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通过正电子发射断层扫描研究皮质中风后远隔脑区的代谢紊乱。

Metabolic disturbances in exo-focal brain areas after cortical stroke studied by positron emission tomography.

作者信息

Nagasawa H, Kogure K, Fujiwara T, Itoh M, Ido T

机构信息

Department of Neurology, Institute of Brain Diseases, Tohoku University, Sendai, Japan.

出版信息

J Neurol Sci. 1994 May;123(1-2):147-53. doi: 10.1016/0022-510x(94)90217-8.

DOI:10.1016/0022-510x(94)90217-8
PMID:8064308
Abstract

We have reported that exo-focal delayed neuronal damage was observed in the ipsilateral thalamus and the substantia nigra of the rat brain after occlusion of the middle cerebral artery (MCA). To determine if that phenomenon also occurs in humans, we measured cerebral metabolic rates for glucose (CMRGlc) in the remote brain areas at a chronic stage after cortical infarction using 2-[18F]fluoro-2-deoxy-D-glucose and position emission tomography (PET). The subjects studied were 11 patients who were affected by unilateral cerebral infarction in the cortex supplied by MCA. There were significant decreases of CMRGlc as compared with control values (p < 0.01), not only in the cerebral cortex directly damaged by the ischemic insult, but also in the ipsilateral thalamus and in the contralateral cerebellum, areas in which no lesions had been detected by MRI or CT scan. The present study indicates that different mechanisms may be responsible for multi-focal metabolic disturbances in the remote areas after stroke. The reduction of CMRGlc in the contralateral cerebellum may be explained by the crossed cerebellar diaschisis theory and in the ipsilateral thalamus as being due to retrograde degeneration associated with the infarcted cortex. We suggest that these multi-focal brain dysfunctions caused by neuronal network disturbances may exacerbate clinical symptoms at a chronic stage of stroke.

摘要

我们曾报道,大脑中动脉(MCA)闭塞后,在大鼠脑的同侧丘脑和黑质中观察到远隔部位延迟性神经元损伤。为确定该现象是否也发生在人类身上,我们使用2-[18F]氟-2-脱氧-D-葡萄糖和正电子发射断层扫描(PET),在皮质梗死的慢性期测量了远隔脑区的脑葡萄糖代谢率(CMRGlc)。研究对象为11例受MCA供血区单侧脑梗死影响的患者。与对照值相比,CMRGlc显著降低(p < 0.01),不仅在直接受缺血性损伤的脑皮质中如此,在同侧丘脑和对侧小脑中也是如此,而MRI或CT扫描在这些区域未检测到病变。本研究表明,中风后远隔部位多灶性代谢紊乱可能由不同机制引起。对侧小脑CMRGlc的降低可能用交叉性小脑失联络理论来解释,同侧丘脑CMRGlc的降低则可能是由于与梗死皮质相关的逆行性变性。我们认为,由神经网络紊乱引起的这些多灶性脑功能障碍可能会在中风慢性期加重临床症状。

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