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1

Lagueny, A., and A. Vital. "Neuropatie tossiche." EMC - Neurologia 8, no. 4 (January 2008): 1–9. http://dx.doi.org/10.1016/s1634-7072(08)70521-x.

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Said, G. "Neuropatie diabetiche." EMC - Neurologia 10, no. 1 (January 2010): 1–9. http://dx.doi.org/10.1016/s1634-7072(10)70501-8.

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Camdessanché, J. P., and J. C. Antoine. "Neuropatie sensitive." EMC - Neurologia 15, no. 2 (April 2015): 1–7. http://dx.doi.org/10.1016/s1634-7072(15)70522-2.

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Bidot, S., and C. Vignal-Clermont. "Neuropatie ottiche." EMC - AKOS - Trattato di Medicina 15, no. 1 (March 2013): 1–6. http://dx.doi.org/10.1016/s1634-7358(13)63940-6.

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Turčanová Koprušáková, Monika, and Egon Kurča. "Paraproteinaemic neuropathies." Neurologie pro praxi 17, no. 1 (February 1, 2016): 28–33. http://dx.doi.org/10.36290/neu.2016.006.

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Mazanec, Radim, Daniel Baumgartner, and Veronika Potočková. "Toxic neuropathies." Neurologie pro praxi 18, no. 1 (March 1, 2017): 20–24. http://dx.doi.org/10.36290/neu.2017.059.

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Banach, Marta, Judyta K. Juranek, and Jakub Antczak. "Drug-induced neuropathies." Family Medicine & Primary Care Review 4 (2015): 284–88. http://dx.doi.org/10.5114/fmpcr/60395.

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8

Serratrice, G., J. P. Azulay, and J. F. Pellissier. "Neuropatie ereditarie sensibili alla pressione (neuropatia tomaculare o allantoidea)." EMC - Neurologia 10, no. 1 (January 2010): 1–7. http://dx.doi.org/10.1016/s1634-7072(10)70502-x.

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9

Saïd, G. "Neuropatie delle vasculiti." EMC - Neurologia 10, no. 4 (January 2010): 1–5. http://dx.doi.org/10.1016/s1634-7072(10)70493-1.

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Kerschen, P., and V. Planté-Bordeneuve. "Neuropatie amiloidi familiari." EMC - Neurologia 12, no. 1 (April 2012): 1–12. http://dx.doi.org/10.1016/s1634-7072(12)60703-x.

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Lozeron, P. "Neuropatie delle ipoglicemie." EMC - Neurologia 15, no. 3 (August 2015): 1–3. http://dx.doi.org/10.1016/s1634-7072(15)72179-3.

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Adam, C., and M. Quirins. "Neuropatie delle vasculiti." EMC - Neurologia 15, no. 4 (November 2015): 1–7. http://dx.doi.org/10.1016/s1634-7072(15)73992-9.

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Mazanec, Radim, Jana Neupauerová, Daniel Baumgartner, Veronika Potočková, Petra Laššuthová, Dana Šafka-Brožková, and Pavel Seeman. "Hereditary motor neuropathies." Neurologie pro praxi 17, no. 6 (December 1, 2016): 354–58. http://dx.doi.org/10.36290/neu.2016.074.

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Boček, Václav, and Ivana Štětkářová. "Neuropathies due to ethanol abuse." Neurologie pro praxi 19, no. 3 (July 1, 2018): 172–74. http://dx.doi.org/10.36290/neu.2018.093.

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15

Fockens, E., F. Fatehi, and S. Attarian. "Neuropatie ereditarie da ipersensibilità alla pressione (neuropatia tomaculare o allantoidea)." EMC - Neurologia 18, no. 4 (April 2018): 1–8. http://dx.doi.org/10.1016/s1634-7072(18)41292-5.

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Bednařík, Josef. "Chronic inflammatory demyelinating neuropathy." Neurologie pro praxi 17, no. 1 (February 1, 2016): 16–21. http://dx.doi.org/10.36290/neu.2016.004.

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Kraus, Josef, Ivana Perníková, and Marie Brožová. "Peripheral neuropathy in children." Neurologie pro praxi 19, no. 3 (July 1, 2018): 175–82. http://dx.doi.org/10.36290/neu.2018.021.

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18

Havlová, Klára. "Peripheral neuropathy from the perspective of a urologist." Urologie pro praxi 17, no. 1 (February 1, 2016): 11–13. http://dx.doi.org/10.36290/uro.2016.003.

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19

Psimaras, D., D. Ricard, and J. Y. Delattre. "Neuropatie periferiche e cancri solidi." EMC - Neurologia 12, no. 4 (November 2012): 1–10. http://dx.doi.org/10.1016/s1634-7072(12)63279-6.

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20

Planté-Bordeneuve, V. "Introduzione agli aspetti genetici delle neuropatie." EMC - Neurologia 8, no. 3 (January 2008): 1–11. http://dx.doi.org/10.1016/s1634-7072(08)70524-5.

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21

Adams, D., P. Lozeron, M. Théaudin, C. Adam, and C. Lacroix. "Neuropatie periferiche nel corso delle disglobulinemie." EMC - Neurologia 11, no. 4 (January 2011): 1–14. http://dx.doi.org/10.1016/s1634-7072(11)70699-7.

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Planté-Bordeneuve, V., and H. Salhi. "Introduzione sugli aspetti genetici delle neuropatie." EMC - Neurologia 15, no. 3 (August 2015): 1–11. http://dx.doi.org/10.1016/s1634-7072(15)72178-1.

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23

Rosińska, Justyna, Maria Łukasik, and Wojciech Kozubski. "Neuropatie w przebiegu zakażeń wirusami pierwotnie hepatotropowymi." Neurologia i Neurochirurgia Polska 46, no. 3 (2012): 263–70. http://dx.doi.org/10.5114/ninp.2012.28916.

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24

Saïd, G., and P. Chemouilli. "Neuropatie periferiche nell’infezione da virus dell’immunodeficienza umana." EMC - Neurologia 10, no. 3 (January 2010): 1–5. http://dx.doi.org/10.1016/s1634-7072(10)70496-7.

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Delmont, E., and S. Attarian. "Neuropatie motorie multifocali con blocco della conduzione." EMC - Neurologia 17, no. 3 (August 2017): 1–7. http://dx.doi.org/10.1016/s1634-7072(17)85563-x.

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26

Kowalska, Berta, and Iwona Sudoł‑Szopińska. "Ultrasound assessment of selected peripheral nerves pathologies. Part II: Entrapment neuropathies of the lower limb." Journal of Ultrasonography 12, no. 51 (December 30, 2012): 463–71. http://dx.doi.org/10.15557/jou.2012.0033.

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27

Metelka, Rudolf, Lubica Cibičková, Jaromíra Gajdová, and Ondřej Krystyník. "Heart rate variability evaluation in the assessment of cardiac autonomic neuropathy in patients with type 2 diabetes." Cor et Vasa 60, no. 4 (August 1, 2018): e335-e344. http://dx.doi.org/10.1016/j.crvasa.2017.05.001.

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28

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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29

Alalwee, Azza, Jonathan D. LeSar, Mina Ghassemi, Eugene Cheng, Steven Stuto, Lawrence Osher, Scott Bastian, Vincent J. Hetherington, and Jill Kawalec. "Foot Temperature Trends in Normal, Diabetic, and Neuropathic Foot Populations." Journal of the American Podiatric Medical Association 106, sp1 (January 1, 2016): 5. http://dx.doi.org/10.7547/8750-7315-2016.1.alalwee.

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INTRODUCTION AND OBJECTIVES: Patients with underlying peripheral neuropathy are subject to changes in foot temperature. (1,2) Of the many forms of neuropathy that affect the lower extremity, the most notable are those types associated with diabetes. The aim of this study was to look for differences in temperatures between uncomplicated diabetic, diabetic neuropathic, and non-diabetic neuropathic feet. METHODS: The feet of 75 subjects were divided into 3 groups: 1) normal (n=50 feet), 2) diabetic (n=50 feet), and 3) neuropathic (n=49 feet). The neuropathic group was further subdivided into diabetic neuropathies (n=20 feet) and non-diabetic neuropathies (n=29 feet). To properly assign subjects to groups, all participants underwent vibratory threshold testing with a biothesiometer. In addition, all diabetic subjects had added glycosylated hemoglobin (hemoglobin A1C) studies performed. Temperature measurements were recorded at nine distinct foot locations (six plantar and three dorsal). Data was statistically analyzed using the Kruskal-Wallis test. RESULTS: For five of the plantar pedal sites tested, temperatures in the diabetic foot were significantly greater than those for the normal controls (p<0.05). At most sites, temperatures in the diabetic foot population tended to be higher than those in both diabetic and non-diabetic neuropathic feet, with the differences between the diabetic foot and non-diabetic neuropathic foot being statistically significant at one dorsal and five plantar sites. Patients in the non-diabetic neuropathic group were not stratified according to their specific neuropathic types. CONCLUSIONS: Diabetic feet, with and without neuropathy, tend to be warmer than the feet of patients with other non-diabetic neuropathies. The finding of no statistical difference between non-neuropathic diabetic and neuropathic diabetic feet is unexpected in that a number of these patients were projected to have an autonomic system component. These null findings suggest the need to further investigate neuropathy solely determined by sensory testing versus tests for autonomic system involvement.
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30

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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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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32

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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33

Said, Gérard. "Focal and multifocal diabetic neuropathies." Arquivos de Neuro-Psiquiatria 65, no. 4b (December 2007): 1272–78. http://dx.doi.org/10.1590/s0004-282x2007000700037.

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Diabetic neuropathy is the most common neuropathy in industrialized countries, with a remarkable range of clinical manifestations. The vast majority of the patients with clinical diabetic neuropathy have a distal symmetrical form that progress following a fiber-length dependent pattern, with predominant sensory and autonomic manifestations. This pattern of neuropathy is associated with a progressive distal axonopathy. Patients are exposed to trophic changes in the feet, pains and autonomic disturbances. Less often, diabetic patients may develop focal and multifocal neuropathy that includes cranial nerve involvement, limb and truncal neuropathies. This neuropathic pattern tends to occur after 50 years of age, mostly in patients with longstanding diabetes mellitus. The LDDP does not show any trend to improvement and either relentlessly progresses or remain relatively stable over years. Conversely the focal diabetic neuropathies, which are often associated with inflammatory vasculopathy on nerve biopsies, remain self limited, sometimes after a relapsing course.
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Giorgio, Cristina, Mara Zippoli, Pasquale Cocchiaro, Vanessa Castelli, Giustino Varrassi, Andrea Aramini, Marcello Allegretti, Laura Brandolini, and Maria Candida Cesta. "Emerging Role of C5 Complement Pathway in Peripheral Neuropathies: Current Treatments and Future Perspectives." Biomedicines 9, no. 4 (April 7, 2021): 399. http://dx.doi.org/10.3390/biomedicines9040399.

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The complement system is a key component of innate immunity since it plays a critical role in inflammation and defense against common pathogens. However, an inappropriate activation of the complement system is involved in numerous disorders, including peripheral neuropathies. Current strategies for neuropathy-related pain fail to achieve adequate pain relief, and although several therapies are used to alleviate symptoms, approved disease-modifying treatments are unavailable. This urgent medical need is driving the development of therapeutic agents for this condition, and special emphasis is given to complement-targeting approaches. Recent evidence has underscored the importance of complement component C5a and its receptor C5aR1 in inflammatory and neuropathic pain, indicating that C5a/C5aR1 axis activation triggers a cascade of events involved in pathophysiology of peripheral neuropathy and painful neuro-inflammatory states. However, the underlying pathophysiological mechanisms of this signaling in peripheral neuropathy are not fully known. Here, we provide an overview of complement pathways and major components associated with dysregulated complement activation in peripheral neuropathy, and of drugs under development targeting the C5 system. C5/C5aR1 axis modulators could represent a new strategy to treat complement-related peripheral neuropathies. Specifically, we describe novel C5aR allosteric modulators, which may potentially become new tools in the therapeutic armory against neuropathic pain.
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35

Devi, Fryda Liana. "Manajemen Nyeri Neuropatik." Jurnal Penelitian Perawat Profesional 3, no. 1 (February 19, 2021): 179–88. http://dx.doi.org/10.37287/jppp.v3i1.370.

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Diketahui jutaan orang di seluruh dunia telah mengalami nyeri neuropatik yang diperkirakan terjadi pada sebanyak 7% dari populasi. Nyeri neuropatik merupakan salah satu jenis nyeri yang timbul akibat adanya lesi atau gangguan primer pada susunan saraf. Nyeri ini dapat terjadi akibat berbagai gangguan, seperti penyakit infeksi, trauma, radikulopati dan kerusakan di sistem endokrin. Tujuan dari literature review iniadalah untuk meninjau lebih lanjut terkait masalah nyeri neuropatik yang umum terjadi sehingga dapat diketahui langkah manajemen masalah ini dengan tepatdi masyarakat.Metode. Penelitian ini merupakan studi literature review yang melibatkan sebanyak 21 sumber pustaka. Kata kunci yang digunakan dalam penelusuran yaitu ‘neuropathic pain dan management dengan tahun terbit antara 2009-2020. Abstrak dan full text jurnal dibaca dan dicermati, kemudian dilakukan analisis terhadap isi yang terdapat dalam tujuan penelitian dan hasil/temuan penelitian. Hasil. Berbagai penelitian menunjukkan farmakoterapi sering kali merupakan salah satu langkah yang efektif yang dapat dengan cepat memberikan dasar untuk implementasi komponen lain dari manajemen nyeri, seperti modalitas terapi fisik dan keterampilan koping pasien.Pendekatan multidisiplin dan multimodal dalam manajemen nyeri neuropati dapat meredakan derajat nyeri untuk sebagian besar pasien yang menderita nyeri neuropati. Beberapa jenis obat yang direkomendasikan dalam pengobatan nyeri neuropatik, antara lain golongan obat anti-depresan, antikonvulsan, obat topikal dan golongan analgetik.
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36

Kowalska, Berta, and Iwona Sudoł‑Szopińska. "Ultrasound assessment on selected peripheral nerve pathologies. Part I: Entrapment neuropathies of the upper limb – excluding carpal tunnel syndrome." Journal of Ultrasonography 12, no. 50 (September 30, 2012): 307–18. http://dx.doi.org/10.15557/jou.2012.0016.

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37

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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38

Seneczko, Franciszek. "Dziedziczne neuropatie czuciowe i autonomiczne – patogeneza, klinika i leczenie. Część II: typy II, IV i V." Dermatologia Praktyczna 10, no. 3 (August 30, 2017): 5. http://dx.doi.org/10.26625/2017.10.3.01.

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Należące do grupy neuropatii czuciowych i autonomicznych (HSAN) typy II, IV i V wykazują zróżnicowania genetyczne, anatomiczne, fi zjologiczne oraz dotyczące obrazów klinicznych. Istotę HSAN2 stanowi głównie upośledzenie funkcji neuronów obwodowych; czuciowych i autonomicznych. Objawy kliniczne rozwijają się w okresie noworodkowym lub we wczesnym dzieciństwie. Również w dzieciństwie ujawnia się HSAN4, ze względu na dominujące objawy zwana także wrodzoną obojętnością na ból z anhydrozą. Z kolei HSAN5, klasyfi kowana jako obojętność na ból z częściową anhydrozą, wykazuje objawy kliniczne podobne do występujących w HSAN4, ale o łagodniejszym przebiegu.
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Ticse, Ray, Renán Pimentel, Pilar Mazzeti, and Jaime Villena. "Elevada frecuencia de neuropatía periférica en pacientes con Diabetes mellitus tipo 2 de un hospital general de Lima-Perú." Revista Medica Herediana 24, no. 2 (June 8, 2013): 114. http://dx.doi.org/10.20453/rmh.v24i2.593.

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Objetivos: Determinar la frecuencia de neuropatía periférica en pacientes con diabetes mellitus tipo 2 y la correlación entre la evaluación clínica con el estudio de la velocidad de conducción nerviosa (VCN). Material y métodos: Estudio descriptivo, transversal. Se evaluaron 62 pacientes con diagnóstico de diabetes mellitus tipo 2. Se utilizó el Michigan Neuropathy Screening Instrument (MNSI), el Michigan Diabetic Neuropatic Score (MDNS) y el estudio de VCN. Además se describieron las variables demográficas, antropométricas y de laboratorio. Resultados: La frecuencia de neuropatía periférica fue 96,8% según la VCN y 45% según el MNSI. La correlación entre el número de nervios afectados según VCN y el score MDNS fue moderada (Spearman r=0,59; p<0,001). Conclusiones: Existe una elevada frecuencia de neuropatía periférica en los pacientes diabéticos evaluados y no hubo buena correlación entre VCN y el score MDNS.
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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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Suturkova, Ljubica, Katerina Brezovska, Ana Poceva-Panovska, Aleksandra Grozdanova, and Sladjana Knezevic Apostolski. "Glycoconjugates as target antigens in peripheral neuropathies." Macedonian Pharmaceutical Bulletin 60, no. 02 (2014): 21–27. http://dx.doi.org/10.33320/maced.pharm.bull.2014.60.02.002.

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Identification and characterization of antigens present at the human peripheral nerve is a great challenge in the field of neuroimmunology. The latest investigations are focused on the understanding of the biology of glycoconjugates present at the peripheral nerve, and their immunological reactivity. Increased titers of antibodies that recognize carbohydrate determinants of glycoconjugates (glycolipids and glycoproteins) are associated with distinct neuropathic syndromes. There is considerable cross-reactivity among anti-ganglioside antibodies, resulting from shared oligosaccharide epitopes, possibly explaining the overlap in syndromes observed in many affected patients. Sera from patients with neuropathies (GBS, chronic inflammatory demielynating polyneuropathy - CIDP, multifocal motor neuropathy - MMN), cross-react with glycoproteins isolated from human peripheral nerve and from Campylobacter jejuni O:19. The frequency of occurrence of antibodies against these glycoproteins is different, depending of the type of neuropathy. Identification of the cross-reactive glycoproteins and possible additional auto antigens could be useful in laboratory evaluation of peripheral neuropathies and help to develop a more effective therapeutic approach.
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42

Beydoun, Said R. "Letter from the Editor-in-Chief." US Neurology 13, no. 01 (2017): 12. http://dx.doi.org/10.17925/usn.2017.13.01.12.

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Said R Beydoun, M.D., Professor and Division Chief, Neuromuscular Disorders, at the Department of Neurology at Keck Medicine of USC, University of Southern California. He is Program Director of the ACGME-accredited Clinical Neurophysiology Fellowship, which trains three physicians each year. As a principal investigator, Dr. Beydoun has participated in various research clinical trials. His clinical and research areas of expertise are in the fields of neuropathy, diabetic neuropathies, neuropathic pain and immune-mediated neuromuscular disorders, such as CIDP, multifocal motor neuropathy and myasthenia gravis. He has been published in several scientific journals on topics related to neuromuscular diseases and neuropathies. He is an elected fellow of the American Academy of Neurology and a fellow of the American Association of Neuromuscular and Electrodiagnostic Medicine. He is a member of the advisory board and the scientific committee of the Myasthenia Gravis Foundation of California. He holds board certification by the American Board of Psychiatry and Neurology in Neurology, Clinical Neurophysiology, Pain Medicine, and Neuromuscular Medicine.
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43

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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Capone, Flávia Varela, Danielle de Araújo Torres, and Marco Antonio de M. T. de Lima. "Neuropatia auditiva: alerta aos pediatras." Revista Paulista de Pediatria 29, no. 4 (December 2011): 669–73. http://dx.doi.org/10.1590/s0103-05822011000400030.

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OBJETIVO: Alertar os pediatras sobre a neuropatia auditiva, doença descrita recentemente e ainda desconhecida por muitos médicos. Descrever seus fatores de risco, características clínicas e diagnósticas, com a finalidade de possibilitar uma intervenção terapêutica precoce e eficaz. FONTES DE DADOS: Realizada pesquisa nas bases de dados PubMed, Lilacs e SciELO utilizando os descritores "neuropatia auditiva" e "auditory neuropathy", entre os anos de 1996 e 2010. SÍNTESE DOS DADOS: A neuropatia auditiva, também conhecida como dessincronia auditiva, descrita em 1996, caracteriza-se clinicamente pela dificuldade na compreensão das palavras, mesmo em casos de perdas auditivas leves ou moderadas. Foi relacionada a diversas neuropatias generalizadas e fatores de risco neonatais, como internação em terapia intensiva, hiperbilirrubinemia, sepse e hipóxia. Após suspeita clínica, o diagnóstico é confirmado pela presença das emissões otoacústicas associada a um potencial evocado auditivo de tronco encefálico ausente ou alterado. Sua terapêutica permanece controversa, tendo como opções a protetização auditiva, o acompanhamento fonoterápico para habilitação ou reabilitação da linguagem e, em casos de insucesso, há relatos de resultados satisfatórios com o implante coclear. CONCLUSÕES: Enfatiza-se a importância do reconhecimento pelo pediatra da neuropatia auditiva, entidade ainda pouco citada na literatura latino-americana da especialidade.
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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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Enax-Krumova, Elena, Nadine Attal, Didier Bouhassira, Rainer Freynhagen, Janne Gierthmühlen, Per Hansson, Bianca M. Kuehler, et al. "Contralateral Sensory and Pain Perception Changes in Patients With Unilateral Neuropathy." Neurology 97, no. 4 (May 19, 2021): e389-e402. http://dx.doi.org/10.1212/wnl.0000000000012229.

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ObjectiveTo test whether contralateral sensory abnormalities in the clinically unaffected area of patients with unilateral neuropathic pain are due to the neuropathy or pain mechanisms.MethodsWe analyzed the contralateral clinically unaffected side of patients with unilateral painful or painless neuropathy (peripheral nerve injury [PNI], postherpetic neuropathy [PHN], radiculopathy) by standardized quantitative sensory testing following a validated protocol. Primary outcome was the independent contribution of the following variables on the contralateral sensory function using generalized linear regression models: pain intensity, disease duration, etiology, body area, and sensory patterns in the most painful area.ResultsAmong 424 patients (PNI n = 256, PHN n = 78, radiculopathy n = 90), contralateral sensory abnormalities were frequent in both painful (n = 383) and painless (n = 41) unilateral neuropathy, demonstrating sensory loss for thermal and mechanical nonpainful stimuli and both sensory loss and gain for painful test stimuli. Analysis by etiology revealed contralateral pinprick hyperalgesia in PHN and PNI. Analysis by ipsilateral sensory phenotype demonstrated mirror-image pinprick hyperalgesia in both mechanical and thermal hyperalgesia phenotypes. Pain intensity, etiology, and affected body region predicted changes in only single contralateral somatosensory parameters. Disease duration had no impact on the contralateral sensory function.ConclusionMechanisms of sensory loss seem to spread to the contralateral side in both painful and painless neuropathies. Contralateral spread of pinprick hyperalgesia was restricted to the 2 ipsilateral phenotypes that suggest sensitization; this suggest a contribution of descending net facilitation from supraspinal areas, which was reported in rodent models of neuropathic pain but not yet in human patients.
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47

Dubey, Divyanshu, Vanda A. Lennon, Avi Gadoth, Sean J. Pittock, Eoin P. Flanagan, John E. Schmeling, Andrew McKeon, and Christopher J. Klein. "Autoimmune CRMP5 neuropathy phenotype and outcome defined from 105 cases." Neurology 90, no. 2 (December 8, 2017): e103-e110. http://dx.doi.org/10.1212/wnl.0000000000004803.

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ObjectiveTo establish the phenotype and clinical outcomes of collapsin response-mediator protein-5 (CRMP5) autoimmune neuropathy in comparison with anti-neuronal nuclear antibody type 1 (ANNA1)–immunoglobulin G (IgG) neuropathy.MethodsPatients with CRMP5-IgG and/or ANNA1-IgGs were identified in our service-line testing, and medical records were reviewed.ResultsOne hundred five patients with CRMP5-IgG neuropathy (88% smokers; 69% having cancer, most commonly small cell lung cancer [75%]) were identified and compared to 51 patients with ANNA1-IgG neuropathy, 27 with coexisting CRMP5-IgG. Patients with CRMP5 had painful axonal polyradiculoneuropathy (65%), mostly asymmetric onset (84%), with neuropathy predating cancer diagnosis by 185 days (range 60–540 days). Most cases (79%) had moderate to severe neuropathic pain, all on neuropathic medications (median 2, range 1–4), opioids in 39%. Nerve biopsies (n = 2) showed microvascular inflammation with axonal degeneration. Compared to ANNA1 alone, CRMP5 neuropathy has a higher prevalence of pain (79% vs 46%, p = 0.008), asymmetric polyradiculoneuropathy (54% vs 12%, p < 0.001), and inflammatory spinal fluids (elevated CSF protein or nucleated cell count 92% vs 60%, p = 0.022). Cerebellar ataxia (21%), myelopathy (19%), and optic neuritis and/or retinitis (11%) were common neurologic accompaniments. CRMP5 cases had significant pain reduction by immunotherapy (p < 0.001). Specifically, high-dose corticosteroid administration was associated with improvement/stabilization in neuropathy impairment scores (p = 0.012) (Class IV). Patients with CRMP5 had better 5-year survival than patients with ANNA1 (67% vs 32%, p = 0.012).ConclusionPainful axonal asymmetric polyradiculoneuropathy is established as the major CRMP5 autoimmune neuropathy presentation and is distinguishable from other paraneoplastic neuropathies, including by ANNA1 autoimmunity. Patients with this phenotype should be prompted for CRMP5-IgG testing to assist in early cancer diagnosis.
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48

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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Simanjuntak, Galvani Volta, and Marthalena Simamora. "Lama menderita diabetes mellitus tipe 2 sebagai faktor risiko neuropati perifer diabetik." Holistik Jurnal Kesehatan 14, no. 1 (April 22, 2020): 96–100. http://dx.doi.org/10.33024/hjk.v14i1.1810.

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Sensory neuropathy in type 2 diabetes mellitus and its correlation with duration of diseaseBackground: Diabetic peripheral neuropathy is a complication of type 2 diabetes mellitus (T2DM) that results in harm to the nervous system. It is a progressive disease, and symptoms get worse over time.Purpose: To exploration the sensory neuropathy in type 2 diabetes mellitus and its correlation with duration of disease.Method: An observational analytic with cross sectional design with population was patients with T2DM without diabetic ulcers in diabetic clinic Sari Mutiara Hospital. The number of samples was 86 respondents by a simple random sampling. Measuring the risk of diabetic peripheral neuropathy used 10 gram monofilament.Results: Showed the majority of the duration of T2DM >5 years (53,5%) and the majority of respondents had neuropathy (54,7%). The results of the Spearman rank correlation test showed that there was a significant correlation between duration of T2DM and risk of diabetic peripheral neuropathy (p-value = 0,023 and r= -0,438). Conclusion: The majority respondents has a diabetic peripheral neuropathy and also has a risk of diabetic peripheral neuropathy who are suffering >5 years. It is recommended that they need a regularly asses and educate to prevent further complication.Keywords: Sensory neuropathy; Type 2 diabetes mellitus; Duration of diseasePendahuluan: Neuropati perifer diabetes adalah komplikasi diabetes yang mengakibatkan kerusakan sistem saraf. Ini adalah penyakit progresif, dan gejalanya bertambah buruk seiring waktu.Tujuan: Untuk mengetahui hubungan lama menderita dengan risiko neuropati pada pasien DM tipe 2.Metode: Desain analitik korelasi dengan pendekatan cross sectional dan populasinya seluruh pasien DM tipe 2 yang tidak memiliki ulkus diabetik di klinik diabetes RSU Sari Mutiara. Sampelnya sebanyak 86 yang diambil dengan teknik simple random sampling. Risiko neuropati perifer diabetik diukur menggunakan monofilament 10 gram.Hasil: Analisis data menunjukkan mayoritas pasien menderita DM tipe 2 yang >5 tahun (53,5%) dan mayoritas pasien telah mengalami neuropati (54,7%). Hasil uji statistik menggunakan korelasi spearman menunjukan adanya hubungan lama menderita DM tipe 2 dengan risiko neuropati (p-value = 0,023<0,05 dan nilai r = -0,438).Simpulan: Mayoritas responden yang mengalami Neuropati perifer diabetes maupun resiko terjadinya Neuropati perifer diabetes pada mereka kelompok yang menderita DM tipe 2 yang >5 tahun. Sangat dianjurkan pada pasien tersebut untuk dilakukan pengkajian secara teratur dan pendidikan untuk mencegah komplikasi lebih lanjut.
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Wilmshurst, Jo M., Robert A. Ouvrier, and Monique M. Ryan. "Peripheral nerve disease secondary to systemic conditions in children." Therapeutic Advances in Neurological Disorders 12 (January 2019): 175628641986636. http://dx.doi.org/10.1177/1756286419866367.

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This review is an overview of systemic conditions that can be associated with peripheral nervous system dysfunction. Children may present with neuropathic symptoms for which, unless considered, a causative systemic condition may not be recognized. Similarly, some systemic conditions may be complicated by comorbid peripheral neuropathies, surveillance for which is indicated. The systemic conditions addressed in this review are critical illness polyneuropathy, chronic renal failure, endocrine disorders such as insulin-dependent diabetes mellitus and multiple endocrine neoplasia type 2b, vitamin deficiency states, malignancies and reticuloses, sickle cell disease, neurofibromatosis, connective tissue disorders, bowel dysmotility and enteropathy, and sarcoidosis. In some disorders presymptomatic screening should be undertaken, while in others there is no benefit from early detection of neuropathy. In children with idiopathic peripheral neuropathies, systemic disorders such as celiac disease should be actively excluded. While management is predominantly focused on symptomatic care through pain control and rehabilitation, some neuropathies improve with effective control of the underlying etiology and in a small proportion a more targeted approach is possible. In conclusion, peripheral neuropathies can be associated with a diverse range of medical conditions and unless actively considered may not be recognized and inadequately managed.
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