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Journal articles on the topic 'Peripheral neuropathic pain'
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Di Stefano, Giulia, Andrea Di Lionardo, Giuseppe Di Pietro, and Andrea Truini. "Neuropathic Pain Related to Peripheral Neuropathies According to the IASP Grading System Criteria." Brain Sciences 11, no. 1 (December 22, 2020): 1. http://dx.doi.org/10.3390/brainsci11010001.
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Neuropathic pain is defined as pain caused by a lesion or disease of the somatosensory system. Neuropathic pain represents a broad category of pain conditions, common complications of peripheral neuropathies, which are characterized by a combination of positive symptoms, including paresthesia and/or dysesthesia and sensory deficits in the painful area. In the present paper, we aimed to assess neuropathic pain frequency and clinical characteristics of peripheral neuropathies due to different aetiologies according to grading system criteria of the International Association for the Study of Pain for a definitive diagnosis of neuropathic pain. Epidemiological studies applying these criteria have been conducted in patients with diabetes, brachial plexus injury, and other traumatic nerve injuries. Neuropathic pain was diagnosed in 37–42% of patients with diabetic peripheral neuropathy, 56% of patients with brachial plexus injury, and 22% of patients with intercostobrachial neuropathy. The most frequent neuropathic pain type was ongoing pain (described as burning or pressing), followed by paroxysmal pain (electric shock-like sensations) and allodynia (pain evoked by brushing and pressure). By providing information on the frequency, clinical signs, and variables associated with neuropathic pain due to different aetiologies, these studies contribute to improving the clinical management of this condition.
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Lee, Ho Seong. "Treatment of peripheral neuropathy: a multidisciplinary approach is necessary." Journal of the Korean Medical Association 63, no. 8 (August 10, 2020): 432–34. http://dx.doi.org/10.5124/jkma.2020.63.8.432.
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The number of patients with peripheral neuropathy or neuropathic pain is increasing. The recommended treatment for peripheral neuropathy and neuropathic pain is proper medications, exercise, physical therapy, and support. Overly invasive interventions can be harmful rather than beneficial to patients. Many doctors do not understand the characteristics of peripheral neuropathy and neuropathic pain. Peripheral neuropathy is not a problem that is confined to a particular department. The most appropriate treatment is a combination of drug therapy, physical exercise, and psychological support. Thus, a multidisciplinary approach is necessary for the effective treatment of peripheral neuropathy and neuropathic pain.
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Jeong, Na Young, Youn Ho Shin, and Junyang Jung. "Neuropathic pain in hereditary peripheral neuropathy." Journal of Exercise Rehabilitation 9, no. 4 (August 31, 2013): 397–99. http://dx.doi.org/10.12965/jer.130057.
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Murphy, Douglas, Denise Lester, F. Clay Smither, and Ellie Balakhanlou. "Peripheral neuropathic pain." NeuroRehabilitation 47, no. 3 (November 13, 2020): 265–83. http://dx.doi.org/10.3233/nre-208002.
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Neuropathic pain (NP) can have either central nervous system causes or ones from the peripheral nervous system. This article will focus on the epidemiology, classifications, pathology, non-invasive treatments and invasive treatments as a general review of NP involving the peripheral nervous system. NP has characteristic symptomatology such as burning and electrical sensations. It occurs in up to 10% of the general population. Its frequency can be attributed to its occurrence in neck and back pain, diabetes and patients receiving chemotherapy. There are a wide range of pharmacologic options to control this type of pain and when such measures fail, numerous interventional methods can be employed such as nerve blocks and implanted stimulators. NP has a cost to the patient and society in terms of emotional consequences, quality of life, lost wages and the cost of assistance from the medical system and thus deserves serious consideration for prevention, treatment and control.
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Baron, Ralf, Christoph Maier, Nadine Attal, Andreas Binder, Didier Bouhassira, Giorgio Cruccu, Nanna B. Finnerup, et al. "Peripheral neuropathic pain." PAIN 158, no. 2 (February 2017): 261–72. http://dx.doi.org/10.1097/j.pain.0000000000000753.
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Castoro, Ryan, Megan Simmons, Vignesh Ravi, Derek Huang, Christopher Lee, John Sergent, Lan Zhou, and Jun Li. "SCN11A Arg225Cys mutation causes nociceptive pain without detectable peripheral nerve pathology." Neurology Genetics 4, no. 4 (July 20, 2018): e255. http://dx.doi.org/10.1212/nxg.0000000000000255.
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ObjectiveThe SCN11A gene encodes the NaV1.9 sodium channel found exclusively in peripheral nociceptive neurons.MethodsAll enrolled participants were evaluated clinically by electrophysiologic studies, DNA sequencing, and punch skin biopsies.ResultsAll affected family members are afflicted by episodes of pain. Pain was predominantly nociceptive, but not neuropathic in nature, which led a diagnosis of fibromyalgia in some patients. All patients had normal findings in nerve conduction studies for detecting large nerve fiber neuropathies and skin biopsies for detecting small nerve fiber pathology.ConclusionsUnlike those patients with missense mutations in SCN11A, small fiber sensory neuropathy, and neuropathic pain, the Arg225Cys SCN11A in the present study causes predominantly nociceptive pain with minimal features of neuropathic pain and undetectable pathophysiologic changes of peripheral neuropathy. This finding is consistent with dysfunction of nociceptive neurons. In addition, since nociceptive pain in patients has led to the diagnosis of fibromyalgia, this justifies a future search of mutations of SCN11A in patients with additional pain phenotypes such as fibromyalgia to expand the clinical spectrum beyond painful small fiber sensory neuropathy.
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Micu, Elena Claudia, and Laszlo Irsay. "The Rehabilitation of Oncological Patients Presenting Neuropathies." Medicine and Pharmacy Reports 87, no. 2 (June 30, 2014): 67–72. http://dx.doi.org/10.15386/cjmed-278.
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The International Association for the Study of Pain (IASP 2011) defines neuropathic pain as “the pain caused by an injury or disease of the somatosensory portion of the nervous system”. The central neuropathic pain is defined as “the pain caused by an injury or disease of the central somatosensory central nervous system”, whereas the peripheral neuropathic pain is defined as “the pain caused by an injury or disease of the peripheral somatosensory nervous system”. The peripheral neuropathy describes any affection of the peripheral nervous system. The etiology is vast, there being a number of over 100 possible causes, which causes the global morbidity rate to reach approximately 2.4%. The chronic nature of the pain superposes the everyday routine and leads to the high intake of medication for pain alleviation. The number of cases of neuroplasia has always increased today. This disturbing diagnosis which can potentiate the signs and symptoms of peripheral neuropathy as well as reduce and limit the treatment options associated with neuropathies. The treatment presupposes a multidisciplinary approach, while the solution to prevent complications involves the control of risk factors and pathophysiological treatment. Chemotherapy-induced peripheral neuropathy (CPIN) is a significant disabling symptom that is tightly connected to the administration of neurotoxic cytostatic agents used for the treatment of neoplasia. CPIN compromises the quality of life and produces pain or discomfort. I have sought to produce a presentation of the medicated and physical-kinetic treatment options that have proved their effectiveness during clinical studies or random trials and can be applied to cancer patients presenting with symptoms associated with peripheral neuropathy, namely with neuropathic pain, and support it with arguments
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Basu, Paramita, and Arpita Basu. "In Vitro and In Vivo Effects of Flavonoids on Peripheral Neuropathic Pain." Molecules 25, no. 5 (March 5, 2020): 1171. http://dx.doi.org/10.3390/molecules25051171.
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Neuropathic pain is a common symptom and is associated with an impaired quality of life. It is caused by the lesion or disease of the somatosensory system. Neuropathic pain syndromes can be subdivided into two categories: central and peripheral neuropathic pain. The present review highlights the peripheral neuropathic models, including spared nerve injury, spinal nerve ligation, partial sciatic nerve injury, diabetes-induced neuropathy, chemotherapy-induced neuropathy, chronic constriction injury, and related conditions. The drugs which are currently used to attenuate peripheral neuropathy, such as antidepressants, anticonvulsants, baclofen, and clonidine, are associated with adverse side effects. These negative side effects necessitate the investigation of alternative therapeutics for treating neuropathic pain conditions. Flavonoids have been reported to alleviate neuropathic pain in murine models. The present review elucidates that several flavonoids attenuate different peripheral neuropathic pain conditions at behavioral, electrophysiological, biochemical and molecular biological levels in different murine models. Therefore, the flavonoids hold future promise and can be effectively used in treating or mitigating peripheral neuropathic conditions. Thus, future studies should focus on the structure-activity relationships among different categories of flavonoids and develop therapeutic products that enhance their antineuropathic effects.
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Falo, Clara P., Raquel Benitez, Marta Caro, Maria Morell, Irene Forte-Lago, Pedro Hernandez-Cortes, Clara Sanchez-Gonzalez, Francisco O’Valle, Mario Delgado, and Elena Gonzalez-Rey. "The Neuropeptide Cortistatin Alleviates Neuropathic Pain in Experimental Models of Peripheral Nerve Injury." Pharmaceutics 13, no. 7 (June 24, 2021): 947. http://dx.doi.org/10.3390/pharmaceutics13070947.
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Neuropathic pain is one of the most severe forms of chronic pain caused by the direct injury of the somatosensory system. The current drugs for treating neuropathies have limited efficacies or show important side effects, and the development of analgesics with novel modes of action is critical. The identification of endogenous anti-nociceptive factors has emerged as an attractive strategy for designing new pharmacological approaches to treat neuropathic pain. Cortistatin is a neuropeptide with potent anti-inflammatory activity, recently identified as a natural analgesic peptide in several models of pain evoked by inflammatory conditions. Here, we investigated the potential analgesic effect of cortistatin in neuropathic pain using a variety of experimental models of peripheral nerve injury caused by chronic constriction or partial transection of the sciatic nerve or by diabetic neuropathy. We found that the peripheral and central injection of cortistatin ameliorated hyperalgesia and allodynia, two of the dominant clinical manifestations of chronic neuropathic pain. Cortistatin-induced analgesia was multitargeted, as it regulated the nerve damage-induced hypersensitization of primary nociceptors, inhibited neuroinflammatory responses, and enhanced the production of neurotrophic factors both at the peripheral and central levels. We also demonstrated the neuroregenerative/protective capacity of cortistatin in a model of severe peripheral nerve transection. Interestingly, the nociceptive system responded to nerve injury by secreting cortistatin, and a deficiency in cortistatin exacerbated the neuropathic pain responses and peripheral nerve dysfunction. Therefore, cortistatin-based therapies emerge as attractive alternatives for treating chronic neuropathic pain of different etiologies.
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Giorgio, Cristina, Mara Zippoli, Pasquale Cocchiaro, Vanessa Castelli, Giustino Varrassi, Andrea Aramini, Marcello Allegretti, Laura Brandolini, and Maria Candida Cesta. "Emerging Role of C5 Complement Pathway in Peripheral Neuropathies: Current Treatments and Future Perspectives." Biomedicines 9, no. 4 (April 7, 2021): 399. http://dx.doi.org/10.3390/biomedicines9040399.
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The complement system is a key component of innate immunity since it plays a critical role in inflammation and defense against common pathogens. However, an inappropriate activation of the complement system is involved in numerous disorders, including peripheral neuropathies. Current strategies for neuropathy-related pain fail to achieve adequate pain relief, and although several therapies are used to alleviate symptoms, approved disease-modifying treatments are unavailable. This urgent medical need is driving the development of therapeutic agents for this condition, and special emphasis is given to complement-targeting approaches. Recent evidence has underscored the importance of complement component C5a and its receptor C5aR1 in inflammatory and neuropathic pain, indicating that C5a/C5aR1 axis activation triggers a cascade of events involved in pathophysiology of peripheral neuropathy and painful neuro-inflammatory states. However, the underlying pathophysiological mechanisms of this signaling in peripheral neuropathy are not fully known. Here, we provide an overview of complement pathways and major components associated with dysregulated complement activation in peripheral neuropathy, and of drugs under development targeting the C5 system. C5/C5aR1 axis modulators could represent a new strategy to treat complement-related peripheral neuropathies. Specifically, we describe novel C5aR allosteric modulators, which may potentially become new tools in the therapeutic armory against neuropathic pain.
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Gonçalves, Décia. "8% Capsaicin Patch in Treatment of Peripheral Neuropathic Pain." Pain Physician 5;23, no. 9;5 (September 14, 2020): E541—E548. http://dx.doi.org/10.36076/ppj.2020/23/e541.
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Background: Neuropathic pain is a complex condition that is difficult to control and has a high impact on quality of life. 8% Capsaicin patch can be a therapeutic strategy in the treatment of peripheral neuropathic pain. Objectives: This study aims to (1) evaluate clinical efficacy and (2) tolerability of 8% capsaicin patch in a Pain Unit. Study Design: Retrospective observational study Setting: Portuguese Pain Unit Methods: A sample of 120 patients diagnosed with peripheral neuropathic pain, underwent treatment with the 8% capsaicin patch between February 2011 and February 2019 in a Portuguese Pain Unit. Patients were included in one of the following groups according to the etiology of pain: postherpetic neuralgia (PHN), chronic post-surgical pain (CPSP), post traumatic neuropathic pain (PTNP), diabetic neuropathy (DN), regional pain syndrome. complex I and II (CRPS I / II), HIVassociated neuropathy (HIVN), lumbar neuropathic pain (LNP), trigeminal neuralgia (TN) and other neuropathies (O). The evaluated parameters were: pain intensity according to unit protocol (numerical rating scale), pain characteristics, location, size of the painful area. The evolution of pain intensity after treatment (patients were considered as responders to therapy if the decrease in NRS was equal to or greater than 30%; patients with a decrease in NRS of 50% or more were also analyzed), the area of pain and the need for adjuvant analgesic therapy, as well as the tolerability to treatment and the identification of eventual predictors of its efficacy were evaluated, at 15 days, 8 weeks and 12 weeks after 8% capsaicin patch. Results: Of the 120 patients in the sample, 40.8% had a ≥ 30% decrease in basal pain intensity 15 days after treatment, 43.3% after 8 weeks and 45.0% after 12 weeks. 30.8% of patients had ≥ 50% decreased basal pain intensity 15 days after treatment, 27.5% after 8 weeks and 30.0% after 12 weeks. Pain area decreased in 36.7% of patients and 18.3% reduced chronic analgesic therapy within 12 weeks after 8% capsaicin patch application. There was only one case of intolerance to the treatment. Limitations: This study has the limitations inherent to a retrospective study. The study period was only 12 weeks and some diagnostic groups included a small number of patients. Conclusion: Treatment of peripheral neuropathic pain with 8% capsaicin patch seem to be effective in the short and medium term, both in decreasing pain intensity and in reducing the painful area. Its application is tolerated by most patients. Key words: 8% capsaicin patch, peripheral neuropathic pain, pain intensity, painful area
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SIMPSON, MARY ANNE. "Conquering peripheral neuropathic pain." Nursing 34, no. 6 (June 2004): 17. http://dx.doi.org/10.1097/00152193-200406000-00009.
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Cvijanovic, Milan, Svetlana Simic, Sofija Banic-Horvat, Zita Jovin, Petar Slankamenac, and Miroslav Ilin. "Contemporary treatment neuropathic pain." Medical review 64, no. 9-10 (2011): 443–47. http://dx.doi.org/10.2298/mpns1110443c.
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Introduction. Neuropathic pain, or pain associated with disease or injury to the peripheral or central nervous system, is a common symptom of a heterogeneous group of conditions, including diabetic neuropathy, trigeminal neuralgia, postherpetic neuralgia and spinal cord injury. Chronic neuropathic pain should not be thought of as a symptom. It should truly be thought of as a disease with a very complicated pathophysiology. Pathophysiology. The mechanisms involved in neuropathic pain are complex and involve both peripheral and central pathophysiologic phenomenon. The underlying dysfunction may involve deafferentation within the peripheral nervous system (e.g. neuropathy), deafferentation within the central nervous system (e.g. post-thalamic stroke) or an imbalance between the two (e.g. phantom limb pain). Clinical characteristics. Neuropathic pain is non-nociceptive, in contrast to acute nociceptive pain, and it can be described as ?burning?, ?electric?, ?tingling?, and ?shooting? in nature. Treatment. Rational polypharmacy is often necessary and actually it is almost always the rule. It would be an exception if a patient was completely satisfied with his treatment. Treatment goals should include understanding that our patients may need to be titrated and managed with more than one agent and one type of treatment. There should be the balance of safety, efficacy, and tolerability. Conclusion. There are many new agents and new applications of the existing agents being currently studied which will most certainly lead to even more improved ways of managing this very complicated set of disorders.
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Rosenberg, Michael L., Vahid Tohidi, Karna Sherwood, Sujoy Gayen, Rosina Medel, and Gad M. Gilad. "Evidence for Dietary Agmatine Sulfate Effectiveness in Neuropathies Associated with Painful Small Fiber Neuropathy. A Pilot Open-Label Consecutive Case Series Study." Nutrients 12, no. 2 (February 23, 2020): 576. http://dx.doi.org/10.3390/nu12020576.
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Peripheral neuropathies associated with painful small fiber neuropathy (SFN) are complex conditions, resistant to treatment with conventional medications. Previous clinical studies strongly support the use of dietary agmatine as a safe and effective treatment for neuropathic pain. Based on this evidence, we conducted an open-label consecutive case series study to evaluate the effectiveness of agmatine in neuropathies associated with painful SFN (Study Registry: ClinicalTrials.gov, System Identifier: NCT01524666). Participants diagnosed with painful SFN and autonomic dysfunctions were treated with 2.67 g/day agmatine sulfate (AgmaSet® capsules containing G-Agmatine® brand of agmatine sulfate) for a period of 2 months. Before the beginning (baseline) and at the end of the treatment period, participants answered the established 12-item neuropathic pain questionnaire specifically developed to distinguish symptoms associated with neuropathy and to quantify their severity. Secondary outcomes included other treatment options and a safety assessment. Twelve patients were recruited, and 11 patients—8 diagnosed with diabetic neuropathy, two with idiopathic neuropathy and one with inflammatory neuropathy—completed the study. All patients showed improvement in neuropathic pain to a varied extent. The average decrease in pain intensity was 26.0 rating points, corresponding to a 46.4% reduction in overall pain (p < 0.00001). The results suggest that dietary agmatine sulfate has a significant effect in reducing neuropathic pain intensity associated with painful SFN resistant to treatment with conventional neuropathic pain medications. Larger randomized placebo-controlled studies are expected to establish agmatine sulfate as a preferred treatment.
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Rachmantoko, Reza, Zamroni Afif, Dessika Rahmawati, Rodhiyan Rakhmatiar, and Shahdevi Nandar Kurniawan. "DIABETIC NEUROPATHIC PAIN." JPHV (Journal of Pain, Vertigo and Headache) 2, no. 1 (March 1, 2021): 8–12. http://dx.doi.org/10.21776/ub.jphv.2021.002.01.3.
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Diabetic Neuropathy is the most common complication from diabetes, which experienced in almost 90% diabetes patient. Evenly pain is one of the most common symptoms of diabetic neuropathic, but the pathophysiology mechanism of pain is not clearly known. The hyptosesis of toxicity of hyperglycemia on development of pain complication has been widely accepted globally, but there is other proposed hypothesis. Basic concept in management of painful diabetic neuropathic is exclusion of the other cause of painful peripheral neuropathy, improving glycemic control for prophylaxis therapy and medication use for alleviating pain. The first choice drug of therapy for alleviating pain are anticonvulsant, like pregabalin and gabapentin, and antidepressant, mainly that work on inhibiting serotonine and noradrenaline reuptake. In conclusion, the better understanding of painful diabetic neuropathic underlying mechanism can help to find a better management that improving the guideline quality in optimalizing pain control.
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Schifilliti, Chiara, Lelio Cucinotta, Viviana Fedele, Carmela Ingegnosi, Salvatore Luca, and Carmelo Leotta. "Micronized Palmitoylethanolamide Reduces the Symptoms of Neuropathic Pain in Diabetic Patients." Pain Research and Treatment 2014 (April 2, 2014): 1–5. http://dx.doi.org/10.1155/2014/849623.
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The present study evaluated the effectiveness of micronized palmitoylethanolamide (PEA-m) treatment in reducing the painful symptoms experienced by diabetic patients with peripheral neuropathy. PEA-m, a fatty acid amide of the N-acylethanolamine family, was administered (300 mg twice daily) to 30 diabetic patients suffering from painful diabetic neuropathy. Before treatment start, after 30 and 60 days the following parameters were assessed: painful symptoms of diabetic peripheral neuropathy using the Michigan Neuropathy Screening instrument; intensity of symptoms characteristic of diabetic neuropathic pain by the Total Symptom Score; and intensity of different subcategories of neuropathic pain by the Neuropathic Pain Symptoms Inventory. Hematological and blood chemistry tests to evaluate metabolic control and safety were also performed. Statistical analysis (ANOVA) indicated a highly significant reduction in pain severity (P<0.0001) and related symptoms (P<0.0001) evaluated by Michigan Neuropathy Screening instrument, Total Symptom Score, and Neuropathic Pain Symptoms Inventory. Hematological and urine analyses did not reveal any alterations associated with PEA-m treatment, and no serious adverse events were reported. These results suggest that PEA-m could be considered as a promising and well-tolerated new treatment for symptomatology experienced by diabetic patients suffering from peripheral neuropathy.
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Smith, MD, Howard S., and Patrick D. Meek, PharmD, MSPH. "Pain responsiveness to opioids: Central versus peripheral neuropathic pain." Journal of Opioid Management 7, no. 5 (September 1, 2011): 391–400. http://dx.doi.org/10.5055/jom.2011.0080.
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Neuropathic pain is initiated or caused by a primary lesion or dysfunction in the nervous system. Neuropathic pain is composed of peripheral neuropathic pain (with a primary lesion or dysfunction in the peripheral nervous system) and central neuropathic pain (CNP; with a primary lesion or dysfunction in the central nervous system). CNP may be further subdivided into supraspinal central neuropathic pain and spinal central neuropathic pain. Opioids have a role in the pharmacologic management of neuropathic pain; however, there is a scarcity of literature on the treatment of CNP with opioids. One of the few statements in the literature regarding the analgesic efficacy of opioids for CNP suggests that despite limited data, the opioid responsiveness for neuropathic pain of central and peripheral etiologies is similar. After reviewing the extremely limited data, it is proposed that although there may be a subpopulation of patients with CNP who have a reasonable analgesic response to opioids, overall, when sensory pain rating is used as the yardstick, CNP appears to respond less well to opioids than peripheral neuropathic pain. Thus, opioids should be considered a second- or third-line agent in any algorithm of the pharmacologic treatment of CNP. Also within CNP, it appears that supraspinal central neuropathic pain may respond less well to a trial of opioids than spinal central neuropathic pain. Moreover, under close monitoring for side effects (eg, constipation), it is suggested that clinicians may want to consider titrating to higher doses of potent opioids before the trial is judged to be unsuccessful for refractory supraspinal central neuropathic pain.
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Kluša, Vija, Juris Rumaks, and Ñina Karajeva. "Neuromidin Attenuates Neuropathic Pain in the Streptozocin-Induced Diabetes Model in Rats." Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences. 62, no. 3 (January 1, 2008): 85–90. http://dx.doi.org/10.2478/v10046-008-0024-z.
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Neuromidin Attenuates Neuropathic Pain in the Streptozocin-Induced Diabetes Model in Rats Diabetic neuropathy, which affects all peripheral nerves and may cause dramatic pain, is one of the most severe pathologies associated with hyperglycaemia, damage in the blood vessels, and inflammation in nerves. Anticonvulsants and antidepressants are still the most commonly used options to manage diabetic neuropathy. However, to improve clinical benefit in the treatment of diabetic neuropathies, as well as to minimize side effects, search for a new type of drugs to protect/treat neuropathic pain is still important. The aim of this study was to investigate neuromidin (ipidacrine, amiridin, NIK-247), an anticholinesterase drug of tetrahydroaminoacridine series, in the streptozocin (STZ)-induced diabetic neuropathic pain model in rats. Neuromidin was administered per os at daily doses 0.3, 1.0 and 3.0 mg/kg for ten days. The dynamics in the development of hyperalgesia (pain threshold) was measured by algesimeter for five weeks. The data obtained show that neuromidin considerably protects the development of peripheral neuropathic pain caused by STZ. The most active dose was the lowest—0.3 mg/kg. Neuromidin did not affect STZ-hyperglycemia, nor the weight gain in animal groups. Neuromidin per se at the doses 0.3 and 1.0 mg/kg showed a short-term analgesic activity. The cholinergic mechanism of neuromidin may be considered as essential in attenuating of diabetic neuropathic pain; other mechanisms remain to be elucidated.
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Kavvoura, Fainia K. "Peripheral Neuropathy & Neuropathic Pain, Into the Light." British Journal of Diabetes 16, no. 1 (March 8, 2016): 45. http://dx.doi.org/10.15277/bjd.2016.068.
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Francis, David A., Anne T. Christopher, and Bradley D. Beasley. "Conservative Treatment of Peripheral Neuropathy and Neuropathic Pain." Clinics in Podiatric Medicine and Surgery 23, no. 3 (July 2006): 509–30. http://dx.doi.org/10.1016/j.cpm.2006.04.004.
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Pjevic, Miroslava, Erzebet Patarica-Huber, Dragana Radovanovic, and Sanja Vickovic. "Neuropathic pain due to malignancy: Mechanisms, clinical manifestations and therapy." Medical review 57, no. 1-2 (2004): 33–40. http://dx.doi.org/10.2298/mpns0402033p.
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Introduction Neuropathic pain in cancer patients requires a focused clinical evaluation based on knowledge of common neuropathic pain syndromes. Definition Neuropathic pain is a non-nociceptive pain or "differentiation" pain, which suggests abnormal production of impulses by neural tissue that is separated from afferent input. Impulses arise from the peripheral nervous system or central nervous system. Causes of neuropathic pain due to malignancy Neuropathic pain is caused directly by cancer-related pathology (compression/infiltration of nerve tissue, combination of compression/infiltration) or by diagnostic and therapeutic procedures (surgical procedures, chemotherapy, radiotherapy). Mechanisms Pathophysiological mechanisms are very complex and still not clear enough. Neuropathic pain is generated by electrical hyperactivity of neurons along the pain pathways. Peripheral mechanisms (primary sensitization of nerve endings, ectopically generated action potentials within damaged nerves, abnormal electrogenesis within sensory ganglia) and central mechanisms (loss of input from peripheral nociceptors into dorsal horn, aberrant sprouting within dorsal horn, central sensitization, loss of inhibitory interneurons, mechanisms at higher centers) are involved. Diagnosis The quality of pain presents as spontaneous pain (continuous and paroxysmal), abnormal pain (allodynia, hyperalgesia, hyperpathia), paroxysmal pain. Clinical manifestations Clinically, neuropathic pain is described as the pain in the peripheral nerve (cranial nerves, other mononeuropathies, radiculopathy, plexopathy, paraneoplastic peripheral neuropathy) and relatively infrequent, central pain syndrome. Therapy Treatment of neuropathic pain remains a challenge for clinicians, because there is no accepted algorithm for analgesic treatment of neuropathic pain. Pharmacotherapy is considered to be the first line therapy. Opioids combined with non-steroidal antiinflammatory drugs are warrented. If patient is relatively unresponsive to an opioid, a trial with adjuvant analgesics might be considered. Tricyclic antidepressants might be selected for patients with continuous dysesthesia, and anticonvulsants might be used if the pain is predominanty lancinating or paroxysmal. The complexity of neuropathic syndromes and underlying etiologic mechanisms warrant clinical trials to determine appropriate treatment.
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Lopes, Arthur, Kleber Duarte, Catarina Lins, Gabriel Kubota, Valquíria Silva, Ricardo Galhardoni, Luciana Mendes Bahia Menezes, Irina Raicher, Manoel J. Teixeira, and Daniel C. Andrade. "Spinal Cord Stimulation as a Treatment Option for Refractory Chemotherapy-Induced Peripheral Neuropathy: Case Report." Arquivos Brasileiros de Neurocirurgia: Brazilian Neurosurgery 39, no. 03 (June 23, 2020): 228–31. http://dx.doi.org/10.1055/s-0040-1709985.
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AbstractColorectal cancer is one of the most common oncological diseases. Chemotherapy is usually recommended as an adjuvant treatment for stage-II, -III, and -IV tumors. Approximately 10% of the patients develop neuropathic pain after chemotherapy, and they may remain refractory despite the administration of drugs that are commonly used to treat neuropathic pain. Spinal cord stimulation is a good treatment option for neuropathic pain of the lower limbs, and it should be trialed in patients with chemotherapy-induced peripheral neuropathy. We report the case of a patient with oxaliplatin-induced neuropathy and neuropathic pain refractory to oral medication who was successfully treated by spinal cord stimulation.
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Kocot-Kępska, Magdalena, Renata Zajączkowska, Joanna Mika, Jerzy Wordliczek, Jan Dobrogowski, and Anna Przeklasa-Muszyńska. "Peripheral Mechanisms of Neuropathic Pain—The Role of Neuronal and Non-Neuronal Interactions and Their Implications for Topical Treatment of Neuropathic Pain." Pharmaceuticals 14, no. 2 (January 20, 2021): 77. http://dx.doi.org/10.3390/ph14020077.
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Neuropathic pain in humans arises as a consequence of injury or disease of somatosensory nervous system at peripheral or central level. Peripheral neuropathic pain is more common than central neuropathic pain, and is supposed to result from peripheral mechanisms, following nerve injury. The animal models of neuropathic pain show extensive functional and structural changes occurring in neuronal and non-neuronal cells in response to peripheral nerve injury. These pathological changes following damage lead to peripheral sensitization development, and subsequently to central sensitization initiation with spinal and supraspinal mechanism involved. The aim of this narrative review paper is to discuss the mechanisms engaged in peripheral neuropathic pain generation and maintenance, with special focus on the role of glial, immune, and epithelial cells in peripheral nociception. Based on the preclinical and clinical studies, interactions between neuronal and non-neuronal cells have been described, pointing out at the molecular/cellular underlying mechanisms of neuropathic pain, which might be potentially targeted by topical treatments in clinical practice. The modulation of the complex neuro-immuno-cutaneous interactions in the periphery represents a strategy for the development of new topical analgesics and their utilization in clinical settings.
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Lejčko, Jan. "Treatment of peripheral neuropathic pain." Neurologie pro praxi 19, no. 6 (December 10, 2018): 440–45. http://dx.doi.org/10.36290/neu.2018.133.
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Gupta, R., and A. Bhaskar. "Chemotherapy-induced peripheral neuropathic pain." BJA Education 16, no. 4 (April 2016): 115–19. http://dx.doi.org/10.1093/bjaed/mkv044.
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Park, Hue Jung. "Chemotherapy induced peripheral neuropathic pain." Korean Journal of Anesthesiology 67, no. 1 (2014): 4. http://dx.doi.org/10.4097/kjae.2014.67.1.4.
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Gilron, Ian, Dalia Wajsbrot, François Therrien, and Jacinthe Lemay. "Pregabalin for Peripheral Neuropathic Pain." Clinical Journal of Pain 27, no. 3 (2011): 185–93. http://dx.doi.org/10.1097/ajp.0b013e3181fe13f6.
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Stacey, Brett R. "Management of Peripheral Neuropathic Pain." American Journal of Physical Medicine & Rehabilitation 84, no. 3 (March 2005): S4—S16. http://dx.doi.org/10.1097/01.phm.0000154905.18445.0f.
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Morales-Vidal, Sarkis, Christopher Morgan, Mathew McCoyd, and Alejandro Hornik. "Diabetic Peripheral Neuropathy and the Management of Diabetic Peripheral Neuropathic Pain." Postgraduate Medicine 124, no. 4 (July 2012): 145–53. http://dx.doi.org/10.3810/pgm.2012.07.2576.
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Teasell, Robert W., and J. Malcolm O. Arnold. "Alpha-1 Adrenoceptor Hyperresponsiveness in Three Neuropathic Pain States: Complex Regional Pain Syndrome 1, Diabetic Peripheral Neuropathic Pain and Central Pain States Following Spinal Cord Injury." Pain Research and Management 9, no. 2 (2004): 89–97. http://dx.doi.org/10.1155/2004/150503.
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The pathophysiology of the pain associated with complex regional pain syndrome, spinal cord injury and diabetic peripheral neuropathy is not known. The pain of complex regional pain syndrome has often been attributed to abnormal sympathetic nervous system activity based on the presence of vasomotor instability and a frequently reported positive response, albeit a temporary response, to sympathetic blockade. In contrast, the pain below the level of spinal cord injury and diabetic peripheral neuropathy are generally seen as deafferentation phenomena. Each of these pain states has been associated with abnormal sympathetic nervous system function and increased peripheral alpha-1 adrenoceptor activity. This increased responsiveness may be a consequence of alpha-1 adrenoceptor postsynaptic hypersensitivity, or alpha-2 adrenoceptor presynaptic dysfunction with diminished noradrenaline reuptake, increased concentrations of noradrenaline in the synaptic cleft and increased stimulation of otherwise normal alpha-1 adrenoceptors. Plausible mechanisms based on animal research by which alpha-1 adrenoceptor hyperresponsiveness can lead to chronic neuropathic-like pain have been reported. This raises the intriguing possibility that sympathetic nervous system dysfunction may be an important factor in the generation of pain in many neuropathic pain states. Although results to date have been mixed, there may be a greater role for new drugs which target peripheral alpha-2 adrenoceptors (agonists) or alpha-1 adrenoceptors (antagonists).
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Freeman, Roy. "The Treatment of Neuropathic Pain." CNS Spectrums 10, no. 9 (September 2005): 698–706. http://dx.doi.org/10.1017/s1092852900019696.
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AbstractNeuropathic pain is responsible for a significant amount of the morbidity associated with generalized and focal peripheral neuropathies. It is a consequence of alterations in neuronal function, chemistry, and structure that occur secondary to nerve injury. These manifestations of neuronal plasticity occur in the peripheral nerve, spinal cord, and brain. A variety of agents from diverse pharmacologic classes, the so-called adjuvant analgesics, have been used to treat neuropathic pain. These include antidepressants, first- and second-generation anticonvulsants, antiarrhythmic agents, topical agents, N-methyl-D-aspartate receptor antagonists, and opioid analgesics. The use of these adjuvant analgesics, either alone or in combination, should result in the alleviation of neuropathic pain in most patients. Recent advances in the understanding of pain mechanisms at multiple central nervous system levels should pave the way toward more effective treatment modalities.
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Izci, M., S. Kanyilmaz Turgut, O. Akan, I. Topal, and O. Kuru. "POS0146 PERIPHERAL NEUROPATHY IN PSORIASIS AND PSORIATIC ARTHRITIS: A SINGLE BLIND, CONTROLLED, ELECTROPHYSIOLOGICAL STUDY." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 286.1–286. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1258.
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Background:It is well known that both psoriasis (PsO) and psoriatic arthritis (PsA) causes morbidity and disability in patients’ lives. Additional pathologies such as peripheral neuropathy (PN) may interfere with disease specific symptoms and may increase the burden of disease. Neuropathic complaints of patients with PsO and PsA are observed during patients’ follow-up (1,2). However, the presence of PN in PsO and PsA is not well defined in clinical studies and clinicians might be neglecting this issue.Objectives:Our aim was to investigate the presence of PN by electrophysiological methods and to examine its relationship with neuropathic pain and with treatments in patients with PsO and PsA.Methods:38 patients with PsA, 36 patients with PsO and 37 age&sex-matched healthy volunteers were enrolled into this prospective, single-blind study. Disease activity was assessed with Psoriasis Area Severity Index (PASI) for patients with PsO and with Disease Activity in Psoriatic Arthritis (DAPSA) score for patients with PsA. Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) score was used to evaluate neuropathic pain. All participants were electrophysiologically examined in Electromyography (EMG) Laboratory by an experienced neurologist blinded for study groups.Results:There were no significant differences on patients age, sex and body mass index among 3 study groups (p>0.05). However, disease duration was significantly longer in PsO group compared to PsA group (median 19.1[1-43] years in PsO vs median 7.5[2-29] years in PsA; p<0.01). PN was detected in 7 patients (19.44%) in the PsO group, 14 patients (34.21%) in the PsA group, and in 1 volunteer (2.7%) in the control group (PsO vs control: p<0.05; PsA vs control: p<0.001, PsO vs PsA: p>0.05) (Table 1). Among patients with PsA, 1 patient had ulnar neuropathy and 1 patient had both carpal tunnel syndrome (CTS) and sensory polyneuropathy. All other PNs detected electrophysiologically were CTS. Neuropathic pain was present in 11 patients (30.56%), 20 patients (52.63%) and in 2 volunteers (5.41%) in PsO, PsA and control groups consecutively (PsO vs control: p<0.05; PsA vs control: p<0.001, PsO vs PsA: p>0.05). PN did not show any significant correlation with disease activity or treatments including biological agents.Table 1.Results of peripheral neuropathy and neuropathic pain in control group and patients with PsO and PsAControl Group (n=37)PsO Group (n=36)PsA Group (n=38)p^p+p&CTS1 (%2.70)7 (%19.44)13* (%34.21)0.028a<0.001a0.153aUlnar Neuropathy001 (%2.63)Polyneuropathy001* (%2.63)Total PN1 (%2.70)7 (%19.44)14 (%36.64)0.028a<0.001a0.097aLANSS Score5 (0:13)6.50 (0:16)13 (3:19)0.170b<0.001b0.004bAccording to LANSSlikely neuropathic pain2 (%5.41)11 (%30.56)20 (%52.63)0.005 a<0.001a0.054a*: Both polyneuropathy and CTS were detected in one patient in the PsA group; Data are given as n (%) and median (minimum: maximum); a: Chi-Square Test, b: Kruskal Wallis Test; p^ value: control vs PsO, p+ value: control vs PsA, p& value: PsO vs PsAConclusion:To our knowledge, this is the first study to investigate simultaneously the presence of neuropathic pain and PN by electrophysiological methods in patients with PsO and PsA. We observed PN and neuropathic pain high in patients with PsO&PsA and among them CTS appears as the most prominent neuropathy. Clinicians should keep this in mind during routine care of patients with PsO and PsA, which may improve patient-centred care. Large, prospective studies are needed to understand the characteristics of these neuropathies and its prognosis.References:[1]Rifbjerg-Madsen S, Christensen AW, Christensen R, Hetland ML, Bliddal H, Kristensen LE, Danneskiold-Samsøe B, Amris K (2017) Pain and pain mechanisms in patients with inflammatory arthritis: a Danish nationwide cross-sectional DANBIO registry survey. PLoS One 12(7):e0180014.[2]Ljosaa TM, Mork C, Stubhaug A, et al. Skin pain and skin discomfort is associated with quality of life in patients with psoriasis. J Eur Acad Dermatol Venereol. 2012;26:29-35.Disclosure of Interests:None declared
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Krøigård, Thomas, Toke K. Svendsen, Martin Wirenfeldt, Henrik D. Schrøder, Camilla Qvortrup, Per Pfeiffer, David Gaist, and Søren H. Sindrup. "Oxaliplatin Neuropathy: Predictive Values of Skin Biopsy, QST and Berve Conduction." Journal of Neuromuscular Diseases 8, no. 4 (July 30, 2021): 679–88. http://dx.doi.org/10.3233/jnd-210630.
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Background: Oxaliplatin-induced peripheral neuropathy negatively affects the quality of life for patients with gastrointestinal cancers and may cause neuropathic pain. Measures of peripheral nerve structure or function, such as intraepidermal nerve fiber density (IENFD) during treatment could reduce neuropathy severity through individualized dose reduction. Objective: The aim was to evaluate the predictive values of IENFD, quantitative sensory testing (QST), and nerve conduction studies (NCS) for significant neuropathy and neuropathic pain. Methods: Fifty-five patients were examined prospectively before, during, and six months following treatment using skin biopsies, QST and NCS. Clinically significant neuropathy six months after treatment was defined as reduced Total Neuropathy Score of more than five and neuropathic pain was assessed according to International Association for the Study of Pain criteria. Results: Thirty patients had a clinically significant neuropathy, and 14 had neuropathic pain. Vibration detection threshold (VDT) before treatment was correlated with clinically significant neuropathy six months after treatment (OR 0.54, p = 0.01) and reductions in cold detection threshold (CDT) after 25% of treatment (OR 1.38, p = 0.04) and heat pain threshold (HPT) after 50% of treatment (OR 1.91, p = 0.03) with neuropathic pain. Cut off values of 5 for baseline VDT and changes of more than –0.05 °C and –0.85 °C in CDT and HPT were estimated. Sensitivity and specificity was low to moderate. There was no correlation between changes in IENFD or NCS and significant neuropathy or neuropathic pain. Conclusions: Vibration detection thresholds and thermal detection thresholds may be useful for prediction of clinically significant and painful neuropathy, respectively. However, low to moderate sensitivity and specificity may limit the predictive value in clinical practice.
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Brandolini, Laura, Michele d’Angelo, Andrea Antonosante, Annamaria Cimini, and Marcello Allegretti. "Chemokine Signaling in Chemotherapy-Induced Neuropathic Pain." International Journal of Molecular Sciences 20, no. 12 (June 14, 2019): 2904. http://dx.doi.org/10.3390/ijms20122904.
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Chemotherapy-induced peripheral neuropathy (CIPN) is a side effect of chemotherapics such as taxanes, vinca alkaloids, and platinum compounds. In recent years, several reports have indicated the involvement of different molecular mechanisms in CIPN. The pathways described so far are diverse and target various components of the peripheral Nervous System (PNS). Among the contributors to neuropathic pain, inflammation has been indicated as a powerful driver of CIPN. Several pieces of evidence have demonstrated a chemotherapy-induced increase in peripheral pro-inflammatory cytokines and a strong correlation with peripheral neuropathy. At present, there are not adequate strategies to prevent CIPN, although there are drugs for treating CIPN, such as duloxetine, that have displayed a moderate effect on CIPN. In this review, we focus on the players involved in CIPN with a particular emphasis on chemokine signaling.
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Feletti, Alberto, Giannantonio Zanata Santi, Francesco Sammartino, Marzio Bevilacqua, Piero Cisotto, and Pierluigi Longatti. "Peripheral trigeminal nerve field stimulation." Neurosurgical Focus 35, no. 3 (September 2013): E10. http://dx.doi.org/10.3171/2013.7.focus13228.
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Object Peripheral nerve field stimulation has been successfully used for many neuropathic syndromes. However, it has been reported as a treatment for trigeminal neuropathic pain or persistent idiopathic facial pain only in the recent years. Methods The authors present a review of the literature and their own series of 6 patients who were treated with peripheral nerve stimulation for facial neuropathic pain, reporting excellent pain relief and subsequent better social relations and quality of life. Results On average, pain scores in these patients decreased from 10 to 2.7 on the visual analog scale during a 17-month follow-up (range 0–32 months). The authors also observed the ability to decrease trigeminal pain with occipital nerve stimulation, clinically confirming the previously reported existence of a close anatomical connection between the trigeminal and occipital nerves (trigeminocervical nucleus). Conclusions Peripheral nerve field stimulation of the trigeminal and occipital nerves is a safe and effective treatment for trigeminal neuropathic pain and persistent idiopathic facial pain, when patients are strictly selected and electrodes are correctly placed under the hyperalgesia strip at the periphery of the allodynia region.
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Julian, Thomas, Rubiya Syeed, Nicholas Glascow, Efthalia Angelopoulou, and Panagiotis Zis. "B12 as a Treatment for Peripheral Neuropathic Pain: A Systematic Review." Nutrients 12, no. 8 (July 25, 2020): 2221. http://dx.doi.org/10.3390/nu12082221.
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Neuropathic pain describes a range of unpleasant sensations caused by a lesion or disease of the somatosensory nervous system. The sensations caused by neuropathic pain are debilitating and improved treatment regimens are sought in order to improve the quality of life of patients. One proposed treatment for neuropathic pain is vitamin B12, which is thought to alleviate pain by a number of mechanisms including promoting myelination, increasing nerve regeneration and decreasing ectopic nerve firing. In this paper, the evidence for B12 as a drug treatment for neuropathic pain is reviewed. Twenty four published articles were eligible for inclusion in this systematic review in which a range of treatment regimens were evaluated including both B12 monotherapy and B12 in combination with other vitamins or conventional treatments, such as gabapentinoids. Overall, this systematic review demonstrates that there is currently some evidence for the therapeutic effect of B12 in the treatment of post-herpetic neuralgia (level II evidence) and the treatment of painful peripheral neuropathy (level III evidence).
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Moulin, Dwight. "Use of Methadone for Neuropathic Pain." Pain Research and Management 8, no. 3 (2003): 131–32. http://dx.doi.org/10.1155/2003/749572.
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Chronic neuropathic pain is often considered to be a common complication of injury to the central or peripheral nervous system and the pain itself is usually assumed to be intractable. Both of these assumptions are inaccurate. For example, numbness and tingling in glove and stocking distribution are common accompaniments of longstanding diabetes mellitus, but only about 10% of patients with diabetic neuropathy consider these sensory changes to be painful (1). Anticonvulsant and antidepressant treatments provide effective analgesia in up to 50% of patients with chronic neuropathic pain (2) and there is a growing body of high-quality evidence that controlled-release opioid analgesics provide substantial pain relief in a further subset of patients (3-6). Even with polypharmacy, this still leaves perhaps 20% to 30% of chronic neuropathic pain sufferers lacking adequate analgesia, and side effects can be problematic. In addition, central pain appears to be more refractory to opioid treatment than pain due to peripheral nerve injury (7).
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Papanas, Nikolaos, and Dan Ziegler. "Emerging drugs for diabetic peripheral neuropathy and neuropathic pain." Expert Opinion on Emerging Drugs 21, no. 4 (October 2016): 393–407. http://dx.doi.org/10.1080/14728214.2016.1257605.
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Bailly, Florian, Alain Cantagrel, Philippe Bertin, Serge Perrot, Thierry Thomas, Thibaud Lansaman, Laurent Grange, Daniel Wendling, Calogera Dovico, and Anne-Priscille Trouvin. "Part of pain labelled neuropathic in rheumatic disease might be rather nociplastic." RMD Open 6, no. 2 (September 2020): e001326. http://dx.doi.org/10.1136/rmdopen-2020-001326.
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Pain in rheumatic diseases is primarily due to mechanical or inflammatory mechanism, but neuropathic pain (NP) component is also occurring in many conditions and is probably underdiagnosed. The purpose of this article is to provide an overview of prevalence, pathophysiological and currently available treatment of NP in rheumatic diseases. When associated with clinical evaluation assessing neurological clinical signs and neuroanatomical distribution, Douleur Neuropathique 4 Questions, painDETECT, Leeds assessment of neuropathic symptoms and signs and Neuropathic Pain Questionnaire can detect NP component. Inflammatory or connective diseases, osteoarthritis, back pain or persistent pain after surgery are aetiologies that all may have a neuropathic component. Unlike nociceptive pain, NP does not respond to usual analgesics such as paracetamol and non-steroidal anti-inflammatory drugs. Entrapment neuropathy, peripheral neuropathy or small-fibre neuropathy are different aetiologies that can lead to NP. A part of the pain labelled neuropathic is rather nociplastic, secondary to a central sensitisation mechanism. Identifying the right component of pain (nociceptive vs neuropathic or nociplastic) could help to better manage pain in rheumatic diseases with pharmacological and non-pharmacological treatments.
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Basu, Paramita, Camelia Maier, and Arpita Basu. "Effects of Curcumin and Its Different Formulations in Preclinical and Clinical Studies of Peripheral Neuropathic and Postoperative Pain: A Comprehensive Review." International Journal of Molecular Sciences 22, no. 9 (April 28, 2021): 4666. http://dx.doi.org/10.3390/ijms22094666.
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Lesion or disease of the somatosensory system leads to the development of neuropathic pain. Peripheral neuropathic pain encompasses damage or injury of the peripheral nervous system. On the other hand, 10–15% of individuals suffer from acute postoperative pain followed by persistent pain after undergoing surgeries. Antidepressants, anticonvulsants, baclofen, and clonidine are used to treat peripheral neuropathy, whereas opioids are used to treat postoperative pain. The negative effects associated with these drugs emphasize the search for alternative therapeutics with better efficacy and fewer side effects. Curcumin, a polyphenol isolated from the roots of Curcuma longa, possesses antibacterial, antioxidant, and anti-inflammatory properties. Furthermore, the low bioavailability and fast metabolism of curcumin have led to the advent of various curcumin formulations. The present review provides a comprehensive analysis on the effects of curcumin and its formulations in preclinical and clinical studies of neuropathic and postoperative pain. Based on the positive outcomes from both preclinical and clinical studies, curcumin holds the promise of mitigating or preventing neuropathic and postoperative pain conditions. However, more clinical studies with improved curcumin formulations are required to involve its use as adjuvant to neuropathic and postoperative drugs.
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Zieglgänsberger, Walter, Achim Berthele, and Thomas R. Tölle. "Understanding Neuropathic Pain." CNS Spectrums 10, no. 4 (April 2005): 298–308. http://dx.doi.org/10.1017/s1092852900022628.
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AbstractNeuropathic pain is defined as a chronic pain condition that occurs or persists after a primary lesion or dysfunction of the peripheral or central nervous system. Traumatic injury of peripheral nerves also increases the excitability of nociceptors in and around nerve trunks and involves components released from nerve terminals (neurogenic inflammation) and immunological and vascular components from cells resident within or recruited into the affected area. Action potentials generated in nociceptors and injured nerve fibers release excitatory neurotransmitters at their synaptic terminals such as L-glutamate and substance P and trigger cellular events in the central nervous system that extend over different time frames. Short-term alterations of neuronal excitability, reflected for example in rapid changes of neuronal discharge activity, are sensitive to conventional analgesics, and do not commonly involve alterations in activity-dependent gene expression. Novel compounds and new regimens for drug treatment to influence activity-dependent long-term changes in pain transducing and suppressive systems (pain matrix) are emerging.
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Simon, Chantal. "Peripheral Neuropathy." InnovAiT: Education and inspiration for general practice 2, no. 9 (August 26, 2009): 538–45. http://dx.doi.org/10.1093/innovait/inp129.
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Peripheral neuropathy is defined as dysfunction of the structure and function of peripheral motor, sensory and autonomic nerves. Although many individual causes of peripheral neuropathy are rare, it is estimated that up to 8% of the population have some degree of peripheral neuropathy or a total of 4.7 million people in the UK alone. There are many different types of peripheral neuropathy but the most common cause is diabetes and up to 60% of diabetic patients have a peripheral neuropathy of some sort. Peripheral neuropathy not only causes problems with everyday functioning but also in many cases causes severe, disabling neuropathic pain. This article aims to provide a simple overview of peripheral neuropathy and its management in primary care.
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Thomas, Sarah E., and Helen Laycock. "The use of high dose topical capsaicin in the management of peripheral neuropathy: narrative review and local experience." British Journal of Pain 14, no. 2 (April 15, 2020): 133–40. http://dx.doi.org/10.1177/2049463720914332.
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Capsaicin, derived from the chilli pepper plant, is available in high concentration (8%) patches to provide topical therapy for neuropathic pain. Its analgesic effects relate to defunctionalisation and nerve terminal retraction of predominantly C fibres in the dermis and epidermis. Systematic reviews and meta-analysis support its use for the management of post-herpetic neuralgia and HIV neuropathy with some evidence for use in painful peripheral diabetic neuropathy. The article concludes with advice on the practicalities of running a topical 8% capsaicin clinic for peripheral neuropathic pain.
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Gormsen, Lise, Flemming W. Bach, Raben Rosenberg, and Troels S. Jensen. "Differential pain modulation in patients with peripheral neuropathic pain and fibromyalgia." Scandinavian Journal of Pain 3, no. 3 (July 1, 2012): 116–23. http://dx.doi.org/10.1016/j.sjpain.2012.01.002.
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AbstractBackgroundThe definition of neuropathic pain has recently been changed by the International Association for the Study of Pain. This means that conditions such as fibromyalgia cannot, as sometimes discussed, be included in the neuropathic pain conditions. However, fibromyalgia and peripheral neuropathic pain share common clinical features such as spontaneous pain and hypersensitivity to external stimuli. Therefore, it is of interest to directly compare the conditions.Material and methodsIn this study we directly compared the pain modulation in neuropathic pain versus fibromyalgia by recording responses to a cold pressor test in 30 patients with peripheral neuropathic pain, 28 patients with fibromyalgia, and 26 pain-free age-and gender-matched healthy controls. Patients were asked to rate their spontaneous pain on a visual analog scale (VAS (0–100 mm) immediately before and immediately after the cold pressor test. Furthermore the duration (s) of extremity immersion in cold water was used as a measure of the pain tolerance threshold, and the perceived pain intensity at pain tolerance on the VAS was recorded on the extremity in the water after the cold pressor test. In addition, thermal (thermo tester) and mechanical stimuli (pressure algometer) were used to determine sensory detection, pain detection, and pain tolerance thresholds in different body parts. All sensory tests were done by the same examiner, in the same room, and with each subject in a supine position. The sequence of examinations was the following: (1) reaction time, (2) pressure thresholds, (3) thermal thresholds, and (4) cold pressor test. Reaction time was measured to ensure that psychomotoric inhibitions did not influence pain thresholds.ResultsPain modulation induced by a cold pressor test reduced spontaneous pain by 40% on average in neuropathic pain patients, but increased spontaneous pain by 2.6% in fibromyalgia patients. This difference between fibromyalgia and neuropathic pain patients was significant (P < 0.002). Fibromyalgia patients withdrew their extremity from the cold water significantly earlier than neuropathic pain patients and healthy controls; however, they had a higher perceived pain intensity on the VAS than neuropathic pain patients and control subjects. Furthermore, neuropathic pain patients had a localized hypersensitivity to mechanical and thermal stimuli in the affected area of the body. In contrast, fibromyalgia patients displayed a general hypersensitivity to mechanical and thermal stimuli when the stimuli were rated by the VAS, and hypersensitivity to some of the sensory stimuli.ConclusionsThese findings are the first to suggest that a conditioning stimulus evoked by a cold pressor test reduced spontaneous ongoing pain in patients with peripheral neuropathic pain, but not in fibromyalgia patients when directly compared. The current study supports the notion that fibromyalgia and neuropathic pain are distinct pain conditions with separate sensory patterns and dysfunctions in pain-modulating networks. Fibromyalgia should therefore not, as sometimes discussed, be included in NP conditions.ImplicationsOn the basis of the findings, it is of interest to speculate on the underlying mechanisms. The results are consistent with the idea that peripheral neuropathic pain is primarily driven from damaged nerve endings in the periphery, while chronic fibromyalgia pain may be a central disorder with increased activity in pain-facilitating systems.
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Niederberger, Ellen, Gerd Geisslinger, David S. Warner, and Mark A. Warner. "Proteomics in Neuropathic Pain Research." Anesthesiology 108, no. 2 (February 1, 2008): 314–23. http://dx.doi.org/10.1097/01.anes.0000299838.13368.6e.
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Neuropathic pain is often caused by nerve injury or dysfunction in the peripheral and central nervous system and is frequently associated with allodynia and hyperalgesia. The underlying molecular mechanisms of neuropathic pain are largely unknown, and therefore, pharmacologic treatment is insufficient in many cases. To elucidate translational and posttranslational modifications in the nervous system that arise after nerve injury, a number of proteomic studies have been performed using different animal neuropathy models. The results of these proteomic approaches are summarized in this review to provide a better overview of proteins that are involved into the pathogenesis of nerve injury and neuropathic pain. This might allow a better understanding of the pathophysiologic signaling pathways in this impairment, facilitate the discovery of specific biomarkers, and thus promote the development of novel pain therapies.
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Kwon, Ohyun. "Pathophysiology of neuropathic pain." Journal of the Korean Medical Association 64, no. 7 (July 10, 2021): 468–76. http://dx.doi.org/10.5124/jkma.2021.64.7.468.
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Background: Neuropathic pain is notoriously difficult to manage properly, not only because of its varied nature and the absence of objective diagnostic tools but also because of extensive reciprocal neuronal interactive pathogenic mechanism from the molecular level to patient’s own psychophysical characteristics. This paper briefly reviews the pathophysiology of neuropathic pain to the level of clinicians’ interest and its potential in clinical practiceCurrent Concepts: Recent research progress now allows us to obtain a bird view of neuropathic pain pathophysiology: peripheral and central sensitization. For peripheral sensitization, a local inflammatory milieu of the injured nerve primarily drives sequential phenotypic changes, which are critical and shared by both neuropathic and inflammatory pain. Central sensitization is led either by the hyperexcitability of the second-order afferent neuron itself or loss of physiological inhibitory control of the transmission of pain signal to the higher nervous system. Peripheral and central sensitization work synergistically but can also introduce neuropathic pain alone.Discussion and Conclusion: The cause of neuropathic pain is diverse, and understanding of its pathophysiology is still insufficient to realize a mechanism-based approach to clinical phenotypes or therapeutic applications. In dealing with chronic neuropathic pain, it is highly desirable to assess key aspects of a patient’s pain based on a plausible mechanism and select the best management method accordingly.
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Morley-Forster, Pat. "Prevalence of Neuropathic Pain and the Need for Treatment." Pain Research and Management 11, suppl a (2006): 5A—10A. http://dx.doi.org/10.1155/2006/718098.
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Recent publications have suggested that more than two million adults in the United States suffer from neuropathic pain, but this number seems to be a significant underestimate. The prevalence of neuropathic pain from diabetes and postherpetic neuralgia alone, using the most conservative estimates of incidence, would equal two million Americans. Lesions of the nervous system responsible for pain genesis can occur either in the central or the peripheral nervous system. The most common causes of peripheral neuropathic pain syndromes worldwide are diabetes, HIV infection, cancer-related neuropathy (due to tumour invasion, surgical nerve damage, radiation or chemotherapy-induced nerve damage) and lumbar degenerative disc disease. Other less common, but significant, sources of suffering are postherpetic neuralgia, complex regional pain syndrome, phantom limb pain and postsurgical nerve trauma. Central neuropathic pain can be caused by stroke (infarct or hemorrhage), multiple sclerosis, spinal cord injury and syringomyelia. Certain pain syndromes such as trigeminal neuralgia and vulvodynia, although clearly neuropathic and a source of tremendous suffering, are not discussed in the present article due to space constraints. There is an unmet need for the treatment of neuropathic pain as evidenced by reports of pain despite the use of opioids and anticonvulsants, continuing psychological difficulties, lack of access to treatments and patients seeking access to complementary therapy.
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Kumar, Senthil P., Prabha Adhikari, P. S. Jeganathan, Z. K. Misri, and Sydney C. D'Souza. "Diabetic Peripheral Neuropathic Pain - An Update." Journal of Medical Science & Research 4, no. 1 (2013): 25. http://dx.doi.org/10.5958/j.2321-5798.4.1.005.
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Slavin, Konstantin V. "Peripheral nerve stimulation for neuropathic pain." Neurotherapeutics 5, no. 1 (January 2008): 100–106. http://dx.doi.org/10.1016/j.nurt.2007.11.005.
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Santillan, Roberto Medina. "Management of Diabetic Peripheral Neuropathic Pain." US Endocrinology 00, no. 01 (2005): 1. http://dx.doi.org/10.17925/use.2005.00.01.1i.
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