Thursday, April 21, 2016

T2*-weighted fMRI time-to-peak of oxygen challenge in ischemic stroke

Absolutely no clue what use this is for helping stroke survivors. Or what part of stroke strategy this is addressing.
http://jcb.sagepub.com/content/36/2/283.full
  1. Qiang Shen1,2,3
  2. Shiliang Huang1
  3. Timothy Q Duong1,2,3,4
  1. 1Research Imaging Institute, University of Texas Health Science Center, San Antonio, TX, USA
  2. 2Department of Ophthalmology, University of Texas Health Science Center, San Antonio, TX, USA
  3. 3Department of Radiology, University of Texas Health Science Center, San Antonio, TX, USA
  4. 4South Texas Veterans Health Care System, Department of Veterans Affairs, San Antonio, TX, USA
  1. Qiang Shen, Research Imaging Institute, University of Texas Health Science Center at San Antonio, 8403 Floyd Curl Dr, San Antonio, TX 78229, USA. Email: shenq3@uthscsa.edu Timothy Q Duong, Research Imaging Institute, University of Texas Health Science Center at San Antonio, 8403 Floyd Curl Dr, San Antonio, TX 78229, USA. Email: duongt@uthscsa.edu

Abstract

T2*-weighted MRI of transient oxygen challenge (OC) showed exaggerated OC percent changes in the ischemic tissue at risk compared to normal tissue. One ambiguity is that regions with high vascular density also showed exaggerated OC percent changes. This study explored time-to-peak (TTP) of the OC percent changes to improve the utility of T2*-weighted OC MRI. Experiments were performed longitudinally at 30 min, 150 min and 24 h after transient (60-min) stroke in rats. Ischemic core, normal, and mismatch tissue were classified pixel-by-pixel based on apparent diffusion coefficient and cerebral blood flow. Major findings were: (i) Delayed OC TTP was localized to and corresponded well with the perfusion-diffusion mismatch. (ii) By contrast, the exaggerated OC percent changes were less localized, with changes not only in the at-risk tissue but also in some areas of the contralesional hemisphere with venous vessel origins. (iii) The OC time-course of the mismatch tissue was biphasic, with a faster initial increase followed by a slower increase. (iv) At-risk tissue with delayed TTP and exaggerated OC was normal after reperfusion and the at-risk tissue was mostly (83 ± 18%) rescued by reperfusion as indicated by normal 24-h T2. OC TTP offers unique information toward better characterization of at-risk tissue in ischemic stroke.

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