Examines metabolic changes in LGI1 encephalitis, suggesting implications for cognitive deficits.
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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Akitomi et al. (2026) studied this question.
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