Abstract
The Neurobiology and Treatment of Restless Legs Syndrome
Highlights
Restless Legs Syndrome (RLS) is a chronic sleepassociated neurological disorder bearing a significant impact on sleep quality, daytime functioning and health-related quality of life
At the level of the orbitofrontal cortices and anterior cingulate gyri, ratings of pain perception demonstrated inverse correlations with opiate receptors density. This suggests that greater severity of RLS symptoms can result in increased endogenous opiate release in brain regions involved in pain processing, which can possibly explain their involvement in the pathophysiology of both motor and sensory symptoms of RLS
Iron is a co-factor for the enzyme Tyrosine Hydroxylase (TH) necessary for DA synthesis alongside other proteins included in general neuronal activity [44]
Summary
Restless Legs Syndrome (RLS) is a chronic sleepassociated neurological disorder bearing a significant impact on sleep quality, daytime functioning and health-related quality of life. Most patients affected by RLS experience Periodic Leg Movements during Sleep (PLMS) or wakefulness (PLMW), this is not an essential diagnostic criterion [3]. Numerous hypotheses have been proposed to explain the underlying pathophysiology of RLS. These include genetic variations, peripheral neuropathy, spinal cord microlesions, brain metabolism fluctuations, iron deficiency and neurotransmitter dysfunctions. This article reviews the literature on the neuobiological underpinnings and available pharmacological therapies of RLS. Both variants of RLS (primary and secondary) will be covered, the main focus will be upon primary RLS and its pathophysiology, in an attempt to identify the most effective treatments available for this common condition
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