Encephalitis frequently manifests as FDG-PET hypermetabolism, but focal hypometabolism can also be observed. Seizure activity must be excluded as a possible cause of hypermetabolism in patients suspected of having encephalitis. Because other conditions that can cause hypometabolism may mimic encephalitis clinically, FDG-PET is more likely to serve as an adjunct to lumbar puncture, EEG, and clinical findings rather than a primary diagnostic tool in the management of patients suspected of having encephalitis.
Brain FDG-PET was acquired in a consecutive case series of 10 cases of suspected encephalitis over a 5-year-period. Cases with positive Lyme serology were excluded. Two expert reviewers graded the FDG-PET studies in blinded fashion with respect to the clinical history. Retrospective review of the clinical history and examination, laboratory findings, electroencephalogram (EEG), and magnetic resonance imaging (MRI) studies was performed. A diagnosis of encephalitis was based on a combination of the clinical and diagnostic examination findings in each case.
Fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET) may be used to establish a diagnosis of encephalitis, yet prior descriptions are mainly limited to small case reports. We explore the role of FDG-PET in the diagnostic evaluation of encephalitis.
Encephalitis was diagnosed in 6 of 10 cases. FDG-PET hypermetabolism was demonstrated in 5 cases of encephalitis, most frequently involving the medial temporal lobes. Multifocal hypometabolism was noted in at least 2 regions in all 6 cases of encephalitis, with at least 4 regions of hypometabolism noted in 5 of 6 cases. Nonencephalitis cases revealed hypermetabolism in only 1 of 4 cases, ascribed to status epilepticus. Hypometabolism was evident in all nonencephalitis cases.