Obeso J A, Rodriguez-Oroz M C, Rodriguez M, DeLong M R, Olanow C W
Department of Neurology and Neurosurgery, Clínica Universitaria and Medical School, University of Navarra, Pamplona, Spain.
Ann Neurol. 2000 Apr;47(4 Suppl 1):S22-32; discussion S32-4.
The anatomical and physiological basis of levodopa-induced dyskinesias (LIDs) in patients with Parkinson's disease (PD) is reviewed in the light of the current model for the organization of the basal ganglia. This model, which was developed in the late 1980s, works relatively well in explaining the motor features of PD but, for example, it does not account for why tremor, rigidity, bradykinesia, gait dysfunction and postural instability present to differing degrees in different patients, and may respond differently to levodopa treatment or surgical procedures. Recent information suggests that LIDs develop as a consequence of pulsatile stimulation of dopamine receptors, with consequent dysregulation of genes and proteins in downstream neurons resulting in changes in neuronal firing patterns. A modified model of the basal ganglia in PD patients with LID is proposed, which incorporates more recent clinical and experimental data.
根据当前基底神经节组织模型，对帕金森病（PD）患者左旋多巴诱发异动症（LIDs）的解剖学和生理学基础进行了综述。该模型于20世纪80年代末提出，在解释PD的运动特征方面效果相对较好，但例如，它无法解释为什么震颤、强直、运动迟缓、步态功能障碍和姿势不稳在不同患者中表现程度不同，并且对左旋多巴治疗或手术程序的反应可能不同。最新信息表明，LIDs是多巴胺受体脉冲刺激的结果，下游神经元中的基因和蛋白质随之失调，导致神经元放电模式改变。本文提出了一个适用于LID的PD患者的基底神经节修正模型，该模型纳入了更多最新的临床和实验数据。
