Temporoporal metabolic abnormalities in temporal lobe epilepsies

Abstract

Positron emission tomography (PET) may be used to map regional cerebral glucose metabolism using 18 F‐deoxyglucose‐PET in patients with partial epilepsy. An area of reduced glucose metabolism, that is commonly more extensive than the underlying anatomical abnormality, is reported in most of the patients with medically refractory partial epilepsy. These functional changes are useful in the delineation of the epileptogenic focus prior to surgery. Nevertheless, in patients with mesial temporal lobe epilepsy (MTLE) without mass lesion, the hypometabolism involves a large area of the temporal lobe, including the mesial structures, the temporal pole and part of the lateral temporal cortex. In such patients with MTLE, subcortical structures and extratemporal lobe areas are also often hypometabolic. The reasons for this large hypometabolism remain debated. In MTLE patients, the most severe hypometabolism is found in the temporo‐polar region. The clinical significance of this temporo‐polar hypometabolism is unknown. The pathophysiology of interictal hypometabolism probably involves several mechanisms, such as neuronal loss, deafferentation, postictal depression, and others epilepsy‐related phenomena. The relationship between interictal temporo‐polar hypometabolism and seizure onset or seizure spread remain speculative.