In autoimmune encephalitis the distribution pattern of changes in cerebral glucose metabolism depends on the associated antibody

1817 Objectives Encephalitis can be associated with antibodies against N-methyl D-aspartate receptors (anti-NMDAR) or leucine-rich glioma inactivated protein 1 (anti-LGI1). In patients with autoimmune encephalitis we evaluated the influence of associated antibodies on cerebral glucose metabolism. Methods 6 females (39±5 yrs) with anti-NMDAR encephalitis and 5 age matched female oncologic patients (41±2) were examined using F-18-FDG-PET/CT (Siemens, Biograph, static scan 60 min. p.i.). Analogue examinations were performed in 3 males (66±6) with anti-LGI1 encephalitis. All data sets were reconstructed employing an OSEM algorithm (4 iterations, 8 subsets). Spatial normalization and smoothing were performed using statistical parametric mapping (SPM2). Significant differences were set by p Results Patients with anti-NMDAR encephalitis showed compared to the reference group a regionally limited (≤200 voxels), bilateral hypermetabolism of the hippocampus and parahippocampus (BA 20, 28, 30, 35 and 36) as well as an extensive (≥2000 voxels) hypometabolism in the precuneus, parietal and posterior cingulate cortex (BA 7, 23, 40). In patients with anti-LGI1 encephalitis we observed hypermetabolism in the precentral region (BA 4, 6) and hypometabolism in the anterior cingulum/frontomesial (BA 10, 11, 24). Direct comparison between the above mentioned groups of encephalitis likewise revealed hypometabolism within BA 7, 23 and 40 in anti-NMDAR encephalitis as well as frontomesial hypometabolism (BA 11, 25) in anti-LGI1 encephalitis (p Conclusions Our results indicate that differences in the regional alterations of cerebral glucose metabolism in patients with autoimmune encephalitis depend on the associated antibody.