Kuwert T, Hömberg V, Steinmetz H, Unverhau S, Langen K J, Herzog H, Feinendegen L E
Institut für Medizin, Forschungszentrum Jülich, Germany.
J Neurol Sci. 1993 Aug;118(1):10-6. doi: 10.1016/0022-510x(93)90238-t.
Using positron emission tomography (PET), the regional cerebral metabolic rate of glucose consumption (rCMRGlc) was measured in 7 subjects suffering from chronic posthypoxic amnesia and in 12 controls. In 6 of the 7 patients regional decreases in rCMRGlc below normal limits were found involving the thalamus in 3 cases, the medial temporal cortex in 2 cases, and the caudate nucleus and cerebellum in one case each. No significant decrease in rCMRGlc was observed in any of the neocortical regions in any of the patients studied. Significant differences between group means of rCMRGlc were found only for the thalamus and the medial temporal cortex. These data suggest that posthypoxic amnesia stems from damage to the medial temporal cortex and its thalamic projection areas and not from neocortical dysfunction, confirming recent theories on the genesis of amnesia in man.
利用正电子发射断层扫描（PET）技术，对7名患有慢性缺氧后遗忘症的受试者和12名对照者的局部脑葡萄糖代谢率（rCMRGlc）进行了测量。在7名患者中的6名患者中，发现rCMRGlc低于正常范围的局部降低，其中3例累及丘脑，2例累及颞叶内侧皮质，1例分别累及尾状核和小脑。在所研究的任何患者的新皮质区域均未观察到rCMRGlc有显著降低。rCMRGlc的组均值之间仅在丘脑和颞叶内侧皮质存在显著差异。这些数据表明，缺氧后遗忘症源于颞叶内侧皮质及其丘脑投射区域的损伤，而非新皮质功能障碍，这证实了最近关于人类遗忘症发生机制的理论。
