摘要
背景:我们描述了4例阿尔茨海默病(AD)患者的交叉小脑裂(Ccd)现象。离子(NIA-AA)标准,结合18F-FDGPET和11C-PIB PET成像. 方法:18F-FDG PET表现为脑代谢模式,左侧大脑额叶顶叶皮质相对减少最为明显,右侧小脑交叉代谢低下。兰姆。11C-PIB PET在左半球呈对称性淀粉样堆积,但相对示踪量(相对脑血流量的代用品)较低。CCD是一种单边现象小脑代谢低下是对侧大脑幕上功能障碍的一种远程效应。这一机制意味着皮质-桥脑-小脑纤维的受累.病理生理学被认为有一个功能或可逆的基础,但也可以反映在继发性的形态学变化。随着新成像技术的发展,ccd是一种公认的现象。技术,虽然很少在神经退行性痴呆中描述。 结果:据我们所知,这是首次用18F-FDGPET和11C-PIB PET显像来描述AD患者的CCD。在功能的基础上解释了我们研究对象中的CCD。因为左半球的神经退行性病变。无结构损害,对称性淀粉样堆积与单侧代谢损害不一致。 结论:CCD可能是由非淀粉样变性引起的.CCD的病理生理机制、临床意义及治疗意义及小脑的作用AD中的Lum需要进一步的研究。
关键词: 小脑diaschisis(CCD),低代谢,幕上病变,对侧,痴呆,阿尔茨海默病。
Current Alzheimer Research
Title:Crossed Cerebellar Diaschisis in Alzheimer’s Disease
Volume: 15 Issue: 13
关键词: 小脑diaschisis(CCD),低代谢,幕上病变,对侧,痴呆,阿尔茨海默病。
摘要: Background: We describe the phenomenon of crossed cerebellar diaschisis (CCD) in four subjects diagnosed with Alzheimer’s disease (AD) according to the National Institute on Aging - Alzheimer Association (NIA-AA) criteria, in combination with 18F-FDG PET and 11C-PiB PET imaging.
Methods: 18F-FDG PET showed a pattern of cerebral metabolism with relative decrease most prominent in the frontal-parietal cortex of the left hemisphere and crossed hypometabolism of the right cerebellum. 11C-PiB PET showed symmetrical amyloid accumulation, but a lower relative tracer delivery (a surrogate of relative cerebral blood flow) in the left hemisphere. CCD is the phenomenon of unilateral cerebellar hypometabolism as a remote effect of supratentorial dysfunction of the brain in the contralateral hemisphere. The mechanism implies the involvement of the cortico-ponto-cerebellar fibers. The pathophysiology is thought to have a functional or reversible basis but can also reflect in secondary morphologic change. CCD is a well-recognized phenomenon, since the development of new imaging techniques, although scarcely described in neurodegenerative dementias.
Results: To our knowledge this is the first report describing CCD in AD subjects with documentation of both 18F-FDG PET and 11C-PiB PET imaging. CCD in our subjects was explained on a functional basis due to neurodegenerative pathology in the left hemisphere. There was no structural lesion and the symmetric amyloid accumulation did not correspond with the unilateral metabolic impairment.
Conclusion: This suggests that CCD might be caused by non-amyloid neurodegeneration. The pathophysiological mechanism, clinical relevance and therapeutic implications of CCD and the role of the cerebellum in AD need further investigation.
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Crossed Cerebellar Diaschisis in Alzheimer’s Disease, Current Alzheimer Research 2018; 15 (13) . https://dx.doi.org/10.2174/1567205015666180913102615
DOI https://dx.doi.org/10.2174/1567205015666180913102615 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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