the initial clinical survey and how to identify the … · module two transcript: neurological...

MODULE twO tRANSCRIPt: NEUROLOGICAL INItIAL SURVEY | COPYRIGht © 2016 FUNCtIONAL NEUROLOGY SEMINARS LP | PAGE 1

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

Transcript – Neurological Initial Survey

Presentation by Dr. Brandon Brock

Okay, so good afternoon. Everybody in their insulin-resistant state? Ready to go? No sleeping? I will shine the laser pointer on you, alright?

Well listen: We have been retracing charted territory. So in other words, we’ve given you a lot of information about the central nervous system, and Dr. Kharrazian and I, when we were talking about how in the world are we going to put this stuff together, we decided that we really wanted to take that central nervous system and just jump into it immediately, because that’s the abyss that everybody’s kind of scared of in the world of neurology. Like the cortex, and when we start getting to the brainstem, it will make it really doable for you. But we’re now going to start venturing out into other systems: a system called the peripheral nervous system.

Remember the very first rule I told you whenever we started doing this is, is the lesion central or peripheral or both? Is it neurological, metabolic, or both? Is one perpetuating the other? So there’s a lot of good research out there that shows that when you have a peripheral nerve lesion, there’s central nervous system consequences. No promotion. On my Facebook page I posted a nice little paper that just came out, that says there’s no more questions. Manual therapy, subluxation reduction, adjustment, exercise, whatever you want to call it, changes brain. And it really is going to change the face of what people think about segmental fixation and so forth.

We’re realizing this: Most everything we do is brain-based, to an extent. Medication is brain-based. Nutrition is brain-based. Certainly what we’re doing better be brain-based, or else we’ve got the wrong name up here, right? But what we found is, the nervous system has its fingers in everything. So it’s…

Is Siri talking to me back there? Okay. No.

So what we’re going to do is this: Every time we get a new form, I’m going to overlap it with a chart. And then when I get treatment, I’m going to overlap the treatment with the form with the chart. We are giving you a very superficial, one-dimensional understanding of the forms. But – now just think about this for a


second – you could have all those frontal lobe symptoms on the questionnaire, but could you have a real genetic issue with neurotransmitters? Yeah. You could. Could you have an insulin issue that is changing monoamines, which is changing neurotransmitters, which is leading to the problem? Yes you could. There will be dimensions that we will add onto these intake forms. I need for everybody to really understand that.

Right now it’s like, “Hey, this looks like it could be this, this, and this,” but you don’t… you need to realize, you need to get to the point to where you can take one of those things that scores really high and learn to break it down and say, “Is it a cardiac issue? Is it an infectious disease issue? Is it an autoimmune issue? Is it a metabolic problem? Is it an ablative tumor?” You know, these are the good differential diagnostic skills that we promised ourselves that we were going to make sure that everybody in here had. There’s no reason why you can’t have them. And by the way, most people in here are coming from a metabolic background anyway. So it’s not a hard transition to say, “This is how this ties into the nervous system,” and then for the functional neurology people, it’s like, “This is how it ties into the metabolic system.” They’re going to be woven together.

So we’re going to kind of jump in and start looking at the peripheral nervous system. Now, my background is peripheral nerves. I love that – you know – the whole concept of peripheral nerve lesions and stuff like that. I did electrodiagnostics for years. So it’s my pleasure to introduce that section. But I’m doing to introduce it in the context, the text, of peripheral nerves and outside of the central nervous system is going to be done in context with what you’ve already learned in the central nervous system. So it’s not like I’m just going to pull it out and say, “Here it is.” I’m going to do that tomorrow. But today I’m going to introduce some of the initial neurological concepts and weave them together with the other parts that we’ve already heard this morning, so it’s a growing story.

Disclaimer. Disclaimer. Everybody’s happy. Alright.

So, these are clinical quickies that you’re going to see, and that you’ve already seen, and that you’re going to see more of. This is kind of Dr. Kharrazian’s stuff, but I just want to throw it up there that we will have things that you need to be checking off and checking on patients. I mean, let me just ask you a random question. Does, for instance, your nail beds… could it have anything to do with your brain? Absolutely it could. If you have hypoxia, it could be a problem. If you have poor capillary refill, it could be a problem. If you have a thyroid issue, making fragility in hair and nails, could it be a problem for brain? Absolutely. So when you see these things, remember: It all runs down to where we’re going. That is, we look at brain. That’s what we’re doing in this program.

So I’m not going to steal the show on this – Dr. Kharrazian’s going to go through it – but here’s mine. And here’s what I want you to be able to get out of this weekend. I’m going to give you some basic stuff right here, real quick. Is there a motor problem? A muscle problem? So whenever your patients come in this week, you’re going to start checking off: Is there weakness? Is there atrophy?

Now, what are these both signs of? Weakness with atrophy that is rapidly because of denervating, not because of disuse. Remember, I have pounded this into everybody. Is it upper or lower motor neuron lesion? It’s lower. Remember, I told you: Is the problem in the peripheral or central nervous system? If it’s lower or upper motor neuron? And then is it left or right brain? Is it anterior or posterior? Inferior, superior, outside, inside? That’s what we’ve been working on this whole time.


So when I say I’ve got a person that’s weak, with atrophy, and there’s fasciculations all over the place, and they’re starting to get weak hands, by the end of the weekend you’ll immediately know what that is. I’m going to give you every peripheral nerve combination, not memorize the problems, but the differences, and you will know them. The difference between nerve root, plexus, radicular – which is nerve root – down into the peripheral nerve, polyneuropathy, ventral horn cell, neuromuscular junction, primary muscle disease. There’s one little bitty thing that differentiates each of them, and you’ll know it instantly. Okay?

Why is this important? Because in the world of neurology, these patients walk into your office every single day. So people say to me, “You know what? My specialty’s not orthopedics.” Good. Don’t care. Doesn’t matter. You can learn what a radiculopathy looks like. It’s pretty straightforward.

So, spasticity: upper or lower? Upper. Okay. Facial involvement will be a big deal, because if you have weakness in a limb with facial weakness, it’s above the foramen magnum. So that’ll tell you: “Do I need to go to the brainstem or the cortex? Or do I need to stay and do the spinal cord?”

Then I’ve got a whole section on spinal cord, not this weekend. You’ve also got to realize: We have a whole section on peripheral nervous system lesions too. So each section that we’re doing, big picture will be whittled down into a smaller, more myopic presentation where we talk just about that for two days.

Is both legs involved? So let’s just go through some scenarios. What if both legs are involved? Could it be cauda equina? Yeah. Could it be a polyneuropathy? Yeah. Could it be a parasagittal meningioma? Yes. So I’m going to challenge you to know. If somebody comes in with bilateral lower extremity symptoms, and it comes all the way up to here, is it a myelitis in the thoracic cord? If it’s in a saddle distribution, maybe it’s cauda equina. If it’s both legs with upper motor findings, then maybe it’s in the brain and there’s a meningioma that’s benign growing in between the two hemispheres. If it’s in a stocking distribution, maybe it’s a polyneuropathy.

Now, you’ll be able to replay this and watch it. And I’m going to say it so that you can do that. So don’t even really try to take a ton of notes. Just enjoy. You can watch it a little bit later.

We’re going to say: Is it on one side? Is it just on the extensors, flexors? Do your myotatic stress responses – that’s what DTRs are now called – do they show this and do we have any tremor? This is all our motor stuff. So for the next month, this is what you’re going to look at on your patient. And I’m going to show you more about what each of these mean as we go, okay? I’m just kind of… just giving you a brief introduction.

Every time we look at motor, we discuss sensory. So now I’m going to say this: Is there any numbness? What is the pattern of numbness? Is it in a dermatome, meaning does it cross the wrist to the fingers to the elbow to the shoulder? So watch this. Real simple. The lesion’s at the wrist: it’s just the digits. The lesion’s at the elbow: it’s the digits and the palm. The legion’s in the neck: it’s digits, palm, forearm.

So I’m going to teach you some very simple rules to help you understand where the lesion is at, okay? Does that help? It’s going to help you immensely, because you’re going to have to now become a human electrician and start wiring all these peripheral nerves together, but when you have some, like, the three basic rules for the three basic entrapments of the three basic nerves of the upper extremities, it becomes


much more easy than saying, “Hey, here’s the radial nerve! Let’s do this giant, long explanation of it,” and people are like, “I can’t do it.”

But we have to know the pattern of numbness and the fiber type. And burning. So numbness and tingling, more large diameter. Burning and temperature loss, more small diameter. Some diseases and polyneuropa-thy affect only small fibers, and some affect only large fibers. I need you to catch that. So, I’m a peripheral nerve. I’ve got small fiber and large fiber types. I’ve got pain and temperature, I’ve got light touch and vibration. Some disease processes will either demyelinate or create an axonopathic presentation in one fiber type or the other. I broke those down for you so you don’t have to go look them up. Cool? Alright.

Cold limb. What could a cold limb be? Could you have a cold limb because of a small fiber type lesion? That’s your autonomic nervous system, by the way. And what controls the vessel diameter? Small fibers. Well, could it be a thyroid condition? Yeah. Could it be a nitric oxide condition? Yeah. So when we start going through this, we’ll do more and more case studies, and each case study will include these forms, and it will force you to think, “It could be this, but no, wait a minute, it’s going to be that.” Or, “Maybe it’s this, or no, no, wait, maybe it’s that.” So you’ll start thinking about the different depths of differentiation, and when you start overlapping you’re going to say, “Wait a minute, this guy’s got diabetes affecting both motor types. It’s in a stocking-glove distribution. Now their legs are numb, it’s moving to their hands, and now because of the diabetes they’ve got inflammation and it’s creating this, that, and the other,” and you start to see this giant collage of problems occurring, and you’re like, “Wow! I just found a neurological problem because of a metabolic disorder that’s not controlled.” And that person comes in to you and you check their blood sugar and it’s 400.

Honest to goodness. Chiropractic neurologist comes into my office. And I check her blood sugar. She’s like, “I’m losing weight, I pee a lot, and, you know, I’m hungry all the time.” And I’m like, “Wow. That sounds like diabetes.” And her blood sugar was 400. But she had already lost all the sensory stuff up to her knees, up to her elbows, and was starting to get a lot of other retinal degeneration, microalbuminism was being challenged in her kidneys: not good. But she came in and said this: “I have MS.” I was like, “Really? Says who?” She’s like, “Says me.” I’m like, “Says you? How’d you know that?” “Well, it’s just what it sounds like.” And then the person she was with, she heard her explanation, and she goes, “Wow. If you were an animal, you’d have diabetes.” I said, “Yeah. You sure would.” 400.

Okay. So gait. Steppage gait. So, are you having to step really high, and you see somebody doing this kind of stuff? Or is it slapping? So I’ll go through all of the gaits with you. Scissor gaits, diplegic gaits, hemiplegic gaits, ataxic gaits; you’ll know all of these. When does a toe deformity matter, when does it not matter? Okay?

I’m going to go through the head… and I need you to understand something. In the vestibular system module, I am going to talk to you about head tilt, and head tilt with skew deviation in one direction or the other, meaning the right eye’s hypertropic with the left head tilt, or the left eye’s hypertropic. They mean two different things. So we will talk about all of the integration from your inner ear, including your otoliths and your canals, but if we make it like that right now, everybody’s going to walk out and say, “I hate otoliths and I don’t like the vestibular system, and I don’t even understand the steppage gait yet.” So we have to take it slow. And we’ll just say this: “Can you see a head tilt? When you look at the head tilt is one eye up


or down? Can you even recognize it?” Then we’ll learn what it means, how you rehab it, the things you do, and it will be very systematic for you.

I’m going to talk about a lot of these things here in just a little bit. What your lids look like, what your facial symmetry looks like, what your pupil symmetry looks like, all the way down. And then we’re going to go through the torso, and find: do you have labored breathing? Are you barrel-chested? Are you a pink puffer? Are you a blue bloater? You guys know those. Do they matter to the nervous system?

If you have emphysema, then guess what? Your oxygen concentration… You have this: You don’t have enough elastic recoil to get oxygen out of your system, so you’re going to retain oxygen. But you’re going to eventually become hypoxic. When you become hypoxic, and you start to get a little bit of neurodegenera-tion, it would be nice to know. I’m going to be real honest with you. If that person’s on their inhaler, and their SPO2 goes up, yay! Happy days, man. I’m just trying to preserve the brain. Have you see these new e-cigs? They cause popcorn lungs. Have you seen this? Nothing’s safe. I’m like, “We finally got something safe.” No. We don’t have anything safe. Apparently.

So, we’re going to look at all these things and say, “Wow. The person’s coming here, they have neurode-generation, and they have signs of emphysema, or they have signs of hypoxia.” Or they have a thrill, and a murmur, and their ejection fraction is down, and now they have a cardiac pathology, and as a result they’re not going to get blood flow to their head, and guess what: neurodegeneration. Their carotid system is not that great. I have one – it’s about a two- to three-hour section of all the vasculature, from here up. Not this weekend, thank God, because it’s not… There’s only so much difficulty we can give. You’ll know how to draw it. By the end of this weekend, you will be able to draw the entire peripheral nervous system. I promise. You may think you can’t, but you will.

Okay. So we go through this. Is there any herniations, like umbilical herniations? Like umbilical herniations? Stretch marks. Can it have anything to do with adrenal function or glandular function? Yeah. I mean, so you look at these things, and you’re like, “Wow. What is the metabolic terrain like? What labs do I need to run?”

You come over there – now, this is the part that I really like. Is this person really oriented? And I used to think this was kind of silly, because I didn’t have these kind of patients, but then I started getting them and I’m like, “Hey, where you at?” And they’re like, “…Utah?” And I’m like, “Utah? This is Texas.” And they’re like, “Oh, close enough.” And I’m like, “Yeah, close enough. What year is it?” And you know what’s funny? A lot of times they’ll tell you the year in which their degeneration started. “It’s 1993.” And you’re like, “Wow. Tell me how old your grandkids are,” or “Which grandkids do you remember their names.” And they’ll go, “Timmy.” And then you look at the family members and there’s, like, Tommy and Johnny and Jimmy, but Timmy’s the oldest. And he was born right around the time that they tell you is the last year that they remember. Pretty interesting stuff.

Now, when people start to jump ahead of that after therapy, you have made a difference in their lives. So pretty cool.

So, do they have delusions or hallucinations? Or do they have, like, grandeur talk? Like, “I’m going to climb this mountain.” And you’re like, “Wow, really? You barely made it to the clinic. I don’t know how you’re going to climb the mountain, but let’s go for it.”


Now we look at this. Look: verbal fluency, verbal repetition, verbal comprehension. What do those three things look like? Those are the three keys to the aphasias. For those of you that watched some of the videos, it was very easy. They were either fluent or they weren’t. They could either do repetitions or they couldn’t. They could either comprehend or they couldn’t. That tells you every one of the aphasias.

So, take seizures and take speech abnormalities, and most of the people tested that are diplomates cannot tell you what they are. Sorry. Everybody thinks that if you have a Broca’s aphasia that you can’t talk. That’s not the truth. You may be saying all kinds of stuff, okay?

You go down a little bit further, and now we have all the swallowing, comprehension… I’m sorry, speech, and then the short-term, long-term memory, which we kind of already talked about, the recalling of facts. All the way down to being depressed, anxious, and so forth.

These are the little things that I want you to start observing based upon last module’s material and this module’s material. Can you go through and just observe these things? I don’t care if you can fix them, I don’t care if you know what treatment it is, and I don’t even really care if you can differentially diagnose them. I just need you to be able to say this: It’s there or it’s not. Because if you start to observe it, and if you recognize it, you’ll start asking the question: “Why is that there? What’s causing it? Now what are we going to do?” So we’re trying to teach you the observations to the whys, so you can determine the whats. “What am I going to do about why this is there?” Okay? And again, think about all of the stuff we could give you right now, very fast, as it – you know – relates to treatment and to diagnosis, and then expect you to just do it. It would be a disaster like it has been in the past.

Okay. So these are the things that we’re going to look at in the next forty minutes. We’re going to look at behavior, peripheral nerve evaluation, posture, gait, muscle symmetry, eyes, torso, and respiration. We’re just going to get a start. A start. Okay? I’m not going to go all the way into each one. I’m just going to say, “Hey, take a look at this. These are the things to consider. Here’s a chart for you.” Because we have lots of lecture time on each individual chart. Each chart I give you will have an entire section of lecture dedicated to it. So I need to tell you that so you don’t get anxious about, “Oh my God, I don’t know everything that he’s talking about.” It’s not designed that way. It’s designed for this. Can you stay in the ballpark with motor, sensory, mental function, torso, respiration, and the observation of gait? If you can do that, awesome. You’ve got the big picture. Okay?

So, here’s what we have. Mental function. And then mental function, it’s like, do we have depression? Do we have anxiety? Do we have are they mentally coherent? Are they delusional or having hallucinations? Is there any memory loss? Is there any emotional trauma? These are the things that we like to know about. I mean, if you have depression, we have to think about things like this: a SERT mechanism. This is your serotonin recycling transporter. So, some people genetically, this breaks. They don’t have it. So they’re just prone to having serotonin issues. That’s one issue. Well, maybe they have an insulin problem. So now we have to go back and see if they have insulin resistance, and now there’s some competition for monoamines, and as a result they don’t have the precursor to serotonin. And then we have to talk about cellular damage and so forth. Some people have malnourishment, some people don’t absorb proteins well, some people have gut infections and it’s actually eating up all the proteins, so they have protein insufficiency, and they don’t have the monoamines for serotonin.


So what I’m telling you is this: There’s depression. There’s that intake form. And that intake form is showing you all the parts of the frontal brain that aren’t well, and so you have to say, “Frontal lobe’s not good. You’re depressed. Now why? Why? Is it because you have a major situation going on in your life? A crisis? Is it situational? Have you been like this your whole life? Have five other people committed suicide and now you’re having the same symptoms and so is your brother and sister? There might be a genetic component to that.” Well, we have tests now, we can look at that kind of stuff.

So, depression and anxiety, really, we can have all kinds of stuff again that cause it, but we have to look at genetic expression, exposure, diet, trauma, inflammation, infection, and then of course neurological function in various areas. This will help us determine.

So when somebody comes in and they’re like, “Man, I’ve got depression and anxiety,” I’m like, “Have you had a head injury?” “Nope.” I’m like, “Okay, have you had a fever?” “Nope, no fevers.” “Um, you know, does anybody in your family have diabetes?” “Yep, everybody has diabetes.” And you check their C-peptide, and you check their glucose, and it’s outrageous. They’re massively diabetic. And you start looking at them, and you’re like, “Man, I think they’ve got, like, systemic inflammation and bad fuel for delivery, and then they have a gut problem, they don’t absorb things, and their iron is low,” and you’re like, “You’re also anemic on top of this. Congratulations.” And they’re like, “Yeah, thanks. I guess.”

So now you’ve got all these things that tie them to the fact that you’ve got to make a frontal lobe better, reduce their depression, clear their anxiety, and make them this – ready? It’s called wellness. You have to go through and change their life. Because it’s not about one pill at that point. I’ve given that one pill. And sometimes it’s necessary, to take somebody out of a crisis, but sometimes you have to go back and say, “You know what? Why are you in that crisis to begin with? Nobody else in your family has this. What does your life look like?” That’s what this is for, so you can learn to think through the process of, “Why are you here in the first place?” Okay?

Mentally coherent. Some people get dementias. Next module we’re going to break all of them down. Some have had trauma. Take the girl I looked at earlier. All of these different things about neurodegeneration, language, tells us a lot about mental capacity. It’s not uncommon for somebody to do this: “You know what? I don’t really know where I am sometimes, and I’m missing words, and I can’t think of the name of objects, and sometimes I can’t think of names, of faces, and at the same time, now I don’t even know really where I’m at where I used to know where I was at.” So you’re like, “Wow, that left brain’s going, now the right brain’s going,” and when you look at that, you say the person’s globally neurodegenerating. And language is a huge part of that. Okay?

So we go through this: memory loss, short-term, declarative, procedural, working. I’ll go through each one of those. And then emotional trauma is a big, big, big one. So, same person comes in, they’re depressed. “Hey, anybody in your family depressed?” “No.” “Diabetes?” “No.” Metabolic intake forms: you don’t see a whole lot. “How’s your relationships?” “With who?” “With your husband.” “Oh, I hate that guy.” And then you start going through this, and you find out there’s massive emotional trauma. Now, emotional trauma creates inflammation. Emotional trauma can change your brain. Emotional trauma can depress people, make them anxious, and change their capacity to cognitively function. So I go through it.


The other thing I don’t have up here is substance abuse. Big thing. You know what we’re finding? A lot of medications are creating neurodecline. A lot of common medications. Probably not going to say them up here, but they’re very common. Some used for cholesterol, some used for indigestion, and some used for anxiety. All of this stuff that I’m talking about in this initial survey have been shown to create this: a possible scenario for neurodegeneration or decline. How many people are on any of those medications, one or all? Over ten million Americans. Congratulations: you should be in business for a long time.

So that’s behavioral. Now let’s look at the peripheral nerve. Okay, so this is your peripheral nerve intake form. So let’s make it simple. Do you have pain in your spine? Yes? Rate it. Why do I care? Do you have nerve root damage, where it coms out of the neuroforamen? Do you have myelopathy? M-Y-E-L-O, not myopathy – that’s muscle disease – but myelopathy. Now, myelo- can also talk about bone marrow. But in this situation, you may have nerve root damage, but you also have spinal cord damage at the same time. So you have upper motor findings below that area, but then a segmental dermatomal finding, and that tells you the level of the spinal cord compression. Don’t worry, I’m going to give you a lot of cases on it. Okay?

And then you ask: Do you have any pain in your arms? Just real simple. If you have pain in your arms it could be from anything, but I just want to know. So I’m starting at the center, and moving my way out. So it’s like, “Yeah, I’ve got pain in my neck,” and “Yeah, I have pain down my arm, and it goes just like this, six-shooter, tk tk.” C6 nerve root. And you’re like, “Cool. I can figure that one out pretty easy.” You can orthopedically challenge it, and we will have hands-on modules where we’ll show you that. And then you say, “Man, you’ve got a radiculopathy, and you’ve got a C6 distribution.” And you might want to do an MRI and see how much damage is there.

Do you have pain in your legs? Same question as it is in your arms.

Do you have pain over your abdomen or torso? So we can’t forget about no-man’s-land when it comes to the central spinal region. Good case. Ready? Person goes to the dentist. They have a dental procedure. They don’t take their antibiotics post-dental procedure, and they get, like, a staph infection. Staph infection gets systemic. It actually lodges into the spinal cord. Now they get some sort of infectious disease, or infectious process in their spinal cord, and now they have a transverse myelitis, or a myelitis. And the doctor never caught it, because they never did a sensory evaluation above their waistline. Or, they never tapped their reflexes and said, “Wow – why do you have hyperreflexia, and why are you numb up to your belly button?”

So these are things that you have to… Listen. When you look at these things, you’re like, “You’ve got pain in your legs? And you’ve got pain in your spine?” And you go through this, you can start to put it together very quickly. I’m going to show you examples of it filled out here, in a little bit. Okay?

Do you have weakness in your back? Core stability. Now, is it in your shoulders and hips? If you just have weakness in the shoulders and hips, with no sensory loss, think primary muscle disease. Primary muscle disease. What does “primary muscle disease” mean? It means it’s a disease of the muscle. Like facioscapu-lohumeral dystrophy, or limb girdle dystrophy. Very uncommon, but it does happen. Muscle disease doesn’t have sensory loss. So they’re losing their limb girdles. So if that’s all they put, you would say, “Wow! Is this a muscle disease?”


Well, then you go down and it’s like, “Do you have weakness in your arms and your legs?” And if they start having weakness in their hands, and they start having tightness in their legs, that is upper motor findings in their legs and lower motor findings in their arms, with atrophy that’s not starting up here, it’s starting down here and coming up this way, that’s ventral horn cell disease. That’s called ALS. So what is the difference between ALS and primary muscle disease? Watch. The weakness starts here versus here. If the weakness starts down here, it’s not muscle disease. If the weakness starts down here versus up here, and there’s no sensory changes, and they’ve got little fasciculations, it’s ALS.

So here in a little bit I’ll give you a string of seven things, and just say, “How do you know the difference between these?” And we’ll run through them. So you look at this, you’re like, “Wow, they’ve got weakness in their arms and legs, but they don’t have weakness in their shoulders, their glutes,” and then we go to the next section and there’s no sensory loss, and then they say they have, like, little bumpity fasciculations. You might start thinking to yourself, “Is this person telling me that they have ALS?” Are you starting to see what I’m talking about?

So, I made this peripheral nerve intake form to do it in a way where, if you do it right, you should be able to give it to the partner next to you if I gave you a demonstration, and you would say, “This looks like nerve root disease.” Or, “This looks like neuromuscular junction disorder.” Or, “This looks like ALS.” Or, “This looks like a primary muscle disease.” Or, “This looks like a polyneuropathy, which one I don’t know.” Okay?

Weakness on one side of the body. Could be a stroke. Could be cortical. Guess what you would want to correlate it with? Your brain intake forms. If somebody has language loss, and they walk in and the right side of their body is weak and spastic, do you think it’s from a peripheral nerve? No, that’s from the central nervous system. We have disorders that just create cramps. And they’re all metabolic. But we have things like this: Complex repetitive discharges from different types of diseases where you have cramps. Okay? Like myotonia. So I have a girl that walks in not so long ago, and I go, “Here, grab ahold of my hand,” because I could see her, she has like, what I call ET… sorry, Yoda hands. Here fingers were just huge, and, like, super muscular. She grabs ahold of my hand, I go, “Let go.” She’s like, “…” and she can’t let go. And then finally she comes off and she had, you know, myotonia congenita. So these people will cramp and have problems with just, you know, freezing and stuff like that.

So then we say, “Do you have a loss of muscle size? Where?” and then notice, over here it says, mild, moderate, severe. Are your muscles jumping? That’s a sort of a fancy way of saying fasciculation. And then we have all these weakness areas, problems talking and swallowing, we’ve already kind of talked about that; that’s in the brainstem.

And then these are sensory questions. Does it go down your leg? Is it on one side of your body? All the way down to bowel and bladder issues, which could be cauda equina, or it could be brain, like frontal lobe. And the micturition centers are even in the brainstem.

So, last but not least, there’s one other category of peripheral nerves that we can have, where I wanted you to see this, and that is, Do you have congenital peripheral nerve damage? Okay? Like, Charcot-Marie-Tooth disease? Well, these people have high arches and hammer toes. And we see that sometimes with Freidrich’s.


So I put this on there to kind of finish it off, to say, “Hey, I have, like, atrophy in my legs, I have motor greater than sensory, and I have high arches and hammer toes. It can only be one thing. It’s just a matter of you breaking it down and determining which genetic variety it is. And by the way, good luck fixing that. Probably not. You may help them in some ways, but you’re not going to cure it.

So we go through all that. So, let’s break down weakness just real quick. It’s in the face. So do I have any weakness in the face, and is it just the face alone, or is it the face with the body? So if it’s the face with the body, you need to figure out where in the central nervous system the problem is. But if it’s just in the face alone, is it in the lower quadrant or is it in both upper and lower quadrant? So if it’s in both, is it the facial nerve, or is it the actual contralateral cortex? If the whole face is involved, it’s the old Bell’s Palsy or facial paresis. If it’s just the lower quadrant, start looking for a contralateral cortical problem. Because the upper portion has dual enervation, one from the contralateral side, one from the ipsilateral side. Okay?

So always look at this and say, “What’s their facial tone like? Are they losing facial tone? Is it asymmetric? What do their lips look like? Do they have herpes lesions on their lips?” Guys, HSV Type 1 increases your chance of neurodegeneration significantly, because it lives in your brain, and it creates neuroinflammation just by holding the virus at bay.

So I look at that and I’m like, “Wow, you’ve got, like, all these, like, blisters all over your face, and you’re neurodegenerating, and you’ve got this and you’ve got that,” and you just go through the whole list. And then I go through the nose and the mouth. You go through the nose, and you notice this: They’ve got, like, these little crusty, like, sort of yellowish lesions all over their nose. And you’re like, “Wow, that looks just like impetigo. No wonder why you’re inflamed. Let’s get rid of that.”

So don’t ignore those things. You may have weakness, you may have lip problems, you may have nose problems. Now, we come over here, and we look at the nose, the mouth, the lips, hair. I’ll talk about the eyes in just a second in a separate section. And then we look at the spine, and we say this: Is there any range of motion? Do they have a scoliosis? Are they really, you know, forward in a camptocormic position? Do they have a dystonia or a dystonic head? Do they have a skew deviation in their eyes?

So you start looking at these things, and you’re like, “Does the spine correlate with the head, and is the head compensating for the spine, or is the spine straight and the head tilted, or vice versa?”

And then we also want to look on there and say, “Is there a spina bifida?” Because a lot of time with neural arch defects, they have B vitamin deficiencies, or problems, and here’s what that will translate into later in life: neurological disease. So maybe they have a bad methylation issue, and as a result of that bad methylation issue, they’re going to get neurodegeneration and problems throughout the rest of their life. So I want to know.

And then we look at their arms. So we’ve got arms, legs, and torso. So when it comes to weakness, I always want to ask this: Is the whole arm weak? That might be the brain. There is no single peripheral nerve that makes the whole arm weak. So it could be spinal cord or brain. If it’s proximal, and the proximal weakness is there but the hand is preserved, and it crosses into several different nerves, you want to say, “Man, is this a brachial plexus, like an upper or lateral brachial plexus lesion? Or is this a primary muscle disease?” A plexus lesion will give you sensory loss with it; a muscle disease will not. And muscle disease will be bilateral,


and become symmetric; a plexus lesion will not. And a plexus lesion will typically be traumatic, but every now and then you’ll get idiopathic amyotrophy, where you had an upper respiratory tract infection, and it crawls into those nerves, and destroys them. So ask the history. Pretty important.

Distal. The hands. It may start off with ventral horn cell disease. Or it might start off with lower nerve root disorder. So, everybody just watch real close. Ready? 5, 5-6, 6-7, 7-8, 8-T1. Real simple. Let’s do it again. Ready? 5, maybe a little 6. 5 and 6, 6 and 7, 7 and 8, 8-T1. Not too difficult, right? As we come up here, we get a little bit higher. On the back, like around the rhomboids, it’s just C5 only. There’s not as much C6. So when we give you all the peripheral nerves, I’ll give you what’s called switch muscles, meaning how do I know if it’s 5 or 6? Well, this muscle will be 4 or 5, and this muscle will be 5 and 6. So if it’s in this muscle but not that muscle, then here’s the problem. You know it’s single nerve root and not the other, or nerve root, or multiple nerve roots.

So anyway, as we go down the legs, we – again – proximal, distal. Is the gait spastic? Is there a slappage gait? I’ll go through what all these gaits look like. And then is there any edema? I’ll talk about what that means. And then the torso. Are they distended, like with SIBO? Are they distended, like with infection? Do they have a thrill, like a cardiac thrill? Do they have an arrhythmia? We’ll talk about , “Hey look, this person’s sick, and they’ve got cardiac pathology. What does that mean? Which cardiac pathologies do you need to know? Do you need to know what AFib is? Well, a little bit. Like, here’s the deal. Don’t take them off their blood thinner for migraines if they have AFib, because there’s a good chance they can have a stroke. Just be careful; that’s all I’m saying. Just be very careful, alright?

And then also the torso. We’ll talk about discoloration and what that means.

So this is some of our weakness patterns. And again, you’re like, “Wow, this is getting a little bit more complicated here.”

Sensory loss. It’s the same as motor loss. Look: right there, right here. Is it over the face? The face only? Or the face and the body? And then we go to torso. Is it a dermatome? Down the arms? Now, is it a nerve root, crossing multiple joints? Is it the plexus, giving you multiple dermatomal patterns, but nothing’s happening to the paraspinals? Is it entrapped here in the elbow or behind the forearm… I’m sorry, behind the brachium? Or is it down here in the wrist? Tomorrow morning I will break those down for you in a very linear pattern, but I just need you to understand right now: When the arms are like this, man, is it proximal or distal? Is it nerve root or is it plexus? What is the weakness pattern telling? Because people will come in with weakness all the time, like every day. And then there’s the difference between an applied kinesiological challenge, and a true denervation weakness. I’ll go through the differences in those too. Some of you actually care to know that.

And then finally we have autonomics and legs. Legs are the same as arms if we’ve got autonomics. When you have peripheral nerve damage, or you have changes in autonomics, you can get change or problems in the blood vessels, skin, nails, the color of the digits, temperature, bowel and bladder.

One of the very first things that happens with a small-fiber autonomic neuropathy is genital dysfunction. Erectile dysfunction. Occurs very, very frequently. Because the sensory information from the genitals is small-fiber. So as soon as somebody gets diabetes, and they get burning in their feet because their small


fibers are firing, they start to have a little bit of genital dysfunction. And by the time the pain is gone, and now they’re starting to get numbness, they’ve lost sexual function. I’ll go through that here in just a minute. I’ve got one case for you. But man, you need to be able to look at the progression of polyneuropathy. I will promise you, if you do neurology, you will have to learn to look at polyneuropathy. An enormous percentage of patients have polyneuropathy. So we’ll go through that.

So, that’s our peripheral nerve evaluation. And now we’ve just got a very simple gait evaluation. So if you look at this, it’s like, “Hey, do you fall a lot?” And they’re like, “Yeah, I fall all the time, and I keep hitting my head.” And then you check them out and they’ve got a subdural, and that’s why they’re sick. Or they’re blacking out. Why are they blacking out? You find out they have a massive cardiac condition. So you need to know if they’re falling, “Tell me about your falls: do you remember falling? What’s going on?”

Do you have a hard time standing on your heels or your toes? Some people say, “Man, I can’t, like, reach the upper cabinet any more.” And you’re like, “Wow. That will tell me a little bit about which muscles might be denervated.”

Do you keep falling to one side over and over and over? So, if you take your brainstem, and you go to where your pons and your mesencephalon attach, everything top of the brainstem up, you’ll fall away from it. Everything down or below, if there’s a lesion, you’ll fall towards it. Simple enough? So you’ll go uhh, uhh. So if it’s where the pontomesencephalic junction is, if it’s below that, you’ll typically fall towards the lesion if it’s below it. If it’s above it, you fall away from it, okay?

Do you have a hard time going up or down the stairs? Now, it’s like this: Okay, so if you have a waddle gait, which is kind of like this – I hate to make fun of gaits; I’m not – and you’re not diplegic, like it’s not spastic, like cerebral palsy, that’s muscle disease setting in. And they can’t go up or down stairs. Now, if they don’t have a waddle gait, but they can’t go up and down stairs, and you say, “Hey, how does your knee feel?” “It’s killing me.” Then they can’t go up and down stairs because their ACL is slipping or something. You see the difference?

So the gait stuff is really good. And it’s like this: Is one or both arms tights or spastic? Like a stroke, or tetra… you’re not going to be tetraplegic and you’re walking. Are your legs spastic alone, like diplegic, like CP? Most people know they have that.

Do your feet slap when you walk? Do you have to high-step when you walk? Do you shuffle when you walk? Classic Parkinson’s. All the way down through Is it hard to turn if you stop walking?

This questionnaire would go good with the brain intake questionnaire. Perfectly. So when you take the brain questionnaire, the peripheral nerve questionnaire, the gait questionnaire, and all the quickies, and you start putting them together, you start saying things like this: “Wow, the person’s got a cortical lesion, and the cortical lesion happened because of a stroke, because it happened rapidly, and they’re hemiplegic, and now they can’t walk well because they have a circumduction gait, and their arm doesn’t move well, and they’re falling away from the side of the stroke. Wow, that’s exactly where it is. And then, when we take the vasculature, and we superimpose it on top of the intake forms, you’ll be able to say this: “It is that artery.” I don’t know how to make it any easier. Okay? All of the blood vessels will be animated, and then they will connect right to the spots that your intake forms we’ve made for you.


So, posture. Do you have a head-forward posture? This is some stuff we want you to look at. And, you know, they get the term camptocormia back from the Civil War days, you know, back when people used to hide out in all the trenches, and they would stay down so long that when they got out, they were kind of still stuck in that posture. They were from the camps. These people, man… This is usually indicative of degenerative disease. So it’s either that or you broke your neck and you have some sort of postural deformity in your neck, like a compression fracture, or something. So you have to do history.

Do you have hip and knee problems? So, posture. So, is there a rotation? A lot of times when the brain shuts down, the shoulders will roll in. The femur will roll out. The tibia will roll in. The ankle will drop, or the foot will drop. So you get plantar fasciitis, medial compartment knee, strain, hip strain, SI joint dysfunction. As your shoulder rolls in, it starts to basically compress the AC joint, So what kind of acromia do you get? You get a type 2 acromia, and then it starts to kind of like lurch down, and it hits the supraspinatus so every time you abduct it goes kkrrr kkrrr on the supraspinatus, and eventually you do what? You tear your rotator cuff.

So, remember a couple of things here. This part of my brain will go over to the contralateral side to give me volitional movement, but this side will fire down to also give me tone. So these are soft pyramidal changes, these are hard pyramidal changes. So if you get that massive, like, language change, language deficit, and all these left-brain findings, and then you start looking at their posture, and they’re not spastic, they don’t have any other problems that are upper motor, but they start to get some autonomic changes, they start to rotate in, they start to stress this, they start to get lactic acid buildup back here, they get hip rotational change, knee rotational changes, foot drop changes, SI joint changes… You look at them and you’re like, “Man. This person’s got some biomechanical alterations because of brain, and they’re not because they’ve had a stroke, it’s because of their asymmetry.

Okay. So then we look at feet and hands, and of course we look at nails, and we want to look at, again, do they have hammer toes? Do they have high arches? Those can be indicative of hereditary motor-sensory neuropathies, which I’ll go through later on.

Are they hyperkyphotic? Are they scoliotic and so forth? And then again, the shoulders. Is it internally rotated? Do they have AC joint pain? Do they have capsular pain? Do they have rotator cuff damage? That can tell you about the progression of some of their neurological problems. Take, for instance, Parkinson’s disease. Typically fifteen to twenty years before the presentation of any symptoms, people have just idiopathic right-shoulder pain for no reason. Okay?

So, we’ve got posture. Let’s look at eyes for a second. Again, basic stuff. I’m not going through everything that we can do on eyes. This is just a beginner’s… like, this is sort of warming you up a little bit.

Do you have lit problems? Like ptosis? Like one lid doesn’t work? Or is one pupil way bigger? Is there any changes in symmetry, or is there any changes in movement? Are the eyes doing the same thing? We have a whole module on this one slide right here. At the very beginning, this will be the opening slide. And we’ll have a whole little quickie form just for all of those. Alright?

But these are things… You’ve got to look at somebody and say, “You know what? Your pupils are the same size, your lids are the same size. One of your lids is curling in versus it’s not. Your cornea is ulcerated. You’ve


got cataract. Your eyelashes have fallen out. You have no eyebrows. I mean, what happened to your facial presentation?”

Torso. Wow. Is it distended? Okay, are you ready? Do you have epigastric pain? This is stomach. This could be ulcer. Do you have pancreatic pain? This could be what? Pancreatic cancer, could be pancreatitis. Come over here, this is liver and gall bladder. So could be you have some sort of liver pathology, bowel duct pathology, gall bladder pathology, gallstone.

You go down a little bit further, this is appendix. You come over here, this could be diverticulitis. Your spleen could be a little bit over here. Your kidneys are in the back.

So a torso exam is going to be very important for you, because all of these things are under control of vagal and neurological function. So when you look at this slide, you’re like, “Wow – I didn’t know the torso was such a window of function of the brain.” And we’ll go through that as well.

Last thing here: respiration. If somebody’s anemic, their respiration’s going to change. If somebody’s anemic, their brain is going to change. If somebody has low cardiac output, their respiration’s going to change. Their rate of respiration matters, because it can change pH. pH can change the rate at which your brain fires. So you have to know these things. So, it’s always good to know if they have asthma, infection, emphysema, do they have cardiac problems? And if it’s just labored because… it’s like my mother. She has congestive heart failure. So whenever I see her respiration go up, I know her hemoglobin’s dropping. You know why her hemoglobin’s dropping? Her retic count’s going up. Her retic count’s going up because she’s bleeding intestinally, because she won’t stop eating gluten. Do you see how that all just connected? Wow.

So, we’ve got ten minutes now to just do a final case study. So I’m going to show you how some of this stuff comes together. Okay? There’s a lot of things in this quickie section, and that’s why we gave you another two hours to look at this again tomorrow. Because I can’t just come blurt these things out and say, “Hey, here’s all these systems – see you later,” and then not stop and come back and say, “Now, let me break down each one of these nerves for you, so that you really get it and understand it,” and say, “Not only did I break these down; let me have a whole nother module where we talk about just the pathologies related to these nerves.” Because this is going to come in to your office over and over and over. I would rather you own it that be scared of it.

But this patient comes in with brain fog. Well, what does that mean? Could be thyroid, right? Could be inflammation. Could be trauma. Could be ischemia. Could be blood sugar. Could be anemia. Hmm. But they have limb pain and numbness in the feet. Now here’s the deal: Polyneuropathies start distal and go proximal, and sensory starts before motor. Most of the time. Did you catch that rule? Distal to proximal, sensory before motor. Most of the time. I’ll give you the one exception tomorrow.

And they say this: Limb pain and numbness in the feet distally, and now it’s starting to go to the hands. So it’ll be in the feet for about this: for about six, seven, eight years, then it starts in the fingertips. And you start saying, “Wow, is it in all the fingertips?” Well, which nerve goes to all the fingertips? None. So it’s two or more nerves and two or more limbs. Polyneuropathy. It starts distal and goes proximal: polyneuropathy. It starts in the legs and then goes to the hands: polyneuropathy. Most of the time. Okay?


So you start thinking to yourself: “Wow – does this person have a polyneuropathy?” And now they’re starting to lose their short-term memory. “Wow, I wonder if they have a polyneuropathy from an underlying metabolic disease?” Hmm. Keep going. Now the patient’s depressed. Frontal decline. The patient’s starting to get foot atrophy and weakness in the legs with no back pain. You’re like, “Wow – they’re starting to get atrophy and distal stuff going on, and there’s no spinal pain. Doesn’t sound like it’s radicular. It’s in more than one nerve root. And their brain’s affected and their limb’s affected. I wonder if this is metabolic? Hmm.”

The patient has vision loss, and you go to them and look at their retina, and they start getting flame hemorrhages, and they start getting dots and blots and all that stuff. They’re getting GI pain. Head forward posture, and now they’re heavy breathing from smoking. And you look at this, and you go, “Why’d you come in?” “Because I have brain fog and I’m depressed.”

Are you starting to see why now, looking at the comprehensive picture is absolutely imperative?

So you’re like, “Cool. Let’s go through and let’s look at the form.” You look at this and you’re like, “Wow, they can’t organize and plan things. Really have a bad time making decisions.” Notice this is the frontal lobe, right? We just went over these. Dr. Kharrazian just went over this. And you’re like, “Man, they can’t make decisions very well.” You skip down here and you’re like, “They have episodes of depression, and then they have mental fatigue, and they don’t have good attention span,” all the way through periods of concentrating. All of this sounds like what? They’re metabolically failing. Why would they be metabolically failing? Do they smoke? Yeah. Could there be something going on with their blood sugar? I don’t know. You’d have to check it.

So you go through this and you’re like, “Wow. No wonder why you can’t pay attention. And I mean, you can’t… Your right brain looks bad,” and then you come over here and there’s some left-brain stuff. This looks kind of global, maybe with the right brain hinged to it. And you come over here, and you’re like, “Wow, you have a problem initiating movements with your arms,” and you run all the way through and you notice down here they have burning body or limbs… or bumping, sorry, bumping. They do have some sensory changes. But they’re bumping into things because their nerves are, like, dying. They don’t know where their foot’s at.

Come down here a little bit further: Difficulty ith balance, probably because they have peripheral nerve damage. You go all the way through this, all the way over to here, and they have cramping in their feet from denervation, from nerves being damages.

This is their peripheral nerve intake form that I just showed you. Watch. Do you have pain in your legs? Yes. Severity is a 5. Do you have weakness in your legs? Yes. Do you have weakness in your feet? Yes. So now you’re saying, “Okay. Is your weakness in your feet more than your hips?” And they’re like, “Yes, it’s definitely more in my feet than in my hips.” And you’re like, “Hmm. Okay.” But they don’t have any pain in their spine. So it doesn’t look like it’s nerve root, but it definitely looks like it’s involving their feet. Interesting. Let’s keep going.

You go down a little bit further, and it’s like: Do you have any loss in your face? Yes, a little bit, V1, V2, and V3. So now you start thinking, “Man, has this person had a stroke?” You come back here: Do you have any sensory loss in your arms? Yes. You find out it’s their hands.


So you go through this, and you ask questions, and they’re like, “Look. I’ve got weakness in my feet, not my hips, not my spine. I’ve got some sensory loss in my feet, some sensory loss in my fingers, and I’m starting to get a little sensory loss in my face. I’m depressed, I’m not doing well, I’m mentally fatiguing, and I’ve got brain fog.”

This is the case I’m building for you. You go through this; no changes on the gait intake form. So, we know their chief complaints. We’ve looked at the history. We’ve looked at the localization form. And now we have to identify, is there any metabolic factors? There has to be a physical exam that’s going to go along with this, that we’ll get to. And then we’ll identify both the metabolic factors and the neurological factors, and the neurochemical pathways.

Now, this person has this. So this is how you use these. Superimpose the intake form with this form, Here’s what you find. They have lower motor findings, they have atrophy in their feet, they have weakness, it’s denervating, they have a loss of joint integrity, and they have all of the findings of lower motor pathol-ogy. They’re hypo-reflexive in the ankles more than the knees. That’s peripheral nerve pathology. That’s polyneuropathy.

And then you go through this and you find out: polyneuropathy. The pattern is this: sensory more than motor. That’s what you find out. And then you go, “Wow. It’s distal, not proximal.” And then you find out this: They have diabetes. And their pattern type is small-fiber and large-fiber, and you find out they have weakness in the legs, distal compared to proximal, and they have sensory loss, distal compared to proximal. And they have autonomic changes, so now they’re getting this: Their nails are falling off, they have bad capillary refill, and this is how gangrene sets in over time. Blood pools, it doesn’t get cleared out, and they start to have autonomic distress, and they fall apart. In the torso.

This person has some epigastric pain, and we find out they have an ulcer, and they have flank pain, because they have SIBO. So now they have inflammation from their gut, they have blood sugar pathology, polyneu-ropathy, respiration rate – remember, I told you they were smokers; we find out their ejection fraction; not praction, sorry – their ejection fraction is down. So now they’re not getting oxygen around very well, and they have emphysema. And we find out that their blood sugar is 550.

So here’s how we wrap it up. This person has a major increase in blood glucose. Now, neurons and the endothelial component of your vasculature is insulin-independent for the most part. So when you get hyperglycated, you increase intracellular glucose in nervous system. And that increases the intracellular sorbitol, which makes the cell swell, and you get a compressive axonopathy, and damage to the intracel-lular mechanisms because of hyperglycation. So the higher your blood sugar goes, you’ll hyperglycate a lot of stuff, but inside neurological tissues, it creates massive damage. Insulin does something completely different, okay?

So, an increase in glucose leads to the conversion of sorbitol, and this causes osmotic pressure changes. Now, when you keep going, the increase in sorbitol does something that decreases what we call diacylglycerol. So glycerol is used to – it’s the triglyceride component of the bilipid membrane – starts to break down. So now we start to get this: Myelin starts to become damaged. So we have axonal damage from the sorbitol, we have myelin damage from the diacylglycerol, and now we get oxidative stress because the capacity of


glutathione, the function doesn’t work. And this happens in the longer nerves first, so it happens in your feet because of hydrostatic pressure. It pools… it happens more distally.

So you’re like this: “Man, I get off my feet and every night I’m burning and tingling.” And you’re like, “Whoa.” And then it starts to eat up the nerves distally. And then it goes up to right about here, and on guys, guess what stops growing right at the level of the stocking? Their hair. So I’ll show you some clinical tricks. Just get something cold, like your tuning fork, and run it on here, and they’ll say, “Can’t feel it. Can’t feel it. It’s warm, warm, warm, cold! Right there!” And it’ll be right where the hairline is. Get your pinwheel, run it up, and like, “Can’t feel it, can’t feel it, can’t feel it. Boom! Right there.” They’ll say, “I can.” You can mark it, and put wshht! This is where small fibers are dying. Wshht! This is where large fibers are dying.

Go up to their hands. If it’s been going on long enough, it’ll start to hit the tips of their fingers. And then you look at their blood sugar, and you’re like, “Oh my gosh.” And then you look at their microalbumen, and you’re like, “Wow, you’ve got protein spilling into your urine.” And then you’re like, “Wow, you’re inflamed. You’ve got brain fog. Wow, you’ve got anemia, because you have emphysema. That’s going to perpetuate your brain fog and depression.”

Do you see how this is a collision and disaster, and it’s creating somebody that ends up with a diabetic neuropathy? It is creating changes in brain, changes in nerve. When you change nerves, you don’t have feedback to the brain. And this is the beginning of us talking about the metabolic imbalances that lead to neurological changes. And this is everything I just told you. Out of a paper, glucose changing sorbitol, osmotic, all the way down to free fatty acids, pyruvic changes, mitochondrial changes, the membranes break down, and now you have the beginning of polyneuropathy.

Now, last statement. Do you see what it did to brain? Did you see what it did to the intake form of frontal lobe? Do you see what it did for brain fog? Can you see what it might do to kidneys? Can you see what it might do to eyes? And oh my gosh, what’s it doing to nerves? And if the nerves are damaged, what’s happening to the feedback to the brain? It’s perpetuating itself, So right now you have about fifteen loops of pathology going on.

Everybody’s seat belt buckled? Okay. That’s it for this section. Thank you.

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the initial clinical survey and how to identify the … · module two transcript: neurological...

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