Chronic inflammatory demyelinating polyradiculoneuropathy: diagnostic and therapeutic challenges for a treatable condition

Vallat, Jean‐Michel; Sommer, Claudia; Magy, Laurent

doi:10.1016/s1474-4422(10)70041-7

Cited by 247 publications

(206 citation statements)

References 145 publications

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“…Motor impairment is a classical feature in CIDP patients, and even patients whose symptoms are primarily sensory frequently develop motor impairment at later stages of the disease 31, 48. The European Federation of Neurological Societies/Peripheral Nerve Society criteria for diagnosing CIDP are based primarily on motor dysfunction 49.…”

Section: Discussionmentioning

confidence: 99%

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Corneal confocal microscopy in chronic inflammatory demyelinating polyneuropathy

Stettner

Hinrichs

Guthoff

et al. 2015

Ann Clin Transl Neurol

105

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ObjectiveThere is an unmet need for better diagnostic tools to further delineate clinical subsets of heterogeneous chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and multifocal motor neuropathy (MMN) to facilitate treatment decisions. Corneal confocal microscopy (CCM) is a noninvasive and reproducible nerve imaging technique. This study evaluates the potential of CCM as a diagnostic surrogate in CIDP and MMN.MethodsIn a cross‐sectional prospective approach, 182 patients and healthy controls were studied using CCM to quantify corneal nerve damage and immune cell infiltration.ResultsPatients with CIDP and MMN had a reduction in corneal nerve fiber (CNF) measures and an increase in corneal immune cell infiltrates. In CIDP, CNF parameters decreased with increasing duration of disease. The number of dendritic cells in proximity to CNFs was increased in patients with early disease and correlated with the degree of motor affection. A further reduction in CNF parameters and an increase in nondendritic cells were observed in patients with painful neuropathy. In CIDP patients with antineuronal antibodies the number of nondendritic cells was increased.InterpretationOur findings suggest that CNF loss may reflect severity of neuropathy and quantification of distinct cells around the CNF plexus may help in stratifying CIDP subtypes, clinical course, and disease activity. However, further longitudinal studies are required before CCM can be considered as a valid surrogate endpoint for patients with CIDP and MMN.

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Section: Discussionmentioning

confidence: 99%

“…Patients were diagnosed with MGUSN when immunoglobulin (Ig)M or IgG was detectable in the serum, with and without antineural antibodies 29, 30. Due to the small sample size, MGUSN patients were subsumed into the CIDP group for further analysis as per previous suggestions 29, 31, 32…”

Section: Methodsmentioning

confidence: 99%

Corneal confocal microscopy in chronic inflammatory demyelinating polyneuropathy

Stettner

Hinrichs

Guthoff

et al. 2015

Ann Clin Transl Neurol

105

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“…During the 1970s increasingly large series of patients were published, notably by Dyck et al [22] at the Mayo Clinic. It is the most common treatable neuropathy worldwide [4,[23][24][25], with a prevalence ranging from 2.0-3.0 to 8.9 per 100,000 people [26]. In a recently reported epidemiological study, mean age of onset was 57.7 years, prevalence increased with age and reached a maximum in the 70-79-year age group [27].…”

Section: Cidpmentioning

confidence: 99%

“…GBS was firstly reported almost 100 years ago [1], while CIDP, MMN, and anti-MAG neuropathy have been progressively identified since 1958, followed by characterization of clinical, electrophysiological, pathological, and immunological features [2]. In the same way, animal models have been elegantly produced by several researchers, and immune therapies have firstly been used in GBS [3], followed by CIDP [4], and more recently in MMN and anti-MAG neuropathy [5,6]. Even though the exact mechanisms underlying the development of immunopathology remain unknown, immunemediated neuropathies are considered treatable.…”

Section: Introductionmentioning

confidence: 99%

Immunotherapy in Peripheral Neuropathies

Léger¹,

Guimarães‐Costa²,

Muntean³

2016

Neurotherapeutics

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Immunotherapy has been investigated in a small subset of peripheral neuropathies, including an acute one, Guillain-Barré syndrome, and 3 chronic forms: chronic inflammatory demyelinating polyradiculoneuropathy, multifocal motor neuropathy, and neuropathy associated with IgM anti-myelin-associated glycoprotein. Several experimental studies and clinical data are strongly suggestive of an immune-mediated pathogenesis. Either cell-mediated mechanisms or antibody responses to Schwann cell, compact myelin, or nodal antigens are considered to act together in an aberrant immune response to cause damage to peripheral nerves. Immunomodulatory treatments used in these neuropathies aim to act at various steps of this pathogenic process. However, there are many phenotypic variants and, consequently, there is a significant difference in the response to immunotherapy between these neuropathies, as well as a need to improve our knowledge and long-term management of chronic forms.

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“…Although CIDP symptoms do not usually reach their most severe until at least 2 months from disease onset, 4-6 about 16 % of patients may have subacute onset and a monophasic course. [6][7][8] In view of the therapeutic options, intravenous immunoglobulin (IVIg) and steroids exert short-term clinical improvement in approximately 60 % of CIDP cases, whereas steroids have no effect on AIDP patients. [9][10][11][12] Although plasmapheresis is an attractive therapy option for non-responders to IVIg, it is not always easy to perform, is often related to complications (because of thrombosis of venous catheter, sepsis, etc.)…”

mentioning

confidence: 99%

The Application of Clinical, Electrophysiological and Nerve Ultrasound Parameters in Distinguishing Acute-onset Chronic from Acute Inflammatory Demyelinating Polyneuropathy

Kerasnoudis¹,

Pitarokoili²,

Gold³

et al. 2015

European Neurological Review

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History-taking and nerve conduction studies are fundamental for the diagnosis and assessment of the severity of acute (AIDP) or chronic inflammatory demyelinating polyneuropathy (CIDP). The diagnostic challenge of distinguishing these two immune-mediated subacute polyradiculoneuropathies remains high, as intravenous immunoglobulin and steroids exert short-term clinical improvement in the majority of the CIDP cases, whereas steroids have no effect on AIDP patients. Accordingly, the precise classification of subacute polyradiculoneuropathies significantly affects the early application of steroids in CIDP. This review aims to give a timely update on the application of clinical, electrophysiological and nerve ultrasound parameters in distinguishing subacute CIDP from AIDP. KeywordsAcute inflammatory demyelinating polyneuropathy, chronic inflammatory demyelinating polyneuropathy, Bochum Ultrasound Score, nerve ultrasound, sural sparing Disclosures: Antonios Kerasnoudis and Kalliopi Pitarokoili have no conflicts of interest to declare. Ralf Gold has received consultation fees and speaker honoraria from Bayer Schering, BiogenIdec, MerckSerono, Novartis, Sanofi-Aventis and TEVA. He also acknowledges grant support from BayerSchering, BiogenIdec, MerckSerono, Sanofi-Aventis and TEVA, all unrelated to this manuscript. Min-Suk Yoon has received speaker honoraria from CSL Behring, all unrelated to this manuscript. This study was not industry sponsored. No funding was received for the publication of this article.Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any non-commercial use, distribution, adaptation and reproduction provided the original author(s) and source are given appropriate credit. Chronic inflammatory demyelinating polyneuropathy (CIDP) is a common, albeit underdiagnosed and potentially treatable, disease having an estimated prevalence of 1.2-2.3 per 100,000. Although CIDP symptoms do not usually reach their most severe until at least 2 months from disease onset, 4-6 about 16 % of patients may have subacute onset and a monophasic course. [6][7][8] In view of the therapeutic options, intravenous immunoglobulin (IVIg) and steroids exert short-term clinical improvement in approximately 60 % of CIDP cases, whereas steroids have no effect on AIDP patients. [9][10][11][12] Although plasmapheresis is an attractive therapy option for non-responders to IVIg, it is not always easy to perform, is often related to complications (because of thrombosis of venous catheter, sepsis, etc.) and is not ubiquitously available.13 Thus the precise aetiological classification of subacute polyradiculoneuropathies significantly affects the early application of steroids in CIDP. This review aims to give a timely update on the application of clinical, electrophysiological and nerve ultrasound parameters in distinguishing subacute CIDP from AIDP. Methods Clinical ParametersThe clinical evaluation of patients who have symptoms or signs of polyradiculoneuropathy requ...

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Chronic inflammatory demyelinating polyradiculoneuropathy: diagnostic and therapeutic challenges for a treatable condition

Cited by 247 publications

References 145 publications

Corneal confocal microscopy in chronic inflammatory demyelinating polyneuropathy

Corneal confocal microscopy in chronic inflammatory demyelinating polyneuropathy

Immunotherapy in Peripheral Neuropathies

The Application of Clinical, Electrophysiological and Nerve Ultrasound Parameters in Distinguishing Acute-onset Chronic from Acute Inflammatory Demyelinating Polyneuropathy

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