ABSTRACT
Our understanding of the phenomenology and etiopathogenesis of the restless legs syndrome (RLS) has greatly advanced since the first modern description of the disorder by Ekbom (1). There is a strong genetic component to the development of RLS, andmany secondary forms are now recognized. In pure idiopathic RLS, there is evidence of dysfunction within dopaminergic pathways and of those controlling iron homeostasis. Initial studies of nondopaminergic medications focused on benzodiazepines, carbamazepine (CBZ), and clonidine. Gabapentin (GBP) later emerged as a viable treatment option for RLS, and by the time the newer dopamine agonists became widely available, physicians had many treatment options available that did not have the potential to cause augmentation. Other nondopaminergic agents (especially antiepileptics) and nonpharmacologic treatments have since been studied in small groups of patients with some efficacy against RLS symptoms, but with insufficient data to advocate routine use.
