Educational scope notice: This is a study note for medical students, not medical advice, diagnosis, or treatment guidance. Clinical management should follow local protocols and current guidelines.
FDG-PET does not diagnose epilepsy; EEG and history do that. It solves the spatial problem EEG cannot: where the seizure focus sits. Between seizures, the cortex surrounding the onset zone shows reduced glucose metabolism, or hypometabolism. The explanation is inhibitory: the epileptogenic lesion fires continuous pathological activity, and surrounding circuits suppress its spread through inhibition, which consumes less energy, with neuronal loss and reduced synaptic density adding to the deficit. The hypometabolic zone runs wider than the lesion itself but reliably overlaps it, which is why PET lateralizes and roughly localizes even when exact margins stay uncertain.
The uptake protocol
FDG needs 30 to 45 minutes from injection to imaging, and the metabolic state at injection imprints the whole scan. The patient must therefore remain seizure-free throughout uptake, including roughly the 15 minutes before injection, or ictal metabolism contaminates the image into an uninterpretable blend. EEG monitoring during uptake is mandatory to certify the interictal state.
Temporal lobe epilepsy
Temporal lobe epilepsy responds best to surgery, with reported cure rates around 90% for well-selected cases. FDG-PET lateralizes the focus as unilateral temporal hypometabolism, succeeding where serial EEG struggles: the two mesial temporal lobes are densely connected, so discharges appear on one side in one recording and the other in the next. Metabolism has no such mirror effect. Correct lateralization is unforgiving, since only one temporal lobe can ever be removed; resecting both would destroy memory, and operating the wrong side leaves the seizures behind. Conversely, bilateral temporal hypometabolism stops surgery even when EEG favours one side, because the contralateral lobe would keep generating seizures. Preventing that futile operation is among PET’s most valuable contributions.
MRI-negative epilepsy and surgical planning
About one-third of drug-resistant patients have a normal MRI, leaving the surgeon with an EEG suggestion and no visible target. PET can reveal hypometabolism where MRI shows nothing, including a hippocampus without signal change or atrophy, and thereby justify surgery that MRI alone would have foreclosed. When MRI does show a lesion such as mesial temporal sclerosis, PET sizes the abnormality: if hypometabolism spans the whole hippocampus, a standard resection sparing its posterior part will likely leave epileptic tissue behind, and the surgeon must widen the resection. Remote hypometabolism elsewhere in the brain tempers expectations symmetrically, suggesting secondary network damage or diffuse pathology that one resection will not cure.
A high-quality MRI stays indispensable for reading PET: without anatomy, metabolic change cannot be assigned to lesion, normal cortex, or artefact. Simultaneous PET-MRI scanners are costly, and computationally registering a separately acquired PET volume onto high-resolution MRI achieves equivalent colocalization, since the brain holds its shape between scans. The rule is to register the lower-resolution PET onto the higher-resolution MRI and then inspect grey matter systematically.
Outside the temporal lobe, sensitivity falls. The extratemporal cortex is larger and more variable, asymmetries are subtler, and boundaries blur, so analysis grows harder. PET still detects focal hypometabolism that helps, especially coregistered, but expectations should be set lower than in the temporal lobe.
Evidence anchors
- NICE. Epilepsies in children, young people and adults (NG217): https://www.nice.org.uk/guidance/ng217