Choice of anesthesia and data analysis method strongly increases sensitivity of 18F-FDG PET imaging during experimental epileptogenesis.

Purpose: Alterations in brain glucose metabolism detected by 2-deoxy-2-[18F]-fluoro-D-glucose (18F-FDG) positron emission tomography (PET) may serve as an early predictive biomarker and treatment target for epileptogenesis. Here, we aimed to investigate changes in cerebral glucose metabolism before induction of epileptogenesis, during epileptogenesis as well as during chronic epilepsy. As anesthesia is usually unavoidable for preclinical PET imaging and influences the distribution of the radiotracer, four different protocols were compared.

Tc-HMPAO SPECT imaging reveals brain hypoperfusion during status epilepticus.

Status epilepticus (SE) is a clinical emergency with high mortality. SE can trigger neuronal death or injury and alteration of neuronal networks resulting in long-term cognitive decline or epilepsy. Among the multiple factors contributing to this damage, imbalance between oxygen and glucose requirements and brain perfusion during SE has been proposed.

Ex vivo characterization of neuroinflammatory and neuroreceptor changes during epileptogenesis using candidate positron emission tomography biomarkers.

Objective: Identification of patients at risk of developing epilepsy before the first spontaneous seizure may promote the development of preventive treatment providing opportunity to stop or slow down the disease.

Methods: As development of novel radiotracers and on-site setup of existing radiotracers is highly time-consuming and expensive, we used dual-centre in vitro autoradiography as an approach to characterize the potential of innovative radiotracers in the context of epilepsy development. Using brain slices from the same group of rats, we aimed to characterise the evolution of neuroinflammation and expression of inhibitory and excitatory neuroreceptors during epileptogenesis using translational positron emission tomography (PET) tracers; F-flumazenil ( F-FMZ; GABA receptor), F-FPEB (metabotropic glutamate receptor 5; mGluR5), F-flutriciclamide (translocator protein; TSPO, microglia activation) and F-deprenyl (monoamine oxidase B, astroglia activation).

Divergent metabolic substrate utilization in brain during epileptogenesis precedes chronic hypometabolism.

Alterations in metabolism during epileptogenesis may be a therapy target. Recently, an increase in amino acid transport into the brain was proposed to play a role in epileptogenesis. We aimed to characterize alterations of substrate utilization during epileptogenesis and in chronic epilepsy.