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Welcome to Wikipedia!

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Hello Medicinechief! Welcome to Wikipedia! Thank you for your contributions. If you decide that you need help, ask me on my talk page, check out Wikipedia:Where to ask a question, or place {{helpme}} on your talk page and someone will show up shortly to answer your questions. Please remember to sign your name on talk pages using four tildes (~~~~); this will automatically produce your name and the date. Below are some recommended guidelines to facilitate your involvement. And remember, no question is "stupid"; if you have anything, absolutely anything that you'd like to know, feel free to drop on by and leave my a message! :D Happy Editing!

Getting Started
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GeorgeMoney ☺ (talk) ☺ (Help Desk) ☺ (Reference Desk) ☺ (Help Channel) 05:24, 28 June 2006 (UTC)[reply]

References

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Please use high quality references per WP:MEDRS such as review articles or major textbooks. Note that review articles are NOT the same as peer reviewed articles. A good place to find medical sources is TRIP database Thanks and welcome to Wikipedia.

Doc James (talk · contribs · email) (if I write on your page reply on mine) 00:41, 26 November 2012 (UTC)[reply]

There are a number of issues with your addition

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One being that it is not properly formatted. Thus will move it here.Doc James (talk · contribs · email) (if I write on your page reply on mine) 00:41, 26 November 2012 (UTC)[reply]

The numbers for the references do not link to anything. Also we do not typically use Med Hypothese as a reference as what is published in it is simply that hypothesis. Please read WP:MEDRS and WP:MEDHOW. Doc James (talk · contribs · email) (if I write on your page reply on mine) 01:17, 26 November 2012 (UTC)[reply]
We should be using secondary sources from the last 5 years. Most of these are fairly old. The other concern is many of them are primary sources rather than secondary ones. Doc James (talk · contribs · email) (if I write on your page reply on mine) 02:41, 26 November 2012 (UTC)[reply]

Text in question

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Extended content

In 2002, Sota Omoigui published a new theory of pain in his book titled: The Biochemical Origin of Pain. [1]. This theory stated that: The origin of all Pain is inflammation and the inflammatory response. Mediators of inflammation include cytokines, neuropeptides, growth factors, transcription factors, Histamine, Serotonin/5HT, arachidonic acid metabolites,kinins, nitric oxide, oxygen radicals and neurotransmitters. Activation of pain receptors, transmission and modulation of pain signals, neuro plasticity and central sensitization are all one continuum of inflammation and the inflammatory response. Irrespective of the type of pain whether it is acute or chronic pain, peripheral or central pain, nociceptive or neuropathic pain, the underlying origin is inflammation and the inflammatory response. Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arise from inflammation and the inflammatory response. Independent Review of the Inflammation Response Theory Page 18 in a Book Publication from Department of Pharmacology, Leiden /Amsterdam Center for Drug Research (LACDR), Faculty of Science, Leiden University and published by the Center for Drug Research, STATES: “we strongly support the hypothesis proposed by OmoiGui, which states that the origin of all pain is inflammation and inflammatory response (5;6).” [2].[3].

Soft tissue or nerve injury causes excitation of sensory nerve fibers.Antidromic firing of these sensory nerves causes release of the inflammatory mediators PG, Cytokines IL-1 beta, TNF alpha, 5 hydroxytryptamine, leukotrienes, and bradykinins. Mediators stimulate the release of other neuropeptides including CGRP, substance P, and cholecytokinin. Neuropeptides induce vasodilation, increase vascular permeability, attract other immune cells such as T helper cells and excite surrounding sensory nerve fibers -- neurogenic inflammation. Peripheral nociceptive impulses travel via A delta and C fibers to synapse in the lamina II and lamina V of the spinal cord. C fibers also synapse in Lamina I of the spinal cord. 2nd order neurons in Lamina I, respond to impulses from the C fibers. Wide dynamic range(WDR) neurons in Lamina V can be activated to produce wind-up. Neuropeptides glutamate and aspartate mediate fast synaptic transmission in lamina V. The neuropeptides bind and activate amino-3-hydroxyl-5-methyl-4-proprionic acid (AMPA) and Kainate (KAR) receptors that regulate Na+ and K+ ion influx. Glutamate and aspartate bind to NMDA receptors. Activated AMPA receptors produce a depolarization that dislodges a magnesium plug from the ion channel of the NMDA receptor. This initiates the entry of calcium ions into the neuron. Intracellular calcium accumulates. A chain of neurochemical and neurophysiologic changes leads to the rapid and independent firing of spinal neurons without stimulation. This results in magnification of all nerve traffic and pain stimuli that arrive in the spinal cord from the periphery. Activation of motor nerves results in excessive muscle tension. More inflammatory mediators are released, generating more nerve traffic and increased muscle spasm. Constant C-fiber nerve stimulation to the spinal cord results in even more release of inflammatory mediators but this time within the spinal cord.The origin of all pain is from inflammation and the inflammatory response. TNF-alpha and Interleukin 1-beta play an important role in rheumatoid arthritis by mediating cytokines that cause inflammation and joint destruction. TNF-alpha, Interleukin 1-beta and Substance P are elevated in the joint fluids in patients with rheumatoid arthritis[4] [5][6][7]. These inflammatory mediators are also elevated in the joint fluid in patients with osteoarthritis albeit to a far less extent. Along with mechanical factors, growth factors and cytokines such as TGF beta 1, IL-1 alpha, IL-1 beta and TNF-alpha may be involved in the formation and growth of osteophytes, since these molecules can induce growth and differentiation of mesenchymal cells. The incidence and size of osteophytes may be decreased by inhibition of direct or indirect effects of these cytokines and growth factors on osteoid deposition in treated animals Cite error: A <ref> tag is missing the closing </ref> (see the help page).</ref>[8] [9]. Inhibition of IL-1 receptor also decreases the production of metalloproteinase enzymes collagenase-1 and stomelysin-1 in the synovial membrane and cartilage. These enzymes are involved in connective tissue breakdown [10][11]. Tendonitis or bursitis may be associated with diseases such as rheumatoid arthritis, gout, psoriatic arthritis, thyroid disease and diabetes. In one study of patients with rotator cuff diseases, the levels of the cytokine IL-1 beta was significantly correlated with the degree of pain. The combined results of immunohistochemistry indicated that both synovial lining and sublining cells produce IL-1beta, while synovial lining cells predominantly produce the anti-inflammatory intracellular InterLeukin-1 receptor antagonist (icIL-1ra) and sublining cells secrete secreted InterLeukin-1 receptor antagonist (sIL-1ra)[12][13]. In other studies, the levels of IL-1 beta were significantly higher in the shoulder joints in patients with anterior instability and chronic inflammation of the joint [14][15]. In another study, immunohistological staining demonstrated the expression of Interleukin-1 beta (IL-1 beta), Tumor necrosis factor alpha (TNF-alpha), transforming growth factor beta (TGF-beta), and basic fibroblast growth factor (bFGF) in subacromial bursa derived from the patients suffering from rotator cuff tear [16]. Back and neck pain most commonly results from injury to the muscle, disk, nerve, ligament or facet joints with subsequent inflammation and spasm. Degeneration of the disks or joints produces the same symptoms and occurs subsequent to aging, previous injury or excessive mechanical stresses that this region is subjected to because of its proximity to the sacrum in the lower back. Herniated disk tissue (nucleus pulposus) produces a profound inflammatory reaction with release of inflammatory chemical mediators most especially Tumor Necrosis Factor Alpha. Subsequent to release of TNF-alpha, there is an increase in the formation of inflammatory mediator prostaglandin and Nitric Oxide. It is now known that Tumor Necrosis Factor Alpha is released by herniated disk tissue (nucleus pulposus), and is primarily responsible for the nerve injury and behavioral manifestations of experimental sciatica associated with herniated lumbar discs [17][18][19]. This has been confirmed by numerous animal studies and research wherein application of disk tissue (nucleus pulposus) to a nerve results in nerve fiber injury, with reduction of nerve conduction velocity, intracapillary thrombus formation, and the intraneural edema formation [20][21]. Fibromyalgia is a chronic, painful musculoskeletal disorder characterized by widespread pain, pressure hyperalgesia, morning stiffness, sleep disturbances including restless leg syndrome, mood disturbances, and fatigue. Several studies have shown that there are increased levels of the inflammatory transmitter Substance P (SP) and calcitonin gene related peptide (CGRP) in the spinal fluid of patients with fibromyalgia syndrome (FMS [22][23] [24]The levels of platelet serotonin are also abnormal [25]. Furthermore, in patients with fibromyalgia, the level of pain intensity is related to the spinal fluid level of arginine, which is a precursor to the inflammatory mediator nitric oxide (NO) [26]. Another study found increases over time in blood levels of cytokines Interleukin -6, Interleukin -8 and Interleukin -1R antibody (IL-1Ra) whose release is stimulated by substance P. Migraine headache is caused by activation of trigeminal sensory fibers by known and unknown migraine triggers. There is subsequent release of inflammatory mediators from the trigeminal nerve. This leads to distention of the large meningeal blood vessels in the skull and brain and the development of a central sensitization within the trigeminal nucleus caudalis (TNC).A clear association between migraine and the release of inflammatory mediator calcitonin gene-related peptide (CGRP) and substance P (SP) has been demonstrated. Jugular plasma levels of the potent vasodilator, calcitonin gene-related peptide (CGRP) have been shown to be elevated in migraine headache. CGRP-mediated neurogenic dural vasodilation is blocked by anti-migraine drug dihydroergotamine, triptans, and opioids [57] . In cluster headache and in chronic paroxysmal hemicrania, there is additional release of inflammatory mediator vasoactive intestinal peptide (VIP) in association with facial symptoms (nasal congestion, runny nose) [58] . Immunocytochemical studies have revealed that cerebral blood vessels are invested with nerve fibers containing inflammatory mediator neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), peptide histidine isoleucine (PHI), substance P (SP), neurokinin A (NKA), and calcitonin gene-related peptide (CGRP). In addition, there are studies reporting the occurrence of putative neurotransmitters such as cholecystokinin, dynorphin B, galanin, gastrin releasing peptide, vasopressin, neurotensin, and somatostatin. Neuropathic pain, in contrast to nociceptive pain, is described as "burning", "electric", "tingling", and "shooting" in nature. It can be continuous or paroxysmal in presentation. Whereas nociceptive pain is caused by the stimulation of peripheral A-delta and C-polymodal pain receptors, by inflammatory mediators, (e.g. histamine bradykinin, substance P, etc.) neuropathic pain is produced by injury or damage to peripheral nerves or the central nervous system. The hallmarks of neuropathic pain are chronic allodynia and hyperalgesia. Allodynia is defined as pain resulting from a stimulus that ordinarily does not elicit a painful response (e.g. light touch). Hyperalgesia is defined as an increased sensitivity to normally painful stimuli. Examples of neuropathic pain include carpal tunnel syndrome, trigeminal neuralgia, post herpetic neuralgia, phantom limb pain, complex regional pain syndromes and the various peripheral neuropathies. Nerve injury is accompanied by a considerable increase in monocytes/macrophages and subsequent release of Interleukin -6 and TNF-alpha. Subsequent to nerve injury, there is increase in nerve traffic. Expression of sodium channels is altered significantly in response to injury thus leading to abnormal excitability in the sensory neurons. Nerve impulses arriving in the spinal cord stimulate the release of inflammatory protein Substance P. The presence of Substance P and other inflammatory proteins such as calcitonin gene-related peptide (CGRP) neurokinin A, vasoactive intestinal peptide removes magnesium induced inhibition and enables excitatory Inflammatory proteins such as glutamate and aspartate to activate specialized spinal cord NMDA receptors. This results in magnification of all nerve traffic and pain stimuli that arrive in the spinal cord from the periphery. Constant C-fiber nerve stimulation to transmission pathways in the spinal cord results in even more release of inflammatory mediators but this time within the spinal cord. The transcription factor, nuclear factor-kappa B (NF-kappaB), plays a pivotal role in regulating the production of inflammatory cytokines[27] . Inflammation causes increased production of the enzyme cyclooxygenase-2 (Cox-2), leading to the release of chemical mediators both in the area of injury and in the spinal cord. Widespread induction of Cox-2 expression in spinal cord neurons and in other regions of the central nervous system elevates inflammatory mediator prostaglandin E2 (PGE2) levels in the cerebrospinal fluid. The major inducer of central Cox-2 upregulation is inflammatory mediator interleukin-1 in the CNS [28]. Basal levels of the enzyme phospholipase A2 activity in the CNS do not change with peripheral inflammation.. The central nervous system response to pain can keep increasing even though the painful stimulus from the injured tissue remains steady. This "wind-up" phenomenon in deep dorsal neurons can dramatically increase the injured person’s sensitivity to the pain. Transection of a nerve fiber (axotomy) results in an increased production of inflammatory cytokines and induces marked changes in the expression of sodium channels within the sensory neurons [71] . Following axotomy the density of slow (tetrodotoxin-resistant) sodium currents decrease and a rapidly repriming sodium current appears. The altered expression of sodium channels leads to abnormal excitability in the sensory neurons [29]. Studies have shown that these changes in sodium channel expression following axotomy may be attributed at least in part to the loss of retrogradely transported nerve growth factor [30]. Abnormal development of sensory-sympathetic connections follow nerve injury, and contribute to the hyperalgesia (abnormally severe pain) and allodynia (pain due to normally innocuous stimuli). These abnormal connections between sympathetic and sensory neurons arise in part due to sprouting of sympathetic axons. Studies have shown that sympathetic axons invade spinal cord dorsal root ganglia (DRG) following nerve injury, and activity in the resulting pericellular axonal 'baskets' may underlie painful sympathetic-sensory coupling [31]. Sympathetic sprouting into the DRG may be stimulated by neurotrophins such as nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), neurotrophin‑3 (NT‑3) and neurotrophin 4/5 (NT‑4/5). Osteoporosis is common with aging and in post Menopausal Women. It is often ascribed solely to abnormalities in calcium metabolism. However osteoporosis is associated with elevated levels of cytokines IL-6, IL-1 and TNF-alpha. IL-6 increases osteoclastic activity. Bone resorption occurs in inflammatory diseases such as Rheumatoid Arhritis, Chronic Regional Pain Syndrome/Reflex Sympathetic Dystrophy (CRPS/RSD). Elevated levels of IL-6 are found in multiple myeloma and in menopause. Estrogens block osteoblast secretion of IL-6 and decreased levels of estrogens occurs in menopause. Osteoporosis accounts for pain in 89% of Menopausal Women. Inflammatory mediators activate bone nociceptors and decrease their threshold for activation. Severe pain arises from fractures of compressed vertebrae or femoral neck, and facet joints. Bisphosphonates are used in the treatment of osteoporosis and act by decreasing IL-6 levels and osteoclastic activity. Another osteoporosis drug Prolia, inhibits transcription factor Receptor activator of NF-Kappa B ligand (RANKL. Receptor activator of NF-Kappa B ligand (RANKL) increases expression of osteoclastogenic cytokines.

Medicinechief (talk) 01:43, 26 November 2012 (UTC)[reply]

  1. ^ The biochemical origin of pain: How a new law and new drugs have led to a medical breakthrough in the treatment of persistent pain. S Omoigui - 2002 - State-of-the-Art Technologies
  2. ^ https://openaccess.leidenuniv.nl/handle/1887/13263
  3. ^ https://openaccess.leidenuniv.nl/bitstream/handle/1887/13263/Chapter.1.pdf;jsessionid=91F3C82E8F729DA596288A5D5EA088DD?sequence=2
  4. ^ Arthritis Rheum. 2006 Feb 15;55(1):53-6. Synovial fluid levels of anti-cyclic citrullinated peptide antibodies and IgA rheumatoid factor in rheumatoid arthritis, psoriatic arthritis, and osteoarthritis.Caspi D, Anouk M, Golan I, Paran D, Kaufman I, Wigler I, Levartovsky D, Litinsky I, Elkayam O.
  5. ^ Osteoarthritis Cartilage. 2012 Nov;20(11):1302-8. doi: 10.1016/j.joca.2012.07.021. Epub 2012 Aug 5. Cartilage and bone markers and inflammatory cytokines are increased in synovial fluid in the acute phase of knee injury (hemarthrosis)--a cross-sectional analysis.Swärd P, Frobell R, Englund M, Roos H, Struglics A.
  6. ^ J Rheumatol. 2010 Jan;37(1):18-25. doi: 10.3899/jrheum.090492. Epub 2009 Nov 16. Increased levels of interleukin 33 in sera and synovial fluid from patients with active rheumatoid arthritis. Matsuyama Y, Okazaki H, Tamemoto H, Kimura H, Kamata Y, Nagatani K, Nagashima T, Hayakawa M, Iwamoto M, Yoshio T, Tominaga S, Minota S.
  7. ^ Rev Prat 1994 Jun 15;44(12):1569-71[Substance P and rheumatic diseases][Article in French]Menkes CJ, Renoux M.
  8. ^ Inflammation 1992 Dec;16(6):587-601. Effects of interleukin-1 beta and tumor necrosis factor-alpha on osteoblastic expression of osteocalcin and mineralized extracellular matrix in vitro.Taichman RS, Hauschka PV.
  9. ^ Calcif Tissue Int 1993 Mar;52(3):227-33 Proliferative responses to estradiol, IL-1 alpha and TGF beta by cells expressing alkaline phosphatase in human osteoblast-like cell cultures. Rickard DJ, Gowen M, MacDonald BR.
  10. ^ Osteoarthritis Cartilage. 2012 Feb;20(2):127-35. doi: 10.1016/j.joca.2011.12.002. Epub 2011 Dec 11. A potential role of chondroitin sulfate on bone in osteoarthritis: inhibition of prostaglandin E₂ and matrix metalloproteinases synthesis in interleukin-1β-stimulated osteoblasts. Pecchi E, Priam S, Mladenovic Z, Gosset M, Saurel AS, Aguilar L, Berenbaum F, Jacques C.
  11. ^ Arthritis Rheum 2001 Oct;44(10):2320-30 In vivo dual inhibition of cyclooxygenase and lipoxygenase by ML-3000 reduces the progression of experimental osteoarthritis: suppression of collagenase 1 and interleukin-1beta synthesis. Jovanovic DV, Fernandes JC, Martel-Pelletier J, Jolicoeur FC, Reboul P, Laufer S, Tries S, Pelletier JP.
  12. ^ Ann Rheum Dis. 2003 Apr;62(4):303-7. Microarchitecture and protective mechanisms in synovial tissue from clinically and arthroscopically normal knee joints. Smith MD, Barg E, Weedon H, Papengelis V, Smeets T, Tak PP, Kraan M, Coleman M, Ahern MJ.
  13. ^ Rheumatology (Oxford) 2001 Sep;40(9):995-1001. Interleukin-1-induced subacromial synovitis and shoulder pain in rotator cuff diseases.Gotoh M, Hamada K, Yamakawa H, Yanagisawa K, Nakamura M, Yamazaki H, Ueyama Y, Tamaoki N, Inoue A, Fukuda
  14. ^ J Shoulder Elbow Surg. 2012 Sep 20. pii: S1058-2746(12)00277-7. doi: 10.1016/j.jse.2012.06.014. [Epub ahead of print] Inflammatory cytokines are overexpressed in the subacromial bursa of frozen shoulder. Lho YM, Ha E, Cho CH, Song KS, Min BW, Bae KC, Lee KJ, Hwang I, Park HB.
  15. ^ J Orthop Res 1999 May;17(3):392-7. Increased interleukin-1beta production in the synovium of glenohumeral joints with anterior instability. Gotoh M, Hamada K, Yamakawa H, Nakamura M, Yamazaki H, Inoue A, Fukuda H.
  16. ^ Kobe J Med Sci 2001 Feb;47(1):25-34 Immunolocalization of cytokines and growth factors in subacromial bursa of rotator cuff tear patients.Sakai H, Fujita K, Sakai Y, Mizuno K.
  17. ^ Spine (Phila Pa 1976). 2008 Sep 1;33(19):2041-6. doi: 10.1097/BRS.0b013e318183bb86.Elevated levels of tumor necrosis factor-alpha in periradicular fat tissue in patients with radiculopathy from herniated disc.Genevay S, Finckh A, Payer M, Mezin F, Tessitore E, Gabay C, Guerne PA.
  18. ^ Pain. 2004 Aug;110(3):578-87. Role of TNF-alpha in sensitization of nociceptive dorsal horn neurons induced by application of nucleus pulposus to L5 dorsal root ganglion in rats.Cuellar JM, Montesano PX, Carstens E.
  19. ^ Spine 2000 Dec 1;25(23):2975-80 2000 Volvo Award winner in basic science studies: Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology. Molecular, histologic, and behavioral comparisons in rats. Igarashi T, Kikuchi S, Shubayev V, Myers RR
  20. ^ Spine 2001 Apr 15;26(8):863-9 Selective inhibition of tumor necrosis factor-alpha prevents nucleus pulposus-induced thrombus formation, intraneural edema, and reduction of nerve conduction velocity: possible implications for future pharmacologic treatment strategies of sciatica. Olmarker K, Rydevik B.
  21. ^ Schmerz 2001 Dec;15(6):425-9 Radicular pain - recent pathophysiologic concepts and therapeutic implications. Olmarker K.
  22. ^ Arthritis Rheum 1994 Nov;37(11):1593-601. Elevated cerebrospinal fluid levels of substance P in patients with the fibromyalgia syndrome. Russell IJ, Orr MD, Littman B, Vipraio GA, Alboukrek D, Michalek JE, Lopez Y, MacKillip F.
  23. ^ Pain 1988 Jan;32(1):21-6 Elevated CSF levels of substance P and high incidence of Raynaud phenomenon in patients with fibromyalgia: new features for diagnosis. Vaeroy H, Helle R, Forre O, Kass E, Terenius L.
  24. ^ J Rheumatol Suppl 1989 Nov;19:94-7 Modulation of pain in fibromyalgia (fibrositis syndrome): cerebrospinal fluid (CSF) investigation of pain related neuropeptides with special reference to calcitonin gene related peptide (CGRP).Vaeroy H, Sakurada T, Forre O, Kass E, Terenius L.
  25. ^ Z Rheumatol 1998;57 Suppl 2:63-6 Neurochemical pathogenesis of fibromyalgia. Russell
  26. ^ Pain 2000 Aug;87(2):201-11. Changes in the concentrations of amino acids in the cerebrospinal fluid that correlate with pain in patients with fibromyalgia: implications for nitric oxide pathways. Larson AA, Giovengo SL, Russell IJ, Michalek JE.
  27. ^ Neuroreport 2001 Jul 20;12(10):2079-84 NF-kappa B decoy suppresses cytokine expression and thermal hyperalgesia in a rat neuropathic pain model. Sakaue G, Shimaoka M, Fukuoka T, Hiroi T, Inoue T, Hashimoto N, Sakaguchi T, Sawa Y, Morishita R, Kiyono H, Noguchi K, Mashimo T.
  28. ^ Nature 410, 471 - 475 (2001) © Macmillan Publishers Ltd. Interleukin-1-mediated induction of Cox-2 in the CNS contributes to inflammatory pain hypersensitivity Tarek A. Samad, Kimberly A. Moore, Adam Sapirstein, Sara Billet, Andrew Allchorne, Stephen Poole, Joseph V. Bonventre & Clifford J. Woolf
  29. ^ Waxman, S.G. (1999) The molecular pathophysiology of pain: abnormal expression of sodium channel genes and its contributions to hyperexcitability in primary sensory neurons. Pain. 6, S133-S140.
  30. ^ Black, J.A., Langworthy, K., Hinson, A.W., Dibb-Hajj, S.D., and Waxman, S.G. (1997) NGF has opposing effects on Na+ channel III and SNS gene expression in spinal sensory neurons. NeuroReport, 8: 2331-2335.
  31. ^ Eur J Neurosci 1999 Mar;11(3):837-46 Adrenergic innervation of rat sensory ganglia following proximal or distal painful sciatic neuropathy: distinct mechanisms revealed by anti-NGF treatment. Ramer MS, Bisby MA.

Hi Medicinechief. James asked me to discuss this with you. He and I, along with many other volunteers, review recent changes to Wikipedia medical articles to check that they conform to our policies and guidelines. As an encyclopedia edited by anonymous volunteers, we are very tightly constrained as to what we can include.

Wikipedia's medical content is, basically, the presentation of the current scholarly consensus on a topic. Where there is significant scholarly disagreement on a point, we present that, giving due weight to all relevant views, according to their degree of acceptance. We reflect the strength of support for a position, where that is made clear in a scholarly overview of the topic.

We derive this (scholarly consensus, different views, and due weight) from expert reviews of the topic published in high-quality peer-reviewed journals, or similar expert overviews. We call such sources "secondary" sources. For a clear exposition of this method, and a description of ideal sources for this approach, see WP:MEDRS.

Until the theory has been extensively reviewed in a high impact peer-reviewed journal, graduate level textbook or similar independent dedicated review, we can't include it. Once the theory has been addressed extensively in such a source, please don't hesitate to bring it to the article's talk page. --Anthonyhcole (talk) 09:16, 27 November 2012 (UTC)[reply]

Hello Anthony, This theory has been extensively reviewed and cited in numerous articles. I am trying to add more refences. For the review, please refer to Page 18 in ARTICLE from Department of Pharmacology, Leiden /Amsterdam Center for Drug Research (LACDR), Faculty of Science, Leiden University STATES: “we strongly support the hypothesis proposed by OmoiGui, which states that the origin of all pain is inflammation and inflammatory response (5;6).” [1].
Medicinechief (talk) 19:29, 27 November 2012 (UTC)[reply]
That chapter you point me to is not a strong enough source to support us covering the theory in Pain. It is described as a thesis, so may be student work, and does not appear to have been published by a scholarly publisher. The kind of source that would support its inclusion would be a recent scholarly review in a relevant specialist, highly-regarded, peer-reviewed journal (Pain, Journal of Pain, Neuroscience, etc.) or a textbook or monograph published by a highly-regarded scholarly press (OUP, Elsivier, etc.), where the review is dedicated to the theory alone or discusses it extensively and puts it in context against other current theories, and is written by author/s not connected with the author/s of the theory.
This is no criticism at all of the theory, I'm just explaining how this encyclopedia works. Wikipedia:Identifying reliable sources (medicine) describes the kind of sources we insist on for biomedical content, and Wikipedia:Neutral point of view and Wikipedia:Fringe theories describe how we deal with new theories and how we apportion weight.
If, once you've familiarised yourself with those important Wikipedia guidelines, you still believe the theory warrants coverage in Pain or another Wikipedia article, ask for more opinions at Wikipedia talk:WikiProject Medicine. That is a forum where volunteers discuss biomedical content on Wikipedia.
On another but related matter; we can devote very little space to pain theory in the main article Pain because it is an overview and needs to at least touch on many aspects of that broad topic. I think an article called Pain theory, giving a detailed description of the history and current state of scientific conceptions of pain is badly needed. (We do have History of pain theory but that has a number of shortcomings.) If you, or anyone you know, are interested in taking that on, I would be very willing to help it fit Wikipedia style and content policies. --Anthonyhcole (talk) 05:24, 28 November 2012 (UTC)[reply]
Hello Anthony....The Leiden University publication is a book published by a scholarly publisher: The Center for Drug Research. You may see the link to the book at: https://openaccess.leidenuniv.nl/handle/1887/13263. This theory has been also been cited by 62 other articles. 108.65.40.195 (talk) 07:06, 28 November 2012 (UTC)[reply]
It is a doctoral thesis which mentions and supports the theory. What is needed for a mention in Pain is a careful assessment of the theory by someone with recognised expertise, that evaluates it and puts it in context. Has the theory, as Sota Omoigui's theory, been carefully analysed by a review devoted to it or analysed in a broader review devoted to current thinking in pain theory, published in a graduate-level textbook or monograph or a highly-regarded journal yet? If not, we will need to wait for that. That is one of the requirements for inclusion of biomedical information in Wikipedia articles. --Anthonyhcole (talk) 06:52, 29 November 2012 (UTC)[reply]
Hello Anthony.....The doctoral thesis by Leiden University exceeds the requirements you state for an independent review of this theory. The thesis is 239 pages and supervised by 7 professors [2]. The research described in this thesis was sponsored by GlaxoSmithKline and conducted at the Division of Pharmacology of the Leiden/Amsterdam Center for Drug Research, Leiden University,The Netherlands and the Department of Drug Metabolism and Pharmacokinetics of GlaxoSmithKline in Harlow, United Kingdom.

I hope the expertise in this thesis is more than enough to convince you. If not, I will request a third party mediator to ensure that this theory of pain is mentioned in the Wikipedia Section on Pain Theories. Medicinechief (talk) 00:46, 10 December 2012 (UTC)[reply]

Continued issues

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We need to use high quality secondary sources. This typically means review articles or major medical textbooks published in the last 5 or at most 10 years. A number of the refs above are primary sources. If you are unfamiliar wit these terms we have articles that describe each. Cheers Doc James (talk · contribs · email) (if I write on your page reply on mine) 13:32, 17 December 2012 (UTC)[reply]

By all means seek more opinions. We have various noticeboards where editors can ask for input, depending on the situation. James is emphasising the sources you're citing. To discuss the appropriateness of those we have Wikipedia:Reliable sources noticeboard. My concern is that the theory has not been considered and evaluated extensively enough in major textbooks and journal reviews, so to address the merits of that view there is Wikipedia:Fringe theories noticeboard. Please only open one discussion - editors on one board will take into account all aspects of policy when discussing the proposed edit.
Both my opinion and James's are based on fundamental guidelines that you should master before opening a thread on one of those boards, if you want to effectively engage with the discussion. James, if I've overlooked an important relevant policy or guideline, would you please chip in?
The references just added are combined primary and secondary sources from the Trip Database recommended by Doc James. I will submit this theory for dispute solution as there is no reason to continue to prevent the addition of this theory.75.22.67.232 (talk) 08:37, 18 December 2012 (UTC)75.22.67.232 (talk) 08:38, 18 December 2012 (UTC)[reply]
There is a simple breakdown of various dispute resolution options at
I think going to one of the relevant noticeboards is the best option at this stage, but you might want to consider one of the others. When you do open a dispute resolution discussion, could you please mention this conversation? --Anthonyhcole (talk) 06:50, 19 December 2012 (UTC)[reply]
  1. ^ https://openaccess.leidenuniv.nl/bitstream/handle/1887/13263/Chapter.1.pdf;jsessionid=91F3C82E8F729DA596288A5D5EA088DD?sequence=2
  2. ^ https://openaccess.leidenuniv.nl/bitstream/handle/1887/13263/Table%2bof%2bcontents.pdf?sequence=27
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