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Persistent Bilateral [18F]THK5351 and Migrating Unilateral [18F]FDG Uptake in Anti-LGI1 Encephalitis
Yusuke Akitomi1, Kenichiro Taira1, Masanori Kurihara1,2
1Department of Neurology, Tokyo Metropolitan Institute for Geriatrics and Gerontology, Tokyo, Japan.
Abstract:
Anti-leucine-rich glioma-inactivated 1 encephalitis (LGI1-E) can cause persistent cognitive deficits, but the mechanisms remain unclear. A 40-year-old woman with LGI1-E presented with subacute cognitive deficits and showed mild left medial temporal lobe (MTL) swelling and fluid-attenuated inversion recovery (FLAIR) hyperintensity on initial magnetic resonance imaging (MRI). Fluorine-18 fluorodeoxyglucose positron emission tomography/computed tomography ([18F]FDG PET/CT) demonstrated left MTL hypermetabolism, whereas [18F]THK5351 PET/CT revealed bilateral MTL uptake. Although immunotherapy improved her symptoms, mild cognitive deficits persisted. FLAIR hyperintensity resolved, but [18F]FDG PET/CT demonstrated transient right MTL hypermetabolism during relapse, whereas [18F]THK5351 PET/CT showed partial decline over time, although relatively increased right-sided uptake persisted throughout follow-up. These findings highlight a dissociation between episodic metabolic changes on [18F]FDG PET/CT and more persistent medial temporal MAO-B-related uptake on [18F]THK5351 PET/CT, which may be associated with residual cognitive deficits.
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