In this episode of CITV, Dr. David Clark takes us through another case review as a preview of what we will learn in the upcoming Carrick Institute Mastery of Peripheral Neuropathy course.
Learn strategies for assessing and treating peripheral neuropathies from Dr. David Clark, Assistant Professor of Neurochemistry.
Tuition for this program includes:
💊3 days of live training with Dr. David Clark
💊2 years of access to the recording after the module
💊Access to the flipped classroom, loaded with content and educational materials
💊25 neurology hours towards the ACNB and ACFN
💊3 months of unlimited access to Medline upon completion of the module
💊Access to our Private Clinical Neurochemistry and Nutrition Facebook Group, where you can share ideas and celebrate your successes with your peers!
For more information, visit carrick.us/MPN
– Hello, my name is Dr Freddys Garcia. Today we’re joined by Dr David Clark. Dr Clark, welcome.
– We’re doing video case reviews, we’re talking all about peripheral neuropathy, let’s get right into it.
– All right, so without further ado, if you saw the last one we did, we went through a couple of cases. So I thought, let’s do another couple of cases. So we’re gonna start with a little background that I think helps contextualize peripheral neuropathy. So I just want to start with, in case you guys don’t have a lot of background. Let’s talk briefly about the symptoms that can indicate peripheral neuropathy. Well there are sensory symptoms as you can probably imagine. You might think of numbness, tingling. There’s also autonomic symptoms related to blood flow and profusion. And you can see peripheral neuropathy in people that have orthostatic hypotension. You could see it in people with impotence. In fact, impotence and erectile is one of the very early signs of diabetic neuropathy that you see in men. And then there’s something called early satiety which means you get full very quickly because you basically have gastroparesis, abnormal sweating is another autonomic sign that can indicate peripheral neuropathy. And then there’s more of the classical neuropathic symptoms such as burning, stabbing pain, electrical pains. So that’s the kind of stuff we’re looking for in patients that could tell us, just generally speaking that there might be a neuropathy involved. Now I pulled this quotation from a paper I’ll give you the citation for, and it makes sense. I want to put this on here so you guys understand why we do what we do for these people. The treatment of choice when you find someone that’s got a neuropathy, that depends on the most effective therapy able to provide the optimal control of the underlying disease which is the big thing that we’ll be talking about in these cases, but also when we do the big peripheral neuropathy class next month. We want to know, is it a central problem? Is it a metabolic problem? If it is a metabolic problem, well which one is it? What we don’t wanna do is become, simply say, if you have neuropathy, this is the treatment we give. That’s entirely too generic, and it wastes a lot of time and it’s not very efficient. So for example, if there’s a vitamin deficiency associated neuropathy, you replace the vitamins. So for example, if someone’s got a B12 problem or a folate problem, you replace those. If there’s a thyroid condition that’s causing their neuropathy, then you make sure they get their thyroid hormones replaced. If there’s toxic nerve damage from, like a medication, or an occupational exposure, then you limit their exposure. Now we’re gonna talk about this in a lot more detail, but that is the main idea, right? Which is, find out what’s causing it. What’s the mechanism? And do the best treatment based on what that mechanism is, not some generic treatment like, everybody that has neuropathy gets this electrical stimulation on their feet. Or everybody with neuropathy gets photobiomodulation on that area of the body. It depends on why you’re doing it. Now in other cases, the aim of the therapy is only symptomatic, attempting to limit the severity of the neuropathic pain. And that’s of course, where a lot of the medications come in. Now obviously, I’m not gonna try to use medications. But some medication fairly effective at helping with how the brain processes these pains signals. So don’t just discount them and blow them off. Although a lot of the people that are gonna make it to your office have already tried those, and they haven’t worked. But just don’t get too cocky. 33% of cases of peripheral neuropathy have an unknown cause.
– I think that’s a pretty large chunk of people.
– It is large.
– Yeah that’s a lot of people that have a quote unknown, now, I won’t give away my magic answer now, but I’ll tell you what I think 33% of those cases have as their mechanism when we do the class. All right, so what’s the common denominator? What is something physiologically we can say about neuropathies? Well there’s gotta be an alteration in either the quantity or the timing of the afferent barrage to the brain, and the brain interprets that and experiences that as abnormal sensation. There can be a decreased barrage. There can be spontaneous barrage of afferent signals that don’t belong. There can be central sensitization of nociceptive pathways either in the cord or in the brain. You can have peripheral sensitization. There’s a lotta different mechanisms, and it’s up to you as the clinician to figure out what’s happening in that patient and do the right thing for them. And there’s a lot of other things that can be going on as well. Now, the real question, as I mentioned earlier with this patient that you have, the patients I’m gonna talk about in a minute, is their problem metabolic/neurochemical? Is it in their brain? Is it in their cord? Is it a peripheral nerve that’s a problem? Is it a focal neuropathy because they have a compression? So we have to know and be able to identify what is the nature of the problem? Or is it both? ‘Cause there’s absolutely no rule that it can’t just be both things. A person could have diabetes and mononeuropathy. They could have diabetes and a compression syndrome. In fact, I’ll just tell you, most people have multiple factors going on working together in a terrible kind of synergy that makes their neuropathic pain and their neuropathy worse. So the answers to those questions determines what your treatment’s gonna be. And hopefully I illustrate that as we go through these cases. So let’s talk about Cheri. Cheri’s 61 years old, here’s her chief complaints. Let’s do a little thinking exercise. She has constant numbness in bilateral lower legs and feet. Constant numbness. She has intermittent numbness in the face and bilateral arms. She has declining balance function. She has a loss of cognitive focus. She’s forgetting words. Has dry brittle hair and dry skin. These are her chief complaints. So where do you start with her? What do you think, Freddys? I have to ask you since you’re the only person on the line.
– Yeah, I’m in the hot seat. So I would think because it’s bilateral presentation already in the lower extremities starting in the upper extremities, I would first start metabolic.
– Why? Why? What makes you say that’s probably not a cord problem or a peripheral nerve? It’s gotta be something more systemic, right?
– I didn’t think a physical issue. ‘Cause there could be structural issues causing the altered sensation. But the unilateral presentation for the lower extremity and upper extremity makes it much less likely.
– Exactly, right? The fact that she’s got it in both hands, both feet. Ah, there’s probably not a disc doing that, right?
– There might be some kind of exotic brain stem tumor but it’s probably not that, if you know your anatomy and stuff. It’s probably not a structural problem, let’s call it. Right it’s more likely gonna be metabolic. So where could you start with her? Well hey you could say hey I’m just gonna do receptor based rehab, right? Well, I don’t know if that’s gonna be the best choice for this lady, right? Because we already just said she has a metabolic problem. And it’s not that affecting the brain doesn’t affect your biochemistry but, that’s probably not the most efficient thing to do. Could you do metabolic? Sure, I mean based on what we just said, it makes a lotta sense to investigate that and find out what else could be going on, right? Automatically we just said hey, we’re not gonna be the technician mechanic that says you’ve got neuropathy, here’s the one treatment I do for that, for everybody. We’re gonna select the best treatment. Could you manipulate her joints? Sure, why not? You could try to just say look, I want to fix the balance function. I’m gonna adjust her legs and feet and see if her balance gets better. It may get better temporarily but I can just about guarantee you that’s not gonna be a permanent, kinda curative long term help for her. Could you do photobiomodulation, AKA laser? Sure you could do that. But I would ask you, why are you doing it? If you think it’s a metabolic problem, let’s figure out what the metabolic problem is. Let’s not just throw laser at her for no reason. Could you do exercise? Sure. There’s a lotta research showing that, especially in diabetic peripheral neuropathies, exercise can be very helpful for those people. But again, we don’t have the answer to our question, what kind of metabolic problem is it? Could you send her out for medication? Sure, that’s what most people are gonna And I’m not saying that’s bad, but I’m just saying, again, just giving her Gabapentin or something like that doesn’t really answer the question, why do you have this metabolic problem? Here at the bottom I’ve listed some common possibilities for metabolic causes and brain cord kinda nerve causes. Let’s just see if any of these match up. We already kinda gave it away. She’s got constant numbness in the bilateral lower legs and feet. You know, there’s not really a lesion I can think of that’s gonna do that. Intermittent numbness, same thing. Declining balance, well she probably has balance problems because she can’t feel her legs and feet, right? It’s not a cerebellum problem primarily. Now the cerebellum can certainly go through diaschisis and be deaffrentated if you have numbness for a long time. But that’s probably not what the core issue is. Loss of focus, well that’s more brain, obviously. And that could be poor profusion. That could be just poor frequency of firing. We don’t know why. They might not even be related, right? The balance and the focus may have nothing to do with the numbness. One of the tendencies people have is they try to make everything relate to everything else. They don’t all the time. And that’s something, that with experience, you learn unless you kinda take my advice now and just say don’t always make everything connect ’cause it doesn’t always connect. So there’s some metabolic causes like diabetes, B12, folate, autoimmune stuff. So you and I just talked about it. And it’s probably not the stuff on the right side of the screen. It’s probably something in the metabolic category but it may not be one of these, maybe something else metabolic. So let’s talk about her history for a second. She’s had 42 knee surgeries. That’s not a typo, she’s had 42 knee surgeries, four shoulder surgeries and two eyelid surgeries and she’s 61. She’s had both knees replaced. She does not have a patella in either one of her legs. Now you may ask yourself why did that happen? Well, she’s never really been diagnosed with any particular conditions. She just had crappy knees. And she’s had all kinds of surgeries on her knees, she doesn’t have a patella in either one of her legs. So you know her gait’s gonna be off. But does that clue us in to anything that helps us understand the metabolic possibilities? Well, maybe, maybe not. In 2011, she had sudden onset of lower leg edema as well as tachycardia. In February of that year she was diagnosed with Graves’ disease, now what is that? That is an autoimmune thyroid condition, it’s a hyperthyroid condition. And that led to her getting radioactive iodine ablation. Now I’m super interested as a clinician when I see someone walk in with neuropathic symptoms and they’ve got a previous diagnosis of an autoimmune condition. ‘Cause now I know that there’s a good chance that her immune system is probably involved in this neuropathy, just without knowing anything else. Real good chance her neuropathy might be immune system mediated. May not, but the odds are pushing us that direction. She developed exophthalmos, you know where your eyes poach out of the orbit, lower leg tingling and pain. Oh, wait a minute! So something happened in here, right? Somewhere around the Graves’ diagnosis is when she started developing a lower leg tingling and some lower leg pain. So even contemporaneously, timeline wise, those things are a little bit closer together. She took high dose steroids which made her take 40 pounds of weight gain. And the leg pain, the lower leg numbness did not change. Now that’s interesting. So she took steroids, and the leg pain and numbness didn’t change. That might make you think that her immune system’s not involved. But here’s what I want to tell you about steroids. Steroids are not the be-all, end-all, alpha omega of immune system medication. I’ve treated hundreds of people on steroids with very elevated immune system markers. Don’t let that fool you, I guess, is my takeaway for that. Ultimately she was diagnosed with, you’re my friend, the 33% of people who have unknown causes, idiopathic peripheral neuropathy. After seeing many doctors, the neurologist said “She probably had an autoimmune based neuropathy,” and I believe he’s right. But did not provide her any kinds of options for treatment. And they won’t. Unless you have like Guillain-Barré or myasthenia gravis, or some of the more exotic, antibody associated neuropathies, they don’t really offer you any treatment other than, Gabapentin, maybe steroids. But you and I both know steroids long-term, they’re not a good choice. Her balance continued to decline, sure. That makes sense. Now even in 2011 when she was taking the highest dose of Gabapentin, she had pain in her legs. Even doing that. Now around 2014, her hair texture started to change abruptly. She was told her thyroid quantities were fine. And she had been taking thyroid replacement since she had the ablation. ‘Cause you guys know when you have Graves’ and they kill your thyroid, you have to now take thyroid hormones. So somethin’ happened, and I’ll just tell you from experience, that little 2014 thing where her hair texture changed, and skin texture, that sounds very thyroid-esque, very thyroid-esque. We don’t have time to jump too much off into that thyroid thing, got a whole class on that the stuff everybody knows. But that makes me interested as well. Let’s stop here for a second. So we thought, hey this could be a metabolic problem. In her history she has a crap load of knee surgeries, diagnosed with Graves’, clearly had some stuff happen with that. We’re not back over into the structural cord lesion stuff, we’re thinking back over here into the metabolic stuff. She notes hair loss in her arms and legs. Now on her legs, and this is an interesting little tidbit for you guys, the level of hair loss, like where it is, correlates with the level anatomically of her neuropathic symptoms. So where her numbness and tingling stop, that’s where the hair loss stops. It’s like a little line in the forest, and you’ll see that a lot in people that have neuropathy that’s kinda chronic because the autonomic changes and the lack of blood flow, they just lose their body hair in that area. She has decreased muscle tone. Now that’s interesting, right? So not just a sensory problem, got a muscle tone problem as well. She has dry mouth, dry eye, and she bruises easily. I’ll just tell you what I make of those at this stage. Dry mouth and dry eye make me real interested in a condition called Sjogren’s which is a variant of rheumatoid arthritis. And neuropathy is definitely known to happen in people with Sjogren’s. The bruising easily thing, we get capillary fragility and stuff as we get older. But also, if your iron level is too low, you’ll bruise easily. So these are all little tidbits that she’s telling us in the history that we can make use of. She can’t tolerate smells. That could indicate a problem with glutathione. She has a tendency to go a very long time without eating so she has diet induced reactive hypoglycemic kinda symptoms, right? So if you don’t eat for eight hours, and you get hungry and you get crabby, and you get hangry. That’s lifestyle induced, you’re just not eating. Doesn’t mean you need adrenal support and this kind of stuff, it just means you’re not eating. Difficulty falling asleep. She has tremors occasionally in the left hand, that’s interesting, right? Now she was not a very good historian about what are we talking about. I couldn’t say was it a four hertz tremor? She doesn’t know. And she didn’t have it when I actually saw her but that’s what she tells me. I say “It looks like,” I showed her how fast it was, and she said “It kinda looks like that.” So maybe it was an accentuated physiological tremor. Now she is already on the gluten-free, dairy-free diet which I think is helpful considering it might be immune system based. But she may not be consuming enough adequate calories. And trust me, she’s not based on what she said a minute ago. She can’t keep her mind on reading or praying. The other day she looked under the table and felt like she’d been thrown into the ocean and couldn’t tell what was up and what was down. That sounds like a canal problem. She’s been given recently a narcotic for the pain in her legs. That, we don’t like. We do not like that, and one thing we know now guys, we have an opioid problem in the country. And a narcotic for the pain, we want to keep her the hell off of that if we can. As I said earlier, she tried a gluten-free diet, lost about 10 pounds brain fog improved. She had energy. But a few months later, her symptoms returned. She still follows a gluten-free milk-free diet because she is lactose intolerant. So I’m gonna ask you this Freddys, does that mean that she should just go back and eat gluten? Does that mean that?
– I’m not really sure.
– No. Just because someone tried a gluten-free diet, we don’t know how strict she was, and here’s the thing. A diet like that, a lotta times people just want to do it for a month, and if it doesn’t cause a complete, 100% turnaround, they say “Well, it didn’t work.” But here’s what I gotta tell you, a gluten-free diet is not usually enough, by itself, in most cases. It’s just not. It’s important, and I always tell my patients, “Look, you’ve gotta have the right diet to get better.” But the right diet by itself is very often, most of the time, it’s just not enough to get you well. So I look at that and go, that’s cool. At least she kinda knows how to do it. But that doesn’t mean I’m gonna just say well screw it. She can eat gluten if she wants. That would be a mistake. She takes levothyroxine, thyroid medication, Cytomel, that’s T3, that’s a thyroid medication, gabapentin, Celebrex, calcium with vitamin D, and that Nucynta which is the narcotic, and Imitrex. So she’s takin’ some stuff, right? She’s taking the thyroid medication ’cause she doesn’t have a thyroid gland. Takin’ the Celebrex ’cause that’s an anti-inflammatory. The narcotic she’s taking for pain. And the Imitrex is obviously a migraine medication. Now her family history is significant for a mother who’s alive but has some dementia. Father with COPD, brother with seizure disorder, and another brother who’s also dairy sensitive. I look at that and I think well, is there any kind of autoimmune stuff in there? Obviously. Not obviously, I mean you can have dementia without autoimmune stuff. You can have seizures without autoimmune stuff. So there’s nothing in there that makes me go “Aha! “More evidence that there’s autoimmune.” Doesn’t matter, ’cause she already had Graves’. So that’s kinda the ultimate evidence. She’s already been diagnosed with an autoimmune condition at one point. And what I’ll tell you guys, just because you take the thyroid out, doesn’t mean the autoimmune problem’s gone. The immune system, when those switches have already been flipped, those aren’t just turned off by taking the gland that’s being targeted out. It certainly can give the immune system less things to target, but it doesn’t just mean oh, you don’t have an autoimmune condition anymore. That’s not how it works. So again, back to our is it metabolic, is it brain cord, what is it? Well again, there’s kinda four priorities. And you guys remember this from last time. There’s kinda four metabolic questions or metabolic priorities we gotta figure out for her. Number one, does she have an autoimmune condition? Well she had an autoimmune condition and she probably still has some kind of autoimmunity happening. What about her red blood cells? We don’t know anything about those yet. We don’t know anything about her ability to make ATP. We don’t know about her B12 or folate. We haven’t tested any of that. What about glucose handling or hypothalamic pituitary axis tone? And by the way, I’ll just tell you guys, I did a class last year on male and female hormone problems and adrenal stuff, get adrenal fatigue out of your vocabulary, just quit saying that. Because really, it doesn’t exist. I know it maybe sound heretical to say that but what you’re really talking about when you’re talking about adrenal problems, you’re talking about hypothalamic pituitary adrenal axis tone. You’re almost never really saying there’s something wrong with the gland itself. Go back to that class if you want. I just want to mention that. And we know there’s some kind of glucose handling, because she doesn’t eat. So she’s kind of diet induced number three. And then GI, liver, well, doesn’t have any overt GI symptoms. And liver function, we’ll just have to look and see what her enzymes look like. So let’s do it. So let’s ask ourselves, is she diabetic? Well we don’t know, we’re gonna have to check her. Is she prediagnosed? No. We have to look at her glucose, her A1c. Here’s some classic symptoms we went over last time I’ll kinda skip those. I misspelled her name as Chero which is kinda cool sounding there at the top. Does she have a B12 problem? We’re gonna have to do her blood work. If she has a B12 problem, the next question is, why? So look, don’t do the lazy kind of functional medicine. There’s a lot of people that do it this way. I wish they wouldn’t. I mean, I guess they can, it still gives me patients when they do it this way. If someone’s got a B12 problem, the solution, the end step is not take B12, you’re fixed. The next step is why is your B12 low? Do you have an autoimmune condition? Do you have a malabsorption problem? What’s going on? Does she have a folate problem? We don’t know, same question. We gotta find out if she has it. And if she does have it, why? Does she have an autoimmune neuropathy? Well, somebody suggested that. And then of course, you have to prove that if you want to. And the way you can prove that is you can do specific antibody testing. It’s specific but expensive. You could spend a bajillion dollars checking all these antibodies for her and you may never find one. But antibody testing is not encyclopedic, it’s not the be-all end-all. You could do a clinical challenge. But I wouldn’t do that with her. Because if she’s got an autoimmune neuropathy, the last thing I want to do is do something on purpose to rattle up her immune system to see if she has a bad reaction to it. That would be bad, you wouldn’t do that. I do talk about how to do these correctly in some other classes, but I wouldn’t do this with her. Or just treat ’em like they got it, right? Just treat ’em with an antiinflammatory protocol that you’re pretty sure has good results and see how she does. So let’s do her labs. White blood cell count’s 4.8. That’s 2/10ths of a point lower than I like it. It’s not all that exciting. Her anion gap is a little bit high, her sodium’s a little bit high. Cholesterol’s a little bit high, but that has nothing really to do with her neuropathy I would wager. Her ferritin’s 92, that’s pretty good. So ferritin’s her iron, right? If it was 20 I would say that’s a problem. 92 in a lady who’s post-menopausal, that’s pretty normal. Now, B12 at 337, what do you think about that? Excuse me, what do you think about that?
– I believe it’s low, isn’t it?
– Well, it’s not low by the lab range.
– But it’s really close. It’s really close, it’s what we call functionally low, or non optimal. Because look, most lab ranges you look at, again guys, most lab ranges are just simply a bell curve. They’re a standard normal distribution. Doesn’t mean it’s a healthy level because oftentimes there’s a gap between what the lab range is established at, and then what the literature says is clinically relevant. For example, there’s literature that says if you’re below 500, you probably benefit from B12. In someone that has neuropathic symptoms, with a B12 of 337, you can bet your pants I’m gonna give her B12. I’m just going to ’cause there’s a high likelihood it’s gonna help. Ooh, what do you think about that one? Folate 3.5. You have to remember those ranges, don’t you?
– Yeah, I can’t dig back to that one.
– She is 5/10ths of a point from being low.
– That’s super close, again.
– Yeah. That is terrible, that’s a terrible, terrible, terrible folate level. So there’s literature to say, that correlates that says look if your folate’s 11 or 10, that’s enough to cause neuropsychiatric problems, by itself, like mood, depression, anxiety. A folate of 3.5 is bad. And your question is, why? Why is her folate so bad? She probably has a malabsorption problem of some kind. And I’ll just tell ya, the odds are, it’s probably some kinda gluten sensitivity if not outright celiac disease. That’s what kinda the prevailing wisdom is now. I saw some papers recently that say hey, someone’s got a folate like this, they probably have gluten sensitivity. And I didn’t write the paper. Somebody else, in a mainstream medical journal wrote it. Then of course, the last thing that I kinda goofed up in the formatting, her homocysteine is 12.9. Now again, I think that’s too high. The lab range for homocysteine is usually like 15. But 12.9 is too high, there’s some pretty good literature that says if you’re above like eight, that’s too high. Now why would it matter in her case? Well her folate is low, and her B12 is low. That’s probably why her homocysteine is creeping up. Why do we care about homocysteine? Well because when it’s high like this, it’s oxidative, it increases oxidative stress. It increases inflammation. It can be bad for NMDA receptor function in the brain. Her vitamin D’s 30.8. Again she’s .8 away from being low. We don’t like a vitamin D of 30.8. Is it technically normal? Yeah. Is it good? No. It is not a good level. Because if she’s got an autoimmune history we do not want her vitamin D looking like that. We want her vitamin D to be better than that. All right. Diabetic, no, no, no. B12, folate, here we go! Right, we got a problem here, right? We just talked about it. What about autoimmune? Well we didn’t do specific antibody testing. We didn’t do an immune system challenge. But her vitamin D is really low and she has that Graves’ history. What’s your impression, Freddys? What do you think makes the most sense to do for her based on what we’ve just discovered? Just generically, if you want to just keep it generic.
– I wouldn’t know, this is why I need to go to the class. I don’t know this stuff,
– All right, so look.
– I’m stumped.
– We’re probably not gonna want to do photobiomodulation right away because we know, we know there are metabolic factors that need our attention, correct?
– Right, I mean maybe you can do it as an adjunct to what you’re gonna do
– Yeah, you could, sure!
– Do it if you want to as an adjunct. But I would not do it as a primary treatment because it’s probably not gonna get you very far. You could do it
– I get that.
– You could do it, you can do whatever you want. But my rule is, why are you doing it? How are you gonna know if it works? How are you gonna know if it worked long term? That’s the questions you have to answer to yourself. Now, she’s got a B12 problem, she’s got a folate problem. She’s got a vitamin D problem, she’s got an autoimmune history. I can tell you what I’m gonna do for her because based on my experience, and what I’ve read, and what I know, it makes sense to go after that stuff. Now, how are we gonna know it’s gonna work? Well we don’t know until we do it. We’ve gotta do it, and then see if she responds. Because I can tell you physiologically it makes sense that B12 could be related to her neuropathy, absolutely. B12’s related to myelination, same thing with folate. So we know physiologically, when we get into the class we’ll go into why those are physiologically related. But that makes sense for us. All right, so my treatment is I say hey, let’s do something anti-inflammatory for her. Just generic, don’t even worry about the specifics of it. Just think anti-inflammatory. And let’s correct that folate, B12 and vitamin D. Let’s give her an anti-inflammatory diet, even more anti-inflammatory than what she’s currently doing. Now, physical exam stuff. ‘Cause I did physically examine her, right? So I use this thing called a Rydel-Seiffer tuning fork on the feet, which I’ll go over and teach you guys in the class. This is more sensitive than just using a regular tuning fork. Because when you do the tuning fork, you overestimate and underestimate the vibration loss. With the Rydel-Seiffer tuning fork, as I’ll show you guys, it’s just more quantitatively, it’s better. There’s like a zero to six scale. Zero means you don’t feel anything. So she feels no vibration on her left great toe. A two means she’s got about, it’s a scale, but two is not good. She should have at least a four. She’s got no sensation on the left, pretty crappy sensation on the right. The left thumb, 3.75, that’s a little diminished. Upper extremities should be a lot more sensitive to vibration than your feet anyway. And hers is diminished on the right and left. Now a gait analysis, of course she has no kneecaps, her gait’s a little bit unsteady, although not ataxic. But when we dual task her, she immediately lurches to her right. So we know there’s a brain component in there, right? ‘Cause if you guys know about dual tasking, we dual task her, she’s gotta split her resources and then she can’t maintain her balance. So she is definitely using a lotta brain power trying to keep herself upright and walking correctly. Did bedside pursuits, she’s got intrusions, horizontally and vertically. I’m not gonna go too deep into that. Saccades, she’s got prolonged latencies horizontally and vertically, just doing it bedside. You can just see that it’s taking her too long to get going. And of course, we have a saccadometer or whatever, you can quantify that, but just at bedside, you know that that’s not right. So you know she’s got a brain problem in addition to all this neuropathic stuff, you know that. The question is, is there a connection? We don’t know yet. Now we did what’s called a MoCA, which is a Montreal Cognitive Assessment, she stored a 24 out of 30 which is basically, it’s not true cognitive impairment, but it’s getting close to mild cognitive impairment. And remember, she said she had problems focusing. She had forgetting words, well, she’s got an honest to goodness brain problem. The MoCA takes about five or six minutes to do. It’s a really useful thing. I think they have a computerized iPad version of it you can do with people. So I recommend you use that if you have anybody, if you’re wondering, huh, I wonder if this person has any kind of cognitive stuff going on? This is a really cheap thing to do. VOG pursuit testing showed normal pursuit gains which was different than she had at bedside. I’ll explain that some other time. I’ll explain that later. Right, so here’s our impression. She’s got a brain problem. She’s got a metabolic problem, where do you start? Well, again, here’s all the different choices. I think based on what we talked about, we could make cases for doing all that, frankly, right? But what I did is the anti-inflammatory supplemental protocol, don’t even worry about the details of it. Fixed the B12, the folate, the vitamin D, the anti-inflammatory diet, all of which, when we have more time I’ll tell you guys about and we’ll talk about it in depth in the class. Here’s what we got after 30 days. I like to do my treatment plans in 30 day chunks because I believe that 30 days is plenty of time to see if there’s gonna be some kind of change or not. It’s not gonna take six months doing metabolic work if you’re doing it right, and it’s actually helping to figure it out! 30 days is plenty of time. So in terms of focus and forgetting words, no change. Well, crap.
– She had two good days though where there was a lot less pain in her legs. Well that’s interesting ’cause she nearly never has any good days where there’s less pain in her legs. Maybe the balance is a bit better, that means no, by the way. When someone uses waffle words like that, it’s not better. If I say to people “Hey, so how much better is that?” And they go that means it’s not better. Right, if I say “How much better is it?” And like “Ah, it’s actually a lot better.” Just recognize when someone’s telling you it’s really not better. And it’s OK, don’t be afraid for someone to say “It’s not better” because that lets you know, if you’re a good doctor, you’re a good clinician, you’re gonna use that information to change what you’re doing, right? The numbness in her face and arms, and the constant numbness in the legs hasn’t really changed. Well, crap again. So what do you do?
– Let me see. I’m stumped!
– All right, here’s the first thing you could do. You could say well, screw it. None of this metabolic stuff works, I’m never doing it again. I’m just gonna laser every person that comes in. I’m gonna adjust every person. Or you could say huh. Well nothing’s happened yet. I wonder if she’s absorbing this stuff. That’s one thing you could ask yourself. And so you could just go ahead and recheck her B12, folate, vitamin D and see have those levels changed at all?
– That’s a good question.
– That’s a reasonable thing to do, right? That’s a reasonable thing to do because you’re assuming someone who has a crappy these things was absorbing the stuff you gave her, but maybe she’s not. It’s totally valid to do that.
– I don’t know why it’s asking me that. So I did add something else, I added one formula that improves endothelial nitric oxide and neuronal nitric oxide, improves profusion. That’s basically why I added this little liquid formula. Could she add back foods? ‘Cause she’s been eliminating foods off this little anti-inflammatory diet. Could I retest labs? Sure! I could give up, I could retest things. She made the decision for me. She said “You know what? “I just want to stick with this for another couple weeks.” I said “All right, cool.” I said “But I think we should go ahead and retest the labs.” I’m not sure if I put that in here. But I went ahead and ran the labs to see what they were gonna be. And then here’s what she says. So this was… About five weeks into it, I don’t know if you guys can read this top part. This is an email she sent me. She says “So I must tell you, “I’m not quite sure what to make of it. “When I was in there at four weeks, “for the 30 day follow up, there was no difference “and I started to slowly add foods back in. “At about five weeks,” She said “Remember I had that day at the mall “with hardly any pain?” She said “Something has happened. “I’m able to be on my feet for several hours “with minimal pain. “They’re numb, but just minimal pain. “I’m scared to add any foods back. “I’ve added a few things. “My goal is to be able to sit at the table “with my feet down, or at my desk. “I can tell that that’s easier. “It’s been six years of pain. “I hope this isn’t temporary. “I cleaned yesterday like I haven’t cleaned in years.” So here’s the thing, it just took a little bit longer for her than 30 days for things to really start to kick in. Now I could go through the rest of the case with you but bottom line is, her folate levels went up, her B12 levels went up. And we kinda got ahead of the process. So she didn’t have to keep taking the same protocol for the rest of her life. ‘Cause I always tell patients, anything I tell you to take, at some point, I’m gonna tell you to not take it. I gotta find out if you still need it or not. And I’ll tell ya, that’s the one thing that every patient that comes to you for this kinda work thinks you’re gonna tell them, is that they gotta take it for the rest of their life. ‘Cause that’s how they’re given medication. But I view this clinical neurochemistry and functional medicine as rehab. So we rehab, do what we can, and then pull stuff away and find out what does the patient really need? Some people need long term support, some people don’t. The only way to find out is to find out, right? I think it’s the ethical, smart thing to do for them. So anyway, the takeaway from that case is, she was willing to give it another week or so and that’s when the turnaround really happened for her. Now, I wanted to have her come back in. I wanted to do other rehab and stuff on her. But just because of financial stuff and other things, she was happy. She was happy with what we got. I tried to impose my goals on her, but she got what she wanted out of it. So good for her, and I guess good for me. So my takeaway is, don’t be a mechanic. Try to narrow down what you’re doing based on what you think the mechanism is. Do your treatment, did it work? And they’re gonna throw you curve balls because what I’ll tell you guys is when I give you cases, I mean, I’ll give you cases like this, this is real stuff. ‘Cause sometimes things don’t work! What do you do then? Right? You go to some classes and they tell you “Well this is what you do.” But they never tell you what you do if it doesn’t work. You have to know your physiology and things and know what is next, what’s the most likely? So that is our first case. This next one won’t take very long. You guys have seen that before. This is Bruce. Bruce is 60 years old again. The odds of neuropathy, and the prevalence of neuropathy goes up a lot after you hit about 50, 60 years old. Just kinda what happens. His complaints are fatigue. Well, that’s completely non-specific. That could be 100 different things. We won’t even go through the list, it’s so big. He has weakness in his legs. Well, OK, is that a motor problem or a sensory problem? Because, just remember guys, and guys I mean gender neutrally, everybody. You cannot have a motor response that’s correct unless you have a correct sensory input, right? If I have abnormal sensation, I can’t have appropriate motor output. He also has difficulty walking, he has decreased sensation in his feet, there we go. He has general stiffness in his legs. He has occasionally stiffness in the hands. He has near constant tingling in the hands, OK! Let me just cut through some things pretty quickly for you. He’s got sensation loss in the feet and tingling in the hands. That is not a cord lesion, right? That’s not a compression. There’s basically different fiber types, roughly different fiber types involved in the upper and lower extremity. That’s probably metabolic, right? Now if he just had tingling in his feet and nothing else, well, there could be a couple things that could do that. But he’s got them in the upper and lower extremities. Here’s the problem with Bruce, he’s employed as a driver for a major freight company. Here’s a guy that’s got weakness in his legs, decreased sensation in his feet, this is not good for him occupationally. This is a problem for him. The thoughts are the thoughts I just gave you. I can’t read that, hold on a second, I have to move this thing out of the way so I can read it. Ah–
– Metabolic versus neuraxis.
– Very likely a metabolic problem. Get it back here. So here’s the history, early 2012, he had the onset of tingling in his right hand, that was his first symptom. Tingling in his right hand. Freddys, how can we tell if the tingling in his right hand is due to a brain problem, a peripheral nerve problem, or a metabolic problem? How can we figure that out?
– For the nerve, you can do testing. You can do electrodiagnostic testing. You can differentiate it that way.
– You could also just see, is it carpal tunnel? You could just do orthopedic compression test, right?
– Right, certainly could do some mechanical things to confirm that. The neurological stuff you’d have to use other tests to confirm his parietal lobes on the left side.
– Right, how would you do that? Just quickly, how would you do that?
– I guess you could do things like compare the left right graphesthesia, things like that?
– All right, do parietal tests, the tingling could be from his motor map. Doesn’t even have to be from his parietal lobe right? You could do frontal lobe tests. The point is, you could figure that out. If you had the body of knowledge, you could go wait a minute. Like if he walked into your office today and he had tingling in his right hand, you would be able to reasonably push yourself into a couple different directions, right? If you’re like OK, the tingling is nondescript, doesn’t fit carpal tunnel. I can’t provoke it, right? I look in his brain, and his saccades are good. His parietal lobe looks good, pursuits are good. Everything looks good. Probably not either one of those things, right? That’s my point. That’s how fast it can be. Now over the next six months, the tingling spread to both hands, both legs and feet. That’s not his brain probably. Now you could make a case that it’s his parietal lobe, you could. But the bigger chance is, the bigger probability is it’s not that, it’s gotta be some kind of metabolic process doing that. ‘Cause that’s a fast spread, right? Now he had been singing in the choir, but had to stop because he became lightheaded when singing. That’s an autonomic symptom. So he may be getting hypotensive as he’s doing these big breaths and singing, he’s changing his venous return. He’s getting lightheaded. He developed leg cramps and muscle twitching. So what do we think? Well, we think that there’s something going on with him metabolically. Now we don’t necessarily know what the name of it is or what condition it is, but there’s something metabolic going on with this guy. And I gotta tell you, for it to happen that fast, my bet is an immune system problem. That’s what I would tell you. Over six months, all this crap happens, that’s probably an autoimmune problem, I think, I think. Now I could be wrong, it could be toxic or whatever. But it’s not like he’s getting other organ systems involved. It’s mainly nervous system, right? So I’m thinking it could be an autoimmune problem. Oh guess what? He was diagnosed about six months later with an anti-MAG neuropathy. That’s an autoimmune neuropathy. Now MAG stands for myelin-associated glycoprotein. So he’s basically got an autoimmune attack on myelin. I’m giving you guys a link. There’s an article that tells you all about it. Later you can just link out to that. Or you guys can provide the link or something. That’s a good article on anti-MAG neuropathy. Now he was recommended IVIG therapy but he refused it mainly because it was really expensive. And secondly when he read about it, as you can, it’s not that helpful for this kind of neuropathy. IVIG is intravenous immunoglobulin therapy and they use it like in myasthenia gravis, Guillain-Barré. But the literature that’s available says that, low chance of it helping in this anti-MAG neuropathy. So he said, “Forget it, I’m not doing it.” He has tried on his own, before he saw me, this thing called the ReBuilder, which is this electrotherapy thing. That didn’t do anything for him. Now let me ask you a question, Freddys. Why would something like this electrotherapy ReBuilder not do anything for him? Does it make sense why it probably didn’t do anything?
– It doesn’t address his particular cause.
– Tada, right. And then he tried low dose naltrexone. Now if you guys don’t know what that is, that is a…
– Wasn’t that involved in drug medications–
– It’s basically, it’s an opioid blocker is what it is essentially.
– Yeah, yeah, that’s what it is, yeah.
– It’s indirectly a T helper one cytokine immune system booster. And so what it does with some people that have a particular, some have a particular skewing of their immune system, it tends to kinda quote unquote, balance things out. And some people respond really well to it. Other people, doesn’t do jack. Other people it actually makes them worse. He also tried a glutathione support supplement that everybody’s heard of, but I’m not gonna name it. Begins with a P and ends with an M. That didn’t do anything for him. He saw a chiropractor who of course told him spinal adjustments would be great for him. But that didn’t do anything for his neuropathy because look guys, none of those, except maybe this one have anything to do with this mechanism for him. Now Bruce didn’t know that these things had very little chance of helping him. He’s just doing stuff that works. Don’t be the doctor version of Bruce which is I’m just gonna do generic stuff for neuropathy without thinking about what the mechanism is. And again, none of that stuff helped. So he, on his own, adopted a gluten-free diet about two months before I saw him. He was taking fish oil, glucosamine, licorice root which I have a problem with because of the immune system effects of that. We don’t know what Bruce can tolerate or not. Alpha lipoic acid which is generally gonna be OK. And arginine, which, again, I would not have him do. On his examination, he’s got hair loss on the legs up to the level of the knee on both legs. Just guess what, that’s where all of his sensory loss is, up to the knee. Right? When we dual task him, he has reduced armswing bilateral, slow gait, lateropulsion to the right. So his brain is being affected, right? Just like in the last case. These people have neuropathies, it’s a great example of your brain cannot exist in a vacuum from sensory information. It needs sensory barrage. The back part of your brain feeds the front part of your brain. And so if you have a neuropathy that’s this severe, it has a very high likelihood of creating diaschisis, and TND, and just all kinds of different problems in different brain areas. But he’s got adequate muscle strength, that’s what’s interesting. He can’t feel a damn thing, but he’s strong in his feet which is good. Which is one of the only reasons I think he can continue to drive, is he’s actually still got strength in his feet and his legs. He’s got pretty hypoactive stretch reflexes at the patella and the ankle. And again, he’s got loss of vibration sense on the right leg from the foot all the way up to the patella. And loss of vibration sense on the left. Mainly at the great toe, he’s got a little bit of vibration on the malleolus and the patella. So the right side is worse. And of course, he has an abnormal heel to shin testing using his right leg because he can’t really feel his leg. So he has a bad motor output based on core sensory input. Brain doesn’t really know where his leg is, et cetera. And he’s got increased latency of upwards and rightwards and leftward saccades. So the guy’s brain is not working very well. Is it related to the neuropathy? Probably. Will all of that correct if you correct the neuropathy? Don’t know. This guy is still a perfect candidate to do some rehab on. And I’ll just tell ya, most people like this that have got this neuropathy, when you do the right things and the neuropathy corrects, this stuff may correct a little bit, but usually they’re gonna need some kind of other things to try to fill in the gap and get the brain firing at the right rate again. Just to tell you guys a thing about anti-MAG neuropathy, when you look at the literature, they present with a predominantly sensory neuropathy which is what Bruce has got. And they have ataxia, which he’s got, when you dual task him, and tremor, which he doesn’t have, with a poor response to immunotherapy. Meaning, poor response to IVIG. Which is why he didn’t want to do it in the first place. And there’s a really, really, really recent citation for that. So what do his labs look like? ‘Cause look, we already know he’s got an autoimmune problem causes neuropathy, I just want to see what else is going on. Because there’s no rule, again, that says he doesn’t have a B12 problem, folate problem, homocysteine problem, a vitamin D problem, that if we fix those, could make this better, or at least help. So his fasting glucose is a little high. His A1c confirms that his glucose is a problem. His homocysteine almost exactly like the last lady, 12.9. That’s a little bit high. His vitamin D, again, is not great. It’s not as low as the last lady but still, I know this guy’s got an autoimmune problem. I want his vitamin D to be like 70 or 80. And that’s not a high level. 70 or 80 is not high. His white blood cell count, 3.7. Why do I mention that? Because people with chronic autoimmune problems, very often have a white blood cell count that’s three point something. The cytokine load tends to suppress your bone marrow a little bit. His neutrophil percentage is pretty high, 80. That’s pretty high. So what do I see? I see a glucose problem, I see a homocysteine problem, a vitamin D problem and some signs of immune system activation, right, the neutrophil percentage. So what do you do, and what do we know? Well, we know Bruce has got an autoimmune problem. We know about these metabolic priorities. I bet that we should probably be looking at, number one, and number three for sure. ‘Cause he’s got a blood sugar problem, and he’s got an autoimmune problem. So what do I do for him? Well I kinda give you a little bit more detail. So I gave him an anti-inflammatory diet and a supplement protocol which had vitamin D, omegas, turmeric, resveratrol, and a formula to try to get his blood glucose down. Because look, when glucose levels are high, it’s inflammatory, promotes oxidative stress. There’s a lot of things that happen. So having an antibody associated neuropathy plus basically diabetes, that is not a good combo. So we’ve gotta do both things. Now here’s after 30 days. The vibration sensation was now intact on his right leg, from his knee down to his ankle.
– So he got that back. He got that back, that’s with no rehab. That’s just doing the metabolic control. Dual tasking no longer caused lateropulsion, and his arm swing was normal. Now sometimes it doesn’t work like that, I have to tell you. But this is a case where it did. His gait was good, and he didn’t lateropulse, his arm swing was good. His muscle stretch response is still hyporeflexive. We can live with that. We’d like to to be better, but they may not get better. Now after 60 days, he got vibration sense back down all the way to his toe. And his saccade latencies became normal, but they were still kind asymmetrical, meaning, everyone’s asymmetrical a little bit. So the guy’s brain changed in addition to the neuropathic stuff changing. Do we know the exact reason why? No. We haven’t done a controlled way to do that. But we know that what we did helped, right? And not only did it help the neuropathy, it also helped the central function as well. OK. Over the next six months, he maintained that. We like that because anti-MAG neuropathy is supposed to be progressive. It’s not supposed to get better. It’s not supposed to stop, it’s supposed to get worse and worse. Now he discontinued the turmeric and resveratrol but continued to maintain the same level of improvement. So again, we took him off some stuff and said hey, how’s he gonna do without this? And he passed his yearly physical required to maintain his truck driving license, which is very good for him and his financial situation. Then one year after I saw him, the physician who’d diagnosed him with that neuropathy said that “Hey man, the neuropathy has failed to progress.” Which kinda blew that guy’s mind a little bit. Because he had never seen a case where it failed to progress. Of course, they usually chalk it up to being chance or something. But I would like to think that our intervention probably is what did that. So that’s a good thing. So here’s the takeaways. Again, you gotta know how to determine if the cause is metabolic or neuraxis. You gotta know what the symptoms are telling you about the possibilities of those. You’ve gotta know how to test for those. Which means to do this really well, and this is what we’ll talk about in class, we’re gonna talk about how do you assess, not just how to run labs, but how do you do it all, right? How do you check for compression? How do you check for brain stuff? I can’t do a full 800 course or whatever. But we’re gonna give you the tools that you need to be able to make these kinda differentials and know, OK, maybe I should do rehab on a guy like Bruce, right? When do I do it? So the takeaways are you gotta know how to treat effectively and efficiently and that’s the whole point of the class that we’re doing in a few short weeks at Cape Canaveral, livestream or on site. I would love to see you guys on site. And that’s what we’re gonna do. We’re gonna go through, you’ve already got a huge flipped classroom I already released, you guys. It’s full of a lot of stuff. So what I’m not gonna do, I’m just gonna go ahead and tell you. I’m not gonna spend a lot of time going through anatomy of this stuff, I really want to get into the pathophysiology and then how do you test, how do you treat? And we’re gonna do not only the labs and the metabolic stuff that you guys have seen, but talk about the structural stuff like compression neuropathies, what do you do for those? Talk about the structural side plus the biochemical side, plus the kind of functional neurological central brain stuff. There’s a lotta stuff for us to cover. We have plenty of time to cover, there’ll be a lot of hands on stuff as well. So I think I just stole your thunder Freddys, you were supposed to talk about that class.
– No, no, no, I appreciate you going over it. And again, we’ve been getting a lot of excited scholars calling the institute because of this program. Because again, everybody’s been going, “Is he really gonna go over the metabolic stuff “and is he gonna do more?” So again, we’re really proud to say that we are gonna be covering the metabolic, the neurology, and the physical medicine. There’s other courses out there. But none of them are gonna put it together cohesively with actual plans of action for each one of those in a three day course. So thank you very much for putting it together. Dr Clark, thank you very much for spending more time with us and doing these case reviews. You stumped me a couple times this time which I’m not happy about.
– You’re the only one here.
– You got me, but normally I’m a little better. So you got me this time.
– No that’s cool. Hey I want to say something, for you guys that are gonna take the class, do read the flipped classroom papers. Because you’ll be able to get so much more out of the class and I won’t be forced to waste time basically explaining basic stuff that you should already know if you’ve read the flipped classroom, right? So if you’re wondering how to read the flipped classroom, just read the abstracts, like Dr Carrick says, read the abstract, read the conclusions. Then go back, look at the images. But do that flipped classroom ’cause you’ll be so much better prepared because I’m gonna show you when and how to use laser, when and how to use pulsed radiofrequency stimulation, when do you use the kinda fast stretch adjustments. When do you use rehab stuff? That’s a lot of time, and I need you guys to do the background in flipped classroom. That’s all I got to say.
– Perfect. And I want to thank you personally ’cause I actually started the flipped classroom. I could imagine it took you a long time to curate all those papers. ‘Cause I can tell they’re hand selected. And it’s actually being really helpful for me. You shouldn’t have stumped me still, so I’m upset about that. But Dr Clark–
– But never again. Never again, right?
– Not again on the same question at least. December 6th, 7th and 8th, Cape Canaveral Florida available on site, come and join us in Florida or via live streaming, if you want to watch it from home in your couch. Dr Clark thank you very much.
– And we’ll catch everybody next time.
– OK see ya, bye bye.