Multifocal demyelinating neuropathy with persistent conduction block

Lewis, Richard A.; Sumner, Austin J.; Brown, Mark J.; Asbury, Arthur K.

doi:10.1212/wnl.32.9.958

Cited by 460 publications

(249 citation statements)

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“…Whether MMN is a variant of CIDP or a totally unrelated disease, however, is still a matter of debate. [1][2][3][4][5][6][7][8][9][10][11]23 The mechanism of action of IVIg therapy is not fully understood, but it is current opinion that it interferes with the immune system, possibly explaining the beneficial effect in a number of immune diseases. 34 The positive response to IVIg in our patients may therefore support the hypothesis that MMN is an immune-mediated disease, as also suggested by its frequent association with anti-ganglioside a n t i b o d i e~l -~ and by the concomitant improvement with decreasing anti-GM, levels in some patients.2J1 Although all our responding patients had increased levels of anti-asialo-GM, antibodies while no reactivity was present in the nonresponding patient, clinical improvement was not associated with a consistent decrease in antibody levels.…”

Section: Resultsmentioning

confidence: 99%

High‐dose intravenous immunoglobulin therapy in multifocal motor neuropathy

et al. 1993

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Article abstract-We treated five consecutive patients with multifocal motor neuropathy (MMN) with high-dose intravenous immunoglobulin (IVIg). Four patients had increased levels of anti-asialo-GM, IgM and two of anti-GM, IgM as well; one patient had no reactivity. We treated them twice with 0.4 g/kg IVIg for 5 consecutive days at a 2-month interval, followed by maintenance infusions up to 6 to 12 months. All patients with high anti-asialo-GM, had a consistent clinical improvement starting 3 to 10 days after the first IVIg course; in one patient, recovery was complete and persistent for 12 months without additional treatment, while in three patients, improvement only lasted 20 to 30 days. There was a similar improvement in these patients after the second course of M g which was maintained by periodic 2-day IVIg infusions. Clinical improvement in these patients was associated with a reduction of conduction block in most, but not all, motor nerves, while antibody titers were not consistently modified by treatment. There was no clinical or electrophysiologic improvement in the patient without antiglycolipid activity after 6 months of M g . IVIg may be a safe and effective therapy for MMN.

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Section: Resultsmentioning

confidence: 99%

High‐dose intravenous immunoglobulin therapy in multifocal motor neuropathy

et al. 1993

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“…From the onset, we aimed to include only patients with "classic" CIDP, having the typical, symmetric, polyradiculoneuropathy, rather than cases of focal or multifocal CIDP (e.g., Lewis-Sumner syndrome) 28 or a distal, sensory predominant form of CIDP (distal acquired demyelinating symmetric neuropathy). 29 In comparing our results with prior observations, our prevalence of 8.9 in 100,000 is higher than most.…”

Section: Discussionmentioning

confidence: 99%

Incidence and prevalence of CIDP and the association of diabetes mellitus

Laughlin¹,

Melton²,

Leibson³

et al. 2009

Neurology

270

181

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“…The diagnoses of CIDP or MMN were based on the respective criteria of the Peripheral Nerve Society/European Federation of Neurological Societies 26, 27, 28. Patients were diagnosed with MGUSN when immunoglobulin (Ig)M or IgG was detectable in the serum, with and without antineural antibodies 29, 30.…”

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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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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Multifocal demyelinating neuropathy with persistent conduction block

Cited by 460 publications

References 0 publications

High‐dose intravenous immunoglobulin therapy in multifocal motor neuropathy

High‐dose intravenous immunoglobulin therapy in multifocal motor neuropathy

Incidence and prevalence of CIDP and the association of diabetes mellitus

Corneal confocal microscopy in chronic inflammatory demyelinating polyneuropathy

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