Lewis S L
Department of Neurological Sciences, Rush-Presbyterian-St Luke's Medical Center, Chicago, IL 60612, USA.
Lancet. 1998 Aug 1;352(9125):397-9. doi: 10.1016/S0140-6736(98)01442-1.
The pathophysiology of transient global amnesia (TGA) has been obscure since the definition of this syndrome more than 30 years ago. Current hypotheses include migraine, seizure, or transient cerebral arterial ischaemia. However, none of these potential mechanisms explain both the absence of other neurological signs or symptoms during TGA, and its frequent precipitating activities: many of which would be expected to result in marked increases in venous return from the arms to the superior vena cava. Patients with TGA also commonly have a Valsalva manoeuvre at the onset of attacks. I suggest that a Valsalva manoeuvre, blocking venous return through the superior vena cava, may allow brief retrograde transmission of high venous pressure from the arms to the cerebral venous system, resulting in venous ischaemia to the diencephalon or mesial temporal lobes and to TGA.
自30多年前短暂性全面性遗忘症（TGA）这一综合征被定义以来，其病理生理学一直不明。目前的假说包括偏头痛、癫痫或短暂性脑动脉缺血。然而，这些潜在机制均无法解释TGA发作时为何没有其他神经体征或症状，以及其频繁的诱发活动：其中许多活动预计会导致从手臂到上腔静脉的静脉回流显著增加。TGA患者在发作开始时也通常会进行瓦尔萨尔瓦动作。我认为，瓦尔萨尔瓦动作通过阻断上腔静脉的静脉回流，可能会使手臂的高静脉压短暂逆行传递至脑静脉系统，导致间脑或颞叶内侧静脉缺血，进而引发TGA。
