FUNCTIONAL NEUROLOGY ANATOMY AND CENTRAL NEUROLOGICAL ... · down, right? Or the areas that suppress pain aren’t working. Okay? So again, next time you see a patient that comes

MODULE ONE TRANSCRIPT – PAIN PAThwAyS | COPyRIghT © 2016 FUNCTIONAL NEUROLOgy SEMINARS LP | PAgE 1

FUNCTIONAL NEUROLOGY ANATOMY AND CENTRAL NEUROLOGICAL PATHWAYS (MODULE ONE)

Transcript – Pain Pathways

Presentation by Dr. Datis Kharrazian

So you guys all have seen patients with pain, and the key thing I wanted to cover though is chronic pain. Abnormal pain. Pain that exists that doesn’t make sense. Right? So someone has an injury, but the injury never goes away. Someone has chronic pain for five years; they can’t get rid of it. What are the mechanisms involved with those things, right?

So pain is obviously suffering, and we all see a lot of pain patients. Pain is the number one motivator for a person to see a healthcare professional, okay? So what you need to understand is pain, and we need to understand pain from receptor to perception, and then the descending pain pathways down.

So every single person in this room has different pain threshold, different pain levels, right? So let’s say if we took some type of instrument that induces pain on your – let’s say – thumb, and you rate your pain from 1 to 100, everyone in this room got the same exact pain stimulus, we would have scores all over the place, right? Some people would do it and they would just laugh, “Haha, that’s cute, that’s funny.” You know. Some people would have the injury and then go, “Oh my God! That’s terrible! Don’t do it! Don’t do it!” That’s the next person. Some people will get a little stimulus of pain there, and they’ll feel it for the next twenty minutes. Some people will get a little pain there and then they have, like, pain for the next three days. So everyone’s a little bit different.

So what are the mechanisms that cause someone to perceive pain, and why does someone feel more pain than another? Right? Now, one of the things that you really want to always consider doing is, when someone has any kind of injury – so they have chronic shoulder pain, or chronic ankle pain, or chronic back pain – on the side of their pain, just as an exercise, take a pinprick, pinwheel, and just see if the rest of their pain is greater on the side of their injury compared to the other side.

So let’s say I have chronic right hip pain. So just for kicks, just for neurological assessment, take out a pinwheel and go, “Hey, does this feel the same as this side?” And they go, “No, it feels sharper on the right side of my face and arm too.” “And how about your legs?” “Oh yeah, it feels sharper on my right side then my left side.” You now know you have a neurological component to their pain. They may injure their hip


from a mechanical insult, but the fact they have chronic pain could be because they’re perceiving pain at a higher rate than they should. Does that make sense?

So usually when the brain’s involved, you tend to see some more global types of perceptions. Now, when you check for pain perception with these brain-related pathways, you don’t want to just see if they feel the pinwheel, you want to compare left to right, okay?

So just for fun, take your fingernail, just kind of stroke your face. Is it different, or is it the same. Stroke your skin. And you have to have some degree of parietal function to tell the difference. If someone does it to you, it’ll be easier for you to notice that. So do you notice a difference between one side or the other? So you shouldn’t. That would be a normal ideal response. Okay.

What I want to go over with you in my section here is, what’s the difference between a normal pain percep-tion, neuropathic pain, hyperalgesia, hypoalgesia, and allodynia? What factors determine inter-individual perception of pain? And How do you identify metabolic versus neurological primary mechanisms for chronic pain?

So first of all, just make sure you guys know the basics of definitions. So let’s first talk about pain. So pain is an unpleasant emotional experience. It’s not necessarily a sense. In neurology, pain is not considered one of your primary senses like smell or taste; it’s emotional. It’s limbic. So your emotional state determines how much pain you feel. So let’s say you have a bad day, and then you, you know, hit your toe on the door. How much will it hurt versus if you’re having a great day and you hit your toe? If you’re having a bad day, you bump your toe, it hurts a lot, right? If you’re having a great day, like, “Oh, that’s terrible, let me walk this off,” right? So the degree of firing of your limbic system pre-existing to the stimulus will determine how much pain perception you get. Does that make sense? Because it’s a limbic, emotional phenomenon.

So for people that have chronic pain syndrome, one of the things you have to consider is, do they have chronic limbic activity? So again, you go back to the person that everything’s terrible. Life’s terrible, you know, job’s terrible, work is terrible, you’re terrible, everything’s terrible. That’s, first of all, going to change on a neurochemical process that’s going to perpetuate pain. Now, you also know the limbic system is involved, so you wouldn’t be surprised to see chronic pain syndromes. Does that make sense? You don’t see happy people with chronic pain syndromes. But then, chronic pain syndromes then create a limbic response, a neurochemical response, that kind of puts them in the cycle as well. And sometimes they can have chronic pain when they actually either do exercise, have opioid responses, have social interaction, and those things actually tend to change their pain perception. Does that make sense?

So the key thing you have to understand is, pain itself is a limbic, emotional process. That’s critical, okay? The degree of pain someone feels isn’t always related to the amount of injury they have to whatever tissue they have. Alright?

Then you have nociceptors. And nociceptors are your pain receptors. There are certain things that will increase or sensitive nociceptors, right? Neurochemical factors. Autonomic factors that can sensitize nociceptors.


Then you have the concept of hyperalgesia, increased pain perception; hypoalgesia, decreased pain perception.

Neuropathic pain, which is injury to actual nervous system that perceives pain, like peripheral nerve, right? Or areas of your pain realization throughout your brain.

And then you have allodynia, which is you’re feeling pain for reasons that don’t really cause pain. Someone touches you and that’s painful. Right? Whereas you should have something painful injure your tissue before you feel pain.

And then sensitization goes back to receptors that are involved. So you have all these different factors.

Now here’s a question for you: Take a pinwheel, you stroke face, arm, or legs on one side, and then you stroke at the other side, and one side they perceive the pinprick more, and one side they feel less. So which one is the hyperalgesia side, which one’s the hypoalgesia side? Which one’s the involved side? I feel pinprick more on this side, and less on this side? Is this side down? Or is this side oversensitive? How do you know? Do you just pick one? I like oversensitive more.

Guys, you’re going to have to take that pinwheel and go midline on their sternum, and which one feels more like your sternum? So you stroke one side, you stroke the other. You stroke this side, and they go, “Yeah, I don’t feel it as much. This side feels more.” And then you go, “What does it feel like midline?” “Oh, midline, it feels like my left.” So what does that tell you? Right side’s up. So that’s how you want to compare these things. You go left to right, and then compare it to midline to know if one side’s actually over or one side’s under. Your midline is your baseline to compare it to. Okay?

Now, let’s go over some just general concepts so you can understand the terms. So, “Doctor palpates over the area of L4-L5 of an individual that has an acute lumbar disk herniation. The patient violently pulls away from the doctor’s hand and screams.” Is this hyperalgesia, hypoalgesia, or allodynia? Should you have pain if someone palpates over an injured disk? Yeah. So this is maybe hyperalgesia. The chemicals from the disk injury are causing pain sensitization in the area, and there’s more pain. It’s normal to expect pain over an injury if you touch it. Right? So there’s a neurochemical mechanical insult from the injury causing more pain realization, right? So it’s not… it’s hyperalgesia due to injury. Okay?

“A child suffering from autism hates to wear clothes and tells her parents that clothes hurt. During the examination, gently rubbing over the patient’s limbs causes the child to pull away and say, ‘ouch.’ “ So is this hyperalgesia or allodynia? Allodynia. Now, this is important, because, you guys, when you see allodynia, you’ve got to know there’s a brain component, or there is something sensitizing the pain receptors. Right? Something sensitizing pain receptors, usually autonomic or metabolic, or something is involved centrally that’s making them feel more pain. Could the parietal lobe close to threshold cause more pain perception? Yes. Now, there’s descending pain pathways, if they’re not working well you can have increased pain perception, allodynia, and mechanisms of that nature.

Here’s another example. “You measure your patient’s blood pressure with a blood pressure cuff, and the patient tells you that their arm ‘really hurts.’ They tell you that their arm is bruised despite no visible signs of injury.” Is this hyperalgesia, allodynia? It’s kind of hard to tell, because depends… you know, most people,


some people that have sensitivity, they might feel some pressure, so sometimes it’s not always that clear. And that’s just important to know. So sometimes very clear, sometimes you don’t know, some people are very sensitive.

Now here’s an example: You take a pinwheel, you stroke someone’s face, they go, “Ooh, that feels sharp. It feels knife-like. Okay? First of all, is that normal to you? No, right? Then the question to ask is, “Tell me when it goes away.” And they go, “I can still feel it.” And you should time it. Like, “Okay, how about now?” “Still feel it.” “How about now?” “Still feel it.” And like a minute goes by, and they’re like, “Yeah, it’s gone.” What did that just tell you? You evoked a receptor site change, and it kept firing and kept firing and kept firing. That either means the areas of the brain that realize pain are continuously firing and not shutting down, right? Or the areas that suppress pain aren’t working. Okay?

So again, next time you see a patient that comes with any kind of pain syndrome, take out your pinwheel, disposable pinwheel – you should all be using disposable pinwheel heads, right? – check one side, check the other. If they have a global difference in one side, you know there’s a neurodegenerative component, right? And then figure out which one’s close to midline, and then do the pinprick, and then ask them when they feel the pinprick go away. Measure that, and that’s your baseline. Do therapy, see if left-to-right balance, and if they still feel it, if it’s gone from a minute to ten seconds. That lets you know you’re activating the right pathways. Does that make sense? Because that chronic hip pain may have been initially injured, and there’s some scar tissue there. The fact that their pain continuously perceives that pain, or can’t inhibit pain at the spinal cord level, could be why they have chronic hip pain, or some kind of chronic disorder.

Okay. How about this? “A patient complains their anterior thigh feels number. Pinprick sensation, vibration sense, and light touch sense are all normal. They also complain that their legs tire quickly when they stand or walk.” What term would describe this pain? Well, it’s not necessarily allodynia. It’s not necessarily hyperalgesia. Their parietal lobe is kind of intact, right? So this could just be motor weakness. So you have to sometimes realize like, if you have motor weakness, sometimes you get numbness. Like here’s a great example. You sit on the toilet for too long, what happens? You get numbness, you get tingling. It’s painful, okay? Those are all motor. You cut off bloodflow to circulation. So this is a case where it’s really more motor, more vascular. It’s not always the ascending or descending pathways.

“Forty-two-year-old woman complains of chronic body pain. The entire body. She has medical history of diabetes and hypothyroidism. She also is a smoker and has a sedentary lifestyle.” You have multiple mechanisms for pain here. Now, I remember speaking to the director of the Scripps Pain Clinic here in San Diego. And he goes, “We’ve done a lot of research. We know one single factor that determines whether chronic pain patients get better or not.” Know what it was? Movement. If they don’t move, they don’t get out of pain. Literally to the point where they throw people in a pool with a lifesaver and say, “We don’t care. Just paddle. Just do something. We know like you have surgeries and you can’t walk, just move.” They will do stuff like that to get them out of chronic pain. Those types of things activate their brain, which then activates descending projections. Okay?

So, we know with chronic pain people, if their brain isn’t firing, especially areas in their frontal, which fire into limbic pathways, they just don’t have the ability to get out of pain, okay? It’s the worst possible thing for a chronic pain patient is sedentary activity. Research is showing the key factor, whether someone gets out of pain, is if they become active and movement of any kind. I had a guy I knew; he was really a great


doctor. He said, “I don’t care if someone’s sick. I’m going to throw them in a wheelbarrow and have them just, like, kick away in a lake.” It’s exactly what these people at Scripps were saying. They throw them in the pool, they get them to move to get out of pain. Okay? It doesn’t matter where the pain is, [? 13:20] or central-based.

Now let’s talk about the factors that determine individual pain perception. So you always have to start with the receptor site. Certain things sensitize nociceptors, right? They make them more sensitive. So one of the things that sensitize nociceptors is reduced cortisol. So what does that mean to you clinically? Someone who has reduced cortisol. So cortisol has an anti-inflammatory effect. So it initially blocks inflammation. It modulates the immune system. So people that have chronically low cortisol are more prone to have pain inflammatory responses and pain perception. So a person has low cortisol, they’re going to have a tendency to have low blood sugar. And as their blood sugar levels drop, they don’t have enough cortisol to bring it back up. So they’re the ones that get shaky, light-headed, irritable, have to eat all the time to keep their blood sugar stable. You may not be able to get a person out of chronic pain if they have low cortisol patterns.

Then you have prostaglandin imbalances. Prostaglandins can increase the inflammatory cascade, and sensitize those nociceptors. Now, the most common prostaglandin imbalance is people that don’t have enough omega-3s. They’re just eating vegetable oils, eating lots of omega-6s, they don’t eat fish, they don’t eat nuts, they don’t eat seeds. But they’ll have French fries when they’re out, they’ll have fried foods. Those types of diets increase a shift in prostaglandins which is pro-inflammatory.

Hypothyroidism increases pain perception. So if they’re not managed properly, and their TSH is off, that can cause chronic pain. Local inflammatory responses, even systemic inflammatory responses, gut inflammatory responses. They can all sensitize pain receptors.

Obesity has been shown to cause adipose sites to increase inflammatory cytokines, which increases pain perception.

Stress raises catecholamines. They increase pain perception.

Glycosylated end products, uncontrolled diabetes. Those sensitize pain receptors.

Dysautonomia, which we’ll talk about more tomorrow, where the autonomic nervous system isn’t gated and dampening sympathetic response. The more sympathetic you are, the more pain perception you feel.

Toxicants. Hypoxia. If someone has an injury to a side of their limb where they don’t have good circulation, they’re going to have more pain. So as neurons don’t… as neurons become impaired in oxygen, they get close to threshold, so they have greater pain perception.

Insulin surges. Someone eats, and they pass out, and eat, and crave sugar, sugar all day… those will cause increased pain sensitization, or nociceptor resensitization.

And any kind of free radical oxidants.


So if someone has a chronic pain syndrome, you want to go and identify these things. So if you have someone who’s a smoker, someone who’s diabetic, someone who’s chronically low hypoglycemic, someone who has prostaglandin imbalances, those are all things that you have to think about just to make their pain receptors not as responsive.

You can literally take this flowchart and just go through the patient. “Tell me about the fats you eat. How’s your blood sugar level throughout the day?” So here’s what they tell you: They hate fish, they hate nuts, and they’re fattening. “Nuts are fattening, and I don’t like the way fish tastes. I don’t eat after six o’clock because that will make me fat, and I don’t eat breakfast. I have one meal a day and it’s a muffin and a coffee. My stress levels are high, and when I have my coffee and muffin I pass out and I wake up and I crave more sugar. I don’t know why my body hurts all the time. I don’t know why I got a back injury and it just won’t go away.” Because what do they have? They sensitized their pain receptors, and then they had a trauma. Combination of those two are now a problem. Does that make sense?

So we start with the receptor, we look at metabolic factors that can sensitive pain receptors, and then we go through the nervous system. So there’s the ascending pathway. You guys all remember the spinothalamic tracts? Right? So basic, basic review. A-delta, C-fibers, they transmit pain in the posterior horn, goes up the spinothalamic tracts, past the projection, the reticular formation, eventually reaches the cortex. Now, there’s a medial pathway and there’s a lateral pathway. But let’s go over the typical lateral spinothalamic tract.

First, tissue injury. You fire the pain fibers, goes up the brainstem, and eventually hits the parietal cortex, right? So it goes up through these spinothalamic pathways, you have the ventral posterior medial, ventral posterior lateral, whether it’s arms or legs or face, goes to the contralateral parietal cortex. You have perception of pain, so “Yeah, I feel pain,” but you don’t have the emotionality of pain. The emotionality autonomic function of pain is the medial pathway.

So when you look at this, you have a medial pathway which is emotional response to pain, and you have a lateral pathway which is the parietal cortex. When someone has a chronic pain syndrome, is it the parietal lobe involved, or is it their limbic system involved? Right? So here’s the thing.

Let’s go over this first. Tissue injury, you have fibers going in to the spinal cord, you get a projection to the somatosensory cortex, parietal cortex, and you recognize that there’s some kind of pain. How much pain you have, how much emotional response you have, is different. So pathways also project from pain pathways to the cingulate cortex, your limbic system, your amygdala, your limbic region, your frontal cortex. That’s where you have the memory-emotional response to pain.

So let me give you a few examples. So someone injures their parietal lobe, and their neurons in their parietal lobe are close to threshold on the right side. Okay? They get a stimulus and injury to their left hand, they may have what? Greater pain perception, okay?

Or another scenario: Their limbic system and their amygdala is firing like crazy. They have pathways where they can’t dampen stress responses, they’re prone to anxiety, whatever things are involved with dampening the limbic system are not working. So now they get a little bit of pain perception, and they have greater pain. Does that make sense?


So either a parietal lobe that’s closer to threshold, or a limbic region that’s firing too much, can lead to greater pain perception than you should have. This is from the ascending pathways up. Okay?

So here’s a good diagram you guys have. Pain pathways come in, hits areas of the brainstem, reticular formation, the medial ones hit the limbic areas, and lateral ones then go ahead to the parietal lobe. So you can feel pain, you can feel the sensation on your limb, know where it is, and then you have the emotionality of how bad it is and how it impacts your life, and how miserable you feel, and all that. Okay?

Now, this is all dictated by what first? How sensitized pain receptors are. So if someone has a parietal lobe close to threshold, their limbic region is firing like crazy, they have anxiety and stress, right? They’re having high amounts of free radicals, they’re hypoxic, right? They have a pulmon… they have asthma and they don’t breathe well, they have a stress response – that can lead to a chronic pain syndrome. And you literally have to unwind each one of those steps. That’s what you want to do in those types of pathways.

Now, that’s all the things up to pain perception, but then there’s the descending pathway for pain. So the cerebral cortex, and the anterior cingulate gyrus and the amygdala, they fire down to areas of the brainstem: the periaqueductal gray, parabrachial nucleus, and the rostral ventral medulla, and they modulate the expression of pain that a person feels.

So normally your brain should suppress pain. Okay? So when it’s firing and it’s healthy, you have pathways and your frontal projections go in your cingulate cortex, go all the way down, they fire into the periaque-ductal gray, and they dampen pain. So that’s one mechanism where you dampen pain neurologically. So that’s called the descending pain suppression pathway. So do you guys get how this works?

So chronic pain could be because receptor sites are sensitized, the parietal lobe is close to threshold, the limbic system is firing aggressively before the injury, or the descending inhibition pathway doesn’t come down. The collaborative… the combination of how sensitized your receptors are, how your parietal lobe is functioning, how your limbic system is firing, and your descending pain and inhibition pathways determine your level of pain perception. And your patient’s. That combination of things.

So I want to also clarify one thing. Some things we’ve been teaching you are regions of the brain, right? We went through all the different regions of the brain: parietal, frontal, temporal. Some are not regions. Some are networks. Dr. Brock went over language networks. Pain is a network. So you have to distinguish what you’re dealing with. These are not regional lesions, these are network imbalances, and so forth.

Okay, so now another pathway where you block pain… you guys all remember the gate theory? That mechanoreceptors are highly myelinated? So they come into the spinal cord faster than C fibers that are not myelinated. So if you have an injury and you rub your hand, and then pain reception is less, right? And this is one of the aspects of movement. So what does movement do? It increases your mechanoreceptor load, it activates your frontal cortex; you activate your frontal cortex, fires into your cingulate, you get better pain inhibition pathways going on, right? You release opioids, you decrease nociceptive sensitization, and the combination of things make a person have less pain.

So this is a great web page if you guys get a chance to see it, but they have these really cool diagrams and videos. So here you can see, what we flick on here, that they illustrate – ooh! – hammer, pain going all the


way to the thalamus, they rub it – aah! That feels better! – it helps! So that’s at the spinal cord level. Which is what your TENS units are, which is all the different electr… you know, heat or… and they all have some type of effect on these mechanoreceptor paths of typical movements.

So that’s your typical gate control theory. I have another one for you. You guys ready?

So this is electrical stimulation of the periaqueductal gray. So if you guys ever look at the midbrain – you guys remember the midbrain slice? The ones with the Mickey Mouse? Okay, the ears? And the peduncles, and you turn around and there’s a mouth, and a little hole, cerebral aqueduct, the mouth, periaqueductal gray? Okay. That’s where you have… when that’s activated, that’s when you have descending pain inhibition pathways.

So here: look at this. They show this illustration, I click on… they electrically stimulate the periqueductal gray, which is what your anterior cingulate gyrus would do, which is what exercise would do, movement would do, and then as they stimulate that, endorphins are released. These endorphins descend down to the posterior horn, and they block pain perception. Okay? So activation of your cortex fires down to the periaqueductal gray, local mechanoreceptor input blocks pain going up to the brain, and those systems are working together. Okay?

Here’s another one. This is the one with the hammer again. There you go – oof! Pain going up, this is the ascending pathway. Now they’re only showing the somatosensory; this also projects into the limbic areas. Activate the brain, you get a descending effect, and you decrease pain perception. Does that make sense to everyone? Okay.

How would you know if a parietal lobe is close to threshold? Because they would have increased perception with pinprick, pinwheel, right? Touch perception, everything will feel more on that side.

So let me give you an example. I have chronic shoulder and knee pain on the right side. They’re both on the right. Take a pinwheel, stroke this side, I feel it. But when you stroke this side, I really feel it. “Which one feels like your midline, which one feels like your sternum?” I go, “The left.” So now you know what? This is close to threshold. Now, I don’t have an emotional experience with it, I just know that it’s more. Does that make sense?

Now, what if you check the pinwheel and it’s… you check and you go through with the pinwheel type response, and they go, “Ow! Ah! Ah!” and you see the person very angry at you. Then you know that there could be some limbic involvement there. So you look at more basal ganglia pathways, things that inhibit the limbic system. So you want to see their emotionality and their ability to perceive these things to kind of compare these two and see if any of those things are different.

Then you find the areas of the brain, and they’re not firing, you activate them – I’ll show you guys a clinical case of this – and you see if their pain perception goes down. So if they have increased pain on this side, I do some kind of brain therapy, whether it’s cognitive, maybe it’s eye movements, it’s something, and I do the pinwheel again, and they go, “Oh! I don’t feel it as bad!” What did you do? You found out the projection that goes to the periaqueductal gray, that is now deep-dampening their chronic pain. If you keep doing that


over and over again, what do you do? You increase mitochondrial biogenesis in those neural networks, you cause more branching, and you start to train their brain to become more plastic in the areas that inhibit pain.

Okay. So how do you identify metabolic versus neurologic? So here’s another key thing. If it’s bilateral, everything is hurting throughout their body, it’s usually metabolic. If it’s one side right to left, it’s neurogenic. So this is what I was telling you: when you see someone come in and they have an injury, you immediately pull out pinwheels, compare one side to the other, and see if there’s a difference; lets you know if there’s a neurological component to it.

So I had a case – what happened to my video? Let me see if I can fix this. Uh-oh. Let me try one more time and see if I can get it. I knew something was going to go wrong today! I was hoping it was going to be Brandon instead of me! That’s why – that’s why it happens! Ah. Okay, let’s have volume on this, please.

Okay, so this is a lady who’s got chronic pain, and she has chronic pain on the right side, okay? So she had some… she was diagnosed with breast cancer. She had some malignant lymph nodes removed in her axilla, and she’s never stopped having pain there, and it’s been some… it’s been almost a year. She has chronic pain after that procedure. Okay? So we want to first see if she has greater pain on one side compared to the other.

Tell me if you feel this here. “It’s my right.”

Do you still feel alright? “I still do.”

Tell me when it starts to go away. “I’d say now.”

Now over here?

About three or four seconds to go away.

“Yeah. More on the right. But it’s gone away quicker than…”

… the other side? Okay. “More on the right, and it’s fading as I say that.”

“More on the right, and it faded pretty quickly.”

What you’re going to do now is, you’re going to go ahead and count backwards.

Okay, so what do you guys notice? She has increased pain perception on the right side. Okay? So what I’m trying to do now is, I’m trying to figure out how I can try to activate her brain to see if I can get her out of her chronic pain syndrome. So she’s complaining of this right arm pain, but when you actually do the pinwheel, it’s global. It’s everywhere. Does that make sense? That’s letting us think there could be a neurogenic component here.

Now one of the things – I’ll show you more components of this case, the whole video, as we go on into the program. It’s a real interesting case – but I just wanted to pinpoint this part of the pain thing. When we had her do gait, just analysis, her arm swings were not working so well, And we had her do mathematics


as she was walking and her arm swings came back. So my first things were, “If I activate her left brain with some mathematic left inferior parietal activity, does that help her pain syndrome?” Okay, so let’s find out.

“Okay.”

By sixes. “Okay.” Okay? “I’m going to do my best.” Go ahead.

Going to count backwards.

“Alright. Starting with 100?” Yeah. “So starting with 94, and 88, and 82, and 86. Oh sorry, 76. And…

She’s missing. That’s diagnostic.

And 70, and 60… 4, and 58, and 52, and – should I keep going?” Yeah. “And…”

So what are we doing? We’re activating her left inferior parietal, trying to get blood flow there, trying to activate, trying to see if we can decrease pain perception on the right side of her body.

“uh, 40… um 8, and 42, and getting a pattern, and maybe [unintelligible] 42, and 30… um 6”

There you go. “And 30… 30.”

Let’s try this again. Is there any difference? “Okay. Much more on the right and lingering.”

Still on the right? No change at all? “No.”

Damn it! Much more on the right! It got worse! I activated her brain, she got worse. I activated her parietal lobe, it got worse. So should I give her that as therapy? What would happen if I gave her that as therapy? What if I just, “Oh, it’s left brain, let me give you the left brain chart of exercises, and here you go, try it.” They’d go back and go, “I hate you. My [? 31:50] never been worse!

So let’s go through and let’s see what happens next.

Let’s try something else. I’m going to have you do this a few times. Look straight ahead

Now I’m going to do optokinetic activity, just going to move this strip back and forth, it’s going to activate parts of the brain, don’t need to worry about those too much. That makes her feel like she’s moving and spinning to one side.

Okay. Try this again. “It’s… it’s nearly the same if not just the same. Maybe… just right at the beginning, I felt more, and then it subsided.”

More equal? “Mm-hm.” Doesn’t last as long? “Yes, yes.”

Okay. Alright. Okay, so that…


So you guys see that? So we found a pathway that, if we activate, helps fire her periaqueductal gray. So we would do that over, and over, and over again, at a rate that doesn’t fatigue her, to then try to get her out of her chronic pain syndrome. Does that make sense?

Now, is there any metabolic factors involved? Maybe. We can’t see in this picture, but her pulse-ox is really bad. Okay? She has respiratory issues. She’s not breathing well. So what is that going to do? It’s going to cause global hypoxia. Global hypoxia’s going to do what to pain fibers? It’s going to sensitize them.

This is her blood pressure. 100 over 62. Is that good? I mean, it’s good to not have a stroke, but it’s hypotensive, which means you have what? Less blood flow to brain. You have less profusion. So now I have hypoxia, two mechanisms. Lungs aren’t getting enough oxygen in, I have a blood pressure that’s low, so getting less profusion, profusion being pressure pushing blood flow to the brain. Right? So you have to have some degree of health. Blood pressure has to be closer to normal for ideal profusion into the brain. Okay?

Now take a look at this. These are her circulation. What do you think? Good? How do those look? Fantastic, yeah? If you like fungal toenails. But they’re terrible. So if you don’t have proper circulation to your distal extremities, you can’t get blood flow, and your blood carries what? Natural killer cells and T-cells to fight off yeast… I mean, nail and fungal growths.

So now we know she has poor circulation, she’s got hypoxia from her respiratory issues, right? And we know that she has probably less profusion from her blood pressure, and those are all things that are sensitizing pain fibers, and we find out a pathway to help her descending pathways. We can’t ignore these. These are all there. These are important.

Take a look at her blood tests. What do you guys see? I’ll try to read it to you. It’s hard to see here. Her white blood cells are down to 3.7. Too low. Something’s chronically impacting her immune system. Her red blood cell count’s low, and her MCV’s high. So that’s a megaloblastic anemia. She has anemia. She has anemia, she has a pulmonary issue, she’s got hypotension, and she’s got a chronic pain syndrome. Okay? Her lymphocytes are low, and her glucose is 66. She’s hypoglycemic. Hypoglycemic – guys, remember that diagram I put to you? That’s real. People have those things. Here’s an example of one. They actually exist.

So now she has low blood sugar, because she probably has what? Low cortisol. Low blood sugar, low cortisol, pain sensitization, hypoxia, poor circulation, pulmonary issues, and a chronic pain syndrome. So is my therapy going to be optokinetic stimulation? No. Because here’s just the thing. When we repeat that test, it doesn’t work any more. So we do a couple of those, and it doesn’t help her pain any more. Which means we have a what? If you look at the flow chart. We have an underlying metabolic thing. She’s getting worse with testing. We have all these underlying metabolic things that need to be addressed. And by the way, here’s her cortisol. Totally low throughout the day.

Low cortisol, low blood sugar, low blood pressure, pulmonary issues, decreased circulation, means the mitochondria doesn’t have what it needs. Guess what? She’s taking B12 for the past year, but she still has megaloblastic anemia and low white blood cells. She has an autoimmune disease, and she has intrinsic factor antibodies. She can’t absorb B12. So we had to put her on B12 shots. We didn’t do any therapy with her because the therapy all made her have more pain. Even though we had a clinical exam finding that kind of changed for a second, it’s not going to last because she doesn’t have fuel.


It took her almost four or five months before she actually had a boost of energy and her anemia got restored with injections. So we had to do… send her out, get some B12 injections, get her blood sugar stable, put her on a high-salt sodium intake to get her levels improved. We put her on some things like glycyrrhiza to try to get her cortisol to hang around longer in her blood stream. We tried to stabilize her blood sugar throughout the day. And after about four months her energy boosts came back, which means now we could do rehab. And then we went in and started to rehab. Does that make sense? Okay.

So that’s the key thing with pain. So in summary, here’s the key concepts: When you have someone who has a chronic pain syndrome, first place you guys want to start clinically is look at the receptors. Are there any things sensitizing them? So you can look at that chart I gave you. Those are the major ones. Then you want to go and see, is there parietal cortex involved? Do they have their limbic system involved? Just simply take a pinprick, compare one side to the other, compare it to midline to determine if one side’s hyper- or hypoalgesic. Find what areas… do your neuro exam, find what areas are involved, activate those areas, see if it changes that perception. If it does, that’s what you can do to activate the periaqueductal gray to dampen pain, and then treat the underlying metabolic pathways. Does that make sense? That’s how we combine neuro and metabolic type of workups, which are pretty critical.

Okay, so that’s the key thing I wanted to share with you guys with pain.

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FUNCTIONAL NEUROLOGY ANATOMY AND CENTRAL NEUROLOGICAL ... · down, right? Or the areas that suppress pain aren’t working. Okay? So again, next time you see a patient that comes