Bolus Gadolinium Effect

If gadolinium contrast is used to increase signal intensity on routine MR images, why does it decrease signal on DSC perfusion images?  

As a paramagnetic agent, gadolinium facilitates both T1- and T2(*) relaxation processes. Which effect predominates depends on its location and concentration.

For conventional MR imaging, gadolinium is imaged at a time when it has relatively low concentration and is distributed widely in the tissue extracellular space. In this environment, T1 shortening effects predominate and gadolinium appears bright on T1-weighted images.

In a Dynamic Susceptibility Contrast (DSC) study, gadolinium is imaged during its first pass through the vascular space. At this time the concentration of gadolinium is high (often exceeding 2-3 mM). This shortens both T2 due to dipole-dipole interactions and T2* due to susceptibility changes from gadolinium compartmentalization within the vessels. Water molecules diffusing nearby experience a changing magnetic field and undergo accelerated transverse relaxation. This translates to signal loss on T2- or T2*-weighted sequences.

Susceptibility-induced distortion of the main magnetic field (B_o) due to intravascular compartmentalization of gadolinium.

Dynamic Susceptibility Contrast (DSC) T2*-weighted source images acquired before, during, and after passage of the gadolinium bolus. At peak (middle image) note decreased signal throughout the brain, especially in blood vessels.

Advanced Discussion (show/hide)»

As you might expect, the relationship between the presence of Gd in a vessel and its T2(*) effects are more complex than the simple discussion above suggests.

First, standard Gd contrast agents are confined to the plasma and do not enter red blood cells. Accordingly, there are susceptibility effects within the intravascular space itself as well as those due to intravascular-extravascular space compartmentalization. The extent of compartmentalization varies with hematocrit. Hematocrit, in turn, differs between larger blood vessels and capillaries.

Field strength is important, as susceptibility effects generally scale with B_o².

The pulse sequence used will also determine the relative contributions of susceptibility from different vessels. GRE sequences will be sensitive to T2* dephasing from all vessels, but especially the larger ones; SE sequences will be more sensitive to T2 effects in small arterioles, venules and capillaries.

Finally, the orientation of blood vessels with respect to B_o affects both intravascular and extravascular susceptibility phenomena. For example, blood vessels oriented parallel to B_o will have no extravascular susceptibility changes while those oriented perpendicularly will exhibit a maximal effect. This curious phenomenon results from the angular dependence of dipole-dipole relaxation described in a prior Q&A.

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References
     Boxerman J, Hambert L, Rosen B, Weisskoff R. MR contrast due to intravascular magnetic susceptibility perturbations. Magn Reson Med 1995; 34:555-566. (explains susceptibility effect differences between large and small vessels).      

     Villringer A, Rosen BR, Belliveau JW et al. Dynamic imaging with lanthanide chelates in normal brain: contrast due to magnetic-susceptibility effects. Magn Reson Med 1988; 6:164-174.

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Related Questions
     Can the T2-shortening effects of gadolinium ever be observed on routine MR imaging? 
     What is the difference between T2 and T2*?   

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