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Figure 2 | BMC Neurology

Figure 2

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 2

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 – tomographic display. Group analysis by statistical parametrical mapping of 18F-fluoro-2-deoxy-d-glucose positron emission tomography shows 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 of investigated patients with anti-N-methyl-D-aspartate receptor encephalitis (A, anti-NMDA, n = 6) and anti-leucine rich glioma inactivated 1 protein encephalitis (B, anti-LGI1, n = 4) compared to age and sex matched controls (n = 5–6). A, Clusters of significant voxels projected onto magnet resonance tomograms in Montreal Neurological Institute space illustrate the typical pattern of temporomesial hippocampal and parahippocampal hypermetabolism as well as widespread hypometabolism in the precuneus, pre- and postcentral, parietal and posterior cingulate cortex of anti-N-methyl-D-aspartate receptor encephalitis patients. B, In anti-leucine rich glioma inactivated 1 protein encephalitis we observed hypermetabolism in the cerebellum, basal ganglia, precentral and occipital areas and hypometabolism limited to the anterior cingulate / frontomesial cortex. C, Direct comparison of anti-N-methyl-D-aspartate and anti-leucine rich glioma inactivated 1 protein encephalitis patients revealed hypometabolism in the precuneus, parietal, occipital and cingulate cortex and hypermetabolism limited to frontotemporal regions. Significant hypermetabolism is indicated by red to yellow and hypometabolism by blue to green color-coding.

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