Concepedia

TLDR

Diffusion-weighted hyperintensity in ischemic tissues may arise from cytotoxic edema due to transmembrane pump failure or microscopic brain pulsations. The study compared diffusion-weighted and T2-weighted MR images and correlated them with 1H and 31P MR spectroscopy over 6–8 h after unilateral MCA and bilateral carotid occlusion in eight cats. Diffusion-weighted images revealed significant hyperintensity within 45 min of ischemia, whereas T2-weighted images did not detect injury until 2–3 h; diffusion-weighted signal ratios were consistently higher and correlated with metabolic disturbances measured by 1H and 31P spectroscopy, but early diffusion- and T2-weighted ratios did not correlate.

Abstract

Diffusion-weighted MR images were compared with T2-weighted MR images and correlated with 1H spin-echo and 31P MR spectroscopy for 6-8 h following a unilateral middle cerebral and bilateral carotid artery occlusion in eight cats. Diffusion-weighted images using strong gradient strengths (b values of 1413 s/mm2) displayed a significant relative hyperintensity in ischemic regions as early as 45 min after onset of ischemia whereas T2-weighted spin-echo images failed to clearly demonstrate brain injury up to 2-3 h postocclusion. Signal intensity ratios (SIR) of ischemic to normal tissues were greater in the diffusion-weighted images at all times than in either TE 80 or TE 160 ms T2-weighted MR images. Diffusion- and T2-weighted SIR did not correlate for the first 1-2 h postocclusion. Good correlation was found between diffusion-weighted SIR and ischemic disturbances of energy metabolism as detected by 31P and 1H MR spectroscopy. Diffusion-weighted hyperintensity in ischemic tissues may be temperature-related, due to rapid accumulation of diffusion-restricted water in the intracellular space (cytotoxic edema) resulting from the breakdown of the transmembrane pump and/or to microscopic brain pulsations.

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