Hot Topic: Neuroplasticity
Posted on: June 12, 2013 by Dennis Doyle, CAT(C), BAHSc, BComm
I was very fortunate to be present at the 30th International Osteopathic Symposium in Montreal last weekend, for the presentation on the topic of neuroplasticity by Dr. Michael M. Patterson, PhD.
Dr. Patterson is a prominent and internationally renowned osteopathic researcher, who previously worked in the spheres of experimental psychology and psychobiology. He has been a teacher in osteopathy since 1971, and has been engaged in neurological research since 1963. Dr. Patterson is has received a number of awards from the American Academy of Osteopathy for his contributions to osteopathic research, and is the author of over 160 publications.
In his presentation, titled “Neuroplasticity: from the synapse to the personality”, Dr. Patterson spoke about the adaptability of the brain and spinal cord. He talked about the potential of our nervous system to adapt in positive and negative ways, about how this affects our pain perception, and about what it means for members of the osteopathic community. I am pleased to share it!
- Dennis Doyle, CAT(C), BAHSc, BComm
May 31, 2013 presentation by Dr. Michael Patterson, PhD on the topic of neuroplasticity:
Good morning! What a wonderful day! It is just like Florida here, same temperature, same humidity. I want to talk to you a little bit about Neuroplasticity. First, though, I wanted to remind Jean-Pierre Barral of a symposium we attended together. This was in Europe in 2005 (photo). It was a wonderful time, it was held at a winery. And then, another picture. This symposium is honouring Viola Frymann. This picture was taken in Montreal in 2002 at the gala. The theme was obviously Harry Potter. It was also a good time.
What is neuroplasticity? It is the ability of the nervous system to alter its function through alterations in its structure. Now this alteration in structure can be at a molecular level, at a whole neuron level, or at a complete system level in the brain. Let’s start in the peripheral nervous system. In the peripheral nervous system, we see examples of neuroplasticity. When we have a wound, damage to the skin for example, various things are released from the damaged tissue. They cause the nociceptors, the pain receptors, to become active and send signals into the spinal cord. These nerve impulses travel in, but they also travel back out at the branches to other nociceptors. And that causes these nociceptors to become sensitized. That’s why when you have a cut on your finger and you wait a little while and you tap it, it hurts. Usually that increased sensitization of the nociceptors goes away after a little while. But it can be long-lasting and lead to permanent changes in those nociceptors. But let’s leave the peripheral nervous system and go into the spinal cord. There are a series of neuroplastic changes that occur in the spinal cord with sensory input. The first are habituation and sensitization. And then, a longer term change is long-term sensitization, then fixation, then cell death and neural sprouting. Most of these changes occur in the dorsal horn of the spinal cord.
Sensitization and habituation, what are they? Well, habituation (we all experience it) is the lessening of input with repeated stimulation. And sensitization is exactly the opposite, with repeated inputs, the neural activity increases. These changes occur pretty rapidly. They should occur within a few seconds of repeated inputs, and they happen within the spinal cord. What happens is, as repeated inputs occur, either there is less neurotransmitter release with each successive input, or there is more neurotransmitter release with each successive input. In the case of habituation, the interneurons lose their excitability, and so less information is transmitted into the pathways going into the brain. Each of you is now experiencing habituation. I want you to think about the feeling of the clothes on your back. Before I said that, how many of you were feeling the clothes on your back? How many of you are feeling them now? That is a process of habituation. It stops input from overwhelming us. Sensitization on the other hand, is the opposite process, where sudden inputs or repeated high level inputs cause more neurotransmitter to be released and hence more information going into the central nervous system. I’ll give you an example of that: “BAM!” You’re all sensitized.
I began with my post-doctoral mentor, studying these processes in the late 1960’s, and this is sensitization: in a spinalized animal, with no information coming down from the brain, repeated noxious stimulation, ankle stimulation, caused the interneurons to increase their firing rate, sometimes two or three times their initial firing rate. And as long as the stimulation continues, the interneuron firing rate remains high. Once the input is stopped, the excitability of those neurons in the spinal cord decreases pretty rapidly. So this is basically a temporary process. But there is another process that begins to occur when there is this repeated noxious stimulation. This is called long-term sensitization. This occurs when you have a stimulation going on for several minutes. Once you put the input in for several minutes, and stop it, the excitability does not go back to baseline. It will drop, but it will stay above its original baseline for hours, and this is a different process. It is a cellular process in the interneurons that changes the excitability of the membranes receiving neurotransmitter. The next process is fixation. This was first described in 1939 by an Italian researcher. She found that if she made a lesion in the cerebellum of a dog, the hind limbs would draw up in a flexed position. If she let the dogs remain like that for three or four hours and then transected the spinal cord, the hind limb would remain flexed. Now, you see, when you transect the spinal cord, you cut off the descending influence from the injured cerebellum. So what has happened is, the interneurons in the spinal cord have become so hyper-excitable that they fire by themselves. And that causes the limb to remain in a flexed position. Not many people believe that this really happened, because when you transect the spinal cord, you should get a flaccid paralysis.
This phenomenon was worked on by a couple of people over the years, and I began working on it in 1979. A graduate student of mine and I looked at the data, and constructed a study to show, we thought, that it really wouldn’t happen. We used a rat model, because rats are a lot less expensive than dogs, making a lesion in the cerebellum, and then waiting awhile, then sectioning the spinal cord and measuring the amount of tension generated in the hind limb. We published our first paper in 1981. We found that in these rats, the lesion in the cerebellum would cause about 20 to 25 grams of force in the hind limb. If we waited only 20 minutes before we cut the spinal cord, essentially the limb dropped to a flaccid paralysis. If we waited only 45 minutes and then cut the cord, the limb remained with a high degree of tension. Very simple study, but it showed the effect. I spent the next 20 years working on this fixation effect, and showed that it was indeed happening within the spinal cord, and we could produce it within spinalized animals, that is, with their cord already transected, by stimulating the skin of the hind limb. Not only that, but with a very high level of stimulation, we could show the effect within 15-20 minutes. So this was a neuroplasticity that occurred pretty rapidly.
Others working on this kind of phenomenon have shown that the effect is caused by gene changes within the cells of the spinal cord; that there is an upregulation of certain genes within the nerve cell that cause more receptors to be put in the cell membrane. Thus the cells become much more sensitive to any neurotransmitter that is in the area. This effect, by the way, can last for weeks, so it is a really long-term change. There is another phenomenon that we know of in the spinal cord called sprouting. When certain events happen, stimulation and so on, we can have actual shoots coming up from neurons in one level of the cord coming up and making synapses onto the cells in other levels of the cord. This primarily happens when cells in areas of the cord that receive mechanostimulation, that is stimulation from stroking or movement sprout up into the level of the cells that receive pain input. When this happens, you begin to get crosstalk between mechanoreceptor pathways and the pain pathways going up to the brain. Then, when the patient moves, he feels not only the mechanical movement but also pain. This may be a permanent change in neuroplasticity.
There is another thing that happens in the spinal cord, actually two. One is classical conditioning in the spinal cord. Classical conditioning is when you pair, put together two stimuli, one that causes essentially no reaction in the organism, and the other that causes a definite reaction in the organism. Pavlov invented classical conditioning, and he would sound a bell and then put food powder in a dog’s mouth. The bell wouldn’t cause any reaction in the mouth, but the food powder would cause the dog to salivate. After awhile, when you pair the bell with the food powder, the bell begins to elicit salivation. This is a very primitive form of learning. Well, a number of people before I started looking at it had tried to show that this process occurred in the spinal cord. In 1970, I began with my mentor, looking at spinal conditioning. In cats, we had a small stimulus to the paw, followed very quickly by a strong stimulus. The strong stimulus elicited a reflex response, and these were in spinalized cats where the spinal cord is cut. In 1973, we published this paper. It shows the rapid increase in response to the small stimulus when it is paired with the large stimulus. When you present the same two stimuli, but not together, you get no such increase. When you present just the small stimulus, you also get no increase. Well, that shows learning in the spinal cord, a definite neuroplasticity.
Another way of doing that is instrumental conditioning. In instrumental conditioning, you shock the paw whenever it comes down to a certain level, using an electrode that contacts the water. When the paw gets shocked, it goes back up. Pretty soon, the spinalized animal learns to hold the paw up; another example of neuroplasticity of learning in the spinal cord. So, in the spinal cord itself, we can have simple and fairly complex neuroplastic changes. But really, the question that we should ask is, can the brain be altered? Traditional thought is that no, the brain cannot be altered, it is hard-wired. While we can certainly learn things, a form of neuroplasticity, the basic function of the brain is not changeable. I want to talk about the pioneers in this area, and if you want to read some good literature on these areas, “The Telltale Brain” is a wonderful book. Ramachandran, who wrote it, is one of the pioneers I’m going to talk about. Another one is “The Brain that Changes Itself”. The third book “The Mind and the Brain” is by Schwarz and Begley.
The first real pioneer that started this whole area of neuroplasticity was Edward Taub. In experiments with monkeys, he showed that by cutting the nerves from the arm of the monkey, so you take away the sensory input, the sensory cortex would undergo changes. So he really began the process of changing our thinking about how the brain functions. Another pioneer I’m going to talk about is Paul Bach-y-Rita. He was an MD, PhD. Early in his career, his father had a bad stroke. He was paralyzed; he couldn’t talk, and had all kinds of other problems. Bach-y-Rita gave him intense rehabilitation over years, and he regained practically all of his function. When he died, the autopsy showed that there was tremendous permanent damage to various areas of his brain. But the rehabilitation process had allowed other areas of the brain to take over the necessary functions and allowed him to be practically normal.
One of the most interesting cases that Bach-y-Rita did was the “wobbler” case. A patient named Cheryl had an infection and was given the drug gentamicin for a long time. This drug destroyed her vestibular system. She couldn’t stand up without holding onto things, she was dizzy, depressed, and it was permanent. The vestibular system, after all, is what gives us our orientation in space. Bach-y-Rita made a helmet that she put on her head, and it had an accelerometer in it. The accelerometer gave information about the position of the head. That was connected to a computer that was connected to a little plate that Bach-y-Rita had her put on her tongue. The plate had little electrodes that stimulated the various areas of her tongue. When her head was upright and still, the middle of her tongue was stimulated. When her head tilted to one side, the stimulation moved to that side of her tongue. This is the information basically that is supplied by the vestibular system. Almost immediately, she could stand up without wobbling. After wearing the helmet for a few minutes, she took it off, and she could still stand up straight for about a minute and a half. Over many sessions of wearing this helmet, the stimulation of her tongue and then taking it off, she was able to maintain the upright position steadily for hours without the helmet. They finally did away with the helmet and put the accelerometer on the tongue plate. Then people could wear this little computer and the wobbling went away.
Bach-y-Rita did the same thing with blind people. Basically he built that plate for the tongue and had a camera that was mounted on glasses. Now you see the plate, with the electrodes, stimulates the tongue with a picture of what the camera sees, and the people don’t anymore sense the stimulation on the tongue, they “see” things in front of them. Brain scans show that when the tongue was stimulated in this way, the visual cortex was activated, and the people could walk along a line, they could reach out and grab things and so on. They saw. Bach-y-Rita called this “sensory substitution”, and he realized the tongue was an ideal portal into the nervous system. Either vestibular, vision, or other senses could be substituted with tongue stimulation. There is a blind person with the tongue sensor (photo).
The next person is Ramachandran, who wrote one of the books that I mentioned. Ramachandran worked a lot with various disease entities, but he also worked with amputees. He realized that when you have an amputation, the sensory input from that amputated limb no longer exists. Now, in the brain, in both the sensory and motor areas, the body is mapped out on the sensory cortex. Note here (picture of sensory homunculus) the hand area is right next to the face. In an amputation situation, there is practically always a phantom limb. The person “feels” that limb. That isn’t too bad, but sometimes the limb that’s amputated develops pain. How do you treat that? Well, there were various types of treatments, successive amputations, and drugs, nothing worked. Go back to the diagram, and again note the face and the hand. This gentleman (photo) had an amputated forearm, and he developed a phantom on his face, of his hand. When this part of his face was touched, he felt in the amputated hand that the thumb was being touched. Ramachandran hypothesized that neurons from the face area grew into the hand area, because it wasn’t being used. So he hypothesized that phantom limb pain develops because the brain is mapping the amputated hand onto a body image. Well, in looking at that, he decided that perhaps he could fool the brain and get rid of that phantom. He developed the mirror box. The box has a mirror, and you see there is the stump (photo), but you put your other hand in, and the patient sees the mirror image of that hand as though it was his amputated hand. That fools the brain into thinking there is a hand, because you see it move when you move the other hand. It appears that the pain then goes away. Again, Ramachandran’s hypothesis is that because consciousness is always behind reality, because it takes about 1/16th of a second to process sensory information, the brain projects things onto a body image, not onto the actual body. By fooling the brain in the mirror box, the brain alters that image. The brain, then, believes that it has the hand.
The last pioneer I want to talk about is Pasqual- Leone. He’s a fairly young guy, born in 1961. He had subjects practice playing the piano, and he did brain scans of the sensory and motor cortices. He found that with practice, the amount of cortex devoted to the fingers increased. But more startlingly, he had subjects just think about playing the piano, and they had the same increases in cortex devoted to the fingers. Again, remember the cortical maps. He found that the key ingredient for having that change in cortical area was paying attention to the task, whether you were doing it or thinking about it. So the human brain can be altered. Well, he found a school where blind people were taught by sighted teachers. The teachers, in order to experience what the blind people experienced, had blindfolds put on for five days. These were very good blindfolds, no visual information coming in. What he found with these teachers was that over that time, the visual cortex began processing tactile and auditory information. So the visual cortex, you see, can process all sorts of information, not just visual input. With humans, the visual sense is so overwhelmingly powerful, that other information is not processed in the visual cortex unless it is not receiving visual information.
How did these changes occur? We don’t know for sure. But what Pasqual- Leone has found is that the changes start, and if the blindfold is taken off, they go away. But, each time the blindfold is put on and the changes occur again, they become more permanent. So it is sort of like spinal fixation. There are a couple of ways that this could occur. One is that there are pathways that are not generally used, but if you force their use, they become powerful enough to transfer information to another area of the brain. Another possibility, of course, is that we build new pathways. But some of these changes occur so rapidly that there is no way the sprouting could occur in that time. But again, with repeated trials, certainly the effect increases. So really, the changes in cortical processing power are sort of like short and long-term memory. The actual picture of our brains is that our brain processing is very plastic. It is undergoing changes all the time that we are not aware of, and our cortex is not made up of completely hard-wired and unchangeable processing centers. Our cortex is made up of sets of operational processors that can process any kind of information.
What does this mean for osteopathy? Well our sense of touch is really an overlooked sense in science, but it is very important in many functions and physiological processes in our bodies. When you palpate, you are receiving information from your patient. I think what we are seeing with this neuroplasticity of brain function suggests that your students should mentally practice palpation and the moves for manipulation. After all, they can do that at home, alone. The more they do it, the more they will be in touch with that information and processing it better in all kinds of areas of the brain. Interestingly enough, a rather radical suggestion, would be to teach students palpation blindfolded so that they begin to route this tactile information to more areas of the brain and increase the processing power.
Our brains change, but I don’t! Thank you very much.