Functional Neurology Explains Why Concussion Symptoms Spiral with Dr. Matt Antonucci | E61

For decades, patients with persistent post-concussion symptoms have been told that their imaging is normal, their brain has healed, and there is nothing more that can be done. But what if we've been asking the wrong questions?

In this episode of Life After Impact, Dr. Ayla Wolf sits down with functional neurologist Dr. Matt Antonucci to discuss his groundbreaking new paper published in Frontiers in Systems Neuroscience, introducing the Network Entrapment by Reflex Dysfunction (NERD) Model. Together, they explore a new framework for understanding why concussion symptoms can persist long after the initial injury has healed. 

Dr. Antonucci explains how the brain functions as an interconnected network rather than a collection of isolated structures, and how disrupted sensory processing, maladaptive feedback loops, and altered neuroplasticity can cause symptoms to spiral over time. The conversation dives into predictive processing, cerebellar function, autonomic regulation, postural instability, chronic headaches, neck pain, light sensitivity, dysautonomia, and why many patients feel trapped in patterns that conventional medicine struggles to explain. 

Topics discussed include:

•  The difference between structural neurology and functional neurology 
•  Why normal MRI and CT scans don't mean the brain is functioning normally 
•  The NERD model and persistent post-concussion syndrome 
•  How the brain becomes trapped in maladaptive feedback loops 
•  Predictive processing and the role of the cerebellum 
•  Why symptoms often worsen under cognitive, physical, or sensory load 
•  Neuroplasticity: when adaptation helps and when it hurts 
•  Dysautonomia, POTS, headaches, neck pain, and sensory sensitivity 
•  The importance of identifying the true source of dysfunction 
•  How this model may apply beyond concussion to conditions such as ADHD, autism, migraine, and chronic neurological disorders 

Whether you're a patient struggling to understand persistent symptoms or a clinician seeking a deeper framework for neurological rehabilitation, this episode offers a fascinating look into what may become one of the most influential models in functional neurology. 

If you’re a patient feeling stuck, or a clinician looking for a clearer concussion recovery model, this is a practical, hopeful listen. Subscribe, share with someone navigating post-concussion symptoms, and leave a review. What “load” situation reliably sets off your symptoms?

The NERD model: reflex circuit dysfunction as a systems-level driver of persistent post-concussion symptoms - Read the paper! 

Dr. Antonucci's Website

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Transcript

A Big Step Forward for Functional Neurology

Dr. Matt Antonucci 0:00

I think what we're really trying to do, our hope, our fingers are crossed, that we can, you know, we can have a spot in history of saying in 2026, this is when it all changed. Um, and this is where functional neurology became was born. Uh, it was published, was validated, and this is where those 1.3 billion people in the world finally get seen and finally get treatment because right now they're not. So that's the hope. That was the hope by publishing this paper. So fingers crossed.

Dr. Ayla Wolf 0:31

Welcome to Life After Impact, the concussion recovery podcast. I'm Dr. Ayla Wolf, and I will be hosting today's episode where we help you navigate the often confusing, frustrating, and overwhelming journey of concussion and brain injury recovery. This podcast is your go-to resource for actionable information. Whether you're dealing with a recent concussion, struggling with post-concussion syndrome, or just feeling stuck in your healing process, know that you are not alone. This podcast can be your guide and partner in recovery, helping you build a better life after impact. Dr. Matt Antonucci, welcome back

Welcome And Why This Paper Matters

Dr. Ayla Wolf 1:10

to Life After Impact. How are you?

Dr. Matt Antonucci 1:12

I'm great. Thank you so much for having me back. Um, super excited to be here again.

Dr. Ayla Wolf 1:16

Yes. Last time you were on the show, we talked about these concepts of uh the hierarchical approach to treating complex, persistent post-concussion cases. You have really flushed out this concept into a specific model that I know you've probably been percolating on for a long time. And you recently published a paper in Frontiers in Systems Neuroscience with Dr. Kenneth J., also on the faculty of the Kerrick Institute. And this is a phenomenal paper. I'm so excited to have you talk us through it, break it down. It's it's very complex. And what was the process like of trying to put all this into a framework?

Dr. Matt Antonucci 2:00

That was the hardest part. Yes, the paper is complex, but the background behind the paper is even more complex. And what I mean by that is persisting post-concussive symptoms are probably the most complex condition that exists in the humankind because it's just so multifaceted. And we start to look at it from a human perspective. Of course, the humans, the way we look at things is in a very linear model. It's like chocolate or vanilla, right? It's it's we're we're very basic in the things that we do it every day. And we marvel at the people that can think deeper into things like philosophers and things like that. But the reality is that when we look at persisting post-concussive symptoms, they don't follow any one course. And in research and science, we call this heterogeneity, meaning that things are never the same. Homogeneity means everything's the same, heterogeneity means that things are different. So heterogeneous concussions are very heterogeneous. And that means that two identical people, I have like, I have two sets of identical twins. And if we're, God forbid, in a car accident and we all are in the car accident the same exact way, they have identical genes. They were raised in the same household. Uh, we were in the same mechanism of injury. Maybe they both went forward and had a seatbelt, maybe hit their head on the back of a front seat the same exact way. They would have completely different concussions, right? Some of them, one of them might have issues with thinking, another one might be hyper-emotional, one might have lightheadedness, another one might have light sensitivity, another one, you know, it's just there's no rhyme or reason why people have the symptoms that we have. So to try to put that into a model that can pass the rigor of peer review for people that don't know you, don't know your work, don't sometimes don't even see these types of patients, for them to read something and say, you know what, this is a solid model. Let's put it out there for the rest of the scientific community to read. Uh, it was huge for us.

Dr. Ayla Wolf 4:01

Yeah, I bet. And you start out the paper kind of introducing this concept of functional neurology. Now, I have the words functional neurology literally in the name of my clinic, which means that people ask me all the time, what is functional neurology? And I think perhaps the best uh almost poetic answer can now be found in your 26-page paper. And so I just want to read what you wrote. I'm gonna quote you and then let you introduce this model that you've been working on. You say too often conventional paradigms attempt to localize dysfunction to static lesions or binary

Functional Neurology Versus Structural Thinking

Dr. Ayla Wolf 4:40

findings. Functional neurology, by contrast, embraces complexity not as a problem to be simplified away, but as the terrain itself. That's beautiful.

Dr. Matt Antonucci 4:51

Yeah, and it's meaningful. And one of the things you'll start to see is if you we talk about it a little bit in the paper, and we have another paper that's going to be going into peer review pretty soon about defining functional neurology. Um, so that'll be hopefully another peer-reviewed paper to be the first ever published definition of what functional neurology is. And that was a that was a byproduct of this paper. What we start to realize is that when we created this paper, we weren't really just identifying how to fix concussions. We were really defining what functional neurology is. We were putting a model around it. Um, so as you kind of read, neurology had a very interesting past. Um, neurology was studied all the way back to the Roman gladiator days. Uh Galen of Alchemyon, which was one of the first uh physicians in the year 200 uh BCE, basically said, you know, I'm studying the brain, and the he thought that the brain secreted fluids that filled up muscles, but he read he he thought this organ over there pumped fluid down through tubes into muscles into your bicep to make your bicep track. So he had this idea that the brain controlled the body. That was the first real like evidence of you know studying urology. If you go back further than that, you know, ancient Egypt, they used to take people's brains out through their nose and discard them and put their other organs like you know, heart and liver in these canoptic jars and put them in them in the tomb with the mommy because they needed them in the afterlife. They didn't need the brain, they needed everything else. So somewhere between there, the brain became important. And then we have this gap in time all the way until the 1800s and 1900s. Um, in that period of time, not going to go too deep into this, but uh realistically, the father of neurology was Jean-Marie Charcot, who practiced at the Sault Petrier hospital in Paris, France. And he basically was the first to perform a neurological examination. The reason why I'm sharing this is that that was when the neurologic examination was born. Touch your nose, look at pupils, follow my finger, all of these tests to figure out what exactly is this organ inside the head that we can't see. What is it doing? How is it functioning? How is it working? Is it broken? And function was tested in neurology all the way till 1971. Every neurologist did a neurological examination, pin prick, muscle testing, reflexes to figure out what the brain is doing. In 1971, the CT scan was developed. And for the first time, neurologists can see pathology in the brain. And when you can see something in literally black and white, it becomes more tangible. It becomes a little easier to diagnose in some cases, but also beneficial for things that we, you know, we need structural neurology for. So there was like this bifurcation in neurology with structural neurology and then you know this neurology of assessing function like EEG and things of that nature. And inside that gap there between the measurement of neurological function and structural neurology lives a lot of people, uh, people with migraines, concussions, autism, ADHD, all of these people have neurological problems with nothing on a CT scan or an MRI. Right? So, what happens to those people and how many are there? Well, the estimates are that there's about 1.3 billion people in the world that have some sort of a neurological problem that is not structural. And those people get caught in this gap because they're told that they're crazy or they need psychological care or there's not really anything wrong, you're perfectly fine because there's nothing on the imaging. So that's what I meant in that quote when I say that all too often we start looking for structural pathology, or things are binary, you're either healthy or broken. Um, and it's not really that simple. Um, and and that persisted all the way into the early 90s when the fMRI was developed, and now structural neurologists are able to start seeing functional changes. And now we're kind of getting this convergence again into what we're calling functional neurology, right? But when we start looking at function versus structure, and it's not to say that they they um are separate things, they must coexist. We we need to know when somebody has a tumor. We need to know when somebody's having a stroke. But the thing is, is we can't just throw all those people that that don't have structural problems um to the wayside and say there's nothing wrong with you. We have to have a model that explains them. And I guess the fortunate thing, but also the fortunate thing that there's nothing structural wrong, but the unfortunate thing with nothing being structural is that there's nothing tangible to say this is the problem. So how do we have to, how do we determine what's wrong with them? Well, we have to go back to doing a really good physical examination. And that's where our model started. Our model started with how can we start to I how do we model what happens when somebody has a shaking of their brain and they're not functioning properly? Where does it all start and how does it unfold if there's nothing there on the imaging?

Dr. Ayla Wolf 9:50

Yeah, that's a big task. And I think you did a fantastic job of really piecing this out system by system and going back to that trajectory of even how people learn neurology as a student learning basic neuroanatomy. It's like you learn the different lobes of the brain, and oh, the occipital lobe is where we have vision and the frontal lobe is where we have executive function. But the reality is that vision is a whole brain activity, you know, sound is a whole brain activity. And so even the way that I think we teach neuroanatomy, it still feels like the teaching of it is so localized, and there could be a whole entire discipline of just functional neuroanatomy that has to be a foundation before people can even understand your paper.

Dr. Matt Antonucci 10:35

Yeah, I mean that's that's kind of true. And it's I think you hit the nail on the head there. Like humans by nature are very reductionalists. We like to understand pieces, right? And it's nice and easy to understand pieces, is understand that the frontal lobe does this, the occipital lobe does that. But what ends up happening, and that is really great for things like structural neurology. Okay, the frontal lobe does this, we have a big tumor in that frontal lobe. This is why you can't do that. That makes perfect sense. However, what we're starting to realize is that the way that the brain actually works, well, let's put it this way. We've understood the way the brain actually works outside of medicine for a long time. Uh, and what I mean

The Brain As A Neural Network

Dr. Matt Antonucci 11:13

by that, if you go on your computer, go to, you know, uh Chat GPT or Claude or any of these um types of Gen AI softwares, you go and put something in there and you ask it a question. And basically what it does is it queries something called a neural network, right? And it's like, wait a second, that sounds pretty familiar. Neural meaning brain, network being a you know, info collection of information. So AI is based upon how our brain actually functions. However, we're not necessarily implementing that in traditional medicine. We're not looking at it as your brain being a neural network. And what do I mean by that? You know, in in neural networking and also the way that our brain works, we have areas, frontal lobe, parietal lobe, whatever it is, that are basically points inside of this big model, but there's connections, right? The frontal lobe connects to the parietal lobe, the occipital lobe connects to the frontal lobe, right? So there's connections, connectivity. And in this model that we call graph theory, and not we and me, but like, you know, people that understand and study this stuff, graph theory, that explains the relationship between these areas. And all of a sudden you start to realize, oh my goodness, I can put Humpty Dumpty back together again because I understand how all of those things connect. Um, and that is kind of by definition how functional neurology is. I always kind of say functional neurology is neurology plus graph theory. So it's just understanding how the anatomical structures talk to each other and function together. And if you understand how they function together, you understand how they dysfunction together and how to put it back together. So that's that's kind of the basis for all of this.

Dr. Ayla Wolf 12:54

Yeah. So let's dive in. Your model's called network entrapment by reflex dysfunction, nerd for short. Was that intentional?

Dr. Matt Antonucci 13:03

Absolutely. Absolutely. We're like, we're like, how could we make this memorable? Because that's usually the hardest thing about some of these different models, either they're hard to pronounce, they're hard to remember. So we basically said we wrote the paper and then we said, what do we call it? Right. And of course, we used a little bit of, you know, Gen AI, Chat GPT, whatever, like, hey, this is this is the theory, you know, what's what's give me some keywords? And it it started talking about network and it started trap talking about dysfunction and reflexes and entrapment. And I was like, wait a second. Nerd. Right. So yeah, so

Naming The NERD Model

Dr. Matt Antonucci 13:34

that's that's okay. So it's easy to remember.

Dr. Ayla Wolf 13:36

Yeah, yep, excellent. So this reframes persistent post-concussion syndrome, uh, conceptualizing it as a hierarchical reflex integrated network dysfunction. And it arises from you talk about disinhibited feedback loops, degraded gain modulation, and constrained capacity. So most people are going to be like, I don't know what you're talking about. So we're gonna let's just like break this down and talk about what these three concepts actually mean, how that translates to the patient's experience.

Dr. Matt Antonucci 14:07

Yeah, absolutely. That and it's not so hard, but obviously, you know, one of the things that I've always realized over the years is that humans have been around for millions

Feedback Loops That Create Symptoms

Dr. Matt Antonucci 14:15

of years, but we've only been speaking for tens of thousands. So our language access is not nearly as developed as our cognitive access. So access. So when we try to explain something like that, it's really hard. But here's here's it nice and simplistically. In order to figure out what this model actually means, you have to understand a couple core concepts. The way the brain works, we have sensory information through our eyes, our ears. Like I can feel myself rubbing my face right now. You know, I can turn my head side to side, I can feel my heads moving. We have sensors, which are we call it the sensory interface, right? This is where we interact with the environment, whether it's internal, external. We can feel, you know, our our belly, you know, when we're hungry, we can see light, but we can also feel like, you know, our change in blood pressure, or we can change, feel a change in chemistry in our blood. Not consciously, but there's sensors there that do that. So we have the input, which is the sensory interface. The real reason why we have that sensory interface is to bring the outside world into our brain so our brain can process it, compare it against what's currently happening, what happened in the past, and then create a motor response. The motor response might be our pupils getting smaller when it's really bright. A motor response might be our heart rate speeding when we get startled. A motor response might be like, hey, you know, put your hands up to block something from hitting your face that you see coming at it. So our brain basically just takes information through sensors, processes it, and creates motor responses. That's the basic thing for the brain. And everybody's understood this for a long, long, long time. But the part that everybody seems to be forgetting is that when you have a motor response, you then sense that motor response. Right? So if I see something coming at my face and I put my hands up, I felt my muscles contract, I felt my hands move, I feel the light from the light that's in my face not in my face anymore. I process all that information. So that's how a healthy brain works. When we start looking at a broken body, you know, somebody that breaks an arm or someone that, God forbid, is in war and their arm gets blown off, the sensory input is not getting to the brain anymore. So the brain can't regularly or accurately control that body part anymore. Great example. I had a situation like this at the Heathrow airport. Um, I fell asleep because it was early in the morning and I had my legs crossed, and they started calling my name for my flight, and I was about to miss my flight, and I stood up really quickly, my leg was asleep, and I look like I had a stroke. I was dragging my leg across the airport. Yeah, because when you can't feel a body part, you can't control it, you can't move it. So that makes a lot of sense when we have broken body can create bad output, and that bad output that gets reingested by the nervous system to tell you, hey, that body part's not working. Nice and easy to understand. It's a little bit more difficult to understand when our brain breaks because we get normal sensory information in. Look at somebody with autism, nothing wrong with their receptors, right? Somebody who has a concussion, there's nothing wrong with your eyeballs, there's nothing wrong with your inner ears, there's nothing wrong with your skin, there's nothing wrong with body parts. The receptors are fine as long as they weren't injured. Of course, you can have like a whiplash, or you can get a lacrosse ball to the eye, right? So these things can happen, what we call comorbid width also with concussion, but they're not the defining characteristics of a concussion. So your receptors are fine in a concussion, but your brain is broken. So what does that mean? Sensory information comes in perfectly normal. Your brain processes that information. However, in the processing of it, it doesn't create the appropriate motor output. Right? Where you might stand up really quickly and like, whoa, you get really dizzy and you go to fall over. Well, because you feel like you're falling over, now you're going to recreate muscle tone to keep yourself from falling over. But guess what? You weren't really falling over. So putting your hands out like that now makes it so that you have different input going into your body. Or to say this a little bit differently, this one's probably a little bit more relatable to somebody. Light comes in through your eyes, your brain processes it and says, ooh, that's really bright. So now you squint your eyes, right? And the squinting of your eyes is now fed back into your brain. And now all of a sudden you're not really seeing very well because it's not bright, but your eyes are closed and halfway dimmed. So you can see this becomes like a we call it a negative feedback cycle. It's a spiral. You start spiraling because you're having bad, you're gonna have good info in, bad info out, bad info in, which creates bad info out again because you can't create good motor activities with bad information in. And this is the thought that kind of came into our head with concussions. It's like these people that have concussions have nothing wrong physically with their brain, but they can somehow seem to like just spiral almost like they're going down the figurative toilet. Like they keep getting worse and worse and worse, no matter what people do to help them. And then at a certain point, they just get stuck. Right? They don't they don't end up dying from concussion, thank goodness, but they just get stuck where they can't get better, but they don't get worse.

Dr. Ayla Wolf 19:18

Yes. I I feel like I need to rename my clinic the Hail Mary Project because the people that come into my clinic are the people that have tried everything else. They're out of ideas, they're out of money, and I'm literally their Hail Mary. They're like, Okay, you're kind of my last hope here. What do you got? And I just had somebody the other day who has been struggling for years and years and years. She's done all kinds of therapy. And she came in, she said, Well, based on everything going on, I think my understanding of what's going on is that, you know, my my occipital lobe is just damaged. My visual processing centers are damaged. And I kind of had to step back and say, Well, if that was the case, you'd be blind and you can see just fine. It's just that visual input creates pain behind your eyes, in your head, uh, and causes cognitive symptoms. And so I said, I think we need to look at this slightly differently. It's not that your occipital cortex is damaged, it's that this integration of all of these inputs and the way that they're getting interwoven, light and vision and pain signals are all just kind of getting intertwined together in these processing loops that have now become kind of cemented in place. And so now you're stuck in this place where vision is causing you discomfort, a horrible place to be in, but it's kind of the perfect example of what you lay out in your paper in terms of how this may not have been the original problem, but this is where the person ends up after years and years and years of these uh incorrect inputs, incorrect response, incorrect feedback, and it just slowly, gradually snowballs, and then it becomes fixed in place.

Dr. Matt Antonucci 21:07

Yeah, exactly. And and that makes perfect sense because if we start looking at from second one after a concussion in a timeline, there's a period of time where everybody in science agrees that we know exactly what happens, right? We have after concussion, we know that there's blood vessel changes, we know that there's functional changes, we know that there's glucose changes, we know that there's inflammation. Happens the same in everybody. And we know that certain amount of people just recover on their own, but everybody should recover by four weeks. At that point in time, if somebody has concussion symptoms longer than four weeks, the blood flow, the you know, the oxidative, the free radical

When Neuroplasticity Locks In Problems

Dr. Matt Antonucci 21:46

creation, all that kind of stuff is not really the problem anymore. It's now the result. And at that point, we have to change our models. We have to change it from acute care to, I just call it after acute care, because it could be subacute, it could be chronic, it's just it's It's just all part of a continuum. And then we have to really understand what the difference is there. And one of the best papers for this was a paper written by this woman, Erin Kinsey from Portland. And she spent years creating this big model of what happens in the timeline of concussion. And what she starts to show is that there's a lot of connections in the early phase and the in the late phase, things just get really, really deep all the way into depression and cognitive dysfunction. So how do you get, how do you get from like inflammation and blood flow changes to depression and working memory issues? And the answer is that in that period of time, your brain did what it does best. It remodels. Our brain is so adaptive. You know, you you can this neuroplasticity, right? And sometimes people like so, oh yay, neuroplasticity. But neuroplasticity is not always a good thing. It's just a thing, it's just a it's a function of our brain. Uh, and some people are like, what are you talking about? Well, if you're learning the multiplication tables, neuroplasticity is amazing. If you went to war and you see all of your service people getting killed over and over and over again, neuroplasticity still occurs, right? And then you have PTSD. So those are kind of like on larger scales. But what we have to realize is that neuroplasticity occurs all of the time. Right now, people listening to this, they're learning neuroplasticity is occurring, right? It just happens all the time. But the problem is that if a part of our brain is injured and goes into hibernation and we start using other parts of the network, then the part that goes into hibernation starts to shrink and the parts that are the other parts that we start to use start to grow. Right. And now we have a very efficient way of processing the world. Um, and I often talk about this as like airports, right? Everybody's familiar with this airport sort of thing. Everybody knows that if you're flying into Atlanta Airport and there's snow for whatever reason or ice and flights are canceled and delay, we know how difficult it is to get to where you're going. A concussion is just like that, where the airport shuts down for a little while. So you might very well say, you know what, maybe Detroit's a better example of this or Minneapolis. I am never gonna fly through Detroit in the wintertime because I always have, and this happened to me. I had to spend 48 hours one time in Detroit airport.

Dr. Ayla Wolf 24:15

No. Yeah.

Dr. Matt Antonucci 24:15

So in the wintertime, I avoid Detroit. But basically, what ends up happening is your brain does like that. Hey, that part of the brain was injured, didn't work very well. I'm gonna use a different pathway. So instead of using the old injured pathway, I'm gonna find something different that becomes very efficient. And basically means that when you look at something, because you're using a different visual prop pathway, it becomes painful instead of it just being vision.

Dr. Ayla Wolf 24:38

Yeah, yeah. And so let's talk about these concepts of nodes. We've talked a little bit about the sensory interface, this input that comes in. And if that input coming in and the way it's processed is incorrect, that we can have an incorrect motor response. And then we sense that incorrect motor response and it kind of creates that particular spiral. It's almost like if somebody isn't mad, but they text somebody else and says, Hey, where are you? And the other person interprets that as, oh my gosh, they're angry at me. So then they fire off like an angry response that then makes the other person angry, and now all of a sudden two people that had no reason to be angry at each other are like fighting.

Dr. Matt Antonucci 25:14

Exactly.

Dr. Ayla Wolf 25:14

It's it's that that

The Five Nodes And The Cerebellum

Dr. Ayla Wolf 25:16

I I try to break this down to, you know, concepts that are easy for my brain to understand.

Dr. Matt Antonucci 25:20

And the thing is to your point, that person might have just gotten into a fight with a coworker, right? So something in the environment triggered them to feel a certain way. Now they're looking at the world from a different lens, and there you go.

Dr. Ayla Wolf 25:35

Yep, exactly. And so one of these nodes is the cerebellum. And one of the things that you talk about, or you you call this the predictive calibration node. And so there is this concept of predictive processing that I think is it's a really important key part of this understanding of this model. And so I'd love for you to expand on this concept of predictive calibration, predictive processing, how important that is, and and how when it's not functioning correctly, that can lead to a lot of functional neurological findings that kind of I think are why so many people maybe feel gaslit or they just they go, they try to seek help and they don't find answers.

Dr. Matt Antonucci 26:18

Yeah, absolutely. We can totally do that. So, you know, with with the different nodes that we talk about, we have the sensory interface, we got the brainstem, we got the cerebellum, we got the what's called the basal basoganglionic phlamicating module and the sterepocortex. So basically five nodes. Um, and they are lined up in a hierarchical fashion where the sensory interface is something that's gonna be most primitive. Then we have brainstem activities, then we have the cerebellum. So typically when information comes into our body through sensory interfaces, it integrates into different parts of the brainstem because it's the oldest part of our brain. It's the part that controls our heart rate, our blood pressure, our pupils, our digestion, all the things that we have no control over. Um and we're not gonna spend a whole lot of time there, but now let's look at the next load, which is known as the cerebellum. The cerebellum receives information from the brainstem, which is why if you have a problem in the brainstem, now the cerebellum starts to become abnormal. But the cerebellum also gets information through certain pathways from our body that bring its subconscious information about joint position sense. Also, where we are in space, we get information from our vestibular system that goes through the brainstem into the cerebellum. So if the cerebellum is getting input that is completely normal, but it itself is injured, which does happen in concussion. Research shows that, you know, we have these, that we have these bridges that go into the cerebellum that get stretched when there's a concussion. So we can have a problem in that cerebellum. What happens is the cerebellum is kind of like the maestro in front of a symphony, right? It doesn't play any instruments, it doesn't make any music, but it controls everything. It controls through the through the maestro, hearing the music, and then re-I guess kind of reinforming the symphony of the speed to process things. That's what the cerebellum does. Just to reiterate, the cerebellum has no outputs to the body. It has inputs from the body, but it has no outputs to the body. So therefore, the maestro doesn't blow a horn, you never hear the maestro. Sometimes you don't even see it, sometimes it's below the stage, right? So that the maestro has no interaction with the audience, just like the cerebellum has no interaction with the world. The cerebellum talks to the basal ganglia and the thalamus and the cerebral cortex. So essentially what it does is it monitors the environment, it predicts what's going to happen next, and it tells the frontal lobe and the brain what to do based on the environment. And then the frontal lobe says, I got it. I'm gonna send this motor plan back to you. Tell me if that's right. And if you don't think it's right, tell me how to fix it. So it's this back and forth conversation that happens like at the speed of light, uh, on the millisecond realm. Um, that back and forth, electrical potential is going back and forth to so that we can actually do something fluidly, so we can talk, so we can regulate our speech, we can we can tell a story in sequence, we can, you know, respond to something in the environment with the appropriate proper amount of emotion. So, I mean, I've had patients that are just like, I have no idea why I cry. And then minutes later I'll be laughing and I don't even know what I'm laughing at. Or sometimes I have people that say, like, you know, ever since my concussion, I just can start doing something, but I get distracted really easy and I forget what to come back to. Well, that's not a necessarily a thinking problem. It's not an ADHD problem. It's an orchestration and coordination problem. And whenever you hear something is orchestrated and coordinated, it's a job of the cerebellum, whether that's your sleep weight cycles, whether it's your menses, whether it's your um, you know, thinking, whether it's your emotion, whether it's your standing or ability to move and grab things, if it's orchestrated and coordinated, it's a job of the cerebellum. So you can kind of see how if that is the node that's injured and we call the primary node, the central node, like the the thing that's causing all of the problems, we call it the hub, right? The hub of dysfunction. If your cerebellum is the hub of dysfunction, you'll have all sorts of disorganization, but no real inability to do something. You can still walk, you can still talk, you can still do things, it's just disorganized.

Dr. Ayla Wolf 30:27

And I think that some of the research that has come out recently, meaning in the last 10 years, is also showing that the cerebellum is also coordinating our thoughts or it's playing a role in coordinating our thoughts. And so, like you were saying, it's like, why am I crying? Why am I laughing? And so are you saying that when the cerebellar functions are are have become dysfunctional, then all of a sudden people's ability to coordinate their own thoughts, coordinate their own emotions is maybe also uh slightly dysfunctional as a as a downstream consequence.

Dr. Matt Antonucci 30:57

Yeah, exactly. And there's a lot more research to support this. So somebody that has the hub being in the cerebral cortex, which could be in like your emotional cortex, if the the lead or the dysfunction or the the issue is primarily there, what ends up happening is sometimes you develop anidenia where you just have no emotions. Right. Uh so that's typically what happens when it's in the emotional part of the brain. It's not like you have a little bit of emotion here, but not a lot of emotion there, right? You either, it's almost kind of like when you, as you've mentioned earlier, when you injure your occipital cortex, you go blind. When you injure your emotional cortex, you just have no emotions. So we start looking at the one of the things we're gonna talk about in another future paper are the signatures of those nodes. Like, what is the signature of the cerebellum node? Well, you all know that now. The signature of the cerebellum node is disorganization, right? The signature of the what we call the basoganglionic thalamic gating module, there's not really any ways to say it because they're like, they're like two peas in a pod that talk to each other. And when one breaks, so does the other. And when one breaks, so does the other. Um, when that node breaks down, we have difficulty gating. What does gating mean? Mean turning the volume down or turning the volume up. So you become light sensitive, sound sensitive, hyper-vigilant, you know, uh hyperactive or slow, whatever. So you have, you just basically have inappropriate gating. That's the signature of that node. And then we have the cerebral cortex node, which that node basically is stop and go, right? It tells us whether to do something or not to do something, very, very broadly speaking. Um, and if that part's broken, you'll say, hand move and it doesn't do it, or you become paralyzed. Or it may be like, okay, fingers tap, right? And you're really slow. But the fact that you can still do it means it's not completely broken. It just means that there's probably something else in the network that's making it slower. So this is where the difference between what we call a lesion, which is binary, you're either that part of your brain's either alive or dead, and functional, which means it's working, but it's not working like it should.

Dr. Ayla Wolf 33:11

Right. And so going back to the finger tapping, sometimes you see that people are slow. Other times you see that they can't keep uh a rhythm. They they'll be dysrhythmic. So is that going back to that cerebellar node?

Dr. Matt Antonucci 33:24

Yes, exactly. So you start looking at the if the rhythm is not right, that's the signature of the cerebellum. If they freeze, that's a signature of the frontal lobe and the basal ganglias interaction. And you see these with Parkinson's disease, um, mainly because the part of the brain with Parkinson's disease creates dopamine, and dopamine fuels all of that beautiful magic. So with that, you'll start seeing all changes in motor function and a lot of other different things, which that's obviously not the topic of this conversation. But uh, just somebody who is a nerd like me that's listening, they're saying, hey, wait, that might not be right. It's just understanding that how it all integrates.

Dr. Ayla Wolf 33:59

Right. And I think that that also highlights the beauty of functional neurology, where you have one test, which is can I bring my two fingers together? And how somebody performs on that test gives you insights into the motor cortex in the frontal lobe, into the whether can they can they do this and how fast is it? Then if they're freezing, that gives you some insights into the basal ganglia. If they do it in a very dysrhythmic pattern, then all of a sudden you might say, oh, there's something going on with the cerebellum. And so it's the same exact test, a very simple test that can be done in five seconds, 10 seconds. And yet it's giving us incredibly valuable functional information about very different parts of the body that requires no fMRA.

Dr. Matt Antonucci 34:41

Correct. And you just, I think you really just did a great job emphasizing that because that test is a Parkinson's test. Right. But all of you watching this right now, open up your fingers and tap them big as fast as you can. Some people are gonna say, hey, mine's a little slower than Dr. A's just was, mine's a little bit faster, mine rhythm's not the same. You don't have Parkinson's disease. Well, you might, but you probably don't. But that's really like the epitome of what we talk about when we say functional neurology. It's understanding the test, not just doing it because it's a test for Parkinson's.

Dr. Ayla Wolf 35:14

Exactly. And then, like uh the patient I mentioned earlier, I had her do this finger tapping test sitting down. I had her do it standing up, I had her do it looking right, I had her doing looking left. Turns out that she has a harder time doing it on her left hand than her right hand, a harder time doing it when her head is turned to the left, and a harder time doing it standing on a foam pad versus sitting down. And so again, same exact test, different environment, different shifting parameters, gives you these different functional clues as to what is going on in the system that then hopefully gives you some insights into how do I kind of enter into that system and start to modulate it a little bit differently.

Dr. Matt Antonucci 35:52

Yeah. And you just gave a great example of the model, right? So the model is just that. It's like what other things influence it. When that person turned their head to the right or left and their brain was like, uh, this is not really processing the way it's supposed to, you start recruiting information from other places. You start losing higher function to support lower function that's just not able to maintain. Uh, and that's the basis of the model. We we talk a lot about, uh, or at least a good section, about load. Like, you know, one of the things that uh drives the system is load, right? And that that exposes some of the vulnerabilities. So I often tell people, like, you know, if you've got a pickup truck and you're driving down the highway and everything is fine, it doesn't necessarily mean your pickup truck is great. What you'll notice is that if you put a bunch of stuff in the back of the pickup truck, it doesn't drive the same and it starts sputtering or whatever. That's because there is something wrong with your engine, but it doesn't happen when you're just driving with no load, right? Just driving normal highway speeds without a load. And this is hallmark for concussion. People will tell you all the time, listen, Doc, I'm fine if I'm just

Load Reveals Hidden Weak Links

Dr. Matt Antonucci 36:57

home in the dark, not doing anything. I feel great. But as soon as I have to do anything, get up or go to school or go to work or even get dressed, or even just, you know, think about a grocery list, I just start to fall apart. Because that's because the model basically represents that they've broken down and functioned to the point where they can only do simple things. Uh, because when they are under load, the system falters and now all they can do is simple things. So the the real solution there is build the system back up, not necessarily give them a pill or make them sit in a dark room or something like that uh to build it back up so that they can do the things that they need to do.

Dr. Ayla Wolf 37:36

Yeah, yeah. And I think that is, you know, the the most common thing I hear from people is I am okay if I'm in a quiet house by myself, not doing much. The second I have to go into the grocery store, uh, now everything falls apart. You know, like Dr. Zlinski says, his his final test at the end of uh intensive is can you go to Costco, right? Can you go into Walmart?

Dr. Matt Antonucci 37:59

Yeah, exactly.

Dr. Ayla Wolf 38:00

So you mentioned something else in your paper that I want to dive into. You talk about how at a cellular level, interneurons become hyperconnected in local hubs with reduced long-range inputs, which leads to a loss of distal inhibitory control. So let's break this down, what that means, and then again, what the outcome is of that.

Dr. Matt Antonucci 38:22

Yeah, and that has to do a lot with what's called Jacksonian dissolution. Um, Hugh Jackson was uh you know, he was a scientist, researcher neurologist, and philosopher back in the early early 20th century. But basically he he posited that when the brain is injured,

Jacksonian Dissolution And Reflex Control

Dr. Matt Antonucci 38:42

um, it basically decreases its complexity and it becomes hyper-localized in its function. What that basically means is that when we injure our brain, all of this beauty to think and marvel and do math and you know, try to figure out the meaning of life and maybe even go shopping, these cortical functions, when the brain becomes injured, our brain goes, Yeah, you know what? I don't have the ability to do that anymore. I'm gonna get, I just need to survive. Right. So what ends up happening is these small pools of neurons become hyper-integrated, and then they reduce the ability to connect with other parts of the brain to allow us to do things. It's called Jacksonian dissolution. And when you have that, that's what disables somebody from doing anything basically meaningful other than just being reflexogenic, meaning just input from the sensory information and uncontrolled output, which is a great example of this, is if you have pots. Everybody's talking about POTS now, postural orthostatic tachycardia syndrome. Basically, you lie down and you stand up. And if you're in the medical world, you go to see the cardiologist for that. Why do you go to a cardiologist? Well, because your heart rate goes up. Well, that's a heart problem, or your blood pressure drops. So wait a second, that's a heart problem. But really, it's not even a heart problem. It's a blood vessel problem. But really, it's not even a blood vessel problem, it's a neurological regulation problem. Right? So when we start looking at POTS and somebody has that sort of a condition, what ends up happening is they become very reflexogenic on a brainstem level. Their ability to regulate their blood vessel diameter and their heart rate and all that kind of stuff from a higher center becomes more integrated on a lower center. So now whenever they stand up, they have exaggerated responses and they don't have the modulation, the basoganglionic thalamic gain modulation and the coordination and orchestration of being able to go from a lying to standing position with their heart rate and blood pressure. So you can see POTS really is a neural system problem, not necessarily a certainly not a heart problem in most cases, but also not necessarily just a focal problem.

Dr. Ayla Wolf 40:52

Mm-hmm. Yeah. And so another example that you mentioned when you talk about this idea that the brain kind of regresses to more primitive control systems is that that also uh basically affects postural instability, like in the case of POTS. But also one of the things that people often talk about is they get a concussion and now they have intractable headaches and their neck is stiff, and it doesn't matter what you do to the neck, it just is always stiff and tight. And so um, this is also kind of going back to these postural kind of programs that are running in the background that the it's like we we kind of lose our ability to know where we are in space, and the brain just says, I'm just gonna kind of lock it all down and kind of regresses to some basic programming.

Dr. Matt Antonucci 41:37

Yeah, absolutely. Because and that typically happens when you have vestibular issues. It can happen when you have oculomotor issues as well, but largely with vestibular issues, because and let's be clear, I mean, we we shortcut when we talk. A vestibular issue doesn't necessarily mean there's something wrong with your inner ears. There may be something wrong with your inner ears, but when we talk from a functional standpoint, we rule out a problem with the inner ear because that wouldn't be functional at that point. That would be structural. You have something wrong with the structure in your inner ear. So in the functional world, when we say somebody has a vestibular problem, we basically mean microphone, wire, amplifier in the brain. Right. And basically there's nothing wrong with the microphone, there's nothing wrong with the wire, but the amplifier volume is a little bit off because maybe you had a concussion and basically the twisting of your brain injured the actual brainstem structures that process it. Most often, when we have a problem with the vestibular system, the problem is in the brainstem's integration into the cerebellum and how those two communicate with each other. So when we start looking at that sort of a problem as a vestibular problem, when we turn our head a certain amount or if we move, or even if we breathe in our heartbeats, when we heartbeat, our actually body is moving, we can measure this on posturiphy. We can, we can put somebody on a balance plate, we can actually see an EKG through their feet on a posturography because we actually move. Well, if you're moving like that back and forth, but your inner ears are not necessarily processing it appropriately, right? We have sensory input movements, we have the integration of the brain saying, hey, this is the wrong or not really right what I'm expecting. Now the output starts to change, and what we start to say is, I gotta lock my neck down because I don't want to move that much, right? So then you start having tight neck. What does the tight neck do? Feeds back into the system. What happens when you feed back in the system? Well, a tight neck starts causing you to have hypermetabolism. We have to have more blood flow and all that kind of stuff, but also becomes more sensitive, like a tightened guitar string. So now every time you move your head, you can start getting a little bit dizzy or have a headache or have things because of the neck. Now, what's the treatment for this? Right? That's what we have to do. That's clinicians and even patients watching this. You have to think about this with your clinician. If what I just said is true and it's a model right now, it hasn't been proven. We talked About how to prove it, but if that model is accurate, if your dizziness when you turn your head or headaches from your or in a tight tight neck scenario occur, if what we say is true, that the vestibular integration is the problem, and that's causing you to have tight neck muscles, and the tight neck muscles are not giving you a headache. Do you reduce the tightness of the neck or do you fix the vestibular integration? And that's where we start having to think a little bit deeper. And it's not easy to think this way. I and a lot of people don't want to think this way because it is a lot of thinking. You have to be like somebody who likes the rubrics cubes and puzzles, like I do. Um, you know, you have to think a little bit deeper like like you do in order to solve this problem. But sometimes the treatment of the neck is the worst thing you want to do because that is your stability, right? If you don't have this and you don't have this, then all you have are your eyes, and now you become super light sensitive. Right? Because you're overbiasing your vision.

Dr. Ayla Wolf 45:02

Right. You downregulated one system, up regulated another system. So, okay, I'm gonna quote you again because I love this quote. You said the nervous system does not descend into chaos, instead, it reorganizes into new, often less efficient but stable configurations. And that's exactly what you're describing here.

Dr. Matt Antonucci 45:20

Yeah, and we we call that, you know, basically constrained adaptation. So essentially, constraining something means you limit it, and an adaptation means that you're just ability to change in the environments. We I kind of alluded to this a little earlier that nobody dies from a concussion, at least not months or years afterwards. We don't have mortality, which is death. We have morbidity, which is a loss of quality of life. So the question is if, and we had to address this in a model because

Environment And The Psychological Default

Dr. Matt Antonucci 45:47

the way the model was written is it's essentially you could just spiral until you just don't function anymore, right? Because if this is a reverberative loop where we lose higher function, then middle function, then lower function, what's to say we just don't lose all function? Well, the thing is we have this constraint adaptation because there are things in the environment that never change, that we always process consistently. Some of them are intrinsic, some of them are extrinsic. And then we'll have one other thing that we talk about here that really affects constraint adaptation, uh, which is environment. We'll talk about that in a second. But ultimately, the fact that we breathe in and breathe out, right, that never really changes. That's always a constant driver. Uh, the fact that night and day always occur, at least you know, if you put your head outside, um, the fact that there's always some sort of gravity there as tissue deformation, there are universal constants that make it so that we have this floor of function. Floor, I mean, obviously, it sounds like it's low, but what does a floor do? It supports you from falling through to the next floor below it. All right, so we have this floor that basically is driven by what we call central pattern generators and environment consistent environmental stimuli. So that basically puts this constraint on there. But one of the other things that solidifies this constraint model is the environment, which explains a lot of different things that we're starting to see now, which means that somebody had something going on with them, then had a concussion, and still have that other something going on with them with the concussion, and now you get a twofer. Uh, I always, the way I explain this to my patients, that your environment is what was always there. Your concussion is just what's new. If your environment was a puddle of gasoline and your concussion was a match, that's a bigger problem because eventually, you know, gasoline in a puddle by itself is inert, eventually it'll evaporate. A match will eventually die out, blow out. But if those two things come together, you have a much bigger problem. So environment determines how much constraint adaptation we have. If you live in a moldy house, if you have Lyme disease, if you are, you know, having some sort of a spousal abuse problem, if you, you know, if you, if you, if you, right? Those are all things that really drive that constraint adaptation a bit lower. So this is why somebody might say, like, I had no problems before my concussion, but now I have all of these problems, and they don't necessarily all attribute to the concussion because that constraint mechanism is broken by something in the environment.

Dr. Ayla Wolf 48:20

Yeah. And then the other piece of that that you talk about is the psychological default that happens. So talk a little bit about that too.

Dr. Matt Antonucci 48:28

Yeah, psych, psyche is a is a really important thing. So a lot of the things that we're talking about are we called bottom-up sort of aspects where we have uh this anatomically speaking, bottom-up. So sensory information comes in through your spinal cord or into your cranial nerves and goes up into your brain. Uh, anatomically speaking, top-down would be things that originate in the cerebral cortex and go downwards to affect all the output. Um, you know, so to say it differently, just to kind of give you just an example, like um I could just get mad about something and smack somebody, right? That's a top-down implementation. It's like, you know, nothing bottom-up other than, you know, whatever the sensory stimulus may be mad, maybe whack somebody, but that's a top-down activity. So our psyche is really a top-down mechanism. It's the ability to think and assign emotion to things and to manifest our future. And uh, from an actual neurophysiological basis, these are called thalamocortical and corticothalamic integrations. So this is basically the thalamus and the cortex. The thalamus sends information up to the cortex, but then the cerebral cortex then sends information back to the thalamus. This is the basis of affirmations, right? So it's like, you know, you want to hang a check on your wall that's for a million dollars that you want to cash one day. Every day you see it, we have cortical reality of that check, and eventually you're gonna start creating behavior. This is your Tony Robbins. This is this is everything that starts to try to change the way you think. And it may not even be that significant. It might just be, you know, this is gonna be a very kind of a sexist comment, but guys see a Ferrari and they want to get one. Women might see a, I don't know, a Chanel bag or something like that. That's what I mean by this as being sexist. There are guys that like Chanel bags, there are women that like Ferraris, but just, you know, just to kind of just give an example here. Um, you know, you might be going through your mid-rife crisis as a guy and say, I want to finally buy that Ferrari. Nobody in my town has a white Ferrari with black wheels, a 488, whatever. And all of a sudden you're on, you get in the car, you're driving to the Ferrari dealership, what do you see? Ferraris. White Ferrari, black wheels 488, the exact one that nobody else in your town has. That's just because your cerebral cortex became attuned to what you were looking for. We're basically started looking for it in the environment. So, what I meant by that in our paper is that if somebody is in a mental state where they don't want to get better, they won't get better. Right. No matter how much therapy you do with them, how much light stimulation or spinning or whatever it might be, it's difficult. It's one of the things that constrains our ability to get better, but it also constrains our ability to get worse. If you have, you know, hope and you have, you know, optimism, you know, a lot of times people with hope and optimism, they at least plateau where someone who is just dwelling on the misery, they can continue to get worse. So that's why we we kind of put that psychological factor in there as a stabilizer or one of the contributions to constraint adaptation.

Dr. Ayla Wolf 51:28

Yeah, that makes sense. Okay, we've covered a ton of information. What is the next step here? You already mentioned a few other papers you're working on, but you also talk at the end of this paper about experimental validation protocols. So, what does that look like? And what what are the the next steps here in taking this model to the next level?

Dr. Matt Antonucci 51:48

Yeah, so um that would be on this in this pathway with the nerd model, that would be it. So, this, I mean, I I've been conceptualizing this paper for a decade. It took us about a year to write it. Um, and in that period of time, when we submitted it for peer review, it took about six months to go for the peer review process. So, in that period of time, one of the things that we said the follow-up was going to be was some sort of

Validation Plans And RCT Results

Dr. Matt Antonucci 52:09

an RCT. Well, we did the RCT, it should be published this month. Uh so we have a randomized control trial implementing the nerd model versus standard of care to see if there's actually a difference between the two. And surprise, surprise, the results say there's a big difference between implementing this model and standard of care for concussion. So that'll be the first RCT to support this model. Uh eventually, what we want to do is get some functional imaging studies where we can actually see if we can identify the fact that these hubs and nodes are relevant to the model. That would be super huge. Um, but we also, in the paper, my my co-author, Kenneth J created a really nice mathematical formula that explains the model in mathematic format. So that can bridge the gap between a theory and actual data modeling. So somebody who is really keen on and knowledgeable in mathematics can look at that equation, especially if they have the ability to process things like um you know deep learning, large language models, uh, gen AI. They can actually build that out inside of a mechanism and utilize patient notes to validate the model. So basically, what would happen is you can plug that equation, plug, that's a seems so easy. They can build that equation inside of a model, get patient data, and see if the outcomes are the same as clinical outcomes. And if that's the case, that would validate the model. And we also have some things in the paper that would say, you know, if we did those things and we don't see this, it falsifies the model. That's science. And we might not be right. We have to test it. And if we're wrong, then we go back to not the drawing board, so to speak, but then we can we can adapt the model based upon the things that we find in order to make a better model.

Dr. Ayla Wolf 53:55

And how did you apply this model in a randomized clinical trial?

Dr. Matt Antonucci 53:59

So we basically did an evaluation. I guess the the shortcut way is I've always been doing this model. You know, I know you've been doing the model. It's just this is the first time it's really been articulated and published. It's what we've always been doing. So essentially what we just said is all right, you know the thing that we've always done was X, Y, and Z. Let's make sure that we can assign X to this, Y to this, and Z to that. So that becomes the nerd group. And then we had the RCT or the control group, which is somebody that just did normal. What we did is we we did a literature review and said, hey, how should someone get treated with the concussion? We followed that. And then what we did is we did a crossover. So the people that got the standard of care, they eventually got nerd treatment. And then the people that got nerd treatment eventually got standard of care to see if the control group got better after getting the control the standard care, and if the nerd people got any better when they did standard of care. And I'm gonna leave you guys hanging for the results of that. But I think I think you kind of know what the outcome is.

Dr. Ayla Wolf 55:02

I wouldn't, I, I, I might place some bets on the outcomes.

Dr. Matt Antonucci 55:06

Yeah, exactly. So that's kind of how we tested that in the RCT.

Dr. Ayla Wolf 55:11

Awesome. And that trial's done. You've written the paper. That's exciting.

Dr. Matt Antonucci 55:16

It should be published this month. It's in the final stages of review. So we're hoping that maybe it's into April right now. So hopefully sometime April, May, we we should have that paper out.

Dr. Ayla Wolf 55:24

Okay. I can't wait to see it.

Dr. Matt Antonucci 55:26

Me too.

Dr. Ayla Wolf 55:29

Awesome. Well, all the work you're doing is, I mean, it's changing the landscape of neurology indefinitely. So thank you so much for all your hard work and the ability to take these very complex situations and actually create a model that hopefully provides a structural framework for clinicians to be able to be more effective at treating these cases of people who oftentimes have feel like they've tried everything and they have plateaued. And it's like to be able to have a framework and a model that more and more people can adopt, not just a small handful of people around the world that are hard to find. Um, that's really what we need in the world today. So thanks

Scaling The Model Beyond Concussion

Dr. Ayla Wolf 56:08

for all your hard work on making that happen.

Dr. Matt Antonucci 56:10

Oh, thank you. And thank you for sharing. But yeah, you you absolutely are right. And granted that this paper was published in a scientific journal and scientists would read it and doctors will read it. Ultimately, this paper was for patients. You know, I know it's a little hard for patients to read, but ultimately what we start to say is that, you know, a doctor, if you can, a doctor will put their hands on one patient at a time. But if you can influence a doctor, you get to influence all of the patients that they they treat. So hopefully we get a lot of clinicians reading the paper, asking questions, studying it, seeing how it applies. We haven't, I mean, for a year now, we've been trying to break this model. We can't break it. We've had optometrists, you know, first question and say, How do I fit into this model? Because I'm changing vision and I change the way people see. We're able to fit them into the model. Physical therapist, acupuncturist, you know, you name it. And ultimately, here's the secret. Don't tell me. We, in order to get this paper published, we had to say the model was for something. You'll never ever get a paper published saying this is a model for everything that exists. But what you'll start to see is the model is holding true for ADHD, it's holding true for autism, it's holding true for peripheral neuropathy, it's holding true for basically every neurological condition that doesn't have imaging findings. And also, it can explain people that have imaging findings as well. Because when you read the paper, there's something called a seed injury. Now, because we had to say that for a concussion, because we know that concussion affects certain areas. However, a seed injury could be a tumor growth in the brain. A seed injury could be an infarct in the brain. And then the model still applies. So I think what we're really trying to do, our hope, our fingers are crossed, that we can, you know, we can have a spot in history of saying in 2026, this is when it all changed. Um, and this is where functional neurology became was born. Uh, it was published, was validated, and this is where those 1.3 billion people in the world finally get seen and finally get treatment because right now they're not. So that's the hope. That was the hope by publishing this paper. So fingers crossed.

Dr. Ayla Wolf 58:23

Yeah, yeah. Well, keep thinking big. It's working.

Dr. Matt Antonucci 58:27

Thanks.

Dr. Ayla Wolf 58:28

Awesome. Well, so good to have you on the show again. I will uh let people know where they can find you. I know you have a website with an amazing blog and a lot of good info. And so I'll include all that. And is there anything else that you want to say before we we wrap up?

Dr. Matt Antonucci 58:44

Oh no, I mean, I just I'm grateful for it. I think uh in the next couple days, I'm going to record a nice presentation for the Kerrick Institute. I'm gonna put that up there for free. So anybody that wants to learn more about this model and kind of dig into it a little bit deeper in an academic standpoint, go to the Carrick Institute's website and you know you'll be able to find the nerd model uh introduction. It hasn't been made yet, so I don't know what it's gonna be called. But ultimately we'll have a free, probably 30 minutes to an hour presentation on this model so that explains it a little bit deeper from a clinician standpoint and uh people can learn a little bit more about it. But also if you um you know if you want to read the actual paper, maybe you can link up to it. But if you I love this by the way, if you go on Google and just type in Antonucci nerd, you'll find it.

Dr. Ayla Wolf 59:29

You'll find the paper.

Dr. Matt Antonucci 59:30

Yeah.

Dr. Ayla Wolf 59:32

Awesome, awesome. Well, I will include a link to the paper. It is open access, so people can just click that link and download it. And uh, it's a very good read. A couple times. Couple times, oh yeah, more than once. Awesome. Have a great rest of your day.

Dr. Matt Antonucci 59:48

Me too.

Dr. Ayla Wolf 59:52

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Medical Disclaimer

Dr. Ayla Wolf 1:00:31

in the notes.