Purpose <p>The loss of synaptic vesicle glycoprotein 2&#xa0;A (SV2A) can lead to dysfunction of GABAergic neurons, but a direct comparison of SV2A and GABA<sub>A</sub> receptor densities in humans has not been assessed. This study evaluated SV2A and GABA<sub>A</sub> receptor abnormalities in patients with drug-resistant epilepsy (DRE) and compared the patterns to glucose hypometabolism.</p> Methods <p>Eleven patients with DRE were retrospectively recruited and underwent PET imaging with [<sup>18</sup>F]fluorodeoxyglucose ([<sup>18</sup>F]FDG), [<sup>18</sup>F]Flumazenil (FMZ), and [<sup>18</sup>F]SynVesT-1. Visual assessments counted abnormal metabolic brain regions based on the Anatomical Automatic Labeling (AAL) atlas, while voxel-level analyses delineated the abnormal metabolic distributions. The relationship between hypo-metabolic distributions and the age of epilepsy onset was analyzed.</p> Results <p>The hypometabolic regions in [<sup>18</sup>F]FDG PET, identified in the AAL atlas, was significantly broader than in [<sup>18</sup>F]FMZ (<i>p</i> = 0.0005) and [<sup>18</sup>F]SynVesT-1 (<i>p</i> = 0.0010) PET, with no statistical difference observed between [<sup>18</sup>F]FMZ and [<sup>18</sup>F]SynVesT-1 PET (<i>p</i> &gt; 0.05). The voxel number in [<sup>18</sup>F]FDG PET was significantly higher than that of the [<sup>18</sup>F]FMZ and [<sup>18</sup>F]SynVesT-1 PET in both hypo-intensity area and severe hypo-intensity area. The ratio of the voxel number between these two area was higher for [<sup>18</sup>F]SynVesT-1 PET compared to [<sup>18</sup>F]FDG PET (<i>p</i> = 0.0195) and [<sup>18</sup>F]FMZ PET (<i>p</i> = 0.0237), and positively correlated with the age of epilepsy onset (<i>r</i> = 0.7397, <i>p</i> = 0.0145).</p> Conclusions <p>[<sup>18</sup>F]FMZ and [<sup>18</sup>F]SynVesT-1 PET images revealed a more restricted pattern of reduced uptake compared to [<sup>18</sup>F]FDG PET in DRE patients. The age of epilepsy onset correlated with a reduction in [<sup>18</sup>F]SynVesT-1 uptake but not in [<sup>18</sup>F]FMZ or [<sup>18</sup>F]FDG uptake.</p>

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Head-to-Head comparison of [18F]FDG, [18F]FMZ, and [18F]SynVesT-1 positron emission tomography imaging in patients with drug-resistant epilepsy

  • Guanglei Li,
  • Zengping Lin,
  • Weiqi Bao,
  • Shize Jiang,
  • Jie Wang,
  • Qi Huang,
  • Yang Yang,
  • Juanjuan He,
  • Yiyun Huang,
  • Yihui Guan,
  • Jie Hu,
  • Fang Xie

摘要

Purpose

The loss of synaptic vesicle glycoprotein 2 A (SV2A) can lead to dysfunction of GABAergic neurons, but a direct comparison of SV2A and GABAA receptor densities in humans has not been assessed. This study evaluated SV2A and GABAA receptor abnormalities in patients with drug-resistant epilepsy (DRE) and compared the patterns to glucose hypometabolism.

Methods

Eleven patients with DRE were retrospectively recruited and underwent PET imaging with [18F]fluorodeoxyglucose ([18F]FDG), [18F]Flumazenil (FMZ), and [18F]SynVesT-1. Visual assessments counted abnormal metabolic brain regions based on the Anatomical Automatic Labeling (AAL) atlas, while voxel-level analyses delineated the abnormal metabolic distributions. The relationship between hypo-metabolic distributions and the age of epilepsy onset was analyzed.

Results

The hypometabolic regions in [18F]FDG PET, identified in the AAL atlas, was significantly broader than in [18F]FMZ (p = 0.0005) and [18F]SynVesT-1 (p = 0.0010) PET, with no statistical difference observed between [18F]FMZ and [18F]SynVesT-1 PET (p > 0.05). The voxel number in [18F]FDG PET was significantly higher than that of the [18F]FMZ and [18F]SynVesT-1 PET in both hypo-intensity area and severe hypo-intensity area. The ratio of the voxel number between these two area was higher for [18F]SynVesT-1 PET compared to [18F]FDG PET (p = 0.0195) and [18F]FMZ PET (p = 0.0237), and positively correlated with the age of epilepsy onset (r = 0.7397, p = 0.0145).

Conclusions

[18F]FMZ and [18F]SynVesT-1 PET images revealed a more restricted pattern of reduced uptake compared to [18F]FDG PET in DRE patients. The age of epilepsy onset correlated with a reduction in [18F]SynVesT-1 uptake but not in [18F]FMZ or [18F]FDG uptake.