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Thread: Is Central Pain a somatization syndrome

  1. #21
    Quote Originally Posted by arndog View Post
    Without getting too mired in semantics, I would amend THC's comment and would replace "neuropathic pain" with the term "peripheral neuropathic pain".

    One could make a case for the term "Neuropathic Pain" is inclusive of both "Central Pain" and "Peripheral Neuropathic Pain".

    I hope/am sure the Professor will pipe in here to straighten it this out in simple, easy to understand language {smiling}.
    that's what i thought. i call my pain neuropathic as that's what doctors recognize. but it is caused by sci.

  2. #22
    I have'nt had the bennefit of the same education that many of you have had.......all I know is....it hurts no matter what you call it. My question is.....does it matter which it is? Would the same medication work if one were actually found? And, how do you know which one you have...can you have both? Sometimes I think I have both, and when you hurt as many places as I do, and many so many others, does it even matter?

    Peripheral sugggests to me.....your limbs.....so how do you explain your toosh, who who, and all the other places that can hurt? I did'nt have this pain until sci......but they call it peripheral neuropathic diesease.

    Nights....and days....when it's killing me, I don't give a dam which it is.....I just want it stopped! But, it just gets worse as time/life passes me by...... I use to hope/pray that a medication would be discovered to help/cure this......but now, not so much. It's hard to hold onto hope when you realize no one is really looking.......

  3. #23
    smoky - it doesn't matter what you call it when you personally are suffering. It doesn't make it better by naming it.

    Just like knowing the name of a wildflower doesn't increase one's true knowledge and experiential joy of witnessing it.

    Humans seem to like to name, characterize, and quantify things. Like how many wooly mammoths are outside of my cave that I have to worry about. I think it is why we won the primate battle and now are the top dogs of the planet. ;-)

    It may be that different drugs will target different types of Neuropathic Pain, and for the research world, it does matter that you are comparing apples to apples.

    But when it boils down to you, in your house burning or freezing or sitting on a porcupine - a name doesn't seem to matter. But sometimes not knowing what it is creates more distress in medical problems.

    About the word peripheral in this setting - it means any nerve that is outside of the central nervous system (brain) or the spinal cord. So the nerves to and from the Toosh are peripheral. So are the nerves to your rib cage. It isn't just arms and legs.

  4. #24
    I must confess I am a believer in very specific terms. There is actually a huge battle going on over this, but I believe there is a pragmatic argument for specific terms, not only for central vs. peripheral, but also for the various Central PAINS, eg. dysesthetic burning vs. lancinating vs pins and needles, vs muscle pain, vs. visceral pains (typically the bladder and rectum) etc. There is a committee of the International Association for the Study of Pain, who sit around and discuss how they are going to name something. The coding process of Medicare and others makes this essential for pain doctors. It also makes a difference for researchers applying for grant money.

    When one has an illness for which there is no vocabulary, the vocabulary that we use as a substitute becomes extremely important for the clinician.

    For the first year, I did not call my central pain "pain" because I had experienced pain and considered this suffering to be quite different. I spent a great deal on textbooks to try to learn about my condition, underwent surgeries etc, all because I did not know what I had, so I was susceptible to believing and following doctors who also did not know what I had.

    A famous doctor finally told me I had central pain. This permitted me to research into the literature. I early came on the research of Dejerine and Roussy, and in these, I FINALLY had something I could recognize. Roussy's series of patients had high cervical lesions, and so following Egger, the two Frenchmen wrote of thalamic pain, including some with very high cervical lesions. From their articles we got the term "onion peel skin" which refers to the fact that not all areas of the skin are affected equally.

    There are zones, which Dejerine compared to the layers of onions. These are felt as gradations of intensity. It is more gradual than the word "layers' would suggest, but "layer" helps the reader to get the idea better. In me, the pain levels are different in the three areas supplied by the three branches of the trigeminal nerve on the face. I can tell where divisions A, B, and C are simply by noting the difference in intensity of dysethetic burning on my face, and in my eyes, mouth and nose and jaw. I can tell you for example that the trigeminal nerve hits the front half of the opening of the ear but not the back half. We also learned from Dejerine and Roussy that the pain of central pain grows more intense as you go further out the nerve supplying the skin area. DandR called this "centripetal pain". All this was learned just by carefully questioning patients. On a number, Roussy performed autopsy after death and frequently found thalamic lesions. Today, even cord lesions are suspected to be affecting the thalamus, usually the VPL and VPM nuclei of the thalamus. However, the brain is subtle and it is hard to pin one function to one area where pain is concerned. Surrounding structures undoubtedly get involved. For example, the subthalamus has very convincing roles in pain. Consequently, there is less use of "thalamic pain" because there is no absolute proof that central pain does not involve some misfunction of the subthalamus.

    Prior to Dejerine, a very smart S. Weir Mitchell, to whom we owe the formation of Johns Hopkins, was working as a civil war doctor. In those days, you sometimes had to face the enemy at close range, where bayonets and tomahawks were a possible threat. In other words, those soldiers had to be very brave. Mitchell had one captain whom he considered the bravest and most fearless man he had ever met. When this captain was struck in the neck, Mitchell was shocked that the captain developed the temperament of the "most nervous girl". Mitchell realized something different was going on. He concluded it was because the pain was so great and persistent. Mitchell called it "pain of central origin".

    Of course, there was plenty of PERIPHERAL nerve injury going on as well, but central pain was different. Mitchell discovered that if you touch the skin of someone with central pain, there is a delay of twenty seconds or so before the pain heightens (called "delay with overshoot"), whereas with peripheral nerve injury, the pain is immediate. This is now known as "Mitchell's sign". Evoked pain comes on slower in central pain patients. The doctor who touches you and doesn't notice anything may fail to keep the stimulation going so he gets a correct reading, if he doesn't know Mitchell's sign.

    A British neurologist publishing in the Lancet (Riddoch) also was struck by the very unique symptoms of patients with central nervous system injury. Riddoch'a article was "A Pain Beyond Pain'. He realized that the durability and elaboration of symptoms put these patients in a special category. He was the first to call it central pain, after Mitchell's "pain of central origin".

    Next, Ron Tasker discovered that pain was carried in the spinothalamic tract. He began to experiment on his patients and learned that radiostimulation of the spinothalamic tract caused NO pain in patients. However, in those with central pain, it recreated the dysesthetic burning. Tasker also concluded that neuropathic pain was different from ordinary pain. Tasker also made firm the idea published earlier in Britain that central pain potentially has spontaneous AND evoked aspects. He also split off lancinating pain from burning dysesthesia.

    Next, John Bonica wrote a book about Central Pain. Cassignari at Harvard did the same. Patrick Wall, the editor of "The Textbook of Pain" began to include chapters from Tasker and others on neuropathic pain. In this chapter, Tasker retained a differentiation between neuropathic pain and the subset, central pain.

    Research began to appear showing abnormal frequencies in the thalamus (called thalamocortical oscillations) in those with central pain.

    Subsequently, Dejerine's term "thalamic pain" began to be limited to those who had strokes to or near the thalamus. For post SCI pain, MS pain, traumatic brain injury pain, and certain other conditions, "central pain" was used.

    The result of this polyglot is that the textbooks seemed to ignore the topic. After all the years, this is still the case.

    Dr. Patrick Wall firmly believed that retention of the term "central pain" was eesential to creating funding for targeted research on the greatly elaborated pain which can follow cord injury. He also believed that the doctors needed to take it further, and find out which TYPES of central pain a person had. There were still neurosurgeons doing brain ablative surgery (typically cingulatomy or thalamotomy) to try to stop central pain. The failure of brain ablation led to doctors attempting to stimulate the very areas which some had removed. Tasker himself tried electrodes in the thalamus to create a paresthesia buzz to block the pain. So to assess the worth of such surgeries, the surgeon needed to be able to say the brain ablation stopped the lancinating pain, but did NOT stop the burning dysesthesia, or whatever. The same was true of drugs. Dr. Wall believed it was essential to be a splitter in order to decide where therapies needed to be developed.

    Neurology, typically working with anesthesiologists, had developed a subspecialty of pain treatment. Soon the physical medicine and rehab specialists began to get involved and we saw devices implanted, either to provide stimulation or medication.

    I do not see how we are going to navigate our way around all this rationally unless we know what we are talking about. Accurate or not, we need to stick with the terms that have developed over time, in order to assess the validity of treatments.

    It is not uncommon for a doctor to say to a patient, well this drug is approved for fibromyalgia, which is thought to be neuropathic, so lets TRY IT for your central pain.

    And so we have everyone on a wild goose chase trying to stop their central pain. This is expensive and disappointing. We KNOW that injury to peripheral nerves can cease in cases where the nerve manages to grow back down the axon sheath to reach an area of the skin, or whatever.

    However, in the central nervous system, the very attempt to repair causes the glia to release growth factors, which are inflammatory, and may even be the CAUSE of central pain. In the cord, opiates inhibit pain. In the brain, opiates inhibit inhibitory tracts, so we get a paradoxical block of inhibition of pain (called disinhibition) which can make pain WORSE.

    Since residents are already very poorly educated on nerve injury pain, and because we as patients do a truly lousy job of describing our central pains, we need to quit shifting terms, and try to find a solution to the confusion.

    Consequently, I always speak of central pain to my doctor. Otherwise, I will be loaded down with medications which may help peripheral nerve injury pain (which has a chance of healing and making the meds, surgery, or whatever look good, while for me it is a waste of time.

    I know of no other area in science where dumbing down terms has made things better. I actually think there are different varieties of central pain, and that eventually we will split it into finer categories.

    So I regard the mushing together of central pain with peripheral nerve injury pain into the term "neuropathic pain" to be disadvantageous. It makes text authors who give passing mention of neuropathic pain think they have somehow said something about terribly severe central pain, when they have not. Omitting information actually misleads clinicians into thinking central pain is no big deal, sort of in the same category as diabetic neuropathy.

    I realize this is controversial. I have been at pain meetings where famous pain specialists nearly got into a fistfight over this. The IASP committee often falls into sharp disagreement over how to categorize things. The fight was disgraceful. The adoption of "neuropathic" pain seems to have eased the emotional and contentious Patrick Wall refereed over TYPES of pain states. After Pat died, tired of the fighting, neuropathic pain has proven to have a healing effect on the harsh debates. However, it has muddied the water for patients.

    I could not be more opposed to referring to central pain simply as neuropathic pain. It is like referring to pancreatic cancer in the same words as basal cell carcinoma. We can do better than "neuropathic pain". We must start by looking inwardly and finding terminology the doctor can understand. Patients do an absolutely terrible job of describing their central pain to their doctors. Most central pain patients have NO idea how much of their pain is ordinary and will respond to opiates, and how much is purely central pain, which may need more than sedation by opiates. IF we use precise terms, the doctor will learn from each patient, and then can provide proper cues to elicit an even better history from the next patient. Eventually, medicine will come up with a vocabulary. We mislead the doctor when we speak of THE PAIN, when we could just as easily learn to say "spontaneous dysesthetic burning", in which case the doctor would eventually realize the burning, which localizes VERY POORLY, is different from the lancinating or lightning pains, which are NOT dysesthetic and localize beautifully

    That is my two cents. I don't want to transfer the fights I saw earlier at meetings to this forum. But PhD rsearchers are humans and are drawn to areas where the need is intense. I cannot think of a single person who has made any progress in central pain, who did not knwo the difference between it and peripheral nerve injury pain.

    This does not mean that the medicines and treatments developed for peripheral nerve injury pain might not help central pain, but we should not just make that assumption. We have to fight to be heard.

    Years ago, I had conversation with Harold Varmus, head of NIH, and was able to convince him to allocate some money for central pain. Much good research has come from that. However, we need a great deal more. This will ONLY happen, if doctors realize that central pain exists.

    I should add that one very good pain doctor (an expert on nypertonic bladder pain) who sometimes edits my own publications disagrees with me and feels we should just say neuropathic pain. We are still friends, but on this topic he disagrees strongly, partly because he is unsure whether hypertonic bladder is central or peripheral nerve injury pain. Of course, he does not have central pain, and I do. So each and every central pain is to me a very specific thing. I think these specific things should have names.

    I may be wrong because central pain is so little known, that the best result will come if we all join together in the cause of neuropathic pain, so research money will be allocated. But I just cannot get over the fact that Yale has shown that fetal ion channels for sodium are produced in central pain but not in peripheral neuropathic pain. The roof structures of the cerebellum are activated in central pain but NOT in peripheral nerve injury pain. We must be very careful not to mislead PhD researchers into thinking these illnesses are the same, or they will become confused and misunderstand their own research.

    The leading resarcher on peripheral nerve injury pain is, in my opinion, Kenneth Hargreaves. He clearly differentiates between peripheral nerve injury pain and central pain.

    I suffered for many years over a problem coming out of the cervical facets, which I assumed was just another aspect of central pain. Knowing that this terrible pain was NOT central pain, allowed me to go for therapies which helped it. I cannot see any advantage to not speaking very specifically. I would argue for greater specificity, not less.

    When I broke my ankle, I got NO therapy, because the doctor assumed I was feeling it so severely because I had central pain. Specific terms would have avoided this.

    When speaking to family and friends, I believe nerve injury pain is a good term, but to my doctors, I want to make sure they know what I am talking about. Of course, in the rapid fire 15 minute managed care appointment, you are lucky if you can even say hello. When I saw Dr. Tasker, his chief resident took most of the MORNING, and Dr. Tasker took a good deal of the AFTERNOON. I doubt today's doctors are so efficient they can cover the territory faster than Ron Tasker. So the economies of managed care is another reason why keeping it all "neuropathic" happens. And the need for more time is why I advocate retaining the term, "central pain". It should clearly indicate an upgrade in the time allowed for evaluation and for treatment. Opiates do not help me--I am just gald I don't have to spend my 15 minutes in an opiate battle with my caregiver like some of you have to. I am guessing you never have time even to talk about the human being who needs the opiate. To quote Alan Parsons, sometimes "One kind word means more to me than all the birds of Paradise" You need a little professional empathy to help you avoid falling into the mindset where you are just marking time until life is over. Happy children around also help on this account (credit C.S. Lewis)
    Last edited by dejerine; 09-05-2011 at 01:03 PM.

  5. #25
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  6. #26
    Dej, thanks for taking the time to clearly state your position on terminology.

    Having happy children around does help. My 20 yr old spent 2 weeks with us before his 3rd year of college. It does help.

    How about a T-shirt that says, "Ask me about Central Pain" ;-)

    Humor also helps....

  7. #27
    What an incredible narrative! Thank you. Wise.

    Quote Originally Posted by dejerine View Post
    I must confess I am a believer in very specific terms. There is actually a huge battle going on over this, but I believe there is a pragmatic argument for specific terms, not only for central vs. peripheral, but also for the various Central PAINS, eg. dysesthetic burning vs. lancinating vs pins and needles, vs muscle pain, vs. visceral pains (typically the bladder and rectum) etc. There is a committee of the International Association for the Study of Pain, who sit around and discuss how they are going to name something. The coding process of Medicare and others makes this essential for pain doctors. It also makes a difference for researchers applying for grant money.

    When one has an illness for which there is no vocabulary, the vocabulary that we use as a substitute becomes extremely important for the clinician.

    For the first year, I did not call my central pain "pain" because I had experienced pain and considered this suffering to be quite different. I spent a great deal on textbooks to try to learn about my condition, underwent surgeries etc, all because I did not know what I had, so I was susceptible to believing and following doctors who also did not know what I had.

    A famous doctor finally told me I had central pain. This permitted me to research into the literature. I early came on the research of Dejerine and Roussy, and in these, I FINALLY had something I could recognize. Roussy's series of patients had high cervical lesions, and so following Egger, the two Frenchmen wrote of thalamic pain, including some with very high cervical lesions. From their articles we got the term "onion peel skin" which refers to the fact that not all areas of the skin are affected equally.

    There are zones, which Dejerine compared to the layers of onions. These are felt as gradations of intensity. It is more gradual than the word "layers' would suggest, but "layer" helps the reader to get the idea better. In me, the pain levels are different in the three areas supplied by the three branches of the trigeminal nerve on the face. I can tell where divisions A, B, and C are simply by noting the difference in intensity of dysethetic burning on my face, and in my eyes, mouth and nose and jaw. I can tell you for example that the trigeminal nerve hits the front half of the opening of the ear but not the back half. We also learned from Dejerine and Roussy that the pain of central pain grows more intense as you go further out the nerve supplying the skin area. DandR called this "centripetal pain". All this was learned just by carefully questioning patients. On a number, Roussy performed autopsy after death and frequently found thalamic lesions. Today, even cord lesions are suspected to be affecting the thalamus, usually the VPL and VPM nuclei of the thalamus. However, the brain is subtle and it is hard to pin one function to one area where pain is concerned. Surrounding structures undoubtedly get involved. For example, the subthalamus has very convincing roles in pain. Consequently, there is less use of "thalamic pain" because there is no absolute proof that central pain does not involve some misfunction of the subthalamus.

    Prior to Dejerine, a very smart S. Weir Mitchell, to whom we owe the formation of Johns Hopkins, was working as a civil war doctor. In those days, you sometimes had to face the enemy at close range, where bayonets and tomahawks were a possible threat. In other words, those soldiers had to be very brave. Mitchell had one captain whom he considered the bravest and most fearless man he had ever met. When this captain was struck in the neck, Mitchell was shocked that the captain developed the temperament of the "most nervous girl". Mitchell realized something different was going on. He concluded it was because the pain was so great and persistent. Mitchell called it "pain of central origin".

    Of course, there was plenty of PERIPHERAL nerve injury going on as well, but central pain was different. Mitchell discovered that if you touch the skin of someone with central pain, there is a delay of twenty seconds or so before the pain heightens (called "delay with overshoot"), whereas with peripheral nerve injury, the pain is immediate. This is now known as "Mitchell's sign". Evoked pain comes on slower in central pain patients. The doctor who touches you and doesn't notice anything may fail to keep the stimulation going so he gets a correct reading, if he doesn't know Mitchell's sign.

    A British neurologist publishing in the Lancet (Riddoch) also was struck by the very unique symptoms of patients with central nervous system injury. Riddoch'a article was "A Pain Beyond Pain'. He realized that the durability and elaboration of symptoms put these patients in a special category. He was the first to call it central pain, after Mitchell's "pain of central origin".

    Next, Ron Tasker discovered that pain was carried in the spinothalamic tract. He began to experiment on his patients and learned that radiostimulation of the spinothalamic tract caused NO pain in patients. However, in those with central pain, it recreated the dysesthetic burning. Tasker also concluded that neuropathic pain was different from ordinary pain. Tasker also made firm the idea published earlier in Britain that central pain potentially has spontaneous AND evoked aspects. He also split off lancinating pain from burning dysesthesia.

    Next, John Bonica wrote a book about Central Pain. Cassignari at Harvard did the same. Patrick Wall, the editor of "The Textbook of Pain" began to include chapters from Tasker and others on neuropathic pain. In this chapter, Tasker retained a differentiation between neuropathic pain and the subset, central pain.

    Research began to appear showing abnormal frequencies in the thalamus (called thalamocortical oscillations) in those with central pain.

    Subsequently, Dejerine's term "thalamic pain" began to be limited to those who had strokes to or near the thalamus. For post SCI pain, MS pain, traumatic brain injury pain, and certain other conditions, "central pain" was used.

    The result of this polyglot is that the textbooks seemed to ignore the topic. After all the years, this is still the case.

    Dr. Patrick Wall firmly believed that retention of the term "central pain" was eesential to creating funding for targeted research on the greatly elaborated pain which can follow cord injury. He also believed that the doctors needed to take it further, and find out which TYPES of central pain a person had. There were still neurosurgeons doing brain ablative surgery (typically cingulatomy or thalamotomy) to try to stop central pain. The failure of brain ablation led to doctors attempting to stimulate the very areas which some had removed. Tasker himself tried electrodes in the thalamus to create a paresthesia buzz to block the pain. So to assess the worth of such surgeries, the surgeon needed to be able to say the brain ablation stopped the lancinating pain, but did NOT stop the burning dysesthesia, or whatever. The same was true of drugs. Dr. Wall believed it was essential to be a splitter in order to decide where therapies needed to be developed.

    Neurology, typically working with anesthesiologists, had developed a subspecialty of pain treatment. Soon the physical medicine and rehab specialists began to get involved and we saw devices implanted, either to provide stimulation or medication.

    I do not see how we are going to navigate our way around all this rationally unless we know what we are talking about. Accurate or not, we need to stick with the terms that have developed over time, in order to assess the validity of treatments.

    It is not uncommon for a doctor to say to a patient, well this drug is approved for fibromyalgia, which is thought to be neuropathic, so lets TRY IT for your central pain.

    And so we have everyone on a wild goose chase trying to stop their central pain. This is expensive and disappointing. We KNOW that injury to peripheral nerves can cease in cases where the nerve manages to grow back down the axon sheath to reach an area of the skin, or whatever.

    However, in the central nervous system, the very attempt to repair causes the glia to release growth factors, which are inflammatory, and may even be the CAUSE of central pain. In the cord, opiates inhibit pain. In the brain, opiates inhibit inhibitory tracts, so we get a paradoxical block of inhibition of pain (called disinhibition) which can make pain WORSE.

    Since residents are already very poorly educated on nerve injury pain, and because we as patients do a truly lousy job of describing our central pains, we need to quit shifting terms, and try to find a solution to the confusion.

    Consequently, I always speak of central pain to my doctor. Otherwise, I will be loaded down with medications which may help peripheral nerve injury pain (which has a chance of healing and making the meds, surgery, or whatever look good, while for me it is a waste of time.

    I know of no other area in science where dumbing down terms has made things better. I actually think there are different varieties of central pain, and that eventually we will split it into finer categories.

    So I regard the mushing together of central pain with peripheral nerve injury pain into the term "neuropathic pain" to be disadvantageous. It makes text authors who give passing mention of neuropathic pain think they have somehow said something about terribly severe central pain, when they have not. Omitting information actually misleads clinicians into thinking central pain is no big deal, sort of in the same category as diabetic neuropathy.

    I realize this is controversial. I have been at pain meetings where famous pain specialists nearly got into a fistfight over this. The IASP committee often falls into sharp disagreement over how to categorize things. The fight was disgraceful. The adoption of "neuropathic" pain seems to have eased the emotional and contentious Patrick Wall refereed over TYPES of pain states. After Pat died, tired of the fighting, neuropathic pain has proven to have a healing effect on the harsh debates. However, it has muddied the water for patients.

    I could not be more opposed to referring to central pain simply as neuropathic pain. It is like referring to pancreatic cancer in the same words as basal cell carcinoma. We can do better than "neuropathic pain". We must start by looking inwardly and finding terminology the doctor can understand. Patients do an absolutely terrible job of describing their central pain to their doctors. Most central pain patients have NO idea how much of their pain is ordinary and will respond to opiates, and how much is purely central pain, which may need more than sedation by opiates. IF we use precise terms, the doctor will learn from each patient, and then can provide proper cues to elicit an even better history from the next patient. Eventually, medicine will come up with a vocabulary. We mislead the doctor when we speak of THE PAIN, when we could just as easily learn to say "spontaneous dysesthetic burning", in which case the doctor would eventually realize the burning, which localizes VERY POORLY, is different from the lancinating or lightning pains, which are NOT dysesthetic and localize beautifully

    That is my two cents. I don't want to transfer the fights I saw earlier at meetings to this forum. But PhD rsearchers are humans and are drawn to areas where the need is intense. I cannot think of a single person who has made any progress in central pain, who did not knwo the difference between it and peripheral nerve injury pain.

    This does not mean that the medicines and treatments developed for peripheral nerve injury pain might not help central pain, but we should not just make that assumption. We have to fight to be heard.

    Years ago, I had conversation with Harold Varmus, head of NIH, and was able to convince him to allocate some money for central pain. Much good research has come from that. However, we need a great deal more. This will ONLY happen, if doctors realize that central pain exists.

    I should add that one very good pain doctor (an expert on nypertonic bladder pain) who sometimes edits my own publications disagrees with me and feels we should just say neuropathic pain. We are still friends, but on this topic he disagrees strongly, partly because he is unsure whether hypertonic bladder is central or peripheral nerve injury pain. Of course, he does not have central pain, and I do. So each and every central pain is to me a very specific thing. I think these specific things should have names.

    I may be wrong because central pain is so little known, that the best result will come if we all join together in the cause of neuropathic pain, so research money will be allocated. But I just cannot get over the fact that Yale has shown that fetal ion channels for sodium are produced in central pain but not in peripheral neuropathic pain. The roof structures of the cerebellum are activated in central pain but NOT in peripheral nerve injury pain. We must be very careful not to mislead PhD researchers into thinking these illnesses are the same, or they will become confused and misunderstand their own research.

    The leading resarcher on peripheral nerve injury pain is, in my opinion, Kenneth Hargreaves. He clearly differentiates between peripheral nerve injury pain and central pain.

    I suffered for many years over a problem coming out of the cervical facets, which I assumed was just another aspect of central pain. Knowing that this terrible pain was NOT central pain, allowed me to go for therapies which helped it. I cannot see any advantage to not speaking very specifically. I would argue for greater specificity, not less.

    When I broke my ankle, I got NO therapy, because the doctor assumed I was feeling it so severely because I had central pain. Specific terms would have avoided this.

    When speaking to family and friends, I believe nerve injury pain is a good term, but to my doctors, I want to make sure they know what I am talking about. Of course, in the rapid fire 15 minute managed care appointment, you are lucky if you can even say hello. When I saw Dr. Tasker, his chief resident took most of the MORNING, and Dr. Tasker took a good deal of the AFTERNOON. I doubt today's doctors are so efficient they can cover the territory faster than Ron Tasker. So the economies of managed care is another reason why keeping it all "neuropathic" happens. And the need for more time is why I advocate retaining the term, "central pain". It should clearly indicate an upgrade in the time allowed for evaluation and for treatment. Opiates do not help me--I am just gald I don't have to spend my 15 minutes in an opiate battle with my caregiver like some of you have to. I am guessing you never have time even to talk about the human being who needs the opiate. To quote Alan Parsons, sometimes "One kind word means more to me than all the birds of Paradise" You need a little professional empathy to help you avoid falling into the mindset where you are just marking time until life is over. Happy children around also help on this account (credit C.S. Lewis)

  8. #28
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    Wow Dejerine....In 2002, my dad had a thalamus lesion in the late stages of his cancer (spread to his brain) and he described pain in his feet similar to mine in my legs.

    I never connected the dots until now. But it makes sense now.

    Very interesting. Fortunately, he did not have a lifetime of suffering. He could not handle it for the couple of months he had it.

    I learn something here almost every day.
    T12-L2; Burst fracture L1: Incomplete walking with AFO's and cane since 1989

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  9. #29
    Quote Originally Posted by darkeyed_daisy View Post
    I learn something here almost every day.
    Same here. I was interested to read in dejerine's post that cord lesions can actually have an effect on the thalamus - I have many of those (and perhaps a thalamic lesion, proper - it's been awhile since my last brain scan).

  10. #30
    Bonnette,

    Hi.

    I usually get hammered for technical answers, but I will attempt to comment on your post. NOne of this is medical advice. See your own doc for that.

    According to existing theory the thalamus is the concentration point for sensations coming in. Pain is one of those and is thought to be mostly in the VPL and VPM nuclei. These are very small structures. The thalamus sits in the middle of your brain, pretty much back from the eyes about two inches. The thalamus does many other things than process pain.

    The resolution ability of imaging today, despite all those million dollar machines is still nowhere near sufficient to see the spinothalamic tract. This tract is not a discrete bundle, but is more like telephone wire. The pain tracts weave their way among other tracts, such as the spinoreticular, which carries burning pain. This anatomic dispersal by itself would bring the tract well below the resolution power of todays scanners.

    Astoundingly, there may be as few as 1100 fibers running in the spinothalamic tract, which is so few you cannot imagine, considering what a big deal pain is. Obviously, a lot of pain function involves communication with those fibers communicating with larger tracts.

    Pat Wall found an ODD number of entry points for the spinothalamic tract into the thalamus, which has never been explained.

    More and more anatomists suspect that the structures AROUND the thalamus are also involved in pain. These structures are called the basal nuclei. And of late, there are studies showing that the anterior part of the posterior division of the subthalamus very definitely is involved in pain. There are also inhibitory tracts of pain scattered around the central nervous system.

    Today, the importance of physical anatomy is being downgraded by what is called chemoarchitecture, which means that chemical pathways are just as important as physical ones. Imaging has a very difficult job with tracing chemical reactions, although fMRI tries to read oxygen subtraction, interpreting this as a sign of activity. The brain is not generally one area one function, but a number of areas typically light up on these studies, so physiologists speculate about what the variables mean, but there is still a lot to be learned. Presently, the body location of pain is in S1, the significance of pain is in S2 in the parietal lobe, and the painfulness of pain is in the insula. Additive to this are the emotional areas of the brain which are reacting to pain. The list gets pretty long. Carl Saab showed that the vermis in the cerebellum tries to inhibit central pain. This has not been followed up to my knowledge.

    The thalamus is a very peculiar organ. For example, when your brain sends out a signal for some motor action, it MUST go through the anterior nucleus of tghe thalamus. When messages come up, the thalamus writes software, on the fly, to somehow facilitate the message.

    When a radiologist calls a thalamic stroke, he is usually seeing a very large injury, perhaps at least 1.5 mm or greater, due to some major block or bleed. Because the individual areas are so small, it is not possible for imaging to tell you if you have anything wrong with a small nucleus (cell arrangement) in your thalamus. Presently, that is purely experimental, and can only be done by inserting a wire into the thalamus and recording frequencies of the signals. The studies are very few. A slow signal, as low as 0.2 to 2 Hertz seems to be associated with pain. Stimulation is sometimes done at 25 Hz when the surgeon is attempting to create a paresthesia (buzz) to block the pain. This is not very successful, the electrodes can come loose, and since the structures are so deep in the brain there is considerable danger in the operation. Patients with high lesions may require as many as eight electrodes, and most surgeons do not want to risk planting eight electrodes deep in the brain. It is my understanding this procedure is not done in the U.S. at this time, and there is probably very good reason. If you are young, and the electrodes are said to average about four years, then you would be looking at far too many deep brain surgeries, but then I am not an expert in this. So don't rely on me in your thinking.

    Finally, in an important paper by Triggs, it was shown that patients with obvious lesions on MRI tended to be completely numb and to have no pain. Those with pain typically had no MRI finding. This would be consistent with an incomplete lesion which would be too small to be seen on MRI. Even if your entire spinothalamic tract were wiped out discretely, it would still be too small to be seen, unless there is some imaging method I am unfamiliar with.

    The diagnosis of central pain is made clinically, not radiologically.

    Identification of a lesion near the thalamus may well be done radiologically, but this does not mean they can tell if the pain tracts are damaged. Stroke in the brain typically is revealed in an area larger than the small pain tracts.

    I am very sorry to hear of your father. We all want our loved ones to avoid pain with dying. Such incidents point to the need for more research to prevent this sort of thing.

    At present, subtle cord damage is usually evaluated electrophysiologically, using somatosensory evoked potentials. This only sees the anterior parts of the posterior columns so it theoretically is not showing the spinothalamic tract; yet, there is reasonably good correlation IF and ONLY IF the reader of the SSEP is trained in reading pain. Most are not. Very few look for the wave which signifies pain. This test is painless.

    Although central pain patients are VERY sensitive to changes in temperature as an evoking stimulus for pain, they paradoxically are less able to discriminate differences in temperature. Most anyone can tell a four degree difference, but many with CP cannot. This test is extremely hard to perform because it requires a stable baseline in the skin and room temp and special equipment. It is only done experimentally.

    What is the solution. More money for researchers so they can begin to measure pain better. The new functional MRI and more advanced tensor analysis studies may begin to help, but again, the real activity may be going on in areas supplied by blood vessels too small to be detected discretely by fMRI. Solution. Once again, more money. Write your congressmen. Talk to the local newspaper or other media.
    Last edited by dejerine; 09-06-2011 at 11:11 PM.

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