Abstracts: Poster Presentations, the Seventh European Paediatric Neurology Society (EPNS) Congress 95 that required artificial ventilation following a short history of fever and coryza and has remained in coma since. Brain Magnetic Resonance Imaging (MRI) showed symmetric T2 signal abnormality on the thalami and brain stem. The same areas subsequently showed T1 haemorrhagic transformation. Influenza A virus was detected on bronchoalveolar lavage three days after presentation. Investigations on blood, cerebrospinal fluid, urine and muscle did not reveal any other infectious, metabolic or autoimmune cause. Antibiotics, antivirals and immunotherapy were given without results. She had previously presented with unexplained acute encephalopathy at 10 months of age following a febrile illness and a prolonged seizure. MRI at the time showed T2 signal abnormality with identical distribution, which resolved over four months following clinical resolution. ANE after Influenza A has been rarely reported outside Japan and beyond infancy. The previous similar presentation with identical MRI lesions in our case raises the possibility of recurrent disease, which has not been previously described in sporadic cases. IAP032 A case of ADEM associated with mycoplasma pneumonia presenting with acute flask paralysis at first, relapsing transvers myelitis and than AHLE C. Mine 1 *, K. Yılmaz 2 , I. Tulay 1 , H. Hulya 1 , K. Ali 3 . 1 Pamukkale University Faculty of Medicine, Pediatrics Department, 2 Pamukkale University Faculty of Medicine, Radiology Department, 3 Pamukkale University Faculty of Medicine, Hematology Department, Turkey ADEM is usually a monophasic illness that may follow many infections or immunization. The common infections include rubeola, rubella, varicella, herpes zoster, mumps, upper respiratory truct infections and Mycoplazma pneumoniae infection. ADEM commonly presents after a latent period after the infection, which may only be a few days. The clinical features in children include multiphocal neurologic signs, lethargy, coma and seizures that often implicate widespread areas of the brain, spinal cord and optic nerves. Acute hemorrhagic leukoencephalitis (AHLE) may be a severe variant of ADEM. The presenting neurologic symptoms of AHLE can be similar to those of ADEM or can mimic an expanding mass lesion. Patient with AHLE deteoriate much more quicly, and coma and death commonly occur within a week. We present a case of ADEM associated with Mycoplasma pneumoniae. It manifested as acute ascending flask paralysis simetrically at first, recurrent transvers myelitis radiologically and than it had rapidly progressive course associated with AHLE at the level of brainstem and all of the spinal cord. The treatment with claritromycin, doxycyline, pulse metil prednisolone, ivig and plasmophresis did not improve the patient’s status. IAP033 Acute disseminated encephalomyelitis (ADEM) or multiple sclerosis (MS)? Part of the same demyelinating spectrum? M. Tzoufi 1 *, I. Nakou 1 , P. Sixlimiri 1 , A. Zikou 2 , M. Argyropoulou 2 , A. Siamopoulou-Mavridou 1 . 1 Child Health Department, University of Ioannina, Ioannina, Greece, 2 Department of Clinical Radiology and Imaging, University of Ioannina, Ioannina, Greece Introduction: The diagnostic differentiation between acute disseminated encephalomyelitis (ADEM) and multiple sclero- sis (MS) is important mainly for prognostic reasons, especially in childhood. Aim of the study: The differentiation of paediatric MS and ADEM, according to their initial presentation, in a small closed area of North Western Greece (Hepirus). Patients and Methods: Three children with ADEM (2M/1F, 10.3-11.8 years) and 4 with MS (3F/1M, 11-13.6 years) were included in this study and followed up for 3.5-8 years. Demographic, clinical, laboratory and imaging features were evaluated, and also the follow up imaging findings and the clinical outcome of the patients. Results: All patients with ADEM presented initially with clinical and laboratory findings of acute encephalitis and 1 of them, two days later, showed further neurological deterio- ration, with transverse myelitis and Horner’s syndrome. MRI of the brain showed in all, multiple lesions in the subcortical white matter. However, the children showed rapid clinical and imaging recovery (within a month). There were no relapses with only one exception, who showed a second similar attack (after 1.5 year), with full clinical and imaging recovery. The children with MS presented all, with established neurological picture (3/4 with optic neuritis, 2/4 with hemiparesis, 1/4 with cerebellar ataxia and vestibular syndrome). CSF studies showed a high IgG index (>0.5). Evoked potentials were informative in 3/4 patients. MRI of the brain showed multiple lesions in the periventicular and subcortical white matter. On follow up MRI examinations, in all patients revealed new lesions associated with clinical relapse in one, while the other three were clinically silent. Conclusion: This small study in children did highlight clinical, laboratory and imaging differences in the initial presentation, between ADEM and MS. However, the follow up period for the children with ADEM is small and it is impossible to predict their possible progress to MS, as the only truly reliable diagnostic test remains time. IAP034 Mitochondrial dysfunction in a child with neuromyelitis optica A. Bhatt 1 *, S. DeRoos 2 , K. Chillag 2 . 1 Michigan State university department of Neurology and Opthalmology, East Lansing, Michigan, USA, 2 Department of Pediatric Neurology, Helen DeVos Children’s Hospital, Grand Rapids, Michigan, USA In this case study, we report a 9.5 year old girl who presented with bilateral optic neuritis at 6.5 years of age. Muscle biopsy revealed dysfunction in ETC complexes 1-4 and she was diagnosed with a mitochondrial cytopathy. She experienced recurrent exacerbations of optic neuritis which responded to treatment with intravenous methylprednisolone. At 8 years of age she developed transverse myelitis and brainstem lesions. Neuromyelitis Optica (NMO) antibodies were present in the serum and CSF and a diagnosis of NMO was made. NMO is an autoimmune neuro-inflammatory condition characterized by optic neuritis and longitudinally extensive transverse myelitis. It has rarely been reported in children, especially with coexistant mitochondrial cytopathy. Ours is the second reported NMO proven case. The mitochondrial dysfunction in our patient may represent an epiphenomenon or a predisposition to NMO and may offer further insight into the pathogenesis of this condition IAP035 Recurrent pseudotumoural hemicerebellitis: case report of a patient with review of the literature G. Haliloglu 1 *, K.K. Oguz 2 , O. Bircan 3 , D. Alehan 3 , M. Topcu 1 . 1 Hacettepe University, Pediatric Neurology, 2 Hacettepe University, Radiology, 3 Hacettepe University, Pediatrics, Ankara, Turkey Background: Acute cerebellitis is an inflammatory process with usually bilateral involvement of the cerebellum. Unilat- eral involvement, so called pseudotumoural hemicerebellitis is extremely rare and must be differentiated mainly from unilateral mass lesions and demyelinating diseases. Case presentation: A 13-year-old girl presented with headache, cerebellar and pyramidal tract involvement. She had a previous episode of transient visual loss and ataxia two years ago and in a month the symptoms revealed without any specific treatment. She had no complaints within the