Disease relevance of Guillain-Barre Syndrome

• Parainfluenza virus type 3: isolation from CSF of a patient with Guillain-Barré syndrome [1].
• Distinct integrin expression patterns are observed in multiple sclerosis and Guillain-Barré syndrome [2].
• Campylobacter infections, Guillain-Barré syndrome, and parenteral gangliosides [3].
• Matrix metalloproteinases MMP-9 and MMP-7 are expressed in experimental autoimmune neuritis and the Guillain-Barré syndrome [4].
• Serum interleukin-2 concentrations in Guillain-Barré syndrome and chronic idiopathic demyelinating polyradiculoneuropathy: comparison with other neurological diseases of presumed immunopathogenesis [5].

Psychiatry related information on Guillain-Barre Syndrome

• Antiganglioside antibodies were present in the sera of 39 of 50 patients with Guillain-Barré syndrome (GBS), in 10 of 12 patients with Alzheimer's disease, and in approximately 30% of the controls [6].
• The most common diagnoses were Wernicke's encephalopathy, thiamine deficiency, and Guillain-Barré Syndrome [7].
• Vivid dreams, hallucinations, psychosis and REM sleep in Guillain-Barré syndrome [8].
• Associations include Multiple Sclerosis, GUillain Barre Syndrome, urethral sphincter dyssynergia, various vulvar pain syndromes (nine cases), post-hysterectomy, Lichen Sclerosis (five cases), spondylolisthesis, vaginismus and genital or pelvic trauma [9].
• Objective laboratory indicators of alcohol consumption (mean corpuscular volume and serum glutamic-pyruvic transaminase (GPT), glutamyltransferase (gamma-GT), and glutamic-oxaloacetic transaminase (GOT] were measured in 18 patients with Guillain-Barré syndrome (GBS) and 710 control patients [10].

High impact information on Guillain-Barre Syndrome

• Multiple sclerosis, Guillain-Barré syndrome and myelin basic protein-specific cellular antibody [11].
• A bacterium lipopolysaccharide that elicits Guillain-Barré syndrome has a GM1 ganglioside-like structure [12].
• The diagnosis in life was unclear, but had over the years been variously considered to be Guillain-Barrè Syndrome (GBS), Friedreich ataxia, or multiple sclerosis (MS) [13].
• To clarify the pathogenesis of Guillain-Barré syndrome (GBS) after parenteral injections of bovine brain gangliosides, we searched for new molecules in bovine brain gangliosides recognized by sera from GBS patients [14].
• We studied genetic polymorphisms in the tumor necrosis factor (TNF) region in 81 Japanese patients with Guillain-Barré syndrome (GBS) and 85 controls [15].

Chemical compound and disease context of Guillain-Barre Syndrome

• Ineffectiveness of high-dose intravenous methylprednisolone in Guillain-Barré syndrome [16].
• To clarify the association between Campylobacter jejuni (Cj) infection and antibodies to ganglioside GM1 (anti-GM1) in Guillain-Barré syndrome (GBS), we have carried out a prospective case-control study of 96 patients with GBS [17].
• Capsaicin for the treatment of pain in Guillain-Barré syndrome [18].
• N-glycolylneuraminic acid-containing GM1 is a new molecule for serum antibody in Guillain-Barré syndrome [14].
• Inappropriate secretion of antidiuretic hormone associated with Guillain-Barré syndrome [19].

Biological context of Guillain-Barre Syndrome

• Between January 1, 1978, and March 31, 1979, 1,034 cases of Guillain-Barré syndrome (GBS) were reported to the Centers for Disease Control by the 1,813 American Academy of Neurology sentinel physicians who participated in the national GBS surveillance program [20].
• Tolerance to self gangliosides is the major factor restricting the antibody response to lipopolysaccharide core oligosaccharides in Campylobacter jejuni strains associated with Guillain-Barré syndrome [21].
• Campylobacter jejuni serotype O19 strains associated with the Guillain-Barré syndrome (GBS) and other strains were examined by restriction fragment length polymorphism (RFLP) analysis of polymerase chain reaction products of the flaA genes and by random amplified polymorphic DNA (RAPD) analysis [22].
• CONCLUSIONS: APOE genotype did not influence susceptibility to Guillain-Barré syndrome or recovery from it [23].
• Macrophage procoagulant activity as a measure of cell-mediated immunity to P2 protein of peripheral nerves in the Guillain-Barré syndrome [24].

Anatomical context of Guillain-Barre Syndrome

• The Guillain-Barré syndrome (GBS) and multiple sclerosis (MS) are thought to result from aberrant immune responses to myelin antigens [25].
• Human T-cell lines reactive with the peripheral nerve myelin protein, P2 protein, were isolated from the peripheral blood of 4 normal persons and 1 patient with Guillain-Barré syndrome [26].
• High-titre anti-GM1 sera from Guillain-Barré syndrome or multifocal motor neuropathy patients, or anti-GM1 rabbit sera were applied to the rat ventral root, where saltatory conduction in single motor fibres was serially observed for 4-12 h (mean 8.2 h) [27].
• Patients with Guillain-Barré syndrome (GBS) induced by rabies vaccines prepared from either suckling mouse brain (SMB) or mature sheep brain (Semple vaccine) and patients with sporadic, idiopathic GBS were studied for antibody to myelin basic protein (MBP), P2 protein, and Schwann cells [28].
• Since macrophages are implicated in primary demyelination in the peripheral nervous system (PNS) in Guillain-Barré syndrome and experimental allergic neuritis, we have investigated the ability of plasmin and of conditioned media from cultured macrophages, in the presence of plasminogen, to degrade the proteins in bovine and rat PNS myelin [29].

Gene context of Guillain-Barre Syndrome

• PMP22 now deserves consideration as an autoantigen in human acute inflammatory demyelinating polyradiculoneuropathy [30].
• CONCLUSIONS: Circulating matrix metalloproteinases (MMP-9) correlates with disease severity in Guillain-Barré syndrome (GBS) [31].
• However, the hallmark of the nuclear response to axonal injury was the formation of numerous nuclear bodies (NBs; 6.37 +/- 0.6, in the AIDP, vs. 2.53 +/- 0.2, in the control, mean +/- SDM), identified as promyelocytic leukemia (PML) bodies by the presence of the protein PML [32].
• Circulating tumor necrosis factor (TNF)-alpha and soluble TNF-alpha receptors in patients with Guillain-Barré syndrome [33].
• Circulating transforming growth factor beta 1 (TGF-beta1) in Guillain-Barré syndrome: decreased concentrations in the early course and increase with motor function [34].

Analytical, diagnostic and therapeutic context of Guillain-Barre Syndrome

• Animal model of axonal Guillain-Barré syndrome induced by sensitization with GM1 ganglioside [35].
• Counterimmunoelectrophoresis (CIEP) was used to determine precipitating antibodies to Mycoplasma pneumoniae retrospectively in sera from 100 patients with Guillain-Barré syndrome (GBS), 125 medical and neurological controls, and 40 normal individuals [36].
• Plasma exchange and prednisone in Guillain-Barré syndrome: a controlled randomized trial [37].
• We then studied sera from 70 CIDP patients, 35 Guillain-Barré syndrome (GBS) patients, and 483 disease (amyotrophic lateral sclerosis, Alzheimer's disease, multiple sclerosis, diabetes, and other polyneuropathies) and normal controls for selective high-titer anti-beta-tubulin using ELISA methodology [38].
• This study found increased spontaneous proliferation of peripheral blood mononuclear cells following intensive plasmapheresis treatment of patients with multiple sclerosis (MS) or Guillain-Barré syndrome (GBS) [39].

References