Unraveling Specific Brain Microstructural Damage in Moyamoya Disease Using Diffusion Magnetic Resonance Imaging and Positron Emission Tomography.


Journal

Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association
ISSN: 1532-8511
Titre abrégé: J Stroke Cerebrovasc Dis
Pays: United States
ID NLM: 9111633

Informations de publication

Date de publication:
Apr 2019
Historique:
received: 09 09 2018
revised: 04 12 2018
accepted: 27 12 2018
pubmed: 27 1 2019
medline: 10 4 2019
entrez: 26 1 2019
Statut: ppublish

Résumé

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 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.

Sections du résumé

BACKGROUND AND PURPOSE OBJECTIVE
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
MATERIALS AND METHODS 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 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 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.

Identifiants

pubmed: 30679013
pii: S1052-3057(18)30738-9
doi: 10.1016/j.jstrokecerebrovasdis.2018.12.038
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1113-1125

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

Auteurs

Shoko Hara (S)

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.

Masaaki Hori (M)

Department of Radiology, Juntendo University, Bunkyo-ku, Tokyo, Japan.

Ryo Ueda (R)

Department of Radiology, Juntendo University, Bunkyo-ku, Tokyo, Japan.

Shihori Hayashi (S)

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.

Motoki Inaji (M)

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.

Yoji Tanaka (Y)

Department of Neurosurgery, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.

Taketoshi Maehara (T)

Department of Neurosurgery, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.

Kenji Ishii (K)

Team for Neuroimaging Research, Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo, Japan.

Shigeki Aoki (S)

Department of Radiology, Juntendo University, Bunkyo-ku, Tokyo, Japan.

Tadashi Nariai (T)

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.

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