Original Article

Journal of Cerebral Blood Flow & Metabolism (2006) 26, 1442–1450. doi:10.1038/sj.jcbfm.9600294; published online 22 March 2006

The relationship between diffusion anisotropy and time of onset after stroke

This work was supported by the Heart and Stroke Foundation of Alberta, Northwest Territories, and Nunavut, Alberta Heritage Foundation for Medical Research (AHFMR), and the Canadian Institutes for Health Research (CIHR), as well as a 'Focus on Stroke' doctoral training award to YAB from the Canadian Stroke Network, Heart and Stroke Foundation of Canada, CIHR, and AstraZeneca. The facility infrastructure was provided by AHFMR, Alberta Science and Research Authority, University of Alberta Hospital Foundation, and Canada Foundation for Innovation.

Yusuf A Bhagat1, Derek J Emery1,2, Ashfaq Shuaib3, Faiz Sher3, Nasir H Rizvi3, Naveed Akhtar3, Tracey L Clare2, Tammy Leatherdale2 and Christian Beaulieu1

  1. 1Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada
  2. 2Department of Radiology and Diagnostic Imaging, University of Alberta, Edmonton, Alberta, Canada
  3. 3Division of Neurology, University of Alberta, Edmonton, Alberta, Canada

Correspondence: Dr C Beaulieu, Department of Biomedical Engineering, Faculty of Medicine and Dentistry, University of Alberta, 1098 Research Transition Facility, Edmonton, Canada AB T6G 2V2. E-mail: christian.beaulieu@ualberta.ca

Received 8 September 2005; Revised 23 December 2005; Accepted 1 February 2006; Published online 22 March 2006.

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Abstract

Diffusion anisotropy changes in stroke lesions less than 24 h after onset have been reported to be elevated, decreased, or both. To address these mixed findings, we sought to characterize temporal changes of diffusion anisotropy by analyzing anatomically distinct ischemic white matter (WM) regions at 3 time phases within the first 34 h of ischemic stroke onset in 26 stroke patients (2 to 5 h, N=7; 7 to 14 h, N=11; 18 to 34 h, N=8). Mean diffusivity (Trace/3 apparent diffusion coefficient (ADC)), fractional anisotropy (FA), and T2-weighted signal intensity were measured for major and subcortical WM in lesions defined by a greater than or equal to30% drop in Trace/3 ADC. Major WM tract lesions with mean decreases of approx40% in relative (r) Trace/3 ADC showed an increased rFA of 1.11plusminus0.18 (P<0.01) during the hyperacute phase (2 to 5 h), whereas rFA declined to 0.90plusminus0.20 (P<0.01) and 0.88plusminus0.12 (P<0.01) in the acute (7 to 14 h) and subacute (18 to 34 h) phases, respectively. Of those patients with lesions in major WM, 4 of 8 patients less than or equal to7 h showed elevated rFA as opposed to none of the remaining 13 patients after 7 h. A greater proportion of the evaluated WM regions-of-interest (ROI) in the hyperacute phase revealed increases in rFA (60%), whereas conversely large proportions of ROIs (55% and 59%) in the acute and subacute phases showed reduced rFA. Similar anisotropy changes were noted in subcortical WM regions in the gyri.

Keywords:

cerebral ischemia, diffusion anisotropy, diffusion tensor imaging, stroke, white matter, DTI

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