Thalamic Metabolic Abnormalities in Children with Epilepsy
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Overview
abstract
Introduction: Hypometabolism of the thalamus has been reported in epilepsy patients detected by 18F-FDG PET imaging. This retrospective study aimed to investigate the thalamic metabolic activity qualitatively and semi-quantitatively in pediatric patients with epilepsy with respect to the control group.
Methods: A total of 57 children with epilepsy (24 boys and 33 girls with a mean age of 9 years) and 50 children without epilepsy (control group) (29 boys and 21 girls with a mean age of 10.5 years) underwent interictal 18F-FDG PET/CT in this retrospective study. Localization of the hypometabolic epileptic focus was performed visually. Bilateral thalamic metabolic activity was evaluated qualitatively (Thalamic FDG uptake in relation to the cerebral cortex) and semi-quantitatively (SUV max, normalized SUV (ratio to ipsilateral cerebellum) and absolute asymmetric index (AAI), 100 x [right - left]/ [1/2 x (right + left)]). Comparisons were made between thalamus metabolic activity and asymmetry in patients with epilepsy and the control group.
Results: 26 patients with epilepsy demonstrated cerebral cortical hypometabolism in the interictal 18F-FDG PET study; 15 patients on the right side, ten patients on the left side, and one on both sides. Of these 26 patients, seven had visually observed asymmetric hypometabolism in the ipsilateral thalamus. Semi-quantitively, asymmetry was more prominent in the epileptic patients using the AAI than in the control group. Average AAIs were 3.4% and 5.7% in the controls and epilepsy patients, respectively. Metabolic activity in thalami was significantly reduced (p-value: 0.001) in epileptic patients than in the control group, with average SUV max of 7.8 and 10.2, respectively. Associated hypometabolism of the ipsilateral thalamus was observed in 77% of epileptic patients with a focal cortical defect semi-quantitively. Focal defects in the frontal lobe cortex showed less correlation with hypometabolism in the ipsilateral thalamus (3 out of 11 patients, 27%), and focal defects in the temporal lobe cortex showed the most correlation with hypometabolism in the ipsilateral thalamus (7 out of 8 patients, 87.5%). Epileptic patients with large focal defects, more severe and intractable disease, and temporal lobe defects demonstrated more severe thalamic hypometabolism quantitatively.
Conclusions: The study suggests associated ipsilateral thalamic hypometabolism may be a supplemental finding on the interictal brain 18F-FDG-PET studies in epileptic patients. Patients with a large focal cerebral cortical defect, temporal lobe defect, or severe medically refractory seizures are more likely to have more severe ipsilateral thalamus hypometabolism. Further investigation with a larger sample size is suggested to investigate if associated thalamic hypometabolism has a prognostic value and can predict response to therapy in patients with intractable epilepsy who are candidates for surgery.
