Relevant bibliographies by topics / Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
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Academic literature on the topic 'Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)"

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Abraham, Alon, Majed Alabdali, Mohammad Qrimli, Carolina Barnett, Hans D. Katzberg, Bruce A. Perkins, and Vera Bril. "Chronic Inflammatory Demyelinating Polyneuropathy in Diabetes Patients." US Neurology 11, no. 01 (2015): 47. http://dx.doi.org/10.17925/usn.2015.11.01.47.

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Diabetes mellitus (DM) is pandemic, and is the leading global cause of polyneuropathy, most commonly, a distal symmetric sensorimotor polyneuropathy (DSP). By contrast, chronic inflammatory demyelinating polyneuropathy (CIDP) is rare, and characterized mainly by symmetrical proximal and distal muscles weakness. There are currently 15 sets of criteria using a variable combination of clinical, electrophysiologic, laboratory, and biopsy features to identify CIDP, but it is unclear if these criteria are the same in patients with and without DM. Slowed conduction velocity, a feature of demyelination, is observed in patients with type 1 DM with poor control, and the clinical characteristics of these patients differ from those who have CIDP and DM, suggesting a different pathophysiology. Treatment response rates in CIDP patients, with and without DM, are as high as 80 %, and it is recommended that treatment be started early to prevent secondary axonal loss. However, patients with type 1 DM with CIDP are far less likely to be treated than CIDP patients who do not have DM. In patients with type 1 DM with polyneuropathy who have prominent weakness or demyelination in electrophysiologic studies, a diagnosis of CIDP and a trial of therapy should be considered.
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Oh, Shin J., Liang Lu, Mohammad Alsharabati, Marla B. Morgan, and Peter King. "Chronic inflammatory axonal polyneuropathy." Journal of Neurology, Neurosurgery & Psychiatry 91, no. 11 (September 11, 2020): 1175–80. http://dx.doi.org/10.1136/jnnp-2020-323787.

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ObjectivesChronic inflammatory axonal polyneuropathy (CIAP) is defined on the basis of the clinical, electrophysiological and nerve biopsy findings and therapeutic responses of ‘immunotherapy responding chronic axonal polyneuropathy (IR-CAP)’.MethodsThe diagnosis of IR-CAP was made when all of three of the following mandatory criterion were met: (1) acquired, chronic progressive or relapsing symmetrical or asymmetrical polyneuropathy with duration of progression >2 months; (2) electrophysiological evidence of axonal neuropathy in at least two nerves without any evidence of ‘strict criteria of demyelination’; and (3) definite responsiveness to immunotherapy.ResultsThirty-three patients with IR-CAP showed similar clinical features of chronic inflammatory demyelinating polyneuropathy (CIDP) except ‘motor neuropathy subtype’. High spinal fluid protein was found in 27/32 (78%) cases. ‘Inflammatory axonal neuropathy’ was proven in 14 (45%) of 31 sural nerve biopsies.DiscussionsIR-CAP could well be ‘axonal CIDP’ in view of clinical similarity, but not proven as yet. Thus, IR-CAP is best described as CIAP, a distinct entity that deserves its recognition in view of responsiveness to immunotherapy.ConclusionDiagnosis of CIAP can be made by additional documentation of ‘inflammation’ by high spinal fluid protein or nerve biopsy in addition to the first two diagnostic criteria of IR-CAP.
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Vedeler, C. A., E. Farbu, and S. I. Mellgren. "Chronic inflammatory demyelinating polyneuropathy (CIDP)." Acta Neurologica Scandinavica 127 (November 29, 2012): 48–51. http://dx.doi.org/10.1111/ane.12049.

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Mathey, Emily K., and John D. Pollard. "New Treatments for Chronic Inflammatory Demyelinating Polyneuropathy." European Neurological Review 8, no. 1 (2012): 51. http://dx.doi.org/10.17925/enr.2013.08.01.51.

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Chronic inflammatory demyelinating polyneuropathy (CIDP) is the most common treatable chronic neuropathy in the western world. There are three treatment options currently available for CIDP: intravenous immunoglobulin, plasma exchange or corticosteroids. Despite the efficacy of these therapies CIDP patients are often left with permanent neurological deficits, have a poor clinical prognosis or in some cases do not respond to treatment. Furthermore, high cost and restricted availability make them unfeasible in some treatment centres, especially in the developing world. Recent advances in the understanding of the underlying pathogenic mechanisms in CIDP have brought a number of novel agents into consideration for use in CIDP. Many of these novel therapies have been used in similar autoimmune disorders and target immunopathogenic pathways common to CIDP. Here we review a number of these novel therapies and their applicability to CIDP.
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Saad, Toni C., William Owen Pickrell, Gareth Payne, and Khalid Hamandi. "Chronic inflammatory demyelinating polyneuropathy: a rare cause of falls." BMJ Case Reports 12, no. 12 (December 2019): e231676. http://dx.doi.org/10.1136/bcr-2019-231676.

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This case of chronic inflammatory demyelinating polyneuropathy (CIDP) shows that a patient’s condition can evolve from the point of admission, gradually manifesting its underlying cause. Our patient’s initial presentation of backpain and lower limb weakness prompted investigations which ruled out compressive myelopathy and neuropathy. As upper limb weakness developed later, along with a more proximal and symmetrical pattern of lower limb weakness, the clinical picture suggested polyneuropathy. The diagnosis of CIDP became apparent only after numerous negative tests and nerve conduction studies which identified demyelination. Diagnosing CIDP enabled the commencement of definitive treatment which led to a good recovery.
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Kohle, Felix, Satoshi Kuwabara, and Helmar Christoph Lehmann. "Chronic inflammatory demyelinating polyneuropathy and pregnancy: systematic review." Journal of Neurology, Neurosurgery & Psychiatry 92, no. 5 (February 9, 2021): 473–78. http://dx.doi.org/10.1136/jnnp-2020-325321.

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Pregnancy largely affects disease activity and clinical course in women with immune-mediated neurological disorders. Chronic inflammatory demyelinating polyneuropathy (CIDP) is rare but the most common chronic immune-mediated neuropathy; however, the effects of pregnancy on CIDP have never been investigated except case reports or series. We here provide a systematic review of the literature from 1 January 1969 to 30 June 2020 that revealed 24 women with CIDP, who had onset or relapse during pregnancy. Of these, 17 (71%) developed CIDP during the first pregnancy, and 8 (47%) had a relapse during subsequent pregnancies. Of the 17 patients, in whom the CIDP subtypes were determined, all of them had typical CIDP. First-line treatments for CIDP, such as corticosteroids, immunoglobulin and plasma exchange were efficacious and safe. We suggest that pregnancy can trigger typical CIDP in some women, and women with CIDP have a higher risk of relapse during pregnancy. The onset or relapse of CIDP during pregnancy is a rare but challenging constellation for physicians.
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Gapeshin, R. A., E. R. Barantsevich, D. I. Rudenko, T. R. Stuchevskaya, E. A. Gavrilova, M. S. Pushkaryov, A. A. Yakovlev, A. V. Gavrichenko, and A. G. Smochilin. "Fatigue in patients with chronic inflammatory demyelinating polyneuropathy." Neurology, Neuropsychiatry, Psychosomatics 13, no. 1 (February 18, 2021): 51–56. http://dx.doi.org/10.14412/2074-2711-2021-1-51-56.

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Chronic inflammatory demyelinating polyneuropathy (CIDP) is a peripheral neuropathy, predominantly motor neuropathy, with a progressive or relapse-remitting course. Fatigue is a condition characterized by a physical or mental feeling of lack of energy or lack of motivation for action, which is often present in patients with CIDP.Objective: to assess the severity of asthenia in CIDP patients.Patients and methods. Examinations were made in 34 inpatients treated for documented CIDP that met the international European Federation of Neurological Societies/Peripheral Nerve Society (EFNS/PNS) criteria. A study group included patients with CIDP, whereas a comparison group consisted of volunteers without psychiatric illness, who were compensated for somatic diseases.Results and discussion. In the patients with CIDP, the level of fatigue was found to be much higher than normal. Approximately half of the CIDP patients had obvious asthenia. However, the level of fatigue did not correlate with the severity of the course of CIDP.Conclusion. The findings suggest that fatigue is important in patients with CIDP that should be taken into account in the treatment of these patients.
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Rizvanova, A. S., D. A. Grishina, and N. A. Suponeva. "Clinical heterogeneity of chronic inflammatory demyelinating polyneuropathy: diagnostic challenges." Almanac of Clinical Medicine 48, no. 1 (March 17, 2020): 56–64. http://dx.doi.org/10.18786/2072-0505-2020-48-007.

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Сhronic inflammatory demyelinating polyneuropathy (CIDP) is the most prevalent acquired dysimmune neuropathy with clinical picture of symmetric motor and sensory disturbances. Since the first description of CIDP, many atypical variants have been described, which may reach up to 50% of cases. Diagnosis of atypical CIDP may be challenging due to different clinical presentation and treatment response. Current researches improve our knowledge about dysimmune neuropathies and highlight the importance of its classification. Nowadays CIDP is considered as a spectrum of disorders rather than a separate disease entity. Up to date, more than 15 diagnostic criteria have been proposed reflecting the complexity of СIDP diagnosis. Many polyneuropathies may mimic CIDP, therefore CIDP is frequently a diagnosis of exclusion. The key diagnostic instrument is electroneuromyography; however, the issues related to results misinterpretation and some technical aspects are the most important in CIDP misdiagnosis. Supportive instrumental and laboratory methods have variable sensitivity and specificity, making challenging CIDP diagnosis, especially its atypical forms. The importance of an early and accurate diagnosis of CIDP is supported by an effective pathogenic treatment, which affects the patient's prognosis and level of disability.
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Stewart, John D., Roger McKelvey, Liam Durcan, Stirling Carpenter, and George Karpati. "Chronic inflammatory demyelinating polyneuropathy (CIDP) in diabetics." Journal of the Neurological Sciences 142, no. 1-2 (October 1996): 59–64. http://dx.doi.org/10.1016/0022-510x(96)00126-8.

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Gapeshin, R. A., E. R. Barantsevich, and A. A. Yakovlev. "PATHOGENESIS, CLINICAL AND LABORATORY FEATURES OF CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY." Scientific Notes of the I. P. Pavlov St. Petersburg State Medical University 25, no. 3 (December 25, 2018): 14–24. http://dx.doi.org/10.24884/1607-4181-2018-25-3-14-24.

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Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired progressive or relapse-remitting immunemediated disease of peripheral nervous system. CIDP has typical and atypical variants. Typical variant includes development of symmetric motor and sensory nerve fibers functions abnormalities. The diagnosis of CIDP reveals on clinical presentation and electrophysiological data. There aren’t any biomarkers of such disease. Cerebrospinal fluid analysis, magnetic resonance tomography of peripheral nerves and nerve biopsy may be additional methods to confirm the diagnosis. Instead of international criteria of CIDP diagnosis and large variety of laboratory and instrumental methods, there are many difficulties to make the appropriate diagnosis. This review discusses current concepts of pathogenesis, clinical diagnostics and laboratory and instrumental methods used for differential diagnosis and confirmation of the diagnosis of CIDP and new areas in CIDP research.
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Dissertations / Theses on the topic "Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)"

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Carmo, Samuel Sullivan. "Características do envolvimento do Sistema Nervoso Central na Polirradiculoneuropatia Inflamatória Desmielinizante Crônica: um estudo mediante técnicas quantitativas de Imagem por Ressonância Magnética." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/17/17140/tde-16092014-170302/.

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A polineuropatia inflamatória desmielinizante crônica (PIDC) é uma síndrome caracterizada fundamentalmente pela disfunção do Sistema Nervoso Periférico e que afeta muito a qualidade de vida dos pacientes. O envolvimento da PIDC com o Sistema Nervoso Central tem sido descrito, maiormente como sendo subclínico, porém não há estudos sobre a caracterização deste envolvimento de uma forma ampla e quantitativa. Avaliamos 11 pacientes com PIDC, todos tratados e sem sinais clínicos de alterações centrais, e 11 controles, pareados em gênero e faixa etária de 19 a 69 anos. Foram adquiridas neuroimagens em uma máquina de Ressonância Magnética de alto campo (3T) usando diferentes técnicas de imagens; volumétricas ponderadas em T1, volumétricas de inversão e recuperação com atenuação de fluidos e ponderadas em T2, relaxométricas de cinco ecos para mapas de T2, de transferência de magnetização e por tensor de difusão. As imagens foram processadas em diferentes ferramentas computacionais e foram obtidos resultados para estudos da difusibilidade, volumetria, morfometria, tratometria e conectividade cerebral, além de achados radiológicos para os pacientes. As análises de grupos foram executadas por; 1) testes paramétricos monocaudais de duas amostras pareadas para os resultados da volumetria, da tratometria e conectividade cerebral; 2) mapeamento estatístico paramétrico para os resultados da morfometria baseada em voxel e; 3) estatística espacial baseada em tratos para os resultados da difusibilidade. Foram detectas alterações em todas as comparações. Os principais achados indicam um envolvimento possivelmente caracterizado por uma perda volumétrica encefálica generalizada, sobretudo nas regiões periventriculares associadas a ventrículos proeminentes acrescido de, um aumento da difusibilidade transversa e oblíqua nos maiores tratos de substância branca e, também há uma perda de densidade na substância branca periventricular e um aumento na substância cinzenta em uma região que sinaliza para o espessamento trigeminal bilateral e, uma redução geral da conectividade cerebral estrutural.
Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) is a severe disease fundamentally characterized by dysfunction of the Peripheral Nervous System and affects greatly the quality of life of patients. The Central Nervous System (CNS) involvement in CIDP has not been described using recent quantitative neuroimaging techniques. We evaluated 11 patients with CIDP, all treated and without clinical signs of central alterations and 11 controls matched for gender and age group of 19 to 69 years. Magnetic Resonance Imaging were performed on a 3T scanner using different imaging techniques; structural 3D T1-weighted, fluid-attenuated inversion recovery, relaxometry with 5 echoes pulse sequence for T2 maps, magnetization transfer weighted and diffusion tensor imaging. The images were processed on different tools and were obtained results for the studies of diffusivity, volumetry, morphometry, tractometry, brain connectivity, and radiological findings of patients. Different statistical group analyses were performed in the quantitative results: 1) Parametric test for volumetry, tractometry and brain connectivity; 2) Parametric mapping for voxel morphometry; 3) Tract-based spatial statistics (TBSS) for diffusion coefficients. Changes were detected in all comparisons. In the patients, our main findings are: generalized loss brain volume more pronounced in periventricular regions associated with prominent ventricles, increased simultaneously perpendiculars and parallel diffusivity in the major tracts of the TBSS analyze, white matter density loss in the periventricular area, some bilateral trigeminal thickening, and general reduction of the brain connectivity. The CIDP affects the global brain and represents a demyelination in the CNS.
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Silva, Alex Eduardo da. "Avaliação genotípica de pacientes com polineuropatia inflamatória desmielinizante crônica: estudo da duplicação/deleção do gene PMP22." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/17/17140/tde-25112014-142430/.

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Introdução: Polineuropatias são doenças do sistema nervoso periférico com etiologias variadas. Dentre elas são freqüentes as inflamatórias e as hereditárias, com prevalência de 0,67-7,7/100000 e 7,9-82,3/100000 para polineuropatia inflamatória desmielinizante crônica (PIDC) e Doença de Charcot-Marie-Tooth (CMT), respectivamente. Existem poucas evidências de sobreposição entre estas duas doenças e também algumas dificuldades diagnósticas em situações específicas. Objetivos: Estudar a freqüência de mutações (duplicações e deleções) do gene PMP22 em uma coorte de pacientes inicialmente diagnosticados como PIDC ou suspeitos de apresentarem as duas condições, os sinais e sintomas sugestivos da sobreposição e os fatores implicados em erro de classificação da neuropatia. Métodos: 111 pacientes com diagnóstico de PIDC foram estudados. DNA foi isolado a partir de leucócitos de sangue periférico segundo protocolo padrão. Duplicações e deleções do gene PMP22 foram avaliadas através de marcadores polimórficos do DNA localizados dentro do cromossomo 17p11.2-12, o qual contém o gene PMP22. Achados clínicos e laboratoriais também foram estudados e comparados entre os grupos. Resultados: Dentre os 111 pacientes estudados, mutações no PMP22 foram encontradas em 10 (9%), sendo duplicações em 9 pacientes e deleção em 1 paciente. Concomitância entre PIDC e CMT foi verificada em 4 pacientes (3,6%), todos com duplicação do PMP22. Os outros 6 pacientes foram diagnosticados como CMT puro (5) ou Neuropatia Hereditária Susceptível à Compressão (1), visto que não apresentaram melhora com o uso de tratamento imunomodulador e/ou imunossupressor (5 casos) ou foi estabelecido diagnóstico alternativo associado (1). Os outros 101 pacientes não tiveram duplicação nem deleção deste gene e, portanto, tinham PIDC apenas. Idade média dos pacientes com PIDC/CMT foi de 23,8±18,0 anos e 43,6±19,3 anos para pacientes sem mutações (p=0,04). Houve diferença estatísticamente significativa na resposta ao tratamento entre os grupos PIDC/CMT X CMT (p=0,008) e PIDC X CMT (p=0,00). Ausência de história familiar e presença de doenças e hábitos ligados ao desenvolvimento de neuropatias periféricas, como diabetes mellitus e ingesta de bebidas alcoólicas, por exemplo, bem como achados atípicos na eletroneuromiografia e na biópsia de nervo podem ter contribuído para a confusão diagnóstica nos casos de CMT puro. Conclusões: Alguns pacientes podem desenvolver PIDC em associação com CMT e se beneficiam do tratamento. A neuropatia hereditária poderia predispor à neuropatia inflamatória, uma vez que estes pacientes tendem a apresentar essa condição em idades mais precoces. Cautela deve ser dispensada àqueles pacientes com suspeita diagnóstica de PIDC que não têm os achados clássicos ou não melhoram com o tratamento, uma vez que podem apresentar outras etiologias para a neuropatia, dentre elas uma neuropatia hereditária, como a CMT.
Introduction: Polyneuropathies are peripheral nervous system disorders with a wide range of etiologies. Among them, inflammatory and hereditary are frequent with prevalence of 0.67-7.7/100000 and 7.9-82.3/100000, for chronic inflammatory demyelinating polyneuropathy (CIDP) and Charcot-Marie-Tooth disease (CMT), respectively. There are a few evidence of ovelapping between these two conditions and also some diagnostic difficulties in specific situations. Objectives: To study the frequency of mutations in PMP22 gene (duplications and delections) among a cohort of patients initially diagnosed as CIDP or suspected to have both conditions, the signs and symptoms related to this ovelapping and factors implicated in misdiagnose. Methods: 111 patients with an initially CIDP suspected diagnosis were studied. DNA was isolated from peripheral blood leucocytes following a standard salting-out protocol. Duplications and delections in the PMP22 gene were analysed by polymorphic DNA markers located within the chromosome 17p11.2-12, wich contains the PMP22 gene. Clinical and laboratory findings were also studied and compared within groups. Results: Among 111 patients studied, 10 (9%) were found to harbor mutations in PMP22 gene, specifically duplications in nine and delection in one. We therefore diagnosed CIDP plus CMT in four patients (3.6%), all of them with a duplicated PMP22 gene. The other six patients were diagnosed as pure CMT (5) or Hereditary Neuropathy with liability to Pressure Palsy (1), as they did not improved with the use of immunomodulatory and/or immunosupressive treatment (five cases) or were found to have alternative associated diagnosis (one patient). The other 101 patients did not show duplication nor delection in this gene, so they had CIDP. Mean age of patients with CIDP/CMT were 23.8±18.0 years and 43.6±19.3 years for patients without mutations (p=0.04). There were statistically significant difference in treatmet response between groups CIDP/CMT X CMT (p=0.008) and CIDP X CMT (p=0.00). The lack of family history and presence of other diseases and habits linked to the development of peripheral neuropathies, as diabetes mellitus and alcohol intake, for instance, as well as atypical findings in electrodiagnostic studies and nerve biopsy may have contributed to misdiagnose in the pure CMT cases. Conclusions: Some patients may develop CIDP in association with CMT and have benefit from treatment. The hereditary neuropathy may predispose to the inflammatory neuropathy as these patients tend to show this condition at younger ages. Caution should be dispensed to those patients with a suspected diagnose of CIDP who do not have the classical disease findings or do not improve with treatment, as they can have alternative etiologies for the neuropathy, among them a hereditary neuropathy as CMT disease.
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Books on the topic "Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)"

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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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Kaplan, Tamara, and Tracey Milligan. Demyelinating Diseases 2: NMO, ADEM, GBS, CIDP (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190650261.003.0014.

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The video in this chapter explores demyelinating diseases, and focuses on neuromyelitis optica (NMO), acute disseminated encephalomyelitis (ADEM), Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP), including their symptoms, causes, and diagnostic tests.
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Katirji, Bashar. Case 18. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0022.

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Immune-mediated polyneuropathies are important to recognize since the majority of them are treatable. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is the prototype of the acquired chronic demyelinating polyneuropathies. It should be distinguished from other acquired demyelinating polyneuropathy such as those associated with monoclonal gammopathy, myeloproliferative disorder, and myelin-associated glycoprotein. This case presents a patient with a chronic demyelinating polyneuropathy associated with monoclonal gammopathy of unknown significance. The discussion includes the clinical and electrodiagnostic criteria for CIDP and distinguishing features from axonal polyneuropathies, other acquired demyelinating polyneuropathies, and inherited demyelinating polyneuropathies such as Charcot-Marie-Tooth disease type I. The case also highlights the diagnostic criteria for conduction block and temporal dispersion based on analysis of compound muscle action potential amplitude, area, and duration.
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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 55-Year-Old Female with Slowly Progressive Weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0010.

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Chronic inflammatory demyelinating polyneuropathy (CIPD) typically presents with both proximal and distal weakness, areflexia, and distal sensory findings. Two-thirds of patients have a progressive course over many months to years, however one-third of patients have a relapsing course with partial or complete recovery. It is important to be aware of several systemic disorders which may be associated with CIDP. Immunoglobulin M antibody–producing neuropathies have a monoclonal protein that is usually detected with serum protein electrophoresis, which may mimic CIDP. This chapter emphasizes the importance of differential diagnosis and workup. Treatment options are also described.
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Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson, and David Ledingham. Disorders of peripheral nerves and motor neuron disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0007.

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This chapter discusses the clinical features and evidence-based drug treatment regimens of polyneuropathies (Guillain–Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), multifocal motor neuropathy, paraproteinaemic neuropathies, and vasculitic neuropathies), mononeuropathies (Bell’s palsy), systemic conditions with peripheral nerve involvement (Sjögren’s and sarcoidosis), and motor neuron disease (MND).
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Shaibani, Aziz. Dyspnea. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0009.

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The most common causes of dyspnea are not neuromuscular but rather are cardiac and pulmonary. However, dyspnea is an important and serious manifestation of many neuromuscular disorders, and it may compound an underlying pulmonary or cardiac problem. The diaphragm is a skeletal muscle under the control ofperipheral nerves(phrenic nerves) and may be targeted by inflammatory neuropathies such as Guillain-Barrésyndrome(GBS), chronic inflammatory demyelinating polyneuropathy(CIDP), and brachial plexitis, myopathies such as acid maltase deficiency and muscular dystrophies, and neuromuscular disorders such as myasthenia gravis. Periodic measurement of pulmonary function isrecommended in neuromuscular clinics.
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Shaibani, Aziz. Dyspnea. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0009.

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The most common causes of dyspnea are not neuromuscular, but rather cardiac and pulmonary. However, dyspnea is an important and serious manifestation of many neuromuscular disorders, and it may compound an underlying pulmonary or cardiac problem. The diaphragm is a skeletal muscle under the control of a peripheral nerve and may be targeted by inflammatory neuropathies such as Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), and brachial plexitis or myopathies such as acid maltase deficiency, muscular dystrophy (MD), and neuromuscular disorders such as myasthenia gravis (MG). Periodic measurement of pulmonary function is a recommended measure in neuromuscular clinics.
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Shaibani, Aziz. Proximal Arm Weakness. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0012.

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Proximal arm muscles include supra and infra spinatii, pectoralis major and minor, teres major and minor, rhomboids, serratus anterior, deltoids, biceps, and triceps. The main function of these muscles is to abduct the arms. The first sign of proximal weakness is difficulty raising arms above the horizontal level. Shoulder conditions like supraspinatus tendonitis are often confused as proximal weakness. In myopathies, usually proximal arm weakness is associated with proximal leg weakness. Motor neuron diseases (MNDs) like amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA) and neuropathies like chronic inflammatory demyelinating polyneuropathy (CIDP) may present with symmetrical proximal weakness. For differentiation, electromyography/nerve conduction study (EMG/NCS) is crucial.
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Shaibani, Aziz. Proximal Leg Weakness. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0013.

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Proximal leg weakness is a common presentation to neuromuscular clinics. Hip flexion, abduction, adduction, and rotation is mainly achieved by the iliopsoas, glutei, and obturator muscles. Hip pathology, especially when painless, may lead to diagnostic confusion that needs a good electromyogram (EMG) of these muscles to be cleared. Most myopathies present with painless proximal leg weakness (difficulty climbing stairs and arising out of a deep chair). chronic inflammatory demyelinating polyneuropathy (CIDP), diabetic amyotrophy, motor neuron diseases (MNDs), and lumbar plexitis may all present similarly. Pain is more typical of these conditions that myopathies. Students should be taught to avoid the assumption that proximal weakness is caused only by myopathies.
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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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Abstract:
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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Book chapters on the topic "Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)"

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Kuwabara, Satoshi, and Sonoko Misawa. "Chronic Inflammatory Demyelinating Polyneuropathy." In Advances in Experimental Medicine and Biology, 333–43. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9636-7_21.

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Braun-Falco, Markus, Henry J. Mankin, Sharon L. Wenger, Markus Braun-Falco, Stephan DiSean Kendall, Gerard C. Blobe, Christoph K. Weber, et al. "Polyneuropathy, Chronic Inflammatory Demyelinating." In Encyclopedia of Molecular Mechanisms of Disease, 1683–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_3174.

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Peters, Nils, Martin Dichgans, Sankar Surendran, Josep M. Argilés, Francisco J. López-Soriano, Sílvia Busquets, Klaus Dittmann, et al. "Chronic Inflammatory Demyelinating Polyneuropathy." In Encyclopedia of Molecular Mechanisms of Disease, 357. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_9089.

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Hund, Ernst F., Hans-Peter Hartung, Allan H. Ropper, and Daniel F. Hanley. "Chronic Inflammatory Demyelinating Polyneuropathy." In Neurocritical Care, 788–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87602-8_68.

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Suzuki, Miki, and Gérard Said. "Chronic Inflammatory Demyelinating Polyneuropathy." In Neuroimmune Diseases, 737–64. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-19515-1_25.

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Dudley, Matthew Z., Daniel A. Salmon, Neal A. Halsey, Walter A. Orenstein, Rupali J. Limaye, Sean T. O’Leary, and Saad B. Omer. "Do Vaccines Cause Chronic Inflammatory Disseminated Polyneuropathy (CIDP)?" In The Clinician’s Vaccine Safety Resource Guide, 213–15. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-94694-8_29.

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Grebenciucova, Elena, and Kourosh Rezania. "Immunopathogenesis and Treatment of Guillain-Barre Syndrome and Chronic Inflammatory Demyelinating Polyneuropathy." In Inflammatory Disorders of the Nervous System, 203–25. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-51220-4_10.

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"Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)." In Imaging in Neurology, 398. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-323-44781-2.50310-7.

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"Polyneuropathy, Chronic Inflammatory Demyelinating (CIDP)." In The APRN and PA’s Complete Guide to Prescribing Drug Therapy. New York, NY: Springer Publishing Company, 2019. http://dx.doi.org/10.1891/9780826179357.0314.

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"Polyneuropathy, Chronic Inflammatory Demyelinating (CIDP)." In The APRN and PA’s Complete Guide to Prescribing Drug Therapy. New York, NY: Springer Publishing Company, 2019. http://dx.doi.org/10.1891/9780826179340.0314.

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Conference papers on the topic "Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)"

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Cameron, Shane, and Rami Haddad. "066 Contactin-1-mediated chronic inflammatory demyelinating polyneuropathy (CIDP) presenting as an acute case of guillain bare syndrome (GBS)." In ANZAN Annual Scientific Meeting 2021 Abstracts. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/bmjno-2021-anzan.66.

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Crump, Nicholas, Richard Macdonell, and Michael Cartwright. "025 A cross-sectional study of patients with chronic inflammatory demyelinating polyneuropathy (CIDP): identifying ultrasonographic features for diagnosis and prognosis." In ANZAN Annual Scientific Meeting 2021 Abstracts. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/bmjno-2021-anzan.25.

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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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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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You might also be interested in the extended bibliographies on the topic 'Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)' for particular source types:
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