Relevant bibliographies by topics / Neuropatie

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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 'Neuropatie'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Neuropatie"

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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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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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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Dissertations / Theses on the topic "Neuropatie"

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Lourenço, Paula Marques. "Aspectos clínico-neurológicos da neuropatia motora multifocal." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17161/tde-05122016-145344/.

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A neuropatia motora multifocal (NMM) é uma neuropatia inflamatória de baixa prevalência, 0,6/100.000 pacientes, caracterizada por uma fraqueza muscular progressiva, assimétrica e distal, sem comprometimento sensitivo. A NMM pode mimetizar a esclerose lateral amiotrófica (ELA), outras variantes da doença do neurônio motor e outras polineuropatias inflamatórias desmielinizantes crônicas, com início assimétrico. A diferenciação é importante, tendo em vista as especificidades da evolução e do tratamento das referidas neuropatias. O principal achado eletrofisiológico é o bloqueio de condução nervosa na ausência de anormalidades sensitivas. A fisiopatogenia da NMM é pouco conhecida. O frequente achado de anticorpos circulantes contra o monoassialogangliosídeo (GM1) é sugestivo de que possa haver seu comprometimento em alterações estruturais nodais e perinodais, com comprometimento multifocal da condução nervosa. O corolário desses distúrbios são paresias e paralisias, também de distribuição multifocal. A Imunoglobulina humana por via endovenosa em altas doses constitui o tratamento de escolha. Novas estratégias de tratamento alternativas são necessárias para prevenir fraqueza muscular permanente e incapacidade. Poucos estudos e revisões bibliográficas têm elucidado as características clínicas da NMM, com a ausência na literatura de publicações de série de casos nacionais. No presente estudo, a partir de uma revisão retrospectiva, serão avaliados os aspectos clínicos- eletrofisiológicos da NMM, a fim de se obter um maior entendimento da evolução da doença.
The multifocal motor neuropathy (MMN) is an inflammatory neuropathy that has low prevalence (0.6 / 100,000 patients). It is characterized by progressive, asymmetric and distal muscle weakness without sensory impairment. The MMN can mimic amyotrophic lateral sclerosis (ALS), other motor neuron disease variants and other chronic inflammatory demyelinating polyneuropathy, with asymmetric start. Differentiation is important, given the specificities of the development and treatment of these neuropathies. The main electrophysiological finding is the nerve conduction block in the absence of sensory abnormalities. The pathophysiology of MMN is little known. The frequent finding of circulating antibodies against monoassialogangliosides (GM1) is suggestive that there may be their involvement in nodal and perinodal structural changes with multifocal impairment of nerve conduction. The corollary of these disorders is paresis and paralysis, with also multifocal distribution. The human immunoglobulin intravenously in high doses constitutes the treatment of choice. New alternative treatment strategies are needed to prevent permanent muscle weakness and disability. Few studies and literature reviews have elucidated the clinical features of MMN and there are no case series publications in the national literature. In this study, from a retrospective review, will be assessed clinic and electrophysiological features of MMN in order to obtain a greater understanding of disease progression.
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Varotti, Emma. "Un ausilio per il controllo della forza di presa della mano durante la deambulazione per persone con neuropatie periferiche." Master's thesis, Alma Mater Studiorum - Università di Bologna, 2021. http://amslaurea.unibo.it/23738/.

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È stato sviluppato un prodotto-servizio pensato principalmente per persone affette da neuropatie periferiche. A seguito di uno studio della sintomatologia e delle difficoltà che incontrano questi pazienti, è emerso che le parti distali del corpo sono quelle più deboli, sia a livello di sensibilità che di forza. Dopo averne analizzato le limitazioni è stato disegnato un ausilio che, attraverso un appoggio antibrachiale regolabile nell’angolazione, permette di ridistribuire i carichi su mani e polsi, diminuendo potenzialmente possibili complicazioni e consentendo una camminata meno problematica. Oltre al prodotto fisico, è stata individuata la forza di presa della mano come una delle abilità fondamentali che viene valutata dal fisiatra per capire qual è l’ausilio adatto per il paziente. Dal momento che questo dato ha anche un valore prognostico, evolutivo e descrittivo delle condizioni di salute del paziente, e siccome il valore di questa forza è strettamente correlato al concetto di esauribilità, dunque è importante capire come varia nel tempo, è stata progettata una versione smart dell’ausilio con impugnatura sensorizzata, che permette di leggere questo ed altri dati, come la frequenza cardiaca e l’ossigenazione del sangue. In questo modo, si possono analizzare questi valori in funzione del tempo, mentre il paziente compie un’attività quotidiana, ovvero una camminata. Il progetto, così  concepito, può essere quindi sì utile per persone affette da neuropatie periferiche, ma più in generale anche per pazienti che presentano problemi nella deambulazione e debolezza muscolare, artriti o patologie cardiopolmonari o neurologiche. A livello di mercato, il sistema è stato concepito per essere sia analogico, e quindi vendibile direttamente all’utente, sia smart, ed essere utilizzato per offrire un servizio ospedaliero atto, appunto, ad analizzare la forza di presa e gli altri parametri, per poter inquadrare al meglio la condizione fisica dei pazienti.
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Blanchet, Fabienne. "Neuropathies périphériques, modèle expérimental de neuropathie à l'acrylamide : application pharmacologique." Paris 5, 1994. http://www.theses.fr/1994PA05P208.

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Chaya, Georges. "Les neuropathies diabétiques : présentation d'une étude clinique portant sur 234 cas." Bordeaux 2, 1989. http://www.theses.fr/1989BOR25309.

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Evangelista, Afrânio Ferreira. "Avaliação do efeito do transplante de células-tronco mesenquimais derivadas de medula óssea em modelo murino de neuropatia periférica diabética." Centro de Pesquisas Gonçalo Moniz, 2014. https://www.arca.fiocruz.br/handle/icict/9646.

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Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
O diabetes é uma doença de alta prevalência que, frequentemente, induz o comprometimento do sistema nervoso periférico. Na neuropatia diabética periférica, os sintomas mais encontrados são os sensitivos, no qual a dor neuropática, condição crônica caracterizada por alodinia e hiperalgesia, é a mais debilitante. Esta, prejudica a qualidade de vida do paciente, sendo muitas vezes não responsiva aos métodos farmacológicos convencionais de tratamento. Diante desse panorama, o desenvolvimento de novas abordagens terapêuticas que possuam ação efetiva neste tipo de dor é de grande relevância. O uso da terapia celular no tratamento de lesões do sistema nervoso tem demonstrado resultados promissores e o potencial terapêutico de células-tronco na neuropatia experimental tem sido proposto. Neste estudo, avaliou-se o efeito de células-tronco mesenquimais derivadas da medula óssea (CMsMO) na neuropatia diabética periférica estabelecida em modelo experimental de diabetes induzido por estreptozotocina (ETZ). Quatro semanas após a indução do modelo por ETZ (80 mg/kg; ip; 3 dias consecutivos), os animais receberam uma administração endovenosa de CMsMO (1 x 106) ou veículo. O tratamento com gabapentina (30 mg/kg; v.o. a cada 12 horas durante seis dias consecutivos) foi usado como padrão ouro. Os limiares nociceptivos térmico e mecânico foram avaliados durante todo o período experimental (90 dias), pelos métodos de hargreaves e von Frey. A avaliação da função motora foi realizada pelo teste de rota-rod. Em diferentes tempos e para todos os grupos experimentais, foram realizadas coletas de segmentos da medula espinal (L4-L5) para dosagem de citocinas por ELISA e segmentos do nervo isquiático foram também coletados para avaliação de alterações morfológicas por microscopia óptica e eletrônica de transmissão. Os dados comportamentais demonstraram que o tratamento com CMsMO reduziu a mecanoalodinia e a hipoalgesia térmica, levando os limiares nociceptivos de animais neuropáticos a níveis similares aos de animais não neuropáticos. Do mesmo modo, a administração de CMsMO normalizou a função motora dos animais neuropáticos. Dados de microscopia mostraram que animais neuropáticos apresentaram atrofia axonal, redução do número de fibras mielínicas e aparente redução do numero de fibras amielínicas no nervo isquiático. Animais neuropáticos tratados com CMsMO tiveram menor ocorrência de atrofia axonal e não apresentaram redução do numero de fibras mielínicas ou amielínicas, em relação aos neuropáticos tratados com salina. Além disso, animais neuropáticos tratados com CMsMO apresentaram menores níveis espinais de IL-1β e TNF-α, e maiores de IL-10 e TGF-β, em relação aos animais neuropáticos não tratados. Esse conjunto de resultados indica que CMsMO produzem efeito antinociceptivo duradouro na neuropatia diabética, seguido de modificações no padrão fisiopatológico da doença, o que aponta a terapia celular como uma interessante alternativa para o controle da neuropatia diabética periférica dolorosa.
Diabetes is a highly prevalent disease which frequently compromises the peripheral nervous system. In peripheral diabetic neuropathy, the most frequent symptoms are sensitive, in which the neuropathic pain, chronic condition characterized by allodynia and hyperalgesia, is the most debilitating. Neuropathic pain affects the quality of patients’ lives, and is often not responsive to pharmacological conventional treatment methods. Against this background, the development of new therapeutic approaches that have an effective action in this type of pain is of great importance. The use of cell therapy in the treatment of lesions in the nervous system has shown promising results and the therapeutic potential of stem cells in experimental neuropathy has been proposed. In this study, we evaluated the effect of mesenchymal stem cells derived from bone marrow (CMsMO) in peripheral diabetic neuropathy established in experimental model of streptozotocin (STZ) induced diabetes in mice. Four weeks after the induction of the model by administration of STZ (80 mg/kg, ip; 3 days) the animals received an CMsMO by intravenous administration (1x106) or vehicle. The treatment with gabapentin (30 mg/kg, orally every 12 hours for six days) was used as the gold standard. The thermal and mechanical nociceptive thresholds were assessed throughout the entire experimental period (90 days), using Hargreaves and von Frey methods, respectively. Motor function evaluation of was conducted using the rotarod test. At different times, were analyzes conducted in spinal cord segments (L4-L5) to determine cytokines profile by ELISA. Sciatic nerve segments were also collected for evaluation of morphological changes by optical and electron transmission microscopy. According to the behavioral data, the CMsMO treatment reduced the mecanoalodinia and the thermal hypoalgesia, leading nociceptive thresholds of neuropathic animals to levels similar to those of non-neuropathic animals. Similarly, CMsMO administration normalized motor function of neuropathic animals. Microscopy data demonstrated that neuropathic animals had axonal atrophy and an apparent decrease of the number of myelinated fibers as well a reduction in the number of unmyelinated fibers in the sciatic nerve, but neuropathic animals treated with CMsMO had a lower incidence of axonal atrophy, showed no decrease in the number of myelinated fibers and no apparent decrease in the amount of unmyelinated fibers in relation to neuropathics treated with saline. Furthermore, neuropathic animals treated with CMsMO presented lower levels of spinal IL-1β and higher levels of TNF-α, and IL-10 and TGF-β compared to neuropathic animals that received saline. These data indicate that CMsMO produces a lasting analgesic effect in diabetic neuropathy, followed by changes in the pathophysiological disease pattern, which indicates cell therapy as an interesting alternative for the control of painful peripheral diabetic neuropathy.
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Fernandes, Fabienne. "Neuropathies diabétiques : à propos de 30 observations avec biopsie nerveuse." Bordeaux 2, 1989. http://www.theses.fr/1989BOR25298.

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Saad, Mehdi. "Détection précoce et quantification objective par mesures chronoampérometriques de l’atteinte neurologique périphérique chez des patients recevant une chimiothérapie neurotoxique." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS060/document.

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Introduction : La chimiothérapie cytotoxique constitue une modalité thérapeutique de nombreux cancers. L’amélioration de la durée de survie des patients a fait apparaître des complications de ces traitements notamment sur le nerf périphérique. Il s’agit d’une complication fréquente et potentiellement sévère qui peut avoir un impact durable. Pourtant, bien que les chimiothérapies neurotoxiques soient connues, il n’existe pas de données précises permettant de prédire la tolérance individuelle. La détection précoce des polyneuropathies chimio-induites (PNCI) est donc capitale pour évaluer les facteurs favorisants. L’utilisation du TNSc (Total Neuropathy Score clinical version) et le Sudoscan® peut notamment permettre la détection de ces PNCI. En effet, le TNSc (Total Neuropathy Score clinical version), un score composite évaluant les petites et grosses fibres nerveuses. Celui-ci a été validé pour déterminer la sévérité de la PNCI. Selon le traitement, l’atteinte concerne les grosses fibres myélinisées ou les fibres fines amyéliniques (FFA). L’examen des grosses fibres est bien standardisé au moyen de l’EMG. Cependant il n’en est pas de même pour le diagnostic d’atteinte des FFA. Le Sudoscan® mesure la conductance cutanée (mesure chronoampérométrique) après une exposition à un courant continu inférieur à 100µA/6V permet d’apprécier la fonction sudomotrice. Des études dans le diabète ont montré que la fonction sudomotrice est directement liée à l’état des FFA, car ces fibres contrôlent les glandes sudoripares. Le Sudoscan® pourrait donc être utilisé pour la détection de PNCI.Objectifs i) Evaluer l’incidence des PNCI par le TNSc selon la dose et évaluer l’atteinte des FFA chez des patients au cours de traitement par Sels de platines ou Taxanes ou Alcaloïdes de pervenche; ii) étudier l’évolution dans le temps des PNCI par le TNSc et par Sudoscan® au cours de la chimiothérapie et à distance de son arrêt; iii) caractériser des facteurs de risque de PNCI; iv) comparer les TNSc et mesures chronoampérométriques selon les traitements reçus v) évaluer l’intérêt des conductances par rapport au TNSc.Résultats Une attention particulière a été portée aux patients sous Oxaliplatine (n=65) et Taxanes (n=28). Nous avons retrouvé une augmentation du TNSc chez tous les patients sous chimiothérapie neurotoxique. Pendant le suivi, 57% des patients sous Oxaliplatine et 58% des patients sous Taxanes atteignaient un TNSc correspondant à une neuropathie clinique. Aucune différence du TNSc entre les patients symptomatiques et asymptomatiques n’a été observée à distance de traitement par Oxaliplatine (≥4mois). De même, on ne retrouvait pas de différences du TNSc entre les patients symptomatiques et asymptomatiques à distance de traitement par Taxanes. D’autre part, l’étude des conductances n’a pas révélé d’évolution en fonction de la dose reçue pour les patients sous Oxaliplatine. En revanche, chez les patients sous Taxanes on retrouvait des différences significatives des conductances en fonction des doses reçues. La mesure la plus basse des pieds pendant le suivi est observée en moyenne 23 jours avant que le TNSc le plus élevé ne soit atteint (p=0,03). On ne retrouve pas de différences des conductances pendant le suivi entres les patients symptomatiques et asymptomatiques à distance de traitement par Oxaliplatine. Toutefois, les patients symptomatiques à distance de traitement par Taxanes avaient des conductances des pieds plus basses que les patients asymptomatiques à distance (p=0.004). Le TNSc est plus élevé selon la dose reçue chez les patients diabétiques que chez les patients non diabétiques. Les conductances des mains et des pieds des patients diabétiques étaient significativement plus basses (p=0.003) chez les patients diabétiques que chez les patients non diabétiques.Conclusion Ces résultats suggèrent que les mesures chronoampérométriques permettent de détecter et quantifier l’atteinte des FFA chez les patients recevant des Taxanes
Introduction : Cytotoxic chemotherapy is a treatment modality for many cancers. The improved survival time of patients showed some complications of these cytotoxic treatments including chemotherapy-induced peripheral neuropathy (CIPN). This is a common and potentially severe complication that can have a lasting impact on the quality of life. Although neurotoxic chemotherapies are known, there is no accurate data to predict individual tolerance. Early detection of CIPN is therefore essential to assess the contributing factors. To this end, the use of the TNSc (Total Neuropathy Score clinical view) and the Sudoscan® can improve the detection CIPN.Indeed, the TNSc (Total Neuropathy Score clinical view), a composite score assessing small and large nerve fibers, has been validated to evaluate the severity of CIPN. The nerve impairment concerns the large myelinated fibers or small fibers, depending on the treatment. The objective assessment of large fibers is standardized by means of the EMG (Electromyography), but it is not the same for the diagnosis of the small fibers impairment.On the other hand, the Sudoscan® measures skin conductance (chronoamperometric measurement) after exposure to a direct current of less than 100μA and 6V, and can assess the sudomotor function. Interestingly, studies in diabetes have shown that sudomotor function is directly related to the status of the small fibers that control the sweat glands. The Sudoscan® could thus be used for the detection of CIPN.Objectives: i) to evaluate the impact, depending on the dose received of chemotherapy, of CIPN by TNSc and assess the impairment of small fibers in patients during treatment with Platinum compounds or Taxanes or vinca alkaloids; ii) to study the evolution of the peripheral neurologic impairment by TNSC and skin conductance measurements during chemotherapy and after the end of the treatment; iii) to characterize risk factors for CIPN; iv) to assess the usefulness of conductance measurements compared to TNSc.Results: Particular attention has been given to patients treated with Oxaliplatin (n= 65) and Taxanes (n= 28), known to damage small fibers. We found an increased TNSc in all patients receiving neurotoxic chemotherapy. During follow-up, 57% of patients receiving Oxaliplatin and 58% of patients receiving Taxanes reach a TNSc corresponding to a clinical neuropathy. However, there was no difference of TNSc during the follow-up between symptomatic and asymptomatic patients, 4 months after the end of the treatment by Oxaliplatin. Similarly, we did not find differences of TNSc during the follow-up between symptomatic and asymptomatic patients, 4 months after the end of the treatment by Taxanes.Regarding conductance values, we didn’t observe changes depending on the dose received for patients treated by Oxaliplatin. However, in patients receiving Taxanes we found significant differences, based on the cumulative dose, for the hands and feet. Indeed, the lowest measure of the feet during the tracking is observed within an average of 23 days before the TNSc reached its highest value (p = 0.03). We didn’t find differences in conductance values during follow-up among symptomatic and asymptomatic patients 4 months after the end of their treatment. However, 4 months after the end of the chemotherapy, symptomatic patients treated with Taxanes had feet conductance values lower than asymptomatic patients (p= 0.004). The TNSc was higher in diabetic patients than in non-diabetic patients depending on the dose received during the follow-up. During the follow-up, the conductance values of the hands and feet were significantly lower (p= 0.003) for these patients than in nondiabetic ones.Conclusion: These results suggest that the chronoamperometric measurements can be useful in the detection and quantification of small fibers impairment in patients receiving Taxanes
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Hutton, E. J. "The skin as a window on mechanisms of neuropathy and neuropathic pain." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1532903/.

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Neuropathies are common, yet the pathogenic mechanisms of many remain incompletely understood. Animal and cell models have provided much useful information about disease mechanisms, and yet translation of this knowledge to clinical practice and disease therapies is often disappointing. One of the difficulties in studying human nerves is limited availability of tissue, due to the morbidity of peripheral nerve (usually sural nerve) biopsy. I sought to evaluate the utility of cutaneous nerves, both generally as a tool to assess the relevance of pathogenic mechanisms identified in animal studies in human disease, and also specifically in evaluating whether immune changes in the skin may play a role in the development of neuropathic pain. Animal models have suggested that proinflammatory cytokines exert algesic effects on nerves, whilst anti-inflammatory cytokines have a counter-regulatory analgesic effect (Üçeyler et al., 2009). More recently, support for a link between variability in systemic and / or local cytokine balance and pain in neuropathy has begun to emerge (Üçeyler et al., 2007c, Üçeyler et al., 2010). Despite some support for a link between painful neuropathies and increased inflammatory and / or decreased antiinflammatory cytokines, it remains unclear whether the immune changes reflect underlying neuropathological processes, a response to nociceptor activation, variability in individual immune response to nerve damage or are a biomarker of another factor indirectly modulating both pain and immune function. It is also unclear whether immune-nerve interactions are unidirectional or bidirectional: does increased nociceptor firing modulate local immune function or does immune response to nerve damage modulate activity of remaining undamaged fibres, or is there a combination of these factors? I sought to understand the effect of acute nociceptor activation on skin immune profile, as well as whether changes in chronic neuropathy would be associated with the presence and intensity of pain.
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Camargo, Marcela Regina de [UNESP]. "Parâmetros espaço temporais da marcha e inter-relação com equilíbrio e força muscular isométrica de tornozelos em diabéticos com neuropatia periférica." Universidade Estadual Paulista (UNESP), 2009. http://hdl.handle.net/11449/87311.

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O Diabetes mellitus é uma enfermidade crônica que leva a alterações sensitivas e motoras. Tais alterações comprometem o equilíbrio e a deambulação predispondo seus portadores à ocorrência de quedas. Esta revisão teve por objetivo levantar, na literatura recente, estudos que visassem avaliar parâmetros da marcha e aspectos envolvidos com a deambulação. Para isso, foi realizada uma busca nas bases de dados MEDLINE, SciELO, LILACS e PEDro, cruzando as palavras-chaves: Neuropatias Diabéticas x Marcha; Diabetes Mellitus x Marcha e Pé Diabético x Marcha. Após passarem pelos critérios de seleção, foram obtidos 15 artigos, os quais foram sintetizados e discutidos, sendo, portanto, incluídos nesta revisão. Ficou claro que a neuropatia diabética leva a déficits na amplitude do passo, velocidade e cadência da marcha em superfícies planas, sem mudanças bruscas de direção ou paradas, e, déficits de equilíbrio e coordenação em aclives, declives e terrenos irregulares. Acarreta, também, aumento dos índices de pressão plantar e, devido à alteração de ativação do tríceps sural, dificuldade na fase de apoio terminal e prébalanço. Assim, o próximo contato inicial ocorrerá de maneira inadequada, com o antepé e sem absorção de choques.
Diabetes mellitus is a chronic disease that leads to sensory-motor changes. These changes affect balance and walking predisposing their patients to falls occurrence. This review aimed to investigate, in recent literature, assessing gait parameters and walking studies involved aspects. For this, a search was conducted in databases MEDLINE, SciELO, LILACS and PEDro, crossing the keywords: Diabetic neuropathies x Gait; Diabetes Mellitus x Gait and Diabetic Foot x Gait. After passing by selection criteria, it was remainder 15 articles, which were synthesized, discussed and is therefore included in this review. It was clear that diabetic neuropathy leads to deficits in the step amplitude, gait velocity and gait cadence on flat surfaces, without sudden changes of direction or stops, and balance and coordination deficits in slopes and uneven terrain. Diabetic neuropathies, provide, also increase plantar pressure rates due to the triceps sural activation change, difficulty in the terminal phase of support and pre-assessment. Thus, the next initial contact occurs in an inadequate way, with the forefoot and without absorption of shocks.
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Houssin, Rémy. "Les neuropathies amyloides familiales : à propos d'un cas de neuropathie amyloi͏̈de familiale de type portugais." Bordeaux 2, 1992. http://www.theses.fr/1992BOR2M200.

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Books on the topic "Neuropatie"

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International, Symposium on Diabetic Neuropathy (3rd 1994 Kanagawa-ken Japan). Diabetic neuropathy: New concepts and insights : proceedings of the 3rd International Symposium on Diabetic Neuropathy, Kanagawa, 3-5 November 1994. Amsterdam: Elsevier, 1995.

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Bakker, R. Scott. Neuropath. New York: Tor, 2009.

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Bakker, R. Scott. Neuropath. New York: Tor, 2009.

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Neuropath. New York: Tor, 2009.

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Neuropath. Toronto: Penguin Canada, 2008.

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Mark, Hallett, and Millender Lewis H. 1937-, eds. Entrapment neuropathies. 2nd ed. Boston: Little, Brown, 1990.

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Pfeifer, Michael A. Diabetic neuropathy. Kalamazoo, Mich: Upjohn, 1985.

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Veves, Aristidis, and Rayaz A. Malik, eds. Diabetic Neuropathy. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-311-0.

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Asbury, Arthur K., Herbert Budka, and Elfriede Sluga, eds. Sensory Neuropathies. Vienna: Springer Vienna, 1995. http://dx.doi.org/10.1007/978-3-7091-6595-9.

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

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Book chapters on the topic "Neuropatie"

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Calcutt, Nigel A., and Sandra Chaplan. "Neuropathic Pain Model, Diabetic Neuropathy Model." In Encyclopedia of Pain, 2075–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_2679.

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Milligan, Erin D., Steven F. Maier, and Linda R. Watkins. "Neuropathic Pain Model, Neuritis/Inflammatory Neuropathy." In Encyclopedia of Pain, 2080–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_2680.

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Chiang, Ming-Chang, Paul-Chen Hsieh, and Sung-Tsang Hsieh. "Neuropathic Pain in Small Fiber Neuropathy." In Small Fiber Neuropathy and Related Syndromes: Pain and Neurodegeneration, 153–64. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-3546-4_14.

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Vatine, Jean-Jacques, Ze’ev Seltzer, and Jeanna Tsenter. "Neuropathic Pain Models, CRPS-I Neuropathy Model." In Encyclopedia of Pain, 2100–2105. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_2685.

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Sawada, Atsushi, and Michiaki Yamakage. "Neuropathic Pain Syndrome: Diabetic and Other Neuropathies." In Chronic Pain Management in General and Hospital Practice, 249–60. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-2933-7_14.

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Greene, D. A., A. A. F. Sima, and M. A. Pfeifer. "Neuropathie." In Spätkomplikationen des Diabetes mellitus, edited by C. E. Mogensen and Eberhard Standl, 103–66. Berlin, Boston: De Gruyter, 1990. http://dx.doi.org/10.1515/9783110847741-008.

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Ramchandren, Sindhu, and Richard A. Lewis. "Chronic Neuropathies – Chronic Inflammatory Demyelinating Neuropathy and Its Variants." In Frontiers of Neurology and Neuroscience, 12–25. Basel: KARGER, 2009. http://dx.doi.org/10.1159/000212313.

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Stracke, Hilmar, and Andreas Schäffler. "Neuropathie-Tests." In Funktionsdiagnostik in Endokrinologie, Diabetologie und Stoffwechsel, 265–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-55914-7_23.

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Gries, F. A., and D. Ziegler. "Diabetische Neuropathie." In Diabetes mellitus, 178–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74610-9_15.

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Ziegler, D., and F. A. Gries. "Diabetische Neuropathie." In Diabetes in der Praxis, 317–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18571-7_26.

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Conference papers on the topic "Neuropatie"

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de Oliveira, Juliana Karina, Suelem Tavares da Silva Penteado, Jakeline Liara Teleken, Suzane Virtuoso, and Thayla Mohana Cardoso de Oliveira. "RASTREAMENTO DE COMPLICAÇÕES CRÔNICAS EM PACIENTES DIABÉTICOS EM UMA FARMÁCIA BÁSICA DO MUNICÍPIO DE CASCAVEL-PR." In II Congresso Brasileiro de Ciências Farmacêuticas On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1031.

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Introdução: O diabetes mellitus (DM) não controlado pode provocar, a longo prazo, disfunção e falência de vários órgãos, estando associado ao aumento da mortalidade e ao alto risco de desenvolvimento de complicações micro e macrovasculares. Diante disso, o bom controle do DM na atenção primária evita hospitalizações e maiores complicações, por isso, a detecção de retinopatia, nefropatia, neuropatia e pé diabético deve ser realizada em tempo oportuno para acompanhamento e seguimento de cada paciente. Objetivo: O objetivo desse trabalho foi rastrear e identificar as complicações crônicas de Diabetes Mellitus em pacientes assistidos pela Farmácia Básica do município de Cascavel-PR. Métodos: Foram coletados os dados sociodemográficos dos pacientes e exame de microalbuminúria para rastreamento de nefropatia. Além disso, para o rastreamento de neuropatia diabética foi aplicado um questionário de Escore de Sintomas Neuropático (ESN) e, para o rastreamento de pé diabético foi aplicado o questionário Michigan Neuropathy Screening Instrument (MNSI). Esse projeto foi aprovado pelo Comitê de Ética, sob o Parecer Consubstanciado do CEP, nº 3.848.285. Resultados: Dos 62 pacientes incluídos no estudo, o gênero feminino foi mais prevalente (64,5%) e a maioria (71,0%) possuíam como comorbidade hipertensão arterial sistêmica (HAS). Em relação às características antropométricas a prevalência de obesidade grau I foi expressiva (24,2%). Em relação às complicações crônicas do DM, foi expressiva a identificação de neuropatia (33; 53,2%), além disso, nefropatia (12; 19,4%) também foi uma complicação crônica relevante identificada. Apenas 1 paciente apresentou histórico atual de pé diabético, com presença de ulceração e deformidade. A retinopatia diabética foi identificada em apenas 2 pacientes com histórico prévio da complicação. Conclusão: O presente trabalho evidencia a prevalência de complicações microvasculares e alerta para a necessidade de rastreamento destas ainda em tempo oportuno, a fim de realizar o manejo e tratamento adequado com o paciente.
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Ponirakis, Georgios, Shazli Azmi, Maryam Ferdousi, Ioannis Nikolaos Petropoulos, Andrew Marshall, Basil Ammori, Handrean Soran, and Rayaz Malik. "The Impact of Bariatric Surgery on Neuropathic Pain and on Objective Markers of Neuropathy." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbop1377.

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Borodai, Olena. "PSYCHO-EMOTIONAL DISORDERS IN PATIENTS WITH POST-TRAUMATIC NEUROPATHIES AND PLEXOPATHIES ACCOMPANIED BY NEUROPATHIC PAIN." In THEORETICAL AND EMPIRICAL SCIENTIFIC RESEARCH: CONCEPT AND TRENDS, chair Tetyana Litovchenko. European Scientific Platform, 2021. http://dx.doi.org/10.36074/logos-28.05.2021.v2.39.

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Carozzi, Valentina Alda, Cynthia Renn, Rhee Peter, Danisha Gallop, Paola Marmiroli, Guido Cavaletti, and Susan Dorsey. "Abstract 934: Electrophysiological, behavioural and molecular characterization of the neuropathic pain in bortezomib-induced peripheral neuropathy." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-934.

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Ford, I., P. G. Newrick, R. Malik, F. E. Preston, J. D. Ward, and M. Greaves. "HAEMOSTATIC PARAMETERS, ENDONEURIAL OXYGEN TENSION AND SURAL NERVE HISTOLOGY IN DIABETES MELLITUS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643107.

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We have examined coagulation parameters in 15 neuropathic (Group A) and 10 complication-free diabetic patients (Group B). Venesection and sample testing were performed under standard conditions. Group A underwent sural nerve biopsy and 14 also had measurements of endoneurial oxygen tension. Factor VIII related antigen was higher in Group A (l-617u/ml ± 0.67) compared to Group B (0.944u/ml ± 0.26); (mean ± SD; p<.0.05) perhaps suggesting endothelial cell damage, although this did not correlate with capillary basement membrane thickness or endothelial cell number nor with endoneurial oxygen levels. Platelets from Group A were more sensitive to arachidonate than those of Group B, showing aggregation thresholds in platelet rich plasma of 0.36 ± 0.17mM and 0.57 ± 0.9mM respectively compared with 0.65 ± 0.37mM in non-diabetic controls.Platelets from Group A subjects also produced more thromboxane B2 in response to arachidonate than Group B or normal controls (37.95 ± 27.5; 25.5 ± 13.0; 16.55 ± 15-5pmol/107 platelets). Blood fibrinolytic capacity measured by euglobulin clot lysis time, was diminished in NIDDs (post-occlusion ECLT 165.7 mins ± 116.0), compared to IDDs (55.5 ± 34.5) (p<0.05) due at least in part to excess of tissue plasminogen-activator inhibitor, although we found no significant difference in ECLT between Group A and Group B. Interaction between haemostatic and microvascular abnormalities in diabetes may contribute to the pathogenesis of diabetic neuropathy.
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Vines, Robert S., Rucsandra R. Marica, and Ha V. Vo. "Comparison of the Duration of Diabetes and PSSD Measurements." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192668.

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In the U.S. there are roughly 15 million diabetics with 10 million of them having mild to severe forms of nerve damage. Almost 4.5 million diabetics suffer from nerve damage in the feet [1]. Early detection of neuropathy is paramount to preventing further damage to the affected limb(s). Neuropathy is a leading factor in amputations, which can be avoided or reduced if neuropathy is detected early and limb care is promoted.
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Strenzke, N., L. Tranebjærg, and M. Bitner-Glindzicz. "Auditorische Neuropathie bei CAPOS-Syndrom." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640630.

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Bonafini, Beatriz L., Giselle L. F. Ronque, and Lucas F. de Oliveira. "Pupilometria Dinâmica para Avaliação do Reflexo Foto Motor na Detecção da Neuropatia Autonômica Diabética e Relação Glicêmica." In Anais Estendidos do Simpósio Brasileiro de Computação Aplicada à Saúde. Sociedade Brasileira de Computação (SBC), 2021. http://dx.doi.org/10.5753/sbcas.2021.16100.

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A Neuropatia Autonômica é uma das complicações da diabetes por ocasionar danos ao sistema nervoso e uma forma de acessá-lo é por meio da análise da reação pupilar. Este estudo teve como objetivo realizar pupilometria dinâmica em pacientes com diabetes. Foi desenvolvido um sistema de aquisição de vídeo que registra o movimento pupilar exposta à estímulos luminosos, sendo aplicado em 45 voluntários no SEMPR-HC da UFPR. 90 vídeos de pupilometria foram obtidos. As CNNs YoloV2 e RetinaNet foram aplicadas as imagens avaliando a detecção da íris e pupila. A RetinaNet obteve melhor performance para IoU de 90%. As diferenças entre os grupos com e sem neuropatia apareceram na máxima dilatação pupilar, plateau e velocidade de re-dilatação.
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Losada, Ana Laura Pereira, and Guilherme Dalpiva. "A EFICACIA DA CINESIOTERAPIA E PROPRIOCEPÇÃO EM PACIENTES COM POLINEUROPATIA DIABÉTICA: UMA REVISÃO SISTEMÁTICA." In II Congresso Brasileiro de Saúde On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1525.

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Introdução: A diabetes mellitus (DM) é uma doença crônica no qual o corpo não produz insulina ou não consegue empregar de forma adequada a insulina que produz. É uma das enfermidades mais diagnosticadas nos últimos anos no mundo todo e afeta uma grande quantidade de indivíduos. a Polineuropatia diabética é uma das complicações mais comuns ocasionadas pela DM gerando diversos sintomas como o déficit de sensibilidade periférica dos MMII, que consequentemente aumenta o risco de quedas entre os portadores da doença. Objetivo: Analisar tratamentos de cinesioterapia e propriocepção, e sua eficácia com déficit sensórios motores causados pela polineuropatia diabética. Materiais e Métodos: Por meio de uma revisão sistemática, através de buscas em bases de dados, foram admitidos apenas ensaios clínicos publicados entre os anos de 2010 e 2020. A busca envolveu as bases de dados SciELO, BVS, PubMed, PEDro e Google acadêmico, utilizando os descritores “Physical Therapy Specialty”; “Diabetic Neuropathies”; “Exercise Therapy”; “Proprioception”; “Adult”; “Aged”. A triagem dos artigos, foi realizada por dois pesquisadores, e foram incluídos ensaios clínicos, teses e doutorados que abordassem trabalho proprioceptivo e de equilíbrio em pacientes neuropatas diabéticos. Resultados: Na análise inicial, a busca resultou em 69 registros potencialmente relevantes, porém 57 foram excluídos e apenas 12 contemplaram os critérios de seleção e destes todos atingiram a pontuação estabelecida na escala PEDro. Conclusão: Por meio desta análise metodológica, foi possível concluir que um trabalho postural, de equilíbrio estático e dinâmico com propriocepção é de fato efetivo, trazendo melhora das disfunções dos portadores de Polineuropatia diabética. Porém, alguns protocolos ainda necessitam de estudos e maior tempo de aplicação para concluir sua eficácia.
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Vaughan, Neil, Venketesh N. Dubey, Tamas Hickish, and Jonathan Cole. "A Smart Device to Substitute the Neurothesiometer." In ASME 2017 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/detc2017-68306.

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This paper presents a patented smart point-of-care testing (POCT) system for the diagnosis and grading of peripheral neuropathy at the patient’s home or care center. The device aims to detect changes or worsening of a patient’s neuropathy. Our system utilizes the vibration motor within a smartphone, applied through a 3D printed probe attachment to detect sensation loss in vibration sensitivity threshold (VST). A smartphone app displays several neuropathy questionnaires to the user to identify and monitor changes in their condition. This paper presents results from comparison between the new smart device and the gold standard Neurothesiometer. Results suggest that the new device performs closely to the gold standard in terms of the frequency and amplitude of vibration.
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Reports on the topic "Neuropatie"

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Pereira, Jéssica Alessandra, Vanessa Soares de Araújo, Uiara Aline de Oliveira Kaizer, and Sônia Regina Pérez Evangelista Dantas. Neuropatia periférica por diabetes: prevenção de complicações. Associação Brasileira de Estomaterapia, 2018. http://dx.doi.org/10.30886/cartilha012018.

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Pereira, Jéssica Alessandra, Vanessa Soares de Araújo, Uiara Aline de Oliveira Kaizer, and Sônia Regina Pérez Evangelista Dantas. Neuropatia periférica por diabetes: prevenção de complicações. Associação Brasileira de Estomaterapia, 2018. http://dx.doi.org/10.30886/cartilha012018.

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Cherninkova, Sylvia, Boryana Zaharova, Radoslava Saraeva, Albena Todorova, Radka Kaneva, Alexander Oscar, and Ivailo Tournev. Leber’s Hereditary Optic Neuropathy in Bulgarian Patients. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, January 2020. http://dx.doi.org/10.7546/crabs.2020.01.16.

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Cook, Alonzo D. Realistic Murine Model for Streptozotocin-induced Diabetic Peripheral Neuropathy. Science Repository OÜ, August 2018. http://dx.doi.org/10.31487/j.rgm.2018.02.006.

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Dy, M.D., M.S., Sydney M., Wendy L. Bennett, M.D., M.P.H., and Ritu Sharma, B.Sc. Preventing Complications and Treating Symptoms of Diabetic Peripheral Neuropathy. Agency for Healthcare Research and Quality (AHRQ), March 2017. http://dx.doi.org/10.23970/ahrqepccer187.

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Wang, Shaomei. Non-Invasive Cell-Based Therapy for Traumatic Optic Neuropathy. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada606407.

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Liou, Gregory I., Saif Ahmad, Mohammad Naime, Nadeem Fatteh, and Sohail Khan. Role of Adenosine Receptor A2A in Traumatic Optic Neuropathies. Fort Belvoir, VA: Defense Technical Information Center, December 2012. http://dx.doi.org/10.21236/ada581642.

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Liou, Gregory I., Saif Ahmad, and Ahmed Elsherbini. Role of Adenosine Receptor A2A in Traumatic Optic Neuropathies. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada600384.

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Floyd, Candance L. Treatment of Neuropathic Pain after SCI with a Catalytic Oxidoreductant. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada622188.

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Yang, In H. Novel High-Throughput Drug Screening Platform for Chemotherapy-Induced Axonal Neuropathy. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada613177.

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