De Reuck J, Vanwalleghem I, Hemelsoet D, De Weweire M, Strijckmans K, Lemahieu I
Department of Neurology, Ghent University Hospital, Ghent, Belgium.
Eur Neurol. 2003;49(3):131-6. doi: 10.1159/000069075.
Despite extensive research, it still remains controversial as to what the precise location of the critical lesions underlying amnesia actually is. The amnesic syndrome is believed to be heterogeneous and due to several distinct functional deficits.
Two patients, a 45-year-old woman and a 56-year-old man, with sudden cardiopulmonary arrest and successful resuscitation, were left with a clear amnesic syndrome as main neurological sequela. During their revalidation period, they underwent a positron emission tomographic (PET) examination, utilizing the (13)NH(3) bolus technique at rest and after intravenous acetazolamide administration.
Both PET studies showed more or less similar features with a decrease in regional cerebral blood flow (rCBF) in the frontal, temporal and parietal lobes. In addition, the rCBF was increased in both thalami of the 45-year-old woman and in the striata of the 56-year-old man. Acetazolamide vasoreactivity was most lost in the frontal lobes.
In the present PET study, we demonstrated that destruction of the inhibitory pathways to the thalamus and basal ganglia by ischaemic-hypoxic frontal lesions could be one of the mechanisms leading to amnesia.
尽管进行了广泛研究，但失忆症关键病变的确切位置仍存在争议。失忆综合征被认为具有异质性，是由几种不同的功能缺陷引起的。
两名患者，一名45岁女性和一名56岁男性，经历了心脏骤停并成功复苏，之后遗留明显的失忆综合征作为主要神经后遗症。在康复期，他们接受了正电子发射断层扫描（PET）检查，在静息状态和静脉注射乙酰唑胺后采用（13）NH（3）团注技术。
两项PET研究均显示出大致相似的特征，额叶、颞叶和顶叶的局部脑血流量（rCBF）减少。此外，45岁女性的双侧丘脑和56岁男性的纹状体中的rCBF增加。乙酰唑胺血管反应性在额叶中丧失最为明显。
在本PET研究中，我们证明缺血缺氧性额叶病变对丘脑和基底神经节的抑制通路破坏可能是导致失忆的机制之一。
