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The Tell-Tale Brain
A neuroscientist's quest for what makes us human
V. S. Ramachandran
Prefrontal cortex can suffer major damage, yet in a casual meeting patient seems normal. But friends and kin will say the person has changed so dramatically they don't recognize him any more. Patient seems to lose all interest in own future, and shows no moral compunctions at all - may urinate in public, laugh at funeral. His language, his memory, even his IQ seem unchanged, but has lost the things that make him 'human': empathy, foresight, morality and dignity.
Interestingly, this lack of empathy, moral standards and self-restraint are also typical of sociopaths, so it is possible that there is a neuro explanation.
When a limb is amputated,the brain still has a body map including it, even though it is no longer receiving signals from it. What then happens is that the areas which are still getting signals take over neighboring space. So a missing hand will appear on patient's face, and touching cheek areas will be reported as touching a missing finger or palm. The body map of penis is right beside foot, and one patient who's foot amputated reported orgasms which spread through that foot as well.
Our power of empathy is so strong that some patients claim that when watch someone else's hand being tapped, they 'feel' it on their phantom limb. Such patients can also get relief by just watching other person's hand being massaged.
Mirror box as first successful amputation of a phantom limb (see below). VSR says don't yet know how it works, but he suspects that the brain gets a whole lot of conflicting info - no signals back from the limb, no result from commands sent to the limb, and finally conflicting visual feedback via the mirror box - and just gives up, and says, "To hell with it, there is no arm."
Vision: if you have 3 projectors - one shining red, one shining green and another blue - you can, by changing the brightness, produce any color at all, even white. So astonishing that people have trouble believing it at first, but it tells us something fundamental about vision. Even though we can distinguish thousands of colors, we have just 3 different color receiving cells in our eyes - one for red light, one for green and one for blue. Using just colored lights to figure out the laws of color vision was one of the early triumphs of science. The rules were deduced way before the actual mechanism was discovered and explained. And it paved the way for color printing using just 3 dyes, and color TV.
Visual info gets to cortex by 'old' and 'new' pathways. The old pathway starts at retina, goes through an ancient midbrain structure called the superior colliculus to the parietal lobes. This pathway is concerned with where an object is going, but not what it is. The new pathway, which is highly developed in all primates, does the analysis and recognition of scenes and objects. This goes from the retina to V1, the first and biggest of our brain visual maps. From there it splits into two substreams, pathway 1 and 2.
Pathway 1 is the 'how' and 'where' stream - you utilise when you dodge something thrown at you, or navigate around obstacles or reach out to grab something. There is a phenomenon called 'blindsight' - 'blind' patients with a damaged path to V1 could still navigate around obstacles etc, even though not consciously aware of being able to see anything. The old pathway is still delivering info, but below level of conscious thought.
Pathway 2 does the classifying - what is this and what does it mean to us? Runs from V1 to the fusiform gyrus, where things are classified - Hawks from handsaws, Joe from Jane, but without assigning any significance to the classifications. It just collects and labels things. Then info goes to the rest of temporal lobes, where various associations are attached - memories about the object.
Pathway 3 bypasses all the processing areas and goes straight to the amygdala, the emotional core of the brain. This can activate the nervous system for fast action if necessary - the "4 Fs" of fight, flee, feed or romance.
Capgras syndrome (where think people close to you have been replaced by aliens) explained by selective damage (stroke or accident) to Pathway 3 - still recognize your mother and have all associations with her, but no longer getting an emotional response. The brain refuses to admit that it could be wrong. The only way brain can reconcile the discrepancy is by concluding that mom's been replaced by an exact replica.
[V.S. RAMACHANDRAN:] I'm interested in all aspects of the human mind, including aspects of the mind that have been regarded as ineffable or mysterious. The way I approach these problems is to look at patients who have sustained injury to a small region in the brain, a discipline called Behavioral Neurology or Cognitive Neuroscience these days.
Let me tell you about the problem confronting us. The brain is a 1.5 kilogram mass of jelly, the consistency of tofu, you can hold it in the palm of your hand, yet it can contemplate the vastness of space and time, the meaning of infinity and the meaning of existence. It can ask questions about who am I, where do I come from, questions about love and beauty, aesthetics, and art, and all these questions arising from this lump of jelly. It is truly the greatest of mysteries. The question is how does it come about?
When you look at the structure of the brain it's made up of neurons. Of course, everybody knows that these days. There are 100 billion of these nerve cells. Each of these cells makes about 1,000 to 10,000 contacts with other neurons. From this information people have calculated that the number of possible brain states, of permutations and combinations of brain activity, exceeds the number of elementary particles in the universe.
The question is how do you go about studying this organ? There are various ways of doing it. These days brain imaging is very popular. You make the person perform some task, engage in conversation or think about love, for that matter, or something like that, or imagine the color red. What part of the brain lights up? That gives you some confidence in saying that that region of the brain is involved in mediating that function. I'm sort of simplifying it, but something along those lines. Then there is recording from single cells where you put an electrode through the brain, eavesdrop on the activity of individual neurons, find out what the neuron is responsive to in the external world. There are dozens of such approaches, and our approach is behavioral neurology combined with brain imaging.
Behavioral neurology has a long history going back about 150 years, a venerable tradition going back to Charcot. Even Freud was a behavioral neurologist. We usually think of him as a psychologist, but he was also a neurologist. In fact, he began his career as a neurologist, comparable in stature with Charcot, Hughling Jackson, Kurt Goldstein. What they did was to look at patients with sustained injury to a very small region of the brain—and this is what we do as well in our lab. What you get is not a blunting of all your mental capacities or across the board reduction of your mental ability. What you get often is a highly selective loss of one specific function, other functions being preserved relatively intact. This gives you some confidence in saying that that region of the brain is specialized in dealing with that function.
It doesn't have to be a lesion; it can be a genetic change. One of the phenomena that we've studied, for example, is synesthesia, the merging of the senses (which I'll talk about in a minute) where's there has been a genetic glitch. It runs in families in whom some gene or genes cause people to hear colors and taste sounds. They've got their senses muddled up. We've been studying this phenomenon.
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One of the peculiar syndromes, which we have studied recently, is called apotemnophilia. It's in fact so uncommon that many neurologists and many psychiatrists have not heard of it. It's in a sense a converse of phantom limbs. In a phantom limb patient an arm is amputated but the patient continues to vividly feel the presence of that arm. We call it a phantom limb. In apotemnophilia you are dealing with a perfectly healthy, normal individual, not mentally disturbed in any way, not psychotic, not emotionally disturbed, often holding a job, and has a family.
We saw a patient recently who was a prominent dean of an engineering school and soon after he retired he came out and said he wants his left arm amputated above the elbow. Here's a perfectly normal guy who has been living a normal life in society interacting with people. He's never told anybody that he harbored this secret desire - intense desire - to have his arm amputated ever since early childhood, and he never came out and told people about it for fear that they might think he was crazy. He came to see us recently and we tried to figure out what was going on in his brain. And by the way, this disorder is not rare. There are websites devoted to it. About one-third of them go on to actually get it amputated. Not in this country because it's not legal, but they go to Mexico or somewhere else and get it amputated.
So here is something staring you in the face, an extraordinary syndrome, utterly mysterious, where a person wants his normal limb removed. Why does this happen? There are all kinds of crazy theories about it including Freudian theories. One theory asserts, for example, that it's an attention seeking behavior. This chap wants attention so he asks you to remove his arm. It doesn't make any sense. Why does he not want his nose removed or ear removed or something less drastic? Why an arm? It seems a little bit too drastic for seeking attention.
The second thing that struck us is the guy would often take a felt pen and draw a very precise irregular line around his arm or leg and say, "I want it removed exactly that way. I don't want you removing too little of it or too much of it. It would feel wrong. I want you to amputate it exactly on that line." And you could test him after a year it is the same wiggly line which he couldn't have memorized, and this suggests already that this is something physiological, and not something psychological that he is making up.
Another theory that is even more absurd (found in some papers, and again, it's also a Freudian theory) is that the guy wants a big stump because it resembles a giant penis. Sort of wish fulfillment. This again is ridiculous, complete nonsense, of course. The question is why does it actually happen? What we were struck by was that there are certain syndromes where the patient has a right hemisphere stroke, in the right parietal cortex. The patient then starts denying that the left arm belongs to him. He says, "Doctor, this arm," he'll often point to it with his right arm and say, "this arm belongs to my mother." Here's a person who is perfectly coherent, intelligent, can discuss politics with you, can discuss mathematics with you, play chess with you, asserting that his left arm doesn't belong to him.
This is different from apotemnophilia. In apotemnophilia the patient says, "This arm is mine, but I don't want it. I want it removed." But there are similarities, there's an overlap, so we suggested that maybe there's something wrong with his body image in the right hemisphere, which alienates the left arm, or the right arm, for that matter, from the rest of the person's body and the sense of alienation leads to the person saying, "I don't want it. Have it removed."
More specifically, messages from the arm and the skin throughout the body, in fact, go to the parietal lobe to a structure, the postcentral gyrus. There's a big furrow or cleft right down the middle of the brain called the central sulcus. Just behind that sulcus there is a vertical, narrow strip of cortex where there's is a complete map of your body's surface. Every point of your body's surface is represented in a specific point on the cortex and there's a complete map called the Penfield Map. That's where touch sensations, and behind it, joint sensations and muscle sensations, are all represented in this somatosensory map.
It turns out if I poke anybody with needle that pain sensation goes to the sensory pain region in the brain, probably in the thalamus and cortex, and then it goes to the amygdala. The amygdala alerts you to the pain and you say, "Ow." Right? And then it goes down to the anterior cingulate that feels the agony of the pain. There's a cascade of events. There's a sensation of pain and then the agony of pain, and then messages go down the autonomic nervous system and make you start sweating, preparing for action, fleeing, fighting, or whatever the required action is. So if you poke somebody with a needle, this whole cascade of events is set in motion. You can measure the skin resistance, which measures the sweating, you start sweating when poked.
Now, when I poked him with a little pencil above the line where he wanted his arm to be amputated nothing happened. Just a little gentle pencil prick. It's not a painful stimulus. Not much happened. There's no galvanic skin response, there's no arousal. But if you touch him below the line where he wants the amputation, there's a huge, big galvanic skin response. You can actually measure the aversion physiologically, not just rely on the subject to report. There's no way you can fake the galvanic skin response. It's the basis of all lie detector tests.
Then, of course, we went straight to the brain and we said let's map it out. And as I said we found S1 was normal, if you go to S2 that's normal. If you go to the superior parietal lobule where the body image is constructed, to some extent the inferior parietal lobule, right parietal, let's say, where the body image is, there is no arm representation in that center. That's what we found. If you touch the arm there's no activity there. If you touch above the line of amputation or touch the normal arm the activity is completely normal. So that region of the brain is abnormal, but we also speculate that the regions of the brain in the frontal lobes and insula/amygdala to which that SPL/IPL projects, there could be an interruption of signals. In either event there's a physiological reason why this happens. This is giving you insight into how the normal brain constructs a body image.
Sometimes you come across a syndrome where you cannot quite know for sure if this is a legit syndrome or not, even though you can find it in the bible of clinical psychologists called DSM, Diagnostic and Statistical Manual, which is the official book for clinicians. If they can label you, give your syndrome a name, they can charge you, charge an insurance company, so there has been a tendency to multiply syndromes.
There's one called, by the way, Chronic Underachievement Syndrome, which in my day used to be called stupidity. It actually has a name and it's officially recognized. Then there is a syndrome called De Clerambault Syndrome. De Clerambault Syndrome refers to, believe it or not, a young woman developing an obsession with a much older, famous, eminent, rich guy and develops the delusion that that guy is madly in love with her but is in denial about it. This is actually found in a textbook of psychiatry, and I think it's complete nonsense. Ironically, there's no name for the converse of the syndrome where an aging male develops a delusion that this young hottie is madly in love with him, but is in denial about it. Surely, it's much more common and yet it doesn't have a name. Right?
There are several theories of synesthesia. One theory is that they are crazy. Maybe, but let's set that aside for a minute. One of the things we learn in medicine is when a patient is trying to tell you something when you think he's crazy, it often means that you're not smart enough to figure it out. Sometimes he's crazy, but usually it means you're not smart enough to figure it out, so look carefully, talk to the patient.
In the case of synesthesia, another odd aspect of it is that it's much more common amongst artists, poets, novelists, and other creative people. In fact, seven or eight times more common. This is controversial, but the strong evidence is that this is true. Now why would that be the case? I mean, one of my students has shown this to be the case, Ed Hubbard; why would this happen? There are several little mini-mysteries here about synesthesia. Why would it run in families? Why would they say numbers are colors or tones are colors for that matter? Why would it be more common in artists, poets, and novelists? So on and so forth. So it's a medical mystery worthy of Sherlock Holmes, waiting to be solved.
The first thing we want to show is these people are not crazy. By the way, another common theory is that they are on drugs like LSD –– acid junkies or pot heads. Sure enough it's more common among people who are high on acid, but that makes it even more intriguing. Why would some drugs produce this merging of the senses, this peculiar phenomenon of numbers evoking colors?
Another theory is they're being metaphorical as when you and I say, "It is the east and Juliet is the sun." Or we just say, "This is a loud tie." The tie isn't loud. It doesn't make any sound. Why do you say it's a loud tie? Or cheese. Cheddar cheese is sharp. Now sharp is a tactile adjective, a sharp nail or something. Why do you use a tactile adjective to describe a taste, a gustatory sensation? You say well, it's a metaphor. That's circular. Why do you want to use a tactile metaphor for a taste sensation?
Explaining synesthesia as just a metaphor doesn't explain anything because it's trying to explain one mystery with another mystery and that doesn't work in science. Another example of a metaphor would be, "It is the east and Juliet is the sun." You don't say, "Juliet is the sun." Does that mean she's a glowing ball of fire? No, you don't say that. You say, "She is warm like the sun. She is radiant like the sun." "Is nurturing like the sun" is a celestial body like the sun (a pun rather than a metaphor) "is the center of my solar system" and so on. The brain forms the right links. Synesthesia, by the way, is a completely arbitrary link between five and red. It's not a metaphor in that sense, so I was uncomfortable with the idea, but I thought there might be something to it. But we'll come back to that later as we go along. About a decade ago, by the way, I proposed there may be unconscious synesthetic propensities in all of us, which has now been amply confirmed in many studies including a recent one from Oxford.
Another theory is they're remembering childhood memories. Maybe they played with refrigerator magnets and five was red, and six was blue, and seven was green and for some reason they're stuck with these memories. Well, this again begs the question of why you and I have played with magnets, but we don't have synesthesia presumably. Most of us don't. We found, by the way, the phenomenon of synesthesia is quite common. You see it in one in 50 people. It's not one in a thousand or one in 10,000. People often don't come out and say that they do because they're worried you might think they're crazy.
So the childhood memories thing doesn't work because, as I said, why would it run in families? Another reason for not believing it, you would have to say the same magnets were being passed from generation to generation and it doesn't make any sense. Metaphor? Maybe they are being metaphorical in some sense. Maybe it's related to metaphors. They're crazy? That's not a real argument. They're on drugs — no, that doesn't work either.
The first thing we wanted to show is they're not crazy. They aren't making this up. We generated a computerized display made up of fives, lots of scattered fives on the screen, and among those fives were scattered some twos. When you look at a two and a five, a five is a mirror of a two in a sense, in terms of its shape. So you have a bunch of outline drawings of fives. Scattered among them are some twos forming a shape. The twos cluster to form a triangle or a square or a circle like your Ishihara color test in traffic, when you're going through a traffic school eye exam for color vision. It's similar to that.
A normal person looking at it, the non-synesthete looking at this, says, "Oh, fives? You mean there are twos in here embedded? Let me see. Oh, there's a two there. There's a two. Okay. Oh, there's a two there. There's another one there." They take 20 or 30 seconds to find the hidden shape. A synesthete who sees five as red and two as green instantly sees a green circle or a green square or a hidden green shape pop out from the background. He's much faster in detecting the circle or the square than you and I are. If he's crazy how come he's better at it than us? Secondly, if you ask him what he sees he says, "I see a green triangle. I see a green square." Phenomenologically, perceptually, he literally sees the green square or the triangle or the rectangle. What this suggests is that it's a sensory experience not a memory association at least in some synesthetes. Jamie Ward has recently replicated our findings.
It turns out there is a heterogeneity of synesthetes, there are some synesthetes that we will call lower synesthetes, in whom the color is actually perceptually evoked and the numbers seem tinged with color—red, green, blue, yellow, chartreuse or indigo. But there are also more conceptual synesthetes where it does seem to be more like a memory association. We were focusing on the perceptual synesthetes, sensory synesthetes because they are easier to study scientifically.
First, we've shown they're not crazy, it's a real phenomenon. (Remember, I had three steps. First, to show it's real. Second, what are the brain mechanisms? Third, what are the broader implications? Why should I care?) We've solved the first problem which is it's a genuine phenomenon.
The second question is what causes it? Well, Ed Hubbard and I were looking at brain atlases and we were struck by the fact that there's a structure called the fusiform gyrus in the brain buried inside the folds of the temporal lobes. This structure, the fusiform gyrus it turns out, is where the color area of the brain is, V4, which was discovered by Semir Zeki. Right next to it, almost touching it, is the number area of the brain. It represents the visual representations of numbers. The two areas are almost touching each other. We said what's the likelihood that the most common type of synesthesia is the number-color synesthesia, and the number region and color region are adjacent to each other in the brain. This seems unlikely to be a coincidence. Then we said maybe there's an accidental cross-wiring between these two regions of the brain.
Now why would this happen? Why do these people have this cross-wiring? That's the next question. A clue first comes from observations made by Francis Galton and has been confirmed since then: it runs in families, it may have a genetic basis. So we said if you take the infant brain, a fetal brain, there's a tremendous redundancy of connections. Everything is connected to everything. It's a crude approximation, but it's almost true. Then what happens is there are pruning genes which prune away the excess connections between adjacent brain regions (or even separated brain regions that were densely connected). This creates a characteristic modularity of the adult brain. Now, if something goes wrong with the pruning gene, if pruning fails to occur in adjacent brain regions, like the color and number area remain connected even in the adult, and if the gene is selectively expressed in the fusiform gyrus through transcription factors, for example, if it's expressed in the fusiform gyrus then you're get a number/color synesthete. Every time your guy sees a number, because of the cross- wiring, the color neurons are going to be activated. Every time he sees a number he sees a color.
What has this got to do with synesthesia? What's going on in a metaphor? You're linking seemingly unrelated concepts and ideas, right? If the same synesthesia gene, instead of being expressed selectively in the fusiform gyrus and producing this quirky phenomenon of number/color synesthesia, if it were to be expressed throughout the cortex, throughout the brain, it's going to create a higher propensity, higher opportunity to link seemingly unrelated ideas and concepts in far flung brain regions. If we think of ideas and concepts as also located in specific brain regions, occupying specific brain regions, and if you have these long-range connections then it permits greater opportunity for linking seemingly unrelated concepts. Hence, the basis of creativity and metaphors. Hence, the eight times higher incidence of synesthesia among artists, poets, and novelists.
In other words, what I'm getting at is, an evolutionary biologist could ask the question what use is this gene? It's seen in one in 50 people. It's fairly common, not rare. Why is it conserved in evolution? If there's a gene in evolution that's useless—it's completely useless to see five as red and six as green—it would have been eliminated from the gene pool eons ago, 10,000 years, 20,000 years ago. Clearly, this gene has been around and has been conserved. Now why? Why is this gene still around if it's completely useless?
Well, one possibility is it confers some outliers in the population with the ability to link seemingly unrelated ideas making them artistic, more creative. But when I give these talks people often ask me why, if it's that good that that gene makes you artistic, creative, and metaphorical, why doesn't everybody have it? Well, it's a silly question because evolution takes time and given another 20,000, 100,000, 50,000 years everybody will have this gene and we'll all be creative. But that's not the right answer. It may be a partial answer, but the real answer, I think, is that you don’t want everyone being creative; we need engineers!
The reason I was attracted to it was because I'm curious about neurological syndromes given my background in clinical neurology, among other things. I began with being intrigued by phantom limbs. Patients would come into the clinic with an arm missing or a leg missing and continue to vividly feel the presence of that missing arm or leg. And again, it has been known for about 100 years and people thought of it as a curiosity, as a case study to be reported during grand rounds: 'Here is a patient with phantom limb.' Nobody knew what to make of it and certainly there was no interest in mainstream neuroscience in phantom limbs.
What we found is quite intriguing: two or three things. One discovery goes back about 15 years. Let's say I'm the guy with the phantom limb, I've lost my left arm and you're the physician. You come and touch the left side of my face. I start feeling the stroking sensation in my phantom thumb! Even though you're stroking my face I feel it in my phantom. If you touch this region, it's my index finger, that's my pinky. There's a complete map of the missing hand on the face. Now, why would this be? Here again is the medical mystery.
In an adult if you remove the arm, the hand area of the brain is now devoid of sensory input. It's hungry for new sensory input and it's not getting any sensory input. The sensory input from the face skin which normally only goes to the adjacent face area in the brain now invades the vacated territory corresponding to the missing hand and activates the hand cells in the brain. That, of course, misinforms higher centers in the brain that the hand is being stimulated. The patient then experiences the sensations as arising from the missing phantom limb. When you touch the face skin the message not only goes to the face area, but also activates the hand area in the brain. So you're getting cross-wiring between the hand area and the face area of the brain.
We did a ten minute experiment to show this, and it challenged the doctrine in neurology that neural connections of the brain are laid down in the fetus and in early infancy and once they've been laid down by the genome there's nothing you can do to change these connections in the adult brain. That's why if you have a lesion in the adult brain, say following a stroke, there's such little recovery of function and why neurological syndromes are so difficult to treat, notoriously difficult to treat.
It was believed there was no plasticity in the brain connections. We showed in our experiment that, in fact, there's a tremendous scope for rewiring. So much so that over a two centimeter distance in brain tissue in the cortex the face input has now invaded the hand territory of the brain. Then we did brain imaging and showed that this invasion had actually occurred, but we already knew this from the psychological experiment. So I guess my mind is primed to think about cross connections in the brain.
Now that's an example of cross connections caused by amputation depriving sensory input. In synesthesia, just like the face and the hand area, the color and the number area are right next to each other. I started thinking, well, maybe this is cross-wiring again. But in this case the cross- wiring is not due to deafferentation by removing the sensory input, but due to genes, given that it runs in families.
Sometimes we're able to devise treatment for the patients. For example, in phantom limbs, two-thirds of the patients with phantom limbs experience excruciating pain. There's no known treatment. I should re-state that: There are 20 known treatments, none of them work. So we started investigating it to develop a treatment for it. But sometimes even just explaining to the patient he's not crazy, telling him, "You've got a phantom limb. The reason for this is something is going on in the brain," is a tremendous relief for him. Somebody has apotemnophilia and wants his arm removed. Telling him, "You're not crazy, it's not Freudian, it's a specific anatomical reason why you're experiencing this." Then you go to the next step and say you have this hypothesis about what's going on. You've tested it, you know what's going on in his brain. But can you actually help the patient?
We said, "Let's use a mirror." So we put a mirror in the center of the table. This is similar to a mirror treatment for phantom pain and for stroke we discovered over a decade ago. You put a mirror in the center of the table and the patient puts his painful dystrophic, swollen, immobilized, paralyzed arm on the left side of the mirror. The shiny side of the mirror is on the right side and the patient puts his right hand on the right side of the mirror, positions it so it mimics the posture and location of the hidden dystrophic painful left hand. He looks inside the mirror and sees the reflection of the normal hand. Suddenly his hand looks normal, no longer swollen. That's obvious because he's looking at the reflection of the normal hand and it looks like you resurrected his normal hand in the mirror, and it's optically superimposed in the position of dystrophic swollen hand.
Now you ask him to send signals to both hands as if he were moving them, clenching and unclenching or rotating while he's looking in the mirror. Now he's going to get the impression - you don't initially ask him to actually move the left hand because if he moved it would be painful, he only moves his right hand - and he imagines his left hand moving. What then happens is the patient gets the visual image that his left hand, which is immobilized and paralyzed, is again obeying the brains command, it looks like it's moving and is not painful. This way you unlearn the learned pain and the learned paralysis. The astonishing thing is that the hand actually does start moving for the first time in his life, first time in decades, first time in years. It works better if you do it very soon after the dystrophy sets in, a few weeks or months afterwards. The hand starts moving again and the pain subsides, and in a remarkable example of mind/body interaction, the swelling also subsides, often in a matter of hours.
This chronic pain disorder is considered intractable, incurable. It has been known for decades. I think it was discovered over 100 years ago, for which people have done dorsal rhizotomy, cut the nerves going to the spinal cord, cut the spinal cord to treat it. They do a sympathetic ganglionectomy that does work to some limited extent. You can treat it equally effectively, if not more effectively, with just a two-dollar mirror. The patient looks inside and moves his normal hand. There have been clinical trials on this from a group in Germany, I believe, on 50 patients. The discovery was originally made on a handful of patients. Since then their have been double blind, placebo controlled crossover trials, which is the best type of clinical trial you can do, and people have found dramatic recovery from this pain in a matter of a few weeks of mirror treatment. Then the pain stays gone for a period of at least six months and then you may need a refill after that. Imagine the amount of pain and agony and invasive surgery this has saved.
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