How Clinicians Can Support Neuroplasticity in Adults

Editor's Note: This text is a transcript of the course, How Clinicians Can Support Neuroplasticity in Adults, presented by Jacqueline Hinckley, PhD, CCC-SLP.

Learning Outcomes

After this course, participants will be able to: 

• Describe if/how new neurons or synapses are formed in the brain of someone with neurological injury or disease.
• Identify one neurochemical change that is associated with social interaction.
• Define “mirror neurons” and describe their functions.

Introduction

Thank you for coming to this webinar. In this course, I am going to be talking about neuroplasticity. Specifically, I've selected a couple of specific updates or new findings that are happening in neuroplasticity, and I want to talk about what they might mean for us as SLPs. Then I want to discuss how we can incorporate those principles into our own practice, regardless of what setting we are in.  And as the title of this course suggests, I am going to focus on adults. This is not a session on how children develop their brains. 

What is Neuroplasticity?

Neuroplasticity simply refers to the ability of the brain to change. We used to only think about plasticity in response to injury.  But, I think it's pretty well known all around our public media now that the brain is constantly changing. So when we say neuroplasticity, that refers to normal development, it refers to what's happening in the brain of an infant or a child who's developing. It also refers to any time someone, child or adult, is learning something new. And it's also an umbrella term that includes what happens after an injury or during brain disease. So, all of those concepts are included in this big umbrella term of neuroplasticity.

What specifically do we mean when we're talking about neuroplasticity? I will boil this down into two simple categories for our purposes. One is structural changes, and that's all about when neurons change.  The other category is chemical changes, and that's all about neurotransmitters and all that is happening within the synapse. So, we will be looking at some examples of both structural and chemical changes.

Structural Brain Plasticity

Structural brain plasticity happens throughout the lifespan. It refers to neurogenesis which is when new neurons are created. It also refers to axonal sprouting and dendritic branching. Neurogenesis, or the birth of new neurons, is usually only associated with the developing child. In fact, maybe the developing embryo or fetus, before the child is born. But in more recent years, there is evidence that shows new neurons are created in the brains of adults as well.  

Neurogenesis. Most of the evidence seems to point to that neurogenesis happening in the hippocampus, which is associated with memory. If somebody has their hippocampus removed, that person is no longer able to lay down any new memories. The hippocampus does a lot, including consolidating new learning. For example, if we learn something during the day, when we sleep, the hippocampus is very active in consolidating that learning and connecting it to things we already know. When we say, "connecting it to things we already know," our experience is that those are somehow mental concepts. But we're talking about actual neurons and actual neurochemicals. Again, there is evidence that throughout adult life, new neurons are being formed in the hippocampal structure. And, this is one structural neuroplasticity form among adults. There is also some early evidence about the changes of neurogenesis and the hippocampus that might be associated with brain diseases in adults, like dementias.

Axonal Sprouting. In addition to forming all new neurons, one thing that can happen is that alive neurons can generate axons. They can make their axons longer, and they can sprout new ones so they can make many new connections.

Dendritic Branching. On the other end, neurons can also sprout new dendrites to make new connections. So we have both of those as possibilities, which are structural changes to the neuron during adulthood. You may already know this, but I want to remind you that if the cell body of the neuron dies, there will be no axonal sprouting or dendritic branching. That neuron is dead. That does happen in injuries and disease. And when that happens, various neurochemical processes and glial cells will take action and clear those dead neurons out, and a scar will form in the brain. So I don't want to be misleading.  But on the other hand, any neuron that is alive, even if its axon was cut or hurt a little bit, it can continue to sprout. Any neurons that weren't hurt can sprout connections.

In summary, when it comes to structural plasticity in adults, the headlines are that even adult humans seem to create new neurons, primarily in the hippocampus. All adults have the potential to make new connections through axons and dendrites, whether we're neurologically healthy, or whether the adult brain has been injured or has a disease.

The important piece to remember is that the brain changes in response to activity. We often think our brains are in charge of the show. But we change the brain anytime we change our activity, our habits, or we learn something new. This is critical. It seems almost simplistic to say it because it does seem like common knowledge in many ways. But it's important because the activities are what we do in therapy, and the activities have to be specific enough to support that brain change.

Mirror Neurons. Another new area of structural plasticity is mirror neurons. Mirror neurons are kind of newer on the scene and in the last 10 or 20 years, and they are a network of neurons that respond when you do something, and when you observe someone else doing something similar. Mirror neurons are fascinating and powerful. The idea of a mirror network, or mirror neurons, helps us to understand so much about how we learn and how important it is for us to use certain techniques that we use in speech-language pathology.

These mirror neurons can be motor or sensory, and they are distributed throughout the parietal and frontal cortices. What's fascinating about these is that if you are watching somebody do something, your mirror neurons activate, and can facilitate your ability to do that action as well. The mirror neuron network has been implicated in various conditions. The fact that we can see someone else, and we have a network of neurons that responds as though we were doing that is very important.

So, researchers have been looking into all the different ways that mirror neurons might contribute to learning, culture, etc. There is fascinating literature on mirror neurons. As an SLP, I can ask myself, "What could I do a little bit differently in my own practice to leverage the power of these mirror neurons?" Because mirror neurons play a big role in motor learning, we can apply this to anything we're doing in speech, swallowing, and recognizing the actions and intentions of others. For example, when we see somebody reaching for a cup, we recognize that as an intention to pick up the cup or to drink. So, researchers are looking into the mirror network to see if this plays a role in our empathy for others and our understanding of what other people are doing.

According to the research, mild cognitive impairment (MCI), or Alzheimer's dementia, seems to have a slow degeneration of the mirror network. Individuals can compensate for that in the early stages. The degeneration seems to go from posterior to anterior a bit. And, remember, it could be sensory or motor neurons. We can have that mirror network activating for how people might be feeling, like sensory feeling. Are they feeling pain? If you watch a movie and something terrible happens, can you "feel that in your gut?"  That is evidence of your mirror network working.

In ALS and Frontal Temporal Dementia (FTD), there is also documented involvement of the mirror network. Interestingly, in Parkinson's Disease, the mirror network involvement seems to be occurring much later. That's probably not too surprising because we know that any signs of dementia or cognitive decline in patients with Parkinson's usually occurs much later in the progression of the disease. So it seems to correspond with that thinking.

You may be wondering about autism. It seems natural to investigate mirror networks in the realm of autism. However, the evidence really doesn't have any suggestion that the mirror network is an obvious contributor to what we think of as autism spectrum behaviors. But stay tuned because who knows what new information will be coming out.

There is also an interesting paper, which is in your reference list, about the mirror network and stuttering. It addresses the impact of exposing people who stutter to stuttering or not stuttering and how that might relate to the mirror network. Again, we don't have any answers, but it's an interesting direction that some researchers have started looking.

Leveraging Mirror Neurons in Therapy. There are many ideas for leveraging mirror neurons in therapy. There are many specific techniques that we use in a variety of different treatment approaches that are probably leveraging the mirror network. Therefore, it's important to not just think about why those techniques will work. We also need to think about why certain strategies might not be working for individuals with some degeneration or disruption of the mirror network.  It is possible that we need to change our techniques and not be frustrated that the patient's not responding. There's probably a good reason for it, and therefore, we need to think of alternative ways to cue or support that patient.

Neurochemical Brain Plasticity

Moving on to the communication between neurons, which is neurochemical and happens in the synaptic space between the two neurons. It's that space between the axon of one neuron and the dendrite of another. In that synaptic space, numerous chemicals are released, modulated, received, and inhibited. It's an unbelievably complex chemical communication that is making the kinds of connections that we all have as humans. So, when we talk about plasticity that is reliant on neurochemistry, the main focus is neurotrophic factors. Neurotrophic simply means neural growth. These factors, or chemicals, help neurons grow.  In other words, they support axon and dendritic synaptogenesis.

Many different neurotrophic factors help neurons grow. They can spring into action when there's injury. They can also spring into action based on activity. Remember I said that the brain changes in response to activity? One of the most exciting areas in neuroplasticity is brain-derived neurotrophic factors (BDNF) which is one of many different chemicals that helps to grow neurons.

BDNF is normally stored in axons and dendrites and is released in response to activity.  It is released in response to activity. Additionally, it is the most abundant growth factor in the brain and is involved in long-term plasticity. Consider this scenario.  You learned to ride a bike when you were young, and you can still ride a bike. That's long-term plasticity. And what's exciting is that BDNF can be measured via blood levels. We can simply take blood serum levels and see if BDNF has increased in response to an activity.

There's a lot of evidence about BDNF, both from animal studies and human studies. With chronic stress, aging, and Alzheimer's dementia, there is a decrease in BDNF in the brain. In other words, there's less of this chemical that supports neuronal growth in those three conditions. On the other hand, antidepressants, exercise, and an enriched environment increase the presence of BDNF and supports neuronal growth. And neuronal growth refers to axonal sprouting and dendritic branching.

Let's look at a couple of specific examples.  The first example is a study in which the researchers were interested in knowing if BDNF increased in the blood of children who received cochlear implants. The sample was made up of some children who got cochlear implants and some children who continued using their hearing aids. They measured BDNF levels from a simple blood draw before and after six months of all of children. Results showed that there were significant increases in BDNF in the children who received the cochlear implants, which seems to support the idea that there is a lot of new brain changing going on in a child who gets a cochlear implant. Remember, BDNF is released in response to activity, and activity doesn't have to be movement. In this case, it was hearing.  

A second example is a bit more relevant to our practice with adults and it's based on the idea that there are two different genetic profiles associated with the genes that help express or produce BDNF in individuals. One genetic profile seems to produce more BDNF in response to activity than another one. So in this particular study, they were studying patients with swallowing disorders who were undergoing pharyngeal electrical stimulation. Some patients had a genetic variation that supported more BDNF, and some patients did not have that genetic variation.  

They were particularly interested in seeing if there was a differential response to the treatment based on this BDNF genetic profile. And there was. I bring this example forward because it's in our field. Still, there are many examples in other disciplines that look to see if these genetic profiles are predictive of responding to certain treatments versus others. So we don't have the answers yet, but I think this is where a lot of research will be happening. And looking into the future, it would be great if we could sort out which treatments are more likely to be effective with one patient versus another based on their BDNF response.

As SLPs, it's important to know that BDNF is released in response to activity, and specifically enriched environment. What is an enriched environment? I have a picture of a hamster cage in my mind. But the term 'enriched environments' comes from working with mice many years ago when experiments were conducted to see if mice who were given strokes or brain injuries did better in a cage by themself, in a cage with toys by themself, or in a cage with toys and other mice. Those were the early days of studying this.

Fortunately, research has progressed quite a bit from then. We now know that enriching the environment through cognitive activity, social connection, and physical activity increases BDNF.  That is important because the BDNF is the most likely neurochemical route to support those new connections in terms of the axons and dendrites making new connections in healthy brains and those with brain injuries and diseases.  

Many things about an enriched environment apply to our practice.  Where and how does the enriched environment occur?  The first is our specific therapeutic interventions with our clients.  But we're not with our clients for many hours during the week. The rest of that time is called ambient experience. McClung and colleagues did an extensive literature review and, from that, created a checklist of ambient factors that clients may or may not have in their favor (2010). 

• Depression
• Exercise/physical activity
• Active/inactive leisure life
• Communication Partners – Spouse
• Communication Partners – Family (family support)
• Communication Partner Attitudes
• Communication Partners – Friends (social network)
• Community support/communication access & accommodation

It's certainly within our scope of practice to screen for depression. We don't diagnose or treat it, but any allied health practitioners can screen for depression or make the appropriate referral. We also don't do direct exercise, but I will discuss physical activity shortly.  An active leisure life is also important.  . So hobbies. Then there are several communication factors that McClung and colleagues found when reviewing the literature on what supports recovery. It's all about communication partners, communication partner attitudes, and communication access and accommodation. So much of that is in our scope of practice.

Specific Therapeutic Interventions

Cognitive activity, physical activity, and social connection are the three main therapeutic interventions. Under the broad category of cognitive are all of our speech and language activities. This is not referring to cognitive goals or working specifically on attention or memory.  This is suggesting that anytime we're working on speech, language, communication, or cognition, those all fit under the broad umbrella of mental activity.  There are many cognitive activities that are subsumed in taks that we think of as very specific language or communication activities. 

But there is a caveat. The brain changes are specific to the task that's being practiced and brain connectivity is specific to task demands. So, we need to think carefully about the time we're spending in therapy and if it is specific to the tasks or activities the person will be doing when they are not in therapy. How specific can we make it because the brain changes in response to what is being practiced.

Let's look at a couple of concrete examples. The first one is picture naming. Usually, if we are working on picture naming with a client it's because we want to improve their naming abilities. That's one of the most common language impairments in neurogenics. However, if you are just taking a pile of cards and asking the person, "What is this a picture of," that is not a context that normally happens in real life.  That decontextualized practice is most likely not exploiting brain plasticity mechanisms as much as we could be exploiting them. Also, it's not as specific, so we shouldn't be surprised when it doesn't carry over. 

Some treatment types may address both cognitive activity and social connection. In addition to all of the wonderful communication partner training, there are many ways that we can connect the mental activity, and do it in a way that will facilitate social connection outside of therapy. And this is critical for us to think about because that will help our clients in the long term. Most of them will not get formal therapy or services in the long term.

One example is called activity-specific treatment. Some literature refers to it as contextualized treatment. Activity-specific treatment uses real-life activities, specifically those that will be used by the client after treatment discharge. You might be wondering, "Isn't that just functional treatment?" But it depends on what your functional treatment looks like.  Functional treatment can have a very broad application.  Some clinicians think that simply picking stimuli that are common to the patient's environment makes it functional.  But if the task is to have the patient name pictures that are put in front of them, that is not functional because no one will ask that client to name those pictures again outside of therapy. So, there is a difference between making a task functional versus making it contextualized.

Consider this example. Let's say we want the person to be able to order their own food. It doesn't have to be in a restaurant. It could be in a hospital or a skilled nursing facility. We could role-play with a printed-out menu from a restaurant they are going to. If they are in a skilled nursing facility, take them in the dining room with the menu or whatever is used in the facility, and practice it there.  The idea is to make it as contextualized as you possibly can.

Another example of a decontextualized task is having a client write the alphabet. That's not necessarily a bad idea, but it's not contextualized because no adult I know of ever needs to sit down and write the whole alphabet. What we do need to have them do is write specific words. If the goal is to print the person's name, have them write their name over and over again. Then that can be embedded into a real context, like signing birthday cards for grandkids, or notes, etc.

A third example of tasks that are decontextualized is following directions. Oftentimes, we discover, based on a test that we have given, that the client did poorly on the subtest of following directions. So, we give the person a list of directions that have no point and no context.  We need to contextualize that task by having the client follow directions in a recipe or directions that get from their room to the recreation room, for example. We want to have them do something that matters to them. When we contextualize treatment, it makes a big difference.

Evidence for Using Contextualized Treatment - TBI. The literature suggests that patients with TBI who received 30% more contextualized treatment during inpatient rehab were more likely to be out of the house 1-2 days per week after discharge.  That is a great outcome.  They also found that patients with more severe disabilities benefited more than those with mild impair. In other words, the more severe the disability, the more you need to contextualize. Sometimes we instinctually do the opposite thinking we have to lay down some domain-specific basics. But for patients with more severe impairments, the more you can get them to do things like being in the kitchen, working on an activity, playing cards, et cetera, the better.

Evidence for Using Contextualized Treatment - Stroke. Here's an example of stroke and aphasia. Activity-focused treatment, such as ordering items from a catalog, transfers over to ordering other things. So, people with aphasia who learned to order clothes were much better at ordering pizza or ordering for themselves in a restaurant. Additionally, they maintained those skills, and the reason for that maintenance was because these were things they actually did outside of therapy.

Work by Mary Boyle and others has shown that discourse treatment (i.e, working in conversation) results in an improvement in word retrieval assessments. In other words, if all I do is work in conversation, the person's picture-naming score will improve. There's a downstream transfer that is being observed.

Activity-focused treatment is also less dependent on cognitive abilities because you have as many cues and context as you can manage and that supports a range of other impairments. So it's important for us to be asking ourselves the question, "How can we support contextualized treatment?"

Ambient Experience

Remember ambient experience is also very important and helps recovery. It is what happens outside of treatment sessions and after discharge.

Ambient factors: A Role for SLP?

• Depression
• Exercise/physical activity
• Active/inactive leisure life
• Communication Partner Training
• Community support/communication access & accommodation
• Screening, referral, counseling, connection to social/support groups
• Requesting rides/finding info/co-treating with PT
• Focus on client’s interests from beginning
• Communication Partner Training
• Train other health care workers, community service people, others

Some of the ambient factors listed are the original list discussed previously and there are some additional ideas also listed.  How we can address ambient factors for recovering and facilitating neuroplasticity? I already mentioned screening for depression. For exercise and physical activity, even though that's not in our scope of practice, maybe you could co-treat with a physical therapist. If you work in an outpatient facility, maybe the client just needs to work on requesting a ride or scheduling an exercise class. Those are things that we can definitely do. Can we focus on the client's interests and hobbies? I've actually worked on building birdhouses so that patients can increase their leisure life. 

Then, of course, is communication partner training, as well as training other healthcare workers, community service people, and others on how to accommodate communication.

The very sad truth is that most of our adult clients with neurogenic communication disorders end up being discharged from therapy and sitting at home on the couch watching TV. And several studies have shown this. They lose their friends, they lose their social connections, and they lose their activities. They may lose their ability to be physically active in the ways that they were before, as well as their employment. So remember we're trying to enrich the environment with mental activity, physical activity, and social connection.

As SLPs, we have a lot in our toolbox that we can offer. All of these things will increase that BDNF and leverage the mirror neurons.  We have to keep asking ourselves, "What am I doing? What is happening this session that is going to contribute to ongoing neuroplasticity after discharge?" And it really boils down to social interaction, and being active mentally.

Summary

In summary, we talked about structural neuroplasticity and neurochemical plasticity.  We need to educate our clients about this topic. They need to know how to keep their brains healthy and what to do for their brains too. We need to educate our colleagues. So many say, "Whatever you get in the first six months, that's it." But that is not true. That's only true if the only important thing is a standardized aphasia battery score, which is not what's important to people in their actual life. If you're measuring things that are important to people in their actual life, they continue growing.

We need to have discussions, journal groups, etc. to help our colleagues modify what they tell clients. I come across clients all the time who are devastated by receiving comments like this. So we need to make sure that we're helping our colleagues talk about this in an evidence-based, and also a person-centered way. It is better to say, "Progress is usually its fastest in the first several months, but it can continue at a slower rate for years."

Questions and Answers

Would looking at actual genetics determine if a person has a greater capacity to produce BDNF?

There is a specific genetic test. But it's probably not the mail-order ones that we can all do. But, yes, that can be assessed.

Are there any medications that increase BDNF production?

The only category of medications that I know about are antidepressants, which are not being prescribed to increase BDNF. It's just that this has been observed. So I think we're a ways away from that, but I would stay on the lookout for that coming in the future.

In the example of naming cars, would you say these would be more effective than showing pictures of the client's car and family car, or if the person likes old cars show those and discuss, and label them?

I would say if at all possible, ask your client what they would prefer.  If the client has trouble communicating, have a couple of pictures of old cars, a couple of pictures of the client's car, and family cars. And you have a couple of piles. Ask them, "Which would you like to talk about today?" I think that's where you're going to leverage the most power.

Are there any resources for increasing contextualized treatment with AAC?

I don't know any off the top of my head. I think that is an area that's needed though. And I do think about these things because sometimes if we're working on AAC and we need to do something so people find the right buttons, or whatever it is that their response modality. But we need to, as quickly as possible,  embed that into the context where they're actually going to do it. For example, if we're building a sentence on an AAC device, we need to create a context where the person has something to talk about and can create a sentence.

Are there any studies on specific nutrition supplements that support BDNF?

People are talking about nutrition supplements, but there is no evidence for that at the moment.

Adults who have a disease can make new neurons?

It depends on what the disease is and this is also an area that we don't have comprehensive information. But they should be able to if that hippocampus is intact.

Can mirror neurons be activated by only watching, or does both watching and doing activate them?

Yes, by watching and doing activate them. So if you're doing something and someone is mimicking you, your mirror network is probably active as well.

I would like to know more about how mirror neurons relate to adult apraxia?

Mirror neurons are critical for mirroring things, which all the techniques for adult apraxia usually rely on postural or kinesthetic cues. There are so many different visual cues that we're trying to model in one way or another. So, I think that it's very active and I think the mirror network would be critical for the treatment of adult apraxia. We don't have enough information to know more specifically than that, but if you have a patient with mild cognitive impairment and adult apraxia, then you might need to know that the person may not be able to respond as well to those treatments. We don't have a lot of evidence for this yet. So, we're trying to take the evidence that we do have about neuroplasticity, and use our best guess for how to leverage this in our practice. But I do think it's really important to keep in mind and is also a great area to stay on top of.