Paulus Walter, Trenkwalder Claudia
Department of Clinical Neurophysiology, University of Göttingen, Göttingen, Germany.
Lancet Neurol. 2006 Oct;5(10):878-86. doi: 10.1016/S1474-4422(06)70576-2.
Therapy-related augmentation of the symptoms of restless legs syndrome (RLS) is an important clinical problem reported in up to 60% of patients treated with levodopa and, to a lesser extent, with dopamine agonists. The efficacy of low-dose dopaminergic drugs for RLS has been established, but the mode of action is unknown. Here, we review the existing data and conclude that augmentation is a syndrome characterised by a severely increased dopamine concentration in the CNS; overstimulation of the dopamine D1 receptors compared with D2 receptors in the spinal cord may lead to D1-related pain and generate periodic limb movements; iron deficiency may be a main predisposing factor of augmentation, probably caused by a reduced function of the dopamine transporter; therapy with levodopa or dopamine agonists should remain at low doses and; iron supplementation and opiates are the therapy of choice to counter augmentation.
与治疗相关的不安腿综合征（RLS）症状加重是一个重要的临床问题，在接受左旋多巴治疗的患者中，高达60%的患者报告有此问题，在接受多巴胺激动剂治疗的患者中，症状加重的比例相对较小。低剂量多巴胺能药物治疗RLS的疗效已得到证实，但其作用方式尚不清楚。在此，我们回顾现有数据并得出结论：症状加重是一种以中枢神经系统中多巴胺浓度严重升高为特征的综合征；与脊髓中的多巴胺D2受体相比，多巴胺D1受体过度刺激可能导致与D1相关的疼痛并产生周期性肢体运动；缺铁可能是症状加重的主要诱发因素，可能是由多巴胺转运体功能降低所致；左旋多巴或多巴胺激动剂治疗应保持低剂量；补充铁剂和使用阿片类药物是对抗症状加重的首选治疗方法。
