Shoko Hara1, Masaaki Hori2, Ryo Ueda2, Shihori Hayashi3, Motoki Inaji3, Yoji Tanaka4, Taketoshi Maehara4, Kenji Ishii5, Shigeki Aoki2, Tadashi Nariai3. 1. Department of Neurosurgery, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan; Department of Radiology, Juntendo University, Bunkyo-ku, Tokyo, Japan. Electronic address: shara.nsrg@tmd.ac.jp. 2. Department of Radiology, Juntendo University, Bunkyo-ku, Tokyo, Japan. 3. Department of Neurosurgery, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan; Team for Neuroimaging Research, Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo, Japan. 4. Department of Neurosurgery, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan. 5. Team for Neuroimaging Research, Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo, Japan.
Abstract
BACKGROUND AND PURPOSE: 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 15O-gas positron emission tomography (PET) to elucidate the specific ischemic brain microstructural damage of MMD in the cortex and the white matter. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND AND PURPOSE: 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 15O-gas positron emission tomography (PET) to elucidate the specific ischemic brain microstructural damage of MMD in the cortex and the white matter. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
Authors: S Hara; M Hori; A Hagiwara; Y Tsurushima; Y Tanaka; T Maehara; S Aoki; T Nariai Journal: AJNR Am J Neuroradiol Date: 2020-08-27 Impact factor: 3.825