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    Real misery of phantom pain

    Medicine & Science

    Real misery of phantom pain
    Nerves: The body's attempt to rewire itself after a stroke, amputation or spine injury can lead to agony without any usual cause.

    Sponsored by

    By David Kohn
    Sun Staff

    August 25, 2003

    Bob Lane thought he had survived almost unscathed. At first, the only damage from his 1999 stroke seemed to be reduced peripheral vision in one eye. But a few months later, the pain began.

    It began as just an odd tingling in his left leg. But over several months, the sensation became more and more painful, until it was excruciating. The strangest part of the phenomenon: Nothing at all was wrong with his leg.

    "It feels like my leg has been burned and I'm wearing sandpaper pants," says Lane, a retired college biology professor who lives in Bainbridge, Ga. Because the brush of a bedsheet can trigger the sensation, Lane rarely sleeps through the night. Even the breeze from a ceiling fan can bring on the pain.

    Over the past 3 1/2 years, he has gone to a half-dozen doctors and tried a dozen different drugs, as well as acupuncture - to no avail. "It's frustrating," he says. "Somehow my brain is sending the wrong messages to my body."

    Lane's experience is not unusual. Thousands of stroke victims every year suffer this mysterious pain. The problem is not limited to them - the malady afflicts hundreds of thousands of Americans, including those with spinal cord injuries, cancer, diabetes, multiple sclerosis and amputated limbs.

    The syndrome is commonly known as "central pain" because it originates in the central nervous system - the spinal cord and brain - rather than in the limbs and trunk. It has confused and vexed doctors and patients for decades.

    "We don't understand it very well, and we don't treat it very well," says Johns Hopkins Hospital neurosurgeon Dr. Frederick Lenz, a recognized specialist in central pain.

    But in the past five years, researchers have begun to unravel exactly how the central nervous system perceives - and creates - pain. Scientists are using this knowledge to develop new treatments, which could eventually ease Lane's sandpaper sensation.

    Those with central pain endure a range of agonizing, baffling sensations. Some describe feeling as if they were on fire, while others report a tingling coldness. One patient found that brushing his teeth sent awful pain to his arms.

    "I get the feeling there are chunks of broken glass in parts of my body," says 38-year-old Lisa Bard, whose spinal cord was damaged in an accident this year. Bard, who lives in Germantown, has tried numerous drugs and therapies. None has done much to alleviate the pain, which flares up without warning.

    Drugs that work well for "normal" pain, such as morphine, typically do little for the disorder. Unwilling or unable to face the excruciating suffering, a significant number of central pain patients commit suicide.

    Until the 1950s, many physicians doubted that the mysterious malady even existed, attributing complaints to hypochondria or malingering. Even today, it is not unusual for doctors to question the reality of their patients' pain.

    "Traditionally, physicians have been taught that if there's no sensory input, the pain isn't real," says anesthesiologist Dr. Christine Sang, a central pain expert at Harvard Medical School.

    Researchers now know that central pain stems from misinterpreted signals in the central nervous system. "It's an illusion - a neural illusion," says neuroscientist Bob Yezierski. "You have a sensation that something is going on, but in fact nothing is going on. The only thing happening is an abnormal activation in the central nervous system."

    For those with spinal cord injuries, central pain is particularly vexing: 60 percent to 90 percent of the 400,000 spinal cord injury patients in this country have the disorder. For many, this pain is more debilitating than the original injury - one study found that almost four in 10 patients would gladly trade pain relief for the chance to regain pre-injury movement.

    For the past decade, Yezierski has studied how spinal cord injuries disturb pain transmission. In experiments on rats, he has found that after an injury, the spinal cord's main inhibitory circuitry breaks down, allowing pain-transmitting neurons to fire much more often than normal. "The brain interprets these abnormal discharges as pain," he says.

    Yezierski, who directs the Comprehensive Center for Pain Research at the University of Florida, is trying to find ways to stop this neuronal machine gun. He's focusing on neurons that have the neurokinin-1 (NK-1) receptor, which seems to play a key role in sending central pain signals. He uses "molecular neurosurgery," attaching a neurotoxin to the neurotransmitter that activates NK--1.

    When this neurotransmitter links with NK-1, the attached neurotoxin gets into the cell and kills it, thus eliminating the excessive pain signals. The early results are promising. In rats, the procedure "had a very significant effect on pain behavior," says Yezierski, who hopes to test the method in human trials.

    The loss of inhibitory circuits is just one piece of the puzzle. Yale University scientists have found that once severed, spinal cord neurons try to reconnect themselves. They succeed, but often link with the wrong neurons.

    "The wiring gets switched," says Yale neuroscientist Bryan Hains. "Instead of touch, the signal becomes pain."

    This mis-wiring might help explain why those with the disorder can feel piercing pain in response to seemingly harmless stimuli such as clothing on skin.

    Hains and his colleagues are trying to stop these garbled signals by clogging the sodium channel, a key structure in the neuron that sends electrical charges to other neurons. They have developed a drug to block these channels in certain pain receptors. When given to rats with injured spinal cords, the substance seems to sharply reduce pain.

    Other researchers are focusing on the brain's role in central pain. Using cutting-edge brain imaging technology, researchers have found that a spinal cord injury can lead to changes in the brain itself.

    Research on monkeys in the late 1990s suggests the damaged spinal cord sends fewer signals to the thalamus, the walnut-shaped brain region that receives and organizes almost all sensory input. Without input, the thalamus becomes hypersensitive, firing more frequently in response to smaller stimuli.

    A similar alteration might occur in stroke victims, says University of Maryland, Baltimore pain researcher Joel Greenspan. He suspects that in the months after the stroke, healthy brain neurons sprout into damaged areas. These invading cells might misinterpret incoming signals, turning innocuous sensations into excruciating ones.

    Greenspan and Lenz are trying to map brain areas where specific pain sensations occur. With such a map, doctors might one day be able to switch off particular sensations: Scientists at the University of California, San Francisco announced last month that they had injected a signal-blocking gene into the rat cortex, halting pain coming from a specific brain region.

    For now, though, doctors must rely on a less exact method to stop the brain's aberrant pain signals.

    Lenz and a few others around the country are trying a new surgical technique, in which electrodes are implanted above the motor cortex. Placed permanently inside the skull, the device sends a signal that seems to jam central pain messages. Lane, the retired professor, is considering the procedure, which succeeds about half the time.

    How does this stimulation surgery work? No one really knows. Despite recent advances, central pain remains a daunting mystery. As Greenspan puts it: "This syndrome illustrates just how little we know about the human brain."

    Copyright © 2003, The Baltimore Sun

    Proofread carefully to see if you any words out.

    "Medicine & Science

    Real misery of phantom pain"

    This meaning the "scientific" ignoring of magic systems,
    (also between people where some can perceive pain of another even over a meter or more away), and declaring whatever they don't comprehend "phantom"?

    Or actually zero according systems reactions
    outside those that might be needed to imagine also some phantom, monster or whatever?

    "Nerves: The body's attempt to rewire itself after a stroke, amputation or spine injury can lead to agony without any usual cause."

    Hm, apart from that I don't get why the rewiring itself
    instead of effects, after some is already there to transmit again,
    for example "messages" in context with damaged systems,
    seems regarded more central,

    I also don't get this "without any usual cause".
    As with such differing as listed, this seems quite a number of persons.

    Seeming usual enough there.

    Didn't really seem like just one single case known,
    where indeed one might think, how unusual.

    Apart from this, with brain damages as stroke or spine injury,
    or other systems damages as an amputation,
    it seems to me somehow not unusual in any particular form,
    that systems damages and pain are felt in context with this.

    Strange and unusual might seem, if systems, though sensitive for the region where the damages occurred, would react alike nothing wrong there.

    "Bob Lane (...) stroke (...) reduced peripheral vision in one eye."
    Being too lazy to try searching through some neuro texts or so,
    I just wondered idly, what brain system(s) tend to have with such?

    Assuming it was not to do with within the eye?

    Also I don't get from this part, where exactly the internal damages are.

    I find this to complicate attempts to try to comprehend patterings
    alike what follows about a leg.

    If one knew, soandso systems got damaged,
    if including ones having relays also with a leg,
    one might start to think about this then.

    Maybe also about stuff alike,
    I think there was this experiment where the abuser front of persons of related kinds cut whiskers and then messed into the brain of women and men of related kinds held prisoners, and then someone trying to cross-deduct something to do with later differing high reactions sensory over to autism.
    High reactions to touch or/and this or that there.

    But without sector data given from where to where the damages extend
    (and the MRI I think in this year was already invented,
    and also magic check attempts if anything of significance is noticed)
    it seems harder to comprehend patterings to some extent or speculate.

    "But a few months later, the pain began."

    (This for example also not telling, if any meds/drugs in this time were taken that can alter receptor molecule numbers.

    Nor, if this is one of the people resting a lot and sort of respecting damaged systems.
    Or one ruthlessly trying to force them to this or that,
    messing massively into the healing processes running.

    In other words, such info not there, seems to make it difficult to guess around,
    if this just came somehow as some wake effect,
    or if there was something in between happening maybe of significance
    to also consider.)

    "It began as just an odd tingling in his left leg."

    Hm, I think I rather leave this now for comments to experienced with such having SCI.

    (As the only sort of tinglings I can first think about, are to do with lacking supply,
    or alike Restless Leg Syndrome.)

    "But over several months, the sensation became more and more
    painful, until it was excruciating. The strangest part of the phenomenon: Nothing at all was wrong with his leg."

    So all sensory relays with brain systems undisturbed. Not alike something from up there not going down there. No damaged relays alike off or shut down, or so. It being excluded that not something was missing in signals down, of importance for something down there. Therefore any disturbances down there via such excluded?

    Again, without listings what sectors got damaged in the brain,
    how is one supposed to seriously think about the issue?

    Hm, but O.K., tried without.

    First options for theories I can think of:

    1.: There were damages to something in the brain, having relays with down there.
    Also that it was just one leg, seeems to speak for this.

    I guess some neuro could be asked, peripheral vision in one (which?) eye
    would blank out with what systems damaged?

    The eyes nerves crossing aside, is there with one eye on a certain side a distinct whatever, which side then deeper in the brain damages might be?

    Close to this region, are there any systems having relay connections with the left leg?

    If so, which?

    2.: A fixing on incoming signals, due to whatever causes,
    over the months might alike highten internal structures for processing such.

    Similar as using a brain system or several often for this or that, that eventually connections between cells might alter.
    From what I understood in hippocampus, not sure how many other sectors maybe also, cell numbers can also alter.
    I heard a more general whatever, that with either success or often using a region for something cell numbers can increase.

    (However being unclear about to how many sectors this was (not) referring)

    Whether connections, or also cells,
    an increase if using systems often for something,
    seems quite standard.

    Therefore it might be speculated, if this happened there.

    3. 1.+2.: It might be also wondered, if brain damages
    caused a differences in relays to the leg, this causing disturbances there.

    Then something as in theory 2 following.

    (As this system might crash at quite inconvient timings,
    I rather send this off. Continuation might follow.)

    [This message was edited by Acid on 08-27-03 at 05:09 AM.]



      "It feels like my leg has been burned and I'm wearing sandpaper pants,"

      -> Autist comment.

      -> Autism literature.

      Also: Which fabrics by various are more disliked or still better tolerated.

      Note: If in genetic history from maybe over a billion years backwards to now,
      taking a 1 m measure, the time from where our ancestors started to wear clothes,
      till now,
      might seem amazingly small on this.

      The wearing of clothes touching against skin
      for hundreds of millions of years was not customary among our ancestors.

      If getting so high problems with it, why not consider some closer to the equator culture ("without winter"), where it is not customary to wear particularily much.

      "a retired college biology professor"

      Some resettling of interest directions might make note various data better.
      For example a shift into a cross of some of neurology and "autism" observations.

      (Mentioned some neuro and "autism" stuff.
      Clothes aversions, or with parts of fabrics aversions, are not this uncommon with the latter.
      Some interesting theories might be found about why such high reactions might be there.

      However with various theories one might be better careful, even if stated alike facts, how erratic they might be.)

      "Because the brush of a bedsheet can trigger the sensation, Lane rarely sleeps through the night. Even the breeze from a ceiling fan can bring on the pain."

      That I don't recall in context with autism yet. And seems weird.

      The guy does not happen to have no partner,
      and some mental crisis in life not just in context with this,
      where a leg fixation might come suited?

      I've been in the Sahara, often no fan for weeks, and though first sweating till 1 a.m., eventually seeming getting used to it better.
      So if a ceiling fan were regarded such a problem, why not switch it off.
      This is also why I wondered, if the guy ain't got some cause for a mental fix on it.

      As a bio smurf it might not be beyond his understanding,
      that non-use might lead to decrease,
      and high use to increase with various connections.
      Nor might be be oblivious, that adrenaline can be quite a blocker against pain.

      However instead of distractions with some adrenaline suited sports and films,
      he seems to be busy with the ceiling fan, where I assume it has a switch-off button.

      With a non-bio one might still assume, hm, maybe never heard about some cellular and cellular connection principles.

      But with a bio? Even if not specialized into cell-bio, I assume the average bio smurf had quite a bit to do with cells and quite some stuff in context.

      Even some acidhead MBD chaot like me, might have the idea to flip open some pages of a neuroanatomy book.

      (Though after some joint just extinguished, might get even more chaotic: )

      ~"A brain stem region, located in the lateral medullary reticlular formation,gives rise to a descending noradrenergic projection that also suppresses pain transmission."

      Guess if I had the problem, I might consider to find me some pics, and try
      if aimings for there and some regulatatory influences can be figured out by me or not.

      ~"Damage to the optic tract or the lateral geniculate nucleus.,
      also due to a vascular accident, produces a defect in the contralateral visual field."

      (Hm, suspected already before something to do with geniculate, therefore go for this

      What's near the lat. geniculate n.? ..."Ventral posterior n.: Input: SPINAL cord, ...
      Output: Primary somatic SENSORY Cortex. Functions: TOUCH, limb position sense, PAIN, and TEMPERATURE sense.

      Patterings match: "It feels like my leg has been BURNED." PAIN. TOUCH. SENSORY.


      For what we might call in German some "phi times" (over the) "thumb" estimate(d) thingie,
      this sector nor far from geniculate looks not incompletely inconspicuous.

      If it were my brain, the thought might occur, smurfing to a hospital, dudes, I wanna get me some MRIs, can you aim your artificial energies of the thingie, for them two thalamus sectors. If all still looks neat and proper there.
      (Though for the typical Westie doc, one'd better word this very differingly.)



        (...) I ain't mean, it gotta be this.

        Ain't recall ever reading one neurobook in my life till the end.
        Some half-stoned flipping through a few pages of one, with alike a pattering whatever, is closer to my usual methodics with such.
        I can find it amusing, if an author goes alike real serious about something, and me thinking but why is no convergence whatever seeking there noticed
        between optic systems correlated whatevers
        and what might cause such pains as described there.

        So I can go quite joking in between, too. As that lateral geniculate is not far from other stuff to do with pain, someone seriously into neuro might know.
        And I thought of this one, more optics correlated, before even reading this close to it is pain correlated stuff.

        But maybe it's something totally differing there.

        I can sometimes just semi-joke around.

        Alike, if a retired college biology professor,
        weren't preoccupied with the ceiling fan,
        but managed somewhen to find the off-switch of this device,
        there might be also ample time to flip through some neuro pages.

        Way more, than some stoned MBD acidhead, somewhere between two joints,
        is willing to spend with such.

        Exaggerated, some professor might be expected, to have various capacities beyond
        some MBD in a THC cloud.

        With medial geniculate between lateral geniculate and ventral posterior n.,
        it seems questionable, anyway, if the sort of arching geniculate makes,
        would be sufficient, and there being options,
        that some damage could hit lateral geniculate and ventral posterior,
        but, at least in this text so far,
        no indicator by me noticed for medial geniculate.

        Though apart from this, can be entertaining to speculate around with wild guesses.

        Just got curious and flipped to Somatic Sensory chapter.

        "Ventral posterior lateral nucleus mediates sensations from the limb and trunk."
        "...": ~ The ventral posterior nucleus ... provides the dominant input to the primary somatic sensory cortex.
        Sensory c.: Areas 3b and 1 play a major role in touch perception.

        {Gee, just had a major word swap error, instead of "touch perception" "pain perception" first coming out. Didn't sleep last night. When getting tired, might be a bunch of word swaps, and not necessarily noticed. Might be better to not take this stuff here too serious, anyway, is more alike some thought game.}

        If not having any relevant role with pain perception, or having some,
        seemed to be argued about there, but I was too lazy to get it well.
        However from there seems to go to insular cortex regions.
        Not sure, wasn't there some article in CareCure mentioning insular cortex
        in context with pain perception?

        Thalamus ... posterior nuclear group (...) of nuclei located caudal and ventral to
        the ventral posterior nucleus.
        These nuclei, which have long been thought to participate in pain perception, are likely to be part of a variety of functional circuits.

        (Another suspicious candidate group or not?)

        Primary Somatic Sensory Cortex: Descending projection neurons: To
        ventral posterior nucleus of the thalamus.

        (Here we go again ...)

        And to: striatum, brain stem, spinal cord.
        From neurons located in layer 5.

        To thalamus from 6.

        Hm, one might wonder, in case ventral posterior got zoinked a badie in the first place,
        if alike a long round is done, down to that leg and back,
        or (//and) if shortcircuiting around in the melon?
        Or IF some of the region got damaged, if any might come there from this leg and being too much for it, and overreactions being sent out from there to neighbours, +via sens.c. to insular c.?

        Hm, entertaining game.