Abstract
Gadolinium (Gd)-based contrast agents (GBCAs) are chemicals injected intravenously during magnetic resonance imaging (MRI) to enhance the diagnostic yield. The repeated use of GBCAs can cause their deposition in the brain, including the cerebellum. Such deposition may affect various cell subsets in the brain and consequently cause behavioral alterations due to neurotoxicity. Caution should thus be exercised in using these agents, particularly in patients who are more likely to have repeated enhanced MRIs during their lifespan. Further studies are required to clarify the toxicity of GBCAs, and potential mechanisms causing neurotoxicity have recently been reported. This review introduces the effects of GBCAs in the cerebellum obtained from in vitro and in vivo studies and considers the possible mechanisms of neurotoxicity involved.
Highlights
This review explores the effects of gadolinium-based contrast agents (GBCAs) on the cerebellum based on the findings of in vitro and in vivo studies and discusses the possible mechanisms involved
The growing literature on the stability and cerebellar deposition of GBCAs as demonstrated by in vitro, in vivo, and human research data presents increasing evidence of potential toxicity associated with GBCA treatment (Figure 2)
It should be noted that the Food and Drug Administration (FDA) stated, “FDA warns that gadolinium-based contrast agents (GBCAs) are retained in the body; requires new class warnings (19 December 2017)”
Summary
Metal-containing contrast agents have been used to enhance magnetic resonance imaging (MRI). The cerebellum is considered a primary region for GBCA deposition in the brain in humans and animals with repeat injections [13,14,15]. The exact chemical nature of the insoluble form has not yet been fully clarified [7,12] These results indicate that both Gd3+ and GBCAs may be deposited in the cerebellum and affect cerebellar function. This study has shown that repeated intravenous injection of linear (gadodiamide) or macrocyclic (gadoterate meglumine) GBCA from pregnancy day 15 to 19 induced deposition of Gd in the offspring brain at postnatal day 28. A previous study has shown the transplacental transfer of GBCA in rabbits [30] These results indicate that GBCA can cross the placenta and deposit in the brain. Further study is required to clarify the mechanisms causing such differences
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