Why does restless legs syndrome emerge in Parkinson's disease? A state-dependent sensorimotor gating reserve...

Restless legs syndrome (RLS) occurs in Parkinson's disease (PD), but its interpretation is complicated by nocturnal off-period discomfort, painful dystonia, akathisia, and leg motor restlessness. We ask whether PD creates a distinct mechanism or lowers the threshold for shared idiopathic-RLS biology. Dopamine may modify this threshold alongside rest, nocturnal state, and movement-related sensory processing. Integrating evidence on iron dyshomeostasis, adenosine-glutamate regulation, thalamo-sensorimotor networks, and sleep-circadian state, we propose sensorimotor gating reserve as an integrative framework for the capacity to prevent low-priority leg signals from engaging action systems. PD may reduce this reserve; RLS susceptibility and nocturnal rest may then cross the symptom threshold, while movement temporarily restores separation. Direct PD-RLS evidence remains limited; the model is a testable hypothesis for a phenotypically defined subset. Three comparisons examine within-patient transitions across asymptomatic rest, symptomatic nocturnal rest, and movement-induced relief, with idiopathic RLS and RLS mimics in PD as controls.