What is Central Sensitization?

In the previous post on allodynia and hyperalgesia, I mentioned that sensitization of nociceptive neurons in the dorsal horn of the spinal cord were crucial for the development of allodynia and likely contribute strongly to hyperalgesia. When pain scientist and clinicians talk about this type of sensitization they often refer to it as “central sensitization”. What, exactly does this mean?

Central sensitization is loosely defined as an increased response to stimulation that is mediated by amplification of signaling in the central nervous system (CNS). While the stimulation does not necessarily need to be of noxious intensity, for central sensitization to be present it should recruit mechanisms that would signal a noxious response. An example of this is the case of allodynia. Under normal conditions a non-noxious stimuli may not recruit electrophysiological activity in nociceptive neurons in the dorsal horn. On the other hand, following an injury, this same innocuous stimulation may recruit activity in these same central neurons. This would be an example of central sensitization and, in this case, the sensitization would provide a mechanism for allodynia. Central sensitization was first described by Clifford Woolf. In a Nature paper in 1983 he showed that a thermal injury in the periphery caused an amplification of painful stimuli evoked activity coupled to an augmentation of the flexion reflex response (recorded by EMG). Because this reflex is mediated by a dorsal horn – ventral horn reflex arc this gave evidence that amplification of pain signaling was occurring in the CNS. Importantly, he also noted that the injury (to only one paw) stimulated an increase in the reflex arc on the contralateral side of the body. Because this occurred on the side opposite the injury, it could not have been mediated by peripheral mechanisms and must have involved amplification of signaling in the CNS. He termed this phenomena “central sensitization” and realized that such mechanisms could give rise to pain amplification similar to what is seen in humans following an injury or in chronic pain conditions.

In the decades that have followed central sensitization has become an important area of research for pain scientists and a route for therapeutic intervention for pain clinicians. Let’s begin with advances in research:

While the body of literature on this topic is too large to cover in full, there have been several major advances that are worth noting. A major theme that has emerged in research on central sensitization is that this phenomena shares cellular mechanisms with learning and memory. For instance, central sensitization occurs in part because of increased activity in glutamate receptors, including increased NMDA and AMPA receptor activity and a crucial role for group I mGluRs (mGluR1/5). Many of the kinases (these are proteins that phosphorylate proteins) that are involved in learning and memory (like CaMKII alpha and ERK) also play a key role in central sensitization. In addition to these molecular targets, neurons that signal central sensitization have also been identified. These neurons are found in lamina I of the spinal cord and they express the substance P (substance P is a neuropeptide released by nociceptive primary afferent neurons) receptor NK-1. Steve Hunt and Pat Mantyh demonstrated this by ablating these neurons with substance P conjugated to saporin (a cellular toxin). Spinal administration of substance P-saporin ablates experimental hyperalgesia in pre-clinical models showing that these neurons are crucial for the full expression of central sensitization.

Work from the group of Jurgen Sandkuhler has demonstrated that the neurophysiological basis for central sensitization involves, in many cases, a specific form of neuronal plasticity called long-term potentiation (LTP). This LTP is similar to that observed in the hippocampus and other CNS regions except that in a subset of neurons this LTP can be evoked by low frequency stimulation (generally LTP is evoked only by high frequency stimulation). This finding was crucial because in conditions of inflammation or nerve injury nociceptors fire continuously but they do so at a relatively low frequency. Hence, these findings tied activity in nociceptors after an injury to a specific type of neuronal plasticity in a specific subset of spinal cord neurons (that are in lamina I and express the substance P receptor NK-1). These findings are summarized in an OA review written by Sandkuhler.

While I have focused thus far on central sensitization as manifest in the dorsal horn of the spinal cord, it is also important to note that central sensitization can occur in other CNS regions as well. For instance, recent work from the labs of Volker Neugebauer and Rob Gereau have shown that the amygdala is critical for the sensitization of nociceptive responses following nerve injury. Moreover, Mary Heinricher’s group has shown that a region of the brainstem, called the rostral ventromedial medulla (RVM), shows plasticity in its responses to painful stimuli after peripheral injury. Because this brain region sends descending fibers into the spinal cord that amplify nociceptive circuits, it is considered the to be involved in descending pain modulation. The RVM is a major target for cannabinoid and opioid analgesics and it is likely that these classes of compounds inhibit pain by attenuating central sensitization-like responses in these neurons.

Mechanisms of central sensitization have become major targets for pain therapeutics. Basic science research has led to the development of targets that are specifically designed to block or attenuate central sensitization. Some examples are NK1 antagonists (which performed poorly in clinical trials, unfortunately), NMDA receptor antagonists and kinase inhibitors (like ERK inhibitors) which are under investigation as novel analgesics. The clinical rationale for preemptive analgesia (in surgical situations) has its basis in the science of central sensitization. The idea here is that the administration of analgesics prior to surgical intervention can block the development of central sensitization that can occur from nociceptor activation during surgery. This approach has been shown to be effective in many clinical trials.

Since its first description, central sensitization has become a unifying theme for pain research and clinical development. We now know that central sensitization underlies many pain conditions ranging from nerve injury induced allodynia to headache. As we continue to gain a fuller understanding of mechanisms that lead to central sensitization it is likely that new avenues for therapeutic intervention will be developed for the treatment of chronic pain that involve blockade or reversal of central sensitization.

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50 responses to “What is Central Sensitization?

  1. Now that is one fine summary of central sensitization. Thank you jp. I especially liked the highlights of work by different folks; the Sandkuhler review looks to be quite helpful.

    Clifford Woolf was actually on my thesis committee, and was typically the only person in the room to really know the pain neurobiology field in any detail. Too bad we only met once a year or so. His lab is located far enough away from the med school quad that we didn’t get to interact terribly much.

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  3. Good job JP.
    What do you think about the old peripheral vs central argument?
    I’ve heard a fair amount of anecdotal clinical evidence that in cases of spontaneous activity in C fibers (as measured by microneurography), peripheral nerve block can completely suppress hyperalgesia/allodynia and other sensory abnormalities for the duration of the block.
    The way I see it, an amplifier only amplifies something that’s already there. So, if peripheral input stops, the spinal cord (central sensitization) can’t amplify anything anymore. Should we be trying to find nociceptor-specific peripheral nerve blocks?
    I’m sure Clifford Woolf would agree…

  4. Short answer, yes and yes.

    Woolf, Bean and Binshtok’s Nature paper on TRPV1 permeation of local anesthetics addressed just this idea.

    The amplifier does need to amplify something (except perhaps in cases where there is some pathology in the CNS, such as stroke). I happen to know an Army doc here who was putting in nerve blocks ASAP all over the battle field in Iraq. He swears that his patients came out better in terms of chronic pain. I would not be surprised at all if this was actually true. Of course that is taking it one step further by stopping the amplifier from ever getting rev’ed up.

  5. The question is how to re-set the amplification to zero?

    I found a few reports on pubmed indicating long-term nerve blockade does not reduce persistent hyperalgesia after neuropathic injury in rat (Anesthesiology. 101(3):806-807, September 2004). I suppose that it’s kind of like trying to forget a phone number once you’ve memorized it. Then I think about the work by Nader (Nature. 2000 Aug 17;406(6797):722-6) where fear conditioning is “deleted” (kinda like retrograde amnesia) by anisomycin in the amygdala. Can this be done for pain?

  6. What seems really strange to me – is that years ago, when I was dealing with a pinched tibial nerve, and no one seemed to believe the extent of my pain, instead the doctors were focusing on a much more minor bone problem that showed up on the x-rays – I wasn’t getting much pain medicine – about 12 tramadols to do me a month – and I was trying not to complain – but I was suffering really bad –

    and I can remember – absolutely remember – sitting up in the bed and looking at my painful foot, and thinking “So this is what pain is.” Now that sounds – yeah – but really it SUNK in – like I KNEW the pain, in an almost biblical sense – lol – and I am absolutely sure that it was that minute that I got fibro. I’ve often thought, did I just lose my mind right then? But I think – I’ve always thought – that what happened was I LEARNED IT (pain). Now any hint of it, I recognize it, if that makes sense. Oh yeah, I know it when I feel it. Even if I shouldn’t feel so much of it.

    I heard a team of 5 anesthesiologists say that I had central sensitization. That’s why I found this article. They couldn’t control my pain, even with nerve blocks, and extra nerve blocks. They nurses up and left the suite, saying they were scared they were going to kill me – that I’d quit breathing.
    I do not normally take opiates, for the record. It wasn’t – couldn’t have been – any sort of tolerance that caused it.

    I barely hit my foot the other day – and I was telling myself it wasn’t hurt, It was fine, it was fine – but I couldnt’ stop the physical response. I ended up hyperventilating and throwing up. I was trying so hard to control my response, but it just kept ramping up. I wish I could learn to control it.

  7. Also – what causes the shivering? When I have this over the top crazy stupid response – I know I am in trouble if I start shivering. If it goes that far, I can’t seem to get any control over it at all.

  8. Kris, thanks for sharing your story! I don’t know what causes the shivering but I have also experienced such an effect when suffering from disc-related pain from time to time. It is quite disturbing. I would speculate that it is related to an autonomic response to pain but I don’t have any evidence to support that except this: there is an area of the brain called the rostral ventromedial medulla (RVM) that is involved in pain facilitation. Many groups are working on targeting this area with drugs for the control of chronic pain. It appears that this area becomes hyperactive in chronic pain syndromes. In addition to the RVMs role in pain facilitation it also plays a role in autonomic control in response to stress. I’m not sure how to approach this experimentally right at this moment but it may be worth some consideration for future experiments.

    So I’m curious, pregabalin (Lyrica) is now being prescribed for fibro. Have you tried it, does it work for you?

  9. Yes, I have tried it. It did seem to work – but after a week or so I found myself staring at a Trix bunny on a coupon and just started bawling. That is not me. I am normally a very happy person – and I had no reason at all to feel that despondant – it scared me very bad, I suspected the lyrica RIGHT away and I looked it up – it is indeed a problem with that drug – it might make the cure worse than the problem, if you understand, and I quit taking it, although I still keep it around, JUST IN CASE I have a terrible flare. There’s no way I’m taking it daily. I think my happiness with my family & home life is the only thing that keeps me going, and I don’t want to risk that!

    Mirapex and tramadol have been the best things for me, and they keep me functional. They really work quite well, until I get my toes run over or something dropped on my foot – some acute pain event – something like that.

    I have noticed, strangely, that when I get burnt, I don’t have that same response. Then it is normal – oh, I got burnt, let me get it under some water. Ouch! You know – same response as I always have had.

    I really wish more researchers would look down the dopamine path. I do think that it is a cns problem.

  10. Kris, this is very interesting. I had a similar experience to your lyrica story with neurontin (gabapentin). I honestly think I didn’t know exactly who I was when I was taking that drug. It worked fine for the pain but I hated it and stopped taking it after about 3 days.

    Tramadol also works well for me but I like it a bit too much. After awhile I started to feel like I was getting high off it and stopped taking it out of fear of addiction.

    I’m curious about your comment about dopamine. I hear this one alot. I get the impression that people automatically associated dopaminergic modulators with CNS action and don’t think of other drugs this way. Tramadol, gabapentin and pregabalin all work in the CNS too. In fact, all of these compounds could be considered to target central sensitization (which is, by definition, a CNS action). That is not to say that there cannot be a role for dopamine in analgesic development. A problem with dopamine is that when you start mucking around with it you can get really bad side effects (extrapyramidal — think Parkinson’s-like side effects — motivational problems or addictive potential). Many people, including me, are trying to develop new CNS targets for analgesia. It is just very difficult to target the CNS and not end up with side effects that no one wants.

  11. Here’s an anecdotal observation of mine, which there is some research about although I don’t know how credible it is: my fibromyalgia-like symptoms nearly disappeared after I started taking 2000 IU a day of Vitamin D. The endocrinologist noted low levels in my blood, and I started taking supplemental Vit D and it seriously changed my life. I am going to write a post about it sometime soon. Between that and my chiropractic treatment, I am starting to feel like a human again, lol.

  12. There’s been research on vitamin D and pain I know – it is pretty recent.

    I’ve never felt anything with tramadol – no high, no nothing, I just feel better. I’ve been on it for 3 or 4 years now, and take less than 1/2 of what I am prescribed normally. I don’t think I’m addicted, because too often I forget to take it like I should. :)

    Neurontin makes me a space cadet – I already have a lot of trouble with brain fog, when I was taking Neurontin, I might as well have been an alzheimer’s patient – I could burn water, just anything. Extreme adhd – that’s what I had on neurontin. It helped the burning, but not the stiffness or aching or mental stuff. Tramadol helps me stay mentally more clear I find.

  13. Hey – if I can every help you in any way, let me know. I was an RN for many years, and web security analyst/technical writer in my past life, b.f. (Before fibro)
    You have my email. I appreciate your putting your talent and knowledge to work on this.

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  15. Hey just happened on this site and have been reading your responses. I have been on Lyrica 50mg for past year, other than not feeling when I burn myself I still fully feel all the nerve pain drs want to increase dosage, but when I try I feel loopy and not in control. I was in a mva while working for the post office. Work comp drs claimed cervical strain and sprain for over a year before allowed to see a chiropractor who turned my life around. Immediately went into surgery for impengement on spinal cord causing neuronal death, with c4c5c6 fusion. I still suffer from herniated disc at L4/5 and L5/S1. They have diagnosed me with central sensitization and although I have undergone almost every injection known to man I have not gotten much releif. Was hoping for some hope I guess. I am an ex-addict so I am leery of taking any meds, had to be hospitalized to get off the morphine after and cannot do nsaids because I only have one kidney. I have ongoing numbness and pain throughout my body and am on a crusade to save my sanity. Vitamin D….I must get this checked out. Hopefully I can find another ray of hope.

  16. Kennie,
    I am sorry to hear of all your pain problems. I have no cervical issues but also suffer from the L4/5 problem and have done a lot of physical therapy to get myself off the shelf when the pain is building to unbearable levels. I might suggest trying to do some pilates or other form of core-strengthening to take some of the strain off your lumbar spine. You should talk to the doctor before going this route but it is helpful for many people.

    In terms of meds I don’t know what else is out there that might be able to help you. What you describe is a very common problem and many people are working hard to find better solutions for pharmacotherapy but the advances have often not been met with clinical success.

  17. Hi juniorprof,

    I appreciate your CS explanation very much – it’s easy to understand but convincing in the level of detail. I am considering sending it to my new sleep doc, who is a neurologist and hadn’t heard of CS. The only thing that makes me hesitant is this – I don’t want her to think that CS only occurs in regard to pain, because I don’t have pain. I discovered by checking the research that CS is also implicated in chronic itch and chronic cough – which I do have (both) My dad has COPD (chronic obstructive pulmonary disease) and has been bothered by coughing. I told him to share the CS story with his doctor. CS may also be implicated in sleep breathing disorders like sleep apnea. BTW, I found all this CS stuff out because the doctor prescribed gabapentin – she thought it would help me sleep better and take care of my hot flushes. Now I can see that the underlying cause of my sleep problems may inadvertently be addressed. I am hopeful! Also, I wanted to wish my best to the other respondents in overcoming their health problems.

  18. I have had neuropathy for nearly three years. i take lyrica (150mg) and elavil (35mg) for the pain. The first day i took lyrica it was like magic, pain completely dissapeared, that magic lasted about a week, then pain came and it comes and goes. Do you have any ideas on what causes this changes?? What makes pain worse some days?

    Regarding to vitamin d, i think i may give a try, but isn’t it a fat soluble vitamin??

    The final question is: do you think this neurotransmissors unbalance could be helped by a tens machine?? and if so, how?

    Sorry if i made mistakes (not a native speaker)

  19. Chronic non-cancer pain is a serious and difficult problem for a growing number of people. We need some fresh approaches. I am working with a person with chronic regional pain syndrome. She has a fentanyl patch (75) and 2 indwelling spinal stimulators (one for her arm the other for her legs). She was up to dilaudid, cymbolta,trazadon and xanax, and was not able to drive anymore at age 35. She is better now after 2 month. Still on fentanyl but off the others and driving again. She is using a patient eduction approach. Please see the Explain Pain by Butler and Mosley (available in audio format -recommended). This can be hope for some that have lost all.

  20. Interesting post, but I noticed the absence of central sensitization regarding Migraine disease. My neuro (headache specialist) said I had central sensitization and allodynia with my migraine. It seems that I perceive many non-noxious stimuli (light, odors, touch) as either painful or very annoying. Could this have anything to do with a recent dx of fibromyalgia? I am on Lyrica (300 mg/day)that helps immensely with the fatigue, but not the pain.

  21. Debbie, central sensitization is generally considered to be an important aspect of migraine pathology and allodynia is a common feature of migraine as well. Photophobia, pain from light, is very poorly understood but there are some indications that this can be treated by analgesics that are thought to target central sensitization. In terms of fibromyalgia, migraine is co-morbid with many other forms of chronic pain so it is hard to separate out what aspects are from what. As for Lyrica, I have heard so many different stories from different people about what this drug helps them with, makes worse, or does nothing at all that I would really like to see some larger studies done to try to test its efficacy more thoroughly.

    • I had a serious high speed RTA nearly five years ago I left the accident as if nothing was wrong weird enough I felt lucky until now ,still unable to work/excercise without intense muscle cramps and burning pain which can have me at breaking point regularly.The pain and cramps are wide spread all down my right hand side of my body from neck to foot and some left side but not as severe .I had surgery on a damaged Brachial plexus nerve which has made my neck/shoulder pain much more severe/I have redness which increases with pain or stress,cramps foot pain which is severely sharp and swellings ,always red hot never wear a coat or anything but short sleeves.I am taking large doses of Gabapentin/targinact/paracetomal/amytriptiline/ibroprofen and mitrazapine my pain is not under control at all..I saw a consultant today who said it is Central Sensitization syndrome and I now have a frozen shoulder.He said I have been left as disabled as a person who had a serious spinal cord injury – I said I suppose but it doesnt make sense he said yes it does perfectly!
      Later on he said he didnt agree with pacing for this syndrome and that I should excercise and carry on the next day regardless of the pain and the next day and so on ,at the moment a 20min swim will leave me in agony for 3-4 days unable to walk comfortably and exhausted only rest brings it down /I said if I did that I would be crying and on my knees he said good keep going! Ive had four children and this pain wears me down against any child birth the severity and constant throb wears me down! what would you recommend I do ? I feel a bit puzzled

  22. Kris-

    Thank you for relating your experience from neurontin. I had the same side effects you describe from BOTH neurontin and Lyrica, which is exactly the same drug as neurontin tweaked to produce a longer half-life. (My boss is a chemical engineer and felt the need to tell me HOW you would go about accomplishing this. I didn’t follow him, just as I seldom follow his chemistry lessons but I nodded and pretended to. My job is just to create certificates for him to sign that things we sell chemically are what we’re selling them as.) I thought I was the only one. Alzheimer’s is a good description. The bad part is, I still don’t remember the times I was on them. My boss had described my behavior and had he not called my doctor and told he she should get me off them I don’t know what might have happened but it couldn’t be good.

    Tramadol doesn’t work for me at all, but I would describe my experience of fentanyl patches the same way. I have never felt any thing whatsoever except my pain is lessened significantly. NO narcotic side effects at all. (except constipation.) It’s my miracle as it makes me feel normal.

  23. I was just diagnosed this week with CS. I am 39 and have thought I had RA for about 3 years. But the constant back pain didn’t make sense.
    I finally found a doctor that didn’t think I was crazy and diagnosed me with this CS.
    He put me on Savella. I have only just begun taking it. Has anyone else heard of it or tried it?

  24. I have been medication free for 8 months now. I do take some turmeric at times for stiffness, but I attribute my improvement to meditation. I got very serious about it – every day, without fail, couple of times a day.

  25. In one of your responses to Kris you stated that ” In addition to the RVMs role in pain facilitation it also plays a role in autonomic control in response to stress.”

    Is it possible that past or present experience with long term stress could pre-dispose someone to develop central desensitization?

    I have failed back surgery syndrome with a lot of pain in my low back and down my right leg. I’m 41 yo now but had mild low back pain since my 20s. I was pretty active with sports, worked as a San Francisco fireman and a competitive olympic style weightlifter. My microdiscectomy was in 2003. I also experienced huge amounts of long-term stress as a kid.

    My idea is that the stress pre-disposed me to developing central desensitization. The broader question is why some people develop central desensitization after a surgery and other don’t.

    One other quick thought. Stress often brings on back pain- not just in me but lots of people. Could that have anything to do with the RVMs dual role?

    Thank you very much for your blog.

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  27. Thanks for the enlightening article and comments. I’m doing reading because my 18-year-old daughter has been diagnosed with CSS and the pain is constantly at least an 8/10, usually worse. She is starting to injure herself (sitting with a twisted foot, etc.) because she is becoming adept at ignoring pain. She can’t take Savella or any other seratonin increasing drugs even at a very low dose or she gets seratonin syndrome. Lyrica, neurontin, and the like have had very very little, if any, effect. All the doctors we have seen here (Mississippi) either have not heard of CSS or don’t have any ideas what to do for it. TENS sounds intresting, but I would be afraid it would stimulate the nerves further – anyone else have any input? I do notice some increase in her headaches, emotional reactivity, and pain if she eats foods with MSG or glutimate relatives. Anyone else notice this? Any suggestions of things to ask the new pain doctor? I know I have said a lot, but this is only a small portion of my questions!

  28. Hi Dart,
    I’m not sure what you mean by CSS but I assume you mean central sensitization. I am not a physician; however, I strongly advise you to seek out a pain specialist for your daughter. This sounds like a very bad situation and she would likely benefit from a specialist. If you are not aware of one in your area you may want to seek advice from either The American Pain Society or The American Pain Foundation. You can find contact info for either one on their webpages. APS cannot give advice on treatments, etc., but they have an extensive resources page that you may find useful:

    http://www.ampainsoc.org/people/

    • Thanks for the quick response and the link to resources — I’ve been reading them today. And yes, I did mean central sensitization – the doctor at Mayo called it Central Sensitization Syndrome. So much to learn, and I appreciate your help in locating another good source in the APS. Thank you!

  29. Thanks JP for the awesome article on CS..best one by far & I have read a lot! Unfortunately I may no more about CS than my neuro & my pain dr as I am not getting effective trtmnt…have chronic migraine w/aura constant 24//7 since 2010 after compl hysterectomy, fibro, vascular & neuro TOS bilateral rib resect w/repeat DVT’s both subclavian veins, severe cervical DDD, lumbar radic from L4 bulge & L5 S1 hern w/annular tear, pain & parasthesia RT leg & foot w/peroneal nerve prob on EMG but neurosurgeons won’t touch me cuz afraid of making worse…think they r afraid of cause CS..too late for that…have tried lyrica, neurontin, ultram, etc etc. & had all kind of inject…read pub med neuro article on ketorolac IV for abort migraine with CS allodynia & dysesthesia etc…got my neuro to write RX but have not tried yet..any thoughts on this trtmnt & how it works?

  30. Deborah Armstrong

    Thank you for a very informative and thorough description of central sensitization syndrome. I understand that some of the current treatment options to reduce stimulation of the CNS is with medications such as topamax, gabapentin and lyrica. Can you comment as to the efficacy of these meds and any other treatment options you are aware of? I should mention that this is more in reference to central sensitization syndrome secondary to a trauma.

  31. I have just been diagnoses with CSS. It took for ever to get the diagnosis, but am so thankful to have a name associated with my many ancillary symptoms that ties them all together. Now phopefully I can find some relief, albeit, I am not expeting the miracle of a full recovery; However, I must say any imporvement would be a huge gain. The one piece of the puzzle I am a little unclear about is, how does CSS relate to Fibromyalgia? Or are they two mutually exclusive issues? I think having this answer would help me understand my syndrome better. Any insight would be most helpful.
    As well, I have a kidney transplant ( which may or may not have played into my getting CSS) any educated thoughts about medicine I could discuss with my doctor, that would not interfere with my immunosuppression meds? One last note, I have significant Brain Fog, any thoughts on how to improve that? My hope is to find a medicine(s) that could help give relief, not interfere with transplant drugs, norworsen my brian fog. If this med exists – it could be a life saver! Thanks in advance for any thoughtful insight.

    • A close relative was diagnosed with CCS by the Mayo Clinic. Dr. Benjamin Wang explained that it was a group of related problems, one of which was fibromyalgia, but also includes chronic fatigue syndrome, interstitial cystitis, etc.
      Things that have helped include regular (but not strenuous) exercise, getting regular sleep – often more than you think you need, watching diet (high acid foods, artificial sweetners and sugars, and MSG and its relatives seem to be triggers for my relative), and reducing stress. Many are helped by extra magnesium and calcium (which have been known to relax the nerves) and the usual meds for fibromyalgia. (The meds are not an option for us because of reactions.) Many also find they need acidophilus and other beneficial intestinal flora. (Here is an article from a chronic fatigue syndrome organization that mentions it toward the end:
      http://www.cfids.org/about-cfids/pain-practitioner-spring2010.pdf) Another article you may find helpful (or confusing) is http://css.dewarlorx.com/therapies.html. I would encourage you to make slow changes, to try one thing at a time and to stop if it seems to make it worse. There has been no magic bullet for us, but the exercise and sleep seem to be key. Hope this helps and you start to see improvement soon.

  32. If lidocaine topical (viscous 2% applied to sensitive trigger areas) helps you, then **mexiletine**, an oral medicine with few if any side effects, may do the trick.
    I have a very clever neurologist who figured this out;; within 20 minutes after I took the first 150 mg capsule, the excruciating, almost heart-stopping pain of trigeminal neuralgia plus vascular migraine were gone. It’s an older drug and used in much larger doses for heart arrhythmias, as well as for pain–since it’s actually lidocaine formulated as an oral medicine.
    After 12 years of this crippling, outrageous pain, I am stunned to have it retreat so nicely. None of my other neurologists used it in their practices; I think it just doesn’t come to mind. I then take 200-300 mg of Neurontin in the evening to help me have proper sleep patterns and replace Ambien.
    I still have an appt with a top neurosurgeon at UCSF in two weeks to be evaluated for the “gamma knife”, which ablates (severs) the nerve at the base of the brain– the new neurologist thinks I may be able to avoid that. I may be able to work and travel again, too. He’s still refining the treatment, using, for example, Namenda, which is an NMDA antagonist, but which takes months to really work; however besides its central neuropathic pain effects it’s used for memory and mental focus — the opposite of Neurontin’s cognitive effect :-)

  33. Christine Allnutt

    Hi, Thank you for such a well written article. I belong to an online support group for people with Post Herpetic Neuralgia (PHN). I was searching for an article for a friend who’s pain no longer follows a single dermatome. Most of the people in the group, by it’s very nature, are people who’s Shingles /PHN has not followed the “normal pattern”. Many are deeply distressed that their pain is not understood by their neurologist or GP/Primary care Physician. Until we started researching as a group I know some people had considered suicide; now we support each other and use articles like yours to take into appointments. (tactfully!). Thank you again,
    yours Sincerely
    Christine Allnutt

  34. Yes lots of interesting information even for those of us with simple (?) PHN. Thankyou – and I am going to research ‘Mexilatene.” Also interested in the post about meditation. it is that getting serious twice a day thing that is hard. BTW I take 150 sustained relese Tramadol and 150 Lyrica twice a day. I manage – a bit dippy. Don’t focus well. An extra Lyrica on a bad day fixes pain, but leaves me lurching all over and mispronouncing occasional
    words (like being drunk and a bit high and giggly) I try to keep it to the 300 mg a day… Yep, thank you for doing this Junior proff
    Sincerely
    Diana

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  44. Diana Thurbon

    I’m going to try the vitamin D too. It must be 8 years since I had shingles. That is 8 years of Postherpetic neuralgia. Lately I’ve noticed 2 things that may be conected. My damaged dermatone was down the front of my leg, it is still sensitive, but I also have pain down the side of my leg and a very tender lower back- do I have sciatica now? Any thoughts. I’m still on same dose of Lyrica, Effexor and Tramadol. If I forget my plls about 3 hours later I’m pretty desperate with stabbing pain in both places.
    .

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