Brain iron stores, while critical for numerous processes involved in proper brain development,  cellular metabolism, and executive function, serve a distinct role in the regulation of motor function.  Both dietary iron deficiency and excessive brain iron accumulation have been implicated in the etiology of movement disorders.  Basal ganglia iron accumulation, most notably in the context of Neurodegeneration with Brain Iron Accumulation (NBIA), is perhaps the best characterization of the link between dysregulated iron metabolism and disordered movement.  However, low basal ganglia iron stores may also play a role in the pathology of movement disorders, particularly in hyperkinetic disorders, such as restless leg syndrome (RLS) and Tourette's Syndrome (TS).