Abstract
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Objectives: To find out that hypometabolism in anterior and medial parts of thalamus would point out specific epileptic focus in cerebral cortex, especially in limbic system and frontal regions. Methods: In all brain interictal FDG PET indicated for epilepsy (during January 2016 and October 2017), we observed hypometabolism of thalamus by visual assessment in 45 patients. 5 of the 45 patients had stereoelectroencephalography(SEEG) tests and were included in our study. We further excluded 3 patients due to brain surgery before FDG PET exam. Remaining 2 patients were finally analyzed in our study. Results: Both patients for analysis had hypometabolism in anterior and medial parts of the thalamus. The first patient had hypometabolism in anterior and medial parts of right thalamus (Figure 1). Besides, hypometabolism in right mesial temporal lobe was noted. His SEEG revealed epileptic electroactivity originating from right frontal cortex(Figure 2) and right hippocampus(Figure 3). The second patient had hypometabolism in anterior and medial parts of the left thalamus(Figure 4). Besides, diffuse hypometabolism involving left frontal region, left insula and left temporal regions was noted. His SEEG revealed epileptic electroactivity originating from left frontal polar region. Glucose hypometabolism in cerebral cortex demonstrated by interictal 18F FDG brain PET may help localize epileptic focus1. We sometimes note thalamic hypometabolism in patients with epilepsy. However, it always turns out that the true epileptic focus is from other part of cerebral cortex and not from the thalamus. It ignites the curiosity about the relationship between hypometabolism of thalamus and the true seizure focus(even far from the thalamus) in epilepsy. Hypometabolism2-7 or hypoperfusion8 in the thalamus were especially observed and discussed in temporal lobe epilepsy in previous studies. However, these studies were discussed in the condition of homogenous hypometabolism/hypoperfusion in the whole thalamus. In our experience, we sometimes observe hypometabolism in only part of the thalamus(not whole thalamus). Thalamus is divided into several nuclei and each nucleus is connected to different parts of the cerebrum. To the best of our knowledge, the present study is the first study of discussing the condition of hypometabolism only in "part of thalamus". Anterior part of thalamus mainly consists of the anterior nucleus, which has nerve connection(such as mammillothalamic tract) to limbic system. Medial part of thalamus mainly consists of the medial dorsal nucleus, which has nerve connection to insular and orbitofrontal cortex. Hypometabolism in these parts of thalamus may be a presentation of malfunction, which would be secondary to pathological change from cortical or subcortical structures to which these thalamic nuclei are connected to. In epilepsy patients, we suspect that hypometabolism in anterior nucleus may be secondary change from epilepsy in limbic system and that hypometabolism in medial dorsal nucleus may be secondary change from epilepsy in frontal region. In our case series study, we partially proved this hypothesis by means of SEEG. Neuromodulation (such as vagal nerve stimulation) and brain surgery may affect the glucose metabolism in the thalamus9,10 and we excluded these conditions from our study. Conclusion: In our preliminary observative study, we found hypometabolism in the anterior and medial dorsal nuclei of the thalamus may have more specific correlation with epilepsy from limbic system and frontal region, respectively. It may help guide epilepsy focus in cerebral cortex once noting hypometabolism in different part of the thalamus.