In rare cases, if high dose steroids do not improve your child’s symptoms, other treatment may need to be considered, such as intravenous immunoglobulins (IVIGs) or plasma exchange. Steroids do not change your child’s risk of a relapse. Steroids have both short and long term side effects so your child will not usually stay on them for a long time. These side effects will be discussed with you in more detail at the time. Your child may then start an oral course of steroid tablets and you will be given a plan of how to reduce these gradually.Ĭhildren usually respond very well to steroid treatment during this acute phase. This will usually be given at high dose for three to five days via a cannula into a vein. Intravenous steroid treatment is often used to treat the acute symptoms of demyelination to try to reduce the inflammation that has occurred. How is MOG antibody demyelination diagnosed? These relapses could happen either months or even years apart and therefore it can be difficult to predict. arm weakness (if higher up the spinal cord)Ĭhildren may also have symptoms such as nausea, vomiting, ataxia (unsteadiness) and extreme lethargy or tiredness.įor many children that have a MOG antibody demyelination episode, it will be a one off and they have no further attack of symptoms (relapse). However, some children may be at risk of further relapses.Symptoms come on quickly and can vary depending on where the inflammation has occurred in the spine. Transverse myelitis is inflammation of the spinal cord. Optic neuritis is demyelination of the optic nerve and can affect one or both eyes. Some children may initially present with acute disseminated encephalomyelitis (ADEM) which is an inflammatory condition that mainly affects the brain and others may have signs of optic neuritis or transverse myelitis. Symptoms of MOG antibody demyelination can be variable from person to person and can range from mild to severe depending on which parts of the brain are affected. NMO-Ab and MOG-Ab could be potential biomarkers to determine visual prognosis in patients with ON.Coronavirus (COVID-19) – information for children, young people and familiesĬoming to GOSH for a day or inpatient admissionĬoming to GOSH for an outpatient appointment In the other 3 groups (NMO-Ab/MOG-Ab, NMO-Ab/MOG-Ab, and NMO-Ab/MOG-Ab), visual acuity did not change significantly (P = 0.53, 0.42, and 0.45, respectively). In the NMO-Ab/MOG-Ab group, visual acuity improved significantly (P < 0.0001). Three (50%) of 6 eyes of patients seropositive for both antibodies did not respond to corticosteroid pulse therapy and plasmapheresis, and visual acuity remained unchanged. Ten (43%) of 23 patients were seronegative for both antibodies. Six (26%) of 23 patients were seropositive for both NMO-Ab and MOG-Ab. MOG-Ab seropositivity was defined by comparing with MOG-Ab level obtained from 8 healthy normal subjects.Įleven (47%) of 23 ON patients were NMO-Ab seropositive, while 8 (34%) of the 23 patients were MOG-Ab seropositive. At presentation, serum NMO-Ab was measured by immunofluorescence using HEK 293 cells transfected with AQP4-GFP, and anti-MOG1-125 antibody was measured by enzyme-linked immunosorbent assay. Thirty-three eyes of 23 patients with ON were studied. We investigated the relationship between NMO antibody (NMO-Ab) and anti-MOG antibody (MOG-Ab) and potential in patients with ON for recovery of vision. MOG antigen is currently considered as a cause of optic neuritis (ON) associated with MS because immunization with MOG antigen derived from oligodendrocytes induces murine ON with myelitis. Myelin oligodendrocyte glycoprotein (MOG) is well known as the causative protein of multiple sclerosis (MS). Damage to astrocytes by anti-aquaporin-4 antibody (AQP4-Ab), also known as NMO antibody, has been implicated as the cause of neuromyelitis optica.
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