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

Abstract

BackgroundPathogenic autoantibodies targeting the recently identified leucine rich glioma inactivated 1 protein and the subunit 1 of the N-methyl-D-aspartate receptor induce autoimmune encephalitis. A comparison of brain metabolic patterns in 18F-fluoro-2-deoxy-d-glucose positron emission tomography of anti-leucine rich glioma inactivated 1 protein and anti-N-methyl-D-aspartate receptor encephalitis patients has not been performed yet and shall be helpful in differentiating these two most common forms of autoimmune encephalitis.MethodsThe brain 18F-fluoro-2-deoxy-d-glucose uptake from whole-body positron emission tomography of six anti-N-methyl-D-aspartate receptor encephalitis patients and four patients with anti-leucine rich glioma inactivated 1 protein encephalitis admitted to Hannover Medical School between 2008 and 2012 was retrospectively analyzed and compared to matched controls.ResultsGroup analysis of anti-N-methyl-D-aspartate encephalitis patients demonstrated regionally limited hypermetabolism in frontotemporal areas contrasting an extensive hypometabolism in parietal lobes, whereas the anti-leucine rich glioma inactivated 1 protein syndrome was characterized by hypermetabolism in cerebellar, basal ganglia, occipital and precentral areas and minor frontomesial hypometabolism.ConclusionsThis retrospective 18F-fluoro-2-deoxy-d-glucose positron emission tomography study provides novel evidence for distinct brain metabolic patterns in patients with anti-leucine rich glioma inactivated 1 protein and anti-N-methyl-D-aspartate receptor encephalitis.

Beyond the limbic system: disruption and functional compensation of large-scale brain networks in patients with anti-LGI1 encephalitis

“…A recent FDG-PET analysis reported hypermetabolism of the sensorimotor cortex in patients with anti-LGI1 encephalitis that, together with contralateral frontal EEG changes and results from polymyographic recordings, are suggestive of a motor cortex origin of FBDS 5. Another FDG-PET study observed hypermetabolism in the precentral gyrus, basal ganglia and cerebellum in patients with LGI1 encephalitis with FBDS 16. Here, precentral hypermetabolism was associated with higher disease severity at follow-up, suggesting that sensorimotor network integrity may serve as a predictor for disease-related disability.…”

The role of PET/CT in the evaluation of patients affected by limbic encephalitis: A systematic review of the literature

“…The 6 patients with anti-NMDA encephalitis involved in the study showed regionally limited hypermetabolism in frontotemporal areas contrasting an extensive hypometabolism in parietal lobes, whereas the other group formed of 4 patients with anti-LGI1 encephalitis demonstrated hypermetabolism in cerebellar, basal ganglia, occipital and precentral areas and minor frontomesial hypometabolism (Wegner et al, 2014). In this study, PET imaging abnormalities of the anti-NMDA receptor encephalitis subgroup did not correlate to those detected by MRI in 4/6 patients in the following lesions: hippocampal T2-hyperintensities bilaterally with diffusion elevation, small single unspecific left paraventricular T2-hyperintensity without contrast enhancement or diffusion restriction, multiple very small subcortical T2-hyperintensities with T1-contrast enhancement and faint T2-hyperintensities in both cingular gyri without contrast enhancement.…”

“…In this study, PET imaging abnormalities of the anti-NMDA receptor encephalitis subgroup did not correlate to those detected by MRI in 4/6 patients in the following lesions: hippocampal T2-hyperintensities bilaterally with diffusion elevation, small single unspecific left paraventricular T2-hyperintensity without contrast enhancement or diffusion restriction, multiple very small subcortical T2-hyperintensities with T1-contrast enhancement and faint T2-hyperintensities in both cingular gyri without contrast enhancement. In two patients however MRI did not show any lesions (Wegner et al, 2014).…”

Global brain atrophy and metabolic dysfunction in LGI1 encephalitis: A prospective multimodal MRI study

“…Structural magnetic resonance imaging (MRI) showed extratemporal T2 hyperintensities in the early phase with faciobrachial (dys)tonic seizures (FBDS) and reduced volume of the whole brain one year after FBDS [6][7][8][9][10]. Glucose metabolism is also abnormal in areas outside of the limbic structures [8,[11][12][13]. Although these data point to global structural and metabolic alterations, no study examined metabolic changes several years after LGI1 encephalitis.…”