Relevant bibliographies by topics / Polyneuropaty

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Polyneuropaty'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "Polyneuropaty"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Polyneuropaty"

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Ziyad, Riyam. "Nervledningsstudie av suralisnerven och dess anatomiska variation." Thesis, Högskolan Kristianstad, Sektionen för lärande och miljö, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:hkr:diva-14046.

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Syftet med studien är att studera normala variationer i suralisnervens anatomi och utifrån detfastställa lämpligaste metoden för neurografi i kliniskt bruk. Vidare vill jag genom studien fåsvar på hur ålder och kroppslängd påverkar suralis sensoriska nerv aktion potential (SNAP)amplituden hos män och kvinnor, hur stimuleringslokationen påverka mätvärdena föramplitud och fortledningshastighet samt hur temperaturen påverkar fortledningshastigheten.Suralisnerven (SN) är den mest studerande sensoriska nerven i nedre extremiteterna hospatienter med perifer neuropati. Nervledningsstudier av SN är ett viktigt diagnostiskt verktygvid både axonal och demyeliniserande form av neuropatier. Det finns en stor spridning avnormalvärdena för SN eftersom den påverkas av olika parameter som ålder, kroppslängd ochhudtemperatur. SN är dessutom känd för sin anatomiska variation som gör att resultatetfeltolkas på grund av minskad eller frånvarande (SNAP).Fyrtio friska frivilliga personer deltog i studien. Medelålder för kvinnor var 47 (intervall 22-64) och 42 (intervall 25-54) för män. Nerven stimulerades från ett antal fördefinierade punkterpå distala halvan av vaden: medialt 14,12 och 10 cm från registretingselektroden och 2 cmlateralt från utgångspunkterna. Registrering utfördes från SN vid laterala malleolen.Studien kunde visa att SN amplitud påverkas av parameter som ålder, kön, kroppslängd ochtemperatur. Den största SNAP- amplituden registrerades från stimuleringsavstånd 10 cmmedialt och lateralt. Stimulering medialt gav större svar än stimulering lateralt.Parametrar som temperatur, ålder längd och köns påverkar normala variationer bland normalapatienter i nervledningsstudier. Studien visar att låga temperaturer ger minskadfortledningshastighet medan amplitudsvar ökar. Det är säkrare att stimulera nerven frånavstånd 10 cm medialt då risken för falskt positivt svar minimeras jämfört med avstånd 14cm. Det är viktigt att känna till suralisnervens anatomiska variationer inför mätningar vidundersökning av polyneuropati, eftersom resultaten annars kan misstolkas.
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Oluwole, O. S. A. "Endemic ataxic polyneuropathy in Nigeria /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-165-9/.

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Gross, M. L. P. "The therapeutic modification of inflammatory polyneuropathy." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599754.

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Wigenstam, Veronica. "Behandling av familjär amyloidos med polyneuropati." Thesis, Umeå universitet, Farmakologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-119817.

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Inledning Familjär amyloidos med polyneuropati (FAP) är en genetisk sjukdom som påverkar deperifera nerverna i kroppen. FAP utbryter pga. en mutation i TTR-genen som kodar förtransthyretin (TTR). Den vanligaste TTR-mutationen heter Val30Met. TTR har entetrametrisk struktur, men när TTR-genen är muterad kommer denna tetramer att brytas upp. Till följd av att tetrameren faller sönder, bildas en onormal substans som heter amyloid. Amyloid lagras i kroppens perifera nerver och orsakar skada. Idag finns två etableradebehandlingar: Levertransplantation och behandling med substansen tafamidis. Idag forskasdet på en ny behandling med substansen diflunisal. Diflunisal är ett NSAID och finns inte på marknaden i Sverige. Syfte Syftet med denna litteratur studie är att undersöka hur familjär amyloidos medpolyneuropati behandlas idag. Frågeställningarna är följande: Hur effektiv är levertransplantation vid familjär amyloidos med polyneuropati? Hur effektiv är tafamidis vid familjär amyloidos med polyneuropati? Har behandling med diflunisal någon effekt motFAP? Vilken verkningsmekanism har diflunisal mot FAP? Metod En litteraturstudie gjordes för att få svar på frågeställningarna. Åtta originalartiklar hittades i databasen PubMed. Filter “Clinical trial” , “human” och “5 years” användes för att begränsa antalet träffar. Sökningar gjordes också i web of science där en originalartikel hittades. Tre hemsidor hittades med hjälp av sökord på Google.se, som användes till inledningen. Resultat Kaplan-Meiers analys användes i tre av studierna för att mäta överlevnadsgraden hos patienter med FAP som genomgått en levertransplantation (LTx). Kontrollgrupper togs medför att jämföra med LTx grupperna. En betydligt högre överlevnadsgrad kunde ses i en LTxgrupp jämfört med en kontrollgrupp. Patienter som genomgått en levertransplantation i sendebut (≥50år) har en lägre överlevnadsgrad än patienter som fått sjukdomen tidigt. Studierna som mätt tafamidis effekt vid FAP visade på en minskad neurologisk försämring, bevarande av funktionen hos små- och stora fibrer samt bevarad quality of life (QOL). Behandling med tafamidis hos patienter som har en sen debut av sjukdomen och en mer avancerad sjukdomsbild gav ej någon effekt. Patienter som fick diflunisal jämfört med placebo i 2 år, visade en minskad progression av neurologisk försämring. De hade även en bevarad livskvalitet. Diflunisal binder till T4 på TTR tetramern. Uppbundit TTR stabiliserasoch kommer inte att brytas upp och starta amyloidgenesen. Diskussion/slutsats Levertransplantation är en bra behandlingsmetod då stora skillnader kan ses mellan LTxgrupper och kontrollgrupper. Tafamidis ger bättre effekt vid FAP än diflunisal och tafamidishar färre biverkningar. Både tafamidis och diflunisal kan stabilisera TTR tetramerer, men iolika grad. Tafamidis kunde stabilisera en högre grad (%) tetramerer. Slutsatsen avresultaten från de beskrivna studierna i detta arbete blir att det är tveksamt att ta in diflunisalsom behandling mot FAP eftersom andra behandlingsmetoder är bättre.
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Lindh, Jonas. "Cryptogenic Polyneuropathy : Clinical, Environmental, And Genetic Studies." Doctoral thesis, Linköpings universitet, Neurologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-71215.

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Objectives: The purpose of this medical thesis was to describe the clinical and neurophysiological features and to evaluate the health related quality of life (HR-QoL) in patients with cryptogenic polyneuropathy. We also wanted to investigate different occupational, and leisure time exposures as determinants for cryptogenic polyneuropathy, and to analyze whether polymorphisms for the null alleles of Glutathione S-Transferase Mu-1 (GSTM1), and Theta-1 (GSTT1), and a low activity genetic variation of epoxide hydrolase (EPHX) affect the risk of developing polyneuropathy. These genes were chosen because their enzymes are important in the metabolism of toxic compounds. Methods: The medical records of all patients aged 40–79 years with the diagnosis of cryptogenic polyneuropathy from 1993 to 2000 were analyzed, and data regarding clinical symptoms, laboratory findings, and neurophysiological findings at diagnosis were collected. 255 cases were found. When the medical records were reevaluated assessment to a protocol 168 patients remained as cryptogenic. Two validated instruments (SF-36 and EQ-5D) for measuring HR-QoL were sent to patients, and a reference group from the general population. Additional clinical information, and data on occupational, and leisure time exposure was obtained from postal questionnaires. Crude odds ratios (COR), and logistic regression odds ratios (LOR) were calculated for exposures with five or more exposed cases and referents taken together. We also tested for genetic polymorphisms of GSTM1 and GSTT1, and epoxide hydrolase exon three, EPHX*3. Results: 68% of the patients were men. The mean age at first symptom was 61 years and at diagnosis 64 years. Distal numbness was the most common symptom, but pain, pedal paresthesias, and impairment of balance were also common. The most common clinical findings were decreased or lost proprioception or sense of vibration (80%), and loss of ankle jerks (78%). Neurography showed mixed sensorimotor polyneuropathy of axonal or mixed axonal and demyelinating type. QOL was significantly affected concerning motor functions, with 42% of the patients reporting problems to walk, 3% having problems with daily activities, and 85% were suffering from pain. Mental health was preserved. Mobility was declining with increasing age, but was not affected by disease duration. Increased risks were found in men for occupational exposure to sulphur dioxide, xylene, methyl ethyl ketone, and herbicides and in women for occupational exposure to lead, nitrous oxide, and insecticides. Interaction between occupational and leisure time exposure were seen for several exposures. No significant correlation was found between GSTM1, GSTT1, and EPHX1 polymorphisms in patients with cryptogenic polyneuropathy compared with controls. A tendency, however, was seen for the GSTT1 null phenotype, which was enhanced among smokers compared to controls (OR 3.7). Conclusions: Cryptogenic polyneuropathy is a slowly progressive sensorimotor nerve lesion of mainly axonal type. Patients with cryptogenic polyneuropathy have a lower QOL compared to the general population, although mental health scores did not differ between the groups. Our results show that known determinants could be confirmed, but also some new appeared i.e. sulphur dioxide, hydrogen sulphide, fungicides, and vibrations in the feet. Moreover our results point to a synergistic effect of various exposures. Our hypothesis is that the GSTT1 null polymorphism may be related to an impaired metabolism of toxic substances and reactive oxygen that could lead to nerve damage in the peripheral nervous system. Our results are indicating that components in cigarette smoke might increase the risk of axonal neuropathy in genetically predisposed patients.
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Bonifácio, Maria João Macedo da Silva. "Studies on amyloid formation in familial amyloidotic polyneuropathy." Tese, Porto : Edição do Autor, 1996. http://catalogo.up.pt/F?func=find-b&local_base=UPB01&find_code=SYS&request=000084315.

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Bonifácio, Maria João Macedo da Silva. "Studies on amyloid formation in familial amyloidotic polyneuropathy." Doctoral thesis, Porto : Edição do Autor, 1996. http://hdl.handle.net/10216/64551.

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Redondo, Ana Clara Corujas. "Familial amyloidotic polyneuropathy : Study of structural determinants in amyloidogenesis." Tese, Universidade do Porto. Reitoria, 2002. http://hdl.handle.net/10216/9586.

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Azevedo, Ana do Carmo Ramalho Moreira. "Familial amyloid polyneuropathy: TTR sequencing and "in silico" analysis." Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/15608.

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Mestrado em Biomedicina Molecular
Familial amyloid polyneuropathy (FAP) or paramiloidosis is an autosomal dominant neurodegenerative disease with onset on adult age that is characterized by mutated protein deposition in the form of amyloid substance. FAP is due to a point alteration in the transthyretin (TTR) gene and until now more than 100 amyloidogenic mutations have been described in TTR gene. FAP shows a wide variation in age-at-onset (AO) (19-82 years, in Portuguese cases) and the V30M mutation often runs through several generation of asymptomatic carriers, before expressing in a proband, but the protective effect disappear in a single generation, with offspring of late-onset cases having early onset. V30M mutation does not explain alone the symptoms and AO variability of the disease observed in the same family. Our aim in this study was to identify genetic factors associated with AO variability and reduced penetrance which can have important clinical implications. To accomplish this we genotyped 230 individuals, using a directautomated sequencing approach in order to identify possible genetic modifiers within the TTR locus. After genotyping, we assessed a putative association of the SNPs found with AO and an intensive in silico analysis was performed in order to understand a possible regulation of gene expression. Although we did not find any significant association between SNPs and AO, we found very interesting and unreported results in the in silico analysis since we observed some alterations in the mechanism of splicing, transcription factors binding and miRNAs binding. All of these mechanisms when altered can lead to dysregulation of gene expression, which can have an impact in AO and phenotypic variability. These putative mechanisms of regulation of gene expression within the TTR gene could be used in the future as potential therapeutical targets, and could improve genetic counselling and follow-up of mutation carriers.
A Polineuropatia amiloidótica familiar (FAP) ou paramiloidose é uma doença neurodegenerativa autossómica dominante com início na vida adulta sendo caracterizada pela deposição da proteína mutada na forma de substância amilóide. A FAP é devida a uma mutação pontual no gene transtirretina (TTR) e até agora mais de 100 mutações amiloidogénicas foram descritas neste gene. A FAP apresenta uma grande variação na idade de início (AO) (19-82 anos, nos casos portugueses) e a mutação V30M pode segregar através de várias gerações de portadores assintomáticos, antes de se expressar num probando. No entanto, este efeito protetor pode desaparecer numa única geração, com os filhos de casos tardios a apresentarem um início precoce. A mutação V30M não explica por si só os sintomas e a variabilidade da AO observada dentro de uma mesma família. O nosso objetivo neste trabalho foi identificar fatores genéticos associados com a variabilidade da AO e a penetrância reduzida. De modo a cumprir este objetivo genotipámos 230 doentes, por sequenciação automática, para identificar possíveis modificadores genéticos dentro do locus da TTR. Após a genotipagem, investigamos uma possível associação dos SNPs encontrados com a AO e realizamos uma intensiva análise in silico de modo a perceber uma possível regulação da expressão génica. Apesar de não termos encontrado nenhuma associação entre os SNPs e a AO, encontrámos resultados não descritos e muito interessantes na análise in silico dado termos observado algumas alterações a nível do mecanismo de splicing, ligação de fatores de transcrição e ligação de miRNAs. Todos estes mecanismos quando alterados podem levar à desregulação da expressão do gene, o que pode ter um impacto na AO e variabilidade fenotípica. Estes mecanismos hipotéticos da regulação da expressão génica no gene da TTR podem ser úteis para no futuro serem aplicados como potenciais alvos terapêuticos, beneficiando o aconselhamento genético e o follow-up dos portadores da mutação.
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Redondo, Ana Clara Corujas. "Familial amyloidotic polyneuropathy : Study of structural determinants in amyloidogenesis." Doctoral thesis, Universidade do Porto. Reitoria, 2002. http://hdl.handle.net/10216/9586.

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Books on the topic "Polyneuropaty"

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Lawson, Erin, and Miroslav "Misha" Backonja, eds. Painful Diabetic Polyneuropathy. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6299-6.

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Evers, Eileen. CIDP (Chronic Inflamatory Demyelinating Polyneuropathy): A guide for patients, relatives and friends. 2nd ed. Leaford: GBS Support Group, 1998.

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International, Symposium on Familial Amyloidotic Polyneuropathy and Other TTR Related Disorders (3rd 1995 Lisbon Portugal). Abstracts from the third International Symposium on Familial Amyloidotic Polyneuropathy and Other TTR Related Disorders: 2nd International Workshop on Liver Transplantation in FAP ; held in Lisbon, 27-29 October 1995. London: Pergamon, 1996.

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Donaghy, Michael. Polyneuropathy. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0453.

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Typically polyneuropathy will cause the combination of distal limb muscle weakness, loss of tendon reflexes, and reduced distal limb sensation. There is variable involvement of the autonomic innervation, damage to which causes a dry, vasodilated foot or hand. Loss of tendon reflexes is a cardinal sign of polyneuropathy, often restricted to the ankle jerks in axonal degeneration, but involving more proximal reflexes in acquired demyelinating neuropathies which may involve more proximal segments or the nerve roots. Clinical features suggestive of demyelinating or conduction block polyneuropathy include: a relative lack of muscle wasting in relation to the degree of weakness because no denervation has occurred; weakness of proximal muscles as well as distal, because of nerve root involvement; and disproportionate loss of joint position and vibration sensations compared to relative preservation of pain and temperature sensations which are carried by unmyelinated fibres.
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Miller, Aaron E., and Teresa M. DeAngelis. Chronic Inflammatory Demyelinating Polyneuropathy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199732920.003.0025.

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The diagnostic approach to a patient with chronic peripheral neuropathy can be daunting, with several candidate etiologies. In this chapter, we review the typical symptomatology, temporal course, examination, and laboratory findings, which raise suspicion for chronic inflammatory demyelinating polyneuropathy, and discuss the available therapeutic modalities.
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Reilly, Mary M. Genetic studies of familial amyloid polyneuropathy. 1996.

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Familial Amyloid Polyneuropathy Therapeutics Market Analysis. https://www.fortunebusinessinsights.com/familial-amyloid-polyneuropathy-therapeutics-market-102086, 2020.

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Miller, Aaron E., and Teresa M. DeAngelis. Acute Inflammatory Demyelinating Polyneuropathy (Guillain-Barré Syndrome). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199732920.003.0024.

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Acute inflammatory demyelinating polyneuropathy (AIDP), also known as Guillain-Barré syndrome (GBS), is a common acute neurological presentation encountered in both the outpatient setting and hospital wards. The hallmark of the disorder is the development of ascending motor paralysis with loss of deep tendon reflexes. In this chapter, we outline the classical clinical and laboratory findings in GBS as well as critical therapeutic and supportive measures along with prognosis.
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Bozzetto Ambrosi, Patricia, ed. Demystifying Polyneuropathy - Recent Advances and New Directions. IntechOpen, 2019. http://dx.doi.org/10.5772/intechopen.73946.

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Lawson, Erin, and Miroslav "Misha" Backonja. Painful Diabetic Polyneuropathy: A Comprehensive Guide for Clinicians. Springer, 2016.

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Book chapters on the topic "Polyneuropaty"

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Carvalho, M., J. Freitas, J. Puig, T. Coelho, P. Fernandes, O. Costa, and Falcão de Freitas. "Spectral Analysis of R-R Variability in Familial Amyloidotic Polyneuropaty, Andrade Type." In Amyloid and Amyloidosis 1990, 839–42. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3284-8_206.

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Nix, Wilfred A. "Polyneuropathy." In Muscles, Nerves, and Pain, 127–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-25443-7_8.

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Benatar, Michael. "Polyneuropathy." In Neuromuscular Disease, 109–47. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1007/978-1-59745-106-2_8.

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Gibbons, Christopher H., and Aristidis Veves. "Epidemiology and Scope of Impact of Painful Diabetic Neuropathy." In Painful Diabetic Polyneuropathy, 3–9. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6299-6_1.

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DiBonaventura, Marco daCosta, and Jeffrey Vietri. "Health Status, Work Productivity, and Costs Associated with Diabetic Peripheral Neuropathy." In Painful Diabetic Polyneuropathy, 107–18. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6299-6_10.

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Tahrani, Abd A., Q. Altaf, and Martin J. Stevens. "Advances in Pharmaceutical Options and Current Clinical Trials for the Treatment of Painful Diabetic Polyneuropathy." In Painful Diabetic Polyneuropathy, 121–38. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6299-6_11.

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Teixeira, Mary Elizabeth. "Nursing and Home Care Perspective of Painful Diabetic Neuropathy." In Painful Diabetic Polyneuropathy, 141–51. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6299-6_12.

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Tesfaye, Solomon. "Impact of Painful Diabetic Polyneuropathy on Patients." In Painful Diabetic Polyneuropathy, 155–66. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6299-6_13.

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Wong, Man-chun, and Joanne W. Y. Chung. "Impact of Treatments for Painful Diabetic Polyneuropathies on Patients." In Painful Diabetic Polyneuropathy, 167–92. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6299-6_14.

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Lawson, Erin, and Miroslav “Misha” Backonja. "Patient Resources." In Painful Diabetic Polyneuropathy, 193–95. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6299-6_15.

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Conference papers on the topic "Polyneuropaty"

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Wang, Xingchen, Olena Kuzmicheva, Matthias Spranger, and Axel Graser. "Gait feature analysis of polyneuropathy patients." In 2015 IEEE International Symposium on Medical Measurements and Applications (MeMeA). IEEE, 2015. http://dx.doi.org/10.1109/memea.2015.7145172.

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Gapeshin, R. A., E. R. Barantsevich, D. I. Rudenko, and T. R. Stuchevskaya. "Timeframes for chronic inflammatory demyelinating polyneuropathy diagnosis." In Scientific achievements of the third millennium. LJournal, 2019. http://dx.doi.org/10.18411/scienceconf-05-2019-20.

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Kuznetsova, Yulia. "CORRECTION OF POLYNEUROPATHY IN WOMEN AFTER BREAST CANCER." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2189.sudak.ns2021-17/218.

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Abdel-Raoof, N. A., N. G. Elnhas, I. M. Elsayed, and Mohamed Abdel Harith. "Influence Of Low Intensity Laser Therapy On Diabetic Polyneuropathy." In THE 8TH INTERNATIONAL CONFERENCE ON LASER APPLICATIONS - ICLA 2011. AIP, 2011. http://dx.doi.org/10.1063/1.3631805.

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Lastiani, Sri Panca, and SM Mei Wulan. "Rehabilitation Management of Chronic Inflammatory Demyelinating Polyneuropathy: A Case Report." In International Meeting on Regenerative Medicine. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007316601040106.

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Bönhof, GJ, A. Strom, N. Papanas, RA Malik, J. Szendrödi, K. Müssig, M. Roden, and D. Ziegler. "Assessment of sudomotor dysfunction using Neuropad and Sudoscan in diabetic polyneuropathy." In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688253.

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Vilas-Boas, Maria Do Carmo, Ana Patricia Rocha, Hugo Miguel Pereira Choupina, Jose Maria Fernandes, Teresa Coelho, and Joao Paulo Silva Cunha. "The first Transthyretin Familial Amyloid Polyneuropathy gait quantification study - preliminary results." In 2017 39th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2017. http://dx.doi.org/10.1109/embc.2017.8037087.

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Correia Monteiro, Jean Michell, Pablo Vinicius da Fonseca, Lissiane Karine Noronha Guedes, Henrique Ayres Mayrink Giardini, and Rosa Maria Rodrigues Pereira. "Importance of sural nerve biopsy in seronegative rheumatoid arthritis and polyneuropathy." In Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.16900.

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Nemtsov, BF, LA Smirnova, and OV Simonova. "THU0133 New approaches in diagnosis of sensor polyneuropathy in rheumatoid arthritis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.1035.

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Gonuguntla, V. T., A. Bernstein, and Y. Kupfer. "Case of Acute Inflammatory Demyelinating Polyneuropathy in SARS COVID 19 Pneumonia." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4073.

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Reports on the topic "Polyneuropaty"

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Abas, Razif, Aspalilah Alias, Mohd Amir Kamaruzzaman, Wong Kah Hui, Siti Nurma Hanim Hadie, Choy Ker Woon, Nor Farid Mohd Nor, and Muhammad Hibatullah Romli. Cranial Polyneuropathy in Bell’s Palsy: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2021. http://dx.doi.org/10.37766/inplasy2021.6.0111.

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Oaklander, Anne L., and Max M. Klein. Undiagnosed Small-Fiber Polyneuropathy: Is it a Component of Gulf War Illness? Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada613891.

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Oaklander, Anne L. Undiagnosed Small Fiber Polyneuropathy: Is it a Component of Gulf War Illness? Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada567336.

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Oaklander, Anne L., and Max M. Klein. Undiagnosed Small-Fiber Polyneuropathy - Is it a Component of Gulf-War Illness. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada589549.

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Oaklander, Anne L. Undiagnosed Small Fiber Polyneuropathy: Is It a Component of Gulf War Illness? Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada553816.

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Barohn, Richard, B. Gajewski, M. Pasnoor, L. Brown, L. Herbelin1, K. Kimminau, O. Jawdat, et al. Comparing Four Medicines to Treat Pain from Cryptogenic Sensory Polyneuropathy—The PAIN-CONTRoLS Study. Patient-Centered Outcomes Research Institute® (PCORI), May 2020. http://dx.doi.org/10.25302/05.2020.cer.130602496.

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