Neuroplasticity and Healing: A Clinical Conversation with Norman Doidge,MD,and Robert Rountree,MD

Norman Doidge, MD, studied classics and philosophy at the University of Toronto, in Ontario, Canada, before receiving his medical degree. He then completed his psychiatric and psychoanalytic training at the Columbia University's department of psychiatry in New York City, followed by 2 years of training as a Columbia–National Institute of Mental Health research fellow and a subsequent year as a clinical fellow in psychiatry. Dr. Doidge has received numerous awards for his clinical and scientific writing and research. He is a psychiatrist and psychoanalyst in the department of psychiatry at the University of Toronto, and on the research faculty of Columbia University's Center for Psychoanalytic Training and Research in New York City.

Robert Rountree: You have written two books, The Brain That Changes Itself and The Brain's Way of Healing . ^1,2 The first book sold over a million copies. You had a parallel track as a writer and a poet, and you are trained as a physician. What inspired you to move along this path?

Norman Doidge: Multiple pathways got me interested in neuroplasticity. At a very practical level, near the beginning of my career, I ran the assessment clinic at the Clarke Institute of Psychiatry, at the edge of the University of Toronto. I found I was seeing depressed people who were having a kind of “crash-and-burn” as they entered the university, and even professors who could not keep up with “publish or perish” demands. I soon realized that a number of these patients actually had adult versions of the same learning disorders, which had only been described in detail in children. When I started looking at the literature, it almost universally claimed that these disabilities were hardwired and that nothing could be done to change them.

Because the disability was “hardwired,” the treatments were called “compensations,” and were designed to work around the damaged circuitry, since there was no way to fix it. The main metaphor for the brain was that it was like an electrical machine with parts, and each part performed a single mental function in a single location in the brain. I was originally a philosophy student, accustomed to examine the premises of arguments, and it was difficult for me to accept this, when I first arrived in medicine, because the brain, of course, is animate, and it grows and it changes.

I knew this machine metaphor began with the philosopher Descartes, impressed as he was with the machines of his day. For the last 400 years, scientists have kept updating the metaphor. The brain is so complex that we reach for metaphors, instead of describing what we know of it in its own terms. So, Descartes described it as a kind of hydraulic mechanism. The nerves were vessels, and they had a fluid current flowing up and down them. With the invention of electrical machines, the brain was described as something with hardwired circuits. With the invention of computers, the brain was described as a biologic computer, and our thoughts were likened to software, with the brain being like hardware.

In all of these metaphors, if there was damage, nothing could be done because machines do many glorious things, but they do not grow new parts. They do not reorganize themselves.

Once I had patients who were dependent upon me, I threw myself into studying the brain and the neuroscience of this so-called hardwiring. I started to be bothered by things that other people were not bothered about. For example, at the Clarke Institute, when patients with psychiatric disorders did not get better, I would hear some colleagues describing their problems as hardwired. The problem was that sometimes patients with very similar conditions would get better, and then hardwiring was not mentioned. I began to realize that “hardwiring” was being used as a metaphor of convenience. As someone who had a background in poetry, I had a nose for metaphors; and, as someone who took philosophy seriously, I knew that metaphors could sometimes conceal as much as they reveal.

I did my training in the department of psychiatry at Columbia University, in part because it was influenced by the presence of Eric Kandel, MD, who was originally a psychiatrist interested in psychoanalysis. Dr. Kandel was a Jew who, as a child, escaped from Vienna—Freud's Vienna—just after the Nazis invaded, and came to America. He wanted to become a psychiatrist and psychoanalyst. However, a few of the analysts who taught him suggested that he had a special gift for experimentation. They said psychotherapy works by learning but that we knew too little about how learning occurs in the brain. Dr. Kandel took up the challenge, and won the Nobel Prize in 2000 for showing that, as animals learned, they changed the number of connections between their neurons. I knew that the psychoanalytic connection to this finding was not insignificant for Kandel. In the late 1800s, Freud had speculated that when we learn new things we change the connections between our brain cells. He called this, “the law of association by simultaneity.” He said that, when two events occur simultaneously, the connections between the neurons in the circuit that are processing these two events become linked more strongly. Dr. Kandel, in fact, picked up on Freud's hypothesis and demonstrated that it was true. (Few people know that Freud was originally a serious neuroscientist before becoming a clinician.)

Given my background, I had philosophical, biologic, psychoanalytic, and clinical reasons for being interested in plasticity. Clinically, the patients with learning problems were often having a very rough time. Someone with an auditory-processing problem who had trouble taking notes in class would be told to bring a tape recorder to class, then spend hours listening to the tape after the lesson, transcribing at a snail's pace. The idea was, because the brain can't change, that person needed to develop a “compensation,” or a way to work around the problem. However, compensation is often cumbersome and exhausting.

Then a breakthrough occurred, as I was searching for better approaches for addressing learning disorders. I heard of the Arrowsmith School—in Toronto, Ontario, Canada—a place that used brain exercises, which were the opposite of compensations, for people with learning disorders. Many people doubted this was possible. However, I immersed myself there, and saw young people who had been up to seven years behind in reading and who, within a year or two, were able to catch up to their peers, and overcame their learning disorders by exercising the weakened areas. This meant that their learning was now actually proceeding much more quickly than their peers. All of these findings and hypotheses pointed toward plasticity, which I define as the property of the brain that allows it to change its structure and function in response to activity and mental experience.

After that, I threw myself into the study of plasticity, to see how far it could go. Could it ultimately affect other psychiatric problems? What about neurologic conditions? The book, The Brain That Changes Itself, ¹ tried to establish that neuroplasticity—a discovery largely made in the laboratories of neuroscientists—had major clinical and cultural implications. I described how it related to obsessive compulsive disorder, a condition in which, through repetition, the brain actually strengthens problematic circuits; how it can be used to help some people recover from stroke and sensory problems; neuroplasticity's role in love, sex, and romance; how the media affects us; how a girl born with half a brain was able learn language although she is missing her left hemisphere; and so on. ¹ This was a case where one hemisphere took over from another. In The Brain's Way of Healing, I was trying to show how this neuroplastic healing occurs. ²

I was able to do this because after The Brain That Changes Itself ¹ was published, I began to correspond with many people, and travel, all over the world, to look at the latest neuroplastic interventions, and I started to notice patterns that had not been described before. I summarized these in what I call the five stages of neuroplastic healing. I also showed these approaches could already help some people with Parkinson's disease [PD], traumatic brain injury [TBI], chronic pain, multiple sclerosis [MS], many kinds of learning disorders, and even some cases of autism.

The first stage of this healing is no surprise to people with an interest in complimentary medicine, because it requires attending to the general cellular health of the neurons and glia. However, neuroscience can now add to that knowledge. For instance, we now know that mental and physical activities trigger brain growth factors. One, BDNF—or brain-derived neurotrophic factor—consolidates the connections between neurons. Another, GDNF—or glia-derived neurotrophic factor—strengthens the cells in the brain, known as the glia. The glia comprise ∼85% of cells in the brain, they support the metabolic functioning of the neurons, and are also involved in communication. Some kinds of brain exercises and various kinds of physical activity both strengthen brain connections and create a healthier cellular environment in the brain. Four stages involve changing the so-called “wiring” in the brain.

Dr. Rountree: Please describe neuroplasticity. Is it more than just making new synaptic connections or growing new dendrites?

Dr. Doidge: Yes, neuroplasticity goes beyond synaptic connections or dendritic growth. Neuroplasticity occurs at many different levels in the brain. For instance, when an animal is trained to make an association between two events, or form a memory, the animal's brain indeed forms new synaptic connections, but there are also changes going on at the DNA level, turning certain genes on and others off to make new proteins, and so on. So plastic change can occur at a DNA level, a molecular level, and a protein level. Change can occur as you say, in the connections between the neurons, that is, synaptic plasticity. However, it can also occur in the myelin, and in the glia, and can also lead to changes within and between large sections of the brain. For instance, as one ages and a certain brain area atrophies, a person can perform the cognitive function that was processed by that area in another brain location. Thus, plasticity can be detected and described all the way up from a micromolecular level to a macro level, and then there is behavioral plasticity. Behavioral plasticity is the product of neuroplasticity.

Dr. Rountree: Are all neurons capable of plasticity?

Dr. Doidge: Yes, that is the way they work, by changing. Neuroplasticity is the modus operandi, or the norm, in the brain. In fact, neuroplasticity is so omnipresent that even many of the things we do not like about ourselves—that we find rigid in ourselves—are also products of our plasticity. For instance, if someone develops a bad habit that is repeated over and over again, we would say that is a behaviorally rigid outcome. However, the reason that the habit is hard to break is because every time it is repeated, the plastic brain makes the circuitry underlying that habit even stronger. So our behavioral rigidity is actually a function of our neuroplasticity. I call this the plastic paradox. We can compare plasticity to snow on a hill in winter. If we decide to ski down a hill when the snow is fresh, we can take many different paths down that hill, because the snow is pliable and plastic. If we had a very good run down that first path, we might try a path very close to that the second and third time. Over time, we start to develop tracks in the snow. Eventually those tracks can get very deep and become like ruts.

Many of our bad habits—and even certain chronic pain syndromes, some psychiatric symptoms, such as obsessions and compulsions, and many of the movement problems that people with strokes, dystonias, or PD have—are actually a function of neuroplasticity going awry. Understanding that plasticity is going awry in these conditions has allowed us to develop new treatments and approaches.

Dr. Rountree: How does this compare with imprinting? Is imprinting neuroplasticity that has gone awry?

Dr. Doidge: Actually, imprinting is neuroplasticity doing its thing well. One of the things we discovered fairly early on is that, during development, there are periods of heightened plasticity and growth. Ultimately, they came to be called “critical periods.”

In neuroplastic terms, a critical period is merely a period of heightened plasticity for a particular brain function, and therefore the experiences during those times are especially formative. Experts in ethology and psychology describe these in different ways, such as developmental windows or periods for imprinting, attachment, or bonding. These are terms for the period of time when the attachment system in animals is especially plastic. Freud showed periods of increased plasticity or formative periods, in childhood, as did Bowlby; Lorenz did it for ethology.

That work is 50–100 years old. It seemed that our early experiences sealed our fate, insofar as they determined brain structure. However, now we know, that as “formative” as they are, the brain circuits they form can be somewhat modified later in life. We are not necessarily stuck with the habits or feelings or attachments or brain structures we originally developed. So even imprinting can be modified to some degree. In the end, that is exactly what a good psychotherapist or a good rehabilitation therapist does: helps facilitate that change. We basically understand that the behavioral rigidities that we are seeing do not necessarily mean that the underlying brain is not plastic.

We are often deceived about this, because plasticity is competitive. For example, if someone learns to pronounce the letter R or L as an English speaker in childhood, that person develops circuits that make that distinction. It is repeated hundreds of thousands of times, and the trained circuits fire faster, stronger, and clearer signals. Chinese-speakers, however, do not make that distinction in the same way English-speakers do. When Chinese people try to pronounce the English R or L, they fire up their Chinese circuitry, which is their strong circuitry, for those sounds, and they mispronounce them. It is very, very hard not to make the same elocution error over and over again, because the circuits for the Chinese way of pronouncing those sounds have a competitive advantage in the brain.

Now, does that mean the brain is not plastic? No. It just means that plasticity has given a competitive advantage to a particular way of doing something. We now know that there are various techniques of blocking those circuits to allow for the development of the proper way of pronouncing those sounds. We can also get over that problem by using plasticity in another brain region. This kind of approach also works in stroke. After a stroke, people neglect their stroke-affected hand, and increasingly compensate by using their “good” hand. However, we have “use-it-or-lose-it” brains, and any chance of recovery of the weakened area is stifled. The trick is to put the good hand in a sling or cast so it cannot be used, and then incrementally train the stroke-affected hand.

Dr. Rountree: Given your feelings about the ability of people to change via neuroplasticity, you seem like a very optimistic person. Do you focus on this optimism in your practice?

Dr. Doidge: That is a common response to my work, so I must credit it to a degree, but I don't like “isms”; they, like ideologies, can give rise to fixed attitudes or moods, and lock a person in. Thinking and empathizing are about responding in real time. I deal with a lot of tragedy—people with brain problems, injuries, and diseases. This is not a happy-go-lucky space in which to dwell. However, in the midst of the despair, I do focus on what might be done. Good therapists have always been interested in reality, which includes both strengths and weaknesses, and that means never losing site of either a patient's strengths or deficits. However, I would say, having studied plasticity, I've become much more aware of hidden strengths.

People often see my views on neuroplasticity and the ability to change as being hopeful or optimistic because they replace a previous pessimistic view that the machine metaphor gave rise to, what I call neurologic nihilism—another “ism” I oppose. This is the insistence by clinicians that, when there is a brain problem, there is nothing that can be done because the brain is a machine, and the machine is broken, and, once broken, machines cannot fix themselves. Books have been written with titles like “the broken brain.” I do not attack neurologic nihilism because of a characterologic optimism; I attack it because this nihilism is simplistic and often wrong. However, the alternative to neurologic nihilism is not some kind of childlike neurologic utopianism. That's an “ism” too. As I say, we are dealing with heavy-duty, often catastrophic conditions, such as PD, MS, chronic pain syndromes, stroke, TBI, learning disorders, and autism. When I see a new patient, I never say, “this will help you,” because every patient and every injury is different. I explain my understanding of what I think is happening in that patient's brain, and, if I know of a new approach, I explain how we believe it works, and I might say, “perhaps this is worth a try.”

Dr. Rountree: Were there any surprises in your work on The Brain's Way of Healing ? ²

Dr. Doidge: As I was writing The Brain's Way of Healing, ² I discovered the importance of energy and its influence on mental activity in brain healing. For example, energy, in various forms, including sound, can help sculpt the brain.

In medical school, we were taught that, if a person lost 90% of the use of his or her right arm, that meant that 90% of the motor cortex, or the sensory motor cortex, or the nerve tracts from those areas must have been damaged. People and textbooks—though we probably knew better—often spoke as though the neurons were digital—on or off—and, if damaged, they were off. Spikes fire or they don't. However, in reality neurons are only completely off and not firing when they are dead. When they are not dead, but in the so-called “off position,” they have a basal firing rate. Then, in the “on position,” the rate is different—either faster (usually) or sometimes slower. After looking at quantitative electroencephalography [EEG] data, reviewing the literature, and seeing people getting better in various new ways, I realized that something else was often occurring when there is a 90% loss of function. For example, let us say someone has a stroke in a certain area of the brain. Some of the cells are indeed dead and firing no signals; but other cells close by are sick and are firing irregular signals. If these irregular signals are picked up by healthy cells, the healthy cells are now getting “junk data” in and will send junk data out, but, thank goodness, there might be some other healthy cells that are not getting junk data in.

In a number of diseases and injuries, a patient ends up with what I call a “noisy brain.” The noisy circuitry functions poorly or not at all. Now, one of the laws of plasticity is that it is a use-it-or-lose-it brain, and when something is not functioning, those circuits go dormant. So, there is a lot of what I would call idling or dormant functioning in many noisy brain conditions. The noisy or poorly synchronized brain has now been shown to be an element of certain kinds of stroke, TBI, autism, learning disorders, and even PD. However, the good news is that if a clinician uses some of the approaches I describe to resynchronize a noisy brain, sometimes someone who has lost, say, 90% of a function, might find that he or she can make radical improvements. So, I no longer automatically accept that a 90% loss of function always means 90% cell damage. That is only true sometimes.

Dr. Rountree: Is this irregular firing a genetic or epigenetic phenomenon?

Dr. Doidge: It can be caused by faulty genetics, or, much more commonly, by experience, caused by a disease or injury. Either way, I think that it is the product of some kind of damage—often cellular damage—to certain brain areas. Also, the areas around the damaged cells might not be totally damaged, but rather partially injured, or “sick,” or have poor oxygen or blood supply or waste disposal. (With respect to stroke we talk about an ischemic penumbra outside the core ischemic zone.) Sometimes, there are genetic risk factors that affect how people are “wired up,” but sometimes, the problem is caused by trauma or disease, such as infection or excessive inflammation. Whatever the cause, this situation can result in death in some networks of the brain. However, if a neuron is merely sick, it still may be firing, but at an irregular or incorrect rate, and this turns out to be a huge problem, but also presents a huge opportunity if it is understood. A number of the interventions I described use patterns of light or sound or electrical energy, delivered noninvasively, often through the senses, to modulate the brain and resynchronize it so it fires properly. Then one can achieve some stunningly fast reversals of problems that have been disabling a patient for years. I described these avenues to the brain in The Brain's Way of Healing. ²

Dr. Rountree: Do you discuss transcranial magnetic stimulation in your books?

Dr. Doidge: I talked about transcranial magnetic stimulation in The Brain That Changes Itself. ¹ In The Brain's Way of Healing, ² my focus was on what I call the five stages of neuroplastic healing that I see the different neuroplastic approaches addressing.

Dr. Rountree: And they are?

Dr. Doidge: As I said, first we must often attend to general cellular and neuronal health; second, we may require neurostimulation to activate dormant or undeveloped circuitry; third is neuromodulation, which involves using patterns of energy to stimulate the existing “reset buttons” in a desynchronized or noisy brain; and fourth is neurorelaxation, a stage that often occurs spontaneously after neuromodulation occurs, allowing the brain to gather energy for the final stage, which I call neurodifferentiation, in which the brain maps form or reform very fine distinctions. This is necessary, because after brain damage or illness, brain maps lose their fine detail and, fortunately, we can restore that fine detail with various kinds of brain exercises or stimulation. Transcranial magnetic stimulation involves boosting or neurostimulating certain areas of the brain that have gone relatively dormant.

An intervention that often requires multiple stages of neuroplastic healing is autism. In my second book, ² I described a few cases of people with autism who made radical improvements. Many people—such as naturopaths and nutritionists, and clinicians who practice functional medicine—have paid attention to the fact that diet can sometimes help diminish autistic symptoms. This involves attending to stage one, general cellular health.

We have learned in recent years in neuroscience something that confirms observations that parents have been making for decades, which is that there is an immense amount of inflammation in many autistic children, and that autism is not simply a brain disease. It is, as Martha Herbert puts it, a whole-body disease, which, therefore, also affects the brain. From autopsies, we know that the brains of most autistic children are highly inflamed, and we see the same thing in animal models. We also know from studies that such children often have specific neuronal antibodies attacking their brains. It is very hard for a brain to “wire up” properly when it is highly inflamed. From scans and quantitative EEGs, we also know that the brains of autistic children are overconnected in certain areas and underconnected in others, an example of the poorly connected brain and the noisy brain. Finally, another thing that truly stands out in the majority of autistic children is hypersensitivity to sounds. For the longest time, this was thought to be one of many symptoms that autistic children suffer from but not necessarily an especially important symptom. However, one will often see autistic children covering their ears and screaming, as they are deeply, deeply tormented by sounds.

It turned out that one of the things that is happening in such children is the following: All human beings have the auditory equivalent of a “zoom lens,” if you will, in the ear. This auditory zoom involves the bones and muscles in the ear that allow us to tune in on particular sound frequencies, so that when a person goes into a party, first it is booming, buzzing confusion, and then the person can focus in on one conversation about love and another one about sports and another one about religion, and so on.

Now, this auditory zoom is compromised in autistic children who have sound hypersensitivities. What they are experiencing are deeply disturbing sounds that they cannot regulate. Recently, Temple Grandin, PhD, at Colorado State University, has emphasized the role of these sound sensitivities in autism. There are different theories as to why these sounds that autistic children are hearing are very disturbing. One of them comes from Stephen Porges, PhD, at the University of North Carolina in Chapel Hill. Most animals have predators and the sounds that predators make are deeply disturbing to them. A lot of the sounds that disturb humans are very low rumbles such as our predators made. These are the sounds that filmmakers put on the audio track when the monster or the alien spaceship is approaching. These sounds are used to deliberately provoke our fight-or-flight reactions.

Once in the flight-or-fight reaction, the brain turns certain circuits on and other circuits off. Dr. Porges has shown that we cannot really relate to other people when we are in that survival mode. We have trouble regulating our auditory zooms, trouble controlling the cranial nerves that have to do with speech and hearing and facial expressions, and we go into an interpersonal shutdown. It is only when the parasympathetic system is turned on that we can actually activate what Dr. Porges calls the Social Engagement System, which allows us to look at other people, hear higher human speech frequencies, and activate the muscles of facial expression.

In The Brain's Way of Healing, ² I described new interventions for severely autistic children. These children may be very disabled and raging and not making a connection with their parents. These children are deeply distressed by sounds and practice stereotypic actions, such as “stimming” and so on. One can use modified sound, which grew out of the work of Alfred Tomatis, to train the auditory zoom in these children. It turns out that modified Mozart is very good for this, if it is especially gated and filtered to alternate between higher and lower frequencies (in a way tailored to each child). After a few days of this, we often start to hear stories from parents saying that their children are no longer covering their ears, or that they hugged their parents for the first time, or had restored sleep.

These interventions are examples of both neurostimulation and neuromodulation of the circuitry that has gone awry in the auditory zoom. Once that is fixed, the fight/flight system is turned off, the Social Engagement System turns on, and the patients can connect with other people. These children's brainstems and their autonomic nervous systems “press the reset button” with the help of the sound, and these patients then learn to differentiate, or neurodifferentiate, human speech. When this happens, the children also start sleeping a very deep restorative sleep, often for the first time in years. This is the neurorelaxation phase, which is preparatory for the kind of learning that these children are going to be able to do. So, it turns out that hypersensitivity to sound is not just a minor symptom—it is a very important one. However, I want to emphasize that I think one has to address any of the stages of neuroplastic healing that have been blocked, and in autism, general cellular health is often a key part of the picture.

Dr. Rountree: One of the things that impressed me about reading your work is that this is not just telling people to think positive thoughts. Please discuss the example of Michael Moskowitz, MD, the chronic-pain specialist.

Dr. Doidge: Yes, Dr. Moskowitz had had a number of physical injuries. One involved jumping off a tank at a Fourth of July parade. In the process, his corduroys got caught on metal, he broke his femur in multiple places, and he was lying on the ground bleeding to death. During this time, his pain was 10 out of 10; however, he noticed that if he stayed perfectly still for an entire minute, the pain would go down to a zero. He almost chuckled at that, because he, a pain physician, had been teaching the gate theory of pain and the idea that there are switches or gates in the brain and nervous system that have to be opened for a person to experience pain. He had been teaching that for years, and now he actually got to experience it himself, in an acute pain situation.

However, he also developed an unrelated chronic pain syndrome. In acute pain, a body part is damaged and there is a signal that tells the brain to stay still until the part is healed or it could cause further damage. A chronic pain syndrome sometimes arises when that nerve is irritated repeatedly, stimulating the pain maps in the brain for the area. Because the brain is plastic, those maps grow and change as they process input from that nerve repeatedly. Those circuits gain a competitive advantage and now they register the pain for longer periods of time and over greater topographical expanses of the body. Dr. Moskowitz' second injury involved waterskiing on a rubber tire. He hurt his neck badly, and over a period of time, the sore area in his neck expanded, so that he also felt pain in his head, his shoulders, and both sides of his neck and back, and just the slightest twinge would last for a very long time. Because of these injuries, Dr. Moskowitz was disabled for years, and he had tried every known treatment, including opioids and nerve blocks. He had also tried many complementary treatments— acupuncture, hypnosis, and massage—and nothing had worked for him.

As a pain physician, he knew that there is not just one pain processing area in the brain. There are about a dozen dual processors that do not just process pain; they process something else as well. Most people have noticed that, when they are in a lot of pain, they are not able to control emotions, concentrate properly, do higher math or geometry, or do certain kinds of visualization. That is because the brain maps in those dual processors are being hijacked for increased pain processing at the expense of other kinds of processing.

So, as an experiment, Dr. Moskowitz tried to see if he could interrupt the hijacking process that goes on when a person develops a chronic pain syndrome. His idea was to use this competitive plasticity to “wind back” the experience of pain. He decided that he would begin with a visual exercise. He visualized pictures of magnetic resonance imaging scans of the brain pain maps when the brain was not in pain, when it was in acute pain with small areas lighting up, and when it was in chronic pain, when those small lit map areas expanded so that they lit up like supernovas. He would visualize those three scans every time he got into pain just to activate the visual cortex and inhibit the pain signal processing, imagining seeing the supernovas retracting to pinpricks.

He could have visualized anything, but he chose to do this, to remind himself that the brain had switches, and to remain motivated by that knowledge. He did this for three weeks, and he noticed almost no effect. However, toward the end of six weeks he was having brief periods, seconds, of being pain-free in his shoulders. After four months, he had minutes free of the pain, and at the end of the year, he was not taking any medications and was completely pain-free. He had learned to “take back” the brain areas that had been hijacked to process pain. However, the trick was that he had to be completely relentless. His attitude toward each pain attack had to change from feeling overwhelmed by it to seeing it as another opportunity to alter his brain circuitry. He would not let a second go by when he had a pain attack without visualizing. So that is an example of how plasticity is not always our friend, as it can give rise to positive or negative problems. However, understanding plasticity is our friend; if one understands how plasticity works, one can overcome some very disabling conditions. In this case, the result was cure without medication or surgery.

Dr. Rountree: Would you discuss the role of neuroplasticity in PD? I understand you have seen changes that have resulted in a person who was disabled with PD, somewhat overcame it, and was told that he must not have had it in the first place.

Dr. Doidge: That retrospective clean bill of health claim is the knee jerk response of the neurological nihilist. Neurologic nihilism is such an established reflex in some people, that when someone who is well-diagnosed gets better, instead of wanting to understand how this occurred, they question the initial diagnosis. That approach confuses diagnosis with prognosis. The most amusing example of that for me was when a physician said that a person who recovered from a neurologic condition with a neuroplastic approach couldn't have had that condition in the first place, implying he was diagnosed by an insufficiently rigorous physician. Well, it turned out that the physician who had made that diagnosis was himself and he had forgotten that he did this. Barbara Arrowsmith Young of the Arrowsmith School, who developed brain exercises for learning disorders, pleaded with researchers to study what she was doing, and she went to the Hospital for Sick Children, and various other places, to get assistance in the early 1980s. This was before plasticity was accepted. The researchers said that it was just not possible that people would get better. So, she brought some people who had gotten better, and then they said that these patients could not have had learning disorders in the first place. However, these children were very well-diagnosed.

Now let me address your question about PD: John Pepper, the person who gained control over his PD, was well-diagnosed, and he has a very competent neurologist. I have a film of her demonstrating his Parkinsonian signs and symptoms.

When dealing with PD in particular, we once used to wonder a lot about what general cellular and neuronal things may have triggered the PD. When I did my training, there was a lot of emphasis on pesticides; since then, we have found other chemicals that can damage the brain and give rise to PD. There are also other theories as to what is going on in PD at a cellular level; some people think there is a prion component, and one theory postulates that the disease moves from the gut into the brain. Whatever the cause, all these theories deal with pathogenesis, and pathogenesis, alas, is very rarely investigated in most patients who have PD.

Rather, we assume it is idiopathic and focus on the pathology. Whatever the cause, for a long time, it has been known that people with PD have about at least an 80% loss of dopamine in part of the basal ganglia and that dopamine facilitates movement. The basal ganglia turns individual movements into automatic involuntary sequences and individual thoughts into sequences of thought.

I described the story of John Pepper, who developed PD early in his 30s. His condition initially responded to levodopa [l-DOPA]; however, it stopped working and he was getting side-effects. He tried all kinds of exercises, and overdid it, exhausting himself, resulting in weakness. At a certain point, his wife discovered a particular exercise program in South Africa, which emphasized the need for rest and building up very, very slowly. At the start, the idea was to walk for 10 minutes per day, with particular attention paid to gait. Mr. Pepper discovered that he could not initiate movements easily or walk involuntarily and that his gait was awful. However, if he paid microattention to each individual movement within an individual step—such as standing straight up, leaning a bit to the left leg, bending the right leg at the hip, raising the right knee, swinging forward, etc.—he could actually move. He started to call that his conscious walking technique. He was bypassing the basal ganglia.

We now know that other parts of the brain than the basal ganglia are involved in these individual voluntary movements. So, over time, as Mr. Pepper learned how to do this conscious walking, he got to the point where he would be walking very fast for an hour and 15 minutes, and he was getting better as long as he maintained the walking. Ultimately, he was able to stop his medication. I am not saying that everyone can do this, but he was able to. I now think we know why that can happen. It turns out that walking triggers these brain growth factors that are so important for brain health. A person with PD is caught in a “noose.” One of the things we all need for brain health is neurotrophic growth factors, but we cannot release them if we cannot move.

John Pepper still has PD. The signs of PD can still be elicited by his neurologist, but if one saw him walking or did not examine him for it, one would not know it. He first had symptoms in his 30s; he is now in his 80s and has been able to have a very full life. There have been a few times that he has been unable to walk. Each time corresponded with something confining him to bed; once it was a chest infection and another time he needed surgery. Over a course of about 6 weeks all the gains he had made disappeared slowly, because he was not walking. Once he was out of bed, he had to build up his walking again, very slowly over 6 weeks or more—as had happened the first time he tried it—in order to obtain the benefit. He now teaches these techniques, and I have since met a number of other people who are able to walk without walkers, who were originally confined to them.

What I find most interesting is that, not only do we need dopamine to move, we need to move to raise our dopamine levels. There is evidence in animal PD models that, when they have PD on one side of the body, if one blocks the animal's movement, it is highly detrimental and dopamine levels drop further. However, if the animals are forced to exercise, their dopamine levels do not drop. If someone develops PD, one can almost guarantee a worse outcome if exercise is ignored and the only treatment is medication.

The other thing about PD is that dopamine is not just necessary for movement. Work at Columbia University and a few other places has shown that having dopamine is necessary for a person to be able to feel that a movement is worthwhile. So, if one does not have enough dopamine and has to answer the phone, that person will not feel that it is worth the effort. We have known for years that dopamine is related to motivational systems involving pleasure and reward. So imagine that one is a person with an illness that both makes it harder to move, because of a low dopamine level, and that makes it harder for one to appreciate that it is worth moving. This person will be caught in a triple feed-forward trap: the person is not moving because of a low dopamine level and, because he or she is not moving, the dopamine level is getting lower—and, on top of it, the person cannot imagine that moving will help.

Conscious walking can break through this problem in many people, and it is an example of how mental and physical activity can, in some cases at least, arrest or diminish the loss of function in what is thought of as a degenerative disease. One could ask, how many people does this help? We have large group studies that show that exercise is very important for patients with PD for improving everyday movement and mood. We also have huge studies showing that people who move have less of a tendency to develop PD. However, my model is that everybody is different and there may be multiple pathways to PD. Some of these pathways may involve chemical exposures, and some of those exposures may be ongoing. So, there is more to helping some people than exercise. Attending to general cellular health is always important. We have to learn a lot more about whether or not some of these chemical exposures can be dealt with by using various forms of chelation or other kinds of nutrients, or immune interventions to maximize living tissue. I do not see that being done right now routinely, in 21^st–century neurology.

Since I met John, I have seen other patients use slightly different kinds of exercise, combined with conscious techniques, and 2 of these patients were also able to stop their medications and function very well. Both were well-diagnosed by neurologists, and 1 patient is a physician in fact. (I have also films of them.) In these cases, the patients' function has improved over time, at least so far. John himself appears stronger to me than he was 5 years ago. Some other patients who have tried exercise and conscious walking have remained on medications but have had better courses of PD. Thus, these improvements are not confined to only one individual—and I am not basing the importance of exercise on case histories alone—this focus on exercise for PD is also based on the large amount of data from humans demonstrating that exercise helps preserve function, on animal data showing that they too can improve, and on the information from this research on how that happens. So, while many people still assert that there is no serious approach to PD other than medication or deep brain stimulation, the literature now shows that this idea is mistaken, at least for some patients. Given all brains are use-it-or-lose-it, I suspect that this is a very large number of people.

Dr. Rountree: This brings me to my last question. You talk in your writings ^1,2 about an emerging specialist that you would call “a neuroplastician.” Is this something that is being talked about?

Dr. Doidge: It's a term I coined to describe the scientists and clinicians who were the pioneers in plasticity. However, there are now some clinicians who are trying to put these different approaches together, but usually these clinicians only know a few techniques because it takes time to learn them well. My hope is that people from many different backgrounds and kinds of training will familiarize themselves with using a number of the techniques I have described. What I am trying to do is to get to know as much as I can about all of the techniques without necessarily being a full-time practitioner in each, which is not humanly possible. I personally have trained in many of the techniques that I have written about to know what they can do. Sometimes training for one technique is quick (such as conscious walking) or can be 200–400 hours, as is the case for one of the best modalities for neuromodulation—neurofeedback. I am trying to see people who have not been helped by other modalities and determine if there are other things they might try. The five stages of neuroplastic healing has been a helpful guide but I do not pretend to have sorted it all out yet. We have gone from a situation with TBI, for example, wherein the mainstream approach is to rest and restore, and that's it. Rest, restore, and pray that one is among those patients who have spontaneous recoveries. I have now documented 9 different approaches to TBI that I discussed in the second book. ² I often try to figure out which one, or which combination, would be most appropriate for a particular patient and the stage of healing that is blocked. No patient is identical and no two brain injuries are identical, so what we need now are principles, more than protocols.

To Contact Dr. Norman Doidge

Norman Doidge, MD

  Website: www.normandoidge.com

Dr. Rountree: I truly want to applaud you for putting all these different modalities together under one roof. It feels like the beginning of a revolution where we want to get people doing neuroplasticity work together and get them talking to each other, to look for common features, and figure out a way to move forward with this. If people would like more information they can go to your website or they can read your books. On your website, you have frequently asked questions and ongoing information in a newsletter.   ■