well as older people. It happens in young people because of acute onset inflammatory conditions that are contributing to the neurodegenerative process. So look at your individuals coming in with hypothyroid, glu-ten sensitivity, inflammatory reactions. They are definitely potential for neuroinflammatory mechanisms… I’m sorry, neuroinflammatory mechanisms definitely apply to the potential for neurodegeneration. Okay?

So those are all the main neurodegenerative diseases, and let’s get into, now, this area here. So, we talked about neurodegenerative diseases, now let’s talk about isolated neuron loss. So here’s the clinical pearl: Remember, patterns of neurodevelopmental delays that may have been improved into adulthood are usually the first regions to show patterns of neurodegeneration into late adulthood. So a question to ask: “Did you have any problems with any subjects in school? Were you good with sports?” And if they tell you what they weren’t very good at, it tells you what parts of the brain didn’t develop very sufficiently. Okay? And those are the things that you would expect that they would show up with.

So when you see people that have loss of function… So, let me give you an example. You work up someone, and their parietal lobes are just totally off. They can’t recognize vibration, or pinprick, or cold sensation. They keep getting injured on that same side because their ankle sprains, or injuries because they can’t feel their limb, but they don’t have any signs of Parkinson’s or dementia. They just have someone who’s got an impaired parietal lobe. Question is: Why? Now, if they’re twelve, what would you think? It’s probably developmental delay. Right? If they start to become older, you always need to consider that’s probably where they had lack of plasticity, and that’s probably where the neurodegeneration is starting to hit, okay? But you always go back to: What is potentially causing that? Because if you don’t go after the mechanisms that could be potentially causing that, then you don’t know… you’re not addressing the mechanisms that are promoting that, and your success in the future.

One of the things that we talked about is, once you identify the region, what do you need to do? Repeat testing to see what? Do they fatigue and crash? Now, if they fatigue and crash really quickly, you’re really thinking that there’s a neurodegenerative issue, because neurodegenerative issues are inflammatory, cells are unstable, and it’s not healthy. So you want to go into it. If they have parietal lobe issues, and they immediately respond and are healthy, you’re probably not thinking it’s neurodegenerated. So just a heads-up. When you do repeat testing and you see unstable neurons in a certain region that isn’t specific to neurodegenerative disease, you start to… If you see them fatiguing and start to think that there’s a neurodegenerative. But if they don’t fatigue after repeat testing, it’s not that big of an issue, they’re somewhat stable, you’re less likely to think it’s a neurodegenerative disease process. Okay?

Now, the metabolic causes that cause unstable neurons, or metabolic factors that cause unstable neurons, are also metabolic factors that promote neurodegeneration. So what you want to do is, you want to have the skill to now combine these forms, and start screening each of these areas, because many people actually have neurodegenerative changes in their brain, but it isn’t associated with a neurodegenerative


disease, okay? So when you look at your areas 44 and 45 for speech, you might have people that [have] difficulty producing words, but again, you won’t see it usually with them until they get fatigued, and if you have someone that has a history of… or you see frontal lobe-related issues, you want to ask them, “What happens when you get tired? You have a hard time producing words?” Like we had a… During our clinical workshop, if someone had a reduced arm swing on the right, and then we started talking to them, and they had a past head injury, and then the question was, “How do you… How’s your speech function when you get tired?” And they go, “Sometimes it’s hard just to produce words.” So that’s an injury that now is probably going to progress into neurodegenerative changes unless that’s stopped, right? So you want to brain… and you want to do activities to make a difference for them.

So, you can look for these in your brain region localization form. They’re listed there for you. And then you can get into examination findings and go through each of those skills. So, this is what we really want you guys to do between now and the next session. We want you do use your brain region localization forms with just all your patients, and start to memorize those symptoms. And once you see those symptoms, we want you to take the forms, and as soon as you see the certain region of the brain, brain region localization form fill out, go to these charts. These charts are organized exactly to your brain region localization form sections. And then even before – maybe you get the forms first – before you do your physical exam, go in there and circle what exams you need to do. Okay?

Once you find out what exam findings you need to do, see if they’re there. If they’re not there, and they have the symptoms, you may need to repeat test it. You need to push it and challenge it a bit more. And as you challenge it, you’re going to look to see what their fatigability is. And after you see as you challenge them, and they’re starting to break down and break down and break down, you probably have some metabolic inflammatory condition that’s a factor there. How quickly they break down and what kind of symptoms they have when they break down determines whether you actually want to do any kind of therapy or not. A lot of these cases that are highly metabolic and inflammatory, if you treat the metabolic inflammatory mechanisms – like, let’s say they have severe dietary protein allergies, gut inflammation, lack of essential fatty acids, all these things, and you address those things with them in a six week period –they may come back and fill out the forms, and they have a totally different brain. But you still saw symptoms in one region, so what do you want to do? You want to go and push it, examine it, and see if they start to come out more, and then determine what their fatigability is by how many reps they can do, and you start to put that all together, okay?

So, fill out the form, patients fill out the form. Areas where you see sections, circle it on your compilation form. Go in there, and do those examination tests, and as you go through the examination tests, then push it and see what the rate of fatigability is, and then you’re going to go into applications, which Dr. Brock is going to go to, and you can then implement applications and make a change. But we really want, as we carry you guys through the process, to go through each of the steps so we can make it easier to teach. We don’t want everyone all over the place with the though process and the applications yet, because it becomes too difficult to do. Okay?

So anyway, in recap, here’s what you need to know: You need to know that not all loss of function of the brain is a neurodegenerative disease, but it can sometimes be neurodegeneration itself. So, neurodegenera-tive diseases have a very characteristic finding. You guys all know the progression of Parkinson’s, right? Starts in the… starts with smell, starts with the gut, you get slowness, starts with one side, goes to the


other, they start to have sleep problems, they start to have motility problems, they get stiffness, they get slowness, and it keeps getting worse year after year. That’s your Parkinsonian pattern. Okay? Dementias, memory, cognitive, it gets worse. But a specific loss of function in one area is not a neurodegenerative disease, but it could be some degree of neurodegeneration. So make those clear with yourself as you work up the patient. And the ones that are neurodegeneration but not neurodegenerative diseases have better outcomes, better prognosis. Usually easier to treat, and those are the ones you want to worry about. The ones that are neurodegenerative have realistic clinical expectations. Okay?

So that takes us to lunch. So what we’ll do is, we’ll break for lunch. If you guys have any questions, just send them to [email protected], and once we get back from lunch, what Dr. Brock is going to do is, he’s going to expand from where I went on. He’s going to say, “Hey, here’s Parkinson’s, here’s dementia, here’s how you diff-di each one of them for what they are.” And that will help you in your assessment skills. Okay?

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