Posters S101 clinical, radiological, electrophysiological features, laboratory findings and response to the same treatment modality. Two of the patients who were at stage-1 and stage-2B completed the treatment regimen and both had a marked improvement in their Neurological Disability Indexes. The third patient who was at stage-2B on admission rapidly progressed to stage 3B at the beginning of the intraventricular interferon therapy. In this patient the therapy was terminated by the approval of his parents at the sixth week of the treatment. When all the features of the patients are considered, the most important factor effecting the response to the treatment seemed to be the stage at admission. SSPE is a relatively more frequent neurodegenerative disease in our country. Further clinical experience is required to determine the most effective treatment modality. Our findings suggest that oral isoprinosine and intraventricular interferon-a therapy may be a good combination for the patients diagnosed at early stages. P256 Anti-NMDA-receptor encephalitis in a 3 year old boy with an inherited microdeletion on chromosome 6, including the HLA cluster H. Verhelst 1 *, P. Verloo 1 , K. Dhondt 1 , B. De Paepe 1 , B. Menten 2 , J. Dalmau 3 , R. Van Coster 1 . 1 Department of Paediatric Neurology, Ghent University Hospital, Ghent, Belgium; 2 Center for Medical Genetics, Ghent University Hospital, Ghent, Belgium; 3 Department of Neurology, University of Pennsylvania, Philadelphia, USA Background: Anti-NMDA-receptor encephalitis was initially described as a paraneoplastic disorder mostly seen in young women associated with ovarian teratoma. Diagnosis is made by detection of autoantibodies directed against the NR1 NR2 heteromers of the NMDA receptor in association with otherwise unexplained features of encephalitis. Early diagnosis is important as the symptoms are potentially reversible after immunomodulating therapy. Clinical case: Propositus was a previously healthy boy who presented at the age of three years, one month after a respiratory infection, with lateralized convulsions, orofacial dyskinesia and periods of agitation with choreoathetotic movements alternating with periods of sleepiness during which there was almost no reaction to stimuli. Over a period of ten days he developed high grade fever. Lab findings confirmed inflammation with high leucocytosis and high inflammatory parameters in blood and mild pleocytosis in cerebrospinal fluid. He was treated with acyclovir, ciprofloxacine, ampicilline and cefotaxime and became fever free but made almost no progress neurologically. An infectious agent could not be detected, therefore, an autoimmune mechanism was suspected. The diagnosis of anti-NMDA-receptor encephalitis was confirmed by the presences of autoantibodies directed against the NR1 NR2 heteromers of the NMDA receptor and treatment with pulse doses of methylprednisolone was started. During the following months he made some progression although very slowly. Array-comparative genomic hybridization in this patient revealed an inherited microdeletion in chromosome band 6p21.32, including the HLA-DPB1 and HLA-DPB2 genes. It is not clear whether the genomic findings in this patient could be considered as a risk factor for developing an autoimmune disease. However, polymorphisms of the HLA class II genes are known risk factors for autoimmune diseases. Moreover, some authors suggest that polymorphisms of the HLA-DPB1 gene correlate with an increased risk for multiple sclerosis. P257 MRI findings in a patient with palatal insufficiency as isolated symptom of post-infectious GQ1b antibody syndrome H. Verhelst 1 *, M. Maes 1 , K. Deblaere 2 , R. Van Coster 1 . 1 Department of Paediatric Neurology, Ghent University Hospital, Ghent, Belgium; 2 Department of Radiology, Ghent University Hospital, Ghent, Belgium Background: Anti-GQ1b immunoglobulin G (IgG) antibodies are positive in more than 90% of Miller Fisher syndrome patients and, therefore, are commonly used as diagnostic marker for this syndrome. Anti-GQ1b IgG antibodies are also associated with ophtalmoplegia in Guillain-Barr ´ e syndrome and with Bickerstaff’s brain-stem encephalitis. Clinically, most patients with anti-GQ1b IgG antibodies develop ophthalmoplegia and ataxia. Since GQ1b gangliosides are present throughout the central and peripheral nervous system, anti-GQ1b IgG antibodies may mediate a continuum of disorders with overlapping features, hence the concept of the anti-GQ1b antibody syndrome. In the patient presented here, palatal insufficiency was the only clinical symptom of a post-infectious GQ1b antibody syndrome. Clinical case: Propositus was a previously healthy boy who presented at the age of 12 years, one week after a bacterial pneumonia, with progressive swallowing difficulties and nasal speech. He also complained of pain in the legs. Clinical examination was normal except of palatal insufficiency. Cerebral MRI confirmed involvement of the nervus glossopharyngeus and vagus showing gadolinium enhancement of both nerves bilaterally and thickening of the nervus vagus bilaterally. The presence of anti-GQ1b IgG antibodies in cerebrospinal fluid confirmed a post-infectious autoimmune etiology although no increase of protein in cerebrospinal fluid was seen. Treatment with intravenous immunoglobulins stabilized the clinical symptoms and no further progression was noticed. After six weeks, total resolution of symptoms was seen. Conclusions: In the absence of increased protein in the cerebrospinal fluid, MRI may be helpful in addition to anti-GQ1b IgG antibodies to confirm the diagnosis of post-infectious GQ1b antibody syndrome, even in mono- symptomatic patients. Early treatment with intravenous immunoglobulins may prevent ophthalmoplegia and ataxia in anti-GQ1b IgG antibodies positive patients. P258 Altered callosal anisotropy in patients with pediatric multiple sclerosis A. Blaschek 1 *, I. Koerte 2 , A. Pomschar 2 , B. Ertl-Wagner 2 , I. Borggraefe 1 , W. Mueller-Felber 1 , F. Heinen 1 . 1 Department of Pediatric Neurology/Developmental Medicine, Dr v Hauner’s Children’s Hospital, LMU, Germany; 2 Institute of Clinical Radiology, Ludwig-Maximilians-University, Germany Objective: The purpose of this study in a group of pediatric patients with multiple sclerosis (MS) is to asses changes in the structural integrity of the corpus callosum (CC). Methods: DT MRI scans were acquired from 5 patients and 5 age-matched healthy controls. DT tractography was used to calculate the mean diffusivity (MD) and fractional anisotropy (FA) of the CC to assess aspects of structural integrity. At time of imaging patients were between 9 and 16 years and diagnosis of MS was confirmed by McDonald criteria. Results: In this series, we find an altered callosal anisotropy of the normal-appearing CC in our patients when compared with controls. Conclusion: Corpus callosum, the largest compact white matter fiber bundle of the human brain involved in interhemispheric transfer, is frequently damaged in the course of MS. In adult patient changes in the architecture