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 Wegner, Florian Wilke, Peter Raab, Said B. Tayeb, Anna Lena Boeck, Cathleen Haense, Corinna Trebst, Elke Voss, Christoph Schrader, Frank Logemann, Jörg Ahrens, Andreas Leffler, Rea Rodriguez-Raecke, Reinhard Dengler, Lilli Geworski, Frank M. Bengel, Georg Berding, Martin Stangel, Elham Nabavi

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Article number136
JournalBMC neurology
Volume14
Issue number1
DOIs
StatePublished - Jun 20 2014

    Fingerprint

Keywords

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

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

Wegner, F., Wilke, F., Raab, P., Tayeb, S. B., Boeck, A. L., Haense, C., Trebst, C., Voss, E., Schrader, C., Logemann, F., Ahrens, J., Leffler, A., Rodriguez-Raecke, R., Dengler, R., Geworski, L., Bengel, F. M., Berding, G., Stangel, M., & Nabavi, E. (2014). 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. BMC neurology, 14(1), [136]. https://doi.org/10.1186/1471-2377-14-136