Search

Testing for IgG+IgM autoantibodies to gangliosides of peripheralnerves (asialo-GM1, GM1, GM2, GD1a, GD1a, GD1b, GQ1b)was performed in 95 patients with GuillainBarr syndrome (GBS)in Moscow. In 70 patients (74%) acute inflammatory demyelinatingpolyneuropathy (AIDP) was diagnosed, and in 25 patients (26%) either acute motor axonal neuropathy (AMAN) or acute motorsensoryneuropathy (AMSAN). The role of antibodies to gangliosidesfor prognosis of the disease course and response to pathogenictreatment was assessed. Antibodies to gangliosides were found in55 patients (57.9%) more often in patients with AMAN/AMSAN(p0.05). The whole range of antibodies was found both in patientswith AIDP and AMAN/AMSAN. Anti-GM1 were found in bothsubtypes of GBS. Anti-GD1b were associated withAMAN/AMSAN (p0.05). There was a correlation between anti-GM1 and diarrhea (p0.05), anti-asialo-GM1 and campylobacteriosis(p0.05). There wasnt found significant correlation betweenanti-GD1 and axonal subtypes, diarrhea in anamnesis, and campylobacteriosis.Association of severe GBS and elderly age, camplylobacteriosisand axonal subtypes was confirmed. AMAN/AMSANsubtypes, severity of the disease, necessity in mechanical ventilationwere characterized by insufficient efficacy of pathogenic therapy.The same factors and elderly age were associated with unfavorableprognosis in terms of absence of unassisted walking in 6 and12months. Anti-GD1a were associated with sever course of the disease,including necessity in mechanical ventilation. Immunologicfactors are not sufficient in prognosis of the treatment efficacy.Antibodies to GM1 were associated with unfavorable prognosis withabsence of unassisted walking in 6 months. Clinical and neurophysiologicaldata is crucial for making diagnosis and prognosisof the GBS course. Testing for autoantibodies to gangliosidescould be helpful in diagnostics of GBS. It is possible to use thattest for revealing axonal type of the disease (anti-GD1b), prognosticationof severe course of GBS (anti-GD1a) and unfavorablerehabilitation of unassisted walking.

The study of anti-glycolipid antibodies has become available to general practice in Russia. Indications for determining antibodies to gangliosidesare Guillain–Barré syndrome, Miller Fisher syndrome, Bickerstaff’s encephalitis, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy. The indication for measuring anti-MAG antibodies is IgM paraprotein-associated polyneuropathy. These immunological tests must be included in diagnostic protocols if the listed dysimmune diseases are suspected.

Introduction: Several studies have suggested that differential weakness in muscles supplied by the same motor nerve supports the diagnosis of multifocal motor neuropathy (MMN).Methods: We describe the clinical, electrophysiological, neuroimaging, and laboratory findings of patients with a lower motor syndrome whose clinical presentation included differential finger extension weakness that we have seen in our neuromuscular clinic.Results: We identified 3 patients with hand weakness and 1 patient with asymmetric weakness of the upper extremity. Conduction blocks (CBs) were identified in 1 patient. Anti-GM1 immunoglobulin M antibodies were detected in 2 of the 3 patients tested. Only 1 patient responded to intravenous immunoglobulin (IVIg). Rituximab was administered in another patient, but we did not detect a response.Conclusions: We suggest that differential finger extension weakness is a feature that may be seen in MMN, even in the absence of CB or response to IVIg. Muscle Nerve 55: 433-437, 2017. [ABSTRACT FROM AUTHOR]

Multifocal motor neuropathy affects myelinated motor axons in limb nerves at multifocal sites. It is characterized by weakness and muscle atrophy, motor conduction block, and antibodies against ganglioside GM1 which is expressed on the axolemma of nodes of Ranvier and perinodal Schwann cells. Treatment by regular IVIg courses results in temporary improvement but cannot prevent slowly progressing weakness due to axonal degeneration. This review discusses possible mechanisms of conduction block and the reasons why motor axons are selectively affected in this disorder. [ABSTRACT FROM AUTHOR]

Abstract: In an effort to use model fluid membranes for immunological studies, we compared the formation of planar phospholipid bilayers supported on silicon dioxide surfaces with and without incorporation of glycolipids as the antigen for in situ antibody binding. Dynamic light scattering measurements did not differentiate the hydrodynamic volumes of extruded small unilamellar vesicles (E-SUVs) containing physiologically relevant concentrations (0.5–5mol%) of monosialoganglioside GM1 (GM1) from exclusive egg yolk l-α-phosphatidylcholine (egg PC) E-SUVs. However, quantifiable differences in deposition mass and dissipative energy loss emerged in the transformation of 5mol% GM1/95mol% egg PC E-SUVs to planar supported lipid bilayers (PSLBs) by vesicle fusion on thermally evaporated SiO2, as monitored by the quartz crystal microbalance with dissipation (QCM-D) technique. Compared to the 100mol% egg PC bilayers on the same surface, E-SUVs containing 5mol% GM1 reached a ∼12% higher mass and a lower dissipative energy loss during bilayer transformation. PSLBs with 5mol% GM1 are ∼18% heavier than 100mol% egg PC and ∼11% smaller in projected area per lipid, indicating an increased rigidity and a tighter packing. Subsequent binding of polyclonal immunoglobulin G anti-GM1 to the PSLBs was performed in situ and showed specificity. The anti-GM1 to GM1 ratios at equilibrium were roughly proportional to the concentrations of anti-GM1 administered in the solution. Fluorescence recovery after photobleaching was utilized to verify the retained, albeit reduced lateral fluidity of the supported membranes. Five moles percentage of GM1 membranes (GM1 to PC ratio ∼1:19) decorated with 1mol% N-(Texas Red sulfonyl)-1,2-dihexadecanoyl-sn-glycerol-3-phosphoethanolamine (Texas Red DHPE) exhibited an approximately 16% lower diffusion coefficient of 1.32±0.06μm2/s, compared to 1.58±0.04μm2/s for egg PC membranes without GM1 (p <0.01). The changes in vesicle properties and membrane lateral fluidity are attributed to the interactions of GM1 with itself and GM1 with other membrane lipids. This system allows for molecules of interest such as GM1 to exist on a more biologically relevant surface than those used in conventional methods such as ELISA. Our analysis of rabbit serum antibodies binding to GM1 demonstrates this platform can be used to test for the presence of anti-lipid antibodies in serum. [Copyright &y& Elsevier]

So far, the pathogenic significance and use for diagnosis of antiganglioside GM1 antibodies (anti-GM1) are unclear. We therefore compared serum IgM and IgG antimonosialo ganglioside GM1 levels of 33 patients with presumed immune-mediated neuropathies, 100 patients with various other central or peripheral neurological disorders, and 110 controls by ELISA. We also measured the complement-activating capacity of anti-GM1 by C5b-9-GM1-ELISA to evaluate its value to distinguish between pathogenic and nonpathogenic autoantibodies. Low levels of anti-GM1 were observed in all disease categories and in controls (healthy blood donors). Twenty-four of the controls including the 10 with the highest serum IgM or IgG anti-GM1 were examined for neurological disorders in a double-blind checkup study. In the patients, elevated IgM anti-GM1 levels were predominantly found in those with neuropathies (NP), but barely in patients with central nervous system disease (CNSD). We found elevated IgG anti-GM1 levels predominantly in patients with NP of inflammatory origin (multifocal motor neuropathy, chronic inflammatory demyelinating polyneuropathy or Guillain-Barré syndrome), rarely in patients with NP of noninflammatory origin or CNSD, but not in the control disease group myasthenia gravis (MG). Median levels of IgM-, IgG-, (IgM+IgG)-, and C5b-9-binding anti-GM1 were significantly higher in patients with inflammatory NP as compared to the controls (p < 0.025). In addition, median levels of IgG- and (IgM+IgG)-anti-GM1 were significantly higher in inflammatory NP versus CNSD. Elevated complement-binding activity was associated with low or elevated IgM and/or IgG anti-GM1. Nevertheless, there was a significant correlation between anti-GM1 level (IgM+IgG) and the respective complement-activating capacity (r = 0.758; n = 243). Estimation of anti-GM1 and their respective complement-activating capacity may be helpful in the diagnosis of inflammatory neuropathies. However, neither an elevated anti-GM1 level nor an increased C5b-9 binding seems specific for a given disease category (e.g. peripheral nerve disease) nor a disease process (e.g. demyelination or inflammation). [ABSTRACT FROM AUTHOR]

Objectives The aim of this study was to correlate the brain atrophy with serum levels of anti-GM1 antibodies in patients with relapsing-remitting multiple sclerosis (RRMS). Methods Plasma sample from 52 patients with RRMS and 65 healthy controls were examined for anti-GM1 antibodies. Patients with RRMS underwent to MRI study with automated method called SIENAX that calculated an estimate of gray matter (GMV) and white matter (WMV) volumes. Results The percentage of RRMS patients with increased anti-GM1 was 37.8%. Elevated levels of anti-GM1 antibodies did not correlate with brain atrophy. Conclusions Anti-GM1 antibodies do not represent a marker of axonal damage in patients with RRMS. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Anti-GM1 Antibody-Negative Acute Motor Axonal Neuropathy After Mycoplasma Pneumoniae Infection," by Y. A. Rajabally and P. Sarasamma published in the previous issue.

Background: Increasing evidence suggests that gangliosides act as important mediators in both de- and remyelination. The scope of the present research was to investigate the presence of immunoglobulin (Ig) M antibodies against GM1, GD1b, and GQ1b gangliosides in the sera of patients with dementia and the possible connection with clinical parameters of the disease., Method: This research topic demonstrates the investigation of 103 patients with dementia and 60 healthy individuals using enzyme-linked immunosorbent assay for the presence of 3 antiganglioside antibodies in their sera., Results: The authors report a positive connection between IgM anti-GM1 and the age (P = .005) and the severity of dementia (P = .005). Most of the patients who revealed increased IgM anti-GD1b levels had Alzheimer's disease (AD; P = .002)., Conclusion: This study indicates that elevated IgM anti-GM1 may be connected with the neurodegeneration in older patients with severe dementia and that AD may also be associated with increased IgM anti-GD1b levels., (© The Author(s) 2014.)