Restless Leg Syndrome in Neurologic and Medical Disorders.

Abstract

Adopting prior models of sleep-wake transitions, a flip-flop switch in synchronized neurotransmitter activity is proposed to underlie restless leg syndrome onset. In this model, leg quiescence homeostasis sustained through concerted activities of several neurotransmitters in basal ganglia is perturbed and produces striatal motor activity along sensory activity associated with thalamocortical circuits (conscious urge and discomfort). This model explains the association of restless leg syndrome with a wide variety of associated pathologies emphasizing that perturbed function and imbalance may occur under different steady states of neurotransmitter levels. Likewise, this concept links various central and peripheral etiologies and integrates the augmenting and transient effects of therapeutic neuromodulators.