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Journal articles on the topic 'Polyneuropaty'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Tawara, Satoru, Yukio Ando, Chie Furusawa, Taro Yamashita, Shuji Suko, Shinichi Ikegawa, Makoto Uchino, Masayuki Ando, and Shukuro Araki. "Variable eipressivity in Met-30 Japanese patients with familial amyloidotic polyneuropaty in kumamoto." Neuromuscular Disorders 6 (February 1996): S41. http://dx.doi.org/10.1016/0960-8966(96)88867-5.

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2

Acosta, F., J. Diaz, P. Parrilla, T. Fuente, R. Robles, P. Ramirez, and F. S. Bueno. "Plasma β-endorphin levels during orthotopic liver transplantation (OLT) in patients with familial amyloidotic polyneuropaty (FAP)." Neuromuscular Disorders 6 (February 1996): S74. http://dx.doi.org/10.1016/0960-8966(96)88919-x.

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3

Damjan, Igor, Milan Cvijanovic, and Marko Erak. "Importance of electromiographic examination in diagnostification and monitoring of chronic inflammatory demyelinating polyneuropathy." Medical review 63, no. 7-8 (2010): 559–64. http://dx.doi.org/10.2298/mpns1008559d.

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Introduction. Polyneuropathies or peripheral neuropathies present a dysfunction or disease of larger number of peripheral nerves or their dysfunction. Considering their morbidity - mortality characteristics they present an important aspect in daily clinical practice. One particular polyneuropathy that deserves special review is chronic inflammatory demyelinating polyneuropathy, which, due to its clinical - laboratory presentation, does not include the group of ?simple? neuropathies, thus requiring further examinations. Neurophysiological testing should be performed using the protocol for neuropathy examinations. Neurophysiological examination, during the electroneurographic examination, shows neurographic parameters referring to polyneuropatic demyelinating type of lesion, while the electromyographic finding records the presence of neuropathic lesions (denervation activity, great action potentials with a reduced sample). Case report. A 54-year-old patient was diagnosed to have a ?complicated? demyelinating polyneuropathy according to the clinical-laboratory findings and electromyographic examination. Exclusion criteria, targeted diagnostic examinations, considering the mentioned peripheral neuropathies, pointed to acute inflammatory demyelinating polyneuropathy. However, the chronic inflammatory demyelinating polyneuropathy was finally differentiated during the clinical and electromyographic monitoring. Conclusion. The presented case is interesting because it shows how one can ?wander? towards the diagnosis, which is eventually made on the basis of electromyographic examination and monitoring as well as according to exclusion criteria, which have differentiated the acute inflammatory demyelinating polyneuropathy from the chronic one.

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4

Hajaš, Gabriel. "Diabetic polyneuropathy." Neurologie pro praxi 19, no. 3 (July 1, 2018): 161–71. http://dx.doi.org/10.36290/neu.2018.003.

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5

Junkerová, Jana, and Eva Kovalová. "Cryptogenic Neuropathy - a retrospective analysis - Transthyretin-related familial amyloid polyneuropathy - differential diagnostic pathway." Neurologie pro praxi 21, no. 4 (September 8, 2020): 307–12. http://dx.doi.org/10.36290/neu.2020.089.

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6

Raputová, Jana, Eva Vlčková, Lenka Šmardová, Aneta Rajdová, and Andrea Janíková. "Chemotherapy-induced polyneuropathy." Neurologie pro praxi 18, no. 1 (March 1, 2017): 25–31. http://dx.doi.org/10.36290/neu.2017.129.

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7

Hanewinckel, Rens, Judith Drenthen, Vincentius J. A. Verlinden, Sirwan K. L. Darweesh, Jos N. van der Geest, Albert Hofman, Pieter A. van Doorn, and M. Arfan Ikram. "Polyneuropathy relates to impairment in daily activities, worse gait, and fall-related injuries." Neurology 89, no. 1 (May 31, 2017): 76–83. http://dx.doi.org/10.1212/wnl.0000000000004067.

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Objective:To extensively investigate the association of chronic polyneuropathy with basic and instrumental activities of daily living (BADL and IADL), falls, and gait.Methods:A total of 1,445 participants of the population-based Rotterdam Study (mean age 71 years, 54% women) underwent a polyneuropathy screening involving a symptom questionnaire, neurologic examination, and nerve conduction studies. Screening yielded 4 groups: no, possible, probable, and definite polyneuropathy. Participants were interviewed about BADL (Stanford Health Assessment questionnaire), IADL (Instrumental Activities of Daily Living scale), and frequency of falling in the previous year. In a random subset of 977 participants, gait was assessed with an electronic walkway. Associations of polyneuropathy with BADL and IADL were analyzed continuously with linear regression and dichotomously with logistic regression. History of falling was evaluated with logistic regression, and gait changes were evaluated with linear regression.Results:Participants with definite polyneuropathy had more difficulty in performing BADL and IADL than participants without polyneuropathy. Polyneuropathy related to worse scores of all BADL components (especially walking) and 3 IADL components (housekeeping, traveling, and shopping). Participants with definite polyneuropathy were more likely to fall, and these falls more often resulted in injury. Participants with polyneuropathy had worse gait parameters on the walkway, including lower walking speed and cadence, and more errors in tandem walking.Conclusions:Chronic polyneuropathy strongly associates with impairment in the ability to perform daily activities and relates to worse gait and an increased history of falling.

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8

CORONEL, BERNARD, ALAIN MERCATELLO, JEAN-CLAUDE COUTURIER, PIERRE-GEORGES DURAND, LAURENT HOLZAPFELL, PIERRE-LOUIS BLANC, and DOMINIQUE ROBERT. "Polyneuropathy." Critical Care Medicine 18, no. 5 (May 1990): 486–89. http://dx.doi.org/10.1097/00003246-199005000-00004.

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9

Visser, Nora A., Nicolette C. Notermans, Ferdinand Teding van Berkhout, Leonard H. van den Berg, and Alexander FJE Vrancken. "Chronic obstructive pulmonary disease is not a risk factor for polyneuropathy: A prospective controlled study." Chronic Respiratory Disease 14, no. 4 (March 15, 2016): 327–33. http://dx.doi.org/10.1177/1479972316636993.

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Polyneuropathy has been observed in patients with chronic obstructive pulmonary disease (COPD). If polyneuropathy occurs as a complication or extrapulmonary manifestation of COPD, one would expect an increased prevalence among patients with a cryptogenic axonal polyneuropathy. This case–control study aimed to investigate the association between COPD and polyneuropathy. We prospectively included 345 patients with cryptogenic axonal polyneuropathy and 465 controls. A standardized questionnaire assessed the presence of COPD and we verified this diagnosis by contacting the family physician. The severity of COPD was based on the Global Initiative for Chronic Obstructive Lung Disease classification. The prevalence of COPD did not differ between patients with polyneuropathy and controls (15/345 vs. 12/465 respectively; odds ratio (OR) 1.7; 95% confidence interval (CI) [0.8–3.7]). Adjusting for age, gender and possible confounders did not affect these results (adjusted OR 1.7, 95% CI 0.7–4.1). The severity of COPD was similar between patients with polyneuropathy and controls. This study does not support the hypothesis that COPD is a risk factor for polyneuropathy.

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10

Bril, Vera. "Status of Current Clinical Trials in Diabetic Polyneuropathy." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 28, no. 3 (August 2001): 191–98. http://dx.doi.org/10.1017/s0317167100001335.

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Peripheral polyneuropathy is the most frequent complication of diabetic mellitus. In spite of many clinical trials of different specific interventions for diabetic polyneuropathy, intensive glycemic control remains the only effective specific therapy currently available for this troublesome complication. This systematic overview reports the status of current clinical trials in diabetic polyneuropathy with an emphasis on those interventions directed towards specific pathophysiological derangements. A discussion of clinical trials of agents directed towards relieving painful symptoms of diabetic polyneuropathy concludes this overview.

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11

Terentyeva, N. V., N. K. Svyrydova, and Y. V. Ponomarenko. "The clinical and functional state of peripheral nervous system during the treatment of patients with diabetic polyneuropathy." East European Journal of Neurology, no. 1(1) (March 20, 2015): 30–32. http://dx.doi.org/10.33444/2411-5797.2015.1(1).30-32.

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The state of the peripheral nervous system and treat- ment of patients with diabetic polyneuropathy is global problem. To study the clinical and functional status of the peripheral nervous system in patients with diabetic distal polyneuropathy we have examined 30 patients with type 2 diabetes. Our research showed the importance of both clinical and electroneuromyographic examination for patients with diabetes who may have or do not to have objective evidence of polyneuropathy. This allows for early detection of initial effects of polyneuropathy and improve treatment tactics.

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12

Gonçalves, Helena. "Rastreio de Polineuropatia Diabética Periférica em Doentes Internados." Medicina Interna 26, no. 4 (December 11, 2019): 297–303. http://dx.doi.org/10.24950/rspmi/o/176/19/4/2019.

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13

Valli, Giorgio, Ornella Strada, and Carlo Pirovano. "Clinical and Neurophysiologic Features in Paraneoplastic Polyneuropathy." Tumori Journal 74, no. 2 (April 1988): 237–41. http://dx.doi.org/10.1177/030089168807400221.

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Three of 8,954 in- patients have been selected as affected by paraneoplastic polyneuropathy. In all of them the polyneuropathy had a steadily progressive course, with symptoms beginning in the lower limbs and spreading to the upper limbs in a few months. An increase in protein content of the cerebrospinal fluid was evident in each case. No other possible causes of polyneuropathy were found, and the association with malignancy was histologically proved in all 3 cases. A bronchogenic (« oat cell ») carcinoma was present in the first patient, who had an almost exclusively motor neuropathy. An osteosarcoma was diagnosed in the second case, and its association with a polyneuropathy seems to be exceptional. A sigmoid adenocarcinoma was discovered in the third patient. Neurophysiologic investigations were indicative of a polyneuropathy with predominant axonic involvement in all 3 cases.

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14

Ito, H., S. Tsukui, T. Kanda, T. Utsugi, T. Ohno, and M. Kurabayashi. "Angiotensin-Converting Enzyme Insertion/Deletion Polymorphism and Polyneuropathy in Type 2 Diabetes without Macroalbuminuria." Journal of International Medical Research 30, no. 5 (October 2002): 476–82. http://dx.doi.org/10.1177/147323000203000502.

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Angiotensin-converting enzyme (ACE) gene polymorphism is thought to be a potent risk factor for nephropathy and retinopathy in diabetes. We investigated the association between polyneuropathy and gene polymorphisms of both the ACE insertion/deletion (I/D) and angiotensinogen (AGT) M235T genes in 84 type 2 diabetic patients without macroalbuminuria (21 with polyneuropathy and 63 without). ACE genotype distribution did not differ significantly between patients with and without polyneuropathy, but the frequency of the I allele was significantly higher in those with polyneuropathy than in those without. In contrast, neither the genotype distribution nor the allele frequencies of the AGT gene differed between the two groups. In logistic regression analysis using a D-additive model, the D allele had a protective effect on polyneuropathy (odds ratio [OR], 0.34; 95% confidence interval [CI], 0.13–0.88). A D-dominant model hypothesis also gave a significant OR (0.28; 95% CI, 0.09–0.90). ACE I/D polymorphism, but not AGT M235T polymorphism, may affect polyneuropathy development in type 2 diabetes without macroalbuminuria.

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15

Himeno, Tatsuhito, Hideki Kamiya, Keiko Naruse, Zhao Cheng, Sachiko Ito, Taiga Shibata, Masaki Kondo, et al. "Angioblast Derived from ES Cells Construct Blood Vessels and Ameliorate Diabetic Polyneuropathy in Mice." Journal of Diabetes Research 2015 (2015): 1–17. http://dx.doi.org/10.1155/2015/257230.

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Background. Although numerous reports addressing pathological involvements of diabetic polyneuropathy have been conducted, a universally effective treatment of diabetic polyneuropathy has not yet been established. Recently, regenerative medicine studies in diabetic polyneuropathy using somatic stem/progenitor cell have been reported. However, the effectiveness of these cell transplantations was restricted because of their functional and numerical impairment in diabetic objects. Here, we investigated the efficacy of treatment for diabetic polyneuropathy using angioblast-like cells derived from mouse embryonic stem cells.Methods and Results. Angioblast-like cells were obtained from mouse embryonic stem cells and transplantation of these cells improved several physiological impairments in diabetic polyneuropathy: hypoalgesia, delayed nerve conduction velocities, and reduced blood flow in sciatic nerve and plantar skin. Furthermore, pathologically, the capillary number to muscle fiber ratios were increased in skeletal muscles of transplanted hindlimbs, and intraepidermal nerve fiber densities were ameliorated in transplanted plantar skin. Transplanted cells maintained their viabilities and differentiated to endothelial cells and smooth muscle cells around the injection sites. Moreover, several transplanted cells constructed chimeric blood vessels with recipient cells.Conclusions. These results suggest that transplantation of angioblast like cells induced from embryonic stem cells appears to be a novel therapeutic strategy for diabetic polyneuropathy.

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16

Girlanda, Paolo. "Acquired polyneuropathy." Clinical Neurophysiology 119 (May 2008): S48. http://dx.doi.org/10.1016/s1388-2457(08)60178-9.

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17

Portenoy, Russell K. "Painful Polyneuropathy." Neurologic Clinics 7, no. 2 (May 1989): 265–88. http://dx.doi.org/10.1016/s0733-8619(18)30813-2.

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18

Galer, Bradley S. "PAINFUL POLYNEUROPATHY." Neurologic Clinics 16, no. 4 (November 1998): 791–811. http://dx.doi.org/10.1016/s0733-8619(05)70098-0.

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19

McAuley, J. H., J. Fearnley, A. Laurence, and J. A. Ball. "Diphtheritic polyneuropathy." Journal of Neurology, Neurosurgery & Psychiatry 67, no. 6 (December 1, 1999): 825–26. http://dx.doi.org/10.1136/jnnp.67.6.825.

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20

Greene, Douglas, and Mark Brown. "Diabetic Polyneuropathy." Seminars in Neurology 7, no. 01 (March 1987): 18–29. http://dx.doi.org/10.1055/s-2008-1041402.

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21

Joob, Beuy, and Viroj Wiwanitkit. "Diphtheritic polyneuropathy." Journal of Pediatric Neurosciences 14, no. 3 (2019): 177. http://dx.doi.org/10.4103/jpn.jpn_136_18.

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22

Piradov, Michael A., Victor N. Pirogov, Lubov M. Popova, and Irina A. Avdunina. "Diphtheritic Polyneuropathy." Archives of Neurology 58, no. 9 (September 1, 2001): 1438. http://dx.doi.org/10.1001/archneur.58.9.1438.

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23

Krendel, David A. "Lymphomatous Polyneuropathy." Archives of Neurology 48, no. 3 (March 1, 1991): 330. http://dx.doi.org/10.1001/archneur.1991.00530150102026.

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24

Shields, Robert W. "Alcoholic polyneuropathy." Muscle & Nerve 8, no. 3 (March 1985): 183–87. http://dx.doi.org/10.1002/mus.880080302.

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25

JUNTUNEN, JUHANI. "Alcoholic Polyneuropathy." Acta Medica Scandinavica 218, S703 (April 24, 2009): 265–72. http://dx.doi.org/10.1111/j.0954-6820.1985.tb08922.x.

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26

Stirling, Sarah L., and Danny McAuley. "Acute polyneuropathy." Anaesthesia & Intensive Care Medicine 7, no. 4 (April 2006): 129–31. http://dx.doi.org/10.1383/anes.2006.7.4.129.

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27

Bakke, Lars. "URAEMIC POLYNEUROPATHY." Acta Neurologica Scandinavica 46, S43 (January 29, 2009): 205. http://dx.doi.org/10.1111/j.1600-0404.1970.tb02188.x.

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28

Schlotter-Weigel, B., and D. E. Pongratz. "Polyneuropathy - Treatment." DMW - Deutsche Medizinische Wochenschrift 127, no. 40 (October 2002): 2076–78. http://dx.doi.org/10.1055/s-2002-34517.

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29

Schlotter-Weigel, B., and D. E. Pongratz. "Polyneuropathy - Diagnostic." DMW - Deutsche Medizinische Wochenschrift 127, no. 40 (October 2002): 2072–75. http://dx.doi.org/10.1055/s-2002-34529.

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30

van Gijn, J. "Sensory polyneuropathy." Practical Neurology 6, no. 6 (December 1, 2006): 388–89. http://dx.doi.org/10.1136/jnnp.2006.106484.

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31

Schilling, F. "Rheumatic Polyneuropathy." Aktuelle Rheumatologie 27, no. 3 (June 2002): 155–57. http://dx.doi.org/10.1055/s-2002-33130.

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32

Armakov, Sergey. "Diabetic Polyneuropathy." Spravočnik vrača obŝej praktiki (Journal of Family Medicine), no. 6 (June 1, 2020): 33–38. http://dx.doi.org/10.33920/med-10-2006-04.

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Diabetes mellitus is a chronic disease that develops against the background of insulin deficiency as a result of a decrease in its production or impaired receptor perception by target cells. As a result of impaired glucose metabolism, a state of chronic hyperglycemia develops, which has a detrimental effect on a number of organs and systems. One of such systems that are negatively affected by an increase in glucose concentration against the background of a general violation of all types of metabolism is the nervous system, in particular, its peripheral part. Approximately every second patient with diabetes eventually develops a state of diabetic polyneuropathy (chronic sensorimotor polyneuropathy or distal symmetric polyneuropathy), which is characterized by progressive degeneration of peripheral nerves with the development of pain, motor disorders and loss of sensitivity.

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33

ZANGIABADI, MD, NASER, MOHAMAD NAEIM AHRARI, MD, and NOUZAR NAKHAEE, MD. "DIABETIC POLYNEUROPATHY;." Professional Medical Journal 15, no. 01 (March 10, 2008): 5–8. http://dx.doi.org/10.29309/tpmj/2008.15.01.2638.

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Introduction: Diabetes mellitus with the prevalence rate of 8.9-12.3% in human population,ultimately leads to the peripheral nervous system involvement in many patients. It causes various types ofpolyneuropathies which may manifest abnormalities such as impaired nerve conduction velocity (NCV) and prolongedF-wave latency. The aim of this study was to investigate the effect of omega-3 fatty acids on NCV and F-wave latency.Material and Methods: This clinical trial was performed on diabetic patients referring to the Diabetes Center of ShahidBahonar Hospital in Kerman/Iran. Subjects were randomly divided to Omega-3 and Control (no treatment) group.Patients in the case group received three capsules of omega-3 daily and for the duration of 12 weeks. NCV and F-wavelatency were determined in all patients before and after the treatment period. The rate of alterations in these variablesin the two groups was analyzed by using statistical tests. Results: Controlling for baseline NCV and F- wave latencymeasures, follow up results showed no significant difference between the Omega-3 and the no-treatment group inaccordance to somatic nerve measures. Conclusion: No significant difference in electro diagnostic indices was foundbefore and after Omega-3 administration. This result may be due to using the combination of docosahexaenoic acid(DHA) and eicosapentaenoic acid(EPA).Short term administration and lack of sufficient time for drug efficacy can beother probable reason. Further studies with the administration of pure forms of EPA or DHA and longer period ofadministration are suggested.

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34

Svyrydova, N. K., Y. V. Ponomarenko, and N. V. Terentyeva. "Clinical and functional status of the peripheral nervous system in patients with diabetic polyneuropathy." East European Journal of Neurology, no. 1(1) (March 20, 2015): 13–17. http://dx.doi.org/10.33444/2411-5797.2015.1(1).13-17.

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It seems impossible at the moment to stem the incidence of diabetes despite the enormous efforts to address this global problem. We have examined 30 patients with type 2 diabetes to study the clinical and functional status of the peripheral nervous system in patients with diabetic distal polyneuropathy. Our works showed the importance of both clinical and electroneuroneuromiographic examination of patients with diabetes who have or do not have objective manifestations of polyneuropathy. This allows for early detection of the initial effects of polyneuropathy. In patients with symptomatic stage of diabetic polyneuropathy, this method allows to establish the pattern, nature, and severity of lesions of fibers of peripheral nerve trunks.

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35

Khramilin, V. N. "Differential diagnosis of polyneuropathies in diabetes mellitus." Meditsinskiy sovet = Medical Council, no. 12 (September 19, 2021): 256–65. http://dx.doi.org/10.21518/2079-701x-2021-12-256-265.

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Diabetic polyneuropathy (DPN) is heterogeneous in its clinical course and clinical manifestations. Depending on the primary lesion of large or small nerve fibers, different onset, course and clinical manifestations of polyneuropathy are possible. In patients with diabetes, the incidence of associated lesions of the peripheral nervous system is high. When verifying the diagnosis of DPN, it is necessary to carry out a differential diagnosis with a number of diseases: paraneoplastic neuropathies, metabolic neuropathies, neuropathies in vasculitis, toxic neuropathies, autoimmune neuropathies, inflammatory neuropathies and hereditary neuropathies. Diabetes is not the only cause of polyneuropathy. Up to 50% of all cases of polyneuropathies in diabetes have additional causes. Diagnosis of diabetic polyneuropathy - diagnosis of exclusion. The development of polyneuropathy in patients with a duration of type 1 diabetes less than 5 years, the absence of nephropathy and / or retinopathy, asymmetry in symptoms and signs, the predominance of motor symptoms, beginning with upper limb lesions, rapid progression should justify the doctor for differential diagnostic search. You should also take into account the characteristics of the patient (old age, vegetarianism and alcohol use), medical and toxic effects (taking metformin> 3 years and> 2 g / day; cytostatics, chemotherapy, heavy metals), family history of neuropathy. Therapeutic tactics should be individualized and take into account the polyneuropathy polyetiology. The purpose of this review is to discuss the most common reasons peripheral neuropathy in diabetes mellitus. The differential diagnosis of the diabetic polyneuropathy is the focus of this article.

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36

Singhal, Neel S., Viktoriya S. Irodenko, Marta Margeta, and Robert B. Layzer. "Sarcoid polyneuropathy masquerading as chronic inflammatory demyelinating polyneuropathy." Muscle & Nerve 52, no. 4 (July 2, 2015): 664–68. http://dx.doi.org/10.1002/mus.24652.

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37

Adamová, Blanka, Eva Vlčková, Jana Raputová, Iva Šrotová, Ladislav Dušek, Jiří Jarkovský, and Josef Bednařík. "How are patients with painful diabetic polyneuropathy treated?" Neurologie pro praxi 18, no. 6 (December 1, 2017): 408–14. http://dx.doi.org/10.36290/neu.2017.118.

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38

Kopecká, Nela, and Edvard Ehler. "Neuropathic pain in a patient with autoimmune polyneuropathy (case report)." Neurologie pro praxi 19, no. 4 (September 1, 2018): 298–301. http://dx.doi.org/10.36290/neu.2018.039.

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39

Taha, Ahmed, Mohamed Taha, Roaa Ahmed, Gianna Meckler, Narothama Aeddula, and Jason Meckler. "Polyneuropathy: A Rare and Challenging Presentation of Essential Mixed Cryoglobulinemia." Journal of Investigative Medicine High Impact Case Reports 9 (January 2021): 232470962110265. http://dx.doi.org/10.1177/23247096211026503.

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A 49-year-old male presented with acute chronic sensory motor bilateral lower extremity polyneuropathy. Electromyography showed bilateral acute sensory motor axonal polyneuropathy. Lumbar spine magnetic resonance imaging showed diffuse bone marrow replacement and bilateral ankylosing spondylitis. Laboratory workup revealed elevated inflammatory markers and low G6PD (glucose-6-phosphate dehydrogenase) level. Due to elevated acute phase reactants, inflammatory polyneuropathy was suspected; patient was treated accordingly with resolution of neuropathy. Three months later, he relapsed and presented with disabling polyneuropathy and renal impairment, which prompted renal biopsy. Renal histopathology revealed the, otherwise mysterious, etiology, essential mixed cryoglobulinemia. Essential mixed cryoglobulinemia was not considered initially due to the absence of classic systemic manifestations of autoimmune disorders.

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40

Liang, Hudong, Lan Wu, Ling-ling Liu, Jinming Han, Jie Zhu, and Tao Jin. "A case report: Non-alcoholic Wernicke encephalopathy associated with polyneuropathy." Journal of International Medical Research 45, no. 6 (April 3, 2017): 1794–801. http://dx.doi.org/10.1177/0300060517699039.

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We report a rare case of non-alcoholic Wernicke encephalopathy (WE) with polyneuropathy. A 24-year-old woman who had recently served a 4-month prison sentence and underwent a short period of dieting manifested slow response, weakness, language disorder and amnesia. Brain magnetic resonance imaging (MRI) revealed typical lesions of WE. Examination of nerve conduction velocity revealed sensory-motor axonal polyneuropathy. The patient was immediately treated with thiamine. Neurological symptoms were alleviated in a few days and abnormal signals were markedly decreased in a follow-up MRI 1 week later. Polyneuropathy symptoms ameliorated during hospital therapy and significantly improved after 4 months. This case suggests that WE may be associated with polyneuropathy in non-alcoholic patients. Early thiamine treatment in symptomatic patients may improve prognosis.

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41

Grbovic, Vesna, Svetlana Djukic, Srdjan Stefanovic, Natasa Zdravkovic-Petrovic, Stefan Simovic, and Aleksandra Jurisic-Skevin. "The effects of combined physical procedures on the functional status of patients with diabetic polyneuropathy." Vojnosanitetski pregled, no. 00 (2021): 5. http://dx.doi.org/10.2298/vsp201124005g.

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Introduction: Diabetic polyneuropathy is a common chronic complication in patients with diabetes mellitus. This study aimed to determine the importance of applied physical procedures on the functional status in diabetic polyneuropathy patients in comparison to the group of respondents with the applied alpha-lipoic acid. Materials and Methods: 60 subjects were divided into two groups: group A - diabetic polyneuropathy patient?s treatment with physical procedures; and group B - diabetic polyneuropathy patient?s treatment with alpha-lipoic acid. The study protocol implied that the study has lasted for three diagnostic and therapeutic cycles, each lasting for 16 days with the time between cycles of 6 weeks. Results: Manual muscle test, range of motion, Michigan Neuropathy Screening Instrument and Berg balance scale values showed statistically significant improvement at the end of testing the group A respondents, while in the group B respondents there was not any improvement shown. Conclusions: The application of the combined physical procedures shows clear benefit for improvement of muscle strength and mobility of the ankle joint in respondents with diabetic polyneuropathy.

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42

Oblaukhova, Veronika I., Duma N. Svetlana, and Svetlana V. Mustafina. "Polyneuropathy on the background of thyrotoxicosis with thiamazole drug treatment." Clinical and experimental thyroidology 14, no. 3 (December 27, 2018): 156–61. http://dx.doi.org/10.14341/ket10012.

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The article is devoted to the clinical case of the development of toxic polyneuropathy in patients receiving thiamazole 25 mg per day in a 43-year-old patient with manifest thyrotoxicosis, which is clinically manifested by severe pain in the muscles of the upper and lower extremities; muscle weakness in the upper limbs. The patient, prescribed by a neurologist, was treated with carbamazepine-retard 400 mg per day for 1 month, and the attending physician decided to replace tiamazole with propylthiouracil 300 mg per day, followed by dose adjustment. The patient categorically refuses surgical treatment or treatment with radioactive iodine. The diagnosis of toxic polyneuropathy was confirmed during the differential diagnosis with inflammatory diseases of the joints and muscles, polyneuropathy on the background of thyrotoxicosis. In the outcome of the treatment, all neurological symptoms were stopped. The observation time on the occasion of polyneuropathy was 1 month, the total time of observation of the patient at the time of publication was 5 years. This clinical case demonstrates the possibility of the development of toxic polyneuropathy in patients receiving thiamazole in the treatment of thyrotoxicosis. Given the low frequency of this complication in clinical practice, it is necessary to draw additional attention of clinicians to this case and recommend including this condition in the differential diagnosis of polyneuropathy.

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Kuprina, N. I., O. A. Kochetova, V. V. Shilov, and E. V. Ulanovskaya. "Professional polyneuropathy: the state of the main arteries of the upper extremities." Russian Journal of Occupational Health and Industrial Ecology, no. 8 (September 25, 2019): 468–72. http://dx.doi.org/10.31089/1026-9428-2019-59-8-468-472.

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Introduction. Professional polyneuropathy of the upper extremities is an example of the most common pathology due to physical overload and functional overstrain of the muscles of the upper extremities.The aim of the study was to study the ultrasound quantitative parameters of the anatomical structures of the arteries in normal and professional polyneuropathy.Materials and methods. Patients with polyneuropathy from physical overloads and functional overvoltage in hospital were examined by ultrasound in B-mode. The results of ultrasonic assessment of the morphological state of the main arteries of the forearm in professional polyneuropathy from physical overload and functional overvoltage are presented. The criteria for the selection of patients in the study were: the presence of severe clinical manifestations of polyneuropathy, confirmed by instrumental methods of the study, the data of sanitary and hygienic characteristics of working conditions, indicating contact with physical overload in the workplace, the absence of chronic diseases of the cardiovascular system (coronary heart disease, rheumatic, oncological, infectious diseases, heart defects, arrhythmias and conduction).Results. The study of ultrasound morphological features of the arteries of the upper extremities in professional polyneuropathy showed an increase in the intima-media complex, compaction of the structure of the vascular wall equally in the radial and ulnar arteries. The revealed changes were determined with the same frequency in men and women. The study of the right and left hands showed the presence of more pronounced changes on the side of the «working hand».Conclusions. Today the method of ultrasound examination of the main arteries of the middle caliber of the upper extremities is the only available and objective method of studying the morphological changes of the vascular system in professional polyneuropathy from functional overvoltage and physical overload. In comparison with the control group in patients with polyneuropathy, a significant decrease in the diameter of the vessels was determined on the limb, which has a predominant load. Ultrasonic changes are detected at the initial stages of professional polyneuropathy of the upper extremities.

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Belskaya, G. N., and E. V. Sakharova. "Alcoholic polyneuropathy. Clinical forms and pathogenetically based approaches to therapy." Meditsinskiy sovet = Medical Council, no. 10 (August 12, 2021): 94–99. http://dx.doi.org/10.21518/2079-701x-2021-10-94-99.

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The number of cases of alcoholism in Russia is gradually decreasing, but still significantly affects the overall health indicators of the population. One of its frequent complications is alcoholic polyneuropathy. The article deals with the pathogenetic mechanisms of the occurrence and development of the disease, its forms, classification, and clinical picture. The damage to the nervous system in patients with alcoholism depends on the frequency of alcohol consumption, the dose, the type of drinks that were consumed, malnutrition, genetic predisposition and individual characteristics that determine the level of alcohol dehydrogenase and aldehyde dehydrogenase. In the clinical picture, a toxic form of alcoholic polyneuropathy is currently distinguished, associated with the direct effect of toxic alcohol metabolites on somatic and autonomic nerve fibers, thiamine deficiency, resulting from a deficiency of B vitamins, and mixed forms. According to the rate of development of clinical manifestations, there are acute forms of alcoholic polyneuropathy (thiamine deficiency) and chronic forms (toxic). The article discusses the possibilities of diagnostics using modern instrumental and laboratory methods of research, primarily electroneuromyography. With the help of this method of investigation, in alcoholic polyneuropathy, signs of axonal damage are most often detected, and in the thiamine-deficient form, it is possible to determine signs of secondary demyelination. The authors emphasize the importance of differential diagnosis with other pathologies. The article highlights the current understanding of the main therapeutic strategies, treatment options for patients with alcoholic polyneuropathy. Therapy of patients suffering from alcoholic polyneuropathy includes refusal of alcohol abuse, normalization of nutrition, medication. For drug therapy, B vitamins and antioxidants are used. The drug with a recognized antioxidant effect is alpha-lipoic acid. A clinical case was analyzed on the basis of our own clinical observation of a mixed form of alcoholic polyneuropathy.

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Thuringer, Amanda, Omar Jawdat, and Mazen Dimachkie. "Transthyretin Familial Amyloid Polyneuropathy Mimicking Chronic Inflammatory Demyelinating Polyneuropathy." RRNMF Neuromuscular Journal 1, no. 3 (July 17, 2020): 26–31. http://dx.doi.org/10.17161/rrnmf.v1i3.13677.

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Vasylieva, N. V., and I. I. Krychun. "PREGABALINS IN THE MANAGEMENT OF DIABETIC AND ALCOHOLIC POLYNEUROPATHY." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 21, no. 2 (June 17, 2021): 24–27. http://dx.doi.org/10.31718/2077-1096.21.2.24.

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Diseases of the peripheral nervous system are ranking a leading position among other neurological nosologies. And polyneuropathy is known as more prevalent and severe disease. Numerous scientific reports highlight issues on different pathological conditions in relation to polyneuropathy, and in particular intoxications, hypovitaminosis (isolated or as complications of certain pathological processes), infectious and hereditary diseases, paraneoplastic syndromes, metabolic disorders, allergic reactions. These diseases when uncontrolled or untreated may result in the development of complications, among which is polyneuropathy. The diagnosis of polyneuropathy is relatively not difficult, because the disease is manifested as distal symmetrical sensory and/or motor impairments with transient disorders of autonomic nervous system. Diabetic polyneuropathy, in particular, is a late complication of diabetes mellitus, which determines the prognosis of the disease. Alcoholic polyneuropathy in a form of acute, subacute or chronic current variants is caused by the combined effects of thiamine toxicity and vitamin deficiency. At the same time, dysmetabolic polyneuropathies differ by variability of clinical manifestations and the general developmental patterns of the nerve conduction block that is determined by the peculiarities of degenerative and regenerative processes under different pathogenetic factors. Differential diagnosis of polyneuropathies is mainly based on the detection of somatic pathology and the comparison of the dynamic changes in the course of the diseases and clinical manifestations. The study has demonstrated diabetic and alcoholic polyneuropathies have clear distinct clinical-neurophysiological patterns. The article also highlights the treatment outcomes of combination therapy with pregabalin for diabetic and alcoholic polyneuropathies.

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Utsugi, Shinichi, Miyoko Saito, and G. Diane Shelton. "Resolution of Polyneuropathy in a Hypothyroid Dog Following Thyroid Supplementation." Journal of the American Animal Hospital Association 50, no. 5 (September 1, 2014): 345–49. http://dx.doi.org/10.5326/jaaha-ms-6035.

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An 8 yr old male golden retriever was evaluated because of chronic, progressive, multiple neurologic signs. Physical examination showed marked obesity and facial swelling with a “tragic facial expression.” Neurologic evaluation revealed the dog had multiple cranial nerve deficits and lower motor neuron signs in the pelvic limbs. Serum biochemical analysis and thyroid function tests were consistent with hypothyroidism. A biopsy from the common peroneal nerve revealed a loss of myelinated fibers, inappropriately thin myelinated fibers, and resolving subperineurial edema. The diagnosis of polyneuropathy associated with hypothyroidism was made. Levothyroxine therapy was initiated. Response to levothyroxine treatment was slow, with most neurologic abnormalities persisting for >6 wk. However, the dog made a full neurologic recovery within 6 mo. Although the occurrence of polyneuropathy in dogs resulting from hypothyroidism has been controversial, the study authors demonstrated that hypothyroid polyneuropathy can occur in dogs as documented in humans. This is the first report describing long-term follow-up information together with detailed pathological features of hypothyroid polyneuropathy in a dog. In hypothyroid polyneuropathy, the response to thyroid replacement may be slow, but a recovery can be expected if treatment is initiated before peripheral nerve fiber loss becomes severe.

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Zilov, A. V. "Autonomic Diabetic Polyneuropathy Variants: Possible Correction." Doctor.Ru 20, no. 2 (2021): 60–66. http://dx.doi.org/10.31550/1727-2378-2021-20-2-60-66.

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Objective of the Review: To analyse the incidence of polyneuropathy in diabetic patients focusing on autonomic neuropathy. Key Points. Polyneuropathy is one of the most common delayed complications of diabetes mellitus (DM); the condition has numerous clinical aspects. Major polyneuropathy studies focus on assessment, prevention and management of pain caused by sensory and sensory-and-motor defects, prevention of ulceration and Charcot foot. At the same time, various autonomic neuropathy variants in diabetic patients have either been studied not thoroughly enough, or are outside of clinical interest. Still, prevention and pathogenic effect from autonomic neuropathy are similar to those used in other types of diabetic neuropathy. We describe major pathogenic links in nerve fibre damaging and clinical forms of autonomic neuropathy. Major studies of the use of α-lipoic acid in DM are presented. Conclusion. α-lipoic acid medications are efficient in slowing down various forms of autonomic neuropathy. Dose-dependent action of these medications, adequate therapy duration (at least 3 months as a course of medication), improved glycaemic control in patients with DM are essential for autonomic neuropathy prevention and slowing down. Keywords: diabetes mellitus; diabetic polyneuropathy; diabetic autonomic polyneuropathy; α-lipoic acid.

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Ehler -editor hlavního tématu, Edvard. "Polyneuropatie." Neurologie pro praxi 19, no. 3 (July 1, 2018): 160. http://dx.doi.org/10.36290/neu.2018.092.

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Chow, Frances, Leila Darki, and Said R. Beydoun. "The Challenge of Distinguishing POEMS from Chronic Inflammatory Demyelinating Polyneuropathy—Importance of Early Recognition and Diagnosis of POEMS." US Neurology 14, no. 2 (2018): 94. http://dx.doi.org/10.17925/usn.2018.14.2.94.

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POEMS is a rare syndrome characterized by the unique constellation of polyneuropathy, organomegaly, endocrinopathy, M-proteins, and skin changes. Correct diagnosis is often delayed in early stages of the syndrome when patients exhibit only isolated polyneuropathy due to the clinical and electrodiagnostic similarities with chronic inflammatory demyelinating polyneuropathy. We describe a case in which early suspicion for POEMS uncovered underlying malignancy, and we review the clinical, electrophysiological, pathological, and laboratory findings characteristic of POEMS. The importance of high clinical suspicion is key in the proper diagnosis and management of this complex syndrome.

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