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Alternatively, the virus infecting the myelin-supporting cells could elicit the release of sequestered myelin antigens into the circulation and trigger autoimmunity.1 24 This matter of pathogenesis remains a subject of extensive research. Relevance of CMV-IgM seropositivity CMV is a prevalent pathogen, and up to 20% of children in the USA would have contracted CMV before puberty. Primary CMV infection is commonly inapparent. When it is symptomatic, it will only cause up to 7% of cases of mononucleosis, manifesting with symptoms identical to those caused by EBV.25 In the laboratory evaluation of acute mononucleosis syndrome, lymphocytosis with a positive EBV IgM is sufficient to establish EBV as the culprit over CMV (regardless of CMV immunoglobulin seropositivity).25 Instances of EBV and CMV coinfection, although rare, could still occur.26 Whether EBV, CMV or a combination of both contributed to this boy's ADEM cannot be determined for sure. However, an EBV mononucleosis syndrome followed by ADEM would be the most likely explanation. Radiological findings in ADEM In our patient, a brain and spine MRI supported the diagnosis of ADEM by showing characteristic diffuse demyelinating disease (figures 1 and ?and22). MRI is the preferred modality for imaging the brain in patients with ADEM since early CT imaging is often normal, as seen in this case. T2-weighted imaging is the preferred sequence to show the hyperintense signals in the MG-132 mouse involved parenchymal region. The lesions normally do not show enhancement in the contrast-enhanced images, and typically do not show restricted diffusion in the diffusion-weighted images either. Finally, it is essential to screen the whole neural axis including the brain and the spinal cord to show the complete extension of the pathological process. Treatment, outcome and prognosis Owing to lack of randomised controlled trials on treatment of ADEM, there is no standard therapy for ADEM. Instead, it is treated similar to MS and other autoimmune diseases. Based on the clinician's expertise and data from small series, different immunosuppressive approaches are pursued for different cases of ADEM and these include steroids, intravenous immunoglobulin (IVIg) or plasmapheresis.2 3 Most paediatric groups described the use of high-dose steroids (intravenous methylprednisolone (10�C30?mg/kg/day up to a maximum dose of 1?g/day) or dexamethasone (1?mg/kg) for 3�C5?days) followed by oral steroid taper for 4�C6?weeks. Based on their experience, full recovery was reported in 50�C80% of patients.2 ADEM has an overall good prognosis and most patients recover, particularly the paediatric population. Based on collective data from case series, approximately two-thirds of patients make a complete recovery.2 10 27 Mortality from ADEM in the paediatric population has been reported at rates from 0% to less than 5% in more recent studies.