Poster sessions S109 children was higher than expected based on previous reports in the UK, indicating an incidence of 0.7-4 cases per million children. ON was the commonest initial presentation and was an isolated finding in four cases, three of them Caucasian. Three children, two of them Caucasian, presented with ADEM without spinal cord and optic nerve involvement and remain well in remission. Two children were diagnosed with MS, having positive oligoclonal bands and radiological features suggestive of “plaques” with additional intraspinal lesions. One child was diagnosed with CIS, having persistent visual impairment and associated spinal cord lesions. Those cases (n = 3) with recurrent demyelination, initial spinal cord or persistent optic nerve disease were all non-Caucasian and presented with severe Vitamin D deficiency (<18 nmol/L). These data indicate that demyelination in children is a more frequent occurrence in East London than would have been anticipated, and highlights the problems of applying broad epidemiological data related to a disease of variable and heterogenous distribution in a regional setting. Furthermore we found Vitamin D homeostasis was an important factor in more severe disease, which will have implications for future treatment and bone metabolism surveillance. Finally, optic nerve disease refractory to initial steroid therapy or spinal cord involvement may be indicative of a greater risk of early recurrence (<1 year). P19.5 MRI abnormalities in children with multiple sclerosis and acute disseminated encephalomyelitis R. Cedenkayevna Bembeeva 1 *, V. Khalilov 1 . 1 Russian State Medical University, Russian Federation Purpose: To compare the peculiarities of the brain white matter abnormalities in child patients with multiple sclerosis (MS) and acute disseminated encephalomyelitis (ADE). Material and Methods: 28 children with clinically confirmed diagnosis of MS and ADE underwent MRI assessments during the period of 2008 2010. 1,5T MRI was performed with Magnevist “Shering AG”. Results: Abnormalities revealed in group of MS patients are similar in many aspects to those in ADE. However, there are some differences. In ADE patients the foci in the white matter usually occupy greater area (up to 1-2 cm) with unclear boundaries and are situated asymmetrically. Subcortical white matter is more often affected while periventricular white matter remains comparatively spared in patients with ADE. In case of MS the abnormalities usually have more clearly outlined edges and are localized in periventricular areas, and subcortically. In ADE the brain cortex and thalamus are often affected. For MS abnormalities in the corpus callosum and internal capsule are typical. MRI with contrast enhancement reveals quantitative advantage of contrast- positive foci in the acute stage of ADE. On repeated MRI assessments to study the disease dynamics, the increase of brain atrophy is noted in a number of MS cases in contrast to ADE. P19.6 Multiple sclerosis in a 12 year old boy with an inherited microdeletion within the NR3C2 gene H. Verhelst 1 *, P. Verloo 1 , B. Menten 1 , R. Van Coster 1 . 1 University Hospital Ghent, Belgium NR3C2 or mineralocorticoid receptor mutations are the principal cause of autosomal dominant or sporadic type 1 pseudohypoaldosteronism. Patients can be asymptomatic or show a salt-loosing syndrome in the neonatal period. Afterwards, patients compensate for their defective miner- alocorticoid receptors by upregulating their mineralocorticoid axis, hence presenting, in most cases, a lifelong increase in renin and aldosterone levels. The renin-angiotensin-aldosterone system (RAAS) is a key hormonal system regulating blood pressure by acting on vasculature, heart, kidney and adrenal gland. However, expression of RAAS components has recently been detected in other tissues such as brain, thymus and immune cells. Moreover, the RAAS has been implicated in several mouse models of autoimmune disease. Series of studies have demonstrated that angiotensin II has a wide variety of proinflammatory properties which may contribute to the development of autoimmune diseases. Notably, an- giotensin II seems to play a role in sustaining autoimmune neuroinflammation in chronic experimental autoimmune encephalomyelitis, a model mimicking many aspects of multiple sclerosis (MS), and angiotensin receptors are up- regulated in infiltrates of plaques from the brains of MS patients. We report on a male patient who presented at the age of 12 year with MS and in whom an inherited microdeletion within the NR3C2 gene was detected, compatible with the diagnosis of type 1 pseudohypoaldosteronism. His mother and her sister, who both developed autoimmune thyroiditis, also carry the microdeletion. The clinical relevance of this microdeletion in developing autoimmune diseases, and especially in developing MS, is discussed. P19.7 Clinical, neuroimaging and laboratory features of childhood acute demyelinating encephalomyelitis and multiple sclerosis: a case series D. Zafeiriou 1 *, E. Vargiami 1 , M. Pashalidou 2 , A. Anastasiou 3 , M. Kotsiou 4 , N. Gombakis 1 , E. Kontopoulos 1 . 1 1st Department of Pediatrics, Aristotle University, Thessaloniki, Greece, 2 2nd Department of Neurology, Aristotle University, Thessaloniki, Greece, 3 Department of Radiology, “Hippokratio” General Hospital, Thessaloniki, Greece, 4 Pediatric Intensive Care Unit, “Hippokratio” General Hospital, Thessaloniki, Greece Objective: Acute disseminated encephalomyelitis (ADEM) is a treatable inflammatory demyelimating disorder seen more commonly in children than in adults. We describe the clinical, neuroimaging and laboratory features, as well as the treatment, outcome and evolution to MS in a childhood ADEM cohort. Patients and Methods: Retrospective case review of 22 patients (age range 21 months - 15 years) with an initial diagnosis of ADEM admitted to a tertiary referral center between 1999 2009. Results: Most frequent presenting features (alone or in combination) included hemiparesis (N = 10), sensory symp- toms (N = 8), ataxia (N = 7), seizures (N = 5), diplopia (N = 4), aphasia (N = 3), speech disorder (N = 3), muscle weakness (N = 2), personality changes (N = 2), tetraparesis (N = 1) and segmental myoclonus (N = 1). Sites of involvement at MRI included the white matter (N = 12 [6 periventricular]), cortex (N = 6), subcortical white matter (N = 10), basal ganglia (N = 5), cerebellum (N = 3), spinal cord (N = 4) and spinal roots (N = 2). All patients received intravenous methylprednisone bolus dose followed by oral corticosteroids tapering. Nine children relapsed 1 to 12 months after cessation of steroids. Six of these children evolved to MS (follow-up 1-8 years). Presence of CSF oligoclonal bands (N = 5; p < 0.001), diplopia (N=4; p < 0.001) and periventricular white matter lesions in MRI (N=6; p < 0.001) had positive predictive value in evolution to MS. Chronic subcutaneous interferon therapy in 4 patients who evolved to MS (follow-up 1-7 years) resulted in a good response with no side-effects. Conclusion: The presence of diplopia, CSF oligoclonal bands and periventricular white matter lesions were predictive of evolution into MS. Corticosteroids were highly effective in the treatment of ADEM, while subcutaneous interferon seems to