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Figure 3 | BMC Neurology

Figure 3

From: Anti-leucine rich glioma inactivated 1 protein and anti-N-methyl-D-aspartate receptor encephalitis show distinct patterns of brain glucose metabolism in 18F-fluoro-2-deoxy-d-glucose positron emission tomography

Figure 3

18 F-fluoro-2-deoxy-d-glucose positron emission tomography in patients with anti-N-methyl-D-aspartate receptor and anti-leucine rich glioma inactivated 1 protein encephalitis – projection onto surface display. Group analysis by statistical parametrical mapping of 18F-fluoro-2-deoxy-d-glucose positron emission tomography in patients with anti-N-methyl-D-aspartate receptor (anti-NMDA, n = 6) and anti-leucine rich glioma inactivated 1 protein encephalitis (anti-LGI1, n = 4) displays significant (p < 0.005, two sample t-test uncorrected for multiple comparisons and an extent threshold of 30 voxels) hypermetabolism and hypometabolism in different brain regions compared to matched controls (n = 5–6). A, Clusters of significant voxel projected onto magnet resonance based images of the brain surface demonstrate regionally limited hypermetabolism in frontotemporal areas contrasting extensive hypometabolism in parietal lobes of anti-N-methyl-D-aspartate receptor encephalitis. B, In anti-leucine rich glioma inactivated 1 protein encephalitis hypermetabolism is predominant in the cerebellum, basal ganglia, the occipital and precentral cortex whereas hypometabolism is restricted to the anterior cingulate/frontomesial cortex. C, Direct comparison between anti-N-methyl-D-aspartate receptor and anti-leucine rich glioma inactivated 1 protein encephalitis patients reveals distinct patterns of extensive hypometabolism in the precuneus, the parietooccipital and posterior cingulate cortex as well as hypermetabolism in frontomesial and temporal areas. Significant hypermetabolism is indicated by red and hypometabolism by blue color coding.

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