Статті в журналах: "DIABETIC 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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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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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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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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Mokhtar, Nazarine, Stephane Doly, and Christine Courteix. "Diabetic Neuropathic Pain and Serotonin: What Is New in the Last 15 Years?" Biomedicines 11, no. 7 (July 6, 2023): 1924. http://dx.doi.org/10.3390/biomedicines11071924.

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The neurotransmitter serotonin (5-hydroxytryptamine, 5-HT) is involved in numerous physiological functions and plays a key role in pain modulation including neuropathic pain. Diabetic neuropathy is a common complication of diabetes mellitus often accompanied by chronic neuropathic pain. Animal models of diabetes offer relevant tools for studying the pathophysiological mechanisms and pharmacological sensitivity of diabetic neuropathic pain and for identifying new therapeutic targets. In this review, we report data from preclinical work published over the last 15 years on the analgesic activity of drugs acting on the serotonergic system, such as serotonin and noradrenaline reuptake inhibitor (SNRI) antidepressants, and on the involvement of certain serotonin receptors-in particular 5-HT1A, 5-HT2A/2c and 5-HT6 receptors-in rodent models of painful diabetic neuropathy.

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Li, Hao, Shulin Liu, Zheng Wang, Yonglai Zhang та Kaiguo Wang. "Hydrogen sulfide attenuates diabetic neuropathic pain through NO/cGMP/PKG pathway and μ-opioid receptor". Experimental Biology and Medicine 245, № 9 (8 квітня 2020): 823–34. http://dx.doi.org/10.1177/1535370220918193.

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Diabetic neuropathic pain is a frequent complication of diabetic neuropathy. The specific manifestations of diabetic neuropathic pain include spontaneous pain and hyperalgesia, which seriously affect the quality of life of patients. Previous publications have shown that H2S has both pro-nociceptive and anti-nociceptive effects. This present investigation aimed to examine the anti-nociceptive effect of H2S on diabetic neuropathic pain. We established a diabetic neuropathic pain animal model with high-glucose, high-fat diet, and STZ, then treated rats with different concentrations of H2S and inhibitors of NOS, sGC, PKG, and opioid receptors. The mechanical allodynia and thermal hyperalgesia of rats were measured to assess the anti-nociceptive effects of H2S. The mRNA and protein expression of NOS and PKG1 were measured to explore their roles in the anti-nociceptive action of H2S. The results revealed that inhalation of H2S gas had anti-nociceptive effect in diabetic neuropathic pain model rats without affecting the blood glucose level and body mass. It increased the mRNA and protein level of nNOS, and the inhibitor of nNOS, 7-NI, abolished the anti-nociceptive effect of H2S. Furthermore, inhibitors of sGC and PKG could also abolish the anti-nociceptive effect of H2S. The expression of PKG1 was found to be increased by H2S, which was reversed by the inhibitors of nNOS, sGC, and PKG. Finally, CTOP, a μ-opioid receptor antagonist, abolished the anti-nociceptive effect of H2S, indicating that the μ-opioid receptor plays a role in the anti-nociceptive effect of H2S. In conclusion, the findings of this investigation suggest that hydrogen sulfide may attenuate the diabetic neuropathic pain through NO/cGMP/PKG pathway and μ-opioid receptor. Impact statement There are currently approximately 425 million diabetic patients worldwide, of which approximately 90% of patients with diabetes suffer from neuropathy. Diabetic neuropathic pain (DNP) is a common complication of diabetic neuropathy. Nearly half of the patients hospitalized with diabetes have pain symptoms or symptoms related to neurological injury, and the incidence increases with age and diabetic duration. Anti-DNP analgesics have either limited therapeutic effects or serious side effects or lack of clinical trials, which has limited their application. Physiopathological mechanisms and treatment of DNP remain a significant challenge. The present confirmed that inhalation of H2S may attenuate the diabetic neuropathic pain through NO/cGMP/PKG pathway and μ-opioid receptor. It provides us the animal study foundation for the application of H2S on the treatment of DNP and clarifies some target molecules in the pain modulation of DNP.

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Shabbir, Syed H. "Psychiatric Underpinnings of Chronic Diabetic Neuropathic Pain." Einstein Journal of Biology and Medicine 30, no. 1&2 (March 2, 2016): 37. http://dx.doi.org/10.23861/ejbm201530639.

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There is increasing evidence that psychosocial factors may be involved in the pathophysiology of chronic diabetic neuropathic pain. Individuals with diabetic polyneuropathy exhibit significantly higher rates of axis I psychiatric disorders, and worsening neuropathic symptoms correlate with worsened psychiatric illness. This association exists even when social-support and quality-of-life measures are controlled. Aberrant supraspinal structures and neuronal networks in diabetic neuropathy mimic those found in other psychiatric illnesses. Response to standard medications and therapeutic approaches remains unsatisfactory, and antidepressants continue to serve as first-line treatment for diabetic neuropathy. The exact interplay between neuropathic pain and psychiatric illness remains unclear and may have a common pathophysiological focus. This area of study needs to be revisited and psychological interventions must be explored as possible treatment options for diabetic neuropathy.

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Zakin, Elina, Rory Abrams, and David M. Simpson. "Diabetic Neuropathy." Seminars in Neurology 39, no. 05 (October 2019): 560–69. http://dx.doi.org/10.1055/s-0039-1688978.

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AbstractDiabetes mellitus is becoming increasingly common worldwide. As this occurs, there will be an increase in the prevalence of known comorbidities from this disorder of glucose metabolism. One of the most disabling adverse comorbidities is diabetic neuropathy. The most common neuropathic manifestation is distal symmetric polyneuropathy, which can lead to sensory disturbances, including diminished protective sense, making patients prone to foot injuries. However, focal, multifocal, and autonomic neuropathies are also common. Diabetic nerve pain and Charcot osteoarthropathy are advanced neuropathic conditions that portend a severe deterioration in quality of life. To combat these symptoms, along with glycemic control and establishment of health care systems to educate and support patients with the complexities of diabetes, there are pharmacologic remedies to ameliorate the neurologic symptoms. Several guidelines and review boards generally recommend the use of tricyclic antidepressants, serotonin/norepinephrine-reuptake inhibitors, α-2-delta ligands, and anticonvulsants as medications to improve painful diabetic neuropathy and quality of life.

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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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Ekinci, Bilge, Bahadir Suleyman, Renad Mammadov, Arzu Gezer, Ali Mendil, Nergis Akbas, Seval Bulut, Cagatay Dal, and Halis Suleyman. "The effect of carvacrol upon experımentally ınduced dıabetıc neuropathy and neuropathıc paın ın rats." Acta Poloniae Pharmaceutica - Drug Research 79, no. 5 (January 20, 2023): 707–15. http://dx.doi.org/10.32383/appdr/155354.

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Diabetic neuropathies are the most frequent complication of diabetes. While numerous metabolic pathways are disrupted in diabetic neuropathy, oxidative stress has been indicated as a significant reason for this condition. In this study, the effect of carvacrol, which has antioxidant effects, on experimental diabetic neuropathy and neuropathic pain was investigated. Alloxan was used to induce diabetes in the experiment. Diabetes was created by administering 120mg/kg of alloxan intraperitoneally (i.p) once a day for 3 days. Rats with a blood glucose concentration above 250mg/kg in the blood taken from the tail veins at the end of three days were considered diabetic. Rats were categorized under healthy control (HG), alloxan-induced hyperglycemia (AG), and alloxan-induced hyperglycemia + carvacrol-treated (ACG) groups. Carvacrol was i.p injected at 50 mg/kg dose to the ACG (n=6) group of rats with hyperglycemia. The same volume of distilled water as the solvent was applied in the same way to AG (n=6) and HG (n=6) rat groups. This procedure was repeated once a day for three months.Carvacrol showed anti-hyperglycemic effect in diabetic rats, protective effect against lowering pain threshold and analgesic activity in rat paws in rats. Carvacrol prevented the oxidant/antioxidant balance from changing in favor of oxidants. The results supported that carvacrol is an agent against alloxan-induced peripheral diabetic neuropathic pain.

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Yu, Wei, Guo-qing Zhao, Rang-juan Cao, Zhi-hua Zhu, and Kai Li. "LncRNA NONRATT021972 Was Associated with Neuropathic Pain Scoring in Patients with Type 2 Diabetes." Behavioural Neurology 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/2941297.

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Background. Long noncoding RNAs were involved in the processes of diabetes. Our study was aimed to explore clinical potential of LncRNA NONRATT021972 in diabetic neuropathic pain and investigate detailed mechanisms. Methods. 154 patients with type 2 diabetes were enrolled as experimental group paired with control. Patients without diabetes but neuropathy were enrolled to explore exclusive role of LncRNA NONRATT021972 in neuropathy. Real-time PCR and ELISA were performed to examine expression of LncRNA and TNF-α in flood. Neuropathic pain scores were calculated with data from NPQ. Streptozotocin was used for SD adult male rats to establish diabetes for NONRATT021972 siRNA or saline treatment. Neuropathic pain behaviors and expression of TNF-α were assessed. Result. Patients with type 2 diabetes had a significantly higher concentration of LncRNA NONRATT021972 in blood and more severe symptoms of neuropathic pain. LncRNA NONRATT021972 was positively associated with neuropathic pain scores of type 2 diabetes. TNF-α level increased in patients with type 2 diabetes. Animal experiment showed that LncRNA NONRATT021972 siRNA attenuated inflammation via decreasing TNF-α and alleviated neuropathic pain. Conclusion. LncRNA NONRATT021972 increased in type 2 diabetes and was positively associated with neuropathic pain scoring in type 2 diabetes. LncRNA NONRATT021972 exacerbated neuropathic pain via TNF-α related pathways.

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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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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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Zhang, Yan Ping, Ariel Eber, Yue Yuan, Zhe Yang, Yiliam Rodriguez, Roy C. Levitt, Peter Takacs, and Keith A. Candiotti. "Prophylactic and Antinociceptive Effects of Coenzyme Q10 on Diabetic Neuropathic Pain in a Mouse Model of Type 1 Diabetes." Anesthesiology 118, no. 4 (April 1, 2013): 945–54. http://dx.doi.org/10.1097/aln.0b013e3182829b7b.

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Abstract Background: Oxidative stress is a key factor implicated in the development of diabetic neuropathy. This study evaluates the prophylactic and antinociceptive effects of the antioxidant coenzyme Q10 (CoQ10) on diabetes-induced neuropathic pain in a diabetic mouse model. Methods: Total 56 mice with type 1 diabetes induced by streptozotocin were used, 20 normal mice were used as control. Mechanical and thermal nociceptive behavioral assays were applied to evaluate diabetic neuropathic pain. Tissue lipid peroxidation, immunohistochemistry, reverse transcription, and polymerase chain reaction were used to evaluate the molecular mechanisms of CoQ10. Data are presented as mean ± SEM. Results: CoQ10 administration was associated with reduced loss of body weight compared with nontreated diabetic mice, without affecting blood glucose levels. Low dose and long-term administration of CoQ10 prevented the development of neuropathic pain. Treatment with CoQ10 produced a significant dose-dependent inhibition of mechanical allodynia and thermal hyperalgesia in diabetic mice. Dorsal root ganglia, sciatic nerve, and spinal cord tissues from diabetic mice demonstrated increased lipid peroxidation that was reduced by CoQ10 treatment. CoQ10 administration was also noted to reduce the proinflammatory factors in the peripheral and central nervous system. Conclusions: The results of this study support the hypothesis that hyperglycemia induced neuronal oxidative damage and reactive inflammation may be pathogenic in diabetic neuropathic pain. CoQ10 may be protective by inhibiting oxidative stress and reducing inflammation by down-regulating proinflammatory factors. These results suggest that CoQ10 administration may represent a low-risk, high-reward strategy for preventing or treating diabetic neuropathy.

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Bellelli, Alessio, Daniele Santi, Manuela Simoni, and Carla Greco. "Diabetic Neuropathic Cachexia: A Clinical Case and Review of Literature." Life 12, no. 5 (May 4, 2022): 680. http://dx.doi.org/10.3390/life12050680.

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A 46-year-old man was admitted to the surgical department because of abdominal pain and anemia, with the radiological finding of a perforated duodenal ulcer, and underwent laparoscopic surgical treatment. Type 2 diabetes mellitus (T2DM) had been diagnosed 5 years earlier and treated with diet. At clinical investigation, the patient was depressed and anorexic; moreover, he complained of lower extremity weakness and bilateral feet pain, burning in nature and accompanied by allodynia. This painful sensation had been preceded by an 8-month history of fatigue and anorexia with profound weight loss of 35 kg. After clinical evaluation and a nerve conduction study, diagnosis of diabetic cachectic neuropathy was made based on the rapid onset of severe neuropathic pain in the context of diabetic neuropathy, marked weight loss, and depressed mood. The therapy with pregabalin and duloxetine had scarce effect and was gradually discontinued. The patient, however, obtained progressive relief and amelioration of neuropathic lower-limb pain concomitant with weight gain. This clinical trend also confirmed the diagnosis of this rare form of diabetic neuropathy. A few cases of diabetic neuropathic cachexia have been reported in the literature and are briefly reviewed here.

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Calabrese, Donato, Silvia Giatti, Simone Romano, Carla Porretta-Serapiglia, Roberto Bianchi, Marco Milanese, Giambattista Bonanno, et al. "Diabetic neuropathic pain: a role for testosterone metabolites." Journal of Endocrinology 221, no. 1 (January 14, 2014): 1–13. http://dx.doi.org/10.1530/joe-13-0541.

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Diabetic neuropathy is associated with neuropathic pain in about 50% of diabetic subjects. Clinical management of neuropathic pain is complex and so far unsatisfactory. In this study, we analyzed the effects of the testosterone metabolites, dihydrotestosterone (DHT), and 3α-diol, on nociceptive and allodynia thresholds and on molecular and functional parameters related to pain modulation in the dorsal horns of the spinal cord and in the dorsal root ganglia of rats rendered diabetic by streptozotocin injection. Furthermore, the levels of DHT and 3α-diol were analyzed in the spinal cord. Diabetes resulted in a significant decrease in DHT levels in the spinal cord that was reverted by DHT or 3α-diol treatments. In addition, 3α-diol treatment resulted in a significant increase in 3α-diol in the spinal cord compared with control values. Both steroids showed analgesic properties on diabetic neuropathic pain, affecting different pain parameters and possibly by different mechanisms of action. Indeed, DHT counteracted the effect of diabetes on the mechanical nociceptive threshold, pre- and post-synaptic components, glutamate release, astrocyte immunoreactivity, and expression of interleukin-1β (IL1β), while 3α-diol was effective on tactile allodynia threshold, glutamate release, astrocyte immunoreactivity and the expression of substance P, toll-like receptor 4, tumor necrosis factor-α, transforming growth factor β-1, IL1β, and translocator protein. These results indicate that testosterone metabolites are potential agents for the treatment of diabetic neuropathic pain.

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Petrikonis, Kęstutis, Arūnas Ščiupokas, Gintautė Samušytė, Jolita Janušauskaitė, Rita Šulcaitė, and Antanas Vaitkus. "Importance of pain evaluation for more accurate diagnosis of painful diabetic polyneuropathy." Medicina 46, no. 11 (November 13, 2010): 735. http://dx.doi.org/10.3390/medicina46110104.

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Pain is a common problem in diabetic neuropathy, but relatively little has been published regarding the extent to which it needs to be addressed in clinical practice. Objective. To assess neuropathic pain profile and its association with quantitative sensory testing in painful diabetic polyneuropathy. Material and methods. Altogether, 61 consecutive diabetic inpatients with symmetric neuropathic complaints were enrolled. Clinical neurological examination and quantitative sensory testing (QST) were performed. Patients were interviewed using the Neuropathic Pain Scale (NPS) and filled in the McGill Pain Questionnaire (MPQ). Results. Of all patients, 49 (80.3%) had clinical diabetic polyneuropathy. Only 17 of these patients complained of lower extremity pain on an initial interview, while 27 marked it in the MPQ. The intensity of deep and superficial pain did not differ, but patients rated deep pain as more unpleasant than superficial (6.27±2.37 vs. 4.30±1.42 on the NPS, P=0.034). Superficial pain NPS items tended to correlate with QST results, while deep pain items did not. Only female gender (OR=7.87) and lower glycosylated hemoglobin level (OR=0.65) were predictive of pain in case of diabetic neuropathy. Conclusions. Standard pain questionnaires were useful in identifying pain sufferers. At the same intensity, deep neuropathic pain was more unpleasant than superficial. Pain manifestation was associated with female gender and lower level of glycosylated hemoglobin.

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Chen, Shao-Rui, and Hui-Lin Pan. "Hypersensitivity of Spinothalamic Tract Neurons Associated With Diabetic Neuropathic Pain in Rats." Journal of Neurophysiology 87, no. 6 (June 1, 2002): 2726–33. http://dx.doi.org/10.1152/jn.2002.87.6.2726.

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Diabetic neuropathic pain is often considered to be caused by peripheral neuropathy. The involvement of the CNS in this pathological condition has not been well documented. Development of hypersensitivity of spinal dorsal horn neurons is involved in neuropathic pain induced by traumatic nerve injury. In the present study, we determined the functional changes of identified spinothalamic tract (STT) neurons and their correlation to diabetic neuropathic pain. Diabetes was induced in rats by intraperitoneal injection of streptozotocin. Hyperalgesia and allodynia were assessed by the withdrawal responses to pressure, radiant heat, and von Frey filaments applied to the hindpaw. Single-unit activity of STT neurons was recorded from the lumbar spinal cord in anesthetized rats. The responses of STT neurons to mechanical and thermal stimuli and the sensitivity to intravenous morphine were determined in diabetic and normal rats. In 12 diabetic rats, mechanical allodynia and hyperalgesia, but not thermal hyperalgesia, developed within 2 wk after streptozotocin injection and lasted for ≥7 wk. Compared to the 32 STT neurons recorded in normal animals, the 37 STT neurons in diabetic rats displayed a higher spontaneous discharge activity and enlarged receptive fields. Also, the STT neurons in diabetic rats exhibited lower thresholds and augmented responses to mechanical stimulation. Intravenous injection of 2.5 mg/kg of morphine suppressed significantly the responses of STT neurons to noxious stimuli in 12 nondiabetic rats. However, such an inhibitory effect of morphine on the evoked response of STT neurons was diminished in 14 diabetic animals. This electrophysiological study provides new information that development of hypersensitivity of spinal dorsal horn projection neurons may be closely related to neuropathic pain symptoms caused by diabetes. Furthermore, the attenuated inhibitory effects of morphine on evoked responses of STT neurons in diabetes likely accounts for its reduced analgesic efficacy in this clinical form of neuropathic pain.

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Taslim Pinzon, Rizaldy, and Angela Angela. "CLOSING THE GAP FOR PHARMACOLOGICAL TREATMENT OF PAINFUL DIABETIC NEUROPATHY : THE POTENTIAL ROLE OF VITAMIN D." MNJ (Malang Neurology Journal) 8, no. 1 (January 1, 2022): 49–52. http://dx.doi.org/10.21776/ub.mnj.2022.008.01.10.

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Painful neuropathic pain is a challenging chronic pain to treat. It is heterogeneous in symptoms and could be resistant to the available treatments regimen. Current pharmacological treatments fail to achieve adequate pain relief in a most patients. The previous review showed that only less than 50% of patients can achieve good pain reduction with standard adjuvant treatment. The available adjuvants analgesic only focus in the symptom control, and do not interfere with the progressing damage of the nerve. Vit D insufficiency is quite frequent in type 2 diabetes patients.diabetes, particularly those with symptoms of DPN. The studies also showed that low serum vitamin D levels are an independent predictor of DPN development. Vitamin D supplementation is necessary for diabetic neuropathy patients since it promotes the synthesis of neurotrophins and neurotransmitters. Additional vitamin D therapy have big role in nerve growth factor and the regulation of neurotrophin and Ca2+ homeostasis in neurons, and provides protection for neurons in the peripheral nervous system. In this review, we do systematically search the studies about Vitamin D for the treatment of painful diabetic neuropathic condition. We used PubMed, Cochrane, Clinical Key, and search Google Scholar for papers that used vitamin D phrases. and painful diabetic neuropathy as our major database for this review and we make a systematic table to explain our review. However, there is still an unmet need in the management of neuropathic pain. The unmet needs maybe caused by the gap between pharmacological treatmnet in pain reduction in painful diabetic neuropathy patients. Therefore, in this review we discuss about the potential use of vitamin D as an add-on therapy to closing the gap in the management of neuropathic pain.

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Habibi, Abdolhamid, Asma Taheri, and Saba Habibi. "Attenuation of Some Inflammatory Markers by Endurance Training in the Spinal Cord of Rats with Diabetic Neuropathic Pain." Contrast Media & Molecular Imaging 2022 (May 18, 2022): 1–9. http://dx.doi.org/10.1155/2022/6551358.

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Nervous inflammation is an important component of the pathogenesis of neurodegenerative diseases including chronic diabetic neuropathic pain. In order to obtain a decrease in the progression of diabetic neuronal damage, it may be necessary to examine therapeutic options that involve antioxidants and anti-inflammatory agents. The aim of this study was to investigate the attenuation of inflammatory factors with endurance training in the spinal cord of rats with neuropathic pain. Thirty-two 8-week-old male Wistar rats (with a weight range of 204 ± 11.3 g) were randomly divided into 4 groups (n = 8), including (1) diabetic neuropathy (50 mg/kg streptozotocin intraperitoneal injection), (2) diabetic neuropathy training (30 minutes of endurance training at 15 meters per minute, 5 days a week for 6 weeks), (3) healthy training, and (4) healthy control. After confirmation of diabetic neuropathy by behavioral tests, training protocol and supplementation were performed. The NLRP3, P38 MAPK, TNF-α, and IL-1β gene expressions were measured by a real-time technique in the spinal cord tissue. One-way analysis of variance and Tukey's post hoc test were used for statistical analysis. Endurance training reduced the sensitivity of the nervous system to thermal hyperalgesia and mechanical allodynia; also, compared to the diabetic neuropathy group, the gene expressions of NLTP3, P38 MAPK, TNF-α, and IL-1β were significantly reduced by endurance training ( P < 0.05 ). Endurance training modulates NLRP3, P38 MAPK, and TNF-α, IL-1β gene expressions and improves the sensitivity of nociceptors to pain factors. Accordingly, it is recommended to use endurance training to reduce neuropathic pain for diabetics.

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Feng, Ling, Wen-Ke Liu, Lan Deng, Jia-Xing Tian, and Xiao-Lin Tong. "Clinical Efficacy of Aconitum-Containing Traditional Chinese Medicine for Diabetic Peripheral Neuropathic Pain." American Journal of Chinese Medicine 42, no. 01 (January 2014): 109–17. http://dx.doi.org/10.1142/s0192415x14500074.

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Diabetic peripheral neuropathy is a common chronic complication of diabetes. Routine clinical management uses analgesics to relieve pain in combination with drugs for nerve repair. The drugs are often not effective for the severe pain cases, and these western medications also have side effects. We report a more effective treatment of diabetic peripheral neuropathic pain using a high dose of a traditional Chinese medicine, aconitum (including both Radix aconite preparata and Radix aconite kusnezoffii), in combination with Huangqi Guizhi Wuwu Tang (i.e., astragalus, cassia twig, white peony root, and spatholobi). In order to achieve stronger analgesic effects, we increased the clinical dosage of aconitum from 15 to 120 g. The aconitum was boiled for 6–8 hours, and licorice was also used to reduce potential toxicities of aconitum. In the four reported cases, the patients' neuropathic pain was remarkably reduced and the EMG profile was also improved with this treatment regimen. Adverse reactions were not observed during the therapy. Thus, aconitum represents a promising and safe treatment for the well-being of patients and their diabetic peripheral neuropathic pain. Future controlled clinical trials using traditional Chinese medicines containing aconitum in treating the neuropathic pain are warranted.

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Roys, MD, Joseph, Marissa Catalanatto, MD, Christian Vangeison, DO, and Emanuel Husu, MD. "The Role of Caudal Epidural Steroid Injections in Diabetic Lumbosacral Radiculoplexus Neuropathy: A Case Report." Pain Medicine Case Reports 6, no. 7 (November 30, 2022): 267–69. http://dx.doi.org/10.36076/pmcr.2022.6.267.

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BACKGROUND: Diabetic lumbosacral radiculoplexus neuropathy (DLSRPN) or diabetic amyotrophy, although relatively uncommon and typically self-resolving, often leads to a period of severe compromise in quality of life. CASE REPORT: We present the case of a 46-year-old woman with 6 months of bilateral lower extremity weakness and neuropathic pain, diagnosed with diabetic lumbosacral plexopathy. Her recovery course was significantly improved by receiving a caudal epidural steroid injection (ESI) to address her pain and decreased function that was not sufficiently controlled by neuropathic agents and oral opioids. CONCLUSIONS: Caudal ESI may have a beneficial role treatment of DLSRPN to facilitate participation in a functional rehabilitation program. KEY WORDS: Diabetic lumbosacral plexopathy, diabetic lumbosacral radiculoplexus neuropathy, diabetic amyotrophy, Bruns-Garland syndrome, proximal diabetic neuropathy, caudal epidural steroid injection, epidural steroid injection, chronic pain

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Kaki, A., M. Nikbakht, A. H. Habibi, and H. F. Moghadam. "Effect of aerobic exercise on innate immune responses and inflammatory mediators in the spinal cord of diabetic rats." Comparative Exercise Physiology 16, no. 4 (July 1, 2020): 293–301. http://dx.doi.org/10.3920/cep190050.

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Neuronal inflammation is one of the pathophysiological causes of diabetes neuropathic pain. The purpose of this research was to determine the effect of aerobic exercise on innate immune responses and inflammatory mediators in the spinal dorsal horn in rats with diabetic neuropathic pain. 40 eight-week-old male Wistar rats (weight range 220±10.2 g) were randomly divided into four groups of (1) sedentary diabetic neuropathy (SDN), (2) training diabetic neuropathy (TDN), (3) training control (TC), and (4) sedentary control (SC). Diabetes was induced by injection of streptozocin (50 mg/kg). Following confirmation of behavioural tests for diabetes neuropathy, the training groups performed 6 weeks of moderate-intensity aerobic exercise on the treadmill. The expression of Toll like receptor (TLR)4, TLR2, tumour necrosis factor (TNF)-α, interleukin (IL)-1β and IL-10 genes in L4-L6 spinal cord sensory neurons was measured by Real Time PCR. Two-way ANOVA and Bonferroni’s post hoc tests were used for statistical analysis. After performing aerobic exercise protocol, the TDN compared to the SDN showed a significant decrease in the mean score of pain in the formalin test and a significant increase in the latency in Tail-Flick test was observed. The expression of TLR4, TLR2, TNF-α and IL-1β genes was significantly higher in the SDN than in the SC group (P<0.05). The expression of the above genes in the TDN was significantly lower than the SDN group (P<0.05). Also, the expression level of IL-10 gene was significantly higher in the TDN than the SDN group (P<0.05). Aerobic exercise improved sensitivity of nociceptors to pain-inducing agents in diabetic neuropathy due to inhibition of inflammatory receptors and increased levels of anti-inflammatory agents in the nervous system. Thus, aerobic exercise should be used as a non-pharmacological intervention for diabetic patients to reduce neuropathic pain.

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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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Santillan, Roberto Medina. "Management of Diabetic Peripheral Neuropathic Pain." US Endocrinology 00, no. 01 (2005): 55. http://dx.doi.org/10.17925/use.2005.00.01.55.

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Diabetes remains the most common cause of neuropathy in the US, and neuropathy is the most common complication and greatest source of morbidity and mortality in diabetic patients. Additionally, emerging studies suggest that impaired glucose tolerance may lead to polyneuropathy, particularly painful small-fiber neuropathy. It is estimated from epidemiological studies that the prevalence of neuropathy in diabetic patients is approximately 30% in hospitalized patients and 20% in community-dwelling diabetic patients.

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Jeon, Eonju, Hyojung Kwon, Imhee Shin, Seokbong Kang, and Hosang Shon. "Effect of Acupuncture on Diabetic Peripheral Neuropathy: An Uncontrolled Preliminary Study from Korea." Acupuncture in Medicine 32, no. 4 (August 2014): 350–52. http://dx.doi.org/10.1136/acupmed-2013-010479.

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Background Diabetic neuropathic pain can severely influence quality of life, and patients may be dissatisfied with treatment. Objective To carry out an observational study of the effects of acupuncture for the treatment of diabetic neuropathic pain, in preparation for a full study. Methods Nine patients with diabetic neuropathic pain were recruited from a Korean diabetic clinic and given 12 sessions of acupuncture over 4 weeks. Their symptoms were evaluated using the Total Symptom Score (TSS) and Michigan Neuropathy Screening Instrument (MNSI) at baseline and 4 weeks after the last treatment. Results Mean TSS scores reduced from 7.99 (SD 3.55) at baseline to 4.95 (SD 4.41), at the 8-week follow-up—a statistically non-significant change (p=0.057). The MNSI scores improved from 6.33 (SD 1.31) before treatment to 4.33 (SD 3.00) after acupuncture treatment—a significant improvement (p=0.010). One participant experienced an exacerbation of diabetic neuropathy symptoms, but two patients gained complete relief of their diabetic peripheral neuropathy (DPN) symptoms. Conclusions The results of this study justify further investigations into the effects of acupuncture on DPN.

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Chitneni, Ahish, Adam Rupp, Joe Ghorayeb, and Alaa Abd-Elsayed. "Early Detection of Diabetic Peripheral Neuropathy by fMRI: An Evidence-Based Review." Brain Sciences 12, no. 5 (April 26, 2022): 557. http://dx.doi.org/10.3390/brainsci12050557.

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With the significant rise in the prevalence of diabetes worldwide, diabetic peripheral neuropathy (DPN) remains the most common complication among type 1 and 2 diabetics. The adverse sequelae of DPN, which include neuropathic pain, diabetic foot ulcers and lower-limb amputations, significantly impact quality of life and are major contributors to the biopsychosocial and economic burden of diabetes at the individual, societal and health system levels. Because DPN is often diagnosed in the late stages of disease progression by electromyography (EMG), and neuropathic pain as a result of DPN is difficult to treat, the need for earlier detection is crucial to better ascertain and manage the condition. Among the various modalities available to aid in the early detection of DPN, functional magnetic resonance imaging (fMRI) has emerged as a practical tool in DPN imaging due to its noninvasive radiation-free nature and its ability to relate real-time functional changes reflecting the local oxygen consumption of regions of the CNS due to external stimuli. This review aims to summarize the current body of knowledge regarding the utility of fMRI in detecting DPN by observing central nervous system (CNS) activity changes among individuals with DPN when compared to controls. The evidence to date points toward a tendency for increased activity in various central neuroanatomical structures that can be detected by fMRI and positively correlates with diabetic neuropathic pain.

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Stalin, Chandrasekeran, V. Gunasekaran, and G. Jayabalan. "Evaluation of Neuroprotective Effect of Ficus benghalensis against Alloxan Induced Diabetic Neuropathy in Rats." International Journal of Pharmacology, Phytochemistry and Ethnomedicine 4 (August 2016): 52–60. http://dx.doi.org/10.18052/www.scipress.com/ijppe.4.52.

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Neuropathic pain in diabetics is characterized by both hyperalgesia and allodynia. This is attributed to both uncontrolled glycemia and the further complications which it leads to. The objective of the study was to evaluate the neuroprotective effect of methanolic leaf extract of Ficus benghalensis against alloxan induced diabetic neuropathy in rats.Material and methods:Experimental diabetes was induced in wistar albino rats by single intraperitoneal injection of Alloxan monohydrate (150 mg/kg). The methanolic extract of leaves of Ficus benghalensis at a dose of 200 and 400 mg/kg body weight was administered at single dose per day to diabetes induced rats for a period of 28 days. Neuropathic pain was assessed in diabetic rats with various painful procedures. hot and cold water tail immersion test, pinprick test, cold allodynia, hot plate test, actophotometer and rota-rod tests were performed to assess the degree of thermal, mechanical, cold hyperalgesia and locomotor activity as well as motor co-ordination.Results:Animals treated with methanolic extract of Ficus benghalensis (200, and 400 mg/kg p.o.) showed good results in different parameters such as thermal allodynia (hot and cold), thermal hyperalgesia and motor co-ordination in comparison with diabetic control group. Thus, from this study we conclude that Ficus benghalensis exhibits significant neuroprotective activities against Alloxan-induced diabetic neuropathy in rats.

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Unal-Cevik, Isin, Diclehan Orhan, Nazire Pinar Acar-Ozen, and Elmas Burcu Mamak-Ekinci. "Small Fiber Functionality in Patients with Diabetic Neuropathic Pain." Pain Medicine 22, no. 9 (April 23, 2021): 2068–78. http://dx.doi.org/10.1093/pm/pnab150.

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Abstract Objectives Diabetic neuropathic pain is associated with small fiber neuropathy. We aimed to assess the functionality of small fibers in patients with diabetes by using a practical method. Design Patients with impaired glucose tolerance (IGT), diabetic neuropathic pain (DNP), type II diabetes mellitus without neuropathic pain, and healthy control were included. Axon-reflex flare responses were induced by the intradermal application of capsaicin and histamine at the distal leg. The associated flare characteristics (flare areas and flare intensities) were recorded by using Laser Speckle Contrast Analysis (LASCA). The pain and itch responses were rated while performing LASCA. To verify the structural properties of the small fibers, proximal and distal skin biopsies were performed. Results DN4, MNSI, NRS, evoked-burning pain scores, and HbA1c levels were the highest in the DNP group. Compatible with length-dependent neuropathy, the distal skin PGP9.5-positive intraepidermal nerve fiber densities (IENFDs) were the lowest, whereas TRPV1-positive IENFDs were the highest in patients with DNP. The distal leg LASCA data showed hypo-functionality in both patients with IGT and DNP and association with disease severity. Conclusions There is an unmet need to practically assess the functionality of small fibers in patients with pain. In this study, a practical and objective method that does not need special expertise for the measurement of the functional properties of small fibers by using axon-flare responses is presented. The LASCA method could potentially facilitate a practical, quick (within 5 minutes), and very early diagnosis of small fiber hypo-functionality in both patients with IGT and DNP.

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Feng, Yi. "The Different Dynamic Changes of Nerve Growth Factor in the Dorsal Horn and Dorsal Root Ganglion Leads to Hyperalgesia and Allodynia in Diabetic Neuropathic Pain." May 2017 4, no. 20;4 (May 10, 2017): E551—E561. http://dx.doi.org/10.36076/ppj.2017.e561.

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Background: Diabetic peripheral neuropathy (DPN) is the most common complication of diabetes and more than half of the patients with DPN have self-reported symptoms referring to painful diabetic neuropathy (PDN). Nerve growth factor (NGF) is a key factor for the nervous system, but the role of it in the neuropathic pain of diabetic patients is unclear. Objective: This study aimed to investigate the relationship between the dynamic expression of NGF in dorsal horn and dorsal root ganglion (DRG) of diabetic rats and hyperalgesia and allodynia in diabetic neuropathic pain. It also aimed to explore the effects of exogenous mouse NGF (mNGF) on NGF expression in dorsal horn, DRG, and mechanical pain threshold. Study Design: Animal research study. Setting: Experimental research laboratory. Methods: The model of diabetes was established by a single intraperitoneal injection of streptozocin (STZ 55 mg/kg). Firstly, the rats were randomly divided into 2 groups: control group (n = 10) and diabetes group (n = 40). The diabetes group contained 4 subgroups: diabetes week 1 group (DM1, n = 10), diabetes week 2 group (DM2, n = 10), diabetes week 4 group (DM4, n = 10), and diabetes week 8 group (DM8, n = 10). Then, the other rats were randomly divided into 2 groups: control group (n = 10) and treatment group (n = 30). The treatment group contained 3 subgroups: saline group (n = 10), low dose mNGF group (mNGF1, n = 10), and high dose mNGF group (mNGF2, n = 10). Mechanical pain threshold was assessed using Von Frey hairs, before the establishment of the diabetes model and 1, 2, 4, and 8 weeks after the establishment. The NGF expression in dorsal horn and DRG was measured by western blot. Results: The mechanical pain threshold decreased one week after the establishment of the diabetes model, which continued for 8 weeks. The NGF expression in the dorsal horn was reduced 2 weeks after diabetes induction and the decreased NGF expression continued for 4 weeks. However, the NGF expression in DRG was reduced one week after diabetes induction and remained at a low level for 8 weeks. Hyperalgesia occurred when the NGF expression in the DRG decreased and further reduction in the NGF expression in the dorsal horn caused concomitant allodynia. The mechanical pain threshold was significantly elevated 2 weeks after mNGF treatment. Limitations: The course of diabetes should be much longer and there is not a precise analysis of the quantitative relation between the NGF expression in the dorsal horn/DRG and hyperalgesia/ allodynia. Conclusion: In diabetic neuropathic pain, the dynamic changes of the NGF expression in dorsal horn and DRG is involved in the development of hyperalgesia and allodynia respectively. Exogenous mNGF may relieve diabetic neuropathic pain by increasing the NGF expression in dorsal horn and DRG. Key words: Nerve growth factor, diabetic peripheral neuropathy, pain, hyperalgesia, allodynia, dorsal horn, dorsal root ganglion Pain Physician 2017; 20:E551

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Sood, Ankita, Bimlesh Kumar, Sachin Kumar Singh, Pankaj Prashar, Anamika Gautam, Monica Gulati, Narendra Kumar Pandey, et al. "Flavonoids as Potential Therapeutic Agents for the Management of Diabetic Neuropathy." Current Pharmaceutical Design 26, no. 42 (December 12, 2020): 5468–87. http://dx.doi.org/10.2174/1381612826666200826164322.

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Flavonoids are secondary metabolites that are widely distributed in plants. These phenolic compounds are classified into various subgroups based on their structures: flavones, flavonols, isoflavones, flavanones, and anthocyanins. They are known to perform various pharmacological actions like antioxidant, anti-inflammatory, anticancer, antimicrobial, antidiabetic and antiallergic, etc. Diabetes is a chronic progressive metabolic disorder that affects several biochemical pathways and leads to secondary complications such as neuropathy, retinopathy, nephropathy, and cardiomyopathy. Among them, the management of diabetic neuropathy is one of the major challenges for physicians as well as the pharmaceutical industries. Naturally occurring flavonoids are extensively used for the treatment of diabetes and its related complications due to their antioxidant properties. Moreover, flavonoids inhibit various pathways that are involved in the progression of diabetic neuropathy like the reduction of oxidative stress, decrease in glycogenolysis, increase glucose utilization, decrease in the formation of advanced glycation end products, and inhibition of the α-glucosidase enzyme. This review entails current updates on the therapeutic perspectives of flavonoids in the treatment of neuropathic pain. This manuscript explains the pathological aspects of neuropathic pain, the chemistry of flavonoids, and their application in amelioration of neuropathic pain through preclinical studies either alone or in combination with other therapeutic agents.

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Mokhtar, Nazarine, Marcin Drop, Florian Jacquot, Sylvain Lamoine, Eric Chapuy, Laetitia Prival, Youssef Aissouni, et al. "The Constitutive Activity of Spinal 5-HT6 Receptors Contributes to Diabetic Neuropathic Pain in Rats." Biomolecules 13, no. 2 (February 15, 2023): 364. http://dx.doi.org/10.3390/biom13020364.

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Diabetic neuropathy is often associated with chronic pain. Serotonin type 6 (5-HT6) receptor ligands, particularly inverse agonists, have strong analgesic potential and may be new candidates for treating diabetic neuropathic pain and associated co-morbid cognitive deficits. The current study addressed the involvement of 5-HT6 receptor constitutive activity and mTOR signaling in an experimental model of diabetic neuropathic pain induced by streptozocin (STZ) injection in the rat. Here, we show that mechanical hyperalgesia and associated cognitive deficits are suppressed by the administration of 5-HT6 receptor inverse agonists or rapamycin. The 5-HT6 receptor ligands also reduced tactile allodynia in traumatic and toxic neuropathic pain induced by spinal nerve ligation and oxaliplatin injection. Furthermore, both painful and co-morbid cognitive symptoms in diabetic rats are reduced by intrathecal delivery of a cell-penetrating peptide that disrupts 5-HT6 receptor-mTOR physical interaction. These findings demonstrate the deleterious influence of the constitutive activity of spinal 5-HT6 receptors upon painful and cognitive symptoms in diabetic neuropathic pains of different etiologies. They suggest that targeting the constitutive activity of 5-HT6 receptors with inverse agonists or disrupting the 5-HT6 receptor-mTOR interaction might be valuable strategies for the alleviation of diabetic neuropathic pain and cognitive co-morbidities.

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Yosifova, Lili, Evgenia Vladeva та Mira Siderova. "EFFECTS OF MLS-LASER ON NEUROPATHIC PAIN IN DIABETIC SENSОMOTOR NEUROPATHY". Journal of IMAB - Annual Proceeding (Scientific Papers) 29, № 3 (8 вересня 2023): 5079–84. http://dx.doi.org/10.5272/jimab.2023293.5079.

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About 20-50 % of patients with diabetes and about 60 % of those with diabetic neuropathy develop neuropathic pain, which is characterized by tingling, burning, sharp, shooting, or stabbing sensations, and even electric shock-like sensations. Painful diabetic neuropathy can significantly affect the quality of life of patients with diabetes, the ability to perform daily activities and negatively affect mood. According to the 2021 consensus of an international panel of experts regarding the treatment of painful distal symmetric polyneuropathy, non-pharmacological forms of treatment should also be considered due to unsatisfactory pharmacotherapy. A number of studies have demonstrated the role of photobiomodulation as a non-pharmacological method of treating painful diabetic neuropathy. The purpose of this placebo-controlled, longitudinal study was to investigate the effect of high-energy MLS-laser therapy on neuropathic pain. Material and methods: A total of 69 cases of patients with type 2 diabetes and painful diabetic neuropathy of the lower extremities were followed, divided into two groups: an experimental - 41 patients received high-energy laser radiation and a control (placebo) group - 28 patients, with a "mock" laser treatment. For objectification of pain, the Bulgarian version of the short form of the McGill pain questionnaire, version SF-MPQ-2, which includes the visual analog scale (VAS), was used. Comparisons between groups were performed with parametric or non parametric tests depending on the distribution of the variables, the number of the compared groups and the study pre test – post test design. Results: The pain index, reported by the McGill questionnaire, in the experimental group, decreased by - 63.2 % at the end of the nine-day treatment and by - 56.1 % at the 90th day after the start of treatment compared to the value before therapy. In the control group, there was a minimal change at the end of treatment (day 21), which did not persist until the end of the observation period (day 90). Conclusions: MLS laser therapy significantly increases the pain threshold and should be considered a safe, non-pharmacological adjunct to standard therapy in patients with painful diabetic peripheral neuropathy.

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Rosenberger, Daniela C., Vivian Blechschmidt, Hans Timmerman, André Wolff, and Rolf-Detlef Treede. "Challenges of neuropathic pain: focus on diabetic neuropathy." Journal of Neural Transmission 127, no. 4 (February 8, 2020): 589–624. http://dx.doi.org/10.1007/s00702-020-02145-7.

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Lee-Kubli, Corinne A., XiaJun Zhou, Corinne G. Jolivalt, and Nigel A. Calcutt. "Pharmacological Modulation of Rate-Dependent Depression of the Spinal H-Reflex Predicts Therapeutic Efficacy against Painful Diabetic Neuropathy." Diagnostics 11, no. 2 (February 11, 2021): 283. http://dx.doi.org/10.3390/diagnostics11020283.

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Impaired rate-dependent depression (RDD) of the spinal H-reflex occurs in diabetic rodents and a sub-set of patients with painful diabetic neuropathy. RDD is unaffected in animal models of painful neuropathy associated with peripheral pain mechanisms and diabetic patients with painless neuropathy, suggesting RDD could serve as a biomarker for individuals in whom spinal disinhibition contributes to painful neuropathy and help identify therapies that target impaired spinal inhibitory function. The spinal pharmacology of RDD was investigated in normal rats and rats after 4 and 8 weeks of streptozotocin-induced diabetes. In normal rats, dependence of RDD on spinal GABAergic inhibitory function encompassed both GABAA and GABAB receptor sub-types. The time-dependent emergence of impaired RDD in diabetic rats was preceded by depletion of potassium-chloride co-transporter 2 (KCC2) protein in the dorsal, but not ventral, spinal cord and by dysfunction of GABAA receptor-mediated inhibition. GABAB receptor-mediated spinal inhibition remained functional and initially compensated for loss of GABAA receptor-mediated inhibition. Administration of the GABAB receptor agonist baclofen restored RDD and alleviated indices of neuropathic pain in diabetic rats, as did spinal delivery of the carbonic anhydrase inhibitor acetazolamide. Pharmacological manipulation of RDD can be used to identify potential therapies that act against neuropathic pain arising from spinal disinhibition.

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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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ten Hoope, Werner, Markus W. Hollmann, Kora de Bruin, Hein J. Verberne, Arie O. Verkerk, Hanno L. Tan, Camiel Verhamme, et al. "Pharmacodynamics and Pharmacokinetics of Lidocaine in a Rodent Model of Diabetic Neuropathy." Anesthesiology 128, no. 3 (March 1, 2018): 609–19. http://dx.doi.org/10.1097/aln.0000000000002035.

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Abstract Background Clinical and experimental data show that peripheral nerve blocks last longer in the presence of diabetic neuropathy. This may occur because diabetic nerve fibers are more sensitive to local anesthetics or because the local anesthetic concentration decreases more slowly in the diabetic nerve. The aim of this study was to investigate both hypotheses in a rodent model of neuropathy secondary to type 2 diabetes. Methods We performed a series of sciatic nerve block experiments in 25 Zucker Diabetic Fatty rats aged 20 weeks with a neuropathy component confirmed by neurophysiology and control rats. We determined in vivo the minimum local anesthetic dose of lidocaine for sciatic nerve block. To investigate the pharmacokinetic hypothesis, we determined concentrations of radiolabeled (14C) lidocaine up to 90 min after administration. Last, dorsal root ganglia were excised for patch clamp measurements of sodium channel activity. Results First, in vivo minimum local anesthetic dose of lidocaine for sciatic nerve motor block was significantly lower in diabetic (0.9%) as compared to control rats (1.4%). Second, at 60 min after nerve block, intraneural lidocaine was higher in the diabetic animals. Third, single cell measurements showed a lower inhibitory concentration of lidocaine for blocking sodium currents in neuropathic as compared to control neurons. Conclusions We demonstrate increased sensitivity of the diabetic neuropathic nerve toward local anesthetics, and prolonged residence time of local anesthetics in the diabetic neuropathic nerve. In this rodent model of neuropathy, both pharmacodynamic and pharmacokinetic mechanisms contribute to prolonged nerve block duration.

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Jaya, Made Krisnaadi, and Nimade Oka Dwicandra. "EFFECTIVITY ANALYSIS OF NEUROPROTECTOR (VITAMIN B COMPLEX AND MECOBALAMIN) AS NEUROPATHIC PAIN SUPPORTIVE THERAPY IN ELDERLY WITH TYPE 2 DIABETES MELLITUS." Asian Journal of Pharmaceutical and Clinical Research 10, no. 12 (December 1, 2017): 320. http://dx.doi.org/10.22159/ajpcr.2017.v10i12.21845.

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Objective: Neuroprotector (Vitamin B complex or mecobalamin)is often used as a supportive neuropathic pain therapy. The effectiveness of this drug remains controversial, especially in geriatrics with Type 2 diabetic neuropathy pains. The aim of this study was to compare the diabetes neuropathic pain reduction in elderly with and without neuroprotective supplementation.Method: The study was conducted by prospective cohort design. 132 agings were observed during 4 weeks at Neurology Polyclinic, Sanglah Public Hospital, Denpasar, Bali-Indonesia. Individuals undergoing the first-line neuropathic pain therapy who received neuroprotector supplementation were included in the exposure group (66 individuals), while those not receiving neuroprotective supplementations were included in the nonexposure group (66 individuals). The pain scores were measured by numeric rating scales instruments. The measured outcome was a decrease in diabetic neuropathic pain scores.Result: Both groups showed reduce on pain scores statistically different compared to baseline pain score (p<0.05). The comparison head-to-head on neuroprotector supplementation group showed significantly greater to reduce the pain score compared to nonexposure group (p<0.05). The relative risk of pain score reduction more than 2 units was 1.37 (confidence interval [CI]95%: 1.05-1.80)and the number need to treat was 5 (CI 95%: 3-28) compared to nonexposure group.Conclusion: Individuals who are undergoing the first-line neuropathic pain therapy and getting Vitamin B complex or mecobalamin supplementation had decreased pain intensity better than without supplementation therapy.

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Sima, Anders A. F. "Neuropathology of Diabetic Neuropathic Pain." Journal of Neuropathic Pain & Symptom Palliation 1, no. 1 (January 2005): 97–99. http://dx.doi.org/10.3109/j426v01n01_15.

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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." Medicine 99, no. 47 (November 20, 2020): e23244. http://dx.doi.org/10.1097/md.0000000000023244.

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SULLIVAN, MICHELE G. "Diabetic Neuropathic Pain Requires Perseverance." Family Practice News 36, no. 11 (June 2006): 23. http://dx.doi.org/10.1016/s0300-7073(06)73282-0.

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Akter, Nazma. "Diabetic Peripheral Neuropathy: Epidemiology, Physiopathology, Diagnosis and Treatment." Delta Medical College Journal 7, no. 1 (March 19, 2019): 35–48. http://dx.doi.org/10.3329/dmcj.v7i1.40619.

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Diabetic peripheral neuropathy (DPN) is a common complication of both type 1 and type 2 diabetes. It affects over 90% of the diabetic patients. It is widely accepted that the toxic effects of hyperglycemia play an important role in the development of this complication, but several other hypotheses have been postulated. It is typically characterized by significant deficits in tactile sensitivity, vibration sense, lower-limb proprioception, and kinesthesia. Painful DPN has been shown to be associated with significant reductions in overall quality of life, increased levels of anxiety and depression, sleep impairment, and greater gait variability. DPN is often misdiagnosed and inadequately treated. Clinical recognition of DPN is imperative for allowing timely symptom management to reduce the morbidity associated with this condition. The management of diabetic neuropathic pain consists basically in excluding other causes of painful peripheral neuropathy, improving glycemic control as a prophylactic therapy and using medications to alleviate pain. First line drugs for pain relief include anticonvulsants, such as pregabalin and gabapentin and antidepressants, especially those that act to inhibit the reuptake of serotonin and noradrenaline. In addition, there is experimental and clinical evidence that opioids can be helpful in pain control, mainly if associated with first line drugs. Other agents, including for topical application, such as capsaicin cream and lidocaine patches, have also been proposed to be useful as adjuvant in the control of diabetic neuropathic pain, but the clinical evidence is insufficient to support their use. The purpose of this review is to examine proposed mechanisms of DPN, summarize current treatment regimen. A better understanding of the mechanisms underlying diabetic neuropathic pain will contribute to the search of new therapies. Delta Med Col J. Jan 2019 7(1): 35-48

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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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Davydov, O. S. "Principles of effective management of neuropathic pain in primary care." Clinical pharmacology and therapy 37, no. 2 (May 21, 2023): 37–42. http://dx.doi.org/10.32756/0869-5490-2023-2-37-42.

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Neuropathic pain caused by disease or damage affecting the somatosensory nervous system is a common problem in the primary care patients. Neuropathic pain can occur in postherpetic neuralgia, Guillain-Barré syndrome, neuroborreliosis, painful diabetic neuropathy, rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, Sjögren's syndrome, after trauma, due to cancer, stroke, etc. The treatment of neuropathic pain involves a comprehensive multimodal approach using pharmacotherapy with antidepressants and anticonvulsants, the most convenient of which is gabapentin, pathogenetic therapy of the underlying disease and non-pharmacological methods. Only integrated approach can provide effective therapy and improve the quality of life of patients with neuropathic pain.

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M. Ben Lafqih, N. Idrissi Dafali, S. Rafi, G. El Mghari, and N. EL Ansari. "Neuropathic pain in patients with diabetes: Utility of DN4 questionnaire." World Journal of Advanced Research and Reviews 17, no. 1 (January 30, 2023): 093–96. http://dx.doi.org/10.30574/wjarr.2023.17.1.1466.

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Diabetic neuropathy is a common complication of diabetes. The objective of our study is to evaluate the prevalence of diabetic neuropathy via the DN4 questionnaire in our diabetic patients and to identify the factors associated with diabetic neuropathy. We included 231 diabetic patients. The average age of the patients was 45.77 years, 67.1% of women, 36.8% type 1 diabetic and 63.2% type 2 diabetic, The average duration of diabetes evolution was 7, 21 years old. The average HbA1c was 10.4%. The prevalence of diabetic neuropathy in our study was 28.1%, it was more frequent in women, in unbalanced patients, and it was significantly correlated with age, type 1 diabetes, consumption of alcohol and duration of diabetes, in our study we found a significant association of diabetic neuropathy with age, duration of diabetes and alcohol consumption

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Nupoor, N. Bhambid, and Gopalkrishna Sripriya. "Interventions to reduce diabetic peripheral neuropathy complaints in type II diabetes mellitus patients: a systematic review." i-manager’s Journal on Nursing 11, no. 4 (2022): 38. http://dx.doi.org/10.26634/jnur.11.4.18373.

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Diabetic neuropathy is the most common complication of diabetes, likely to affect every segment of the central nervous system. Studies have shown that 30 - 40% of diabetics show symptoms of diabetic peripheral neuropathy. About 70% of patients who suffer from diabetes show some degree of neuropathy. Appropriate interventions to reduce diabetic peripheral neuropathy complaints are important in type II diabetic mellitus patients. The purpose of this systematic review is to identify the interventions to reduce diabetic peripheral neuropathy complaints in type II diabetes mellitus patients. The literature search was confined to the English language from 2001 - 2021. Several databases were searched to find relevant studies, including PubMed, Embase, Science direct, Medline and Web of Science for systematic reviews. All quantitative studies whose aim was to reduce diabetic peripheral neuropathy complaints by using non pharmacological interventions were included. Interventional studies with at least one outcome related to pain or sensory perception due to diabetic peripheral neuropathy were included in the review. The search identified 225 articles. After removing duplicate articles, 190 articles were picked out from the search. Each of the articles was screened out for titles and abstracts of 190 studies. Among these, 140 articles were excluded for various reasons. Hence, the “full text” of the 50 articles was evaluated for eligibility. Most of the articles, i.e., 42 articles were excluded due to absence of resonance with the subject matter and were not relevant to the topic. The remaining 8 articles were finally included in the review. Interventions to minimise diabetic peripheral neuropathy symptoms in type 2 diabetes mellitus patients were proposed in this review. The majority of the interventions focused on foot massage for neuropathic pain, and the typical intervention lasted 2 - 8 weeks, with a significant reduction in pain perception in individuals with type 2 diabetic peripheral neuropathy.

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Hussain, Mazhar, Muhammad Arshad Qureshi, Abdul Qudoos Arain, and Habib-Ur Rehman. "TYPE 2 DIABETIC PATIENTS." Professional Medical Journal 25, no. 11 (November 10, 2018): 1689–95. http://dx.doi.org/10.29309/tpmj/18.4812.

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Background: Peripheral neuropathic pain is a devastating complication intype 2 diabetic patients with significant morbidity and mortality. Objectives: To investigate theeffect of oral vitamin D supplementation on symptoms of peripheral neuropathic pain in type 2diabetic patients. Study Design: Prospective randomized placebo controlled trial. Setting:Diabetic Clinic of Sheikh Zayed Medical College/Hospital Rahim Yar Khan. Period: Overa period of 6 months from Jan-July 2017. Methods: 116 vitamin D deficient type 2 diabeticpatients with symptoms of peripheral neuropathic pain were divided in to two groups toprescribed either oral vitamin D3 capsule 50000IU weekly or Placebo capsule for a periodof 12 weeks. Symptoms of diabetic neuropathic pain were assessed by neuropathysymptoms score (NSS) and neuropathy disability score (NDS) while Vitamin D status wasestimated by measuring the serum total 25(OH) D concentration. The primary end pointwas changes in NSS and NDS while secondary end point was changes in HbA1C and 25(OH) D concentrations from baseline. Results: After 12 weeks of vitamin D therapy, vitaminD improved its own level in interventional group (28.5±12.5 to 48.2±15.6) vs placebo group(30.6±16.2 to31.5±12.6) with p-value (0.001). This rise was accompanied by improvementin HbAIc (8.2±1.8 to 7.5±2.2) vs Placebo (7.8±1.5 to 8.0±1.8) with p-value (0.004) and NSSscore (6.02±1.5 to 4.52±0.8) vs placebo (5.82 ±1.8 to 5.65±1.5) with p-value (0.002). Howeverno significant changes were seen in NDS in both study groups. Conclusion: Oral vitamin D3therapy has positive impact on its own status as well as symptoms of peripheral neuropathicpain in type 2 diabetic patients.

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Jain, Rakesh. "Pain and the Brain: Diabetic Neuropathic Pain." Journal of Clinical Psychiatry 69, no. 8 (August 15, 2008): e22. http://dx.doi.org/10.4088/jcp.0808e22.

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Gawel, Weronika, Sylwia Zdun, Klaudia Walczak, Zuzanna Wesołowska, and Przemysław Jędruszczak. "Mirogabalin - the use of a new gabapentinoid in the treatment of diabetic neuropathy and postherpetic neuropathy and other conditions." Quality in Sport 9, no. 1 (January 20, 2023): 53–62. http://dx.doi.org/10.12775/qs.2023.09.01.007.

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Introduction: Mirogabalin is a new drug from the gabapentinoid group first registered in Japan in 2019. It has found use in the treatment of peripheral neuropathic pain in diabetic neuropathy and postherpetic neuropathy. Purpose: In this article, we review studies on the efficacy and safety of mirogabalin in the treatment of registered indications and its potentially new applications. Materials and Methods: We reviewed the literature available in the PubMed database, using the key words: "mirogabalin", "neuropathy" "pregabalin". Results: Mirogabalin has been registered for the treatment of neuropathic pain in diabetic neuropathy and postherpetic neuropathy. The literature shows that it is effective and safe in the above-mentioned indications. Its use has also been described: in the treatment of neuropathic pain of other etiologies with intolerance to pregabalin, as a coanalgesic in the treatment of pain in the course of cancer, and in neuropathy caused by chemotherapy. It has been shown to be effective in all of the aforementioned cases. Studies have shown no clinically significant effect of mirogabalin in the symptomatic treatment of fibromyalgia pain. It has a good safety profile and a low number of adverse effects. Conclusions:. Mirogabalin is a drug that has the potential to improve the efficacy of treatment of neuropathic pain due to various causes. There is a need to continue conducting studies on larger groups of patients in order to make wider use of its potential in clinical practice.

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Corbett, Cynthia F. "Practical Management of Patients With Painful Diabetic Neuropathy." Diabetes Educator 31, no. 4 (July 2005): 523–40. http://dx.doi.org/10.1177/0145721705278800.

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Purpose Painful diabetic neuropathy (PDN) has a significant impact on patients’ quality of life, affecting sleep, mood, mobility, ability to work, interpersonal relationships, overall self-worth, and independence. The purpose of this article is to provide diabetes educators with current and essential tools for PDN assessment and management. Methods Medline and CINAHL database searches identified publications on the assessment and treatment of PDN. Identified research was evaluated, and information pertinent to diabetes educators was summarized. Results Recent advancements in assessment of neuropathic pain include identifying characteristics that distinguish between neuropathic and nonneuropathic pain. In the absence of treatment, research demonstrates that nerve damage may progress while pain diminishes. Many disease-modifying and symptom-management treatment options are available. Conclusion Good glycemic control is the first priority for both prevention and management of PDN. However, even with good glycemic control, up to 20% of patients will develop PDN. PDN recognition and assessment are critical to optimize management. Although several treatment modalities are available, few patients obtain complete pain relief. Recent advances in understanding the mechanisms underlying neuropathic pain should lead to better treatment and patient outcomes. Combination therapy, including nonpharmacologic modalities, may be required. Research evaluating the efficacy of combination therapy is needed.

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