Glucose and [C-11]flumazenil positron emission tomography abnormalities ofthalamic nuclei in temporal lobe epilepsy

Objectives: To analyze interictal patterns of thalamic nuclei glucose metab olism and benzodiazepine receptor binding in patients with medically intrac table temporal lobe epilepsy (TLE) using high-resolution 2-deoxy-2[F-18]flu oro-D-glucose (FDG) and [C-11]flumazenil (FMZ) PET. Background: Structural and glucose metabolic abnormalities of the thalamus are considered importan t in the pathophysiology of TLE. The differential involvement of various th alamic nuclei in humans is not known. Methods: Twelve patients with TLE und erwent volumetric MRI, FDG and FMZ PET, and prolonged video-EEG monitoring. Normalized values and asymmetries of glucose metabolism and FMZ binding we re obtained in three thalamic regions (dorsomedial nucleus [DMN], pulvinar, and lateral thalamus [LAT]) defined on MRI and copied to coregistered, par tial-volume-corrected FDG and FMZ PET images. Hippocampal and amygdaloid FM Z binding asymmetries and thalamic volumes also were measured. Results: The DMN showed significantly lower glucose metabolism and FMZ binding on the s ide of the epileptic focus. The LAT showed bilateral hypermetabolism and in creased FMZ binding. There was a significant correlation between the FMZ bi nding asymmetries of the DMN and amygdala. The PET abnormalities were assoc iated with a significant volume loss of the thalamus ipsilateral to the sei zure focus. Conclusions: Decreased [C-11]flumazenil (FMZ) binding and gluco se metabolism of the dorsomedial nucleus (DMN) are common and have strong l ateralization Value for the seizure focus in human temporal lobe epilepsy. Decreased benzodiazepine receptor binding can be due to neuronal loss, as s uggested by volume loss, but also may indicate impaired gamma-aminobutyric acid (GABA)ergic transmission in the DMN, which has strong reciprocal conne ctions with other parts of the limbic system. Increased glucose metabolism and FMZ binding in the lateral thalamus could represent an upregulation of GABA-mediated inhibitory circuits.