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脑干梗死与交叉性小脑神经机能联系失联络。一项单光子发射计算机断层扫描脑灌注研究。

Brain stem infarction and diaschisis. A SPECT cerebral perfusion study.

作者信息

Fazekas F, Payer F, Valetitsch H, Schmidt R, Flooh E

机构信息

Department of Neurology, Karl-Franzens University, Graz, Austria.

出版信息

Stroke. 1993 Aug;24(8):1162-6. doi: 10.1161/01.str.24.8.1162.

Abstract

BACKGROUND AND PURPOSE

We studied six patients suffering from pure, unilateral brain stem infarction to explore the association of remote cerebral and cerebellar blood flow changes with damage at different sites of this region of the brain.

METHODS

We used single-photon emission computed tomography and [123I]iodoamphetamine to measure regional differences in tracer uptake. Qualitative image analysis and calculated asymmetry indexes were correlated to the location of the infarcted area on magnetic resonance imaging and to the patients' clinical findings.

RESULTS

Significant perfusion asymmetries were noted in the two patients with infarction in the upper pons but not in those with lesions below this level. They comprised a contralateral cerebellar and ipsilateral supratentorial hypoactivity that was most marked in the frontoparietal cortex. There was no clear relation between the patterns of cerebral or cerebellar tracer uptake and specific neurological findings.

CONCLUSIONS

Remote perfusion changes after pure brain stem infarction may be seen both infratentorially and supratentorially and depend on the lesion site rather than on the neurological deficit. In this context, our study confirmed damage to the corticopontocerebellar pathways as the key event in the genesis of a crossed cerebellar diaschisis. The exact mechanisms causing ipsilateral cerebral hemispheric diaschisis await further clarification.

摘要

背景与目的

我们研究了6例单纯性单侧脑干梗死患者,以探讨远隔部位的大脑和小脑血流变化与该脑区不同部位损伤之间的关系。

方法

我们使用单光子发射计算机断层扫描和[123I]碘安非他明来测量示踪剂摄取的区域差异。定性图像分析和计算得出的不对称指数与磁共振成像上梗死区域的位置以及患者的临床发现相关。

结果

在2例脑桥上段梗死患者中发现了显著的灌注不对称,但在梗死部位低于此水平的患者中未发现。它们表现为对侧小脑和同侧幕上低活性,在额顶叶皮质最为明显。大脑或小脑示踪剂摄取模式与特定神经学发现之间没有明确的关系。

结论

单纯脑干梗死后的远隔灌注变化可在幕下和幕上均出现,且取决于病变部位而非神经功能缺损。在此背景下,我们的研究证实皮质脑桥小脑通路受损是交叉性小脑失联络发生的关键事件。导致同侧大脑半球失联络的确切机制有待进一步阐明。

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