scholarly journals Determining T2 relaxation time and stroke onset relationship in ischaemic stroke within apparent diffusion coefficient-defined lesions. A user-independent method for quantifying the impact of stroke in the human brain

2019 ◽  
Vol 8 (1-2) ◽  
pp. 11-28 ◽  
Author(s):  
Michael J. Knight ◽  
Robin A. Damion ◽  
Bryony L. McGarry ◽  
Rose Bosnell ◽  
Kimmo T. Jokivarsi ◽  
...  
Keyword(s):  
Diffusion Coefficient ◽  
Relaxation Time ◽  
Apparent Diffusion Coefficient ◽  
Human Brain ◽  
Ischaemic Stroke ◽  
Independent Method ◽  
T2 Relaxation Time ◽  
T2 Relaxation ◽  
Apparent Diffusion ◽  
The Impact

Changes in the apparent diffusion coefficient of water and T2 relaxation time in gerbil hippocampus after mild ischemia

Neuroreport ◽  
2000 ◽  
Vol 11 (15) ◽  
pp. 3333-3336 ◽  
Author(s):  
Lidong Zhu ◽  
Nobuhito Saito ◽  
Osamu Abe ◽  
Toshiyuki Okubo ◽  
Haruyasu Yamada ◽  
...  
Keyword(s):  
Diffusion Coefficient ◽  
Relaxation Time ◽  
Apparent Diffusion Coefficient ◽  
T2 Relaxation Time ◽  
T2 Relaxation ◽  
Apparent Diffusion

Apparent Diffusion Coefficient, Fractional Anisotropy and T2 Relaxation Time Measurement

2007 ◽  
Vol 17 (4) ◽  
pp. 230-238 ◽  
Author(s):  
Xiao-Qi Ding ◽  
Jürgen Finsterbusch ◽  
Oliver Wittkugel ◽  
Christian Saager ◽  
Einar Goebell ◽  
...  
Keyword(s):  
Diffusion Coefficient ◽  
Relaxation Time ◽  
Apparent Diffusion Coefficient ◽  
Fractional Anisotropy ◽  
Time Measurement ◽  
T2 Relaxation Time ◽  
T2 Relaxation ◽  
Relaxation Time Measurement ◽  
Apparent Diffusion

scholarly journals Secondary Reduction in the Apparent Diffusion Coefficient of Water, Increase in Cerebral Blood Volume, and Delayed Neuronal Death after Middle Cerebral Artery Occlusion and Early Reperfusion in the Rat

1999 ◽  
Vol 19 (12) ◽  
pp. 1354-1364 ◽  
Author(s):  
Menno van Lookeren Campagne ◽  
G. Roger Thomas ◽  
Harold Thibodeaux ◽  
James T. Palmer ◽  
Simon P. Williams ◽  
...  
Keyword(s):  
Diffusion Coefficient ◽  
Relaxation Time ◽  
Cerebral Blood Volume ◽  
Vascular Occlusion ◽  
T2 Relaxation Time ◽  
T2 Relaxation ◽  
Early Reperfusion ◽  
Occlusion Time ◽  
Contrast Enhanced ◽  
Apparent Diffusion

It has been reported recently that very delayed damage can occur as a result of focal cerebral ischemia induced by vascular occlusion of short duration. With use of diffusion-, T2-, and contrast-enhanced dynamic magnetic resonance imaging (MRI) techniques, the occlusion time dependence together with the temporal profile for this delayed response in a rat model of transient focal cortical ischemia have been established. The distal branch of the middle cerebral artery was occluded for 20, 30, 45, or 90 minutes. Twenty minutes of vascular occlusion with reperfusion exhibited no significant mean change in either the apparent diffusion coefficient of water (ADC) or the T2 relaxation time at 6, 24, 48, or 72 hours after reperfusion ( P = 0.97 and 0.70, respectively). Ninety minutes of ischemia caused dramatic tissue injury at 6 hours, as indicated by an increase in T2 relaxation times to 135% of the contralateral values ( P < 0.01). However, at intermediate periods of ischemia (30 to 45 minutes), complete reversal of the ADC was seen at 6 hours after reperfusion but was followed by a secondary decline over time, such that a 25% reduction in tissue ADC was seen at 24 as compared with 6 hours ( P < 0.02). This secondary response was accompanied by an increase in cerebral blood volume (CBV), as shown by contrast-enhanced dynamic MRI (120% of contralateral values; P < 0.001), an increase in T2 relaxation time (132%; P < 0.01), together with clear morphological signs of cell death. By day 18, the mean volume of missing cortical tissue measured with high-resolution MRI in animals occluded for 30 and 45 minutes was 50% smaller than that in 90-minute occluded animals ( P < 0.005). These data show that ultimate infarct size is reduced after early reperfusion and is occlusion time dependent. The early tissue recovery that is seen with intermediate occlusion times can be followed by cell death, which has a delayed onset and is accompanied by an increase in CBV.

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