TY - JOUR
T1 - Dynamic oxygen-enhanced MRI of Cerebrospinal fluid
AU - Mehemed, Taha M.
AU - Fushimi, Yasutaka
AU - Okada, Tomohisa
AU - Yamamoto, Akira
AU - Kanagaki, Mitsunori
AU - Kido, Aki
AU - Fujimoto, Koji
AU - Sakashita, Naotaka
AU - Togashi, Kaori
N1 - Funding Information:
This study was partly supported by Toshiba Medical Systems Corporation, the employer of Naotaka Sakashita who has a joint patent application about this research with Toshiba Medical Systems Corporation. There are no further patents, products in development or marketed products to declare. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials, as detailed online in the guide for authors. The details of patent application is as follows: “MAGNETIC RESONANCE IMAGING APPARATUS AND IMAGE PROCESSING APPARATUS” “Japanese patent application No. 2013-170529.”
PY - 2014/6/23
Y1 - 2014/6/23
N2 - Oxygen causes an increase in the longitudinal relaxation rate of tissues through its T1-shortening effect owing to its paramagnetic properties. Due to such effects, MRI has been used to study oxygen-related signal intensity changes in various body parts including cerebrospinal fluid (CSF) space. Oxygen enhancement of CSF has been mainly studied using MRI sequences with relatively longer time resolution such as FLAIR, and T1 value calculation. In this study, fifteen healthy volunteers were scanned using fast advanced spin echo MRI sequence with and without inversion recovery pulse in order to dynamically track oxygen enhancement of CSF. We also focused on the differences of oxygen enhancement at sulcal and ventricular CSF. Our results revealed that CSF signal after administration of oxygen shows rapid signal increase in both sulcal CSF and ventricular CSF on both sequences, with statistically significant predominant increase in sulcal CSF compared with ventricular CSF. CSF is traditionally thought to mainly form from the choroid plexus in the ventricles and is absorbed at the arachnoid villi, however, it is also believed that cerebral arterioles contribute to the production and absorption of CSF, and controversy remains in terms of the precise mechanism. Our results demonstrated rapid oxygen enhancement in sulcal CSF, which may suggest inhaled oxygen may diffuse into sulcal CSF space rapidly probably due to the abundance of pial arterioles on the brain sulci.
AB - Oxygen causes an increase in the longitudinal relaxation rate of tissues through its T1-shortening effect owing to its paramagnetic properties. Due to such effects, MRI has been used to study oxygen-related signal intensity changes in various body parts including cerebrospinal fluid (CSF) space. Oxygen enhancement of CSF has been mainly studied using MRI sequences with relatively longer time resolution such as FLAIR, and T1 value calculation. In this study, fifteen healthy volunteers were scanned using fast advanced spin echo MRI sequence with and without inversion recovery pulse in order to dynamically track oxygen enhancement of CSF. We also focused on the differences of oxygen enhancement at sulcal and ventricular CSF. Our results revealed that CSF signal after administration of oxygen shows rapid signal increase in both sulcal CSF and ventricular CSF on both sequences, with statistically significant predominant increase in sulcal CSF compared with ventricular CSF. CSF is traditionally thought to mainly form from the choroid plexus in the ventricles and is absorbed at the arachnoid villi, however, it is also believed that cerebral arterioles contribute to the production and absorption of CSF, and controversy remains in terms of the precise mechanism. Our results demonstrated rapid oxygen enhancement in sulcal CSF, which may suggest inhaled oxygen may diffuse into sulcal CSF space rapidly probably due to the abundance of pial arterioles on the brain sulci.
UR - http://www.scopus.com/inward/record.url?scp=84903522967&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0100723
DO - 10.1371/journal.pone.0100723
M3 - 学術論文
C2 - 24956198
AN - SCOPUS:84903522967
SN - 1932-6203
VL - 9
JO - PLoS ONE
JF - PLoS ONE
IS - 6
M1 - e100723
ER -