The Adenosine Hypothesis of Restless Legs Syndrome

Abstract

R estless Legs Syndrome (RLS) is a very prevalent neurological disorder. According to the RLS epide- miology, symptoms, and treatment study, 5% of U.S. and European patients reported experiencing RLS symptoms at least weekly.1 RLS can be pathophysiologically sepa- rated into two clinical phenomena: deficits of sensorimo- tor integration that produce akathisia and periodic limb movements during sleep (PLMS) and an enhanced arousal state (hyperarousal).2 Akathisia is described as a feeling of restlessness and an urgent need to move. PLMS have very specific charac- teristics: they consist on repetitive episodes of leg move- ment activity (at least four in a row) with a duration of up to 10 seconds and an intermovement interval of 5–90 seconds.3 Hyperarousal manifests as a short sleep time with episodes of arousals during sleep, related but not caused by PLMS; thus, in about half of all cases, the onset of the episodes of arousal precedes the onset of the leg movements.3 Hyperarousal also manifests as a lack of expected profound sleepiness during the day. Thus, the average total sleep time of RLS patients is <6 hours and, yet, they do not show significant daytime sleep- iness on objective meassures.