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We report the case of a 55-year-old man presenting pseudopsychiatric behavior disorders of subacute-onset. MRI showed a FLAIR (fluid-attenuated inversion recovery) hyperintensity in the left hippocampus. The diagnosis of limbic encephalitis was raised, and the patient was referred for an 18F-FDG PET/CT. PET/CT depicted an increased uptake of the left mesiotemporal structures and also an increased uptake of both cerebellum and striatal areas. This pattern was compatible with an anti–leucine-rich glioma-inactivated 1 antibody encephalitis that was later confirmed.

We report the case of a 64-year-old man referred for optic ataxia, constructional apraxia, and spatial orientation disorders evolving for 2 months. Benson syndrome (posterior cortical atrophy) was initially suspected. Brain 18F-FDG PET/CT depicted an asymmetric decreased uptake pattern consistent with Creutzfeldt-Jakob disease. 14-3-3 proteins were detected in the cerebrospinal fluid. Clinical evolution was quickly unfavorable. The patient died 1 month after the PET/CT, and Creutzfeldt-Jakob disease was confirmed on postmortem examination of brain tissue.

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