MRI characteristics can help in differentiating MOG-AD from other neuroinflammatory disorders, including multiple sclerosis and neuromyelitis optica. To avoid misdiagnosis, MOG antibody testing should be undertaken in selected cases presenting clinical and paraclinical features that are felt to be in keeping with MOG-AD, using a validated cell-based assay. Recent advances in MOG antibody testing offer improved sensitivity and specificity. Residual disability develops in 50-80% of patients, with transverse myelitis at onset being the most significant predictor of long-term outcome. Disease course can be either monophasic or relapsing, with subsequent relapses most commonly involving the optic nerve. Although no age group is exempt, median age of onset is within the fourth decade of life, with optic neuritis being the most frequent presenting phenotype.
#Mog disease life expectancy full#
Any medication started would be discussed in full detail if needed.Myelin oligodendrocyte glycoprotein (MOG) antibody disease (MOG-AD) is now recognised as a nosological entity with specific clinical and paraclinical features to aid early diagnosis. These types of medicine are used to control your child’s immune system and to damp down inflammation. Medicines that may be used include azathioprine, mycophenolate mofetil or in some cases rituximab. If a child continues to have relapses, then maintenance treatment may be required to prevent further relapses. Both these treatments will be explained in full detail if needed.įor many children, after an initial attack, it can be difficult to predict if further attacks will happen so it is not always beneficial to start a long term treatment. 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.
#Mog disease life expectancy how to#
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. Staying safe at GOSH and outside the hospitalĬoming to GOSH for a day or inpatient admissionĬoming to GOSH for an outpatient appointment Our new visiting guideline after COVID-19
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