Ranking of positron emission tomography (PET) in epilepsy diagnostics

Studies using positron emission tomography (PET) have advanced our pathophysiological and biochemical understanding of focal and generalised epilepsies. H(2)(15)O PET allows quantification of cerebral blood flow (rCBF), and (18)F-fluorodeoxyglucose (FDG)-PET quantification of cerebral glucose metabolism. Ictal H(2)(15)O PET studies are difficult because of its short half-life (2 min), ictal (18)F-FDG-PET are difficult to interpret due to its prolonged uptake. H(2)(15)O and 18F-FDG-PET are only indirect markers of neuronal activity. Neurotransmitters are directly responsible for modulating synaptic activity and PET allows quantification of specific ligand-receptor relationships which are important for epileptogenesis and spread of epileptic activity. Clinically important are: (1) (11)C-flumazenil (FMZ), which images GABA(A)-receptors, and (2) (11)C-diprenorphin (DPN), which has similar affinity to mu-, kappa- and delta-opioid receptors. Co-registration of structural information is essential for the exact interpretation of functional PET data. Correction for partial volume effects is important if there are structural pathological changes, e.g. hippocampal sclerosis. Partial volume effects are non-linear and are of particular importance for small structures, leading to under- or even overestimation (spill-over) of true activity. In this review, we first present PET studies in idiopathic generalised epilepsies, followed by a summary of PET studies investigating glucose metabolism, rCBF and neurotransmitter changes in focal epilepsies.