Pathophysiology of immune-mediated demyelinating neuropathies-Part II: Neurology

Franssen, Hessel; Straver, Dirk C.G.

doi:10.1002/mus.24068

Cited by 35 publications

(35 citation statements)

References 167 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Immunemediated inflammation and neurodegeneration is considered to play a central role in the pathogenesis of this disease, although the precise mechanisms remain unclear [2,3].…”

Section: Introductionmentioning

confidence: 99%

Comparison of clinical, electrophysiological, sonographic and MRI features in CIDP

Pitarokoili

Schlamann

Kerasnoudis

et al. 2015

Journal of the Neurological Sciences

View full text Add to dashboard Cite

“…Immunemediated inflammation and neurodegeneration is considered to play a central role in the pathogenesis of this disease, although the precise mechanisms remain unclear [2,3].…”

Section: Introductionmentioning

confidence: 99%

Comparison of clinical, electrophysiological, sonographic and MRI features in CIDP

Pitarokoili

Schlamann

Kerasnoudis

et al. 2015

Journal of the Neurological Sciences

View full text Add to dashboard Cite

“…67 Pathologic findings suggest that POEMS syndrome involves predominantly intermediate nerve segments and nerve trunks due to the VEGF-mediated breakdown of the blood-nerve barrier. 25,68 This finding contrasts with some other immune-mediated neuropathies in which antibodies can easily access distal nerve terminals and nerve roots where the blood-nerve barrier is vulnerable. 25,63 VEGF increases microvascular permeability, damages endothelial cells, and is important in angiogenesis.…”

Section: Poems Syndromementioning

confidence: 89%

“…25,68 This finding contrasts with some other immune-mediated neuropathies in which antibodies can easily access distal nerve terminals and nerve roots where the blood-nerve barrier is vulnerable. 25,63 VEGF increases microvascular permeability, damages endothelial cells, and is important in angiogenesis. The level of VEGF, which may a driving factor in the disorder, is diagnostically useful.…”

Section: Poems Syndromementioning

confidence: 89%

“…The anti-MAG antibody neuropathies show absent or remarkably reduced sensory nerve action potentials that are indicative of axonal damage in diffuse nerves of the lower limbs. 22,24,25 Motor nerve conduction studies show greatly prolonged distal motor latencies suggestive of distal-dominant demyelination. A terminal latency index (TLI = distal distance/[forearm motor conduction velocity × distal motor latency]) of <0.26 is highly specific for anti-MAG antibody neuropathy with a demyelinating pattern.…”

Section: Neuropathy Associated With Mgusmentioning

confidence: 99%

“…It has been hypothesized that distal nerve fibers are more vulnerable to anti-MAG antibodies due either to greater permeability of the blood-nerve barrier or more-prominent MAG expression. 25,28 In addition, the anti-MAG antibody impairs neurofilament phosphorylation, resulting in neurofilament accumulation followed by disturbed axonal transport in neurons, which in turn may induce axonal degeneration in more-distal regions of the longer axis.…”

Section: Neuropathy Associated With Mgusmentioning

confidence: 99%

See 2 more Smart Citations

Paraproteinemic neuropathy

Pyun

Kim

2017

Ann Clin Neurophysiol

View full text Add to dashboard Cite

Paraproteinemia is caused by a proliferation of monoclonal plasma cells or B lymphocytes. Approximately 10% of idiopathic neuropathies are associated with paraproteinemia, where a certain paraprotein acts like an antibody targeted at constituents of myelin or axolemma in peripheral nerves. The relationship between paraproteinemia and peripheral neuropathy remains unclear despite this being of interest for a long time. Neurologists frequently find paraproteinemia during laboratory examinations of patients presenting with peripheral neuropathy, especially in the elderly. The possibility of a relationship with paraproteinemia should be considered in cases without an explainable cause. We review the causal association between paraproteinemia and neuropathy as well as clinical, laboratory, and electrophysiologic features, and the treatment options for paraproteinemic neuropathy.

show abstract

Immunomodulation of inflammatory leukocyte markers during intravenous immunoglobulin treatment associated with clinical efficacy in chronic inflammatory demyelinating polyradiculoneuropathy

et al. 2016

View full text Add to dashboard Cite

ObjectiveThe objective of the study was to profile leukocyte markers modulated during intravenous immunoglobulin (IVIg) treatment, and to identify markers and immune pathways associated with clinical efficacy of IVIg for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) with potential for monitoring treatment efficacy.MethodsResponse to IVIg treatment in newly diagnosed IVIg‐naïve and established IVIg‐experienced patients was assessed by changes in expression of inflammatory leukocyte markers by flow cytometry. The adjusted INCAT disability and Medical Research Council sum scores defined clinical response.ResultsIntravenous immunoglobulin modulated immunopathogenic pathways associated with inflammatory disease in CIDP. Leukocyte markers of clinical efficacy included reduced CD185+ follicular helper T cells, increased regulatory markers (CD23 and CD72) on B cells, and reduction in the circulating inflammatory CD16+ myeloid dendritic cell (mDC) population and concomitant increase in CD62L and CD195 defining a less inflammatory lymphoid homing mDC phenotype. A decline in inflammatory CD16+ dendritic cells was associated with clinical improvement or stability, and correlated with magnitude of improvement in neurological assessment scores, but did not predict relapse. IVIg also induced a nonspecific improvement in regulatory and reduced inflammatory markers not associated with clinical response.ConclusionsClinically effective IVIg modulated inflammatory and regulatory pathways associated with ongoing control or resolution of CIDP disease. Some of these markers have potential for monitoring outcome.

show abstract

Pathophysiology of immune-mediated demyelinating neuropathies-Part II: Neurology

Cited by 35 publications

References 167 publications

Comparison of clinical, electrophysiological, sonographic and MRI features in CIDP

Comparison of clinical, electrophysiological, sonographic and MRI features in CIDP

Paraproteinemic neuropathy

Immunomodulation of inflammatory leukocyte markers during intravenous immunoglobulin treatment associated with clinical efficacy in chronic inflammatory demyelinating polyradiculoneuropathy

Contact Info

Product

Resources

About