• B C Chu and K Miyasaka.
• Department of Radiology, Hokkaido University School of Medicine, Sapporo, Japan.
• No To Shinkei. 1998 Sep 1; 50 (9): 787-95.

AbstractDiffusion is a measure of motion freedom and is a sensitive parameter to characterize the tissue at the microscopic level. The methods of measuring in vivo diffusion by magnetic resonance imaging (MRI) have been based mainly on the addition of two motion-probing gradients (MPG) to the spin echo sequence to produce signal attenuation for the spins moving at random. The resultant MR images reflect the intravoxel incoherent motions (IVIM), which contain both water molecule diffusion and perfusion in the capillary network, and can be quantified by an apparent diffusion coefficient (ADC). Diffusion weighted MRI, acquired from IVIM MR imaging by the addition of the very strong MPG predicate water diffusion and anisotropy. High signal or reduced ADC can be observed in case of the slower diffusion. The anisotropy depends upon the orientation of the subjects and the gradients. Greater signal attenuation (faster diffusion) can be observed when the relative orientation of white matter tracts to the MPG is parallel as compared to that obtained with a perpendicular alignment. This anisotropy may preclude the detection or delineation of an ischemic lesion. Diffusion tensor trace has been designated to eliminate this anisotropy effect. In ischemic animal models, low signal (fast diffusion) and high signal (slow diffusion) have been noted in the vasogenic edema and cytotoxic edema, respectively. High signal appears only in case of cerebral blood flow below 15-20 ml/100 g per minute, a value identical to the threshold of tissue at high energetic metabolism and ion homeostasis. ADC value decreases following the cerebral vessel occlusion, or remains unchanged when collateral circulation develops. It has been speculated that reduction in ADC reflects the water shift from extracellular space to intracellular space due to the membrane permeability and/or intracellular osmolality increase. These results suggest that diffusion weighted MRI correlates well with the cell metabolism, and cytotoxic edema plays an important role in the acute cerebral stroke. In clinical setting of acute cerebral ischemia, diffusion weighted MRI may detect superacute infarction by showing high signal (slower ADC) over the 6 hours following the insult, whereas conventional MRI generally fails to do so. In chronic liquefied cerebral infarction, increased ADC, or attenuated signal are the most frequent findings, suggestive of an elevated diffusion. Therefore, diffusion weighted MRI improves early diagnosis of stroke and help differentiate acute from chronic stroke. One disadvantage of diffusion weighted MRI is motion artifact, which may be reduced by the introduction of a navigator echo to correct for the phase shift caused by the first imaging echo, or by the utility of ultrafast imaging technique, such as echo planar. Another shortcomings is the susceptibility artifact incorporating the diffusion weighted MRI. The eddy current may also result from the strong gradients, producing shiftlike artifact. Such artifacts can be compensated for by appropriate shaping of the current pulses sent into the gradient coils, or by use of shielded gradients. As with rapid progresses in perfusion imaging of ischemia penumbra, misery perfusion and luxury perfusion, new insight into the diffusion weighted MRI will be significant.

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