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首页> 外文期刊>European journal of neurology: the official journal of the European Federation of Neurological Societies >Mismatch of cognition and neural networks in asymptomatic middle cerebral artery steno‐occlusive disease
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Mismatch of cognition and neural networks in asymptomatic middle cerebral artery steno‐occlusive disease

机译：无症状中脑动脉闭塞性疾病中的认知和神经网络不匹配

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Background and purpose The role of intracranial steno‐occlusive disease in cognitive impairment and dementia is unclear and has not been well studied. Methods A total of 32 consecutive patients (13 males, aged 54?±?12?years) with asymptomatic steno‐occlusive middle cerebral artery (MCA) disease, defined as 70% stenosis on maximum intensity projection images or a complete signal loss of MCA trunk on magnetic resonance angiography, and 20 age‐ and education‐matched normal controls (12 males, 60?±?8?years old) were compared for neuropsychological performance, gray matter volume and neural network analysis. Results The patient group did not show a significant decrease in gray matter volume or cognitive tests except for their performance on the grooved pegboard test. However, graph analysis of resting‐state functional magnetic resonance imaging showed significant decreases in network strength, global efficiency and the clustering coefficient, as well as a longer characteristic path length ( P ??0.05). The diffusive decrease pattern was particularly located in interhemispheric connectivity and there was no compensatory hyperconnectivity in any brain regions. Conclusion In asymptomatic steno‐occlusive MCA disease, cognition and neural network changes are mismatched and have underlying pathophysiological mechanisms that are different from those of neurodegenerative disease.
机译：背景以来，颅内胸腔闭塞病在认知障碍和痴呆症中的作用尚不清楚，并未得到很好的研究。方法总共32例连续32名患者（13名男性，54岁，54岁？在磁共振血管造影上的MCA躯干和20岁和教育匹配的正常对照（12名男性，60次，60？±8？岁），用于神经心理学性能，灰质体积和神经网络分析。结果患者组没有显示出灰质体积或认知测试的显着降低，但在沟槽Pegboard测试上的性能之外。然而，静态功能磁共振成像的图分析显示了网络强度，全局效率和聚类系数的显着降低，以及较长的特征路径长度（P？＆ 0.05）。扩散减少图案特别位于血液间连接性，并且在任何脑区中没有补偿纤维凝固性。结论在无症状的旋转闭塞MCA病，认知和神经网络变化不匹配，并具有与神经变性疾病不同的病理生理机制。

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