Qing Lv, Xinlin Wang, Tetsuya Asakawa* and Xiao Ping Wang* Pages 372 - 382 ( 11 )
Restless legs syndrome (RLS)/Willis-Ekbom disease is a neurologic disorder characterized by a strong desire to move when at rest (usually in the evening) and paraesthesia in their lower legs. The most widely used therapies for first-line treatment of RLS are dopaminergic drugs; however, their long-term use can lead to augmentation. α2δ Ligands, opioids, iron, glutamatergic drugs, adenosine, and sleep aids have been investigated as alternatives. The pathogenesis of RLS is not well understood. Despite the efficacy of dopaminergic drugs in the treatment of this disorder, unlike in Parkinson’s disease dopaminergic cell loss in the substantia nigra has not been observed in RLS. The etiology of RLS is likely complex, involving multiple neural pathways. RLS-related genes identified in genome-wide association studies can provide insight into the mechanistic basis and pathophysiology of RLS. Here we review the current treatments and knowledge of the mechanisms underlying RLS.
Restless legs syndrome, dopaminergic drugs, nondopaminergic drugs, mechanisms, genetic factors, augmentation.
Department of Neurology, TongRen Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, Department of Neurology, TongRen Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, Department of Neurosurgery, Hamamatsu University School of Medicine, Handayama, 1-20-1, Higashi-ku, Hamamatsucity, Shizuoka 431-3192, Department of Neurology, TongRen Hospital, Shanghai JiaoTong University School of Medicine, Shanghai