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Since Riccardi's1 landmark article in 1981 delineating the clinical manifestations of what we now call neurofibromatosis type 1 (NF1) and neurofibromatosis type 2, we have made great strides in our understanding of the genetic and molecular underpinnings of these distinct conditions. This knowledge has led to the emergence of plausible biologic agents that target specific points in ras-activated downstream pathways for the treatment of various complications of NF1, such as plexiform neurofibromas and optic pathway gliomas (OPGs).2 Yet, despite this progress, clinicians caring for these children continue to struggle with more basic questions, such as how best to follow these individuals and when to intervene. This is most evident in the care of children with NF1 OPGs.
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- © 2016 American Academy of Neurology
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