18F-FDG PET/CT in Anti–Leucine-Rich Glioma-Inactivated 1 Antibody Encephalitis

Caquot, Pierre-Ambroise; Zizi, G.; Lelièvre, Maxime; Dejust, S.; Morland, David

doi:10.1097/rlu.0000000000003469

Cited by 4 publications

(3 citation statements)

References 8 publications

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“…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

FDG-PET-Bildgebung der limbischen Enzephalitis

Buchert¹,

Rauer²,

Meyer³

2023

Radiopraxis

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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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Section: Zerebrale Fdg-petunclassified

FDG-PET-Bildgebung der limbischen Enzephalitis

Buchert¹,

Rauer²,

Meyer³

2023

Radiopraxis

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“…Brain 18 F-FDG-PET imaging reports uncovered abnormal metabolic patterns of anti-VGKC encephalitis, which may be symptom-specific. [14][15][16][17] In the total of 34 patients, basal ganglia hypermetabolism was observed in 28 subjects (82%), and 68% of patients showed medial temporal lobe (MTL) hypermetabolism, the pattern of which appeared earlier than in MRI. It has also been reported that isolated basal ganglia hypermetabolism was more frequently observed in subjects with FBDS (Figures 1 and 2).…”

Section: Anti-voltage-gated Potassium Channel Encephalitismentioning

confidence: 99%

Positron emission tomography in autoimmune encephalitis: Clinical implications and future directions

Liu

et al. 2022

Acta Neuro Scandinavica

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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

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“…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