Transcript
Speaker: Welcome to the NeuroPowerHour. I'm your host and neurological navigator, Dr. Michael Powers, physical therapist, board certified in neurologic physical therapy and clinical electrophysiology.
Speaker: Let's get started. Today, I'm excited to be talking about neuroplasticity. The last four episodes, we've been talking about stroke and key to stroke rehab and across many other neurologic conditions.
Speaker: is this concept of neuroplasticity. Today I'll be covering neuroplasticity in terms of three kind of buckets. I'll be talking about neuroplasticity mechanisms, the factors impacting neuroplasticity, and then concluding with the role of aerobic exercise and intensity on neuroplasticity.
Speaker: Neuroplasticity is the ability of the central nervous system to undergo structural and functional change in response to new experiences. This is important that we understand the definition.
Speaker: Used to be that we thought, well, once someone's injured their brain or something's happened, there's nothing else we can do. But we've learned that the central nervous system is incredible. We already knew that for a long time, but we're really learning a lot more in terms of what drives neuroplasticity and how neuroplasticity is achieved.
Speaker: As we talk about this definition, I do want to highlight the key factor that the central nervous system is undergoing these changes in response to new experiences. As physical therapists, I'd like us to consider that as we're working with our clients and patients, we are able to provide opportunities for this experience-dependent neuroplasticity, and we're continually learning more and more in terms of how to really optimize this neuroplasticity.
Speaker: Let's then talk about the mechanisms of neuroplasticity, and there's five key mechanisms I want to go through, and these include synaptic plasticity, structural plasticity, neuronal plasticity and network adaptations, neurogenesis, and functional reorganization.
Speaker: Now, if understanding the key mechanisms isn't really your thing and you're more interested in the nuts and bolts or the key factors relating to neuroplasticity, feel free to jump ahead to the next section of the podcast.
Speaker: But I do find it fascinating to appreciate and realize that there's multiple mechanisms. So there's not just one thing going on when we're talking about neuroplasticity. There's many different avenues or processes that are happening in terms of neuroplasticity.
Speaker: Let's start then by talking about synaptic plasticity. And this is the modulation of synaptic strength via long-term potentiation and long-term depression. When we're talking long-term potentiation, we're basically saying there's increased receptor density and neurotransmitter release at these activated synapses.
Speaker: Essentially here, when we're talking synaptic plasticity, we're either strengthening synaptic connections or weakening these synaptic connections. The strengthening can occur during skill acquisition and practice, and this would be considered adaptive synaptic plasticity.
Speaker: So let's say i i don't have a neurologic injury. Let's take a baseline without a neurologic condition, and I'm learning how to shoot free throws. Over time, I'm going to be strengthening synaptic connections involved with the skilled movement,
Speaker: of coordinating across multiple joints, the timing, the accuracy, the sequencing that enable me to improve my ability to make that free throw.
Speaker: Now, this strengthening of synaptic connections can also be maladaptive or something we don't want to see, and that can occur with central sensitization and chronic pain conditions.
Speaker: So again, synaptic plasticity, strengthening of synaptic connections during skill acquisition, and this is why, as we talk about evidence-based treatment of neurologic conditions,
Speaker: The task oriented approach, which emphasizes high repetitions of salient task practice, gives you the best results. And we see here that this is really tapping into the strengthening of synaptic connections. Now with synaptic plasticity,
Speaker: We can also have weakening of synaptic efficacy, and this is adaptive when reducing synaptic efficacy to refine motor skills. Let's go back to that free throw example.
Speaker: Maybe as I'm shooting the free throw, I don't really need a lot of activity in certain areas. I need to prune out the inefficient movements. So there's weakening of synaptic ah efficacy, and that's helpful as we're refining motor skills. We reduce co-contractions.
Speaker: We're moving so more smoothly, but this can be maladaptive in conditions such as Alzheimer's disease. Let's move on to structural plasticity. And structural, that should be a key, that we're talking physical changes.
Speaker: So structural plasticity is physical changes in neural architecture. Here we're getting the actual formation of new synapses. The fancy term for that is synaptogenesis.
Speaker: We're also getting dendritic branching and synaptic pruning. So think about we're forming new synapses. There's new branches coming and connecting, but we're also pruning some of these branches. So maybe overly simplistic, but I think of a bonsai tree here that's growing out, but also being pruned at the same time.
Speaker: Following a stroke, some of the peri-infarct areas may demonstrate dendritic sprouting. and formation of new synapses, and this really can help with the restoration of language and or motor capabilities.
Speaker: Moving on to neuronal plasticity and network adaptations. Individual neurons have the ability to modify in response to learning, experience, and environmental input.
Speaker: And this is believed to be via two mechanisms, intrinsic plasticity and network level plasticity. So with intrinsic neuronal plasticity, again, we're at the individual neuron level, and that's achieved through adjustments in excitability and firing properties.
Speaker: If we zoom out to network level plasticity, there's a shift in functional connectivity between brain regions. So this is larger scale.
Speaker: so when we talk neuronal plasticity and network adaptations, we're We're thinking individual neurons can demonstrate plasticity via changes in excitability and firing properties.
Speaker: And then at the bigger level, at the network level, there's changes in functional connectivity between brain regions. For example, after a stroke impacting motor areas, adjacent cortical regions and contralateral motor networks can are recruited to assume lost function.
Speaker: Thinking about therapeutic strategies to really help drive this neuronal plasticity and network adaptations, brain-derived neurotrophic factor seems to play a key role in neuronal plasticity.
Speaker: This can be increased via certain pharmacologic agents, certain drugs, and or activities. so we're going to be talking a lot later about the role of activities and therapeutic activities in BDNF.
Speaker: Also, intensive skill training drives neuronal plasticity and network adaptation. So again, we're coming back to this task-oriented approach. We're seeing that it hits multiple mechanisms of neuroplasticity.
Speaker: Also, mindfulness and cognitive behavioral therapy can be beneficial for driving neuronal plasticity and network adaptations, especially useful in terms of maladaptive thoughts and behaviors.
Speaker: Moving on to neurogenesis, this is the generation of new neurons. This process declines with age, but it remains impactful with respect to learning, memory, emotional regulation, and cognitive flexibility.
Speaker: If we can upregulate BDNF, that's going to be helpful with neurogenesis. So again, we're seeing the importance of BDNF as it relates to neuroplasticity. Exercise, complex spatial tasks, and social interactions are also helpful in the process of neurogenesis. By contrast, chronic stress and elevated cortisol can diminish neurogenesis.
Speaker: neurogenesis, particularly in the hippocampal region, so that would have an adverse impact on memory formation. Then finally, let's talk about functional reorganization. The brain reallocates tasks to other regions. And this is a little bit similar to what we discussed already at network level plasticity.
Speaker: So essentially, we've got a brain region that its main job maybe is in one area, but the brain will reallocate tasks and say, well, we got we got this area that called out sick.
Speaker: You're taking over. You're in the game. You're going to have to work on those TPS reports. ah Sorry about that, but you're taking over. the This adaptive shift can be enhanced by targeted therapies. Particularly, we're talking about therapies such as constraint-induced movement therapy.
Speaker: And we'll touch on this later in this episode. However, this functional reorganization can also be maladaptive such as in cases of phantom limb pain, where someone perceives the sensation of pain from a limb that is no longer there, such as after an amputation. So this functional reorganization, just like many other areas of neuroplasticity, and this is a point I probably didn't make strongly enough, neuroplasticity, we really want to think can be adaptive, or it can be an adjustment in a fashion that leads to increased function,
Speaker: better performance, or it can be maladaptive, which leads to decreased function impaired a ability. So as we're going through talking about neuroplasticity, somewhat of an assumption that I'm making as I'm discussing it is that we are wanting adaptive neuroplasticity.
Speaker: But I'd like you all to keep in mind that neuroplasticity absolutely can be maladaptive. Again, we'll see that a lot with chronic pain in the literature. Conditions such as depression and anxiety are talked about at length. That's why the mindfulness or cognitive behavioral therapy is mentioned as being a positive driver towards changes in a positive fashion in neuroplasticity.
Speaker: So again, just keep that in mind that as we're working with our clients and patients, we're moving towards adaptive neuroplasticity and we're probably thinking of the things we want to achieve. And i I would argue we should. We want to move towards what we want, but we should be keeping in mind that there's absolutely maladaptive neuroplasticity and the things that we're engaging with in therapy, we want to really keep maladaptive processes off the table as much as possible. To summarize, then, the mechanisms of neuroplasticity, we discuss synaptic plasticity, structural plasticity, neuronal plasticity and network adaptations, neurogenesis, and functional reorganization.
Speaker: And if we had to distill a lot of the drivers of what's happening here, are a lot of the drivers of adaptive neuroplasticity, Many of these mechanisms were improved by increases in brain-derived neurotrophic factor, or BDNF. Many of these processes were improved via exercise. And we also discussed the importance of practicing skills and tasks.
Speaker: And then finally, a brief mention was made about chronic stress, elevated cortisol having a negative impact on neuroplasticity. Coming up next, I'd like to discuss and go into greater detail the key factors which can help drive adaptive neuroplasticity.
Speaker: Let's start then by looking at lifestyle factors in neuroplasticity. So before we zoom into therapeutic interventions or thinking about what we can do in therapy, let's talk about general lifestyle factors. And I really like this type of discussion because I think this applies to people independent of whether you've had a central nervous system injury or not.
Speaker: I also think there's a lot of overlap here with pain neuroscience. I think central nervous system, neurologic conditions, pain neuroscience, we're talking about the importance of neuroplasticity. So again, a lot of overlap.
Speaker: So let's start by looking at these lifestyle factors. First up, we're going to talk about sleep, and it seems like everyone's gotten on the sleep bandwagon lately, which is great. Now there's almost a rebound concern of are people overly stressing about sleep? Are those aura rings or your sleep trackers making you more stressed?
Speaker: I'm going to stay out of that discussion and just mention that sleep is imperative. for memory consolidation and synaptic pruning. So I mentioned previously, sometimes I think about synaptic pruning as that bonsai tree, just getting rid of things that aren't necessarily needed.
Speaker: So sleep is really where you're gonna get that memory consolidation, synaptic pruning. Recently, I was working with some students in lab as they were getting ready for a practical. And some of them were saying, I've done all my studying the night before. I don't cram the day of.
Speaker: And I think that's a very helpful strategy because we're really looking at that memory consolidation as we sleep. You're really laying the foundation there. So not a lot of point if you've got an exam or something coming up. Don't need to do a lot of cramming the day of.
Speaker: Get all that content in beforehand. use your sleep to consolidate the memory. Diet and nutrition. So diet's really going to be key in shaping synaptic health and neurogenesis.
Speaker: And there are findings suggesting that high-fat, high-sugar diets promote oxidative stress and impair plasticity. I do think that in some of these areas I'm going to be talking about seem to be getting more attention in general, in general media,
Speaker: in social media within health and wellness, which is great. So here, i have noted that there's been a lot of pushback on processed foods, ultra processed foods, and we can argue, well, what's the definition of these foods anyway? However, it does warrant mention that high fat, high sugar diets do seem to impair neuroplasticity and promote oxidative stress. So general lifestyle factor of looking at good diet and nutrition is going to be important for neuroplasticity. Physical exercise, and now I'm kind of rubbing my hands together, getting excited. We're in the physical therapy wheelhouse here.
Speaker: Physical exercise is one of the most potent enhancers of neuroplasticity. Let's underline that. We're going to come back to that. I'm going to talk about aerobic exercise, intensity of exercise.
Speaker: But physical exercise stimulates BDNF release. I previously mentioned how important BDNF is across multiple mechanisms of neuroplasticity.
Speaker: So physical exercise is one of the most potent enhancers of neuroplasticity. The lifestyle factor of stress management is going to be important more for avoiding or minimizing the impact of chronic stress, such as elevated cortisol levels and how chronic stress can lead to maladaptive changes in fear and anxiety-related circuits.
Speaker: Once you start getting the fear-anxiety-related circuits going, you could be moving towards things such as kinesiophobia or the fear of movement. You could now be impacting the concept of having a positive affect.
Speaker: If we think about optimal theory, which has been covered in another episode, we could start seeing a breakdown or an impact on motor function if we get increases in fear and anxiety and worrying about what's happening So stress management is going to be a key lifestyle factor that can impact neuroplasticity.
Speaker: Then finally, social engagement and cognitive changes. Social engagement and cognitive changes bolster adaptive changes in brain structure and function and of particular importance. And they're finding this out as they're looking at what helps people thrive in retirement, what keeps people happy later in life, that the social engagement, cognitive changes helps mitigate age-related declines in neuroflexibility, and perhaps just as important or perhaps via the same mechanism, it increases people's overall happiness, and we get that positive effect.
Speaker: We get improved movement if we look back at optimal theory. So it's kind of a virtuous cycle here. So to recap lifestyle factors, look at sleep, diet, physical exercise, stress management, and social engagement.
Speaker: And let me pause here a little bit to, if we think about, maybe we've got someone with a neurologic condition. Let's say someone's had a stroke. Maybe they're having difficulty eating, chewing, swallowing, so that's going impact diet.
Speaker: Maybe they're depressed, so their sleep is impacted. That's impacting their stress management. Their mobility has declined, so they're no longer going out in the community. Their participation is limited.
Speaker: You can see how all of these are going to interact with each other to really drive down or impair neuroplasticity. So as we're working with this patient, this kind of example patient, we're going to absolutely prescribe and use physical exercise because we know that drives BDNF.
Speaker: But I would argue we need to touch on sleep, diet, and for sure, social engagement. We got to do something to break the cycle of fear, anxiety, depression, and really improve overall quality of life. Sometimes when I'm presenting on materials in class and I'll touch on quality of life or the importance of participation, it may be challenging to understand or perceive for students why that's important when you're maybe more worried about, well, I want to improve this person's ability to walk.
Speaker: I need to learn about my hands-on techniques. But if we zoom out and we take a look at neuroplasticity, hopefully you can see the importance of this social engagement. And this is why in the episode on stroke, I mentioned that the O'Sullivan textbook and many other clinicians will recommend starting at the participation level when you're thinking about planning your examination and treatment,
Speaker: Because who cares if someone can get five degrees of dorsiflexion back if they're stuck in their house and their overall quality of life hasn't improved. However, if that five degrees of dorsiflexion now enables someone to walk 10 or 15 minutes longer, improves their six-minute walk test, let's say, improves their 10-meter walk speed, and they're able to go out in the community and re-engage, then Now we've kind of lit the candle that's going to drive further improvements in motor function. Now their mood is elevated.
Speaker: They have some meaning. They're engaging in the community. We've tapped into some neuroplasticity via that social engagement. And so hopefully you can see the importance there. And you'll probably hear I'm getting a little soapboxy again. But I really feel like as we're moving through working with our patients, no matter what the condition is, our North Star should be this is a person that has things that they want to do.
Speaker: And the more that we can really hone in on that participation, what's important to them, the better our outcomes will be. And for sure, the more we're going to tap into neuroplasticity.
Speaker: Of course, I'm going to come back to the Sheetz et al. article. That's something I keep coming back to. We just want to highlight here neuroplasticity after central nervous system injury. I'm moving off of the lifestyle factors, talking now more about what we're looking at in the physical therapy domain.
Speaker: And I'm just highlighting four key points from that paper that came out looking at the neurologic evidence in physical therapy. And our four key things I want us to keep in mind are recovery is going to be heavily influenced by specificity, amount, and intensity of task practice.
Speaker: Recall when we talked about the mechanisms of neuroplasticity, I mentioned multiple times the importance of working on skills and tasks. So we're not, for the love of everything, we're not sitting there doing 10 reps of seated long arc quads, okay? We are working on standing at the kitchen getting something out of the counter properly. We're working on things that are important to the patient, and we're working at it at a high intensity level and just a lot, a lot of repetition. Other thing we want to consider is that movement errors are going to be vital, especially as they relate to influencing walking ability.
Speaker: We learn from our mistakes. So allowing, even thinking about imposing movement errors, so really ramping up that task difficulty enhances and influences walking ability. Related to that, we want to highlight the importance of increasing task difficulty.
Speaker: and inducing errors. So yes, we want patients to have some success. We want to see some quote unquote good movement, although that's even debatable. But we, as much as possible, quickly ramp up the task difficulty, make some errors or allow the patient to make some errors so they can learn from those errors.
Speaker: And then finally, strength and coordination and not spasticity are the primary impairments that limit function. When we're talking about experience-dependent plasticity, so recall within the definition of neuroplasticity, we talked that the central nervous system essentially modifies itself based on experience.
Speaker: And there's some key principles here, and I'm not going to go into too much detail because I've got 10 want to highlight. They make intuitive sense. I want you to just keep these in mind as you're looking at developing treatment plans for your patients, as you're looking at tapping into neuroplasticity.
Speaker: Let's then talk about the 10 principles. First one, pretty easy to remember, use it or lose it. If we have a failure to drive specific brain functions, it's going to lead to functional degradation. So it makes sense, use it or lose it.
Speaker: Makes intuitive sense, it's backed up by the evidence. Its related cousin is use it and improve it. So training that drives a specific brain function can lead to an enhancement of that function.
Speaker: Here we're back to that task-oriented training, really working on skills and tasks. So that's use it and improve it. Specificity. Nature of training experience dictates the nature of the plasticity.
Speaker: If I work on shooting free throws, i I'm going to get better at shooting free throws. That's task specificity. So really thinking about whatever it is we're wanting to improve.
Speaker: being specific about it, and then we're going to layer on high repetitions. So the number of repetitions matter. We're not doing three sets of 10 of something.
Speaker: We're doing tens, hundreds, maybe thousands of repetitions. Think back to yourself of any high-level skill acquisition. I'm going to use that free throw example. this The ability to shoot a free throw takes an inordinate amount of repetition. So think about this with your patients. You've heard me mention many times, think about your patients athletes.
Speaker: So don't stop at low repetitions. Their sport may be getting to the front door, walking down the driveway to the mailbox, and we're not going to get better at that with a few repetitions. We need high repetitions.
Speaker: Along those same lines, intensity matters. The introduction of plasticity requires sufficient training intensity. I'm going to talk about that a lot when we talk about aerobic exercise, and we're going to highlight again high-intensity gait. We're going to come back to that.
Speaker: Time matters. There's evidence that different forms of plasticity occur at different times during training. Salience matters. The training experience must be salient or important to the patient or client to induce plasticity. and This is pretty much jokingly, but I will jokingly say at lab, don't play the drinking game of taking a drink every time you hear me say salient because I say salient a lot, but really driving home the importance of we want to be doing something that's important for the patient.
Speaker: Let's say we're working on upper extremity function after stroke and the person we're working with likes to play cards to whatever extent possible. Are we able to introduce playing cards in our treatment session?
Speaker: And maybe we're working on balance as well. Is it possible we could be working on playing cards in a standing position and getting that two for that two for one that I always like seeing?
Speaker: So salience playing with cards instead of reaching for cones. And if we wanted to work on reach, then we're playing cards and maybe we're doing it in such a way that they're having to reach across the table for cards or reaching across midline if we're also working on scanning.
Speaker: So don't get stuck on, hey, we're just going to reach for cones. Cones are fine, but think about how we can make it more salient. Age does matter. Training induced plasticity occurs more readily in younger brains. However, it doesn't mean it won't happen in older brains. We just understand younger brains are going to be a little bit more plastic.
Speaker: We also then have transference. Plasticity in response to one training experience can enhance the acquisition of similar behavior. So the ability, perhaps that one skill or one training experience, we may be able to transfer that to others.
Speaker: However, we want to keep in mind there is also interference. That plasticity in response to one experience can interfere with the acquisition of other behaviors. As it relates to transference and interference, these are probably a little bit more challenging to tap into or to know because we also understand that specificity is the key driver. So we know what we practice we get better at.
Speaker: It may be challenging. You may just want to be on the lookout for, okay if I'm training something adjacent or different, is that going to be transference? Am I going to be able to pull that into another task or is that going to bring in some form of interference?
Speaker: To recap real briefly then, 10 principles i want you to think about and have in your back pocket are use it or lose it, use it and improve it, specificity, repetition matters, intensity matters, time matters, salience, age, transference, and interference.
Speaker: Before we dive into talking about aerobic exercise, high-intensity gait training, I wanted to touch on a few specific treatments that drive neuroplasticity after stroke or that have good evidence for improving neuroplasticity after stroke.
Speaker: task-specific training, and constraint-induced movement therapy. For those of you that aren't familiar, constraint-induced movement therapy or CIMT is the, you minimize or eliminate use of the non-involved side and really shape movement and have the patient focused on salient movements of the involved upper extremity for a set time period per day in a set number of weeks.
Speaker: And there's CIMT, there's modified CIMT. This task-specific training and CIMT, there's robust evidence for promoting cortical reorganization and functional recovery.
Speaker: So again, we're back to that task-specific training. I've been banging that drum throughout. And I think sometimes it's challenging for students to appreciate how important this task training is because it doesn't always appear like exercise or it doesn't appear like a protocol.
Speaker: And maybe it seems too open-ended to think about, well, how is this going to be a treatment? I'm just having someone work on a functional task. But this is, again, a key driver of neuroplasticity, especially tasks and skills that are important to the patient. Mirror therapy, where there's a use of either a mirror box or some form of mirror, and the person is looking at the mirror, so it appears that the involved extremity is moving in a functional fashion because they're actually observing the non-involved extremity moving.
Speaker: There's some YouTube videos of this. It's really interesting when you see the videos, especially I have one video that I've seen where the person takes their other hand out of the mirror box and it kind of messes with your brain. So this mirror therapy stimulates sensory motor cortical activation. It can really help in terms of reshaping or working on that sensory homunculus.
Speaker: Virtual reality, this is another beneficial treatment, lot of good evidence here. helps drive neuroplastic change by facilitating repetitive task-oriented practice while providing multisensory feedback.
Speaker: And it's also fun for many patients Using VR is going to be very fun. And then finally, aerobic exercise contributes to motor recovery and cognitive enhancement and, very importantly, increases levels of brain-derived neurotrophic factor.
Speaker: I want to conclude with a section really emphasizing aerobic exercise, intensity of treatment, and touching again on high-intensity gait training.
Speaker: Let's start by considering the role of aerobic exercise in neuroplasticity. Aerobic exercise induces a cascade of events, leading to increased BDNF gene expression within the central nervous system.
Speaker: Take-home point is aerobic exercise is our best tool to really pump up BDNF within the central nervous system. And I've talked at length about the importance of BDNF as it relates to neuroplasticity. So aerobic exercise, in addition to these improvements in BDNF, aerobic exercise is going to improve cognition, neuroplasticity, and motor learning abilities.
Speaker: I did want to take a little detour, a little side quest, and note that resistance training also can be important, and resistance training augments executive function and working memory. And many studies have found that aerobic exercise combined with resistance training gives multiple benefits as well. However, the evidence as it relates to BDNF is really going to be we're going to focus on aerobic exercise, but I didn't want to leave resistance training. i didn't want to not mention resistance training at the risk of using a double negative there, but we're highlighting the role of aerobic exercise.
Speaker: There are some considerations about when you do the aerobic exercise. So I'll link a study here that mentioned that you can use aerobic exercise before therapy. So let's say you're working with someone with a stroke, performing aerobic exercise before therapy. motor rehabilitation may improve motor function by really tapping into aerobic exercise induced increases in capacity for neuroplasticity. So you can do aerobic exercise, think about you're getting more BDNF, you're kind of getting primed for neuroplasticity.
Speaker: You could also potentially do aerobic exercise after the motor training to facilitate the memory consolidation process. I don't know that I would get too hung up on where I put aerobic exercise within the treatment plan.
Speaker: What I would argue, though, is to move away from this consideration of, hey, we're going to get on the bike for a little bit to warm up. I just had to catch myself because this is a clean podcast. There's no cursing.
Speaker: But no, we're not going to do that. We're We're not warming up. If you're going to do aerobic exercise, let's get to some intensity. Let's drive that BDNF.
Speaker: Let's actually use it for neuroplasticity and not to take up some time or to slowly loosen up or to say, OK, we're going to get ready for the real stuff, because most likely people that are saying, hey, I'm going to use this exercise to get you warmed up.
Speaker: By the time they're warmed up, you're probably not even doing a high enough intensity within your therapy treatment to increase BDNF or to drive real aerobic changes. So get this concept of warming up legitimately off the table. like let's Let's just stop with that.
Speaker: do Do your aerobic exercise for a reason. And that reason, again, within patient tolerance, should be at a high intensity to drive BDNF. I wanted to mention a systematic review. This was published in Stroke in 2022. They looked at a let's see, it was 687 patients across six randomized trials.
Speaker: What I found interesting about this review is that one session, so a single session of high-intensity aerobic exercise, increased BDNF concentration.
Speaker: So we're not talking about needing to do multiple sessions to see changes, at least within BDNF concentration. One session is enough. And remember, this is high intensity. This is getting that heart rate up.
Speaker: So going back to my prior point, my prior soapbox of don't just do this to warm up, get this at a high intensity to really drive those BDNF increases.
Speaker: Let's return to a mention of the high-intensity gait training. Recall that Hornby et al. in 2020 reviewed benefits in ambulation for people with chronic central nervous system conditions such as stroke, traumatic brain injury, and incomplete spinal cord injury.
Speaker: And what was recommended was walking practice at moderate to vigorous intensity, so 60% to 80% of heart rate reserve 70% to 85% heart rate max.
Speaker: heart rate max or walking practice with VR-based feedback. So we're tapping into that VR consideration that I mentioned earlier as well. So let's hone in on those numbers, 60% to 80% heart rate reserve or 70% to 85% heart rate max. these This is our recommended intensity for walking practice.
Speaker: I would argue if we're looking at aerobic exercise for driving BDNF, so I'm kind of combining or looking at both high-intensity gait but also aerobic exercise, we're looking at 60% to 80% heart rate reserve, 70% to 85% heart rate max.
Speaker: seventy to eighty five percent heart rate max If you're engaged in aerobic exercise for your patients that you're trying to tap into neuroplasticity, should be monitoring vitals. You could be looking at rate of perceived exertion, and there's discussions we could have there on how it correlates with heart rates. But really looking at your heart rates, are you hitting that 60% to 80% heart rate reserve 70% to 85% heart rate max?
Speaker: or seventy to eighty five percent heart rate max Related to GATE, in 2022, Henderson et al. compared outcomes between usual care and high-intensity training for patients post-stroke.
Speaker: What I found interesting here is that they looked at not only ambulation outcomes, but they looked at non-locomotor outcomes. These were patients who were less than two months post-stroke, and they were followed prospectively over 18 months.
Speaker: So there was a usual care, so usual care physical therapy, it compared to a group that were slotted into high-intensity training. There was a significant statistically significant improvement in 10-meter walk, 6-minute walk, transfers, and stairs in the high-intensity training group.
Speaker: The improvement in transfers and stairs was measured via FIMS scores. So that's pretty interesting that not only did they find with this high-intensity gait training group, not only did they improve locomotor outcomes, but they improved in transfers and stairs.
Speaker: And if we think back to previous discussions I've made on this show, there is emerging evidence that we can leapfrog over developmental improvements. So we don't necessarily need to be able to stand perfectly before we walk.
Speaker: This was kind of a premise of more traditional approaches such as NDT. There's thoughts of proximal stability before distal mobility. And those general guidelines are applied pretty often and can serve as guidelines. But from a functional perspective or a true outcome perspective, what we're finding is this high intensity, being upright, something about the reciprocal action of walking really lights up the central nervous system.
Speaker: And we're seeing carryover. We're seeing transference, right? Remember that term from before talking about neuroplasticity. We're seeing transference of we're working on high intensity, Kate, but improvements are transferring to other tasks, other upright tasks, such as transfers and stairs.
Speaker: The authors in this study suggested that traditional therapeutic strategies targeting impairments and functional impairments do not provide adequate practice and or reps of any single task, nor does it reach higher cardiovascular intensities.
Speaker: And this is probably ultimately the take-home message as we think about really setting up our treatment plans to tap into neuroplasticity. We've probably set the bar much too low in terms of number of repetitions, the amount of practice,
Speaker: and the amount of intensity as it relates to heart rate. So if you remember nothing else from today's show, I really want you to take away the importance of high repetitions, just tons of practice on things that are important to the patient at a high intensity.
Speaker: You do those two things And you're really going to be tapping into multiple mechanisms and multiple drivers of neuroplasticity. You do that, layer on these lifestyle factors, don't sleep on talking to your patients about sleep, diet, stress management, social connections.
Speaker: You do those things and you're going to be in a great spot for really helping your patients for improving your outcomes and tapping into neuroplasticity. To summarize then, neuroplasticity is the ability of the central nervous system to undergo structural and functional changes in response to new experiences, and that's important, it's experiences. There's multiple mechanisms involved in neuroplasticity, and therapists should emphasize high repetition, task-specific and salient practice,
Speaker: With high intensity, aerobic exercise appears of particular benefit with respect to neuroplasticity as there's robust evidence for increases in brain-derived neurotrophic factor.
Speaker: High-intensity gait training has been found to improve locomotor and non-locomotor outcomes for patients' status post-stroke. And there's a lot of debate within the neuro community on how much time to spend on functional tasks such as bed mobility and transfers versus getting people up as much as possible with this high intensity gait training, especially as we've seen that Locomotor training can yield improvements in non-locomotor function.
Speaker: I think this is an area that's going to continue to be debated, contested, however you want to name it, within physical therapy. And my North Star, and this could change, but my North Star, I'm landing on really the importance of high repetition, task-specific training, and at high intensities.
Speaker: And I'm not saying don't work on bed mobility, but because there's opportunity cost to everything we do and we have limited resources, including our time, including number of therapy sessions, when in doubt, the evidence does appear to favor high intensity, getting someone upright,
Speaker: high repetitions, so all things being equal, I'm not going to spend a lot of my time with hands-on facilitating of bed mobility when there's other things available to me in terms of treatment interventions that have more robust evidence behind them.
Speaker: Thanks again for listening to the NeuroPowerHour. I'm your host, Dr. Michael Powers, and I hope to catch you next time to continue learning.
Speaker: you
