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MODULE TWO TRANSCRIPT: BROCK 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. Brandon Brock So we’re going to go through this, and we’re going to do some cases in neurology, and we’re going to kind of add together all the things that we’ve learned. I’m going to through in some things that we haven’t learned, show you a lile bit of stuff that we’re going to be doing later on. We okay? We rolling? Okay, perfect. So really, this is the me you period where we can kind of downshiſt a lile bit, not get into a big hurry, think about what it is that we’re looking at, and really kind of go through this in a way to where we can methodically break it down so at the end of the module, you have the opportunity to say, “I’m either learning some stuff or I’m not.” Now, I’ve been watching people and it’s amazing the rate at which people are learning. Learning the rules, learning the intake forms, learning the localizaon, learning the regions, learning how to set… kind of connect some of the dots together, and then learning how to think on your feet a lile bit, where if it’s one thing and it’s in the frontal lobe, for instance, could there be something else creang those symptoms? Or, if there is frontal lobe symptoms, what maybe is the underlying causave factor? So, those are the things that I see as feedback from teacher to students, or from learner to learner, that is really nice. It’s nice to see people start to get it and start to click. Because you’d be surprised how difficult it is at this stage to see people start to click a lile bit, right? So, the cool thing is, is that you’re geng all the, you know, the assessment and the understanding and then when the treatment and the physical exam starts coming along, and you’re like, “Man, I was a metabolic doctor, now I’m a neurological praconer as well.” I promise you, what every you’re weak at, you will get beer. There’s very few people that are coming here from both angles. Most people are much stronger in one angle than they are the other. It doesn’t maer, okay? Because you’re going to be able to step up to the plate on both eventually. So, we go through this, we’ll take our me, and we’ve got three cases, and these three cases are really spread out and have a lot of different factors and we’re going to have to start connecng some dots. Is

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Page 1: THE INITIAL CLINICAL SURVEY AND HOW TO IDENTIFY THE LESION BEFORE EXAMINATION (MODULE ... · 2016-05-28 · MODULE twO tRANSCRIPt: BROCK CASE StUDY ... (MODULE TWO) Transcript –

MODULE twO tRANSCRIPt: BROCK 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. Brandon Brock

So we’re going to go through this, and we’re going to do some cases in neurology, and we’re going to kind of add together all the things that we’ve learned. I’m going to through in some things that we haven’t learned, show you a little bit of stuff that we’re going to be doing later on. We okay? We rolling? Okay, perfect.

So really, this is the time you period where we can kind of downshift a little bit, not get into a big hurry, think about what it is that we’re looking at, and really kind of go through this in a way to where we can methodically break it down so at the end of the module, you have the opportunity to say, “I’m either learning some stuff or I’m not.”

Now, I’ve been watching people and it’s amazing the rate at which people are learning. Learning the rules, learning the intake forms, learning the localization, learning the regions, learning how to set… kind of connect some of the dots together, and then learning how to think on your feet a little bit, where if it’s one thing and it’s in the frontal lobe, for instance, could there be something else creating those symptoms? Or, if there is frontal lobe symptoms, what maybe is the underlying causative factor? So, those are the things that I see as feedback from teacher to students, or from learner to learner, that is really nice. It’s nice to see people start to get it and start to click. Because you’d be surprised how difficult it is at this stage to see people start to click a little bit, right?

So, the cool thing is, is that you’re getting all the, you know, the assessment and the understanding and then when the treatment and the physical exam starts coming along, and you’re like, “Man, I was a metabolic doctor, now I’m a neurological practitioner as well.” I promise you, what every you’re weak at, you will get better. There’s very few people that are coming here from both angles. Most people are much stronger in one angle than they are the other. It doesn’t matter, okay? Because you’re going to be able to step up to the plate on both eventually.

So, we go through this, we’ll take our time, and we’ve got three cases, and these three cases are really spread out and have a lot of different factors and we’re going to have to start connecting some dots. Is

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that okay with everybody? So, what I want you to do is, follow along, try to connect the dots, see if you can anticipate where the problem is before we get there, and start thinking to yourself, “What would I do if this patient was in my office? Meaning, “What would I think about their issue?”

Okay. What do you see in the history and the intake? Now, we’re not giving you a lot of physical exam stuff, so I can’t say, “What do you see in the physical exam?” We’re not there yet. It’s another layer on the cake that we will eventually get to. How do we determine the prognosis on this patient? How severe is it? What’s their metabolic fatigue? What can I do? how bad is it? “Is somebody really, really, really messed up? So these are all the things that we’re going to have to start looking at, and how do we know when to treat or not to treat, based on a conservative model, meaning, we’re not doing surgery or something crazy like that, okay? It’s just not what we do.

Alright. Let’s watch this video.

Put your finger out there. Hold this finger there. Hold, hold, hold. Hold your thumb right there. Hold tight, tight, good. Hold your fingers in like this. Hold them tight. Good. Now bring your wrist like this. Hold that pose. Hold.

I don’t think it really matters.

Good, now turn your hand over. Go like this. Hold that really tight. Okay, relax. Where’s your numbness at? Point towards it. “Right here, and here.” And where’s your arm hurt at? “Over here.” Okay. All through here? “Um-hm.” Okay, that’s good. Stop.

Okay, the biggest question si, what do you notice about her voice? She smokes. Sorry. Now listen. Right now, just write down where the lesion is. You want me to play it again? How many of you want me to play it again? How many of you just know? Okay, what was was with… Let’s break it down. Because we’ve got time. I told you, we’re not in a hurry.

By the way, this is the real deal. This is a real… This is not me playing around with somebody saying, “Hey, fake this.” This is a real patient. Okay? This lady comes in, and obviously isn’t doing so good.

Put your finger out there.

Okay, what’s weak? Right there. Is that ulnar or median? That’s ulnar. Oh man.

Hold this finger there. Hold, hold, hold.

What’s that? That’s like, a kitten. She can barely resist anything. That’s her trying her hardest. You see it? Now, what’s the next muscle I test?

Hold your thumb right there. Hold tight, tight, good.

She makes it.

Hold your fingers in like this. Hold them tight. Good.

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Now, what am I going to go ahead and to? What are those? C8…

Now bring your wrist like this. Hold that pose. Hold.

C7

Good, now turn your hand over. Go like this.

My extensors, my radial, still part of C7.

Hold that really tight. Okay, relax. Where’s your numbness at? Point towards it. “Right here, and here.”

The numbness is the palm and the digits. So the only muscles that are weak are related to what nerve? Ulnar. Where’s… Was the digital component the same as the palmar component? So is it at the wrist? Everybody watch. Okay. This nerve, it comes up, and it curls across, okay? And so it gives a little branch and it innervates this hypothenar, and then it comes across and it goes to the first dorsal and to [? 06.18] similar Merkel’s, okay? And then you’ve got a sensory branch that is digital to these two.

So a type one block is over here so the only muscle weak is the first dorsal. A type two block – look, see? Two fingers up. It’s down lower on the motor branch, so both muscles are weak. A types three block is down here at the pisiform hamate region. What’s that called? Guyon’s canal, right? It’s there, so now I have sensory loss to the digit here, half the digit here, this muscle’s weak, and this muscle’s weak. That’s type three. Type four, is just the sensory branch to the digits. The motor is not involved. It depends on how you fall or hit, or how it’s compressed. Four different entrapments. Ready? One, two – both of these muscles – three, weak and sensory loss, and four is just sensory loss. The one at the canal is typically three. That’s in your notes pretty well. I have it drawn out. But I wanted to go through it with you, because a lot of people don’t get it.

Now, does she have a lesion at the wrist? Does she? No, she doesn’t have a legion at the wrist. How do I know that? Because the palmar and the dorsal ulnar don’t run through these canals. They’re recurrent branches. So she says this is equal to this. “Where do you hurt?” She’s pointing to her elbow; she doesn’t really know where, and she has weak ulnar. But I mean, does that get any… How many of you can just get it like that now? By the way, is there stuff you can do to help this patient? Yeah. But let’s see how severe it is. Because I recorded the EMG and the NCV. So watch this.

Now, I have no idea what people are saying in the background on this, okay? So…

“…Feel that one, yeah. Bending in the hand.” “Good. When I’m training…”

I’m going to turn it down a little bit. She might be talking about her dogs, or some chickens or something like that. Now, what I’m doing is an inching technique. So I think this: I think between here and here there’s a problem. But I don’t know where. It could be somewhere anywhere in this segment. So I’m going to start here, then go here, then go here, then go here, then go here, then go here, then go here. And I’m going to watch the amplitude and where it drops I can mark it every centimeter. It’s called inching. Just watch.

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I’m just showing you this, not to make you an electromyographer; I just want you to see the pathology in motion, okaky?

“In the army you have to go to the gas chamber.” “I know it.”

See, they’re already talking about the death penalty. Just ignore it, okay?

“So I’m sure I feel like formal military turned out to be a cop, it’s like…”

Time to go into the gas chamber…

Okay, so here’s another one. So you’ve got to kind of stimulate it until you get to where it’s as good as it’s going to go. Now, does that second wave look about as good as the first wave? About as good. Let’s keep watching, okay? Here goes the next one. This is above the lesion. What can you say about that? There is a significant proximal amplitude drop and a delay in the latency. When I see this, I go, “Oh no. No wonder why it’s weak. This is clear conduction block. You see it? Look: right here. No amplitude. This is above. This is up here. And I’m trying to stimulate through the damaged area. I go down a little bit more distal, and then this is down at the wrist. So right up here, boom. This is a conduction block, and the conduction velocity’s probably about thirty meters per second. Should be above fifty.

So now I see that, and I’m like, “Ah man, let’s inch it. Let’s go all the way through.” There’s one. Let’s go up a little bit higher. I’m going to turn up the juice there a little bit. I’m going to shock her hard enough. Until she goes, “uhhhhh,” then you know you haven’t shocked her hard enough. So there it is again. I’m like, “Okay, cool. That one looks good.” Shock her a couple of extra times, just for good measure.

Let’s do another one. We’ll go up a little bit higher. Does that one look like the other one? Yep. So now we’re going all the way through that region. Little bit higher, little bit higher, little bit higher. Not bad. Losing a little bit of amplitude. We’ll store it.

Let’s go to the next one. I just keep working my way until I find where it is. And every time I go to one, I’m just marking it. That one still looks pretty good. Now we’re past the cubital tunnel. Uh-oh, what’s happening right there? Now we are starting to get amplitude drop, and watch this. If I can get that cursor to move. See how this, this, this, they all line up in a straight line and then boomp, it goes up to this way and it kinks out? Now there’s a latency and an amplitude drop. This is the area where the nerve is getting beat up. So I can go back and I can precisely mark: right there is where it is.

Everybody… I’m just kind of showing this to just to see how works. This is why you order a nerve conduction velocity study. Look at the amplitude drop as you go further down compared to distal. And that’s all done in a segment this big. Okay?

So here is another segment. She might have skipped this one. This is the EMG to it. Now I’ll turn this up a little bit. Again, I don’t know what they’re talking about.

“Four months every third time. I don’t know what the time range…” “How many tests?” [mumbling] “I’m okay.” [mumbling] Okay now, push [mumbling]

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Am I actually in the muscle yet? Am I now? It’s going whooossh. It doesn’t sound like kk kk. It doesn’t sound crisp yet. So I’m still digging around for the muscle. Now, this is in her hand. And she’s like, “Ahhhhh.” I mean, it doesn’t feel good for her, okay? But I’ve got to get in there, because I want to see if there’s any active denervation. Because if there is, I’m going to send her out to get that transposed; to get that nerve transposed. But if it’s not, then I’m going to treat it conservatively. So now, are we looking for prognosis? First of all, could you find where the lesion was? Yeah. Now we’re just looking at severity. That’s all. So come back over here… Let’s just keep sticking her.

So, what you hear there is just… What you hear there is just me tearing through the muscle a little bit, trying to get it to fire.

Still looking for it. Still tearing it around. Not there yet. Now am I there? Did you all hear the difference? Can you just close your eyes and hear it from across the room? Now, how many of you can hear more than one phase in the motor unit? It’s going grrk grrk grrk grrk grrk grrk grrk. In other words, look at that. That is, if you look at this right here, that’s a polyphasic motor unit. There was no active denervation, but it’s polyphasic.

Lets watch. [knocking] Now, you want to try to really get that… You want to try to get it down to where it’s a single motor unit, so you can analyze that single motor unit. There’s your single motor unit. Is it more than just up and down? So now what I’ll do is, I’ll take it, change the markers. click a button, and watch this three-dimensonal picture. Click! There’s your motor units gathered.

“You push him…”

That is a polyphasic motor unit. It’s not actively denervating; it has reinnervated. Is that good news for her? This is your perfect patient to treat. You don’t have to worry about her hand disappearing, you don’t have to worry about it vanishing. Here’s what you can say: “I can take care of this.”

There’s another one right there. See the two motor units together? They have reinnervated because there’s been damage. Watch. We’ll stack it. Change the markers. Nice and beautifu. That is two neighborhoods growing together because one has lost its innervation and it reinnervated.

So, just a quick jog. How many of you could get the ulnar nerve? Now, we do the EMG. Active denervation means this: You stick a needle in the muscle, and it just starts… it’ll just spontaneously fire for no reason. A little bitty fibrillation or a little bitty sharp. She didn’t hve that. But she had the polyphasic motor units, demonstrating that it’s a chronic issue, it’s reinnervated, there’s conduction block there. We can do some stuff conservatively to help his patient. If it doesn’t work, she may have to go in and see somebody, but it’s just cool to be able to say, “You know what? I don’t think you’re going to lose any muscle tissue.”

So that’s what you would ask. “Look, you need an electrodiagnostic study. I need to know if you’re going to lose any tissue. I found that your ulnar nerve is super duper weak.” Now, I like doing electrodiagnostic studies. You don’t have to. But I’m just saying, that’s a good example of saying, “Wow. I found the conduction block and now it’s in the retrocondylar groove. I know that we can do some stuff to decompress this and make the nerve function a little bit better, and hopefully get your hand stronger, and I’m not worried about your hand wasting away, because it’s not actively denervating.” Cool? Alright.

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So, now let’s get into a case here. So, chief complaints: right side insidious onset of symptoms, no trauma. Numbness in the back of the hand and the forearm on the right side. So they have numbness in the back of the hand and the forearm on the right side. It doesn’t follow a cleared dermatomal pattern. It doesn’t hurt. It’s numb. Okay, so just stop for about ten10 seconds; write down three or four differentials. I’m just giving you patterns. This is what the patient says. “I came in; I’m numb, right here. It’s back here. It’s crazy.”

Wow man, that was a loud hug.

So, the patient has now weakness with extension of the fingers and weakness with the wrist. Extension, like this. So, they’ve got numbness back here, and they’ve got problems with extension, so they’ve got a wrist drop. What are you already thinking? It’s median nerve, right? How many of you think it’s median nerve? Well, how many of you think it’s ulnar nerve? How many of you think it’s the musculocutaneous nerve? How many of you think it’s the radial nerve? There you go. The radial nerve. Remember, I told you it goes down the back of the arm. It controls extensors, okay?

So look: We don’t know that yet though. We’re still looking at the patient. So, there’s weakness plus he’s getting atrophy of the extensor muscles of the forearm, he’s getting a waiter tip hand. He has adequate flexion though, so he’s like this. And say, “Turn your arm over and keep your hand just like that, and they go like this.” And say, “Now wiggle all your fingers. And now separate them.” What you just did is, this is C7, ulnar, and median nerve. This right here, radial. You just, in one movement, ruled it all out. Watch.

They’re like this. “Lift it up.” “I can’t do it.” “Okay, keep it just like that and turn it over. Now keep it there. Can you do that?” “Yeah.” If it was C7, it would fall. “Now I want you to pull your fingers apart and wiggle them. And they’re like, “I can do it.” Now, they have a hard time extending them, but inflection, they can do it. You’re like, “Your intrinsics, your lumbricals are intact, your median, your ulnar’s intact. C7’s intact. Now say, “Just curl in your fingers.” They do this. C8’s intact. But they can’t extend the wrist. Now, if you say, “Just let go,” it’ll fall like this, and when they turn it over it’ll go right back.

Do you see how we just evaluated that right there? You’ve got it on replay. You can see it over and over and over again. Okay.

So wait a minute. This patient is a factory worker and deals with metals all day. Hmm. The patient has depression and a lack of creativity and imagination. Recently he noticed that his entire right arm has lost some coordination. He’s had some heart flutters and some issues related to poor digestion. He’s been constipated and feeling a little bit bloated.

Now first of all, what are you concerned about in these last few little deals here? How many of you are concerned about the fact the works with a lot of metals? Okay, now for the extra bonus points of the day, who wants to tell me about which metal you are very concerned about here? Lead. Lead in kids causes encephalopathy. Lead, for some reason, in adults causes radial neuropathy. Ahhh, man. Not a good time to play with toys from certain countries, right?

Okay now, could the depression be as a result of something else? Or could it be as result of something related? I don’t know. But if they have depression, and cortical… a reduction in cortical function, depending on what side is, it might perpetuate the problem in that arm, or it might do different things to it. We don’t

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know. Now, could the person have heavy metal problems and end up having depression as a result? Could they just be exposed to a lot of environmental toxins? Maybe.

Well, they’re not really doing well in regards to some of their cardiac. They already have what could be an arrhythmia here, and they have poor digestion. Now, we don’t know what that means, but that they say they’re constipated and they feel bloated. So maybe they have gastroparesis, maybe hey have hypochlor-hydria, maybe they have a bowel overgrowth. I don’t know. The bottom line is this: It’s an inflammatory mechanism potentially. But I also have to look at and say this: Is their brain that bad that they don’t have good gastric function any more?

So you have to look at it from both directions. So we’ve got assessment forms. And this is what the patient says. They’ve got a little bit of difficulty planning and organizing, and they’re really not that motivated, and they have some difficulty with getting a sound or melody of thoughts – they perseverate a little bit and you notice it during the exam. They can’t finish tasks, they have some depression, and they have some mental fatigue. Really big is difficulty with creativity in intuition on the right side.

So, let me ask you a question. Is there any signs of frontal lobe pathology? And then you’ve got to start looking at this, and you’re like, “Is it global? It looks like it’s both sides to me. Could there be a right side? Now, but wait a minute Dr. Brock. You’re saying this is his right arm, correct? I mean, is that what we said?” We said that this is his right side. How in the world could a decrease in right brain perpetuate? Could it perpetuate this wrist drop? Yeah. Listen: If you go look right in… even some of Netter’s texts, it’ll tell you that the reticular formation comes down ipsilateral. Now, the cortical spinal system goes contralateral, and gives the ability mainly to control your hands. The rubrospinal system is more proximal. But the reticular system will descend ipsilaterally, and what it’ll do is this: Your cortex will go to your corticoreticular pathways, and your reticular pathways will activate tone on that whole side, and give you volitional movement via the corticospinal system on the other side. And then on this side it will give you the ability to have extensor activation, and defacilitate the corticospinal and rubrospinal systems from the other side so you’re not stuck like this. So if you have a right side that’s decreased a little bit, and a right sided pontomedullary system that’s decreased a little bit, and then a little bit of soft pyramidal changes, your extensors will get even a little bit weaker on top of the already induced radial nerve lesion.

Are you seeing how the two can stack? Man. Let’s keep going. So you go over here and it’s like, let’s ask some questions about, you know, frontal lobe, and of course they’re having a hard time moving, when you look at these questions. Now is this because of brain, or is this because of nerve? Because brain doesn’t give you that radial specific issue. It doesn’t say this: Had sensory loss right along one of the four cutaneous patches. It doesn’t just give you a waiter tip hand. It’ll give you global reduction in slowness or apraxia, and then you have the other cognitive findings with it.

So what we’ve got to start saying is, “Is this guy unfortunate enough to have two situations going on, and now their colliding?” See, that’s when I want you to be able to see the difference. I don’t want to give everything where it fits absolutely perfectly. I want to give you things that make you think, and say, “Man, this may or may or may not be related. I may not be able to do anything for the radial nerve. I might just have to treat this guy for his cortical changes. I don’t even know.” Well, this person has a difficulty in posi-tion of the limb, no duh. They can’t even extend their wrist, okay? That does not mean that they have a

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somatosensory problem. Now, let me ask you this? If this limb is damaged for a long period of time, what’s going to happen to the contralateral brain over a period?

Let me tell you something just real quick clinically. What we do is this: If this nerve is damaged and we know it’s going to reinnervate at the rate that I told you – one millimeter per day, one centimeter per week, one inch per what? Month? – and I’m like, “Wow, we’ve got to so something to save the contralateral part of the brain,” we’ll do some mirror imaging stuff, so that as we put a mirror here and then we have… or, we’ll put a mirror actually right here, and we’ll have them move the good limb, so if we’re looking right here, they’re looking in the mirror, they’re moving their good limb up and down and up and down and all around, but their brains sees it and says, “This looks like my right arm.” So the parietal system and the frontal system is preserved, due to visual processing into the motor output of that limb, so you don’t lose brain representation of that while it’s reinnervating.

Is that a cool enough clinical trick? I’m starting to give you a few, because I know what’s going to happen. People are going to leave here and be like, “They didn’t talk about anything clinical.” Well, there you go. There’s one little bitty deal. Now, do you think I need to give something that’s going to allow neurological function to get a little bit better? Like, do you think some essential fatty acids might be better? Some mitochondrial enhancers might be better? Decreasing inflammation might be a little better? And getting some other substrate, because these nerves are going to have to be rebuilt, and there’s going to have to be a massive increase in nucleus and cellular function to replicate enough protein to go down, go through the band of Bungner, go back down and then reinnervate that muscle. so I’ve got to buy some time with the cortex, and I’ve got to increase nutrition so that they don’t fail in the middle of it. If they metabolically fail, it’s over. It’ll never reinnervate, and they’re stuck like this forever, and then you’ve got to just let it go.

So, we’re looking at this again. Man, difficulty with writing, difficulty with a simple drawings. By the way, they’re right-handed. This is just saying which side of the cortex that is. Difficulty with simple drawings. They can’s draw because they can’s use their arm but you’ve got to wonder what it’s going to start doing to certain parts of the frontal lobe and parietal lobe, because they can’t utilize that component of their hand. Listen: handedness is related the language. As a matter of fact, that’s how we start rehabbing language. When I start talking to you about rehabbing language, I’m going to teach you how to use your hand. The hand, the shape, the big picture, the small picture, and the way you do it in certain visual fields will allow us to go to different portions of the cortex to start to rehab language. Now you know why I want you to know which freaking language deficit do you have. Because if you don’t know, and you’re like, “Hey we’re doing hand exercises,” it’s not working. It’s not doing anything. You’re not even in the right area. Okay? So hang in there. We’re going to get to that.

You go over here; the rest of the stuff doesn’t look to bad. Over here, they’re clumsy with their hand because they can’t use it. Now they’ve got this: slow bowel movements and constipation and chronic digestive complaints and racing heart and difficulty sleeping. So does brain have anything to do with limbic and autonomic function? Yeah, it does. Now, let me tell you my problem here. When I started looking at this, and I go, “Well, I can understand why this guy’s got a little bit of a, you know, he’s a little nervous. I mean, come on. the guy’s arm doesn’t work the right way any more, he’s forever stuck in a waiter’s tip hand, which is probably not the best thing to do. I mean, he can’t do a lot of things. It’s just not cool. So I can see the anxiety in that. But if the brain is starting to fail and sympathetics are starting to get dominant,

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and I’m starting to get vasoconstriction what am I worried about now when it comes to healing a nerve that’s damaged?

Now I’m like this: “Wait a minute. I’m not getting enough fuel for delivery.” The person’s

sympathetically dominant, and they’re shunting blood away from everything that needs blood, like their guts, their cord, their nerves… and it’s not going to where it needs, so I’m worried about this: I’m building a mall down the street. I need a six-lane highway. It’s only a two-lane road. Make sense? So we’ll give… I’ll teach you exercises to control autonomics. We’ll teach you exercises to preserve the contralateral brain. We’ll talk to you about things to help the nerve regrow, and nutrition to help that occur. Does that sound like a realistic program?

By the way, if this is induced by anything other than trauma or whatever else, there’s not much to do about. It’s idiopathic. Okay?

Well, here’s their epileptiform activity. They don’t have any, but they took it in anyway. They have no atonia. They have no clonic-tonic findings. They don’t have any myotonic or myoclonic or any kind of other congenital. They have nothing else going on.

Except for somebody’s car alarm going off. Every module, I promise, something will happen. to pursue a storm off every module I promise something will happen. It’s amazing. At least it’s not something going on in the room next door. Okay. Yeah. I just jinxed myself. Oh God. What’s funny, the owner’s not even going to come look. Okay.

So, “Do you have weakness in your arm?” “Yes, it’s severe.” Now, when they start saying “severe,” you start saying, “Whoa, man. There may be some massive damage here.” You go down a little bit further. “Do you have a loss in muscle size?” “Severe. Right arm.” Now you start saying, “Oh gosh, it’s denervating.” You go down a little bit further. “Do you have sensory loss?” “Yes, it’s on the back of the arm, and then there’s another patch right here, and then there’s another patch right here.” Now, these types of pathologies tend to be up higher, more proximal, around the spiral groove or the quadrangular, triangular space. You’ll get a whole patch that will start to die right in here, okay? Go down a little bit further. “Do you have some sensory loss?” We already talked about that.

So this right here, pretty easy so far. How many of you got the ulnar nerve one a minute ago? How many of you can start to get this one now? So the ulnar nerve one, they’re like this. Okay? Okay? Ah, can’t do it. Ready? Can’t do it. They might be able to do that. They can’t do this. This person’s here. They can turn it over here, and they can do this, but they can’t turn it back over and do that. Median nerve, they have a hard time just doing this. They’ll come out like that with an ape hand. Apes don’t have prehensile grip, so they can’t bring their thumb this way and do this. So with median nerve lesions it just stays out here, and they can’t scoop it around like that. Pretty straightforward? Okay.

So, is there any lobes of the brain involved? Well yeah, there’s a lobe involved. We know the cortex is maybe not doing so good. We know that there’s some cellular fatigue probably. There’s got to be some excitotoxic stuff going on. Maybe the cerebellum’s involved. By the way, if you have peripheral nerve damage, you by default are going to get cerebellar changes. They may or may not be terrible, but remember, the feedback

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from that limb is now going to be different, so the cerebellum is going to plastically remodel based upon your what? There’s a great paper out that says this: “Hey, if we cut a nerve, we change the brain.” They proved it. Every time we cut a nerve, the brain rewires. Ooh, we don’t want that to happen. We know there’s some autonomic fluctuations. There’s a lot of motor fluctuations. There’s going to be a little bit of pain and some limbic stuff over time. Of course all the tone and compartment changes are there as well.

So the chief complaints point us toward what nerve? Radial nerve. And you should be able to localize it by the history. How many of you really can localize this by the history? Yeah. And you can localize the region. The general survey helps tell you the severity of it. And we went through all this stuff in regards to cognition. So we’ve localized it. Now, what might be some underlying metabolic factors that you’re concerned about? Let’s just stop and talk about this for a second. What are you concerned that it might perpetuate this thing from a metabolic perspective?

How many of you think anything in the gut – now some of you are thinking, “Oh God, I’m so happy he’s talking about the metabolic part. I get that.” There could be some gut stuff, some SIBO stuff, which could create inflammation. Or there could be an infectious disease. Who knows where this guy’s been, what he’s done, what he’s got, what’s happened. He also works in a place that could be toxic. He could have a toxic environment.

Okay, so maybe he has hypochlorhydria. Maybe he has a gut infection. I don’t know. Let’s run some labs. We’ll do that, and find out, and we’ll show you that later on. The physical examination with lab tests is going to show us everything we need to know, and then we’re going to identify all those factors, wrap them up into one big story, and start saying this: “Let’s get rid of the things that caused it. Let’s start rehabbing the area if we can, and if we can’t, let’s teach you how to cope. Because guess what? That’s what some people will have to learn to do. Sorry.

Ah, here he is. You ready?

Let me see you just open the hand up.

Okay, so what can you do right there? By the way this guy, these giant metal caldrons, he fell headfirst into one. And broke his arm. Guess where he broke his arm. Please don’t break your arm right here. It’s not cool, because there’s a nerve that adheres to the periosteum, and the nerve that adheres to the periosteum is your radial nerve, so if you compound fracture that, you may compound sever the nerve. So now, think about this. I’m a functional neurologist, but this guy comes in, and you don’t know what nerve it is instantly. I don’t… It doesn’t matter what kind of ologist you are. If it has the word neurologist with it, you have to get this one. Okay? If there’s going to be secondary cortical changes with a decrease in limb function there’s going to be cerebellar changes. And by the way, this guy’s not going to be able to use his limb the right way, and he is a manual laborist. Okay. So let’s keep watching.

Lay it flat. Open your fingers up. Open them. “If I try to open them…”

He can’t. You see the extensor? The extensor pollicis is gone.

Put your hands over here.

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So it’s coming across. And he can move his fingers open, Now he turns it over. What happens?

Can you lift your wrist up? “That’s the problem.”

That’s the problem.

“There’s been an unbelievable improvement, because…”

Hey, how many of you saw it? He was like this. His thumb was in here, and he can’t extend the pollicis. It’s wrapped in, and he’s like this. He’s like, “Okay, cool.” He turns it over and he’s like, he’s trying to lift it up with his leg, like this. He can’t do it. So let’s take another look at it.

“But it’s pulling that way.” Okay. Let me have you lift that up.

So I’m just like this: “Come on, dude. Come on.”

“You want to lift my hand.” No, no, no. That’s good. You’re doing your best. Now I want you to pull your fingers apart.

Why did I ask him to pull his fingers apart? Right here. Why did I have him do that? Pull your fingers apart. His ulnar and median nerve’s intact. He can turn it over. 7’s intact. He can’t lift it up. Guys, you don’t need to know anything else but that. That’s it. He’s right here. Median ulnar work. His thumb is tucked in. He turns it over, 7 is there. He turns it back this way, he can’t lift it up. It’s radial. So my thing is, people are like, “Peripheral nerves are so scary.” No they’re not. You can do this.

Okay, now I want you to pull your thumb out.

He can’t do it.

Okay. “I can’t” That’s fine.

What do you notice up here? This guy’s arm got mangled. Now, I want to show you the EMG at rest. At rest.

You see all those little waves up and down? That is all one hundred percent active denervation. Those are positive sharps and fibs, right across. Now, here he is, just trying to activate the muscle. Push! That’s me inserting the needle. Those are all resting potentials. He’s trying to activate the limb right now. Do you see any motor units? It is one hundred percent active denervation, and zero percent motor units. What’s your prognosis? Blblblblbl.

Here’s my deal: Nerve was severed. I’m sorry. I hope it grows back. I don’t know that it will.

So, this is a peripheral nerve lesion. It is bad. The one I showed you a minute ago is one that is not as bad. Which one is going to have a greater probability for a good outcome? The first one. This guy, this is probably it. Are you following me? Now, how many nerves did we go through just in that one case? All of them. In the last two cases, we went through every one of them. Taught you some simple tricks; just easy things to do, man. I mean, really, really simple things. And how many of you can now get it like that? Ulnar nerve,

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radial nerve, median nerve, what the hand looks like, all the stuff. I’ll review these concepts a little bit more whenever Datis and I do some summarization. And you know, when you go through this, and you look at it, here’s the NCV. Ulnar nerve is not so bad. A little bit blocked. So we know this guy has lower motor findings. He has atrophy. He has weakness, He’s denervated. He has loss of joint integrity. There’s sharp, fibs, all this active denervation. He’s hyporeflexive, and he has hand weakness.

Now, which nerve, which muscles in his hands are denervating? None. It’s the muscles in the forearm that are making his hand look like this. It’s not the muscles in the hand. Remember? He can move these. So the hand problems you see are because of the denervation of the muscles up here. Hmm. Mononeuropathy. Single location. Partial weakness extensor. So now, look at this. Just watch. Just go through it. Here it is. Ready? It’s a mononeuropathy. It’s the radial nerve. It’s the spiral groove. Did you see how I just did that? That’s why you have this chart. Mononeuropathy, radial nerve, spiral groove. I am concerned about some metabolic factors. I want to test his lead levels and everything else in his environment, because here’s the deal: He fell, and there was trauma. I told you he worked in an environment where there might be heavy metals, but that’s probably not the cause. But I love to throw that out there as a distractor, because everybody says, “Ooh, it’s lead neuropathy. It’s lead neuropathy. It’s lead neuropathy.” Lead neuropathy is very, very, very uncommon. You usually get it from what? Well water.

So man, threw a little bit of salt on that one. No so bad, but we know the neurological exam is going to involve what we just saw. We’re going to get to all these exam findings. You already know what they are. Extensor weakness, all the other nerves are intact, there’s patches of cutaneous loss that relate to the radial nerve, and then all the other frontal, parietal, temporal, and cortical signs we’ll show you later.

Hmm. Can they get worse with repeat testing? Actually it stays bad the whole time. I’m worried about a soft pyramidal paresis causing problems. He definitely has impaired neuron endurance and I’m worried about his capacity to actually recover. This is the kind of guy you’ve got to start saying things like this: “Look man, I’m not so sure this is going to turn out so good for you.”

Now, what you need to do to get rid of… I mean, if the arm stays like this, the flexors start to develop dominance over the extensors, so what happens? Sometimes we’ll brace it into extension, and we’ll start to activate the extensor with electrical current, and we’ll do mirror imaging therapy, and we’ll do some stuff to control autonomics, and then pump them full of nutrition that will help these neurons repair what they have to repair. And if it’s going to get better, it’s going to get better. If it’s not, it’s not. What do you think I’m going to do once a week, as I’m monitoring this? I’m just going to stick a needle in there, do an EMG, and if I start to see active denervation go down and reinnervation occur, here’s what I’m going to do. Woohoo! If you never see those motor units come back, you’re going to go, “Woo hoo.” Not so good. Rehabilitate that limb.

Here’s is your elec… This is right in your notes. This is your electrodiagnostic approach to somebody with a mononeuropathy. We’ve looked at the anatomy, we know the populations of neurons, we understand the physiology, you know the pathology of the trauma… Look, there could be some toxic exposure. And over here, we know if it’s symmetric or not. It’s only related to one nerve. It’s not a polyneuropathy. We know… It doesn’t matter if it’s distal or proximal. It’s related to just the radial nerve. We know it’s not one of these things where it’s all the nerves affected, like idiopathic demyelinating condition.

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So in other words, all of these rules that I gave you for neuropathic patterns on this slide, it doesn’t apply because you know it’s the radial nerve. We know the location, we know the pattern. I showed you the prognosis. We know the fibers. We know the nerve component. We know the severity. We already know there could be some underlying factors that can make it worse and that are working against us, and we have to run some labs, and we have to pull this all together and say, “Dude, your prognosis is not good. You’ve got these things working against you. It’s called the autonomic nervous system. Bad blood flow. You may have some environmental exposure. That could screw you up.”

And then you go through it and you get all the things, and say, “This is what’s going to keep you from healing, if it’s not just for the sheer fact that you can can’t heal.” When you do that, the guy goes, “Thank you for working me completely, for being honest with me, for giving me a prognosis. If anybody can help me, it’s you.”

Now, if this is something that just happened, I might send them to a micro neurosurgeon, because sometimes they can reconnect the outer covering of the nerve. Sometimes they cannot. And if I think this is completely sheared, I’ll send them off. Fair enough?

Now, how many of you were in the ballpark on that peripheral nerve case? Did we take our time? Didn’t get into a hurry? Nice and smooth? And here’s what we found: You guys all were getting it. That’s what’s important.

Alright. That’s one case. Dr. Kharrazian, he has another.

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