Objective: The main novelty of the case is to demonstrate the relationship between tuberculosis and GABA B receptor encephalitis, which has never reported before. Patients and Methods/Material and Methods: 34 years lady admitted for first episode status epilepticus. She had nasopharyngeal carcinoma, completed radiotherapy 5 years ago, no evidence of recurrence. CSF revealed mild pleocytosis and positive GABA B receptor antibody. EEG showed moderate encephalopathy with electrographic seizure. MRI brain showed bilateral hippocampal T2/ FLAIR hyperintensities. No co-existing paraneoplastic antibody. She was treated with IV methylprednisolone, followed by IVIg and plasmapheresis. CT thorax revealed multiple lung nodules with cavitation suggestive of PTB, confirmed with bronchoscopy and bronchial washing (TB Genexpert positive). Thus started on antitu- bercular treatment. Repeated CT after 1 month showed improve- ment. She was discharged with oral steroids and antiepileptics. She presented after 1 month for refractory seizures, requiring second plasmapharesis. She remained mildly encephalopathic but seizures controlled. Planned for second line immunosuppressant if further relapse. Results: It is unclear whether the relationship between tuberculosis and GABA B encephalitis is of coincidence or causality. Conclusion: Impaired cell mediated immunity with cumulative high dose of steroids in our patient are known predisposing risk of tuberculosis infection, especially in Sabah (TB endemic area). On the other hand, infection as trigger for limbic encephalitis due to cross reactivity with neuronal antigen also remains a possibility. doi:10.1016/j.jns.2017.08.2542 2512 WCN17-3491 SHIFT 7 - AUTOIMMUNE DISORDERS Anti-VGKC-antibody mediated limbic encephalitis in a Sudanese patient: Rarity in sub Saharan Africa O. Seidi. University of Khartoum, Soba University Hospital- Neurosciences, Khartoum, Sudan Background: Anti-Voltage Gated Potassium Channel (VGKC) anti- body associated limbic encephalitis (LE) is a rare disorder with protean clinical presentations needing a high degree of clinical suspicion and advanced immunological tests to confirm. We report the case of a sixty eight years Sudanese gentleman who developed subacute cognitive changes with bizarre movements of his face and limbs, followed by myoclonic jerks with frequent falls. He was diabetic with excellent control. He had faciobracial dystonic movements with myoclonic jerks on the limbs and infrequently spreading to the whole body. The rest of the general and neurological examinations were unremarkable. Abstracts / Journal of the Neurological Sciences xxx (2017) 757–944 903