MRI FindingGadolinium deposition in the brain
Introduction
Gadolinium is a heavy metal with atomic number 64 that belongs to the lanthanide family. It is the main ingredient in most magnetic resonance imaging (MRI) contrast agents. Like other lanthanide metals, the stable oxidation state of gadolinium is +3 and the ionic radius is 0.99 Å. The ionic radius of gadolinium is almost equal to that of Ca2+, and Gd3+ can compete with Ca2+ and become toxic in biological systems. To reduce the toxicity of Gd3+, it has to be administered to humans in chelated forms to avoid the presence of free gadolinium. [1], [2], [3]. Several types of gadolinium-based contrast agents (GBCAs) have been developed to satisfy these conditions. GBCAs are divided into linear and macrocyclic types, and generally, macrocyclic GBCAs are more stable than linear GBCAs. GBCAs have been produced commercially since 1988. GBCAs have been used internationally for more than 25 years in more than 100 million patients [1], [2], [3]. As the use of GBCAs has increased, more gadolinium has been released into the environment, with increased concentrations being noted in sea water or river water over the last 20 years [4].
Section snippets
Gadolinium deposition evaluated with brain MRI
In 2014, we first reported the association of unusual brain MRI findings in patients with a history of GBCA administration [5]. Increased signal intensity in the dentate nucleus and globus pallidus on unenhanced T1-weighted images (T1WI) showed a positive correlation with previous exposure to linear chelate type GBCAs (gadopentetate dimeglumine or gadodiamide), even in patients with normal renal function. Previously, high signal intensity in the dentate nucleus on T1WI had been attributed to a
Transmetallation
The mechanism of gadolinium deposition in brain has not yet been well clarified. Since the degree of brain gadolinium deposition was shown to vary according to its chelate structure, the degree of dechelation probably plays a role. Frenzel et al. [42] evaluated the dechelation rate of GBCA after a 15-day incubation period at 37 °C in human serum in vitro. They found that 20% of gadodiamide (linear) was dechelated after 15 days of incubation.
In vivo, the presence of other metal ions that compete
Techniques
As the signal changes in these regions can be very small, the parameters of the MRI acquisition are very important. A sensitive protocol is needed to evaluate a small signal change due to a small amount of gadolinium deposition. In our experience, the conventional spin-echo sequence is the most appropriate. T1-weighted fluid attenuation inversion recovery (T1FLAIR) or spoiled gradient recalled echo (SPGR) sequences probably lack the sensitivity for weak T1 signal differences [50]. Ramalho et
Conclusions and future directions
Knowledge regarding gadolinium deposition in patients with normal renal function has increased dramatically since 2014. Gadolinium is now known to accumulate gradually in patients with normal renal function. High signal intensity on T1WI in the dentate nucleus, globus pallidus, and pulvinar of the thalamus correlates with a history of GBCA administration, and measuring their intensity can roughly estimate the amount of gadolinium deposition. The pathological analyses have revealed that residual
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