Hara Shoko, Hori Masaaki, Ueda Ryo, Hayashi Shihori, Inaji Motoki, Tanaka Yoji, Maehara Taketoshi, Ishii Kenji, Aoki Shigeki, Nariai Tadashi
Department of Neurosurgery, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan; Department of Radiology, Juntendo University, Bunkyo-ku, Tokyo, Japan.
Department of Radiology, Juntendo University, Bunkyo-ku, Tokyo, Japan.
J Stroke Cerebrovasc Dis. 2019 Apr;28(4):1113-1125. doi: 10.1016/j.jstrokecerebrovasdis.2018.12.038. Epub 2019 Jan 21.
Chronic ischemia may induce brain microstructural damage and lead to neurocognitive dysfunction in patients with Moyamoya disease (MMD). We applied neurite orientation dispersion and density imaging (NODDI) and O-gas positron emission tomography (PET) to elucidate the specific ischemic brain microstructural damage of MMD in the cortex and the white matter.
Thirty-one patients (16-63years old, 9 males) and 20 age- and sex-matched normal controls were enrolled in this study. NODDI evaluates quantitative parameters reflecting neurite and axonal density, network complexity and the interstitial fluid in all participants. Of 31 patients, 12 newly diagnosed patients were evaluated with PET, also. We evaluated correlations between the microstructural parameters of NODDI and the hemodynamic and metabolic parameters of PET, the relationship between NODDI and clinical severity of each hemisphere (Normal, Asymtpomatic, Symptomatic, and Infarcted) as well as neurocognitive performance.
All NODDI parameters significantly correlated with PET parameters (absolute r = 0.46-0.83, P ≤ .048) and clinical severity (P < .001), suggesting that neurite and axonal density and network complexity decreased, and the interstitial fluid increased, as the ischemic burden became severe. NODDI parameters reflecting neurite and axonal density and network complexity significantly correlated with neurocognitive profiles (r = 0.36-0.64, P ≤ .048), but the interstitial fluid component did not.
Chronic ischemia in patients with MMD may induce decreased neurite and axonal density, simplified network complexity, and may lead to neurocognitive dysfunction. The increased interstitial fluid accompanying hemodynamic impairment may not be identical to the decreased neurite density and might be driven by another mechanism.
慢性缺血可能导致烟雾病（MMD）患者脑微观结构损伤并引发神经认知功能障碍。我们应用神经突方向离散度与密度成像（NODDI）和O气正电子发射断层扫描（PET）来阐明MMD患者皮质和白质中特定的缺血性脑微观结构损伤。
本研究纳入了31例患者（年龄16 - 63岁，男性9例）和20名年龄及性别匹配的正常对照者。NODDI评估所有参与者反映神经突和轴突密度、网络复杂性及细胞外液的定量参数。31例患者中，12例新诊断患者也接受了PET评估。我们评估了NODDI的微观结构参数与PET的血流动力学和代谢参数之间的相关性、NODDI与每个半球临床严重程度（正常、无症状、有症状和梗死）之间的关系以及神经认知表现。
所有NODDI参数均与PET参数显著相关（绝对r = 0.46 - 0.83，P≤0.048）以及临床严重程度相关（P < 0.001），这表明随着缺血负担加重，神经突和轴突密度及网络复杂性降低，而细胞外液增加。反映神经突和轴突密度及网络复杂性的NODDI参数与神经认知特征显著相关（r = 0.36 - 0.64，P≤0.048），但细胞外液成分与神经认知特征无关。
MMD患者的慢性缺血可能导致神经突和轴突密度降低、网络复杂性简化，并可能导致神经认知功能障碍。伴随血流动力学损害的细胞外液增加可能与神经突密度降低不同，可能由另一种机制驱动。
