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MODULE twO tRANSCRIPt: KHARRAZIAN CASE StUDY | COPYRIgHt © 2016 FUNCtIONAL NEUROLOgY SEMINARS LP | PAgE 1

THE INITIAL CLINICAL SURVEY AND HOW TO IDENTIFY THE LESION BEFORE EXAMINATION (MODULE TWO)

Transcript – Case Study

Presentation by Dr. Datis Kharrazian

Okay. So, the case that I’m going to go over with you guys is the case that was in the pre-course material. I don’t know how many of you guys have gone through that. But in the pre-course material, we wrote up the history. So, what I usually have in my practice is, I have what’s called a case review process. I have patients send me in their entire… I ask like thirty or forty… somewhere… I don’t know; a lot of questions. And then I have them send that to me typed, because sometimes I work with a lot of compromised brain patients, and I don’t have the time to sit down and figure it all out, because it will take half a day to get all the history out of them. So I want them to send me a history ahead of time. It’s also a way for me to screen patients to make sure that I get the most motivated, dedicated patients in. Sometimes it takes people several weeks to go through all the paperwork with their capacity, but I’d rather have all the information before they come in.

So, I’ll start sharing with you some of the patient histories people write, and the way they write the informa-tion, if they repeat or miss things, or have grammar mistakes or things, also is diagnostic to you, right? You don’t get to see the handwriting because they’re being typed, but at least you can see them.

So, what I did with this pre-course material is, I sent the person’s case history that he presented, and then I go over the first exercise in the pre-course quiz to go through it and try to figure out what regions of the brain were involved. And then there was a part two, where I wrote all the answers and why each of those regions were involved, and then there was a part three where I gave you all the exam findings. So what I’m going to do now is, I’m going to show you the actual case on video, and what we did, and all the things for it. So if you want to review this case with more detail, go back to the pre-course material part one, part two, and part three, and then you can watch this on replay and you kind of see the big picture and the whole thought process.

I’m going to take this entire patient with you through the entire flow charts, all the way to the end. Past the initial survey, from the exam to treatment, and then I’ll show you some of the outcomes and what we did with him. I saw this patient right a week before Module One, so I’ve only been working with him for a short period of time.


So, when you look at the patient… What I’m going to do is, I’m going to take you through this. So, we’re going to go over the chief history, we’re going to localize the region from the history. We’re then going to go into the general survey, and then we’re going to find all the things from the initial survey, then we’re going to localize the region, and then we’re going to go into the blood flow mechanisms, what exercise you want to do pre-synaptically, we go into metabolic issues, I’ll show you the exercises we did, and I’ll show you the dietary nutritional things we did. So the whole way through the entire flow chart. Okay?

So, chief complaints. “My chief complaints are severe constant fatigue, brain fog, and low cognitive function.” This is what he writes are his chief complaints. “I’m a thirty-year-old man, although I feel like a ninety-five-year-old man.” It’s just to give you some perspective. He’s trying to share with you how he feels, what he’s going through.

So right now, we’ve gone through the flow chart, patient’s chief complaints, first thing we want to find out. So his chief complaint is severe and constant [fatigue], brain fog, low cognitive function, okay? So now let’s keep going through the history, because we want to now do what? We want to clinically localize the region with the history. Everybody with me so far? Okay.

So from the history, here’s a few things that are very diagnostic for us. “All along from elementary through high school I suffered from ADD,” – attention deficit disorder – “digestive problems, and asthma. I was a bed wetter until almost thirteen years old. I had to use machines for my asthma. I grew out of asthma when I reached middle school.” Let’s just stop right there.

ADD, or attention deficit disorder. Where’s the attention region of the brain? Frontal cortex. So right away we know there’s a frontal cortex issue. Digestive problems, we don’t know if it’s a brain-gut axis or gut-to-brain axis. And asthma, which is oxygenation, but allegedly it’s under control now. He was a bed wetter. Bed wetter, micturition centers are in the frontal lobe, and they’re right in the medial parasagittal areas, the micturition centers, right next to the feet, homuncular distribution. That’s why a lot of these kids are toe-walkers. So a lot of toe-walkers, and people that are… and kids that are bed wetters, or… have the collateral presentations, because of the parasagittal development delay. Okay?

“Throughout my life I also had tics off and on. Some were facial tics with my eyes, and others were vocal tics.” What part of the brain is involved with tics? So this is a hyperkinetic movement, so we know that the basal ganglia indirect pathway’s involved too. Okay?

“Recently I supplemented with magnesium, which has helped eliminate tics for the most part.” So this is something you really want to be sure if it’s accurate or not. Now, magnesium, if you guys know your path-ways, magnesium is one of the cofactors in enzymes for glutamic acid decarboxylase, which is the enzyme they make that converts glutamate to GABA. Glutamate excites the basal ganglia pathways, and GABA which inhibits it. So, I don’t know if it’s just severely magnesium-deficient, or if this was just coincidental. It’s one of the things he puts in his history. Okay?

“I’ve gone through two nose procedures, both for breathing. In 2007 after my second nose surgery, and injury fractured my nose, which caused a deviated septum to this day.” This is a significant deviation of the septum, where it’s pretty much blocked. So he had to go in for another surgery so he can actually breathe through his nose.


“My hands and feet are constantly cold, and I have a deviated septum that affects my breathing.” So what does this tell you about metabolic issues related to brain? Circulation’s involved to the brain, and now he’s got hypoxia potentials to brain, because he’s not getting oxygen through his nose. And we do a lot of oxygenation through our mouth and our nose, so we’ve got one of these major inspiratory pathways compromised. You guys see?

“My energy is constantly low. I have constant brain fog. I have constant digestive challenes with lost of belching and burping, even after small healthy meals.” So the constant brain fog; you guys, it could be caused by inflammation, it could be caused by hypoxia. Anything that impacts neurotransmission, right? And then digestive challenges with lots of belching an burping, so we don’t know if there’s distension in the gut causing it, we don’t know if it’s vagal system firing on its own, but those are in his history.

“To be completely honest, I have been somewhat a late bloomer in my life.” So what does it mean in society to be a late bloomer? What do you need to be active and do things and to not be a late bloomer? What part of your brain needs to be active? Frontal cortex. So right away, we’re seeing, like, a pattern of ADD from childhood, and now developing into adult ADD, or to say it really straightforward, from an anatomical point of view, a frontal cortex that just hasn’t had a chance to fully develop and develop plasticity, right? If the frontal cortex doesn’t develop plasticity, then getting motivated, planning, being… driving yourself to do things, all of these things become very, very difficult. And this is what he’s suffering from.

“I don’t drink or smoke, any coffee… Coffee does not agree with my body, or any caffeine in general.” So what does this mean to you? Well, it is he can’t metabolize caffeine out of his body? Like, is he a slow metabolizer? Is it the flavonoids in coffee that could be an autoimmune stimulant for TH2-dominant people? We have to figure out more, but we just know there’s some issues with caffeine, right?

“Growing up I’ve always had brain fog and delayed cognition.” Cognition – what area of the brain? Frontal. “This, along with severe fatigue and low energy, has taken over my life to the point where it holds me back from my destiny and potential.” So, you guys, this is pretty straightforward from the history. What do you have? You have frontal cortex involvement.

“I have ambitious goals, but I don’t have the stamina and energy to sustain me in any way.” What is this? This is brain endurance. “I have always know I have great potential, but my poor health, low energy, and body weakness are holding me back so much that I am moving at a snail’s pace.”

Previous diagnosis: Add, generalized anxiety disorder, asthma, severe deviated nasal septum.

Now; here’s the family history. “My mom has lupus.” And it’s pretty significant. It’s pretty severe. “On my father’s side there is plenty of neurological problems, including tics, ADHD, anxiety, and panic attacks.” So, what does this tell you about the father’s side, and the mother’s side? Well, the mom’s side tells you that there’s an autoimmune susceptibility there, right? There’s an inflammatory susceptibility there. Now, it doesn’t mean that he may have it, but it’s something that makes you more aware of what could be going on. On his dad’s side, he’s got plenty of neurological problems: tics, ADHD, anxiety, and panic attacks.”

So, there are certain genotypes that have increased or decreased sensitivity of certain receptors. There are families that have anxiety disorders all through their family history, because they don’t have efficient GABA


receptors. Or, their catecholamine receptors are much more sensitive than other people. So there are all these different uniquenesses. And if you look at the research on genetic potentials for psychiatric disorders, that’s what they find. They’re finding that a lot of people have these psychiatric disorders, whether it’s anxiety, or depression, or attention deficit, because within the family gene pool, certain receptors are not as efficient as other people, so they have some of these symptoms. So there’s a potential that there’s a genotype type of sensitivity there, but these types of genotypes don’t necessarily cause them; it’s genotype plus diet, lifestyle, environment, which then creates a phenotype. So we know that there’s a phenotypic expression that he’s having this focus and attention delay, so at the end of the day, we’re seeing hypoxia related issues, we’re seeing frontal cortex, we’re seeing history of basal ganglia indirect pathways… Are you guys following along with me? Okay, great.

So, he found that “mediation helps me, as well as prayer.” Meditation and prayer are what type of activities? Frontal cortex. Not to take away from the benefits of prayer, or meditation for other reasons that are not neurological, but when you focus on an event like this, whether it’s praying to someone or meditating, that’s all frontal. So a lot of times, when you ask what things have helped, it gives you a clue to what you can do to improve rehab. There’s two questions I think are most critical for me when I work with patients. “What things have helped you”; “What things have made you worse?” If I know those two things, it saves me a lot of time. And the things that help, help me understand the odds.

Anti-inflammatory diet has helped, so what am I thinking? He’s got some degree of inflammation. Frontal cortex activation helps, so I know I can use that pathway, right? And he also says coffee enemas help, which activates motility and gets a vagal response, increases blood flow to the brain. These things are all important. Okay?

Now, you guys understand that when someone does a coffee enema, that the coffee enema… the coffee activates the enteric nervous system, they get distention, you actually get afferents going from the gut to the vagus. When the vagal nuclei in the brainstem activates, you get a massive vasodilation effect in the brain too. That’s why some people who like to do coffee enemas will do them and say, “I think much clearer, I focus better,” and that is really a clue to you that they have probably poor cerebral circulation, because as they increase that pathway, they felt positively better. Right? This is what he’s telling us. It’s not so much that he’s detoxing, necessarily, it’s just the fact that it’s an autonomic type of response. Okay?

Now, “I find…” “I have found when I take supplements during the day I feel sleepy and fatigued afterwards. That’s why I take most of my supplements at night. Even supplements that are supposed to help with energy fatigue me immediately afterwards.” You guys, these happen all the time from autonomic dysregulation. So when you increase your load of supplements or food or nutrients, you have to immediately get blood flow to your gut. And if you have autonomic imbalances, you can shunt blood irregularly. So a lot of people that have some autonomic dystonia or dysautonomia to some certain degrees, when they eat food or take supplements, and they just crash, it’s not related to the insulin surge, but as their brain function goes down, you can suspect that there could be some issues with autonomics. So we’ll go over those.

So, let’s go to where we are. We have the flow chart, we have the patient’s chief complaints: severe and constant fatigue, brain fog, low cognitive function. So now let’s localize the regions with the patient history. So, we know it’s frontal cortex. Do we know if it’s left or right? Or is it both? We don’t know. We know that there’s a basal ganglia indirect pathway in childhood; we suspect there could be some brain-gut axis


issues. So from the history, we should start to localize this. That make sense? We haven’t done the exam, we haven’t done a treatment protocol, but we’re thinking, “Hey, those are some factors there.”

Now, you guys, the frontal cortex, when it’s not developed well, the frontal cortex can lead to secondary basal ganglionic presentations. So the frontal cortex is what fires the striatum, the striatum of the basal ganglia then fires into the loops that make the basal ganglia efficient. So with kids that have frontal cortex issues, many times their frontal cortex is impaired. They can’t activate that striatum of the basal ganglia and get that thing going, so they’ll have tic disorders, whether it’s vocal or motor tics, or any type of basal ganglionic types of imbalances. As the frontal cortex gets healthier, they can fire into the striatum, and those patterns go away. So I wouldn’t consider with this person, with such severe frontal cortex issues and developmental delays… I would probably assume that those hyperkinetic basal ganglionic disorders are secondary – right? – and they’ve all pretty much for the most part are no longer present.

Now, during the history, did we identify any neurochemical pathways of the region? And did we identify any metabolic factors that could impact the region, from the history? Yeah. Well, we found he was caffeine-intolerant, so maybe he has issues with metabolizing caffeine through biotransformation pathways, so he’s a slow metabolizer. Your biggest clue would be, take a… he drinks coffee and then he’s just up for the next three days, right? That could also be that there’s a history of catecholamine sensitization genetically. Those are all possibilities with his history, because his father has those.

Magnesium improved tics, and we’re not really too sure about that, but magnesium also have major impacts in vasodilation. We know a lot of basal ganglionic disorders can be from hypoxia. So the middle cerebral artery has this very important branch, the lenticulostriatal branch, and if that isn’t efficient getting blood flow, you can get basal ganglionic symptoms to present. So a lot of times, if people have chronic migraines, magnesium has a vasodilating effect on blood vessels, which improves circulation. So we don’t know. We just know that he reports that there’s magnesium issues there. So what’s the harm of him taking magnesium, if he feels like it’s helping, you know? I don’t think there’s an issue.

Now, he’s got history of asthma, he’s got… his nasal pathways are blocked, he’s got some digestive chal-lenges, and he’s got poor circulation. Could these things impact his brain rehabilitation? So, we right off the bat we know, hey, we’ve got to get this person’s frontal cortex healthier. We’ve got to do some things to improve plasticity in his frontal cortex. And the next question is, what could get in the way? What has contributed to his developmental delay? Are there any factors? So, what does the brain need? Well, the brain needs oxygen, needs glucose, needs activation. We’re not seeing any glucose issues, but we’re definitely seeing some poor circulation, some lack of nasal circulation of oxygen to his brain.

Now, let’s talk about… Let’s go on to the initial survey. So, let me just stop right here. Right here, that was Module One. You listen to the history, you know your neuroanatomy, you identify the regions, identified some metabolic factors, and now we’re playing the game as we work him up. Module Two: Let’s go into the initial survey.

So let’s look at his face, and his facial… Well, tell me first of all, what do you guys see? Before the exam and after the exam. Is there a change in how tired he looks? So just from an exam he looks completely exhausted. Okay? Now, do you guys see a facial weakness? Before the exam, what side is it on? What side is it on after the exam? Is there a difference? Is it more on one side versus the other? So when you guys


are looking at facial weakness, it’s best to take a look at it half of a face at a time. So the question is, which side does he look younger? The left? Or the right? Does he look younger here? Younger here? Or younger here? He looks younger here and older here. The side that’s older is the side of the facial paresis. So it’s on the left. You guys see that?

Okay. Now, here he is after the exam. Compare that: younger, older, to that. Now switch to the right. You guys see that? That’s telling you, you guys, this guy is fatiguing from just the examination. His brain is cooked on… just from an exam. So you can just see globally, he’s tired, his eyelid’s dropping, you see just… exhausted, you see the lid lags developing, you see overall facial paresis. But you have to see this left to right.

Now, if someone wrote in a report he had facial paresis in the lower two-thirds of the muscles on the left, and then he had it on the right, you would think, “Yeah, come on. Right. Come on, tell me. That doesn’t happen.” But pictures are very telling. This is also very important: If you guys videotape patients, it really does help. I like to videotape patients in my office and if they… ask if they allow me to use it for teaching I will. If they don’t, use it to compare them down the road. Okay? And a lot of times, if a spouse comes with them, it’s also great for them just to have their spouse videotape, like, their gait or just to have normal findings, and they keep it in their phone for themselves. When they come back, you can have them tape again and they can compare, and they can actually see their own change. Right? It’s really nice to see that.

So, right off the exams… So, from the history, you guys, you know it’s frontal lobe, and then just from the initial facial… just looking at his face, without doing anything complicated, we can see he’s just getting completely exhausted in a very short period of time.

So, take a look at his gait. These have volume, if you want to… What do you guys see?

This time when you come back, I want you to do the alphabet out loud, every other letter. A, C, E…

Okay.

“A, C, E, G, I, K, L… M…”

Oh. I’m going to plug it in. Can you hear it now? Play it again. So, here’s just… So what I do when I look at gait, first thing I do is, I just see how they’re walking, get a general feel of what’s going on. Then what I do is, I start with the arms. Is their arm swing from one side to the other? Then I look at the legs and see if the strides are different. Then I look at their head position and see if their head’s turned to one side or the other as they’re walking, okay? Then I go in there and I look at their stance to see if it’s wide stance or if they start scissoring, if there’s any hikes or spikes with their movements. And then I look at their feet to see if there’s any abnormal stomping, right? And, I mean, that’s just the general thing, and then other things just start to show up.

Now, once a person does gait, one of the tasks we have them do is, we have them double-task, and double-tasking usually brings out more gait imbalances. So I’ll have them do the alphabet every other letter. Let’s watch that again. So, go through each of those steps.

Just walk how you want.


Do you guys see there’s no arm swing on the right?

[unintelligible]

Do you see how he’s got a hip hike?

Come back. This time when you come back, I want you to do the alphabet out loud, every other letter. A, C, E… “A, C, E, G…”

It’s like his arm swept to the side.

“…I, K…”

So what area of the brain would cause that?

“…L, N, P, R…”

So here’s the thing: If his arm was just stiff and not moving, you wouldn’t see any angulation. But what do you see with him? You see some angulation. So you could have a basal ganglia indirect pathway impact firing of tone, and then you just see less movement. Right? Or general stiffness. But he doesn’t have general stiffness, he’s got a little angulation. So that’s kind of like a spastic posture. So what you’re seeing here is a contralateral effect of the motor strip, right? So this is frontal, motor strip, and you’re seeing some kind of clinical presentations that are on the contralateral side. Everybody with me? Okay.

So, let’s move on. So that’s his gait. So, does this confirm your initial history? That’s it’s frontal cortex involvement of some kind? So you’re seeing endurance issues with his face, you’re seeing that his arm is having lack of activity there. You see some spastic posture. You see some hiking that’s taking place with him, probably because of motor weaknesses involving him lower extremities.

So we can now add in a few things to this initial survey, just from just what we saw. So, facial tone weakness that continues to change during history and exam, because of fatigue. Reduced arm, right arm swing with tilt and mild sway to the left. You guys saw that he was swaying to the left. Normal speech. Positive mood. Normal mental processing with fatigue during history and exam. So he’s getting tired from the history and exam. No signs of metabolic disease. Like we don’t see anything really significantly different with his hair or his skin or his nails or his eyes, or all the things we talked about, right? We’re just seeing somewhat… person looks somewhat healthy, he’s just getting tired through the exam. You guys see how we’re going through this flow chart? Okay.

So, we did the chief complaint, we identified the region from the history, we did some nutritional and metabolic factors from the history, we now did a general survey. So let’s continue on, and the final area that we think is involved is what area? Frontal cortex. Now, just from his exam findings, his arm swing, which side do you think is more involved? Left or right? Left. Okay?

Now, I want to show you some exam findings. So, I want to show you what we saw with some saccades. So, I’m having him do this once, and then I’m having him do it again, and again, and again. So for a total of


four. So what am I doing? I’m doing repeat testing. Why am I doing repeat testing? Because it’s going to tell me what they can handle and what they can’t handle. Okay?

Now, this goes by pretty quick, so let me slow it down for you. Because it’s going to be boom-boom-boom-boom. Okay? What you’ll see with him is, when he goes to the left, the saccades… first saccades are pretty good. Second saccades, his brain’s fatiguing, so when he goes to the left he turns his head. Third saccade he turns his head even more, he’s fatiguing more. Then I tell him to stop moving his head, and then the saccade to the left just slows down. Okay? Watch.

First one. See the head turn? See the head turn? There you go. Okay, so you see the head turn more. If you watch over again… But that’s how subtle these findings are. But when you know it’s frontal, you’re looking at these things really, really critically, and you’re going into, “What’s going on with him as I do more?”

So, what’s happening is, if you look at this, he’s getting worse and worse with each one. So that’s something to think about.

Now, here’s what we did. You guys remember this flow chart, identifying neuron fatigue? So we did an exam finding; we checked saccades. It was normal, but we suspect… Now, why are we doing saccades, by the way? Well, saccades are generated by the contra… by the frontal eye fields. So the right frontal eye field in the frontal lobe pushes eyes quickly to the left, and the left frontal eye field pushes the eye to the right. So I’m trying to figure out what’s going on with his frontal lobe, because his history is really showing these things.

Now, what I like to do is, I like to find out where the area is, do my full exam, figure out fatigue, and then I do a complete neurological exam and rule out everything else in case I missed something. So I always do a full complete neurological exam. I don’t like it when people just do localized exams. I think that’s a poor workup. Right? So I like to find my area, and then rule out everything else, just to make sure we haven’t missed anything, okay?

Now, what we found with him is, he had normal saccades, but when we repeat tested him, the abnormal findings started to develop – you guys saw the head rotation – which means he has impaired neuron endurance. So we may want to do rehabilitation within limits, and consider metabolic factors. Right? So we might go, “Hey, maybe we want you to just do a couple saccades,” or maybe we don’t want to do any, because he keeps getting progressively worse and worse. That’s going to be a call you’ll have to make as a clinician. Okay? And then see how the patient feels after they do them. An interesting thing is, when he does them, he feels like, “Oh my God, when I do these, my brain really feels like it’s waking up,” which is a good sign, versus, “I’ve done four of these saccades, and I just want to shut… I just want to close my eyes and lie down.” So his response was, “Wow, these eye movements are really making my brain, like, wake up? So for me as a clinician, I’m thinking maybe I’m not so close to doing a few of these just slightly and see how he does. Okay?

Now, we didn’t go into optokinetics. And this is unfortunately really hard to see with the video, but he’s doing okay with these optokinetics, and then you just see him fatigue at the end. We do them horizontal and then we do it vertical. He’s looking at the red and white strip. Look at his eyes.


Do you see his eyes just stop moving? Do you see… able to do them. And then we do them vertical. He’s about to fall asleep. His brain is exceeding his endurance. And now he’s just… did a couple vertical ones. You can see he’s done. Okay? So you’ve got to consider: how would you rehabilitate this guy? Would you wait? Would you do some endurance things? Would you do some metabolic things? This is all things to consider, but now you’re going, man, this maybe not be the person where you do in there and do tons of aggressive neurological rehab as part of your workup. Okay?

So again, with saccades, with optokinetic tapes normal, we do repeat testing, it became worse. We’re considering that there may be some metabolic issues.

Now, one possibility is their abnormal findings – like the first time they’re doing they’re totally abnormal, and as we do them he just gets worse and worse and worse or has new symptoms develop, like vertigo – those people, like if… I’ll give an example. If you go down here on this flow chart, if we had an abnormal optokinetic activity initially, and we kept doing it several rounds and rounds of him, and new symptoms developed, like now all of a sudden he has vertigo, and he’s got that ring in his ear, we’re just saying that’s unstable. We don’t want to rehab that any more. We don’t want to use that type of therapy for rehab. It would be like this is not where we go with this.

Or, if we had him to optokinetics, and he got worse, and we might want to address neurological metabolic factors first, and… so he’s fatiguing with them as we do them, but he’s not necessarily getting to the point where he’s crashing. He’s actually saying he feels like his brain’s kind of waking up. So I’m heading more towards, I might do some rehab with him, with some metabolic support. There’s going to be a clinical judgment call you have to make with these. Okay?

Now, here he is. What I’m having him do is, we’re checking his vestibulo-optical reflexes. He’s doing them by himself actively, then I do them passively. And the vestibulo-optical reflexes should look nice and smooth, you know, perfect, symmetrical from one side to the other. They shouldn’t deviate up, they shouldn’t deviate down, there shouldn’t be any pauses. Those all look good. But you’ll see after the first second or two, you’ll see his eye dilate, and you’ll see ptosis develop. But his vestibulo-ocular reflexes are pretty good.

So here we go.

So, look at that left… the pupil on the right, your right. You see how that’s dilating? And then… we’re trying to see if he’s got any nystagmus. I did head shaking. I wanted to see if he had any head shaking-induced nystagmus.

You dizzy now? “Not too much.”

No dizziness.

I’m going to do the same thing. I’m going to move the chair for you.

I’m doing it for him. Passively move the chair. Looking at his optokinetic reflexes, and then you guys will see that eye isn’t dilating more, because he’s getting an autonomic response, and he starts… even starts to have a little deviation. Notice this there? So again, we’re seeing his vestibular system is pretty intact, which tells


you what, if you’re trying to activate his frontal cortex? You could probably use his vestibular system as a way to feed into his frontal cortex. So, you guys remember that pathway, we talked about gait? Cerebellar pathways fire to what? Opposite brain, contralateral brain. So we go, “Hey, you know his frontal cortex is not in good shape, but we can probably use his vestibular system that’s in pretty good shape, to activate it, as one of a potential possibilities of treatment.

So, as… So anyway, those are a couple of examination findings that we found with him, and at the end of the day, where we are with identifying his region is, you know what? He’s got some endurance impairments here, so we know there’s definitely a metabolic factor here, and especially with what? Circulation, oxygen to his brain. But as we do some of these therapies, he’s not… his exam findings are changing, but he’s saying he’s feeling better; that they’re actually having some awake… some circulation, blood flow response to his brain, so for me to have a tendency to say I might actually do some therapy with him, maybe in combination with some nutritional, dietary, lifestyle things to make a difference there.

Now take a look at his pulse-ox reading. His pulse-ox reading is ninety-five percent. Okay? His lungs are clear. Heart sounds are clear. But he’s got pulse-ox ninety-five percent. Hands are very cold. So one of the things – and his resting heart rate is eighty-seven. His resting heart rate is eighty-seven. So he’s not, again… We’re concerned about oxygen delivery here as an issue.

One of the things I use… you guys see these? This thing here? This is a wall thermometer to look for leaks. You can buy it at Home Depot. Surface thermometer. I put it on people’s limbs. So look at his blood flow to his limb. His temperature’s eighty-seven degrees. We should see this in the nineties. And it’s a ten-degree difference between his foot and his knee. So what does he have? He has impaired circulation. This is a really easy way to show circulation issues. So these are like forty bucks. Surface thermometer. Put it on someone’s feet, and then compare it to their knee; put it on their hand, compare it to their elbow, and you can see if there’s any difference in temperature. Normal, that his temperature should be consistent all the way through. You see the distal tissues are colder, then you know you have poor circulation.

So now I’ve got poor circulation, I’ve got a pulse-ox of ninety-five, I have a frontal cortex not developing, and he’s fatiguing on my exam. So do you think there’s a metabolic factor related to his brain? Yes. And we know what area of their brain is involved: It’s the frontal cortex. Okay.

Now, we go back to this diagram here. Healthy and unhealthy resting membrane potentials. So we know he is having poor ATP production in his brain. He’s fatiguing. He’s getting exhausted. His brain’s not developing. And it’s not developing the frontal cortex. He doesn’t have executive function, so he wants to do things in life, but he doesn’t have the brain plasticity to make it happen, okay? Now, right away we look at, well, could it be poor circulation? Could it be anemia? Could it be dysglycemic? Could it be lack of activity? Could be inflammation, autoimmunity. So we can all agree just from the findings, he’s got some poor circulation issues, right? Now, he’s not anemic on previous lab work. So we’re not concerned about anemia, but he has some poor circulation. So here’s the thing. He has poor circulation, he has low pulse-ox, lungs are clear, heart’s clear, and no anemia.

So this is how we do it. This is how I do it. If I see poor circulation, lungs are clear, heart’s fine, and I don’t have any types of anemia that are going on, then I’m trying to work on their nitric oxide pathways to improve their circulations. Okay? That’s what we’ll do with this therapy. So, he’s got poor neuron endurance, he


doesn’t have the ability to handle stimulation for a long period of time. So if he’s trying to read, or trying to focus, and trying to accomplish his goals, what’s going to happen with him? He’s going to fatigue. Just looking back and forth for a few times just makes him fatigue. Right? So, we know we have an endurance-related issue.

So now, the decision that we make clinically is, do we do… What kinds of things do we do nutritionally; what kinds of things do we do to improve his brain endurance? Do we do it with rehab? Do we do rehab first? Or do we do nutrition first? So that’s where you have to make the call. Right? Because all chronic cases have overlap.

So we decided to rehabilitate him with limits that consider metabolic factors. When I say “we,” I mean myself and the patient. Because I discuss this with him: “How do you want to do this? Because I’m kind of torn. How do you feel after we do these brain exercises? Do you feel like they’re getting better? Do you feel like they’re making a difference for you? What do we need to do?” He goes, “Well, I feel a lot better doing them. Immediately I feel more alert.” So we decided to consider some of these metabolic factors that we’ll go over with you in a second here, in combination with some therapy, but being very conscious of fatigability. Okay?

Now, let’s go through where we’re at with this flow chart.

We know that his chief complaint was severe and chronic complaint, brain fog, low cognitive function. We know we identified it to the frontal cortex primarily throughout the history. We saw things in the initial survey that lead to frontal cortex. We know there’s some metabolic factors with caffeine intolerance, we think magnesium made a difference. He has some nasal septum block. And then we go into the exam.

So the question actually is: Do I want to do exercises to activate the involved regions? So what I’m trying to activate with him will be the frontal cortex. I want to get his frontal cortex involved. Now, is it the right or is it the left? Because it’s actually both. Both his left and right frontal cortex were impaired. I don’t have all the exam findings at the time, but I just want you to understand. And we found some specific issues with pathways from the cerebellum to his cortex that we wanted to activate, so we found his left cerebellum and right cortical integration was off, and we wanted to use his cerebellar pathways to make a response to kind of wake up his brain.

So what I gave him for therapy was saccades in all directions. So saccades in all directions means I’m going to activate the frontal eye field on the left and the frontal [eye field] on the right. And the blood flow to those areas are the middle cerebral arteries. So I’m going to have him do this all throughout the day, because what is it going to do with oxygenation to the brain? As he does these activities, he’s going to get blood flow there. So, if you guys look at PET scan research, what do they do? They have a person do something and see where blood shunts to. So whatever area of your brain you activate, like if I just move my arm right now, you did a PET scan, I’d have blood flow to this area shunted that way. So his frontal cortex is not developing well, so I’m going to have him do saccades in all directions, get those frontal eye fields going. So I fire middle cerebral artery shunting to both these anterior branches, to his frontal cortex, so I can start to nourish his brain, okay?


Then I give him optokinetic activity to the right to improve his left cerebellar integration with his right frontal cortex, and then I give him visual fixation with tandem walking to activate his frontal cortex.

So, one of the things that happened with him is, he had severe ataxia, but the minute he looked at his thumb, his ataxia stopped. So when he activated that frontal cortex pontine cerebellar loop, it normalized. So visual fixation activates the frontal cortex. So we have him a frontal cortex visual fixation with some cerebellar exercises to get those two integrated, so I can start rehabbing that loop. Remember that loop with gait? The cerebellum to the frontal cortex to the pons back to this? So now I’m going frontal cortex to pons to cerebellum, getting frontal eye fields going, and I’m getting that left cerebellum to right cortex, getting to that cerebellar cortical loop, to just get that activity to his frontal cortex.

Now, from a metabolic factor and diet and nutritional considerations, this is what I decided to do. I wanted to first… well, I wanted to open up his nasal pathways best I could, the best way we can, so surgery is a candidate, and then we’ll also put a little clearing pathway block on his nose. Nitric oxide support, because I want to improve his circulation. I put him on a modified ketogenic diet, because he did have some degrees of blood sugar and stability, even though he was eating well, and I wanted to stabilize his blood sugar. I wanted to give him… continue with his anti-inflammatory diet. He felt coffee enemas were really making a big difference for him, and days when his brain wasn’t working he would do them and he would improve his clarity. So we know that’s having a vagal vascular response. So if it’s helping him, we don’t want to deny that for him. We’re not doing it for toxicity reasons. And then we had him use a CPAP. He had a CPAP but he never used it, so we just said, “Hey, you’ve got to start sleeping with that, because you’re not getting enough oxygen to your brain.”

So, you guys see what we’re trying to do? We’re trying to get oxygen to his brain, get blood flow to his frontal cortex, develop plasticity in his frontal cortex. Okay?

My clinical impression: Reduced cerebral endurance and stamina due to hypoxia from severe deviated nasal septum; poor systemic and cerebral circulation; potential genetic polymorphisms impacting dopaminergic or GABAergic dynamics with family history of tics, ADD, anxiety, and panic attacks. But you’ve got to work with what you’ve got. Brain-gut axis impairment with loss of oral tolerance.

So you also, if you read his history, and there’s part one and part two and three in the pre-course material, he has multiple food sensitivities and he’s on a very clean diet, and he has to be. So we suspect there’s some oral tolerance issues with that as well.

Now, here we are in the office, and we did some treatment with him right away. So you can take a look here. There’s some volume on this one.

So I’m doing optokinetic, trying to get that left cerebellar-frontal cortex integration going. He had a startle response that starts to change. He’s happy. It’s better. He had a little bit of clonus…

“…already better.” “Yeah.”

…clonus improved right away. He had hyperreflexia; that’s improved.


…it’s through his whole body. [unintelligible] “Yes.”

That’s his mother.

“It was so…”

His mom noticed he had hyperreflexia; his whole trunk [unintelligible]. He’s happy, you see? Because he’s seeing change happen to his symptoms, to his clinical exam findings, right away.

“You just have to make sure to do exactly what the doctor says, asks you to do.”

He had light-sound sensitivity. That’s pretty much gone.

[conversation]

So, I’m going back and doing some of the exam findings, and the thing is, his mom is a doctor, so she knows what all these findings are. So she sees the hyperreflexia; it’s gone. She sees the light-sound sensitivity is changing. So they’re really, really, you know, excited and happy, because at some point you don’t think there’s any hope.

So let me show you his pre-treatment gait and his post-treatment gait. This is just right after I did what I just showed you. Okay? Let me show you his first gait again, so you guys can see it.

…just go ahead and walk.

Do you guys see the sway to the left…

…come back…

…tilt to the left…

“He’s moving like his…”

…lack of arm swing on the right. You guys all see that?

Go again.

Swaying to the left, tilt.

Come back. This time, when you come back, I want you to do the alphabet out loud, every other letter: A, C, “A, C, E, G, I, K, L, N, P, R…”

Okay? Here he is after what I just showed you. So his arm swing’s starting to come back. You guys see that? He’s not tilting as much.

“It’s much better.”


So that’s the key thing. We do an exam finding; we want to see what changes. If it changes it, you know that’s the therapy you’re going to use. If it doesn’t change a finding, it’s not going to be the therapy you use. And once you find the therapy you use, you figure out how much of it you can do before they crash, or if you do that first, or if you do metabolic things. Does that make sense? The hard part is not finding what area of the brain is involved. You guys are already good at that, finishing with the second module. Okay? The hard part… the heart of this is knowing what to do first, how to follow through with it, and how things are.

So anyways, these are some of the exercises I gave him to do, to activate his frontal eye fields. I’m doing that because I want blood flow to go to his frontal lobes throughout the day.

… then you go back and forth like… Do it before your eyes get tired. Then when your eyes get tired, switch.

See how his head’s moving? We don’t want him to do that.

“Oh, okay. Good.”

So when I see his eyes get tired, and he starts getting worse, I stop him. And afterwards I’m telling him how many he can do.

Side to side, up and down.

I’m just trying to light up his frontal lobes.

If some days you feel you can do more before your eyes get tired… “How many minutes a day, or how much? I was about to say, one or…” You repeat it… “The more the better?”

The more frequently the better, based on his endurance.

…move towards your right…

And then we gave him an app to do some brain rehab, and we’re going to one side.

So you guys, it’s not a hemispheristic model for this case, for me. I’m trying to get both his frontal cortexes… He’s got a metabolic frontal delay. It happens to be his left cerebellum and right aren’t integrating, but I want to get both sides to work.

Now, when he… See how unstable he is, when he tries to stay in that position? He had ataxia when he was walking, but when he looks at his thumb, he doesn’t have any ataxia anymore. So as he gets his frontal cortex involved to feed into the cerebellum, it’s fine. So one of the exercises we gave him was to walk while he’s staring at his thumb, to get that cerebellar-frontal cortex integration working together.

So his brain rehab is basically this: We gave him saccadic eye saccades, eye movement to the left, right, up, down, oblique up to the right, oblique down to the left. These exercises are used to activate the left and right frontal eye fields. I’m doing this to activate the anterior branch of the middle cerebral artery, to get blood flow to those frontal cortexes, because of oxygenation issues inactivity.


Optokinetic activity with OptOK app. Pull screen with moderate speed to one side. I’m sorry, to the right. This exercise activates integration between the left cerebellum and right frontal cortex via that long name – you guys remember? – that dentatorubro… That’s the pathway from the cerebellum to the frontal cortex and back, that large triangle loop.

Visual fixation with tandem walking. This exercise is to increase integration with midline cerebellum activity with the frontal cortex.

Visual fixation with tandem standing on a foam cushion. This exercise is to increase integration with his midline cerebellum and frontal cortex.

Now, here’s my metabolic strategies. And again, we decided them both together.

Nutritionally support his endothelial nitric oxide activity to aid in systemic and cerebral circulation. So things like vinpocetine, things like ginkgo, activate endothelial nitric oxide. Synthase; we’re trying to get his circulation to improve, especially to his brain, while we’re doing all this.

Modified ketogenic diet, eat every two to three hours to stabilize blood sugar levesl. Measure ketone levels with ketone strips. So he’s going to be eating mostly proteins and veggies, avoiding all sugars and carbs. He’s going to get into a modified ketone state. We want to make his brain as efficient as possible when his endurance is this compromised. Okay?

And then exercise with oxygen for a minimum of five to ten minutes with high intensity. So having him put on an oxygen mask, and then exercise with heart rate to flood his brain with oxygen. And he can do that in the morning, he can do that in the afternoon, to really get some circulation and blood flow to his brain.

Now, best scenario is, he does some high-intensity exercise, like getting his heart rate up while he’s wearing an ox… with breathing oxygen, then he’s done, then he does some activity to get some blood flow to his frontal lobes, then he does all those exercises now that his brain’s flooded with nutrients and oxygen and glucose, and he can develop some plasticity. Okay?

Wear Breathe Right strips. The Breathe Right strips are the ones you put on your nose to open up your nasal passages. And then oxygen concentrated during sleep with Breathe Right strips; it’s actually the CPAP.

Continue with anti-inflammatory diet; continue with regular coffee enemas. That also gets the blood flow circulation aspect of brain.

So, do you guys see what we did with him so far?

Okay. Here’s the text he sends me the first day. “Hi, Dr. Kharrazian. This is Robert. Thank you very much for yesterday. I had an unbelievable breakthrough. I woke up today and did all of the exercises and slept last night with the oxygen machine. I already have much more energy. Here is my email for the report, not sure if it is in the file.”

So right away, the first day there’s already a positive outcome. And then this is him with a month followup. It’s audio here.


“Okay, so I came here about a little over a month ago, and I’m thirty years old. I always said that I was like a ninety-year-old. I felt like my energy level, concentration level, was very not according to my age group. And so I came here with a lot of mental fog, a lot of fatigue, chronic fatigue, low energy, and just lethargic. And immediately after coming here and starting with the first week and second week, the exercise that I was going, it little by little transformed my energy and my mental focus. I’m much more sharper, much more energy, much more consistent in what I do day to day, and I can function much better to a thirty-year-old, not a ninety-year-old.”

First day you had a good response? “Very good response. I did the exercises, the eye saccades, the move-ments, I changed my diet, eliminated the sugar and the dairy, and mainly meats, fats, and proteins. And then combined that with the exercises and the breathing, more oxygen intake. It changed a lot. Changed everything.”

Okay. So you see the though processes. So what I wanted to show you guys was the clinical thought process, through that flow chart, all the way through. Okay? These types of things are not a big deal. So you guys will all, if you do functional neurology, will do this type of stuff. It’s not something to “wow” over; it’s easy, it’s straightforward.

Now, you guys see how easy that was when you go through a thought process that’s efficient? Where is the region of the history, what does the initial survey show you, what do the exam findings show you, do you have a metabolic issue, when does it fatigue, when do you do one versus the other – metabolic or neurological – when do you combine them together? And that’s basically, you know, a case to kind of blend those things for you.

So hang in there, you guys. We have just two sections left to cover. We have a quick review section, and then once we do the review, we’ll go right into the questions and we’ll be done for the day. Okay.

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