Abstract:Aims
To identify the metabolic pattern and prognostic predictors in anti‐gamma‐aminobutyric‐acid B (GABAB) receptor encephalitis using 18F‐fluorodeoxy‐glucose positron emission tomography (18F‐FDG‐PET).
Methods
Twenty‐one patients diagnosed anti‐GABAB receptor encephalitis who underwent 18F‐FDG‐PET at first hospitalization were retrospectively reviewed. 18F‐FDG‐PET images were analyzed in comparison with controls. Further group comparisons of 18F‐FDG‐PET data were carried out between prognostic subgroups.
Resu… Show more
“…Patients with increased metabolism in the MTL tend to have poor outcomes after a median follow-up of 33 months. 31 In a study of five patients with anti-GABA B receptor encephalitis, three patients showed abnormalities on PET, including two temporal hypermetabolism and one cortical hypometabolism. 32 Another patient with small cell lung cancer who presented with 3 weeks of progressive seizures, memory impairment, and behavioral disorder was diagnosed with anti-GABA B receptor encephalitis.…”
“…Group analysis also confirmed MTL hypermetabolism and frontal–parietal hypometabolism (Figure 3). Patients with increased metabolism in the MTL tend to have poor outcomes after a median follow‐up of 33 months 31 . In a study of five patients with anti‐GABA B receptor encephalitis, three patients showed abnormalities on PET, including two temporal hypermetabolism and one cortical hypometabolism 32 .…”
Section: Visual Assessment Of Brain 18f‐fdg‐pet Metabolic Patterns By...mentioning
Autoimmune encephalitis is an immune-mediated inflammatory disease of the central nervous system caused by abnormal immune response against surface or intracellular antigens. 1 In addition to the previously discovered classical paraneoplastic encephalitisassociated antibodies, a variety of autoimmune encephalitis-related antibodies have been reported in recent years, including antibodies targeting N-methyld-aspartate receptor (NMDAR), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR), leucine-rich glioma inactivated 1 (LGI1), contactin-associated proteinlike 2 (CASPR2), gamma-aminobutyric acid receptor (GABAR) A/B, dipeptidyl-peptidase-like protein-6 (DPPX), glycine receptor (GlyR), glutamic acid decarboxylase 65 (GAD65), dipeptidyl-peptidase-like protein-6 (DPPX), IgLON5 et al. 2 The clinical manifestations, severity, and prognosis with specific antibodies are different, but in general, early detection and early treatment are the principles to handle this disease. However, it has to be admitted that there are still difficulties in the early diagnosis of autoimmune encephalitis, although we have made improvements and revision in the diagnostic criteria based on the clinical criteria defined by Graus et al. 3 in 2016 to avoid excessive reliance on the detection of autoimmune antibodies from serum or cerebrospinal fluid (CSF). The problems focus on the heterogeneity of clinical manifestations, low positive rate of imaging evidence, and lack of specificity of EEG. For example, autoimmune encephalitis may involve
“…Patients with increased metabolism in the MTL tend to have poor outcomes after a median follow-up of 33 months. 31 In a study of five patients with anti-GABA B receptor encephalitis, three patients showed abnormalities on PET, including two temporal hypermetabolism and one cortical hypometabolism. 32 Another patient with small cell lung cancer who presented with 3 weeks of progressive seizures, memory impairment, and behavioral disorder was diagnosed with anti-GABA B receptor encephalitis.…”
“…Group analysis also confirmed MTL hypermetabolism and frontal–parietal hypometabolism (Figure 3). Patients with increased metabolism in the MTL tend to have poor outcomes after a median follow‐up of 33 months 31 . In a study of five patients with anti‐GABA B receptor encephalitis, three patients showed abnormalities on PET, including two temporal hypermetabolism and one cortical hypometabolism 32 .…”
Section: Visual Assessment Of Brain 18f‐fdg‐pet Metabolic Patterns By...mentioning
Autoimmune encephalitis is an immune-mediated inflammatory disease of the central nervous system caused by abnormal immune response against surface or intracellular antigens. 1 In addition to the previously discovered classical paraneoplastic encephalitisassociated antibodies, a variety of autoimmune encephalitis-related antibodies have been reported in recent years, including antibodies targeting N-methyld-aspartate receptor (NMDAR), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR), leucine-rich glioma inactivated 1 (LGI1), contactin-associated proteinlike 2 (CASPR2), gamma-aminobutyric acid receptor (GABAR) A/B, dipeptidyl-peptidase-like protein-6 (DPPX), glycine receptor (GlyR), glutamic acid decarboxylase 65 (GAD65), dipeptidyl-peptidase-like protein-6 (DPPX), IgLON5 et al. 2 The clinical manifestations, severity, and prognosis with specific antibodies are different, but in general, early detection and early treatment are the principles to handle this disease. However, it has to be admitted that there are still difficulties in the early diagnosis of autoimmune encephalitis, although we have made improvements and revision in the diagnostic criteria based on the clinical criteria defined by Graus et al. 3 in 2016 to avoid excessive reliance on the detection of autoimmune antibodies from serum or cerebrospinal fluid (CSF). The problems focus on the heterogeneity of clinical manifestations, low positive rate of imaging evidence, and lack of specificity of EEG. For example, autoimmune encephalitis may involve
“…Die zerebrale MRT mit T1-, T2, FLAIR-und diffusionsgewichteten Sequenzen ist Teil der Basisdiagnostik bei Verdacht auf eine LE [16,20,38], wobei nur die FLAIR-Sequenz Bestandteil der o. g. diagnostischen Kriterien ist [16]. Initial zeigen etwa 50-75% der Patienten mit limbischer Enzephalitis eine unilaterale oder bilaterale Hyperintensität in der T2/FLAIR-MRT [13,41,46,47], meist ohne Kontrastmittelaufnahme. Mittels Volumetrie des Hippocampus und hippocampler Subfelder sowie voxelbasierter Volumetrie der grauen Substanz anhand T1w-MRT konnten auch strukturelle Veränderungen (Atrophie) nachgewiesen werden, die möglicherweise als Hinweise für das Auftreten und Fortschreiten eines Neuronenverlustes dienen können [41].…”
Section: Zerebrale Mrtunclassified
“…2, Abb. 3) [47,48,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80]. Dabei kann sowohl ein Hyper-, seltener auch ein Hypometabolismus mesiotemporal auftreten [76,77,81].…”
Section: Zerebrale Fdg-petunclassified
“…Insbesondere für den Nachweis extratemporaler Befunde wird der Einsatz voxelbasierter statistischer Verfahren zusätzlich zur rein visuellen Beurteilung der FDG-▶ Abb. 5 Typischer Befund in der zerebralen FDG-PET bei Anti-NMDA-Rezeptor-Enzephalitis PR A XIS Tipp Durch den Nachweis einer extratemporalen Beteiligung bei der limbischen Enzephalitis liefert die FDG-PET bei etwa 50% der Patienten eine Zusatzinformation über die strukturelle MRT hinaus [47,75,78,81,88].…”
Bei der limbischen Enzephalitis liefert die zerebrale FDG-PET essenzielle Informationen zur Unterstützung von Diagnose, Prognose und Therapiekontrolle. Mit zunehmender Bedeutung der limbischen Enzephalitis als „not to miss“-Diagnose wird der Stellenwert der zerebralen FDG-PET bei dieser Fragestellung weiter steigen. Zudem kommt der FDG-PET-Ganzkörperaufnahme bei Verdacht auf eine paraneoplastische Genese und unauffälligem Tumorscreening in den Routineuntersuchungen eine Schlüsselrolle zu.
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