Relevant bibliographies by topics / Neuropathic pain

Academic literature on the topic 'Neuropathic pain'

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Published: 4 June 2021
Last updated: 20 July 2024

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Journal articles on the topic "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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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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Litovchenko, T. A., O. M. Borodai, and O. L. Tondiy. "Quality of life of patients with post-traumatic neuropathies and plexopathies accompanied by chronic neuropathic pain syndrome." INTERNATIONAL NEUROLOGICAL JOURNAL 17, no. 2 (May 19, 2021): 21–24. http://dx.doi.org/10.22141/2224-0713.17.2.2021.229890.

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Background. The modern concept of quality of life research creates opportunities for studying various aspects of patients’ lives, assessing the patient’s condition in dynamics and raises new questions about developing further approaches to a comprehensive assessment of the quality of life of patients with various neurological pathologies, in our case, the patients with post-traumatic neuropathy and plexopathies. Materials and methods. Seventy-three men with neuropathies and plexopathies were examined, who were divided into two groups. Group I included 44 patients with post-traumatic neuropathy and plexo-pathy. The second (control) group included 29 patients with compression-ischemic neuropathies and plexopathies without manifestations of chronic neuropathic pain. Patients underwent clinical and neurological examination, electroneuromyography, ultrasound. DN4 and PainDetect questionnaires were used to determine the neuropathic nature of the pain, and a visual analog scale was used to assess pain severity. The quality of life was assessed according to the MOS SF-36 questionnaire. Results. The study showed a significant reduction in the quality of life of patients with post-traumatic neuropathy and plexopathy accompanied by chronic neuropathic pain. The quality of life of patients compared to the control group is significantly lower on the scales of physical functioning, role functioning due to physical condition, the intensity of pain, mental health. In both groups, patients with neuropathies and plexopathies according to the MOS SF-36 questionnaire had reduced quality of life. In group I, chronic neuropathic pain was diagnosed in 32 patients (72.7 %). The indicators of pain corresponded to VAS 7.85 ± 1.52 points, according to the questionnaire DN4 — 7.83 ± ± 1.06, PainDetect Test — 23.20 ± 3.55.
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Pebrianti, Sandra, Bambang Aditya Nugraha, and Iwan Shalahuddin. "Manajemen nyeri neuropati pada pasien diabetes melitus tipe 2: Studi literatur." Holistik Jurnal Kesehatan 14, no. 2 (July 27, 2020): 276–82. http://dx.doi.org/10.33024/hjk.v14i2.2828.

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Management of neuropathic pain in patients with diabetes mellitus patients type 2: A literature studyBackground: An increase in the population of people with diabetes mellitus (DM), has an impact on increasing the most serious complications of diabetic neuropathy. Studies reveal that 16% to 26% of patients with diabetes neuropathy experience pain. People with DM who experience diabetic neuropathy pain will feel very uncomfortable and disturbed, neuropathic pain causes complaints not only physically, but also the mood and quality of life of patients. Therefore, it is important to identify the management of neuropathic pain in patients with type 2 diabetes mellitus to improve the quality of life of patients.Purpose: This literature review is to identify the management of neuropathic pain in type 2 DM patients.Method: Tracking this literature review using databases such as Google Scholar, Pubmed and Proquest with inclusion criteria that focus on the management of neuropathic pain in DM patients, publication years between 2010-2020 in Indonesian and English, quasi experiment design and Randomized controlled trial . Obtained as many as 87 articles, 32 met the criteria of the year and as many as 19 were the last complete articles found as many as 10 articles which were in line with the focus of the search.Results: Neuropathy management interventions were grouped into exercise, relaxation distraction techniques, percutaneous electrical stimulation and supportive education.Conclusion: Exercise, relaxation distraction techniques, percutaneous electrical stimulation and educational supportive interventions become one of the interventions that can be considered to use in the management of neuropathic pain in type 2 diabetes mellitus patients to improve comfort and quality of life.Keyword: Management; Neuropathic Pain; Patients; Diabetes mellitus type 2Pendahuluan: Peningkatan populasi penyandang diabetes melitus (DM), berdampak pada peningkatan komplikasi yang paling serius yaitu neuropati diabetik. Studi mengungkapkan bahwa 16% hingga 26% pasien dengan neuropati diabetes mengalami rasa nyeri. Penyandang DM yang mengalami nyeri neuropati diabetik akan merasa sangat tidak nyaman dan terganggu, nyeri neuropati menimbulkan keluhan tidak hanya fisik, namun juga mood dan kualitas hidup pasien. Oleh karena itu, menjadi penting untuk mengidentifikasi manajemen nyeri neuropati pada psien diabetes mellitus tipe 2 untuk meningkatkan kualitas hidup pasien.Tujuan: Dengan studi literatur untuk mengidentifikasi manajemen nyeri neuropati pada pasien DM tipe 2.Metode: Penelusuran dengan menggunakan basis data seperti google scholar, Pubmed dan Proquest dengan kriteria inklusi yang berfokus pada manajemen nyeri neuropati pada pasien DM, tahun publikasi antara 2010-2020 dalam bahasa Indonesia dan bahasa inggris, desain quasi experiment dan Randomized controlled trial. Didapatkan sebanyak 87 artikel, 32 memenuhi kriteria tahun dan sebanyak 19 merupakan artikel lengkap terakhir ditemukan sebanyak 10 artikel yang sesui fokus pencarian.Hasil: Intervensi manajemen neuropati dikelompokan menjadi exercise, teknik distraksi relaksasi, stimulasi listrik perkutan dan suportif edukatif.Simpulan: Exercise, tekhnik distraksi relaksasi, stimulasi listrik perkutan dan intervensi suportif edukatif menjadi salah satu intervensi yang dapat dipertimbangkan untuk digunakan pada manajemen nyeri neuropati pada pasien diabetes mellitus tipe 2 demi meningkatkan kenyamanan dan kualitas hidup.
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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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Pergolizzi, Jr., Joseph V., and Jo Ann LeQuang. "Sigma Antagonists for Treatment of Neuropathic Pain Syndromes in Cancer Patients: A Narrative Review." Journal of Cancer Research Updates 11 (October 27, 2022): 70–77. http://dx.doi.org/10.30683/1929-2279.2022.11.10.

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Almost 40% of cancer patients have neuropathic pain or mixed pain with a neuropathic component, which can be intense, debilitating, and challenging to treat. New studies on sigma receptors show these enigmatic ligand-binding protein chaperones may be helpful drug targets for new pharmacologic options to reduce many types of neuropathies, including chemotherapy-induced peripheral neuropathy (CIPN) and other cancer-related neuropathic pain syndromes. Our objective was to review the literature, including preclinical findings, in support of sigma-1 receptor (S1R) antagonists in reducing neuropathic pain and sigma-2 receptor (S2R) agonists for neuroprotection. The mechanisms behind these effects are not yet fully elucidated. The role of S1R antagonists in treating CIPN appears promising. In some cases, combination therapy of an opioid—which is a true analgesic—with a S1R antagonist, which is an anti-hyperalgesic and anti-allodynic agent, has been proposed. Of interest, but not well studied is whether or not S1R antagonists might be effective in treating CIPN in patients with pre-existing peripheral diabetic neuropathy. While neuropathic syndromes may occur with hematologic cancers, the role of S1R agonists may be effective. Sigma receptors are being actively studied now for a variety of conditions ranging from Alzheimer’s disease to Parkinson’s disease as well as neuropathic pain.
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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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More, Akanksha, Gaurav Kasar, Aman B. Upaganlawar, and Chandrashekhar Upasani. "Management of Neuropathic Pain Using Natural Products in Different Animal Models: A Review." Neuro Advances 1, no. 1 (August 25, 2023): 2–14. http://dx.doi.org/10.53365/nadv/168472.

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The focus of this review is on how natural products and their bioactive ingredients can treat neuropathic pain disorders by acting as neuroprotective agents. which includes information about neuropathic pain and their types, namely central neuropathy and peripheral neuropathy with their mechanistic involvement of various pathways may contribute to the development of neuropathic pain. It also includes information about treatment modalities for peripheral neuropathy i.e., first-line therapy includes, tricyclic antidepressant, antiepileptic, anticonvulsants and serotonin- noradrenaline reuptake inhibitors (SNRIs) and second-line therapy (opioids, topical capsaicin, lidocaine patch). Several alternative remedies exist, includes non-pharmacological treatments that play a key part in the reduction of neuropathic pain. Bioactive ingredients, provide great efficacy with minimal side effects correlated with synthetic compounds. The main focus is on animal models utilised for the evaluation of neuropathic pain, Which include several animal models such as, Streptozotocin Induced diabetic neuropathy in rats and mice is a widely used animal model for assessment of neuropathic pain. Other animal models include, Alloxan-Induced Diabetic Neuropathy, the Spinal Cord Injury (SCI) model, the Chronic Construction Injury model (CCI), the Partial sciatic Nerve Injury model (PNI), Anticancer agents induced neuropathy (vincristine and paclitaxel and Oxaliplatin-induced Neuropathic pain and spinal nerve ligation (SNL) model of neuropathic pain.
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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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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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Dissertations / Theses on the topic "Neuropathic pain"

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Casey, Sherelle. "Cannabinoids for Neuropathic Pain." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/24007.

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Neuropathic pain is a severe chronic syndrome and is poorly served by current pharmacotherapeutics. There is some evidence that the cannabis constituents tetrahydrocannabinol (THC), cannabidiol (CBD), and their combination relieves neuropathic pain. However, there is little to no animal evidence for their effectiveness and side effects in neuropathic pain models. In this thesis, a systematic analysis of THC and CBD was performed in a mouse neuropathic pain model. Systemic subcutaneous and oral THC had high anti-allodynic efficacy, but was accompanied by side effects. By contrast, CBD had lower anti-allodynic efficacy, but lacked side effects. Isobolographic analysis demonstrated synergistic analgesia for combination THC and CBD for subcutaneous but not oral administration. Thus, combination THC:CBD had a high therapeutic window when delivered subcutaneously but not orally. Finally, both THC and CBD produced high efficacy anti-allodynia without side effects administered via intrathecal or intraplantar injection. The actions of THC were mostly cannabinoid CB1 receptor mediated, while the actions of CBD were not cannabinoid receptor mediated. An in vitro electrophysiological identified potential cannabinoid targets in sensory neurons. Activity at T-type calcium currents, but not other calcium currents or tetrodotoxin-resistant sodium currents, may account for some of the anti-allodynic activity of THC and CBD. Overall, this thesis provides pre-clinical evidence that the phytocannabinoids THC and CBD alone may be useful as an adjunct therapy for treatment of neuropathic pain, and provides insight as to the ideal ratio and differing benefits and challenges of different administration routes. It also provides some insight into the cellular mechanisms of activity of these phytocannabinoids.
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Searle, Robert David. "Acute neuropathic pain following surgery." Thesis, University of Leeds, 2013. http://etheses.whiterose.ac.uk/6321/.

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Chronic neuropathic pain occurring after an operation is a common problem, however little data is available describing the nature or prevalence of acute neuropathic pain following surgery. In this thesis, I explore the measurement scale properties of a commonly used neuropathic pain screening tool, and use this tool to describe the prevalence of acute and chronic neuropathic pain following thoracic surgery. I also explore how best to diagnose acute neuropathic pain with a Delphi survey of expert opinion and confirmatory observational cohort study. The results show that the Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) neuropathic pain screening tool demonstrates acceptable fit to the Rasch measurement model in the chronic postoperative pain population, but only has reliability consistent with use at a group level. Using this tool, I demonstrate that 8% of thoracic surgery patients experience acute neuropathic pain an average of 3 days after surgery, with 22% developing neuropathic pain by 3 months. Experiencing acute neuropathic pain significantly increased the odds of developing chronic neuropathic pain (odds ratio 7.7 [95% confidence interval 1.5-39.7]). A Delphi survey of specialists identified 9 items considered important in the diagnosis of acute neuropathic pain, and suggests that unlike diagnosis in the chronic pain population, a poor response to opioid medications was an important indicator of neuropathic pain. Preliminary results from a matched cohort study confirm this, by demonstrating that verbal descriptors of neuropathic pain are significantly more common in patients with poorly controlled postoperative pain despite strong opioid use.
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Chan, A. W. "Neuropathic pain in diabetes mellitus." Thesis, Cardiff University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496046.

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Turcotte, Dana. "Multiple sclerosis-induced neuropathic pain." The Consultant Pharmacist, 2004. http://hdl.handle.net/1993/23316.

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Neuropathic pain (NPP) is a chronic syndrome suffered by patients with multiple sclerosis (MS), for which there is no cure. Underlying cellular mechanisms involved in its pathogenesis are multifaceted, resulting in significant challenges in its management. In addition to its complex pathophysiology, the clinical management of MS-induced NPP is further complicated by the lack of clinical therapeutics trials specific to this population. The primary aim of the work underlying this thesis was to contribute to the evidence-based management of individuals with MS-induced NPP through the completion of two clinical therapeutics trials in this population. A secondary aim was to describe pain variability in this patient population through the development and validation of a pain variability algorithm tool. Resulting from this work, we demonstrated that nabilone – a synthetic oral cannabinoid – represents an effective, well-tolerated and novel treatment for MS-induced NPP. Additionally, we show that the SSRI paroxetine was poorly tolerated in our patient population, with a correspondingly high attrition rate. As a result, we were unable to determine any treatment effect in this trial due to insufficient recruitment due to drop-out. Lastly, we were able to define and describe pain instability in this cohort, noting that approximately 30% of individuals with MS-induced NPP experiencing highly variable daily pain. The results of these projects provide novel information for this patient population. Patients currently living with the daily burden of MS-induced NPP would benefit from additional trials ensuing from this, and other, research in order to initiate a momentum for much-needed clinical research in this complicated patient cohort.
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López, Álvarez Víctor Manuel. "Activity-dependent treatments for neuropathic pain." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/457957.

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El inicio y el mantenimiento del dolor neuropático después de una lesión de nervio periférico implica muchos mecanismos tales como cambios en la transducción, sensibilización central o periférica y numerosos cambios plásticos a nivel central. Los tratamientos farmacológicos habituales no son suficientes para aliviar los efectos de la hiperalgesia o alodinia producida por el dolor neuropático. Es por ello que en esta tesis se estudian dos tratamientos dependientes de actividad como son el ejercicio en cinta rodante y la estimulación eléctrica para observar los efectos hipoalgésicos obtenidos y los mecanismos moleculares implicados en estos beneficiosos cambios. En los dos primeros capítulos de esta tesis se muestra un nuevo protocolo de ejercicio en cinta rodante en el que aumentamos la velocidad progresivamente durante una hora (iTR). Se ha demostrado que otros protocolos de cinta rodante mejoran la recuperación funcional después de una lesión del sistema nervioso periférico, pero dependiendo de la intensidad y la duración, se han descrito diferentes efectos. En el primer capítulo, utilizando un modelo experimental de dolor neuropático consistente en la sección y reparación del nervio ciático en una rata (SNTR), se encontró que el protocolo de iTR reduce la hiperalgesia por recodificación neural espontánea, reducción de niveles de neurotrofinas para contrarrestar la reinervación colateral nociceptiva, prevención de la disrupción de cotransportadores de cloruro como NKCC1 y KCC2 para mantener la inhibición central y por contrarresto de la reactividad microglial en áreas centrales. iTR también redujo positivamente la hiperalgesia en el área ciática lateral, demostrando que el efecto hipoalgésico de iTR no se limita exclusivamente al bloqueo de la reinervación colateral nociceptiva en la periferia. Los cambios en los circuitos sensoriales centrales también son importantes. Es por ello que en el segundo capítulo encontramos que el iTR también aumentó la actividad de las proyecciones serotonérgicas y noradrenérgicas desde los centros del tronco encefálico restaurando parcialmente la desinhibición central inducida después de la lesión del nervio. En el tercer capítulo de esta tesis, evaluamos el uso de la estimulación nerviosa periférica (PNS) como tratamiento pasivo dependiente de actividad para el dolor neuropático. El resultado terapéutico junto con el patrón de activación del nervio periférico, están estrechamente relacionados con las diferencias en el tipo y ubicación del electrodo y la intensidad o frecuencia de estimulación. Para ello evaluamos dos modelos experimentales diferentes como candidatos. El modelo de lesión de nervio intacto (SNI) fue la elección inicial, pero la estimulación electrica tuvo efectos muy discretos en la reducción de la hiperalgesia mecánica en comparación con el modelo SNTR. En un trabajo preliminar, se discernió la frecuencia de estimulación que produjese la mejor reducción de la hiperalgesia con estimulación aguda después de la lesión. Posteriormente, mejoramos el tipo de electrodo y la ubicación de éste mediante el diseño de un sistema para hacer estimulación crónica. Se presentaron algunos resultados para los protocolos agudos y repetitivos de estimulación aguda y crónica pero el mejor protocolo de estimulación para reducir la hiperalgesia mecánica fue el protocolo iCES. De forma similar a iTR, iCES consiste en un patrón de estimulación de frecuencia creciente. Se encontró que iCES desencadena una serie de cambios a nivel central, como la restauración de la expresión de KCC2 y el receptor β2 que actúan directamente sobre el aumento de la liberación de GABA en la médula espinal facilitando junto con la disminución de la actividad microglial y astrocitaria, la reducción de hiperalgesia mecánica producida después de SNTR.
The onset and maintenance of neuropathic pain following a peripheral nerve injury involves many mechanisms such as changes in transduction, central or peripheral sensitization, and numerous plastic changes at the central level. Usual pharmacological treatments are not sufficient to alleviate the effects of hyperalgesia or allodynia produced by neuropathic pain. Therefore, in this thesis two activity-dependent treatments such as treadmill exercise and electrical stimulation are studied to observe the hypoalgesic effects produced and the molecular mechanisms involved in these beneficial changes. In the first two chapters of this thesis a novel protocol of treadmill exercise is shown, by increasing the velocity progressively during one hour (iTR). It has been shown that other protocols of treadmill ameliorate functional recovery after peripheral nervous system injury but, depending on intensity and duration, different effects have been described. In the first chapter, using an experimental model of neuropathic pain consisting in the section and repair of the sciatic nerve in a rat (SNTR), we found that iTR protocol reduces hyperalgesia by recoding of spontaneous neural activity, reducing neurotrophins levels to counteract nociceptive collateral sprouting, preventing the disruption of chloride cotransporters like NKCC1 and KCC2 to maintain central inhibition and counteracting microglial reactivity at central areas. iTR also positively reduced hyperalgesia in the lateral sciatic area demonstrating that the iTR hypoalgesic effect is not exclusively limited to the blockade of collateral sprouting in the periphery. Changes at central sensory circuits are also important. At the second chapter we found that iTR also increased the activity of serotonergic and noradrenergic projections from brainstem centers partially restoring the central disinhibition induced after the nerve injury. In the third chapter of this thesis, we evaluate the use of peripheral nerve stimulation (PNS) as a passive activity-dependent treatment for neuropathic pain. The therapeutic outcome together with the pattern of peripheral nerve activation, are closely related to the differences in the type and location of electrode, intensity and frequency of stimulation. For this purpose we evaluated two different experimental models as candidates. The spared nerve injury model (SNI) was the initial choice but PNS had very discrete effects in the reduction of mechanical hyperalgesia compared to SNTR. In a preliminary work, we discerned the frequency of stimulation producing the better reduction of hyperalgesia with acute stimulation after injury. Then, we improved the type of electrode and location by designing a system to make chronic stimulation available. We show some results for acute, repetitive acute and chronic stimulation protocols but the best stimulation protocol in reducing mechanical hyperalgesia was iCES protocol. Similarly to iTR, iCES consists of an increasing-frequency pattern of stimulation. We found that iCES triggers a series of changes at central levels, such as the restoration of expression of KCC2 and β2 receptor that act directly on the increase of GABA release in spinal cord facilitating together with the decrease of microglial and astrocytic reactivity, the reduction of mechanical hyperalgesia produced after SNTR.
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Wallace, Victoria C. J. "Peripheral nerve demyelination and neuropathic pain." Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/27605.

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Chronic neuropathic pain, characterised by allodynia (perception of innocuous stimuli as painful) and hyperalgesia (facilitated responses to painful stimuli), is poorly understood and is usually resistant to classical analgesics. Such abnormal pain phenomena can be associated with human demyelinating conditions such as Charcot-Marie-Tooth disease. Using mouse models of peripheral nerve demyelination, we have provided evidence for the consequent establishment of neuropathic pain and investigated possible underlying mechanisms. The first model investigated was the Prx-null mouse. The murine periaxin gene (Prx) is expressed in Schwann cells and encodes L- and S-periaxin, two abundant PDZ-domain proteins thought to have a role in stabilisation of myelin in the peripheral nervous system (PNS). Prx-null mice show progressive demyelination in peripheral nerves and electrophysiological investigations indicate the presence of spontaneous action potential discharge; abnormal activity thought to be critical for the development of persistent pain states. Consistent with the time course of demyelination, Rrx-null mice display an increased behavioural reflex sensitivity to cutaneous mechanical and noxious thermal stimulation. To further investigate the link between demyelination of peripheral nerves and neuropathic pain, we have also characterised a novel model of focal peripheral nerve demyelinating neuropathy. Focal demyelination of the sciatic or saphenous nerve was induced with lysolecithin (lysophosphatidylcholine) and resulted in an increased behavioural reflex sensitivity to both thermal and mechanical tests, peaking at 9-14 days following treatment. Nerve morphology was investigated using light and electron microscopy, which revealed 30-40% demyelination of the treated nerve, (without lysolecithin-treated axon loss) coinciding with peak behavioural changes. Changes in the excitability of saphenous nerves were revealed, with spontaneous action potential discharge of 2-3 impulses per second present at peak behavioural change. No associated change in peripheral activation thresholds or conduction velocity was observed. In both models, immunohistochemical investigations revealed no cell loss in the dorsal root ganglia (DRG) and no evidence for axonal damage. Similar methods revealed changes in the expression of neuropeptide Y, and the sodium channels Nav1.3 and Nav1.8 in DRG neurones. Such changes may account for increased nerve excitability and are known to occur in other models of nerve injury. However, these changes in the demyelinating models occur in a more restricted manner, specifically in the cells of formerly myelinated fibres. Intrathecal injections of the selective NMDA receptor antagonist, [R]-CPP, indicated that NMDA receptor-dependent changes are crucial for the development of a neuropathic pain-like state following peripheral nerve demyelination. Intrathecal administration of pharmacological agents indicated a role for the transcription factor NFkB in the production of the behavioural reflex sensitivity of lysolecithin-treated mice, as well as identifying the endogenous cannabinoid system as an effective inhibitory regulator and potential analgesic target. This study describes the first mouse models of peripheral nerve demyelination designed for the study of neuropathic pain and reveals phenotypic changes in DRG, which may contribute to the development of a neuropathic pain-like state. Therefore, these models may be useful for the evaluation of novel therapeutic targets for the treatment of demyelination-associated neuropathic pain.
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Taylor, Anna. "Peripheral mechanisms of trigeminal neuropathic pain." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97105.

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Trigeminal neuropathic pain is a unique type of neuropathic pain resulting from damage to primary afferents of the trigeminal nerve that innervates the head and neck region. It is characterized by intractable, unremitting pain in the absence of any overt tissue damage, and represents a significant clinical and societal burden. A thorough understanding of the mechanisms driving this condition is required to adequately treat, and ideally cure, this condition. The skin of the lower lip is innervated by several classes of primary afferents, including myelinated Aβ fibers, thinly myelinated Aδ fibers, and unmyelinated C fibers, which together are able to transduce the variety of innocuous and noxious stimuli encountered in the environment. Nociceptive stimuli are largely mediated by the unmyelinated C fibers, which have been further divided into 2 groups based on neurochemical and anatomical criteria, called the peptidergic and non-peptidergic C fibers. Given that nerve lesions initiating neuropathic pain conditions most often occur in the periphery, changes in the peripheral nervous system following nerve injury are particularly relevant in driving this aberrant pain condition. Therefore, the overall objective of this thesis is to explore the peripheral changes in an animal model of trigeminal neuropathic pain. The results of this thesis are presented in three chapters. The pattern of innervation of non-peptidergic C fibers in the skin of uninjured rats has been described, as well as how this fiber population changes following nerve injury. Concomitant ectopic autonomic fibers were observed in close apposition to the regenerating sensory fibers, and correlated with the behavioral phenotype of the animals. GDNF levels in the skin rapidly increased following nerve injury, and provided a possible mechanism for the ectopic parasympathetic fibers and regenerating non-peptidergic C fibers. Ablation of the non-peptidergic C fibers led to specific sprouting of parasympathetic fibers, but no change in behavior, however ablation of non-peptidergic fibers in neuropathic animals led to an exacerbated pain response. These results suggest an important role for non-peptidergic fibers and autonomic sprouting in neuropathic pain, and identifies GDNF as a potential factor for mediating these changes.
La douleur trigeminale neuropathique est une forme unique de douleur qui résulte d'un dommage aux afférents primaires du nerf trijumeau innervant la région de la tête et du coup. Cette douleur constante qui se manifeste en l'absence d'un dommage aux tissus périphériques représente un fardeau social et économique important. Une compréhension rigoureuse des mécanismes qui mènent à cette condition sera nécessaire pour mieux la traiter et préférablement la guérir.La peau de la lèvre inferieure est innervée par des afférents primaires appartenant à différentes classes, incluant les fibres myélinisées Aβ, les fibres légèrement myélinisées Aδ, ainsi que les fibres C non myélinisées. Ensemble, ces fibres peuvent transmettre une variété de stimuli nociceptifs ou inoffensifs tels que rencontrés dans l'environnement. Les stimuli nociceptifs sont majoritairement transmis par les fibres C non myélinisées, lesquelles peuvent être divisées en 2 catégories, peptidergiques ou non peptidergiques, selon des critères neurochimiques et anatomiques. Puisque les lésions nerveuses qui déclenchent la douleur neuropathique se produisent le plus souvent en périphérie, les changements au niveau du système nerveux périphérique sont centraux au développement de la condition douloureuse. Ceci étant dit, l'objectif général de cette thèse est d'explorer les changements périphériques qui se produisent dans un model animal de douleur trigeminale neuropathique.Les résultats de cette thèse sont présentés dans trois chapitres. L'innervation de la peau par les fibres C non peptidergiques chez le rat normal a d'abord été décrite. Ensuite, les changements subis par cette population suivant un dommage au nerf ont été documentés. Suite à un dommage nerveux périphérique, des fibres autonomiques ectopiques ont été observées en proximité des fibres sensorielles en régénération, et ce changement corrélait temporellement avec le phénotype comportemental des animaux. Les niveaux cutanés de GDNF ont rapidement augmenté après le dommage nerveux, fournissant un mécanisme potentiel permettant la régénération des fibres C non peptidergiques et la migration ectopique des fibres parasympathiques. L'ablation des fibres C non peptidergiques a déclenché la pousse des fibres parasympathiques sans changer le comportement des animaux. Par contre, l'ablation de ces fibres chez des animaux neuropathiques a exacerbé la réponse douloureuse de ceux-ci.Ces résultats suggèrent une participation importante des fibres C non peptidergiques et de la migration autonomique dans la douleur neuropathique. De plus, GDNF est rapporté comme étant un facteur pouvant produire ces changements.
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Hutton, E. J. "The skin as a window on mechanisms of neuropathy and neuropathic pain." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1532903/.

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Neuropathies are common, yet the pathogenic mechanisms of many remain incompletely understood. Animal and cell models have provided much useful information about disease mechanisms, and yet translation of this knowledge to clinical practice and disease therapies is often disappointing. One of the difficulties in studying human nerves is limited availability of tissue, due to the morbidity of peripheral nerve (usually sural nerve) biopsy. I sought to evaluate the utility of cutaneous nerves, both generally as a tool to assess the relevance of pathogenic mechanisms identified in animal studies in human disease, and also specifically in evaluating whether immune changes in the skin may play a role in the development of neuropathic pain. Animal models have suggested that proinflammatory cytokines exert algesic effects on nerves, whilst anti-inflammatory cytokines have a counter-regulatory analgesic effect (Üçeyler et al., 2009). More recently, support for a link between variability in systemic and / or local cytokine balance and pain in neuropathy has begun to emerge (Üçeyler et al., 2007c, Üçeyler et al., 2010). Despite some support for a link between painful neuropathies and increased inflammatory and / or decreased antiinflammatory cytokines, it remains unclear whether the immune changes reflect underlying neuropathological processes, a response to nociceptor activation, variability in individual immune response to nerve damage or are a biomarker of another factor indirectly modulating both pain and immune function. It is also unclear whether immune-nerve interactions are unidirectional or bidirectional: does increased nociceptor firing modulate local immune function or does immune response to nerve damage modulate activity of remaining undamaged fibres, or is there a combination of these factors? I sought to understand the effect of acute nociceptor activation on skin immune profile, as well as whether changes in chronic neuropathy would be associated with the presence and intensity of pain.
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Liu, Xue Jun. "Peripheral regulation of inflammatory pain and neuropathic pain by adenosine." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ66636.pdf.

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Bennett, Michael I. "The development of a pain scale for identifying neuropathic pain." Thesis, University of Birmingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487879.

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Books on the topic "Neuropathic pain"

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Toth, Cory, and Dwight Moulin, eds. Neuropathic Pain. Cambridge: Cambridge University Press, 2013. http://dx.doi.org/10.1017/cbo9781139152211.

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I, Bennett Michael, ed. Neuropathic pain. Oxford: Oxford University Press, 2006.

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Misha-Miroslav, Backonja, ed. Neuropathic pain syndromes. Philadelphia: Saunders, 1998.

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Peripheral neuropathy & neuropathic pain: Into the light. Shrewsbury, England: TFM Publishing Ltd, 2015.

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Smith, Daryl I., and Hai Tran, eds. Pathogenesis of Neuropathic Pain. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-91455-4.

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Chemotherapy induced neuropathic pain. Boca Raton: CRC Press, 2012.

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Galer, Bradley S. A clinical guide to neuropathic pain. [New York]: McGraw Hill, Healthcare Information Programs, 2000.

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1966-, Malmberg Annika B., and Chaplan Sandra R, eds. Mechanisms and mediators of neuropathic pain. Basel: Birkhäuser Verlag, 2002.

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de Castro, Jeimylo, and Yasser El Miedany, eds. Advances in Chronic and Neuropathic Pain. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-10687-3.

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Malmberg, Annika B., and Sandra R. Chaplan, eds. Mechanisms and Mediators of Neuropathic Pain. Basel: Birkhäuser Basel, 2002. http://dx.doi.org/10.1007/978-3-0348-8129-6.

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Book chapters on the topic "Neuropathic pain"

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Irwin, Anna, and Christian Renwick. "Neuropathic Pain: Peripheral Neuropathies." In Anesthesiology In-Training Exam Review, 311–14. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-87266-3_59.

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Haanpää, Maija, and Rolf-Detlef Treede. "Neuropathic Pain." In Clinical Pain Management, 281–89. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444329711.ch34.

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Eckman, Theodore, and Jianguo Cheng. "Neuropathic Pain." In Academic Pain Medicine, 327–32. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18005-8_42.

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Öztürk, Şerefnur. "Neuropathic Pain." In Neurological Disorders in Clinical Practice, 57–61. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23168-6_9.

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Abrecht, Christopher R., and Srdjan S. Nedeljkovic. "Neuropathic Pain." In Pain Medicine, 541–43. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-43133-8_145.

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Gupta, Rajesh. "Neuropathic Pain." In Multiple Choice Questions in Pain Management, 71–88. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56917-8_5.

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Marcus, Dawn A. "Neuropathic Pain." In Chronic Pain, 173–91. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-465-4_10.

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Grass, Gerald W. "Neuropathic Pain." In Essentials of Pain Management, 515–44. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-0-387-87579-8_23.

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Briani, C., L. Padua, C. Pazzaglia, and L. Battistin. "Neuropathic Pain." In Handbook of Neurochemistry and Molecular Neurobiology, 405–24. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-30377-2_19.

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Gupta, Rajesh. "Neuropathic Pain." In Pain Management, 11–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-55061-4_4.

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Conference papers on the topic "Neuropathic pain"

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Sawada, Yosuke, Hiroshi Hosokawa, Kiyoshi Matsumura, and Shigeo Kobayashi. "Molecular Mechanism of Neuropathic Pain." In International Conference on Informatics Education and Research for Knowledge-Circulating Society (icks 2008). IEEE, 2008. http://dx.doi.org/10.1109/icks.2008.24.

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Ramyashree, R. M., and Rammurthy Kulkarni. "Ketamine: Resurgence in Neuropathic Pain Management." In ISACON KARNATAKA 2017 33rd Annual Conference of Indian Society of Anaesthesiologists (ISA), Karnataka State Chapter. Indian Society of Anaesthesiologists (ISA), 2017. http://dx.doi.org/10.18311/isacon-karnataka/2017/ep032.

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Guimarães, Mário Vicente Campos, Josué Andrade Martins, Ana Lívia Piovezan de Oliveira, and Cecília Procópio Cardoso. "Neuropathic pain as consequence of rifle injury: a case report and literature review." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.585.

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Rifle injuries are relatively common in emergency cases. It may result in several acute damages or it could lead to chronic consequences to the patient. This paper reports a case of a rifle injury on the leg that resulted in neuropathic pain and venous insufficiency. To treat this patient, a multidimensional approach was prefered, using comprehensive therapy, drug treatment and neuromodulation. The case reported in this paper was gathered by appreciation of the patient’s records and interviews and was discussed in the light of the most recent literature. Neuropathic pain is caused by lesion or disease of the somatosensory nervous system, according to The International Association for Study of Pain that affects over 7 to 8 percent of general populations and corresponds to 20 to 25 percent of chronic pain, most frequently in women and man older than 50-years, diagnosed exclusively via clinical criteria. It might be classified by the clinical manifestations: spontaneous pain, evoked pain, after sensations, hyperpathia and referred pain. The details of pathophysiology of neuropathic pain are yet to be clarified once most of the data in the matter comes from animal testing and should be interpreted carefully, majorly in the long-term assessments. It is clear, though, that several mechanisms are involved in the pathogenic process, depending on anatomical location and etiology, and that different classifications of neuropathic pain could be clustered to form several subgroups based on the symptoms combination, each reflecting different mechanisms. Understanding these underlying mechanisms is crucial to a proper treatment of the patient. In this paper, we report a patient who suffered from a fire gun injury in the left feet resulting in a neuropathic pain. A 40-year-old male comes to the office referring to allodynia, hyperalgesia, burning pain and paroxysmal pain, characterizing persistent neuropathic pain, intensity 8 in the one-to-ten scale, and edema during the day in the left inferior member. The patient reports being shot, one year and half before, with a 5.56 caliber rifle at the left feet, riching the fifth metatarsal No remarkable finding was present in the medical history prior to the incident. At physical examination, it was perceived that the patient developed venous insufficiency, for which was prescribed a ⅞ compression socks (30- 40 mmhg). The neuropathic pain was firstly treated with pregabalin 50 mg/ day and Duloxetine 30 mg/day, showing relevant response. Then, electroneuromyography revealed intermedial dorsal cutaneous nerve injury, being managed with a local block, prepared with 8 ml of 2% Lidocaine and 2 ml of 4 mg Dexamethasone, and a 30 Hz neuromodulation, terminating the pain. Ballistic knowledge is essential to a proper management of gunshots injury. In this case report, the patient suffered a 5.56 caliber rifle injury, a high-velocity gun, resulting in an intermediate dorsal cutaneous nerve and the fifth metatarsal lesion. In these injuries, the projectile transfers energy to the affected tissue, expanding and crushing it. This brief expansion creates a subatmospheric pressure resulting in bacterial and foreign material suction into the wound. It is worth to note that gunshot-related injuries in the feet, due to scarce soft tissue, numerous bones and articulations, are more propense to vascular and neural lesions. Although pathophysiological mechanisms of neuropathic pain are not fully understood, it is described post-traumatic peripheral ectopic nerve activity and central sensitization that could help to understand the pain origin. Moreover, coexisting psychological and emotional triggers might be associated with neuropathic pain association. As the electroneuromyography shows, the intermediate dorsal cutaneous nerve, the smallest branch of the fibular nerve, was injured at the fifth metatarsal level rising neuropathic pain. In addition, as mentioned above, gunshot injuries might lead to bacterial invasion, triggering the inflammatory response. In this setting, it is important to point out that evidence suggests inflammatory mediators and proinflammatory cytokines as an inductor factor for pain hypersensitivity. Another possible gunshot related etiology that must be considered is lead toxicity in the composition of gun projectiles, which is reportedly associated with neuropathies. For its heterogeneity of etiologies, mechanisms and presentations, it is essential to understand the underlying causes and its consequences to a proper treatment resulting in partial or full pain relief. In this case, the patient was treated with Duloxetine, a serotonin-norepinephrine reuptake inhibitor and first line to treat neuropathic pain, and pregabalin, an anticonvulsant used to inhibit neuronal excitatory transmission. The synergistic action of these drugs is superior compared to monotherapy. Auxiliary, a local block was performed using Lidocaine analgesic, sodium channel blocker, and Dexamethasone, an antiinflammatory corticosteroid, testifying in favor of mechanical and inflammatory pathogenic mechanism originated by the gunshot injury. Finally, it is worth noting that gunshot wounds might give rise to venous insufficiency as a result of vascular injury and must be carefully considered in order to provide the proper treatment, revascularization for exemple. Another possible cause is deep venous thrombosis and leg injury accounts as a risk factor. In this case, it was opted for compression therapy, a conservative treatment, for increased venous return. Concluding that, neuropathic pain is a heterogeneous condition with a limited action mechanism understanding. It is required from the physicians to comprehend the multiple dimensions and main etiology of this disease in order to provide a proper treatment. As gunshots may contribute to the rise of several damage mechanisms, this case report highlights the importance of acknowledging ballistic properties and possibilities wound-related.
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Qu, Guangzhi, Hui Wu, Ishwar Sethi, and Craig T. Hartrick. "Neuropathic Pain Scale Based Clustering for Subgroup Analysis in Pain Medicine." In 2010 International Conference on Machine Learning and Applications (ICMLA). IEEE, 2010. http://dx.doi.org/10.1109/icmla.2010.51.

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Rocha, T. Martins, S. Pimenta, M. Bernardes, A. Bernardo, M. Barbosa, R. Lucas, and L. Costa. "AB0368 Predictors of neuropathic pain in rheumatoid arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2634.

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Stuertz, Elise D., Israel Olayide, Kathryn Braden, Daniela Salvemini, and Christopher K. Arnatt. "Development of GPR183 antagonists to treat neuropathic pain." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.543600.

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Silveira Lopes, Jordana Alícia, Daniela de Oliveira Werneck Rodrigues, Amanda do Carmo Gusmão, Augusto Cézar Apolinário dos Santos, Nathalia Noyma Sampaio Magalhães, Olivia Franco dos Santos, Renato Lourenço de Medeiros, Rodrigo de Martin Almeida, Tássia Mariana Moreira da Paz, and Thaís Sette Espósito. "NEUROPATHIC PAIN AMONG PATIENTS WITH SICKLE CELL DISEASE." In Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.17217.

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Melkani, Indu, Gagandeep Kaur, Sukhanpreet Kaur, Ruhi Rana, Bimlesh Kumar, Shubham Kumar, Narendra Kumar Pandey, Kardam Joshi, Dhara Patel, and Omji Porwal. "Neuropathic pain and diabetes: A complicated clinical condition." In 14TH INTERNATIONAL CONFERENCE ON MATERIALS PROCESSING AND CHARACTERIZATION 2023. AIP Publishing, 2024. http://dx.doi.org/10.1063/5.0192553.

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Bouden, S., S. Ben Massoud, S. Mhamdi, L. Rouached, A. Ben Tekaya, I. Mahmoud, R. Tekaya, O. Saidane, and L. Abdelmoula. "AB0707 PREVALENCE OF NEUROPATHIC PAIN IN RHEUMATOID ARTHRITIS." In EULAR 2024 European Congress of Rheumatology, 12-15 June. Vienna, Austria. BMJ Publishing Group Ltd and European League Against Rheumatism, 2024. http://dx.doi.org/10.1136/annrheumdis-2024-eular.5224.

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Vadalouka, A., and P. Kritikou. "B373 Chronic neuropathic pain management: results from one center participating in the neuropathic pain registry of the hellenic society of pain management and palliative care." In ESRA Abstracts, 39th Annual ESRA Congress, 22–25 June 2022. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/rapm-2022-esra.449.

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Reports on the topic "Neuropathic pain"

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Zheng, Ruo-xiang, Jia-wei Xu, Bi-yao Jiang, Wei Tang, Chun-li Lu, Xiao-yang Hu, and Jian-ping Liu. Mind-body therapies in traditional Chinese medicine for neuropathic pain: a systematic review of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0016.

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Review question / Objective: The purpose of this review is to comprehensively evaluate the effectiveness and safety on mind-body therapies of traditional Chinese medicine for neuropathic pain. Condition being studied: According to the definition by the International Association for the Study of Pain (IASP), neuropathic pain is a kind of pain caused by lesions or diseases affecting the somatosensory nervous system. It has brought considerable negative impacts on patients and society. Neuropathic pain is a prevalent disease and can be induced by a variety of clinical conditions such as spinal cord injury (prevalence rate: 53%), induced peripheral neuropathic pain (prevalence rate: 38%), diabetic peripheral neuropathic pain (prevalence rate: 10%-26%), chemotherapy postherpetic neuralgia (3.9-42.0/10,000 people per year), prosopalgia (3-5/10,000 people per year), and so on. However, current recommended medicines for neuropathic pain management could cause dependence and adverse events. Thus, alternatives would be helpful for both patients and clinicians. Mind-body therapy in traditional Chinese medicine (TCM) has a long history in clinical practice for relieving pain and their effectiveness has not been systematically reviewed.The purpose of this review is to comprehensively evaluate the effectiveness and safety on mind-body therapies of traditional Chinese medicine for neuropathic pain.
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Floyd, Candance L. Treatment of Neuropathic Pain after SCI with a Catalytic Oxidoreductant. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada622188.

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Xing, Ying, Hongping Liu, Yifei Wang, and Tiancai Wen. Effects of acupuncture on pain in diabetic peripheral neuropathy: a systematic review and meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0019.

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Review question / Objective: The purpose of this review is to determine the efficacy and safety of acupuncture on diabetic peripheral neuropathy (DPN) pain compared with analgesics or sham acupuncture.Randomized controlled trials are the only types of studies included in this review. Condition being studied: Diabetic peripheral neuropathy (DPN) is a common complication of type 1 and 2 diabetes. It is also the main cause of lower limb amputation and disability in patients with diabetes. Epidemiological evidence shows that up to 50% of patients with diabetes developed neuropathy during their long-term course of disease. The cause of DPN is not completely clear, but older age, longer diabetic duration and worse postprandial glucose control has been proved to be closely related to DPN. Distal symmetric polyneuropathy is the most typical manifestation of DPN, and about 10% to 30% of the affected patients may experience symptoms of neuropathic pain. Pain can be described as burning pain, electrical or stabbing sensations, parasthesiae, hyperasthesiae, and deep aching pain of the feet and lower limbs at night. This irreversible and unbearable pain greatly affects patients' sleep and quality of life.
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Ding, Ning, Cuicui Zhang, Lingxi Zhang, and Anqin Dong. The effect of cognitive behavioral therapy on neuropathic pain: A Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2021. http://dx.doi.org/10.37766/inplasy2021.5.0102.

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Wang, Liqin, Zhaohong Gao, Xiangru Niu, Meiqi Yuan, Yan Li, Fei Wang, Chuang Guo, and Zhen Ren. Acupuncture for diabetic neuropathic pain: protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2020. http://dx.doi.org/10.37766/inplasy2020.9.0043.

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Huang, Jiapeng, Chunlan Yang, Kehong Zhao, Ziqi Zhao, Yin Chen, Tingting Wang, and Yun Qu. Transcutaneous Electrical Nerve Stimulation in Rodent Models of Neuropathic Pain: A Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2021. http://dx.doi.org/10.37766/inplasy2021.11.0104.

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Yerofeyeva, Anna-Maria V., Sergey V. Pinchuk, Svetlana N. Rjabceva, and Alla Yu Molchanova. Neuropathic pain correction method using mesenchymal stem cells and cannabinoid receptor CB2 stimulation. Peeref, March 2023. http://dx.doi.org/10.54985/peeref.2303p4142545.

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Kovanur Sampath, Kesava, James Hale, Steve Tumilty, Gerard Farrell, Oliver Thomson, Angela Gisselman, Suzie Belcher, and Rajesh Katare. miRNAs that are dysregulated and/or dysfunctional in chronic neuropathic pain: A scoping Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0103.

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Jia, Hongying, GY Yang, and YT Xiao. A Meta-analysis of the Effect of Mindfulness Therapy on Neuropathic Pain of Patients. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2023. http://dx.doi.org/10.37766/inplasy2023.5.0052.

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Chou, Roger, Jesse Wagner, Azrah Y. Ahmed, Ian Blazina, Erika Brodt, David I. Buckley, Tamara P. Cheney, et al. Treatments for Acute Pain: A Systematic Review. Agency for Healthcare Research and Quality (AHRQ), December 2020. http://dx.doi.org/10.23970/ahrqepccer240.

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Abstract:
Objectives. To evaluate the effectiveness and comparative effectiveness of opioid, nonopioid pharmacologic, and nonpharmacologic therapy in patients with specific types of acute pain, including effects on pain, function, quality of life, adverse events, and long-term use of opioids. Data sources. Electronic databases (Ovid® MEDLINE®, PsycINFO®, Embase®, the Cochrane Central Register of Controlled Trials, and the Cochrane Database of Systematic Reviews) to August 2020, reference lists, and a Federal Register notice. Review methods. Using predefined criteria and dual review, we selected randomized controlled trials (RCTs) of outpatient therapies for eight acute pain conditions: low back pain, neck pain, other musculoskeletal pain, neuropathic pain, postoperative pain following discharge, dental pain (surgical or nonsurgical), pain due to kidney stones, and pain due to sickle cell disease. Meta-analyses were conducted on pharmacologic therapy for dental pain and kidney stone pain, and likelihood of repeat or rescue medication use and adverse events. The magnitude of effects was classified as small, moderate, or large using previously defined criteria, and strength of evidence was assessed. Results. One hundred eighty-three RCTs on the comparative effectiveness of therapies for acute pain were included. Opioid therapy was probably less effective than nonsteroidal anti-inflammatory drugs (NSAIDs) for surgical dental pain and kidney stones, and might be similarly effective as NSAIDs for low back pain. Opioids and NSAIDs were more effective than acetaminophen for surgical dental pain, but opioids were less effective than acetaminophen for kidney stone pain. For postoperative pain, opioids were associated with increased likelihood of repeat or rescue analgesic use, but effects on pain intensity were inconsistent. Being prescribed an opioid for acute low back pain or postoperative pain was associated with increased likelihood of use of opioids at long-term followup versus not being prescribed, based on observational studies. Heat therapy was probably effective for acute low back pain, spinal manipulation might be effective for acute back pain with radiculopathy, acupressure might be effective for acute musculoskeletal pain, an opioid might be effective for acute neuropathic pain, massage might be effective for some types of postoperative pain, and a cervical collar or exercise might be effective for acute neck pain with radiculopathy. Most studies had methodological limitations. Effect sizes were primarily small to moderate for pain, the most commonly evaluated outcome. Opioids were associated with increased risk of short-term adverse events versus NSAIDs or acetaminophen, including any adverse event, nausea, dizziness, and somnolence. Serious adverse events were uncommon for all interventions, but studies were not designed to assess risk of overdose, opioid use disorder, or long-term harms. Evidence on how benefits or harms varied in subgroups was lacking. Conclusions. Opioid therapy was associated with decreased or similar effectiveness as an NSAID for some acute pain conditions, but with increased risk of short-term adverse events. Evidence on nonpharmacological therapies was limited, but heat therapy, spinal manipulation, massage, acupuncture, acupressure, a cervical collar, and exercise were effective for specific acute pain conditions. Research is needed to determine the comparative effectiveness of therapies for sickle cell pain, acute neuropathic pain, neck pain, and management of postoperative pain following discharge; effects of therapies for acute pain on non-pain outcomes; effects of therapies on long-term outcomes, including long-term opioid use; and how benefits and harms of therapies vary in subgroups.
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