CRPS Two Years, Pain Free on Low Dose Naltrexone


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Girl with CRPS cold type two years, pain free on naltrexone 3 mg

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KR, 17 year old seen 11/4/11, with Complex Regional Pain Syndrome [CRPS] involving left lower limb from foot to hip, onset 3/09. She has nonspecific immune system abnormalities and many food sensitivities that caused leaky gut syndrome and 30 lb weight loss with certain foods causing the stomach to be rock hard and vomit. Elimination diet allowed her to regain 30 lbs.

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CRPS diagnosed February 2011, two years after first symptoms. The leg was cold, purple, mottled with allodynia. Pain had been 9 on scale of 10 for weeks prior to my visit when she was started on prednisone 60 mg x 1 week, 40 mg 1 week, and a few days on 20 mg, dropping her average pain to 4/10. Pain at my visit 11/4/11, ranged from 4 to 9, average 5, that was 40% better after prednisone. She takes a wheelchair to school and for distance, is able to walk short distances with cane, and without cane she concentrates walking slowly to avoid limp. She is very bright, highly motivated and described the limb as cold, aching, throbbing, shooting, stabbing, sharp, tender, burning, exhausting, tiring, miserable, unbearable. Pain severely interfered with walking, work, sleep, enjoyment of life, general activity, and relations with others. At rare times, the limb would jump. Numbness was present posteriorly off and on, especially when sitting, not present when standing.

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She had good health until mononucleosis at age 13 in October 2007. A few weeks later irritable bowel syndrome began (IBS-C), then CRPS began after injury March 2009, reinjury July 2009, then no problems until February 2011. The initial injury occurred when roughhousing with a friend, and her foot pulled her toes in a dorsiflexed position. The next day it was swollen and purple with bruising pain after the first injury. She was in a boot for several weeks. CRPS improved, she went to Peru climbing Machu Pichu when she was reinjured again. The foot was swollen, burning with allodynia. She was taken to a hospital in Chile where they wrapped the foot, advised to take Advil. Once home, she went to physical therapy. It resolved in 6 weeks.

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February 2011, fulfilling PE for high school, she tried out for swim team. Day two, she had pain from kicking in the water and was never able to get back into the water. She was in crutches the next 2.5 months and began physical therapy three times weekly since then. Pain began in the sole of the foot, but a slip and fall in the rain caused pain to spread to the hip. A flare in the past month caused pain much more in the left knee after prolonged sitting for tests. She now takes her wheelchair to school which she began to use early October 2011. She was in the chair consistently two weeks, now only as needed, and never uses it at home. She has used a cane since later April when she got off her crutches. In hot weather, the cold left lower limb sweats profusely. No hair changes. On prednisone, toes nails grow faster. She has used warm and cold compresses to relieve pain. She failed gabapentin when it caused her to be nonfunctional on 900 mg/day with no relief. Lyrica caused hives. Nortriptyline caused personality change, becoming very mean, an Atilla the Hun, opposite her usual good nature. Cymbalta 20 mg – severe dry throat, thick mucous, medications lodged in esophagus. Tried Tramadol 25 mg TID and Naproxen 500 bid.

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Incidentally, she saw a neurologist at Children’s Hospital in 2009 due to sudden onset of diplopia that was found due to allergy to contacts, and resolved with new contacts. She saw an allergist in 2010, and tested positive for nonspecific autoimmune disorder: ANA 1:160 speckled, positive for food sensitivities, and after four months of stopping certain foods, ANA was negative: gluten, dairy, garlic, broccoli, lima beans, banana, asparagus, pineapple, oyster, mushroom. While eating those foods she had IBS-C, stomach would harden, causing vomiting, and she lost 30 lbs, was 120 before —- it is part of the leaky gut syndrome that prevented her to absorb certain nutrients. She has regained weight and all symptoms resolved. She does not have dry mouth or dry eyes. She is sensitive to normal doses of medications like her grandmother.

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Exam: Toes are cold on the left. At the moment, no changes in hair, skin color, temperature, sweating. Stretch reflexes symmetrical, brisk in both lower limbs. She uses a cane but is able to walk slowly without limp, carefully, holding both arms stiffly at her side as she concentrates on walking. Sensory examination was not detailed due to patient discomfort and long trip from home that was very tiring.

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Treatment: Prednisone was rapidly tapered off. Begin 1 mg low dose naltrexone [LDN]. Begin N-acetyl cysteine [NAC] 600 mg x 3/day for “cold” CRPS – it is reported to take 3 or 4 months to help.

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Reponse: Mom wrote a few days later, “On the way home from our visit in La Jolla, K started to experience sensation in her leg. You had asked her at the appointment if she had numbness and she could feel some in the back of her leg. She didn’t realize the extent of it. The Naltrexone [1 mg] seems to be awakening areas of her leg. She has felt more muscle pain as well. She feels this may be because she is able to use more muscles in her leg with the increased feeling. She also had her foot stepped on the next day (Saturday). In the past, she would have been incapacitated with the pain for a couple weeks. With the Naltrexone, she felt very little pain at all. We were both very excited to see these changes. 🙂 She is at about a level 3 to 4 in pain.”

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Encouraged mom to continue increasing LDN as tolerated.

11/16/11, ” K is pain free at 3 mg of Naltrexone. We are not sure of any side effects at that level as she has a cold/flu and has had nausea and headaches. She does not have any sleep issues so far. K thought the Delsym was making her lightheaded. She will start it again as soon as she is feeling better.…

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Needless to say, it makes me very happy to know I am able to help someone in pain, especially a child.

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11/21/11: “We are thrilled too! The only things she is taking is the NAC and the naltrexone. When she tried 2mgs the pain receded to just the upper back of the leg. She also noticed the minor cut she had that day burned a lot. At 3mg all pain just vanished. I can’t tell you how excited we are. Her muscles are a bit sore in the leg as she is exerting herself more in physical therapy…. I am interested to see K’s next autoimmune text results in 6 months. I am wondering whether her Autoimmune test results will be negative from taking the naltrexone.”

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1/15/12, “K has been using the LDN at 4 mg and it is working better for her….Once K has recovered from the mononucleosis and is back on her feet again she will know for sure whether her leg pain is gone when standing in one position. If not, she will try the dose at 5 mg and let you know how that goes.”

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The material on this site is for informational purposes only, and is not a substitute for medical advice,
diagnosis or treatment provided by a qualified health care provider.
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Gliopathic Pain — when Neuropathic Pain Treatment Fails


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Coming soon, though these stand on their own:

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Modulation of microglia can attenuate neuropathic pain symptoms and enhance morphine effectiveness.

Abstract

Microglia play a crucial role in the maintenance of neuronal homeostasis in the central nervous system, and microglia production of immune factors is believed to play an important role in nociceptive transmission. There is increasing evidence that uncontrolled activation of microglial cells under neuropathic pain conditions induces the release of proinflammatory cytokines (interleukin – IL-1beta, IL-6, tumor necrosis factor – TNF-alpha), complement components (C1q, C3, C4, C5, C5a) and other substances that facilitate pain transmission. Additionally, microglia activation can lead to altered activity of opioid systems and neuropathic pain is characterized by resistance to morphine. Pharmacological attenuation of glial activation represents a novel approach for controlling neuropathic pain. It has been found that propentofylline, pentoxifylline, fluorocitrate and minocycline decrease microglial activation and inhibit proinflammatory cytokines, thereby suppressing the development of neuropathic pain. The results of many studies support the idea that modulation of glial and neuroimmune activation may be a potential therapeutic mechanism for enhancement of morphine analgesia. Researchers and pharmacological companies have embarked on a new approach to the control of microglial activity, which is to search for substances that activate anti-inflammatory cytokines like IL-10. IL-10 is very interesting since it reduces allodynia and hyperalgesia by suppressing the production and activity of TNF-alpha, IL-1beta and IL-6. Some glial inhibitors, which are safe and clinically well tolerated, are potential useful agents for treatment of neuropathic pain and for the prevention of tolerance to morphine analgesia. Targeting glial activation is a clinically promising method for treatment of neuropathic pain.

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Microglia: a promising target for treating neuropathic and postoperative pain, and morphine tolerance.

Source

Department of Anesthesiology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA.

Abstract

Management of chronic pain, such as nerve-injury-induced neuropathic pain associated with diabetic neuropathy, viral infection, and cancer, is a real clinical challenge. Major surgeries, such as breast and thoracic surgery, leg amputation, and coronary artery bypass surgery, also lead to chronic pain in 10-50% of individuals after acute postoperative pain, partly due to surgery-induced nerve injury. Current treatments mainly focus on blocking neurotransmission in the pain pathway and have only resulted in limited success. Ironically, chronic opioid exposure might lead to paradoxical pain. Development of effective therapeutic strategies requires a better understanding of cellular mechanisms underlying the pathogenesis of neuropathic pain. Progress in pain research points to an important role of microglial cells in the development of chronic pain. Spinal cord microglia are strongly activated after nerve injury, surgical incision, and chronic opioid exposure. Increasing evidence suggests that, under all these conditions, the activated microglia not only exhibit increased expression of microglial markers CD 11 b and Iba 1, but also display elevated phosphorylation of p38 mitogen-activated protein kinase. Inhibition of spinal cord p38 has been shown to attenuate neuropathic and postoperative pain, as well as morphine-induced antinociceptive tolerance. Activation of p38 in spinal microglia results in increased synthesis and release of the neurotrophin brain-derived neurotrophic factor and the proinflammatory cytokines interleukin-1β, interleukin-6, and tumor necrosis factor-α. These microglia-released mediators can powerfully modulate spinal cord synaptic transmission, leading to increased excitability of dorsal horn neurons, that is, central sensitization, partly via suppressing inhibitory synaptic transmission. Here, we review studies that support the pronociceptive role of microglia in conditions of neuropathic and postoperative pain and opioid tolerance. We conclude that targeting microglial signaling might lead to more effective treatments for devastating chronic pain after diabetic neuropathy, viral infection, cancer, and major surgeries, partly via improving the analgesic efficacy of opioids.

 

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The material on this site is for informational purposes only, and is not a substitute for medical advice,
diagnosis or treatment provided by a qualified health care provider.
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For My Home Page, click here:  
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