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Journal articles on the topic 'Chronic inflammatory demyelinating neuropathy'

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Published: 4 June 2025

Last updated: 15 July 2025

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

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BABA, Masayuki. "Chronic Inflammatory Demyelinating Poly neuropathy: Treatable Hypertrophic Neuropathy." Internal Medicine 38, no. 5 (1999): 384–85. http://dx.doi.org/10.2169/internalmedicine.38.384.

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Oh, S. J., J. L. Joy, and R. Kuruoglu. ""Chronic sensory demyelinating neuropathy": chronic inflammatory demyelinating polyneuropathy presenting as a pure sensory neuropathy." Journal of Neurology, Neurosurgery & Psychiatry 55, no. 8 (1992): 677–80. http://dx.doi.org/10.1136/jnnp.55.8.677.

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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 (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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Hughes, R. A. C., C. M. Gabriel, N. A. Gregson, and K. J. Smith. "Treatment of inflammatory neuropathy." Multiple Sclerosis Journal 3, no. 2 (1997): 88–92. http://dx.doi.org/10.1177/135245859700300206.

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Experimental autoimmune neuritis (EAN) provides an accurate model for understanding the mechanism of acute and chronic inflammatory demyelinating polyradiculoneuropathy (AIDP and CIDP). Treatments aimed at every stage of the immune process in EAN have been effective in inhibiting or treating the disease, including antibodies directed against cell adhesion molecules on the endothelium, inhibition of T cells, removal or blockade of antibodies, depletion of complement and interference with the release or action of macrophage effector molecules. In human disease the only proven treatments are plasma exchange and intravenous immunoglobulin (IVIg) in AIDP, and either of these regimens and also corticosteroids in CIDP. However the outcome from AIDP and CIDP remains unsatisfactory with existing immunosuppressive regimens. This problem arises from the fact that while demyelination appears to be effectively and promptly repaired by remyelination, it may be accompanied by axonal degeneration which can cause severe persistent disability. In addition to limiting demyelination, it will also be important to develop strategies to protect axons from degeneration and to enhance regeneration.

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Kieseier, B. C., M. C. Dalakas, and H. P. Hartung. "Immune mechanisms in chronic inflammatory demyelinating neuropathy." Neurology 59, Issue 12, Supplement 6 (2002): S7—S12. http://dx.doi.org/10.1212/wnl.59.12_suppl_6.s7.

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Mathis, Stephane, Laurent Magy, Laho Diallo, Sami Boukhris, and Jean-Michel Vallat. "Amyloid neuropathy mimicking chronic inflammatory demyelinating polyneuropathy." Muscle & Nerve 45, no. 1 (2011): 26–31. http://dx.doi.org/10.1002/mus.22229.

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Grishina, D. A., and N. A. Suponeva. "Neurophysiological differential diagnostic markers in hereditary neuropathy with liability to pressure palsies and chronic inflammatory demyelinating polyradiculoneuropathy." Neuromuscular Diseases 13, no. 1 (2023): 52–67. http://dx.doi.org/10.17650/2222-8721-2023-13-1-52-67.

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Background. Today, the issues of differential diagnosis of chronic hereditary and acquired demyelinating neuropathies are still relevant. The variety of phenotypic variants of chronic inflammatory demyelinating polyradiculoneuropathy and hereditary neuropathy with liability to pressure palsies, their remitting course and the non-specificity of neurophysiological changes necessitate the identification of clear markers that can help in the differential diagnosis of the neuropathies under discussion already at the stage of the analysis of the electroneuromyographic study data.Aim. To determine neurophysiological differential diagnostic markers in the manifestation of chronic inflammatory demyelinating polyradiculoneuropathy and hereditary neuropathy with liability to pressure palsies.Materials and methods. A retrospective analysis of the data of neurophysiological examination of 25 patients with hereditary neuropathy with liability to pressure palsies and 25 patients with chronic inflammatory demyelinating polyradiculoneuropathy.Results. A combination of such indicators as the age of the onset of the disease <33 years, the latency of the dM-wave with m.ADM ><3.7 ms and with m.AH ><4.8 ms (AUROC >0.7), the value of the conduction velocity along of the motor fibers of the ulnar nerve at the level of the elbow joint <37.5 m/s (AUROC >0.8), the conduction velocity along of the sensory fibers of the median nerve at the level of the wrist <48 m/s (AUROC >0.8), absence of conduction block along the median nerve in any area, and also the presence along the ulnar nerve at the level of the elbow joint is characteristic of hereditary neuropathy with liability to pressure palsies and allows to exclude chronic inflammatory demyelinating polyradiculoneuropathy.Conclusion. Neurophysiological markers have been identified that can help in the differential diagnosis of two chronic remitting demyelinating neuropathies: chronic inflammatory demyelinating polyradiculoneuropathy and hereditary neuropathy with liability to pressure palsies. However, only a combined analysis of clinical, anamnestic and paraclinical data makes it possible to establish a final diagnosis.

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Md, Shamshir Alam, Malik Garima, Tanwar Priyanka, et al. "A review on Chronic Inflammatory Demyelinating Polyradiculoneuropathy." International Journal of Current Science Research and Review 06, no. 01 (2023): 259–74. https://doi.org/10.5281/zenodo.7533109.

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<strong>ABSTRACT: </strong>Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a kind of inflammatory neuropathy that has a gradual start and symmetrical sensory involvement. However, there are several clinical variances, suggesting that CIDP may represent a spectrum of linked disorders rather than a single disease entity. While the prevailing idea of CIDP pathogenesis is that cell-mediated and humoral processes interact in an abnormal immune response to damage peripheral neurons, the proportional roles of T cell and autoantibody responses are yet unknown. T cell responses to specified myelin antigens are responsible in animal models of spontaneous inflammatory neuropathy. Antibodies to Schwann cell, compact myelin, and nodal antigens have been found in different human inflammatory neuropathies. The roles of the cellular and humoral immune systems in the development of CIDP are discussed in this review. It is believed that, in the future, the identification of clinical phenotypes and the underlying disease processes would aid in the development of diagnostic and therapy options for CIDP.

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ORMAN, Gözde, and Gülten SUNGUR. "Inflammatory Optic Neuropathy." Güncel Retina Dergisi (Current Retina Journal) 9, no. 1 (2024): 41–46. http://dx.doi.org/10.37783/crj-0435.

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Optic neuritis is the primary inflammation of the optic nerve. Chronic Recurrent Isolated Optic Neuropathy is an inflammatory optic neuropathy characterized by its recurrent and/or chronic nature, as well as corticosteroid sensitivity. Relapses that occur after the reduction or cessation of steroids and more severe visual loss compared to demyelinating optic neuritis are characteristic features. Although patients initially tend to respond well to steroids, cumulative damage can lead to poor visual outcomes and permanent loss of the retinal nerve fiber layer and ganglion cell layer. Diagnosing inflammatory optic neuropathies is crucial, as maintenance immunosuppressive therapy should be initiated in patients with relapses to protect against permanent vision loss in many types.

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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 (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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Lehmann, Helmar Christoph, David Burke, and Satoshi Kuwabara. "Chronic inflammatory demyelinating polyneuropathy: update on diagnosis, immunopathogenesis and treatment." Journal of Neurology, Neurosurgery & Psychiatry 90, no. 9 (2019): 981–87. http://dx.doi.org/10.1136/jnnp-2019-320314.

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Chronic inflammatory demyelinating polyneuropathy (CIDP) is an immune-mediated neuropathy typically characterised by symmetrical involvement, and proximal as well as distal muscle weakness (typical CIDP). However, there are several ‘atypical’ subtypes, such as multifocal acquired demyelinating sensory and motor neuropathy (Lewis-Sumner syndrome) and ‘distal acquired demyelinating symmetric neuropathy’, possibly having different immunopathogenesis and treatment responses. In the absence of diagnostic and pathogenetic biomarkers, diagnosis and treatment may be difficult, but recent progress has been made in the application of neuroimaging tools demonstrating nerve hypertrophy and in identifying subgroups of patients who harbour antibodies against nodal proteins such as neurofascin and contactin-1. Despite its relative rarity, CIDP represents a significant economic burden, mostly due to costly treatment with immunoglobulin. Recent studies have demonstrated the efficacy of subcutaneous as well as intravenous immunoglobulin as maintenance therapy, and newer immunomodulating drugs can be used in refractory cases. This review provides an overview focusing on advances over the past several years.

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El-Wahsh, Shadi, Cecilia Cappelen-Smith, and Judith Spies. "Chronic inflammatory demyelinating polyradiculoneuropathy presenting as predominantly sciatic monomelic neuropathy." BMJ Neurology Open 2, no. 1 (2020): e000045. http://dx.doi.org/10.1136/bmjno-2020-000045.

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BackgroundChronic inflammatory demyelinating polyneuropathy (CIDP) is a common yet underdiagnosed cause of potentially treatable chronic sensorimotor neuropathy. The classical form of the disease is characterised by symmetrical weakness in both distal and proximal muscle groups accompanied by sensory dysfunction and diminished tendon reflexes lasting more than 2 months.MethodThe diagnosis of CIDP is supplemented by electrodiagnostic studies and biopsy findings confirming demyelination, in accordance with well-established diagnostic criteria. Atypical presentations of CIDP often pose a diagnostic challenge.ResultsIn this paper, we present a case of isolated lower limb involvement due to CIDP to raise awareness of this focal lower limb variant. Of particular, significance is the use of lumbosacral plexus MRI to assist in the diagnosis.ConclusionFocal CIDP is an atypical presentation that should be considered in patients presenting with chronic monomelic neuropathy and should be investigated with electrodiagnostic studies, lumbar puncture, nerve biopsy and MRI of the nerve roots and plexuses.

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Parker, Vivien, Jodi Warman Chardon, Julie Mills, Claire Goldsmith, and Pierre R. Bourque. "Supramaximal Stimulus Intensity as a Diagnostic Tool in Chronic Demyelinating Neuropathy." Neuroscience Journal 2016 (June 16, 2016): 1–5. http://dx.doi.org/10.1155/2016/6796270.

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Objective. The ability to correctly identify chronic demyelinating neuropathy can have important therapeutic and prognostic significance. The stimulus intensity value required to obtain a supramaximal compound muscle action potential amplitude is a commonly acquired data point that has not been formally assessed as a diagnostic tool in routine nerve conduction studies to identify chronic neuropathies. We postulated that this value was significantly elevated in chronic demyelinating neuropathy. Methods. We retrospectively reviewed electrophysiology laboratory records to compare the stimulus intensity values recorded during median and ulnar motor nerve conduction studies. The groups studied included normal controls (n=42) and the following diagnostic categories: chronic inflammatory demyelinating neuropathy (CIDP) (n=20), acquired inflammatory demyelinating neuropathy (AIDP) (n=13), Charcot Marie Tooth (CMT) type 1 or 4C (n=15), carpal tunnel syndrome (CTS) (n=11), and amyotrophic lateral sclerosis (ALS) (n=18). Results. Supramaximal intensities were significantly higher in patients with CMT (median nerve: 43.4 mA) and CIDP (median nerve: 38.9 mA), whereas values similar to normal controls (median nerve: 25.3 mA) were obtained in ALS, CTS, and AIDP. Conclusions. Supramaximal stimulus intensity may be used as an additional criterion to identify the pathophysiology of neuropathy. We postulate that endoneurial hypertrophic changes may increase electrical impedance and thus the threshold of excitation at nodes of Ranvier.

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Herraets, Ingrid J. T., H. Stephan Goedee, Johan A. Telleman, et al. "Nerve ultrasound improves detection of treatment-responsive chronic inflammatory neuropathies." Neurology 94, no. 14 (2020): e1470-e1479. http://dx.doi.org/10.1212/wnl.0000000000008978.

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ObjectiveTo examine the diagnostic accuracy of nerve ultrasound in a prospective cohort of consecutive patients with a clinical suspicion of chronic inflammatory neuropathies, including chronic inflammatory demyelinating polyneuropathy, Lewis-Sumner syndrome, and multifocal motor neuropathy, and to determine the added value in the detection of treatment-responsive patients.MethodsBetween February 2015 and July 2018, we included 100 consecutive incident patients with a clinical suspicion of chronic inflammatory neuropathy. All patients underwent nerve ultrasound, extensive standardized nerve conduction studies (NCS), and other relevant diagnostic investigations. We evaluated treatment response using predefined criteria. A diagnosis of chronic inflammatory neuropathy was established when NCS were abnormal (fulfilling criteria of demyelination of the European Federation of Neurological Societies/Peripheral Nerve Society) or when the degree of nerve enlargement detected by sonography was compatible with chronic inflammatory neuropathy and there was response to treatment.ResultsA diagnosis of chronic inflammatory neuropathy was established in 38 patients. Sensitivity and specificity of nerve ultrasound and NCS were 97.4% and 69.4% and 78.9% and 93.5%, respectively. The added value of nerve ultrasound in detection of treatment-responsive chronic inflammatory neuropathy was 21.1% compared to NCS alone.ConclusionsNerve ultrasound and NCS are complementary techniques with superior sensitivity in the former and specificity in the latter. Addition of nerve ultrasound significantly improves the detection of chronic inflammatory neuropathies. Therefore, it deserves a prominent place in the diagnostic workup of chronic inflammatory neuropathies.Classification of evidenceThis study provides Class IV evidence that nerve ultrasound is an accurate diagnostic tool to detect chronic inflammatory neuropathies.

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Kim, Se Hoon, Ha Young Shin, Seung Min Kim, Ki-Han Kwon, and Yang Ki Minn. "Leprotic neuropathy misdiagnosed as chronic inflammatory demyelinating polyneuropathy." Leprosy Review 83, no. 1 (2012): 93–97. http://dx.doi.org/10.47276/lr.83.1.93.

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Alonso-Navarro, Hortensia, Angel Fernández-Díaz, Manuela Martín-Prieto, Juan José Ruiz-Ezquerro, Tomás López-Alburquerque, and Félix Javier Jiménez-Jiménez. "Tremor Associated With Chronic Inflammatory Demyelinating Peripheral Neuropathy." Clinical Neuropharmacology 31, no. 4 (2008): 241–44. http://dx.doi.org/10.1097/wnf.0b013e3181585b71.

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Léger, Jean-Marc. "Multifocal motor neuropathy and chronic inflammatory demyelinating polyradiculoneuropathy." Current Opinion in Neurology 8, no. 5 (1995): 359–63. http://dx.doi.org/10.1097/00019052-199510000-00006.

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Wang, Liu, Dan Wang, Yuyi Ruan, et al. "Progressive muscle weakness and amyotrophy during pregnancy as the first manifestation of systemic lupus erythematosus: A case report and review of literature." Science Progress 104, no. 4 (2021): 003685042110502. http://dx.doi.org/10.1177/00368504211050276.

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Background: Systemic lupus erythematosus is a common autoimmune disease involving multiple systems. Clinical involvement of the central and peripheral nervous systems is not unusual, but peripheral neuropathy in systemic lupus erythematosus with chronic inflammatory demyelinating polyneuropathy is uncommon. Our study aimed to illustrate the clinical features, diagnosis, and treatment of systemic lupus erythematosus combined with chronic inflammatory demyelinating polyneuropathy, and to aid in the identification of peripheral neuropathy in systemic lupus erythematosus. Methods: This article reports a case of systemic lupus erythematosus with onset in pregnancy, with chronic inflammatory demyelinating polyneuropathy as the first manifestation. We then analyze the identification of common peripheral neuropathy in systemic lupus erythematosus in detail, based on a literature review of confirmed cases of systemic lupus erythematosus combined with chronic inflammatory demyelinating polyneuropathy. Results: A 34-year-old woman presented progressive muscle weakness and muscular atrophy in the extremities during pregnancy, 3 years previously. At 4 months after onset, she had completely lost the ability to hold objects and walk, and had slight numbness in the limbs, without paresthesia. Her condition was misdiagnosed as “motor neuron disease” at the time. Three years after onset, her condition was revisited because of nephrotic syndrome, and she was diagnosed with nephrotic syndrome and peripheral nerve injury caused by systemic lupus erythematosus. After immunosuppressive treatment with corticosteroids and intravenous cyclophosphamide, her symptoms of muscle weakness were markedly improved. This article summarizes the characteristics of systemic lupus erythematosus combined with chronic inflammatory demyelinating polyneuropathy that have been reported in the literature, from the aspects of morbidity, disease progression, nerve injury, laboratory examinations, and treatment response. Conclusions: Our identification of a common peripheral neuropathy in systemic lupus erythematosus will help to improve clinicians’ understanding of various peripheral neuropathies in systemic lupus erythematosus. It will also aid in the early diagnosis and treatment of such patients, thus improving their long-term prognosis.

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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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Solmaz, Ismail, Elif Soyak Aytekin, Deniz Çağdaş, et al. "Recurrent Demyelinating Episodes as Sole Manifestation of Inherited CD59 Deficiency." Neuropediatrics 51, no. 03 (2019): 206–10. http://dx.doi.org/10.1055/s-0039-3399583.

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AbstractDefects in the regulatory components of the complement system can lead to inflammatory diseases. We present a patient who had four episodes of demyelination in the central nervous system as the only manifestation of inherited CD59 deficiency. Relapsing encephalopathy partially responsive to intravenous immunoglobulin and steroid treatments on the background of parental consanguinity suggested an inherited immune dysregulation. Next generation sequencing revealed homozygous mutation in the CD59 gene, confirmed by lack of CD59 expression on flow cytometry. Inherited CD59 deficiency is a rare autosomal recessive condition characterized by chronic hemolysis, recurrent strokes, and relapsing peripheral demyelinating neuropathy mimicking Guillain–Barré syndrome or chronic inflammatory demyelinating polyneuropathy. Recurrent central nervous system demyelinating episodes as the only manifestation has not been reported to date in inherited CD59 deficiency. This entity should be considered in the differential diagnosis of patients with early-onset recurrent neurological diseases with central or peripheral origin.

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Gapeshin, R. A., E. R. Barantsevich, D. I. Rudenko, et al. "Fatigue in patients with chronic inflammatory demyelinating polyneuropathy." Neurology, Neuropsychiatry, Psychosomatics 13, no. 1 (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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Hassianni Mercy L. Tobing, Noer, Agus Yudha Wijaya, Christina Aritonang, and Yoyok Hendro. "CHRONIC INFLAMMATORY DEMYELINATING POLYRADICULOPATHY." Jurnal Kedokteran Universitas Palangka Raya 9, no. 1 (2021): 1257–64. http://dx.doi.org/10.37304/jkupr.v9i1.2865.

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Chornic inflammatory demyelinating polyradiculoneuropathy (CIDP) merupakan penyakit immune-mediated neuropati (neuropati karena gangguan imunologis), penyakit yang jarang, langka dan bentuknya bermacam-macam (heterogen), tetapi dapat diobati. Selama abad 20 pengenalan CIDP masih terbatas, sehingga sebutan nama penyakit berbeda-beda. Deskripsi klinis dan histopatologis sering bercampur dengan penyakit mirip seperti sindrom Guillain-Barre’. Untuk mendiagnosis penyakit CIDP perlu dilakukan pemeriksaan eletromiografi (EMG) menilai kecepatan hantar saraf dan merupakan pemeriksaan diagnostik pasti. Ultrasound saraf dan MRI dapat pula membantu dalam diagnosis. CIDP terbagi dalam dua tipe yaitu tipikal CIDP dan varian atipikal CIDP. Varian atipikal CIDP dengan fenotipen berbeda menjadi tantangan dalam melakukan diagnosis.

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Luigetti, Marco, Manuela Papacci, Stefano Bartoletti, Alessandro Marcaccio, Angela Romano, and Mario Sabatelli. "AL amyloid neuropathy mimicking a chronic inflammatory demyelinating polyneuropathy." Amyloid 19, no. 1 (2012): 53–55. http://dx.doi.org/10.3109/13506129.2011.650247.

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Nardelli, E., P. Agazzi, A. Polo, et al. "HYPERTROPHY OF SPINAL ROOTS IN CHRONIC INFLAMMATORY DEMYELINATING NEUROPATHY." Journal of the Peripheral Nervous System 5, no. 1 (2000): 45. http://dx.doi.org/10.1046/j.1529-8027.2000.00513-41.x.

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Bedlack, Richard S., Tuan Vu, Simon Hammans, et al. "MNGIE neuropathy: Five cases mimicking chronic inflammatory demyelinating polyneuropathy." Muscle & Nerve 29, no. 3 (2004): 364–68. http://dx.doi.org/10.1002/mus.10546.

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Ryan, Monique M., and H. Royden Jones. "CMTX mimicking childhood chronic inflammatory demyelinating neuropathy with tremor." Muscle & Nerve 31, no. 4 (2005): 528–30. http://dx.doi.org/10.1002/mus.20292.

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Mazzeo, A., and G. Vita. "C5b‐9 TERMINAL COMPLEX ACTIVATION IN CHRONIC INFLAMMATORY DEMYELINATING NEUROPATHY." Journal of the Peripheral Nervous System 7, no. 1 (2002): 80. http://dx.doi.org/10.1046/j.1529-8027.2002.7011_33.x.

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Background: Complement activation plays an important role in the pathogenesis of some peripheral nerve disorders. Activated terminal attack complex (C5b‐9) was detected in the cerebrospinal fluid and in peripheral nerve of patients with Guillain‐Barré syndrome, suggesting its involvement in the tissue‐damaging processes. Recently, complement activation products have been described on and around amyloid deposits in acquired and hereditary amyloid neuropathy in which this may contribute to the injury of axons. Objective: The aim of this study was the investigation of patients with CIDP by immunohistochemistry for evidence of complement activation. Materials and Methods: We performed immunohistochemistry on frozen nerve specimens of 5 patients with CIDP compared with 3 patients with chronic inflammatory axonal neuropathy and 3 with HSMN, by using a panel of monoclonal antibodies raised against C5b‐9, macrophages, B, CD4 and CD8 cell subsets. Normal frozen nerves were used as controls. Results: C5b‐9 expression was found with strong signal in the perineurium, endoneurial vessel walls and in some epineurial vessels in inflammatory demyelinating and axonal neuropathies. C5b‐9 immunoreactivity was also present in the perineurial cells of HSMN and, with very low intensity, in normal control nerves. Conclusion: Our findings suggest that complement activation is an important factor in the cascade of events leading to immune‐mediated demyelination in CIDP and axonal damage in some chronic axonal neuropathies. Less‐specific positive perineurial immunoreactivity was detected in HSMN. Evidence of complement activation in inflammatory neuropathies may be helpful in the diagnosis.

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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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Watanabe, Shohei, Masanaka Takeda, Tomoko Saito, Akiko Kimura, and Hiroo Yoshikawa. "“Chronic” optic neuropathy in chronic inflammatory demyelinating polyneuropathy: A case report." Neurology and Clinical Neuroscience 1, no. 2 (2013): 78–81. http://dx.doi.org/10.1002/ncn3.16.

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Gable, Karissa. "Chronic Immune-Mediated Demyelinating Neuropathies." CONTINUUM: Lifelong Learning in Neurology 29, no. 5 (2023): 1357–77. http://dx.doi.org/10.1212/con.0000000000001290.

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ABSTRACT OBJECTIVE This article is an overview of chronic demyelinating neuropathies and highlights the phenotypic categorization, diagnosis, and treatment of chronic immune-mediated neuropathies. The clinical and diagnostic characteristics of other chronic demyelinating neuropathies that are common mimics of immune-mediated neuropathies are also discussed. LATEST DEVELOPMENTS The underlying pathophysiology of chronic demyelinating neuropathies is heterogeneous, and components of both humoral and cellular immune responses are thought to play a role in the immune-mediated types of chronic demyelinating neuropathy. The role of the humoral response is highlighted with a specific focus on the relatively recent discovery of antibody-mediated antinodal and paranodal demyelinating neuropathies. Additionally, new diagnostic criteria for some of the chronic demyelinating neuropathies, as well as ways to differentiate chronic inflammatory demyelinating polyradiculoneuropathy from other chronic demyelinating polyneuropathies, are discussed. ESSENTIAL POINTS Chronic demyelinating neuropathies can present with overlapping clinical characteristics with seemingly subtle variations. It is clinically important to differentiate these types of neuropathies because the treatment and management can vary and affect prognosis.

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Kim, Jee-Eun, and Jong Seok Bae. "Clinical Scales for Peripheral Neuropathy - Revision 2021." Journal of the Korean Neurological Association 39, no. 2 Suppl (2021): 2–14. http://dx.doi.org/10.17340/jkna.2021.2.16.

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Outcome measurements are essential to monitor the clinical course or the treatment response of peripheral neuropathy. Even though there are no designated standard scale for peripheral neuropathy currently, several clinical scales were validated to use for outcome measurements based on many researches. Here, we reviewed clinical scales commonly used and fulfilled clinimetric properties in peripheral neuropathy, especially focusing on inflammatory neuropathy (Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy). Each scale was classified according to the International Classification of outcome measure model - the International Classification of Functioning, Disability and Health to achieve a comprehensive concept of clinical scale in peripheral neuropathy.

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Wang, Cong‐Cong, Bin Liu, Xiao‐Li Li, Bing Yang, Yan‐Bin Li, and Rui‐Sheng Duan. "Chronic inflammatory demyelinating polyneuropathy‐like neuropathy in IgG4‐related disease." CNS Neuroscience & Therapeutics 28, no. 1 (2021): 172–74. http://dx.doi.org/10.1111/cns.13747.

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Verma, A., R. Tandan, A. M. Adesina, W. W. Pendlebury, T. J. Fries, and W. G. Bradley. "Focal neuropathy preceding chronic inflammatory demyelinating polyradiculoneuropathy by several years." Acta Neurologica Scandinavica 81, no. 6 (2009): 516–21. http://dx.doi.org/10.1111/j.1600-0404.1990.tb01011.x.

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Tsai, Der-Chong, Po-Kang Lin, Kon-Ping Lin, Ko-Pei Kao, and Jorn-Hon Liu. "Optic neuropathy in a patient with chronic inflammatory demyelinating polyneuropathy." Eye 14, no. 6 (2000): 911–12. http://dx.doi.org/10.1038/eye.2000.252.

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Hergüner, M. Özlem, Faruk İncecik, and Şakir Altunbaşak. "Cyclosporin Treatment in Three Children With Chronic Inflammatory Demyelinating Neuropathy." Pediatric Neurology 41, no. 3 (2009): 223–25. http://dx.doi.org/10.1016/j.pediatrneurol.2009.03.016.

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Nobile-Orazio, Eduardo, Francesca Gallia, Francesco Tuccillo, and Fabrizia Terenghi. "Chronic inflammatory demyelinating polyradiculoneuropathy and multifocal motor neuropathy: treatment update." Current Opinion in Neurology 23, no. 5 (2010): 519–23. http://dx.doi.org/10.1097/wco.0b013e32833dd218.

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Okhovat, Ali Asghar, Hiva Saffar, and Farzad Fatehi. "Amiodarone‐Induced Neuropathy with chronic inflammatory demyelinating polyneuropathy‐like presentation." Neurology and Clinical Neuroscience 8, no. 3 (2020): 160–63. http://dx.doi.org/10.1111/ncn3.12373.

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Kerasnoudis, Antonios. "Nerve ultrasound in a case of chronic inflammatory demyelinating neuropathy." Muscle & Nerve 47, no. 3 (2012): 443–46. http://dx.doi.org/10.1002/mus.23624.

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Gabre�ls-Festen, A. A. W. M., F. J. M. Gabre�ls, J. E. Hoogendijk, P. A. Bolhuis, P. J. H. Jongen, and H. M. Vingerhoets. "Chronic inflammatory demyelinating polyneuropathy or hereditary motor and sensory neuropathy?" Acta Neuropathologica 86, no. 6 (1993): 630–35. http://dx.doi.org/10.1007/bf00294303.

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Topa, Antonietta, Raffaele Dubbioso, Rosa Iodice, Lucio Santoro, and Fiore Manganelli. "Chronic inflammatory demyelinating polyneuropathy mimicking an acute painful diabetic neuropathy." Neurological Sciences 36, no. 8 (2015): 1509–10. http://dx.doi.org/10.1007/s10072-015-2122-4.

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Tozza, Stefano, Emanuele Spina, Aniello Iovino, et al. "Value of Antibody Determinations in Chronic Dysimmune Neuropathies." Brain Sciences 13, no. 1 (2022): 37. http://dx.doi.org/10.3390/brainsci13010037.

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Chronic dysimmune neuropathies encompass a group of neuropathies that share immune-mediated pathomechanism. Chronic dysimmune antibody-related neuropathies include anti-MAG neuropathy, multifocal motor neuropathy, and neuropathies related to immune attack against paranodal antigens. Such neuropathies exhibit distinguishing pathomechanism, clinical and response to therapy features with respect to chronic inflammatory demyelinating polyradiculoneuropathy and its variants, which represent the most frequent form of chronic dysimmune neuropathy. This narrative review provides an overview of pathomechanism; clinical, electrophysiological, and biochemical features; and treatment response of the antibody-mediated neuropathies, aiming to establish when and why to look for antibodies in chronic dysimmune neuropathies.

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KUMARI, W., T. DAS, A. DAS, JS RANA, M. LAKHAIR, and M. IRFAN. "THE FREQUENCY OF DIFFERENT CAUSES OF PREDOMINANT MOTOR NEUROPATHY IN PATIENTS PRESENTING AT TERTIARY CARE HOSPITAL." Biological and Clinical Sciences Research Journal 2024, no. 1 (2024): 1014. http://dx.doi.org/10.54112/bcsrj.v2024i1.1014.

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Predominant motor neuropathy (PMN) encompasses a variety of neuropathies primarily affecting motor nerves, leading to muscle weakness and functional impairment. Identifying the causes of PMN is crucial for diagnosis and treatment planning. Objective: The present study aims to determine the frequency of different causes of predominant motor neuropathy in patients at a tertiary care hospital. Methods: This cross-sectional study was conducted at the Department of Neurology, Civil Hospital Karachi, from March 27, 2022, to September 27, 2022, following ethical approval from the institutional review board. A total of 139 patients aged 15-70 years, of either sex, diagnosed with PMN were included through non-probability consecutive sampling. Patients with predominant sensory neuropathy or mixed neuropathies were excluded. Data were analyzed using statistical methods to determine the frequency of various causes of PMN, with particular attention to gender and diabetes status. Results: The most frequent cause of neuropathy was Acute Motor Axonal Neuropathy (AMAN) (26.6%), followed by Acute Inflammatory Demyelinating Polyneuropathy (AIDP) (21.58%), Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) (19.4%), and Charcot-Marie-Tooth disease (16.5%). Less common causes included multifocal motor neuropathy (8.6%), porphyria (3.6%), lead intoxication (2.88%), and familial amyloid neuropathy type 2 (0.7%). There were significant differences in the frequency of neuropathy causes based on gender (p = 0.011) and diabetes status (p = 0.006). Conclusion: The study identified Acute Motor Axonal Neuropathy as the most frequent cause of predominant motor neuropathy, followed by Acute Inflammatory Demyelinating Polyneuropathy. These findings underscore the importance of recognizing specific causes of PMN for appropriate management.

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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 (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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Sawma, Tedy, Mariam Kanso, Jawad Khalife, and Mohammad Khalife. "Chronic inflammatory demyelinating polyneuropathy caused by hepatocellular carcinoma." BMJ Case Reports 16, no. 2 (2023): e251770. http://dx.doi.org/10.1136/bcr-2022-251770.

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Paraneoplastic syndromes are rare abnormal endocrine or immune responses triggered by neoplasms. Chronic inflammatory demyelinating polyneuropathy (CIDP) is one such example. CIDP is an acquired, immune-mediated neuropathy affecting the peripheral nerves and nerve roots. It is associated with many types of cancers, especially haematological malignancies. We report the case of a man in his 60s who presented to the emergency department with acute symptoms of upper and lower extremity paresis and decreased sensation in the toes and tips of his fingers. Laboratory tests were normal. Electrodiagnostic studies showed diffuse motor and sensory dysfunction in all extremities; a diagnosis of CIDP was consequently made. Imaging studies showed a large left lobe liver mass. Subsequent biopsy revealed histopathological findings characteristic of hepatocellular carcinoma. After failure of medical treatment with intravenous immunoglobulin and corticosteroids, laparoscopic resection of the tumour was planned, performed and resulted in complete resolution of symptoms. At 18 months postoperatively, the patient was asymptomatic.

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Suponeva, Natalia A., Daria А. Grishina, Yulia V. Ryabinkina, Alina S. Arestova, Evgeniya A. Melnik, and Taisiya A. Tumilovich. "Chronic inflammatory demyelinating polyneuropathy with an acute onset. Clinical case." Terapevticheskii arkhiv 94, no. 4 (2022): 544–51. http://dx.doi.org/10.26442/00403660.2022.04.201457.

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Chronic inflammatory demyelinating polyneuropathy (CIDP) is a heterogeneous treatable dysimmune neuropathy. The variety of clinical forms and course of the disease can be challenging for proper diagnosis and early treatment. In a quarter of cases CIDP starts acutely, mimicking GuillainBarr syndrome. The early diagnosis is especially important regarding differences in treatment and prognosis of these conditions. In this article, we present a clinical case of acute onset CIDP with a detailed analysis of the differential diagnosis between acute and chronic immune-mediated neuropathies.

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Tikhonova, Olga A., Dmitry S. Druzhinin, Evgenia S. Druzhinina, and Maria А. Rukosueva. "Chronic Inflammatory Demyelinating Polyneuropathy Induced by Immune Checkpoint Inhibitors: Case Reports." Annals of Clinical and Experimental Neurology 18, no. 1 (2024): 98–104. http://dx.doi.org/10.54101/acen.2024.1.11.

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Neurological immune-related adverse events (irAE) are rare but potentially fatal complications associated with the use of immune checkpoint inhibitors (ICI). Recently, there has been a trend towards an increase in the incidence of these cases. We present two case reports of demyelinating polyneuropathy in patients with skin melanoma treated with pembrolizumab or nivolumab. Unawareness of neurological irAE induced by ICI leads to delayed diagnosis and medical treatment, and this may result in persistent neurological deficit or even patients’ death. Neurological irAEs include myasthenia gravis, aseptic meningitis, encephalitis, myelitis, inflammatory demyelinating neuropathy, myositis or their combinations, etc. Considering their variability in patients treated with ICI and poor representation in publications, each case report can be of practical value.

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Jamall, Selene, Nancy Baker, Gordon Peterson, Bryan Tsao, and Jeffrey Rosenfeld. "Aggressive Acquired Demyelinating Neuropathy Caused by NF-155: Initially Treatment-Resistant." Journal of Clinical Neuromuscular Disease 25, no. 2 (2023): 59–62. http://dx.doi.org/10.1097/cnd.0000000000000464.

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Objectives: Anti–neurofascin-155 IgG4 (NF-155) antibody disease has previously been associated with a subset of patients with chronic inflammatory demyelinating polyradiculoneuropathy. We report a case of NF-155 positive polyneuropathy that initially presented as an acute inflammatory demyelinating polyradiculoneuropathy. The patient responded appropriately to treatment but subsequently progressed over a 3-month period, resulting in quadriplegia, areflexia, and oculobulbar paralysis. Methods: Case report and literature review. Results: A 40-year-old male presented with acute bilateral arm and thigh weakness, areflexia, and distal sensory loss. Treatment with intravenous immunoglobulin (IVIg) for acute acquired demyelinating neuropathy resulted in initial improvement but subsequent decline. Lack of response to additional IVIg and plasmapheresis (PLEX) prompted testing for NF-155. Treatment with rituximab and steroids resulted in virtually complete recovery. Conclusions: Early testing for nodal and paranodal proteins is indicated in patients who present with acute acquired demyelinating neuropathy but fail to respond to conventional treatments, such as IVIg or PLEX. Identification of nodal and paranodal antibodies should prompt treatment with rituximab and steroids to increase likelihood of recovery.

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Bagella, Caterina Francesca, Davide G. Corda, Pietro Zara, et al. "Chronic Inflammatory Demyelinating Polyneuropathy after ChAdOx1 nCoV-19 Vaccination." Vaccines 9, no. 12 (2021): 1502. http://dx.doi.org/10.3390/vaccines9121502.

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Recently several patients, who developed Guillain–Barré syndrome characterized by prominent bifacial weakness after ChAdOx1 nCoV-19 vaccination, were described from different centers. We recently observed a patient who developed a similar syndrome, later in the follow up he showed worsening of the neuropathy two months after the initial presentation. Repeat EMG showed reduced nerve sensory and motor conduction velocities of both upper and lower limbs, and a diagnosis of chronic inflammatory demyelinating polyneuropathy (typical CIDP) was made according to established criteria. Our report expands on the possible outcomes in patients who develop Guillain–Barrè syndrome after COVID-19 vaccinations and suggest that close monitoring after the acute phase is needed in these patients to exclude a chronic evolution of the disease, which has important implications for long-term treatment.

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Orzheshkovskyi, V. V. "СOMPARATIVE CHARACTERISTIC OF NERVE CONDUCTION STUDIES AT CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY AND HEREDITARY MOTORSENSORY NEUROPATHY TYPE 1". National Journal of Neurology 1, № 18 (2018): 22–28. http://dx.doi.org/10.61788/njn.v1i18.03.

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Results of the carried-out comparative analysis of nerve conduction studies indicators of 78 patients with demyelinating polyneuropathy (40 patients with the chronic inflammatory demyelinating polyneuropathy (CIDP) and 38 with hereditary motor and sensory neuropathy (NMSN) of type 1). It is revealed that nerve conduction studies characteristics of CIDP and NMSN of type 1 have similar lines in connection with the similar mechanism of a pathogeny - demyelination. The distinctive characteristic is uniformity of distribution of demyelinationat NMSN of type 1 in the form of uniform reduction of motor nerve conduction velocity (NCV) and compound motor action potential in the majority of the lesion peripheral nerves of extremities and high correlation dependence of indicators of NCV on tibialis on a longitudinal axis and with NCV on n.medialis and amplitude indicators at stimulation of n.medialis at patients with NMSN of type 1; patients with CIDP have a high variability and a symmetry of defeat with existence of conduction blocks and high correlation communication of amplitude indicators at stimulation of n.tibialis in distal and proximal departments.

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