Evolution of temporal lobe hypoperfusion in transient global amnesia: a serial single photon emission computed tomography study

Evolution of temporal lobe hypoperfusion in transient global amnesia: a serial single photon emission computed tomography study
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DOI:
10.1111/jon2000104238
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发表时间:
2000-10-01
影响因子:
2.4
通讯作者:
McCluskey, LF
McCluskey, LF
中科院分区:
医学4区
文献类型:
--
作者:
Jovin, TG;Vitti, RA;McCluskey, LF

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以前的功能性神经影像学研究在短暂性全面遗忘症(TGA)没有回答的核心问题,关于TGA的病因,即:是否观察到的灌注不足的内侧颞叶结构反映了一个主要的缺血性过程,或者它是否代表一个继发性的现象,从局部代谢减少。作者在TGA发作期间、发作后24小时和发作后3个月对一名66岁男性进行了Te 99-m-bicisate脑单光子发射计算机断层扫描(SPECT)。据作者所知,这是唯一一项在24小时内进行随访SPECT扫描的报告研究。初步研究显示双侧内侧颞长袍灌注不足,24小时后部分消退,3个月时恢复正常。SPECT扫描异常的分辨率与记忆丧失的分辨率相关。这些研究结果与以前报道的SPECT,正电子发射断层扫描(PET),和扩散磁共振成像(MRI)的研究表明,内侧颞叶结构的主要部位的病理在TGA同意。作者认为,在这种情况下,导致局部代谢减少的过程,如皮质扩散性抑制,构成了主要的病理生理机制。
Previous functional neuroimaging studies performed during transient global amnesia (TGA) have not answered the central question regarding the etiology of TGA, namely: whether the observed hypoperfusion in the mesial temporal lobe structures reflects a primarily ischemic process or whether it represents a secondary phenomenon resulting from locally decreased metabolism. The authors performed Te 99-m-bicisate brain single photon-emission computed tomography (SPECT) scanning in a 66-year-old man during an episode of TGA, 24 hours after the episode and 3 months after the episode. To the authors' knowledge, this is the only reported study in which a follow-up SPECT scan was performed within 24 hours. The initial study showed bilateral mesial temporal robe hy poperfusion that partially resolved after 24 hours and returned to normal at 3 months. Resolution of the SPECT scan abnormalities correlated well with resolution of the memory loss. These findings agree with previously reported SPECT, positron-emission tomography (PET), and diffusion magnetic resonance imaging (MRI) studies that indicate the mesial temporal lobe structures as the major site of pathology in TGA. The authors suggest that a process causing-decreased local metabolism, such as cortical spreading depression, constitutes the primary pathophysiologic mechanism in this case.