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[脑动脉瘤破裂后发生的尿崩症——特别提及术前病例]

[Diabetes insipidus following the rupture of cerebral aneurysms--with special reference to preoperative cases].

作者信息

Miyasaka Y, Beppu T, Matsumori K, Nakayama K, Asahi S, Takano S

出版信息

No Shinkei Geka. 1984 Mar;12(3 Suppl):369-76.

PMID:6462345
Abstract

The authors reported 4 cases with preoperative diabetes insipidus (DI) following the rupture of cerebral aneurysms. In addition, the incidence of preoperative DI and the mechanisms as the cause of DI in cases with the ruptured cerebral aneurysms were also discussed. In the 114 cases underwent clipping of the ruptured cerebral aneurysms more than 14 days after the bleed, only 4 cases (3.5%) developed DI preoperatively. The time period between last subarachnoid hemorrhage and the onset of DI ranged from 23 to 35 days. This delayed onset of DI after subarachnoid hemorrhage was different from previous reports. A few of mechanisms had been suggested through which DI could be brought about in cases with cerebral aneurysm. That is; direct compression to the hypothalamo-hypophysial system by a giant aneurysm. compression and destruction of the hypothalamus by a hematoma or hemorrhage, ischemic changes in the hypothalamo-hypophysial system caused by vasospasm. In the present 4 cases, no had giant aneurysms. Although CT scan revealed subarachnoid clot in all cases, it did not show apparent hypothalamic lesion except case 1 who had small hematoma in the region of the basal frontal interhemispheric fissure. Symptomatic vasospasm was recognized in 3 cases. However, one of them had mild vasospasm restricting in M1 portion and case 3 was free of any vasospasm. Furthermore, the time period from the identification of vasospasm until the onset of DI ranged from 2 to 3 weeks. These results suggest that another mechanism in addition to a hemorrhage, hematoma and/or vasospasm may exist.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

作者报告了4例脑动脉瘤破裂后术前出现尿崩症(DI)的病例。此外,还讨论了脑动脉瘤破裂病例中术前DI的发生率及其病因机制。在114例出血超过14天后接受脑动脉瘤夹闭术的患者中,只有4例(3.5%)术前出现DI。末次蛛网膜下腔出血至DI发作的时间为23至35天。蛛网膜下腔出血后DI的这种延迟发作与先前的报道不同。有人提出了一些可能导致脑动脉瘤患者发生DI的机制。即:巨大动脉瘤直接压迫下丘脑-垂体系统;血肿或出血对下丘脑的压迫和破坏;血管痉挛引起的下丘脑-垂体系统缺血性改变。在目前的4例病例中,均无巨大动脉瘤。虽然CT扫描在所有病例中均显示蛛网膜下腔有血凝块,但除病例1在额底半球间裂区域有小血肿外,均未显示明显的下丘脑病变。3例出现症状性血管痉挛。然而,其中1例仅有局限于M1段的轻度血管痉挛,病例3未出现任何血管痉挛。此外,从发现血管痉挛到DI发作的时间为2至3周。这些结果表明,除了出血、血肿和/或血管痉挛外,可能还存在其他机制。(摘要截断于250字)

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