neuromyelitis optica was made and patient was planned forRituximab therapy.

Second patient is a 35 years old female, presented toneurology clinic with history of recurrent optic neuritis forwhich she was followed up by ophthalmologist. After 16months she was admitted with acute transverse myelitis andoptic neuritis. Initial NMO IgG was �ve. MRI brain showednonspecific T2 hyperintensities. MRI spine showed diffuse T2hyperintensties from C5 through T10. She was treated with IVmethyl prednisolone, and because the response was notfavorable, IV immunoglubulins was given, and maintained onprednisolone (tapering dose) and mycophenolate. On outpatient follow up she continued to have mild residual weak-ness. After a year she developed another attack of paraplegiaand optic neuritis; and was started on interferon. A repeatNMO IgG was +ve. After 2 months she developed anotherattack of paraplegia. And after 4 months it also recurred. Shewas offered treatment with Mitoxantrone but refused.

Third patient is a 24 years old female, transferred to ourhospital with 2 months H/O acute transverse myelitis and opticneuritis for which she was admitted to a local hospital andreceived IV methyl prednisolon. MRI brain showed multiplewhite matter T2 hyperintensities. MRI spine showed diffuse T2hyperintensities C2 to T1 and T7–T12. Patient refused lumbarpuncture. She was seen in neurology clinic after 2 months with3 weeks H/O Lt optic neuritis and received IV methylprednisolone. NMO IgG was +ve and was started on interferon.Seen again after 4 months. Doing well, ambulant withoutsupport. Patient lost to follow up. She subsequently deterio-rated and was started on Rituximab.

Fourth patient is a 46 years old female, admitted withurinary retention, generalized weakness, and altered sensor-ium. MRI brain: non-specific T2 white matter changes. MRIspine: extensive T2 hyperintensities from C2 to T1 and from T8to T10 with contrast enhancement. Treated with methylprednisolone. Had gradual progressive recovery. After 4 monthshad another attack of transverse myelitis. MRI spine: T2hyperintensities from lower medulla to T10. Received IV methylprednisolone. CSF oligoclonal bands was +ve. NMO IgG was+ve. ANCA-PR3 A6 was +ve. Cyclophosphamaide treatmentwas attempted but was not tolerated by patient and wasstopped.

Neuromyelitis optica should be suspected in any patientpresenting with optic neuritis, transverse myelitis or both withan MRI brain not suggestive of multiple sclerosis. Neither apositive oligo clonal band in CSF, nor an initial negative NMO IgGtest can exclude the diagnosis of NMO, as the former may bepresent in 35% of patients with NOM and the last can turnpositive later on in the disease coarse. The diagnosis of NMOwarrants early initiation of a disease specific therapy to preventrelapses.

http://dx.doi.org/10.1016/j.msard.2014.09.159

P011

A large series of Toxocara canis myelitis

R. Jabbour, R. Sawaya, B. Yamout, S. Kanj-Sharara,S. Atweh

Lebanon

Background/objectives: The etiology of isolated myeli-tis is often difficult to find. Helminthic infections of thespinal cord are thought to be very rare. The diagnosis isusually suspected in patients with myelitis and CSF and/orblood eosinophilia. In the current case-series study, wereport 20 cases of isolated Toxocara myelitis recruited atthe American University of Beirut, with full description ofthe clinical presentation, laboratory data, MRI findings, andresponse to antihelminthic treatment.Design and methods: Clinical and laboratory data werecollected for 20 patients who presented with evidence ofspinal cord disease. The clinical presentation includedsensory, motor, and autonomic dysfunction, predominantlyin the lower extremities.Results: Patients exhibited a subacute or chroniccourse; this was either slowly progressive or remitting-relapsing with mild to moderate disability. The patientsunderwent extensive blood and CSF studies as well as MRI ofthe spinal cord and brain. Eosinophilia was not a universalfinding; only 2 patients had a high eosinophil count in theCSF, although blood eosinophilia was seen in 6 patients. Allpatients tested positive for Toxocara canis antibodies in theblood and CSF. MRI of the spinal cord revealed a singlecharacteristic lesion with fusiform enlargement that wasisointense on T1-weighted images and hyperintense on T2-weighted images. Nodular enhancement was seen aftergadolinium injection. MRI of brain was normal in all thecases. Treatment with albendazole, with or without ster-oids, resulted in marked neurologic improvement andnormalization of the MRI in all patients.Conclusions: The finding of a single inflammatory MRIlesion in the spinal cord with positive Toxocara canisserology in the blood and CSF in cases of subacute orchronic myelitis suggests the diagnosis of Toxocara myelitis,irrespective of the presence of eosinophilia. All these casesshowed good clinical outcomes once treated with antihel-minthic agents.

http://dx.doi.org/10.1016/j.msard.2014.09.160

P012

Pediatric onset multiple sclerosis patients tend tohave slower disease progression

R. Alroughani, S. Ahmed, J. Al-Hashel

Kuwait

Background: Data on the difference between pediatricand adult onset multiple sclerosis (MS) in terms of diseasecourse and progression is scare in our region.Objective: To compare the demographic and clinicalcharacteristics between pediatric-onset and adulthood-onset MS.

S. Taghavifar et al.742