g(m1)-ganglioside and Paraplegia

Guillain-Barré Syndrome (GBS) is a prototype of post-infectious autoimmune disease. A 76-year-old woman was treated for a renal abscess and developed muscle weakness in all four extremities, 18 days after the onset of infection. She was diagnosed with GBS on the basis of acute flaccid paralysis, hyporeflexia, nerve conduction studies (reduced amplitude of compound muscle action potentials), and high titers of IgG antibodies to GM1 and GalNAc-GD1a. GBS rarely occurs after sepsis and this case represents the first report of rapidly progressive GBS following Escherichia coli urosepsis.

Topics: Abscess; Aged; Autoantibodies; Disease Progression; Escherichia coli Infections; Female; G(M1) Ganglioside; Gangliosides; Guillain-Barre Syndrome; Humans; Immunoglobulin G; Immunosorbent Techniques; Immunotherapy; Kidney Diseases; Neural Conduction; Paraplegia; Reflex, Abnormal; Time Factors

To determine the serum cytokine profiles of patients with spinal cord injury (SCI) and varying clinical presentations relative to healthy, able-bodied, age-matched control subjects.. Cross-sectional study.. Clinical research unit.. People with SCI (N=56) and different clinical presentations, and healthy, able-bodied, age-matched control subjects (N=35).. Not applicable.. Serum levels of the proinflammatory cytokines interleukin (IL) 1beta, IL-6, tumor necrosis factor alpha (TNF-alpha), the anti-inflammatory cytokines IL-4 and IL-10, the regulatory cytokine IL-2, the IL-1 receptor antagonist (IL-1RA), and autoantibodies against myelin-associated glycoprotein and GM(1) ganglioside (anti-GM(1)) immunoglobulin (IgG and IgM), as determined by enzyme-linked immunosorbent assay. The relationship between elevated serum cytokine levels and clinical variables was also studied.. SCI subjects exhibited serum concentrations of IL-6, TNF-alpha, IL-1RA, and anti-GM(1) (IgG) that were greater (P<.05) than control group values. Elevated cytokine concentrations were not associated with high white blood cell counts, level of injury, or American Spinal Injury Association classification; they were evident in SCI subjects who were asymptomatic for medical complications, but were further elevated in subjects with pain, urinary tract infection (UTI), and pressure ulcers.. Elevated levels of circulating proinflammatory cytokines and autoantibodies are present in the serum of SCI subjects without medical complications, and are further elevated in SCI subjects with neuropathic pain, UTI, or pressure ulcers, relative to healthy, able-bodied control subjects. These findings may be indicative of a protective autoimmunity, simply a consequence of occult or evident infection, or evidence of cytokine dysregulation that may contribute to an immune-mediated impairment of axonal conduction.

Topics: Adult; Autoantibodies; Cervical Vertebrae; Cross-Sectional Studies; Cytokines; Enzyme-Linked Immunosorbent Assay; Female; G(M1) Ganglioside; Humans; Interleukin 1 Receptor Antagonist Protein; Interleukin-8; Male; Myelin-Associated Glycoprotein; Paraplegia; Pressure Ulcer; Quadriplegia; Reference Values; Spinal Cord Injuries; Thoracic Vertebrae; Tumor Necrosis Factor-alpha; Urinary Tract Infections

Remyelination of the CNS is necessary to restore neural function in a number of demyelinating conditions. Schwann cells, the myelinating cells of the periphery, are candidates for this purpose because they have more robust regenerative properties than their central homologs, the oligodendrocytes. Although the ability of Schwann cells to remyelinate the CNS has been demonstrated, their capacity to enter the adult spinal cord in large numbers and effect functional recovery remains uncertain. We used cholera toxin B-subunit conjugated to saporin to demyelinate the rat lumbar spinal cord, remove macroglia, and produce paraplegia. After the removal of oligodendrocyte and astrocyte debris by invading macrophages, there was a spontaneous entry of Schwann cells into the spinal cord, along with axonal remyelination and concomitant functional recovery from paraplegia occurring within 75 d. The Schwann cells appeared to enter the dorsal funiculi via the dorsal root entry zone and the lateral funiculi via rootlets that had become adherent to the lateral spinal cord after the inflammation. In the following weeks, Schwann cell myelin surrounding central axons was progressively replaced by oligodendrocyte myelin without lapse in motor function. Our results show that endogenous Schwann cells can reverse a severe neurological deficit caused by CNS demyelination and enable later oligodendrocyte remyelination.

Topics: Animals; Astrocytes; Cell Count; Cholera Toxin; Demyelinating Diseases; Female; G(M1) Ganglioside; Immunotoxins; Injections, Spinal; Lumbosacral Region; Macrophages; Male; Myelin Sheath; N-Glycosyl Hydrolases; Oligodendroglia; Paraplegia; Plant Proteins; Rats; Rats, Sprague-Dawley; Recovery of Function; Ribosome Inactivating Proteins, Type 1; Saporins; Schwann Cells; Spinal Cord; Substance P