Epilepsy duration impacts on brain glucose metabolism in temporal lobe epilepsy: results of voxel-based mapping

Abstract

Objective: [(18)F]Fluorodeoxyglucose positron emission tomography ([(18)F]FDG-PET) is a valuable method for detecting focal brain dysfunction associated with epilepsy. Evidence suggests that a progressive decrease in [(18)F]FDG uptake occurs in the epileptogenic cortex with an increase in the duration of epilepsy. In this study, our aim was to use statistical parametric mapping (SPM) to test the validity of this relationship in a retrospective study of patients with temporal lobe epilepsy (TLE).

Methods: [(18)F]FDG-PET scans of 46 adult patients with pharmacoresistant unilateral TLE (25 RTLE and 21 LTLE) were subjected to SPM analysis.

Results: Forty-six patients were diagnosed with nonlesional TLE, 16 of whom had hippocampal sclerosis (HS). The average duration of epilepsy was 17.4 +/- 12.3 years (3-46 years), <5 years in 10 patients and >or=10 years in 30 patients. Visual analysis of [(18)F]FDG-PET scans revealed hypometabolism in the epileptogenic temporal cortex in 31 (67%) patients. After SPM analysis of all [(18)F]FDG-PET images, hypometabolism was unilateral and reported in lateral and mesial structures of the epileptogenic temporal cortex in addition to the ipsilateral fusiform and middle occipital gyrus. Subsequent analysis revealed that temporal lobe hypometabolism was present only in patients with longer epilepsy duration (>or=10 years) in parahippocampal gyrus, uncus, and middle and superior temporal gyrus (P < 0.05 corrected). Epilepsy duration was inversely correlated with decreased glucose uptake in the inferior temporal gyrus, hippocampus, and parahippocampal gyrus of the epileptogenic temporal cortex (P < 0.05). Age at seizure onset did not affect the correlation between epilepsy duration and glucose uptake except in the inferior temporal gyrus (P < 0.05).

Conclusion: Voxel-based mapping supports the assertion that glucose hypometabolism of the epileptogenic temporal lobe cortex and other neighboring cortical regions increases with longer epilepsy duration in TLE.

Fig. 1.

Statistical parametric map of paired t-test results used to examine interhemispheric asymmetry. (A) Glucose hypometabolism (shown in red) is present in the epileptogenic temporal cortex lateralized to the left (original images of LTLE and flipped images of RTLE combined). The number of voxels remained above the threshold, indicating decreased metabolic activity in the epileptogenic temporal cortex (left). (B) The SPM results are superimposed onto the realigned MRI data to demonstrate (left) temporal lobe hypometabolism at the coordinate level of [−36, 0, −40]. (C) The three-dimensional brain illustrates the distribution of glucose hypometabolism.

Fig. 2.

Statistical parametric map of paired t-test results used to examine interhemispheric asymmetry in [¹⁸F]FDG-PET images subgrouped on the basis of epilepsy duration. (A) Glucose hypometabolism (shown in red) is present in the epileptogenic temporal cortex lateralized to the left (original images of LTLE and flipped images of RTLE combined) in longer epilepsy duration (≥10 years). The number of voxels remained above the threshold, indicating decreased metabolic activity in the epileptogenic temporal cortex (lateralized to the left). (B) The SPM results are superimposed onto the realigned MRI data to demonstrate (left) temporal lobe hypometabolism at the coordinate level of [−36, −10, −24]. (C) Glucose hypometabolism was not present with short epilepsy duration (<5 years). The number of voxels remained below the threshold, indicating no evidence of decreased metabolic activity in the epileptogenic temporal cortex (lateralized to the left).

Fig. 3.

Statistical parametric map used to examine the correlation with epilepsy duration independently for MTLE and NTLE subgroups: glucose hypometabolism (shown in red) is seen in the epileptogenic temporal cortex with increasing epilepsy duration in patients with (A) NTLE and (B) MTLE. The number of voxels remained above the threshold, indicating decreased metabolic activity in the epileptogenic temporal cortex. The SPM results are superimposed onto the realigned MRI data to demonstrate temporal lobe hypometabolism.