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椎基底动脉系统短暂性脑缺血发作的发病机制。

Pathogenesis of transient ischemic attacks within the vertebrobasilar arterial system.

作者信息

Naritomi H, Sakai F, Meyer J S

出版信息

Arch Neurol. 1979 Mar;36(3):121-8. doi: 10.1001/archneur.1979.00500390039002.

Abstract

Regional cerebral blood flow (rCBF) was measured by xenon 133 inhalation in 36 patients with vertebrobasilar arterial insufficiency (VBI), three patients with brain stem infarction, and 15 age-matched normal controls before and after inducing postural hypotension. Probes mounted over the suboccipital area by means of a helmet were used to measure rCBF over the brain stem and cerebellar regions. When lying flat, rCBF values measured over both cerebral hemispheres and the brain stem-cerebellar regions in patients with VBI were not significantly different from normal controls. Unlike carotid transient ischemic attacks, regional flow reduction rarely persisted for three weeks after transient ischemic symptoms in patients with VBI. When postural hypotension was induced, rCBF became significantly reduced in patients with VBI whether or not they were treated with papaverine. Dysautoregulation was restricted to vertebral, basilar, and posterior cerebral arterial distribution in patients with VBI of 1 to 12 months' duration, but was more widespread and involved both cerebral hemispheres in long-standing VBI. Hemodynamic factors and dysautoregulation appear to play a part in the pathogenesis of symptoms of VBI.

摘要

对36例椎基底动脉供血不足(VBI)患者、3例脑干梗死患者及15例年龄匹配的正常对照者,在诱发体位性低血压前后,通过吸入氙133测量局部脑血流量(rCBF)。使用通过头盔安装在枕下区域的探头来测量脑干和小脑区域的rCBF。平卧时,VBI患者双侧大脑半球以及脑干 - 小脑区域测得的rCBF值与正常对照者无显著差异。与颈动脉短暂性脑缺血发作不同,VBI患者短暂性缺血症状出现后,局部血流减少很少持续三周。诱发体位性低血压时,无论是否用罂粟碱治疗,VBI患者的rCBF均显著降低。病程为1至12个月的VBI患者,其自主神经调节功能障碍局限于椎动脉、基底动脉及大脑后动脉分布区域,但在病程较长的VBI患者中更为广泛,且累及双侧大脑半球。血流动力学因素和自主神经调节功能障碍似乎在VBI症状的发病机制中起作用。

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