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目的采用静息功能磁共振成像低频振幅技术,通过观察双侧海马硬化(HS)颞叶癫痫(TLE)患者脑血氧水平依赖(BOLD)信号活动的改变,探讨TLE脑活动的神经机制。资料与方法采用低频振幅算法,对9例双侧HS的TLE患者及9名正常志愿者静息功能磁共振成像数据进行对比分析,观察TLE患者发作间期痫样放电时(IED)振荡幅度增高及降低的区域。结果TLE患者伴发IED时BOLD信号振荡幅度改变的区域基本呈双侧对称分布。振幅增加的区域包括:双侧海马、杏仁核、扣带回等边缘系统,双侧中央运动区、颞叶皮层,丘脑及中脑结构。振荡幅度降低的区域包括:扣带回前部(ACC)、内侧前额叶(MPFC)及顶下小叶(IPC)等经典缺省模式区域,而后扣带回(PCC)和楔前叶(Pcu)则未包含其中。结论低频振幅功能磁共振成像技术可以对癫痫引起脑的活动改变情况进行观察。振幅增高的脑区反映大脑对癫痫活动的产生、传播等易化作用,振幅降低区域反映了特定脑区功能的抑制,尤其是缺省模式功能的受抑制。这些改变反映了大脑易化与抑制两个系统对癫痫的脑功能进行调节。
Objective To investigate the neurological mechanism of brain activity in TLE by observing the changes of cerebral blood oxygenation (BOLD) signal activity in patients with bilateral temporal hippocampal (TM) temporal lobe epilepsy (TLE) by using the low frequency amplitude technique of resting functional magnetic resonance imaging. Materials and Methods The low frequency amplitude algorithm was used to compare the resting magnetic resonance imaging data of 9 TLE patients with bilateral HS and 9 normal volunteers to observe the increase of IED oscillation amplitude in interictal TLE patients And reduced area. Results The area of BOLD signal oscillation amplitude in patients with TLE was basically bilateral symmetrical distribution. Areas of increased amplitude include: bilateral hippocampus, amygdala, cingulate gyrus and other border systems, bilateral central motor area, temporal cortex, thalamic and midbrain structures. The areas of reduced amplitude of oscillation include classical default mode regions such as the anterior cingulate (ACC), medial prefrontal cortex (MPFC) and inferior parietal (IPC), while the posterior cingulate gyrus (PCC) It is not included. Conclusions Low-frequency amplitude functional magnetic resonance imaging can observe changes of brain activity induced by epilepsy. The brain regions with increased amplitude reflect the facilitation of the epilepsy activity and transmission in the brain. The region with reduced amplitude reflects the inhibition of the function of specific brain regions, especially the suppression of the default mode function. These changes reflect the brain’s ability to regulate epilepsy in both systems of facilitation and suppression of the brain.