Solheim Ole, Skeidsvoll Tora
Department of Neurosurgery, University Hospital of Trondheim, St. Olavs Hospital, Olav Kyrres gt 17, N-7005 Trondheim, Norway.
Med Hypotheses. 2005;65(6):1142-9. doi: 10.1016/j.mehy.2005.05.042. Epub 2005 Aug 2.
Transient global amnesia (TGA) is a disorder of unknown aetiology, characterized by sudden loss of anterograde memory, in the absence other neurological signs or symptoms, followed by complete recovery in less than 24h. Precipitating actions such as strenuous physical activity or valsalva-like manoeuvres are frequently reported. Since first described in 1958, by Fisher and Adams, the possible pathophysiology has undergone much speculation. Nonconvulsive epileptic seizures, migraine, paradoxical embolism thorough a patent foramen ovale, and transient ischemic attacks have been proposed as potential mechanisms. One of the latest hypotheses is that venous congestion causes either ischemia or induces spreading depression in the medial temporal lobes. It has been demonstrated that retrograde flow in the internal jugular veins occurs more frequently during valsalva manoeuvres in TGA patients than in controls, supporting a dysfunctional venous circulation as part of the pathogenesis. However, earlier hypotheses typically fail to explain the relatively low recurrence rate of TGA, lack of comorbidity and the relation to precipitating events. If cerebral venous hypertension was the solely cause of TGA it would presumably be much more common with very high recurrence rates among those predisposed of the condition. Structural changes observed in MRI and SPECT studies along with reports of mild cognitive impairment lasting much longer than the amnestic episodes, indicate that TGA is less transient and perhaps somewhat less benign than earlier believed. Many cases of TGA seem to be associated with factors of increased risk of cerebral venous thrombosis, such as polycythemia, antiphospholipid antibodies, venous hypertension, female sex and more. We suggest that most cases of TGA may be due to small thrombi in the deep cerebral venous system. Small venous thrombi may difficult to visualize even when using modern imaging technology. Further studies of TGA patients with for example blood analysis of D-dimer together with MR venography or CT venography could be done to evaluate this new hypothesis.
短暂性全面性遗忘症（TGA）是一种病因不明的疾病，其特征为突然出现顺行性记忆丧失，且无其他神经系统体征或症状，随后在24小时内完全恢复。经常有报告称剧烈体育活动或类似瓦尔萨尔瓦动作等诱发因素。自1958年费希尔和亚当斯首次描述以来，其可能的病理生理学一直备受猜测。非惊厥性癫痫发作、偏头痛、通过卵圆孔未闭的反常栓塞以及短暂性脑缺血发作都被认为是潜在机制。最新的假说之一是静脉淤血导致内侧颞叶局部缺血或引发扩散性抑制。已有研究表明，与对照组相比，TGA患者在瓦尔萨尔瓦动作期间颈内静脉逆行血流更为频繁，这支持了静脉循环功能障碍是发病机制的一部分。然而，早期的假说通常无法解释TGA相对较低的复发率、缺乏合并症以及与诱发事件的关系。如果脑静脉高压是TGA的唯一病因，那么它可能会更常见，并且在易感人群中复发率会非常高。MRI和SPECT研究中观察到的结构变化以及轻度认知障碍持续时间远长于遗忘发作的报告表明，TGA并非像早期认为的那样短暂，也许也并非那么良性。许多TGA病例似乎与脑静脉血栓形成风险增加的因素有关，如红细胞增多症、抗磷脂抗体、静脉高压、女性等。我们认为大多数TGA病例可能是由于大脑深静脉系统中的小血栓所致。即使使用现代成像技术，小静脉血栓也可能难以显现。可以对TGA患者进行进一步研究，例如检测D - 二聚体的血液分析以及磁共振静脉造影或CT静脉造影，以评估这一新假说。
