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Neurology 2003;61:S49-S55
© 2003 American Academy of Neurology

Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represent the opinions of the authors and are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology.

Restless legs syndrome and PD

A review of the evidence for a possible association

Diego Garcia-Borreguero, MD, Per Odin, MD and Carolina Serrano, MD

From the Department of Neurology, Fundación Jiménez Díaz, Madrid, Spain (Drs. Garcia-Borreguero and Serrano), and Department of Neurology, Central Hospital, Bremershaven, Germany (Dr. Odin).

Address correspondence and reprint requests to Prof. Diego Garcia-Borreguero, Sleep Disorders Unit, Dept. of Neurology, Fundación Jiménez Díaz, Universidad Autónoma de Madrid, Avda. Reyes Católicos 2, 28040 Madrid, Spain.

Restless legs syndrome (RLS) is a common neurologic disorder whose prevalence has been estimated at 4 to 10% of the general population. Although its pathophysiology remains unknown, dopaminergic mechanisms are believed to play a central role. Furthermore, dopaminergic drugs have shown therapeutic efficacy in various large-scale therapeutic trials, and dopamine agonists now represent the first line of treatment. Several studies performed over the past years have suggested an association between RLS and Parkinson’s disease (PD). However, the evidence is still limited and large controlled studies are needed to show the prevalence rates of PD in RLS patients versus controls. Furthermore, in contrast to PD, some brain imaging studies have revealed a mild striatal dysfunction in RLS. Preliminary neuropathologic evidence also suggests that the dopaminergic dysfunction does not involve neuronal degeneration at that level. Therefore, neuronal degeneration in other dopaminergic pathways than the nigrostriatal might be relevant in the pathogenesis of RLS in PD.




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