Abstract
Objective
This study evaluates the diagnostic performance and prognostic value of brain 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) at the initial diagnosis of patients with nonlesional late onset epilepsy (NLLOE).
Methods
In this cohort study at the University Hospital of Nancy, France, newly diagnosed NLLOE patients, >50 years old, were consecutively included from June 2017 to January 2021 and systematically underwent brain 18F-FDG PET. They were categorized into four presumed etiological NLLOE subtypes: neurodegenerative subtype (NDS; patients with a diagnosis of neurodegenerative disease), microvascular subtype (MVS; patients with ≥3 cardiovascular risk factors and ≥2 vascular lesions on magnetic resonance imaging), inflammatory subtype (IFS; patients meeting international criteria for encephalitis), and unlabeled subtype (ULS). A systematic patient follow-up (at least 2 years) allowed assessment of cognitive outcomes under antiseizure medication by comparing for each patient the proportion of preserved/altered scores between initial and second neuropsychological assessment. Brain 18F-FDG PET was analyzed using a combined visual and semiquantitative approach at the individual level.
Results
Eighty-seven patients were included (NDS, n = 18; MVS, n = 22; IFS, n = 7; ULS, n = 40). A normal 18F-FDG PET was observed in 46% of patients, with the final diagnosis of 88% of these patients excluding a neurodegenerative or inflammatory disorder. 18F-FDG PET had a negative predictive value of 94% for a cognitive decline at follow-up, similar for the overall population (n = 71) and the ULS population (n = 32). Moreover, a PET hypometabolic pattern suggestive of a neurodegenerative disorder was indicative of cognitive decline at follow-up in 74% of cases.
Significance
18F-FDG PET as part of the initial diagnosis of NLLOE patients may have a significant impact on both NLLOE diagnosis and cognitive prognosis. For almost half of NLLOE patients, a normal 18F-FDG PET could help to exclude neurodegenerative and inflammatory epilepsy etiologies as well as future cognitive decline.
MAR