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Open Access Research article

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

Florian Wegner1*, Florian Wilke2, Peter Raab3, Said Ben Tayeb1, Anna-Lena Boeck1, Cathleen Haense4, Corinna Trebst1, Elke Voss1, Christoph Schrader1, Frank Logemann5, Jörg Ahrens5, Andreas Leffler5, Rea Rodriguez-Raecke1, Reinhard Dengler1, Lilli Geworski2, Frank M Bengel4, Georg Berding4, Martin Stangel1 and Elham Nabavi4

Author Affiliations

1 Department of Neurology, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany

2 Department of Medical Physics, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany

3 Institute of Neuroradiology, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany

4 Department of Nuclear Medicine, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany

5 Department of Anaesthesia and Critical Care Medicine, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany

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BMC Neurology 2014, 14:136  doi:10.1186/1471-2377-14-136

Published: 20 June 2014

Abstract

Background

Pathogenic 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.

Methods

The 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.

Results

Group 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.

Conclusions

This 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.

Keywords:
Anti- leucine rich glioma inactivated 1 protein (LGI1); Anti- N-methyl-D-aspartate (NMDA) receptor antibody; Paraneoplastic syndrome; Autoimmune limbic encephalitis; Brain glucose metabolism; 18F-fluoro-2-deoxy-d-glucose positron emission tomography (FDG-PET)