Tomographic cerebral blood flow measurements in patients with ischemic cerebrovascular disease and evaluation of the vasodilatory capacity by the acetazolamide test.

S Vorstrup
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Abstract

Cerebral blood flow (CBF) was measured in a series of patients with ischemic cerebrovascular disease using xenon-133 inhalation and single photon emission computer tomography. The spontaneous course of CBF changes in a consecutive series of stroke patients was evaluated. A quite heterogeneous pattern of flow changes was observed: In patients with large cortical/subcortical infarcts, extensive hypoperfused areas were observed, often significantly larger than the corresponding hypodense lesion on the CT scan. Smaller CT lesions caused relatively smaller flow changes. Patients with lacunar infarcts showed only a discrete reduction of CBF, but comprising most of the ipsilateral hemisphere. Repeated CBF studies in the chronic phase showed, that the clinical improvement commonly noted in stroke patients is not related to a CBF increase. On the contrary, the CBF lesions tended to become somewhat larger and more demarcated even in cases where the finding of a normal angiogram and a transient state of hyperemia suggested a dissolution of the intracerebral embolus. The pathogenetic mechanisms for these persisting low flow areas in CT intact structures was discussed. One possibility was a selective neuronal cell damage in the peri-infarct areas caused by the ischemic insult. Such lesions would leave the structures macroscopically intact, but decrease both the metabolic demands and CBF. However, this interpretation finds little support in recent microscopic neuropathological studies in man. A more likely possibility was then considered to be disconnection (diaschisis) where the reduced flow is due to a decreased neuronal function caused by undercutting of afferent or efferent nervefibers. A crossed cerebellar diaschisis was observed in all patients with major infarcts in the forebrain. These findings were observed already in the acute phase, but persisted quite unchanged throughout the subacute and chronic phases. The patients with lacunar infarcts showed cerebellar diaschisis in the acute phase only, suggesting that a transient suppression of remote areas is possible too. In order to differentiate between permanent flow changes caused by a functional impairment and a possible hemodynamic component, CBF was measured before and after administration of a potent cerebral vasodilator, acetazolamide (Diamox). In normal cases tested with Diamox, an even CBF increase is noted throughout the hemispheres, while the cerebral metabolic rate for oxygen remains stable. In patients having a severe stenosis or occlusion of the internal carotid artery, this vasodilatory stress test will identify the patients having poor collateral capacity via the circle of Willis.(ABSTRACT TRUNCATED AT 400 WORDS)

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缺血性脑血管病患者的断层扫描脑血流测量和乙酰唑胺试验对血管舒张能力的评价。
采用氙-133吸入和单光子发射计算机断层扫描技术测量了一系列缺血性脑血管病患者的脑血流量。对连续系列脑卒中患者的自发性脑血流变化过程进行了评估。血流变化的模式非常不均匀:在皮质/皮质下大面积梗死的患者中,观察到广泛的低灌注区,通常明显大于CT扫描上相应的低密度病变。CT病灶越小,血流变化越小。腔隙性梗死患者仅表现出离散性脑血流减少,但包括大部分同侧半球。在慢性期反复的CBF研究表明,卒中患者通常注意到的临床改善与CBF增加无关。相反,即使在正常血管造影和短暂充血提示脑内栓塞溶解的情况下,CBF病变也往往变得更大,更有界限。讨论了CT完整结构中这些持续低流区的发病机制。一种可能是缺血损伤引起梗死周围区域选择性神经元细胞损伤。这种损伤会使结构在宏观上保持完整,但会降低代谢需求和CBF。然而,这种解释在最近的人类显微神经病理学研究中发现很少支持。一种更可能的可能性被认为是断连(分离),其中流量减少是由于传入或传出神经纤维被切断引起的神经元功能下降。所有前脑梗死患者均出现交叉小脑缺血。这些发现已经在急性期观察到,但在亚急性期和慢性期一直保持不变。腔隙性梗死患者仅在急性期出现小脑缺血,提示局部区域也可能出现短暂性抑制。为了区分功能性损伤引起的永久性血流变化和可能的血流动力学成分,在使用强效脑血管扩张剂乙酰唑胺(Diamox)前后测量CBF。在正常情况下,用Diamox测试,整个半球的CBF均匀增加,而大脑对氧的代谢率保持稳定。对于内颈动脉严重狭窄或闭塞的患者,血管舒张压力测试将通过威利斯环识别侧支能力差的患者。(摘要删节为400字)
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Proceedings of the Annual Meeting of the Norwegian Neurological Association. November 2010. Oslo, Norway. Selected articles from the Annual Meeting of the Norwegian Neurological Association, November 2009, Oslo, Norway. Selected articles from the Annual Meeting of the Norwegian Neurological Association, 26-30 November 2007, Oslo, Norway. Advances in the pathophysiology of status epilepticus. Childhood convulsive status epilepticus: epidemiology, management and outcome.
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