Anxiety Disorders and CBT

Anxiety Disorders and CBT

We need information repeated on a regular basis to memorize something solidly. It's the intimate hallmark of how we learn. It may even shed some insight on certain mental disorders commonly experienced such as anxiety disorders.

Phobias afflict many people. We believe that people who suffer from anxiety disorders such as phobias are victims of an overacting fire-together/wire-together tendency in their brains.

In the middle of the last century, Aaron Beck and Albert Ellis developed a type of psychotherapy that uses this fire-together/wire-together tendency as a weapon against anxiety disorders. It's called cognitive behavior therapy (CBT). The assumption behind CBT is that what you think governs what you feel.

For example, if you have a phobia of dogs, you have negative automatic thoughts about dogs (that's the thinking part), so when you see one, anxiety is generated (that's the feeling part), To have those anxious feelings go away, you first have to attack their source: your negative thinking. CBT calls this faulty thinking.

The therapy teaches you to entertain other not-so-self-defeating ways of looking at dogs. CBT does not ask you to block out the fearful feelings. You couldn't; they're wired. It does challenge you to start thinking consistently of alternative choices of viewing a tough aversive subject. You need to make it a habit.

If you successfully challenge faulty thinking on a regular basis, the faulty thinking eventually goes away. Research shows that applied consistently, the anxiety also goes away – and of its own accord,

When done consistently in the hands of a trained therapist, CBT is a potent weapon. Research shows that it's amongst the most effective therapies for anxiety disorders that exist. It's also helpful for depression and bipolar disorder, and even certain types of schizophrenia are responsive.

(From Your Best Brain, Course Guidebook, by Professor John J. Medina).

Genetics play a large role in determining intelligence, and both nature and nurture influence complex human behavior. We have yet to untangle the relative contributions of each to intelligence.

Inner Child vs. Inner Adult

Boost Your PFC to Rein in Your Inner Child and Boost Conscientiousness

This information is designed to help you win the war in your head between the adult, thoughtful part of your brain (the PFC), which knows that you should do, and your pleasure, which are run by a spoiled, demanding inner child who always wants what he wants whenever he wants it.

Your brain's pleasure centers are always looking for a good time:

• They want to jump off a cliff.
• They love going fast on a motorcycle in the rain.
• They crave the ice cream.
• They want the double cheeseburgers.
• They will stand in line for the fresh cinnamon rolls.
• They focus on having the second piece of cake.

Left unchecked, your inner child is often whispering to you like a naughty little friend:

• “Do it now...”
• “It's okay...”
• “We deserve it...”
• “Come on, let's have some fun...”
• “You're so upright...”
• “Live a little...”
• “We already had one bowl of ice cream. Just one more won't hurt...”
• “We'll behave better tomorrow. I promise...”

Without adult supervision, your inner child lives only in the moment and he can ruin your life. I have a friend who shared her daughter-in-law got sick with the flu and had to remain in bed upstairs. Her four-year-old son decided to “take over” the house while his mother was otherwise occupied with a pounding headache, fever, and vomiting. When his father came home, there was ice cream melting in puddles on the kitchen countertop; the pots and pans were arranged in a pyramid formation in the middle of the floor; cartoons were blaring on TV at full volume; and clothes, toys, and blankets (made into tents and forts) were strewn everywhere. Absolute anarchy and chaos This is a great visual of what happens to your life when your PFC is not functioning: Your inner child takes over while your inner adult is napping. The resulting mess is something to behold.

To balance your pleasure centers, and tame your inner child, the PFC helps you think about what you do before you do it. It thinks about your future, not just about what you want in the moment. Instead of thinking about the chocolate cake, it is the rational voice in your head that helps you:

• Avoid having a big belly.
• Remember that “food is medicine” and that you'll be in a sugar-induced, cranky, sleepy mood an hour after eating that cake.
• Remind your inner child of delicious but healthier alternatives that will both taste good and nourish your body.
• Be concerned about your bulging medical bills.
• Say “no” and meant it.

When your PFC is strong, it reins in your inner child, so that you can have a fun, passionate, meaningful life but in a thoughtful life, measured, conscientious way. To live a long healthy life, it s critical to strengthen your PFC and put your inner child into time-out whenever he acts up.

It is also critical to watch your internal dialogue and be a good parent to yourself. Dr. Daniel G. Amen have taught parenting classes for many years and the two rods that embody good parenting, even for your inner child, are “firm” and “kind”. When you make a mistake with food or with your health, look for ways to learn from your mistakes but in a loving way.

(Use Your Brain by Daniel G. Amen, M.D., excerpt).

Inner Child and Inner Adult. Photo by Elena.

Dinosaur Syndrome Revisited

The Dinosaur Syndrome Revisited:  Big Body, Little Brain, Become Extinct

Over the last decade there is growing evidence that shows the harmful effects of too much fat on your body. In a study of 1,438 Japanese men, researchers found significant decreases in brain size in the PFC and temporal lobes (learning and memory). Nora Volkow, director of the National Institute on Drug abuse, and colleagues found that in healthy adults a high BMI (body max index) was inversely correlated with activity in the PFC. Elevated BMI has also been associated with myelin abnormalities in the PFC of healthy normal and elderly adults.

The goal of our study was the test the hypothesis that an elevated BMI is associated with lower blood flow to the PFC in a healthy group of people on brain SPECT imaging. To that end, we compared our group of “healthy” subjects who had a high BMI with people in our “healthy” group of normal weight. The results of our study were very clear. The high BMI group had statistically significant lower activity in the PFC compared with the normal group.

Obesity is becoming a worldwide epidemic and is a risk factor for many chronic condition, including cardiovascular disease, depression, and neurodegenerative diseases like Parkinson's and Alzheimer's. It has recently found to be worse for your liver than alcoholism.

We were not able to determine if problems in the PFC led to increased impulsivity and subsequent obesity or if being overweight or obese directly caused brain changes. Both scenarios may be true. The fact that we used a healthy-brain group and specifically excluded ADHD or other behavioural disorders argues against the premorbid hypothesis, but other studies have shown an association between ADHD and obesity. Still other authors report that fat tissue directly increases inflammatory chemicals, which likely have a negative effect on brain structure and function.

One of the major problems with being overweight or obese is that there is evidence that it damages your PFC, which we know is the major decision-making part of the brain. So if you do not get your weight under-control, it will become harder and harder to use get your own good judgment over time to get and stay healthy. Now is the time to start enhancing your health and longetivity, not at some arbitrary point in the future, which most likely will never come.

The Day of the Flowers. Photo by Elena.

ADHD, PFC Problems, and Early Death

ADHD is associated with low activity in the PFC. Initially, ADHD was thought of as a childhood disorder that most kids outgrew by the time they turned twelve or thirteen. The hallmark symptoms of ADHD are short attention span, being easily distracted, disorganization, hyperactivity (trouble sitting still), and poor impulse control. People with ADHD, like Jose, often exhibit excitement-seeking or conflict-seeking behavior; they also tend to have trouble with time (they are often late and turn in assignments at the last minute). Over the last three decades it has become clear that many ADHD children continue to have debilitating symptoms for the rest of their lives. They tend to outgrow the physical hyperactivity but not the problems with disorganization, inattention, distractibility, and impulse control. Untreated ADHD has been associated with a higher incidence of:

• Drug and alcohol abuse (impulsivity and to calm feelings of hyperactivity)
• Relationship problems (impulsivity and conflict seeking)
• School failure (attentional problems and impulsivity)
• Job-related problems (problems with time, attention, and impulse control)
• Medical problems (associated with chronic stress, plus more head trauma with the excitement-seeking behavior)
• Obesity (lack of impulse control)
• Depression (chronic failure)
• Lack of conscientiousness (all of the above).

In the book Daniel G. Amen wrote with noted neurologist Rod Shankle, “Preventing Alzheimer's, the authors argued that ADHD is likely associated with Alzheimer's disease because of its connection with many of the illnesses that put people at risk for it, such as alcohol abuse, obesity, depression and head trauma. This is very important, because when ADHD goes untreated, a person will not be able to control his or her impulses, setting him up for significant health problems, poor decisions, and earlier death. If you or someone you love has symptoms of ADHD, it is important to be treated. Natural ways to treat ADHD include intense aerobic exercise, a very healthy diet, a multivitamin, fish oil, and supplements (such as green tea, rhodiola, L-Tyrosine) or medication (such as Ritalin or Adderall) to enhance PFC function.

Once you realize the absolutely critical role of the PFC to longevity, you then need to do everything possible to protect it and rehabilitate it if necessary.

(Use Your Brain by Daniel G. Amen, M.D. Excerpt).

Way to healthy live. Photo by Elena.

Dialectical Behavior Therapy

Doing Dialectical Behavior Therapy

 

Natural contingencies are the powerful natural consequences that occur within each therapeutoc interaction that are also similar to how things work in nontherapy relationships. Self-involving self-disclosure is one way the DBT therapist uses natural contingencies to benefit the client.

Interactions with the therapist or aspects of the therapy itself (e.g. Session frequency or length, payment) may evoke some of the same behaviors that trouble the client in other relationships. For example, the client takes an angry, demanding tone when he makes a request of the therapist that is an imposition of the therapists's time. Others in the client's life are turned off and withdraw from him when he does this to them; his angry tirades inhibit others from giving him feedback; he feels lonely and incapable of keeping good relationships. This is a key place to use self-involving self-disclosure to help the client see the contingency between his behavior and its effects. The therapist might say, “Your voice tone sounds quite angry and demanding as you ask me to do this for you. Were you aware of how your tone comes across? When you ask me in this way, it makes me feel less like doing it. If you asked in a way that showed you realize it may be an imposition, you'd get more of what you want from people.”

It is beneficial when the client engages in behaviors with the therapist that are similar to those that cause problems in other relationships because a well-known aspect of reinforcement is that the closer in time and place the behavior is to its consequences, the greater the effect of those consequences. The key is to be aware, from chain analysis and formulation in advance, of what you are trying to strengthen and what you do not want to reinforce. For example, in one case, others would not respond to an emotional pain of a person unless this person became dramatically upset and made extreme statements such as “I'm going to kill myself if she says that again!” The contingency in therapy should be different: you would want to tune in and respond to distress with plenty of help without in having to escalate.

Loneliness. Photo by Elena.

Therefore, warmth, care, and attention should be at a good baseline frequency so that low-level requests and expressions of difficulty regularly produce appropriate help. You would closely monitor the client's current vulnerability factors and antecedents so that when the chain to the pattern is triggered, you can quickly attend to emotional pain but block extreme statements. For example, when this person begins to tell you about an interpersonal conflict similar to those that have led to extreme statements and suicide threats, you might say “I'd really like to help you get things to go the way you want in this situation, so that you do not have to escalate but instead really get what you need.” You would stay responsive and warm to the client's appropriate expression, and become cooler when extreme statements are made, even actively blocking them. “When you threaten suicide, it makes us have to assess the risk. To me that takes a lot of time and distracts from what's most important, which is that you are upset by a real problem – could you tell be about it without the threats.

What happens close in time to the incident is more likely to affect the behavior's future probability. Treatment effects will be stronger, therefor, if client's problem behaviors and improvements occur during the session, where they are closest in time and place to the available reinforcement that the therapist can provide. Nowhere is this more visible than when the therapist and client negotiate solutions to problems in their therapy relationship by by explicitly discussing how each person's responses reinforce our fail to reinforce the other's motivation and engagement in therapy.

Some people have objections to contingency management, as if deliberately responding in a contingent way is harmful or deceitful. This objection ignores the fact that we are all responding contingently all the time with everyone anyway. If I am sharing something about myself, you are either responding in a way that makes me more likely to continue to share or less likely to continue to share; this happens whether either of is is aware of the effects or not. As therapists, we want to be as aware as we can be so that we harness our responses to the client's benefit rather than simply responding to alleviate our own discomfort. A good base rate of genuinely noncontingent positive regard is a prerequisite to effective use of contingency management. Unless the client experiences you as genuinely invested in his or her best interests, contingency management feels manipulative or coercive.

Doing Dialectical Behavior Therapy (A Practical Guide by Kelly Koerner)

Oblivion. Photo by Elena.

Cognitive Modification

Cognitive Modification

Effective behavior is sometimes inhibited by faulty beliefs and assumptions. In DBT cognitive modification is based on logical consistency or consistency with one's true or wise-mind beliefs (e.g., “Is this belief what I believe in my wisest moments?”) and on effectiveness (“Is this this belief useful to meet my goals?” This emphasis on finding what is valid is due in part to clients' sensitivity to invalidation. Focusing intervention on what is wrong with the client's interpretations, especially through Socratic questioning, is too evocative and aversive for many. Although the DBT therapist may sometimes challenge problematic beliefs with reason or through dialectical persuasion – conversations that create the experience of the contradictions inherent in the client's position. For example., in the last chapter a client described getting immediate relief from emotional pain when she burnt herself with a cigarette; she said it was no big deal. The therapist the asked the client would she burn her little niece's arm to help feel better, if the child was in great emotional pain? The client replied, “I just wouldn't do it. It's not right.” The conversation heightened the client's emotional tension and discomfort of holding a double standard. In dialectical persuasion, the therapist highlights the inconsistencies among the client's own action, beliefs, and values.

In addition, the therapist helps the client develop guidelines on when to trust and when to suspect her interpretations. For example, the skill “check the facts” distills many basic cognitive modification strategies into a self-help intervention. Further, in DBT, the therapist actively teaches the client to become better able to discern contingencies, clarifying the if-then effects of their behavior in the therapy relationship as well as in the client's other relationships. Clients learn to observe and describe their own thinking style, and implicit rules, to notice when their thinking is ineffective, and to confront and challenge problematic thoughts in order to generate a more functional or dialectical sense of truth. The client leans to increasingly rely on wise mind, an intuitive knowing that.

Yet change interventions can be experienced as highly invalidating. The therapist's attempts to help can  feel critical and can seem to confirm that the client has not tried hard enough – just as others have always said. Clients with histories of pervasive invalidation can be exquisitely sensitive. For this reason, active, disciplined, and precise validation of what is “right” or “correct” about the client's current responses in required to motivate emotion regulation and thereby create conditions for other change.

From Doing Dialectical Behavior Therapy (A Practical Guide by Kelly Koerner).

Reflections about our life... Photo by Elena.

What Is a Good Night's Sleep?

What Is a Good Night's Sleep?

Let's define the perfect snooze. Like many people, you may be so used to your own sleep patterns, however imperfect, that you don't know what you might be missing.

For most people, the best sleep takes eight hours, runs from dark to dawn – ideally from ten p.m. Or earlier to six a.m. or so – and leaves you feeling great. You should actually start to feel sleepy within about three hours after the sun sets as your sleep-promoting brain chemicals are triggered by by the reduced light. When you actually hit the pillow, it should take only a few minutes for you to get to sleep. Once you get to sleep, you should stay asleep through the night (without bathroom trips!). Ideally, you'll go through a series of vital sleep sequences that take at least eight hours to complete (children need twelve hours). At least six of those hours should be ininterrupted.

There are five stages of sleep that constitute a sleep cycle, and you need to go through four to five sleep cycles in one night. You'll usually pass through the first two superficial sleep stages in your first half hour of sleep. Then, hopefully, you'll drop into two progressively deeper sleep stages and stay there for most of the next few hours. This first half of the night, literally between ten p.m. and two a.m., potentially provides the most restorative sleep, because only while you sleep deeply can your immune system, your growth hormones, and other repair crews emerge to heal your body from the day's ravages. Finally, you dream in the REM (rapid eye movement) stage, which seems to be designed particularly for psychic repair. These five stages repeat throughout the night, though the second half of the night has more rapid ups, downs, and dreams than the first half.

If you sleep poorly, your mind and body are deprived of crucial cellular repairs that can be made only if you sleep long and deeply. You know what happens when you can't bring your car into the shop for its routine maintenance? You run it into the ground and shorten its “life span”. Same thing here. So you should find out what's really keeping you up. But first let's get clear on what your particular sleep disturbance looks like.

In desperation we look into the hoary old idea of remote-controlled mining. Photo by Elena.

What is your sleeplessness like?

Do you sleep habits include any of the following basic flows?:

Are you a night owl? If so, like many people, you may not think that you have a sleep disturbance at all. You may actually consider your late nights a blessing. It can be fun – you get things done, you get some time alone when everyone else is asleep (unless you've spawned some baby night owls). But it's not fun in the morning if you need to get up so early that you can't get a full eight hours of sleep. Chances are, you are chronically undersleeping and feeling out of sync with your spouse – and the rest of the world. Being a night owl is a key symptom of either abnormally low serotonin or excessively high stress-coping hormones.

On the other hand, you may lie awake in frustration most nights for too long. Do you go over and over worries about the past day or the next day before you can finally get to sleep? Or do you just lie there? Do anxiety, pain, panic, or disturbing dreams wake you up in the night or too early in the morning? Or do you take too long to get back to sleep or not get back to sleep at all? Are you a restless, thrashing sleeper or a light one? Do you wake up at the slightest sounds?

Are you proud to call yourself a “morning person” who wakes up very early no matter what time you get to sleep?

Do you rarely get more than six hours of sleep a night? Do you wake up worried or anxious and have to get up and exercise or work on whatever is bothering you? Finally, are you one of the four million poorly adjusted shift workers who try to sleep during the day? Whatever part of your night's sleep you're missing, you should think about it.

Why aren't you getting enough sleep?

If you answered yeas to any of the above questions, you are likely to ave at least one deficiency in your body's sleep-producing chemistry. Let's start with the most common cause of sleep disturbance. It has to do with the brain chemical serotonin. But serotonin is an antidepressant, you might be thinking, what does it have to do with sleep? What you may not know is that this extraordinary biochemical mood marvel is also the only substance from which your brain can produce its most potent knockout drop: melatonin.

Your sleep is supposed to be induced by a biochemical concert that features gradually increasing levels of melatonin, starting in the afternoon and reaching crescendo at about ten p.m. Melatonin is produced out of serotonin by your pineal gland, a pea-size structure embedded deep within your brain. The pineal gland, which consists of pigment cells similar to those found in your eyes, is light sensitive. Very gradually throughout the afternoon a and evening, as light gives way to darkness, the transformation of serotonin into melatonin is supposed to increase until it lullabies you to sleep. But here's the catch: Melatonin can be produced in adequate amount only if you have enough serotonin on hand from which to make it.

(From The Mood Cure, by Julia Ross, m.a. Author of the Diet Cure).

We can't appreciate the condition of sleep. Photo by Elena.

Mental Illness

Mental Illness

One in every hundred people will develop schizophrenia in their lifetime. At the beginning of the 21st century, three hundred thousand Canadians aged sixteen to thirty have been diagnosed with schizophrenia. The average time between onset of symptoms and fist effective treatment is one to two years, but be much longer.

Males and females are equally likely to be diagnosed with schizophrenia. But males tend to have an earlier age of onset, in the teens or early twenties for men, and in the twenties or early thirties for women. Nearly 80 per cent of people with schizophrenia experience a major depressive episode at some point in their lives.

Approximately four out of every ten people with a diagnosis of schizophrenia attempts suicide, and approximately one in ten people diagnosed with schizophrenia die of suicide, making it the leading cause of premature death for people with with schizophrenia. Besides, suicide in this population is rarely attributable to florid psychotic symptoms (hallucinations, delusions); it is more likely to occur in periods of remission or improved functioning. Depression and hopelessness are important factors in suicide by people with schizophrenia.

Tom Ko has worked with 160 families in his job as therapy supervisor at the Calgary Early Psychosis Treatment and Prevention Program. Many – but not all – of his clients are young enough to be living at home with parents and siblings. Ko, who has a master's degree in social work, encourages the whole family to attend psychoeducation sessions with him. “Not all siblings have strong emotional reactions to the illness,” says Ko, a social worker. “But all have some reaction to a psychotic illness in the family.”

How Siblings Are Affected

Here are some of the common emotions and issues raised by the siblings:

1. Anger of parents (“Why don't they take control and fix this?”) and at the unwell sibling (“Why doesn't he just get better?”) “They get angry a lot because things have changed, “Ko says. “They want their brother or sister back.”
2. Grief and sadness: “Because the family isn't the same, and they can sense that.” Ko says that children go through a grieving process just as parents do. “When things change and everything's up in the air, they do get depressed.”
3. Fear that they'll become mentally ill. “Not the seven-year-old but the fourteen-year-old says, “Will I get it?” And we are always upfront.” (Research shows that if you have a first-degree relative with schizophrenia, you in turn have a 10-per-cent chance of winding up with the disorder; this compares to a 1-per-cent chance for someone with no diagnosed relatives.)
4. Guilt that they contributed to their sibling's disorder, or made it worse. For example, two brothers may have been fighting just before one is diagnosed (which is not uncommon because the sibling relationship changes with the onset of symptoms). “We try to tell them, “ You didn't know; of course you got into fights; everybody does, but it didn't cause the illness.
5. Loss of normal family relationship: When parents are tied up with hospitals and meds and caring for their unwell child, says Ko, “It's easy to forget there are other kids involved... Often they (the siblings) will say “we used to have family dinners together, do this and that together.” We try to get them back to those family routines so that everything goes back to normal as much as possible.”
6. Confusion because they know something is wrong but no one is explaining what or why. “They find it very difficult to understand sometimes. They can tell their brother or sister is different, they can tell their family is different, and they wonder. But it just becomes a family secret that no one talks about. They want to know what's going on.”

People can recover. Most of the people who have recovered have been at the depths of depression or the depths of some other illness, and they have made it back to find a life worth living with meaning and purpose. Illustration by Elena.

Mental Disorder

Mental Disorder: What It Feels Like?

Unless you've been there, it can be pretty difficult to imagine what it's like to suffer from a mental disorder. What does it truly feel like to experience the delusions or voices that come with schizophrenia? To soar with the unbridled euphoria of a mania? To shake with the heart-numbing fear of a panic attack?

Short of actually having the disorder, there are very few ways of comprehending what it's like to be inside someone else's head. We could rattle off lists of clinical symptoms, but that would get dull pretty fast. It also wouldn't really give you a visceral sense of the experience.

Yet all of us are curious. Scientists, in fact, have tried to give other folks a taste of what mental disorder feels like. One of the most intriguing efforts is a virtual-reality setup which, using specially enhanced audio and visual effects, attempts to transport the subject into the mind of someone with schizophrenia. You actually hear those internal voices in a manner that those with the disorder say comes close to their reality.

Some sources will tell you that manic depression, or bipolar disorder, as it's also known, rarely shows itself much before the the age of eighteen. But ask any of my friends, reachers, or family – any of those brave souls who traveled with the ill person through his or her life – and they will vigorously dispute that claim.

A rapid cycler, mood changes are like gunfire in the trenches – bang, bang, bang. Light, dark, light, dark. Nobody knows if it's possible to switch a light on and off as quickly as brain manages to switch between euphoria and devastation.

These people spend part of their lives feeling as though they will never join the human race. It's as though they live in a cage where they can hear the world but the world cannot hear them. After years, they see this simply as a manifestation of their illness, which has a way of making the ordinary seem threatening and frightening. Paranoia is more than an occasional visitor. People affected have sat on the subway, convinced that others were laughing at them; they have left parties after an hour, certain that the guests thought the ill persons had no right to be among them. Manic depression can make that girl in The Exorcist (at her writhing, screaming, priest-hating worst) look like someone you would ask to babysit their three-year-old. But these people own their illness. And it will be part of them for the rest of their lives. People can't turn their back on it.

People have been asked if they see their illness as a tragedy, or at least as something that's robbed them of anything of vital importance. Sometimes they do. But stress is a killer; it can initiate the descent into depression, the rise into mania. These people have learned to be vigilant about avoiding those situations that will exacerbate their disease.

The illness also destroys relationships, chewing them up, spitting them out. These people mourn the friendships they have lost. Their behavior – especially when manic – has alienated friends and relatives. In some cases, the ill persons have never been able to reconnect with them.

And yet, many of them can't say that they think of themselves as tragically touched. It is like being born with red hair or brown, one eye or three; you know nothing different, so what does it matter^ We all have a cross to bear. They will carry their cross for all their life.

There's a saying you sometimes hear in the mental health world: Label belong on soup cans, not people. Illustration by Elena.

Rejuvenation

Rejuvenation

At the beginning of the twentieth century the world's most outstanding neuroanatomist, Nobel Prize winner Santiago Ramon y Cajal, who laid the groundwork for our understanding of how neurons are structured, turned his attention to one of the most vexing problems of human brain anatomy. Unlike the brains of simpler animals, such as lizards, the human brain seemed unable to regenerate itself after an injury. This helplessness is not typical of all human organs. Our skin, when cut, can heal itself, by producing new skin cells; our fractured bones can mend themselves; lost blood can replenish itself because cells in our marrow can become red or white blood cells.

But our brains seemed to be a disturbing exception. It was known that millions of neurons die as we age. Whereas other organs make new tissues from stem cells, none could be found in the brain. The main explanation for the absence was that the human brain, as it evolved, must have become so complex and specialized that it lost the power to produce replacement cells. Besides, scientists asked, how could a new neuron enter a complex, existing neuronal network and create a thousand synaptic connections without causing chaos in that network? The human brain was assumed to be a closed system.Ramon y Cajal devoted the later part of his career to searching for any sign that either the brain or spinal cord could change, regenerate, or reorganize its structure. He failed.

In his 1913 masterpiece, Degeneration and Regeneration of the Nervous system, he wrote, “ In adult brain centers the nerve paths are something fixed, ended, immutable. Everything may die, nothing may be regenerated. It is for the science of the future to change, if possible, this harsh decree.”

There matters stood.

The neuronal stem cells I see are vibrating with life. They are called “neuronal” stem cells because they can divide and differentiate to become neurons or glial cells, which support neurons in the brain. The ones I am looking at have yet to differentiate into either neurons or glia and have yet to “specialize,” so they all look identical. Yet what stem cells lack in personality, they make up for in mortality. For stem cells don't have to specialize but can continue to divide, producing exact replicas of themselves, and they can go on doing this endlessly without any signs of aging. For this reason stem cells are often described as the eternally young, baby cells of the brain. This rejuvenating process is called “neurogenesis,” and it goes on until the day that we die.

Paradoxically, sometimes losing neurons can improve brain function, as happens in the massive “pruning back” that occurs during adolescence when synaptic connections and neurons that have not been extensively used die off, in perhaps the most dramatic case of use it or lose it. Illustration by Elena.

Neuronal stem cells were long overlooked, in part, because they went against the theory that the brain was like a complex machine or computer, and machines don't grow new parts. When, in 1965, Joseph Altman and Gopal D. Das of the Massachusetts Institute of Technology discovered them in rats, their work was disbelieved.

Then in the 1980s Fernando Nottebohm, a bird specialist, was struck by the fact that songbirds sing new sons each season. He examined their brains and found that every year, during the season when the birds do the most singing, they grow new brain cells in the area of the brain re responsible for song learning. Inspired by Nottebohm's discovery, scientists began examining animals that were more like human beings. Elizabeth Gould of Princeton University was the first to discover neuronal stem cells in primates. Next, Eriksson and Gage found an ingenious way to stain brain cells with a marker, called BrdU, that gets taken into neurons only at the moment they are created and that lights up under the microscope. Erikson and Gage asked terminally ill patients for permission to inject them with the marker. When these patients died, Erikson and Gage examined their brains and found new, recently formed baby neurons in their hippocampi. Thus we learned from these dying patients that living neurons form in us until the very end of our lives.

The search continues for neuronal stem cells in other parts of the human brain. So far they've also been found active in the olfactory bulb (a processing area for smell) and dormant and inactive in the septum (which processes emotion), the striatum (which processes movement), and the spinal cord. Gage and others are working on treatments that might activate dormant stem cells with drugs and be useful if an area where they are dormant suffers damage. They are trying to find out whether stem cells can be transplanted into injured brain areas, or even induced to move to those areas.

To find out if neurogenesis can strengthen mental capacity, Gage's team has set out to understand how to increase the production of neuronal stem cells. Gage's colleague Gerd Kempermann raised aging mice in enriched environments, filled with mice toys such as balls, tubes, and running wheels, for only forty-five days. When Kempermann sacrificed the mice and examined their brains, he found they had a 15 percent increase in the volume of their hippocampi and forty thousand new neurons, also a 15 percent increase, compared with mice raised in standard cages.

Mice live to about two years. When the team tested older mice raised in the enriched environment for ten months in the second half of their lives, there was a fivefold increase in the number of neurons in the hippocampus. These mice were better at tests of learning, exploration, movement, and other measures of mouse intelligence than those raised in unenriched conditions. They developed new neurons, though not quite as quickly as younger mice, proving that long-term enrichment had an immense effect on prompting neurogenesis in an aging brain.

(Rejuvenation. The Brain That Changes Itself by Norman Doidge, M.D., excerpt).

Keeping unused neurons supplied with blood, oxygen, and energy is wasteful, and getting rid of them keeps the brain more focused and efficient. Illustration by Elena.

Neuropathic Pain

Neuropathic Pain

There are a whole host of haunting pains that torment us for reasons we do not understand and that arrive from we know not where – pains without return address. Lord Nelson, the British admiral, los his right arm in an attack on Santa Cruz de Tenerife in 1797. Soon afterward, Ramachandran points out, he vividly began to experience the presence of his arm, a phantom limb that he could feel but not see. Nelson concluded that its presence was “direct evidence for the existence of the soul,” reasoning that if an arm can existe after being removed so then might the whole person exist after the annihilation of the body.

Phantom limbs are troubling because they give rise to a chronic “phantom pain” in 95 percent of amputees that often persists for a lifetime. But how do you remove a pain in an organ that isn't there?

Phantom pains torment soldiers with amputations and people who lose limbs in accidents, but they are also part of a larger class of uncanny pains that have confused doctors for millennia, because they had no known source in the body. Even after routine surgery, some people are left with equally mysterious postoperative pains that last a lifetime. The scientific literature on pain includes stories of women who suffer menstrual cramps and labor pains even after their uteruses have been removed, of men who still feel ulcer pain after the ulcer and its nerve have been cut out, and of people who are left with chronic rectal and hemorrhoidal pain after their rectums were removed. There are stories of people whose bladders were removed who still have an urgent, painful chronic need to urinate. These episodes are comprehensible if we remember that they too are phantom pains, the result of internal organs being “amputated”.

Normal pain, “acute pain,” alerts us to injury or disease by sending a signal to the brain, saying, “This is where you are hurt – attend to it.” But sometimes an injury can damage both our bodily tissues and the nerves in our pain systems, resulting in “neuropathic pain,” for which there is no external cause. Our pain maps get damaged and fire incessant false alarms, making us believe the problem is in our body when it is in our brain. Long after the body has healed, the pain system is still firing and the acute pain has developed an afterlife.

The phantom limb was first proposed by Silas Weir Mitchell, an American physician who tended the wounded at Gettysburg and became intrigued by an epidemic of phantoms. 

Physicians have long known that a patient who expects to get pain relief from a pill often does, even though it is a placebo containing no medication. Illustration by Megan Jorgensen.

Civil War soldiers' wounded arms and legs often turned gangrenous, and in an age before antibiotics, the only way to save the soldier's life was to amputate the limb before the gangrene spread. Soon amputees began to report that their limbs had returned to haunt them. Mitchell first called these experiences “sensory ghosts,” then switched to calling them “phantom limbs.”

They are often very lively entities. Patients who have lost arms can sometimes feel them gesticulating when they talk, waving hello to friends, or reaching spontaneously for a ringing phone.

A few doctors thought the phantom was the product of wishful thinking – a denial of the painful loss of a limb. But most assumed that the nerve endings on the stump end of the lost limb were being stimulated or irritated by movement. Some doctors tried to deal with phantoms by serial amputations, cutting back the limbs – and nerves – farther and father, hoping the phantom might disappear. But after each surgery it reemerged.

Ramachandran had been curious about phantoms since medial school. Then in 1991 he read the paper by Tim Pons and Edward Taub about the final operations on the Silver Spring monkeys. Pons mapped the brains of the monkeys who had had all the sensory input from their arms to their brains eliminated bu deafferentation and found that the brain map for the arm, instead of wasting away, had become active and now processed input from the face – which might be expected because, as Wilder Penfield has shown, the hand and facial maps are side by side.

Ramachandran immediately thought that plasticity might explain phantom limbs because Taub's monkeys and patients with phantom arms were similar. The brain maps for both the monkeys and the patients had been deprived of stimuli from their limbs. Was it possible that the face maps of amputees had invaded the maps for their missing arms, so that when the amputee was touched on the face, he felt his phantom arm? And where, Ramachandran wondered, did Taub's monkeys feel it when their faces were stroked – on their faces, or in their “deafferented” arm?

Pain, like the body image, is created by the brain and projected onto the body. This assertion is contrary to common sense and the traditional neurological view of pain that says that when we are hurt, our pain receptors send a one-way signal to the brain's pain center and that the intensity of pain perceived is proportional to the seriousness of the injury. We assume that pain always files an accurate damage report. This traditional view dates back to the philosopher Descartes, who saw the brain as a passive recipient of pain. But that view was overturned in 1965, when neuroscientists Ronald Melzack (a Canadian who studied phantom limbs and pain) and Patrick Wall (an Englishman who studied pain and plasticity) wrote the most important article in the history of pain. Wall and Melzack's theory asserted that the pain system is spread throughout the brain and spinal cord, and far from being a passive recipient of pain, the brain always controls the pain signals we feel. 

Their “gate control theory of pain” proposed a series of controls, or “gates”, between the site of injury and brain. When pain messages are sent from damaged tissue through the nervous system, they pass through several “gates”, starting in the spinal cord, before they get to the brain. But these messages travel only if the brain gives them “permission,” after determining they are important enough to be let through. If permission is granted, a gate will open and increase the feeling of pain by allowing certain neurons to turn on and transmit their signals. The brain can also close a gate and block the pain signal by releasing endorphins, the narcotics made by the body to quell pain. How much pain we feel is determined in significant part by our brains and minds – our current mood, our past experiences of pain, our psychology, and how serious we think our injury is.

When a mother soothes her hurt child, by stroking and talking sweetly to her, she is helping the child's brain turn down the volume on its pain. Illustration by Megan Jorgensen.

Constrained-Induced Therapy

Constrained-Induced Therapy

The principles of constraint-induced therapy have been applied by a team headed by Dr. Friedemann Pulvermüller in Germany, which worked with Dr. Taub to help stroke patients who have damage to Broca's area and have lost the ability to speak. About 40 percent of patients who have a left hemisphere stroke have this speech aphasia. Some, like Broca's famous aphasia patient, “Tan”, can use only one word; others have more words but are still severely limited. Some do get better spontaneously or get some words back, but it has generally been thought that those who didn't improve within a year couldn't.

What is the equivalent of putting a mitt on the mouth or a sling on speech? Patients with aphasia, like those with arm paralysis, tend to fall back on the equivalent of their “good”arm. They use gestures or draw pictures. If they can speak at all, they tend to say what is easiest over and over.

The “constraint” imposed on aphasiacs is not physical, but it's just as real: a series of language rules. Since behaviour must be shaped, these rules are introduced slowly. Patients play a therapeutic card game. Four people play with thirty-two card, made up of sixteen different pictures, two of each picture. A patient with a card with a rock on it must ask the others for the same picture. At first, the only requirement is that they not point to the card, so as not to reinforce learned nonuse. They are allowed to use any kind of circumlocution, as long as it is verbal. If they want a card with a picture of the sun cnd can't find the word, they are permitted to say “The thing that makes you hot in the day” to get the card they want. Once they get two of a kind, they can discard them. The winner is the player who gets rid of his cards first.

Therapy is always useful. Illustration by Elena.

The next stage is to name the object correctly. Now they must ask a precise question, such as “Can I have the dog card?” Next they must add the person's name and a polite remark: “Mr. Schmidt, may I please have a copy of the sun card?” Later in the training more complex cards are used. Colors and numbers are introduced – a card with three blue socks and two rocks, for instance. At the beginning patients are praised for accomplishing simple tasks; as they progress, only for more difficult ones.

The German team took on a very challenging population – patients who had had their strokes on average 8.3 years before, the very ones whom most had given up on. They studied seventeen patients. Seven in a control group got conventional treatment, simply repeating words; the other ten got CI therapy for language and had to obey the rules of the language game, three hours a day for ten days. Both groups spent the same numbers of hours, then were given standard language tests. In the ten days of treatment, after only thirty-two hours, the CI therapy group had a 30 percent increase in communication. The conventional treatment group had none.

Based on his work with plasticity, Dr. Taub has discovered a number of training principles: training is more effective if the skill closely relates to everyday life; training should be done in increments; and work should be concentrated into a short time, a training technique Dr. Taub calls “massed practice,” which he has found far more effective than long-term but less frequent training.

Many of these same principles are used in “immersion” learning of a foreign language. How many of us have taken language courses over years and not learned as much as when we went to the country and “immersed” ourselves in the language for a far shorter period? Our time spent with people who don't speak our native tongue, forcing us to speak theirs, is the “constraint.” Daily immersion allows us to get “massed practice.” Our accent suggests to others that they may have to use simpler language with us; hence we are incrementally challenged, or shaped. Learned nonuse is thwarted, because our survival depends on communication.

(Midnight Resurrections, The Brain That Changes Itself, by Norman Doidge, M.D., excerpt).

I can see what you want to say. Illustration by Elena.

Brain Decodes Skin Sensations

How the Brain Decodes the Skin Sensations

Bach-y-Rita determined that skin and its touch receptors could substitute for a retina, because both the skin and the retina are two-dimensional sheets, covered with sensory receptors, that allow a “picture” to form on them.

It's one thing to find a new data port, or way of getting sensations to the brain.  But it's another for the brain to decode these skin sensations and turn them into pictures. To do that, the brain has to learn something new, and the part of the brain devoted to processing touch has to adapt to the new signals. This adaptability implies that the brain is plastic in the sense that it can reorganize its sensory perceptual system.

If the brain can reorganize itself, simple localizationism cannot be a correct image of the brain. At first even Bach-y-Rita was a localizationist, moved by its brilliant accomplishments. Serious localizationism was first proposed in 1861, when Paul Broca, a surgeon, had a stroke patient who lost the ability to speak and could utter only one word. No matter what he was asked, the poor man responded, “Tan, tan,” When he died, Broca  dissected his brain and found damaged tissue in the left frontal lobe. Skeptics doubted that speech could be localized to a single part of the brain until Broca showed the the injured tissue, then reported on other patients who had lost the ability to speak and had damage in the same location. That place came to be called “Broca's area” and was presumed to coordinate the movements of the muscles of the lips and tongue. Soon afterward another physician, Carl Wernicke, connected damage in another brain area farther back to a different problem: the inability to understand language. Wernicke proposed that the damaged area was responsible for the mental representations of words and comprehension. It came to be known as “Wernicke's area.” Over the next hundred years localizationism became more specific as new research refined the brain map.

"We see with our brains, not with our eyes" (Bach-y-Rita, surgeon brain neuroplastician.) Illustration by Elena.

Unfortunately, though, the case for localizationism was soon exaggerated. It went from being a series of intriguing correlations (observations that damage to specific brain areas led to the loss of specific mental functions) to a general theory that declared that every brain function had only one hardwired location – an idea summarized by the phrase “one function, one location,” meaning that if a part was damaged, the brain could not reorganize itself or recover that lost function.

A dark age for plasticity began, and any exceptions to the idea of “one function, one location” were ignored. In 1868 Jules Cotard studied children who had early massive brain disease, in which the left hemisphere (including Broca's area) wasted away. Yet these children could still speak normally. This meant that even if speech tended to be processed in the hemisphere, as Broca claimed, the brain might be plastic enough to reorganize itself, if necessary. In 1876 Otto Soltmann removed the motor cortex from infant dogs and rabbits – the part of the brain thought to be responsible for movement – yet found they were still able to move. These findings were submerged in the wave of localizationist enthusiasm.

Bach-y-Rita came to doubt localizationism while in Germany in the early 1960s. He had joined a team that was studying how vision worked by measuring with electrodes electrical discharge from the visual processing area of a cat's brain. The team fully expected that when they showed the cat an image, the electrode in its visual processing area would send off an electric spike, showing it was processing that image. And it did. But when the cat's paw was accidentally stroked, the visual area also fired, indicating that it was processing touch as well. And they found that the visual area was also active when the cat heard sounds.

The Brain that Changes Itself by Norman Doidge, M.D. Stories of Personal Triumph from the Frontiers of Brain Science.

Nobody will torture cats. Photo by Elena.

Dreams in Psychology

Dreams in Psychology

Why are dreams so important in analysis. Patients are often haunted by recurring dreams of their traumas and awaken in terror. As long as they remain ill, these dreams don't change their basic structure. The neural network that represents the trauma – such as Mr. L's dream that he was missing something – is persistently reactivated, without being retranscribed. Should these traumatized patients get better, these nightmares gradually become less frightening, until ultimately the patient dreams something like At first I think the trauma is recurring, but it isn't; it's over now, I've survived . This kind of progressive dream series shows the mind and brain slowly changing, as the patient learns that he is safe now. For this to happen, neural networks must unlearn certain associations – as Mr. L. unlearned his association between separation and death – and change existing synaptic connections to make way for new learning.

What physical evidence exists that dreams show our brains in the process of plastic change, altering hitherto buried, emotionally meaningful memories, as in Mr. L.'s case?

The newest brain scans show that when we dream, that part of the brain that processes emotion, and our sexual, survival, and aggressive instincts, is quite active. At the same time the prefrontal cortex system, which is responsible for inhibiting our emotions and instincts, shows lower activity. With instincts turned up and inhibitions turned down, the dreaming brain can reveal impulses that are normally blocked from awareness.

Scores of studies show that sleep affects plastic change by allowing us to consolidate learning and memory. When we learn a skill during the day, we will be better at it the next day if we have a good night's sleep. “Sleeping on a problem” often does make sense.

A team led by Marcos Frank has also shown that sleep enhances neuroplasticity during the critical period when most plastic change takes place. Huben and Wiesel blocked one eye of a kitten in the critical period and showed that the brain map for the blocked eye was taken over by the good eye – a case of use it or lose it. Frank's team did the same experiment with two groups of kittens, one group that it deprived of sleep, and another group that got a full amount of it. They found that the more sleep the kittens got, the greater the plastic change in their brain map.

Scientists blocked one eye of a kitten and showed that the brain map for the blocked eye was taken over by the good eye. Photo by Elena.

The dream state also facilitates plastic change. Sleep is divided into two stages, and most of our dreaming occurs during one of them, called rapid-eye-movement sleep, or REM sleep. Infants spend many more hours in REM sleep than adults, and it is during infancy that neuroplastic change occurs most rapidly. In fact, REM sleep is required for the plastic development of the brain infancy. A team led by Dr. Gerald Marks did a study similar to Frank's that looked at the effects of REM sleep on kittens and on their brain structure. Marks found that in kittens deprived of REM sleep, the neurons in their visual cortex were actually smaller, so REM sleep seems necessary for neurons to grow normally. REM sleep has also been shown to be particularly important for enhancing our ability to retain emotional memories and for allowing the hippocampus to turn short-term memories of the day before into long-term ones (i.e., it helps make memories more permanent, leading to structural change in the brain).

Each day, in analysis, Mr. L, worked on his core conflicts, memories, and traumas, and at night there was dream evidence not only of his buried emotions but of his brain reinforcing the learning and unlearning he had done.

We understand why Mr. L. at the outset of his analysis, had no conscious memories of the first four years of his life: most of his memories of the period were unconscious procedural memories – automatic sequences of emotional interactions – and the few explicit memories he had were so painful, they were repressed. In treatment he gained access to both procedural and explicit memories from his first four years. But why was he unable to recall his adolescent memories? One possibility is that he repressed some of his adolescence; often when we repress one thing, such as a catastrophic early loss, we repress other events loosely associated with it, to block access to the original.

But there is another possible cause. It has recently been discovered that early childhood trauma causes massive plastic change in the hippocampus, shrinking it so that new, long-term explicit memories cannot form. Animals removed from their mothers let out desperate cries, then enter a turned-off state – as Spitz's infants did – and release a stress hormone called “glucocorticoid.” Glucocorticoids kill cells in the hippocampus so that it cannot make the synaptic connections in neural networks that make learning and explicit long-term memory possible. These early stresses predispose these motherless animals to stress-related illness for the rest of their lives. When they undergo long separations, the gene to initiate production of glucocorticoids gets turned on and stays on for extended periods. Trauma in infancy appears to lead to a supersensitization – a plastic alteration – of the brain neurons that regulate glucocorticoids. Recent research in humans shows that adult survivors or childhood abuse also show signs of glucocorticoid supersensitivity lasting into adulthood.

That the hippocampus shrinks is an important discovery. Depression, high stress, childhood trauma all release glucocorticoids and kill cells in the hippocampus, leading to memory loss. The longer people are depressed, the smaller their hippocampus gets. The hippocampus of depressed adults who suffered prepubertal childhood trauma is 18 percent smaller than that of depressed adults withous childhood trauma – a downside of the plastic brain : we literally lose essential cortical real estate in response to illness.

If the stress is brief, this decrease in size is temporary. If it is too prolonged, the damage is permanent. As people recover from depression, their memories return, and research suggests their hippocampi can grow back. In fact, the hippocampus is one of two areas where new neurons are created from our own stem cells as part of normal functioning.

Antidepressant medications increase the number of stem cells that become new neurons in the hippocampus. Rats given Prozac for three weeks had a 70 percent increase in the number of cells in their hippocampi. It usually takes three to six weeks for antidepressants to work in humans – perhaps coincidentally, the same amount of time it takes for newly born neurons in the hippocampus to mature, extend their projections, and connect with other neurons. So we may, without knowing it, have been helping people get out of depression by using medications that foester brain plasticity. Since people who improve in psychotherapy also find that their memories improve, it may be that it also stimulates neural growth in their hippocampi.

(Turning Our Ghosts into Ancestors. The Brain That Changes Itself by Norman Doidge, M.D., excerpt).

We are often haunted by important relationships from the past that influence us unconsciously in the present. Photo by Elena.

Autism

Autism and Case of Autism

Redesigning the brain

The mystery of autism – a human mind that cannot conceive of other minds – is one of the most baffling and poignant in psychiatry, and one of the most severe developmental disorders of childhood. It is called a “pervasive developmental disorder,” because so many aspects of development are disturbed: intelligence, perception, socializing skills, language, and emotion.

Most autistic children have an IQ of less than 70. They have major problems connecting socially to others and may, in severe cases, treat people like inanimate objects, neither greeting them nor acknowledging them as human beings. At times it seems that autistics don't have a sense that “other minds” exist in the world. They also have perceptual processing difficulties and are thus often hypersensitive to sound and touch, easily overloaded by stimulation. (That may be one reason autistic children often avoid eye contact: the stimulation from people, especially when coming from many senses at once, is too intense). Their neural networks appear to be overactive, and many of these children have epilepsy.

Because so many autistic children have language impairments, clinicians began to suggest  the Fast ForWord program for them. They never anticipated what might happen. Parents of autistic children who did Fast ForWord told Merzenich that their children became more connected socially. He began asking, were the children simply being trained to be more attentive listeners? And he was fascinated by the fact that with Fast ForWord both the language symptoms and the autistic symptoms seemed to be fading together. Could this mean that the language and autistic problems were different expressions of a common problem?

Two studies of autistic children confirmed what Merzenich had been hearing. One, a language study, showed that Fast ForWord quickly moved autistic children from severe language impairment to the normal range. But another pilot study of one hundred autistic children showed that Fast ForWord had a significant impact on their autistic symptoms as well. Their attention spans improved. Their sense of humor improved. They became more connected to people. They developed better eye contact, began greeting people and addressing them by name, spoke with them, and said good-bye at the end of their encounters. It seemed the children were beginning to experience the world as filled with other human minds.

The incidence of autism has been climbing at a staggering rate that can't be explained by genetics alone. Photo by Elena.

Case of Autism

Lauralee, an eight-year-old autistic girl, was diagnosed with moderate autism when she was three. Even as an eight-year-old she rarely used language. She didn't answer to her name, and to her parents, it seemed she was not hearing it. Sometimes she would speak, but when she did, “she had her own language,” says her mother, “which was often unintelligible.” If she wanted juice, she didn't ask for it.  She would make gestures and pull her parents over to the cabinets to get things for her.

She had other autistic symptoms, among them the repetitive movements that autistic children use to try to contain their sense of being overwhelmed. According to her mother, Lauralee had “the whole works – the flapping of the hands, toe-walking, a lot of energy, biting. And she couldn't tell me what she was feeling.”

She was very attached to trees. When her parents took her walking in the evening to burn off energy, she'd often stop, touch a tree, hug it, and speak to it.

Lauralee was unusually sensitive to sounds.  “She had bionic ears,” says her mother. “When she was little, she would often cover her hears. She couldn't tolerate certain music on the radio, like classical and slow music.” At her pediatrician's office she heard sounds from the floor upstairs that others didn't. At home she would go over to the sinks, fill them with water, then wrap herself around the pipes, hugging them, listening to the water drain through them.

Lauralee's father is in the navy and served in the Iraq war in 2003. When the family was transferred to California, Lauralee was enrolled in a public school with a special-ed class that used Fast ForWord. The program took her about two hours a day for eight weeks to complete.

When she finished it, “she had an explosion in language,” says her mother, “and began to speak more and use complete sentences. She could tell me about her days at school. Before I would just say, :Did you have a good day or a bad day?” Now she was able to say what she did, and she remembered details. If she got into a bad situation, she would be able to tell me, and I wouldn't have to prompt her to get it out of her. She also found it easier to remember things.” Lauralee has always loved to read, but now she is reading longer books, non-fiction and the encyclopedia. “She is listening to quieter sounds now and can tolerate different sounds from the radio,” says her mother. “It was an awakening for her. And with the better communication, there was an awakening for all of us. It was a big blessing.”

By Norman Doidge (excerpt from The Brain That Changes Itself).

Better communication can help to an awakening. Illustration by Elena.

Tactile Vision

Tactile Vision Experiments

In 1969, “Nature”, Europe's premier science journal, published a short article that had a distinctly sci-fi feel about it. Its lead author, Paul Bach-y-Rita, was both a basic scientist and a rehabilitation physician – a rare combination. The described a device that enabled people who had been blind from birth to see. All had damaged retinas and had been considered completely untreatable.

The “Nature” article was reported in “The New York Times”, “Newsweek”, and “Life”, but perhaps because the claim seemed so implausible, the device and its inventor soon slipped into relative obscurity.

Accompanying the article was a picture of a bizarre-looking machine – a large old dentist's chair with a vibrating back, a tangle of wires, and bulky computers. The whole contraption, made of castaway parts combined with 1960s electronics, weighed four hundred pounds.

A congenitally blind person – someone who had never had any experience of sight – sat in the chaire, behind a large camera the size of those used in television studios at the time. He “scanned” a scene in front of him by turning hand cranks to move the camera, which sent electrical signals of the image to a computer that processed them. Then the electrical signals were conveyed to four hundred vibrating stimulators, arranged in rows on a metal plate attached to the inside of the chair back, so the stimulators rested against the blind subject's skin. The stimulators functioned like pixels vibrating for the dark part of a scene and holding still for the brighter shades.

The power of positive thinking finally gains scientific credibility. Mind-bending, miracle-making, reality-busting stuff... Straddles the gap between science and self-help... Illustration by Elena.

This “tactile-vision device,” as it was called, enabled blinded subjects to read, make out faces and shadows, and distinguish which objects were closer and which father away. It allowed them to discover perspective and observe how objects seem to change shape depending upon the angle from which they were viewed. The six subjects of the experiment learned to recognize such objects as a telephone, even when it was partially obscured by a vase. This being the 1960s, they even learned to recognize a picture of the anorexic supermodel Twiggy.

Everyone who used the relatively clunky tactile-vision device had a remarkable perceptual experience, as they wen from having tactile sensations to “seeing” people and objects.

With a little practice, the blind subjects began to experience the space in from of them as three-dimensional, even though the information entered from the two-dimensional array on their backs. If someone threw a ball toward the camera, the subject would automatically jump back to duck it. If the plate of vibrating stimulators was moved from their backs to their abdomens, subjects still accurately perceived the scene as happening in front of the camera. It tickled near the stimulators, they didn't confuse the tickle with a visual stimulus. Their mental perceptual experience took place not on the skin surface but in the world. And their perceptions were complex. With practice, subjects could move the camera around ans say things like “That's Betty; she is wearing her hair down today and does not have her glasses on; her mouth is open, and she is moving her right hand from her left side to the back of her head.”

True, the resolution was often poor, but as Bach-y-Rita would explain, vision doesn't have to be perfect to be vision. “When we walk down a foggy street and see the outline of a buildings,” he would ask, “are we seeing it any less for the lack of resolution? When we see something in black and white, are we not seeing it for lack of color?”

(The Brain that Changes Itself, Stories of Personal Triumph from the Frontiers of Brain Science), by Norman Doidge, M.D.)

“When we walk down a foggy street and see the outline of a buildings, are we seeing it any less for the lack of resolution?". Illustration by Elena.