Intramuscular interferon beta-1a in chronic inflammatory demyelinating polyradiculoneuropathy

Hughes, Richard; Gorson, Kenneth C.; Cros, Didier; Griffin, John W.; Pollard, John D.; Jm, Vallat; Maurer, S.; Riester, Katherine; Davar, Gudarz; Kp, Dawson; Sandrock, Alfred

doi:10.1212/wnl.0b013e3181d1a862

Cited by 91 publications

(59 citation statements)

References 24 publications

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“…Antigenic targets in CIDP have been recently reviewed (Pollard, 2007;Hughes et al, 2010). The therapeutic response of patients with CIDP to plasma exchange strongly suggests that humoral mediators such as antibodies play a role in the pathogenesis of this disease.…”

Section: Antigenic Targets In Cidpmentioning

confidence: 99%

CIDP – the relevance of recent advances in Schwann cell/axonal neurobiology

Pollard

Armati

2011

J Peripheral Nervous Sys

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Early pathological studies in patients with acute and chronic inflammatory demyelinating neuropathies, and the animal model experimental autoimmune neuritis (EAN) showed similarities in the process of demyelination. These studies focused on compact myelin proteins and peptides as targets of immune attack in Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and EAN. However, serological studies in patients with subsets of GBS highlighted the importance of gangliosides -glycolipids enriched in non-compact Schwann cell regions and the node, paranodal, and internodal axolemma. In the acute motor axonal neuropathy (AMAN) rabbit model, antibodies to the ganglioside GM1 bind in the nodal region, impair Na channel clustering and disturb Schwann cell/axon organisation. Schwann cell neurobiological studies now highlight the importance of adhesion molecules, including neurofascins, gliomedin, contactins, and NrCAM to Schwann cell/axon integrity. Changes to nodal fine structure by immune responses against such molecules may provide a mechanism for reversible conduction failure or block. Recovery of patients with CIDP or multifocal motor neuropathy (MMN) following treatment may sometimes be better explained by reversal of conduction failure than remyelination or regeneration. This review considers the importance of the intricate molecular arrangements at the nodal and paranodal regions in inflammatory neuropathies such as CIDP. Early images of compact myelin stripping and phagocytosis, may have diverted the research focus away from these vital non-compact myelin Schwann cell areas.

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Section: Antigenic Targets In Cidpmentioning

confidence: 99%

CIDP – the relevance of recent advances in Schwann cell/axonal neurobiology

Pollard

Armati

2011

J Peripheral Nervous Sys

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“…It showed an improvement in clinical grading but not in grip strength scores. Then, a large RCT was conducted in 67 patients with IVIGdependent CIDP, followed for 32 weeks, with either 30 or 60 mg of IFN-β1a once or twice weekly [60]. IFN-β1a was not more effective than placebo in reducing the mean dose of IVIG, with 47 % of patients in both groups not needing to restart IVIG after their suspension after 16 weeks of therapy with IFN-β1a.…”

Section: Long-term Therapy For Cidpmentioning

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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“…A negative randomized controlled trial of oral methotrexate 15 mg weekly was reported in CIDP [109]. A recent studied evaluating the effects of intramuscular interferon-beta-1a (Avonex) at low (30 micrograms weekly), intermediate (30 micrograms twice weekly or 60 micrograms weekly) and high dose (60 micrograms twice weekly) on IVIg dose in CIDP did not show a significant benefit [104,105,110]. High dose cyclophosphamide without stem cell rescue can lead to long-term remission with refractory CIDP [97] with improved quality of life [112].…”

Section: Treatmentmentioning

confidence: 99%

Chronic Inflammatory Demyelinating Polyneuropathy

Markvardsen

Harbo²,

Holbech³

et al. 2013

Encyclopedia of Pain

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Chronic Inflammatory polyneuropathies are an important group of neuromuscular disorders that present chronically and progress over more than 8 weeks, being referred to as chronic inflammatory demyelinating polyneuropathy (CIDP). Despite tremendous progress in elucidating disease pathogenesis, the exact triggering event remains unknown. Our knowledge regarding diagnosis and management of CIDP and its variants continues to expand, resulting in improved opportunities for identification and treatment. Most clinical neurologists will be involved in the management of patients with these disorders, and should be familiar with available therapies for CIDP. We review the distinctive clinical, laboratory, and electro-diagnostic features that aid in diagnosis. We emphasize the importance of clinical patterns that define treatment responsiveness and the most appropriate therapies in order to improve prognosis.

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Intramuscular interferon beta-1a in chronic inflammatory demyelinating polyradiculoneuropathy

Cited by 91 publications

References 24 publications

CIDP – the relevance of recent advances in Schwann cell/axonal neurobiology

CIDP – the relevance of recent advances in Schwann cell/axonal neurobiology

Immunotherapy in Peripheral Neuropathies

Chronic Inflammatory Demyelinating Polyneuropathy

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