Disease relevance of Optic Neuritis

• These results demonstrate that clinical manifestations of CNS autoimmune disease will vary depending on the identity of the target autoantigen and that MOG-specific T cell responses are involved in the genesis of isolated optic neuritis [1].
• Adeno-associated viral-mediated catalase expression suppresses optic neuritis in experimental allergic encephalomyelitis [2].
• The pathology found in our models closely reflects the spectrum of multiple sclerosis (MS) pathology: Classical MS as well as variants such as optic neuritis, Devic's disease and Marburg's type of acute MS are mimicked in rats immunized with MOG antigen [3].
• We describe a patient with systemic lupus erythematosus who developed transverse myelitis and optic neuritis [4].
• Disk swelling in patients with hypoparathyroidism has often been attributed to papilledema but rarely to optic neuritis [5].

High impact information on Optic Neuritis

• In addition, the rate of new episodes of optic neuritis in either eye was higher in the group receiving oral prednisone, but not the group receiving intravenous methylprednisolone, than in the placebo group (relative risk for oral prednisone vs. placebo, 1.79; 95 percent confidence interval, 1.08 to 2.95) [6].
• Intravenous methylprednisolone followed by oral prednisone speeds the recovery of visual loss due to optic neuritis and results in slightly better vision at six months [6].
• Optic neuritis associated with dideoxyinosine [7].
• In the present study, we show that, in rats suffering from myelin oligodendrocyte glycoprotein (MOG)-induced optic neuritis, systemic application of erythropoietin (Epo) significantly increased survival and function of retinal ganglion cells (RGCs), the neurons that form the axons of the optic nerve [8].
• This study demonstrates that CNTF has a neuroprotective effect on affected RGCs during acute optic neuritis [9].

Chemical compound and disease context of Optic Neuritis

• Oral prednisone alone, as prescribed in this study, is an ineffective treatment and increases the risk of new episodes of optic neuritis [6].
• The pathophysiology of acute optic neuritis. An association of gadolinium leakage with clinical and electrophysiological deficits [10].
• CONCLUSIONS: Intravenous cyclophosphamide pulse therapy seems to be an effective treatment for optic neuritis refractory to corticosteroids, oral immunosuppressants, or both [11].
• Increase of manganese superoxide dismutase, but not of Cu/Zn-SOD, in experimental optic neuritis [12].
• Bilateral postinfectious optic neuritis and intravenous steroid therapy in children [13].

Biological context of Optic Neuritis

• Twenty-three patients with multiple sclerosis (MS) and 1 patient with isolated optic neuritis (mean age 37.5 yrs, average duration of disease 10 yrs) were tested with auditory and visual cognitive event-related potentials (ERPs) using an oddball paradigm [14].
• Horizontal saccadic and smooth pursuit eye movements were studied in 84 patients with multiple sclerosis (MS) and 21 patients with optic neuritis (ON) [15].
• Visual fields were examined with a tangent screen in 54 patients with multiple sclerosis (MS) or optic neuritis (ON) [16].
• All 7 MS patients had abnormal visual evoked response, 3/4 abnormal somatosensory evoked response and 5/6 intrathecal immunoglobulin production, when examined at onset of optic neuritis or at follow-up [17].
• Immunological effects of oral high-dose methylprednisolone in acute optic neuritis and multiple sclerosis [18].

Anatomical context of Optic Neuritis

• Cerebrospinal fluid antibodies to myelin basic protein in acute idiopathic optic neuritis [19].
• Myeloid CSF dendritic cells were elevated in optic neuritis, neuroborreliosis and other inflammatory neurological disorders, while plasmacytoid dendritic cells were elevated in all neuroinflammatory conditions studied, with especially high numbers in neuroborreliosis [20].
• Comparison of these studies in both groups shows no statistical differences and supports the concept that cell-mediated hypersensitization to central nervous system myelin basic protein, however initiated, is a factor in the pathogenesis of retrobulbar neuritis [21].
• Simvastatin treatment does not protect retinal ganglion cells from degeneration in a rat model of autoimmune optic neuritis [22].
• CONCLUSIONS: There is a relative lack of restriction of TCRBV usage by CSF lymphocytes in the very earliest stages (<7 days) of acute optic neuritis [23].

Gene context of Optic Neuritis

• Forty-nine of 55 patients with optic neuritis had increased CSF anti-MBP and the remaining 6 had increased anti-PLP [24].
• Optic neuritis is associated with myelin basic protein and proteolipid protein reactive cells producing interferon-gamma, interleukin-4 and transforming growth factor-beta [25].
• Characterization of the mitochondrial genome in childhood multiple sclerosis. II. Multiple sclerosis without optic neuritis and LHON-associated genes [26].
• Optic neuritis: chemokine receptor CXCR3 and its ligands [27].
• We studied the expression of CCR2 on leukocytes in blood and cerebrospinal fluid (CSF) from patients with monosymptomatic optic neuritis and MS, and the concentration of CCL2 in the CSF from these patients [28].

Analytical, diagnostic and therapeutic context of Optic Neuritis

• RESULTS: Two patients, 39 and 23 years of age, were seen with acute optic neuritis 1 month and 2 weeks, respectively, after anthrax booster vaccination and successfully treated with intravenous methylprednisolone [29].
• Adenoviral gene therapy with catalase suppresses experimental optic neuritis [30].
• We studied immunological changes in 50 patients with optic neuritis or multiple sclerosis who underwent lumbar puncture before and 1 week after completing a 15-day course of oral high-dose methylprednisolone treatment [18].
• The Aulhorn flicker test: possibilities and limits. Its use in optic neuritis for diagnosis, differential diagnosis, monitoring the course of the disease, and assessing the effect of oral prednisolone [31].
• Her optic neuritis improved following oral administration of prednisolone and retrobulbar injections of dexamethasone [32].

References