The fluorescence was read with EUROIMMUN LED fluorescence microscope at 20 and 40 magnification. Open in a separate window Figure 1 Detection of anti-NMDAR antibodies by indirect immunofluorescence (Autoimmune Encephalitis Mosaic 1 kit from EUROIMMUN). %) was the most common presenting symptom; status epilepticus occurred in 23 (60.5%) patients during the course of the illness. Fourteen (35.9%) patients were N-methyl-D-aspartate receptor (NMDAR) antibody-positive and all were negative for the other antibodies tested. Conclusions: One-third of patients presenting with acute noninfective encephalitis would be positive for NMDAR antibodies with the remaining two-thirds with clinically suspected autoimmune encephalitis being antibody-negative. You will find few markers in the clinical and investigative profiles to distinguish antibody-positive and -unfavorable patients. Keywords: Autoimmune, encephalitis, NMDA antibody, seizures Introduction The discovery of autoantibodies specific for the neuronal cell membrane surface or synaptic proteins has led to the emergence of the novel concepts of autoimmune epilepsy[1] and autoimmune encephalitis. The pathogenesis of the unexpected and fulminant disorder characterized by altered sensorium, cognitive and behavioral impairment, focal neurological deficits, epileptic seizures, and status epilepticus had been an enigma. Previously cited as rare entities, recent literature[2,3] shows that autoimmune factors may account for a majority of the nonviral encephalitides. The antigens that are frequently identified in such cases include the N-methyl D-aspartate receptor (NMDAR);[4] the -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR); the -aminobutyric acid receptor-B (GABAB receptor); and proteins that associate with voltage-gated potassium channel (VGKCs) leucine-rich glioma-inactivated protein 1(LGI1) and contactin-associated protein-like 2 (Caspr2).[5,6] It is often difficult to distinguish these from mimics like obscure central nervous system (CNS) infections, mitochondrial encephalopathy, and occult focal cortical dysplasia by clinical features alone. Failure to identify the etiology as autoimmune may deprive the patient of treatment for any potentially curable entity. Our objective was to screen a large number of patients admitted to neurology rigorous care support with fulminant seizures that eluded specific diagnosis in order to identify and characterize those with autoimmune encephalitis. Materials and Methods Establishing of the study The study was Tauroursodeoxycholate carried out in the Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum which is a tertiary neurology referral center in South India. Patients All patients admitted in the neuromedical rigorous care unit (ICU) of the Department of Neurology, between December 2009 and June 2013, were screened to identify patients with unexplained status epilepticus or encephalitis-like presentation. Children below 2 years of age (in view of the difficulty Tauroursodeoxycholate in obtaining the adequate quantity of blood sample and more heterogeneous etiologies of encephalopathy and seizures), persons with encephalitis due to an infective pathology, and epilepsies related to structural, genetic, or metabolic causes were excluded. We applied the criteria proposed by Zuliani et al.,[7] and certain additional criteria[8] to identify possible cases associated with neuronal surface antibodies. The criteria were: Acute or subacute (less than 12 weeks) onset of symptoms; CNS inflammation as evidenced by at least one of the following: Inflammatory cerebrospinal fluid characteristics (lymphocytic pleocytosis, cerebrospinal fluid (CSF) specific oligoclonal bands, or elevated IgG index); Magnetic resonance imaging (MRI) characteristics suggesting inflammation (T2 hyperintensities, contrast enhancement, or restricted diffusion); Inflammatory neuropathology CLIP1 lymphocytic infiltrates or other signs of immune activation in brain biopsy specimens; Exclusion of other causes of encephalitis or other CNS conditions mimicking encephalitis; and Good response to immunotherapy. Of the 1,227 patients admitted Tauroursodeoxycholate in the ICU, 47 patients fulfilled the above criteria Tauroursodeoxycholate for possible autoimmune encephalitis presenting seizures. Thirty-nine of these.