Abstracts

RATIONALE: Although previous reports have shown that bioenergetics in the hippocampus in patients with temporal lobe epilepsy (TLE) is significantly impaired, little is known about the energetic state of other structures involved in the propagation of seizures. Recently both animal and human studies have shown that the thalamus may have a significant role in the propagation of seizures in TLE. Although FDG-PET studies have shown decreases in thalamic glucose uptake, it is unclear if this reflects a decrease in activity or damage of the thalamus. Therefore, the goal of this study was to map the energetic changes in the hippocampal formation and thalamus. At the end of this activity the participants should be able to discuss the relationship between energetic impairment in the thalamus and hippocampus in TLE.
METHODS: 31P MRSI were acquired with a 4T Varian MR system in 12 patients with intractable temporal lobe epilepsy and 10 controls using 12cc voxels and an acquisition time of 46min. For anatomical visualization 3D T1 images were acquired with an isotropic resolution of 1.5 mm. For analysis, 23 regions of interest were selected. Bilaterally, the amygdala, head of the hippocampus (pes), body of the hippocampus, anterior and posterior temporal lobe, thalamus, basal ganglia, parietal and frontal white matter were analyzed. Midline volumes were also selected for prefrontal gray matter, anterior, medial and posterior cingulate, and occipital gray matter. The degree of bioenergetic impairment was calculated from the PCr/ATP ratio.
RESULTS: PCr/ATP was reduced to the greatest extent the ipsilateral amygdala, followed by the ipsilateral pes, hippocampus and thalamus with decreasing severity. A similar pattern was seen in the contralateral hemisphere, albeit to a lesser extent. The ipsilateral amygdala and pes were significantly reduced in comparison to controls, while the ipsilateral hippocampal body and thalamus were significantly reduced in comparison to the contralateral volumes (p[lt]0.02 and 0.03, paired two tailed T-tests) but not control values. The pes was also reduced ipsilaterally relative to the contralateral lobe (p[lt]0.05). No significant changes were detected from the other volumes.
CONCLUSIONS: The data demonstrate that bioenergetic impairment in temporal lobe epilepsy extends beyond the hippocampal formation and includes the thalamus. The involvement of the thalamus is consistent with PET data which reported nearly identical frequencies of hypometabolism in the thalamus (63%) and hippocampus (70%) in TLE patients. However, if the decrease in FDG uptake solely reflected decreased neuronal glucose consumption in the absence of damage, no change in bioenergetics would be anticipated. The presence of bioenergetic impairment in the thalamus suggests that the thalamus[ssquote]s ability to meet its energetic needs has been compromised. Since the thalamus may function as a critical propagation point in TLE, the observed energetic impairment in the thalamus may be a contributing factor to the poor seizure control in these patients.
[Supported by: Charles A Dana Foundation and the National Institutes of Health P01-NS39092, R01-NS40550]