Neurochemical characteristics of pathological tissues in epilepsy: A preliminary 1H MR spectroscopy study at 7 T

被引:0
|
作者
Xin, Lijing [1 ]
Reymond, Philippe [2 ,3 ]
Boto, Jose [2 ,3 ]
Grouiller, Frederic [3 ,4 ,5 ]
Vulliemoz, Serge [3 ,6 ]
Lazeyras, Francois [3 ,5 ]
Vargas, Maria Isabel [3 ,7 ]
机构
[1] Ecole Polytech Fed Lausanne, Ctr Biomed Imaging, Lausanne, Switzerland
[2] Geneva Univ Hosp, Div Neuroradiol, Geneva, Switzerland
[3] Univ Geneva, Geneva, Switzerland
[4] Univ Geneva, Swiss Ctr Affect Sci, Geneva, Switzerland
[5] Ctr Biomed Imaging Geneva, Geneva, Switzerland
[6] Geneva Univ Hosp, Neurosci Dept, Div Neurol, Geneva, Switzerland
[7] Clin Grangettes Hirslanden, Geneva, Switzerland
基金
瑞士国家科学基金会;
关键词
Epilepsy; MR spectroscopy; Non lesional; Cortical dysplasia; 7; T; FOCAL CORTICAL DYSPLASIA; TEMPORAL-LOBE EPILEPSY; HUMAN BRAIN; GLUTAMATE; MICRODIALYSIS; GABA;
D O I
10.1016/j.ejro.2025.100640
中图分类号
R8 [特种医学]; R445 [影像诊断学];
学科分类号
1002 ; 100207 ; 1009 ;
摘要
Background and purpose: This study aims to evaluate the neurochemical characteristics of pathological tissues by 1H magnetic resonance spectroscopy (MRS) in patient with pharmaco-resistant focal epilepsy at 7 T. Methods: Thirteen patients with drug-resistant epilepsy and focal seizure successfully underwent MRS examinations at 7 T MRI scanners. 1H MR spectra were acquired from two voxels (lesion side and contralateral side) using the semi-adiabatic spin-echo full-intensity localized spectroscopy (sSPECIAL) sequence. Metabolite levels were quantified from LCModel and reported as to total creatine ratio. Results: In comparison to the contralateral side, lesions in focal cortical dysplasia demonstrated significantly reduced macromolecule and N-acetyl aspartate, significantly increased total choline and glycine + myo-inositol, and a distinct reduction trend of glutamate. Conclusions: We conclude that performing MRS at high magnetic field offered the potential to reveal metabolic alterations in epilepsy lesions that may help to further understand the underlying pathophysiology of the disease.
引用
收藏
页数:5
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