Document Detail

Physiological noise in oxygenation-sensitive magnetic resonance imaging.
MedLine Citation:
PMID:  11590638     Owner:  NLM     Status:  MEDLINE    
The physiological noise in the resting brain, which arises from fluctuations in metabolic-linked brain physiology and subtle brain pulsations, was investigated in six healthy volunteers using oxygenation-sensitive dual-echo spiral MRI at 3.0 T. In contrast to the system and thermal noise, the physiological noise demonstrates a signal strength dependency and, unique to the metabolic-linked noise, an echo-time dependency. Variations of the MR signal strength by changing the flip angle and echo time allowed separation of the different noise components and revealed that the physiological noise at 3.0 T (1) exceeds other noise sources and (2) is significantly greater in cortical gray matter than in white matter regions. The SNR in oxygenation-sensitive MRI is predicted to saturate at higher fields, suggesting that noise measurements of the resting brain at 3.0 T and higher may provide a sensitive probe of functional information.
G Krüger; G H Glover
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Magnetic resonance in medicine : official journal of the Society of Magnetic Resonance in Medicine / Society of Magnetic Resonance in Medicine     Volume:  46     ISSN:  0740-3194     ISO Abbreviation:  Magn Reson Med     Publication Date:  2001 Oct 
Date Detail:
Created Date:  2001-10-08     Completed Date:  2002-06-04     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8505245     Medline TA:  Magn Reson Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  631-7     Citation Subset:  IM    
Copyright Information:
Copyright 2001 Wiley-Liss, Inc.
Lucas MRS Center, Department of Radiology, Stanford University, Palo Alto, California, USA.
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MeSH Terms
Brain / anatomy & histology*,  physiology*
Magnetic Resonance Imaging*
Grant Support

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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