[Pathophysiology of restless-legs syndrome. Review of current research].
The primary pathomechanism of restless legs syndrome is unclear. Neurophysiological, pharmacological, and imaging studies have demonstrated a complex interaction between central and peripheral structures. The degree of integration of central and peripheral mechanisms is not known. Altered excitability at a spinal level modulated by supraspinal rhythms of the brainstem possibly plays an important role. There is no anatomical structural lesion and it is more likely that circadian disturbances of dopaminergic and/or opioidergic neurotransmission are involved.
Winkelmann
J
J
Max-Planck-Institut für Psychiatrie, Neurologie, Kraepelinstrasse 10, 80804 München. janew@mpipsykl.mpg.de
Trenkwalder
C
C
D000328:Adult; D021081:Chronobiology Disorders / Q000150:complications* / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism; D004569:Electroencephalography; D004576:Electromyography; D020022:Genetic Predisposition to Disease; D006801:Humans; D020189:Nocturnal Myoclonus Syndrome / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D012148:Restless Legs Syndrome / Q000150:complications / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D014055:Tomography, Emission-Computed; D015899:Tomography, Emission-Computed, Single-Photon; D014511:Uremia / Q000150:complications
D004298:Dopamine