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酶法血液去纤维蛋白化在皮质下动脉硬化性脑病中的作用

Effects of enzymatic blood defibrination in subcortical arteriosclerotic encephalopathy.

作者信息

Ringelstein E B, Mauckner A, Schneider R, Sturm W, Doering W, Wolf S, Maurin N, Willmes K, Schlenker M, Brückmann H

机构信息

Department of Neurology, University Hospital of the RWTH Aachen, Federal Republic of Germany.

出版信息

J Neurol Neurosurg Psychiatry. 1988 Aug;51(8):1051-7. doi: 10.1136/jnnp.51.8.1051.

Abstract

Plasma hyperviscosity is a striking abnormality in patients suffering from subcortical arteriosclerotic encephalopathy (SAE) and is thought to perpetuate the chronic ischaemic demyelinating process of the periventricular white matter. Ancrod, a defibrinating enzyme, was given to 10 patients with SAE in an attempt to reduce plasma fibrinogen, which would thus normalise hyperviscosity. This was paralleled by a significant improvement of the initially abnormal retinal arteriovenous passage time, as well as a significant augmentation of the CO2-induced cerebral vasomotor response. This did not lead, however, to any clinical improvement with respect to performance of neuropsychological tests, recurrences of strokes during a 6 month observation period or improvement of various audiological parameters. The findings indicate that hyperviscosity in patients with SAE is merely an epiphenomenon. A potentially reversible, chronic penumbral state of the brain tissue apparently does not exist in SAE.

摘要

血浆高黏滞度是皮质下动脉硬化性脑病(SAE)患者的一个显著异常表现,被认为会使脑室周围白质的慢性缺血性脱髓鞘过程持续存在。对10例SAE患者给予去纤酶Ancrod,试图降低血浆纤维蛋白原,从而使高黏滞度恢复正常。这伴随着最初异常的视网膜动静脉通过时间显著改善,以及二氧化碳诱导的脑血管舒缩反应显著增强。然而,这在神经心理学测试表现、6个月观察期内中风复发情况或各种听力学参数改善方面并未带来任何临床改善。这些发现表明,SAE患者的高黏滞度仅仅是一种附带现象。SAE中显然不存在潜在可逆的脑组织慢性半暗带状态。

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Lacunar strokes and infarcts: a review.腔隙性卒中与梗死:综述
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