Dostrovsky Jonathan O, Hutchison William D, Lozano Andres M
Department of Physiology, Faculty of Medicine, University of Toronto, Ontario, Canada.
Neuroscientist. 2002 Jun;8(3):284-90. doi: 10.1177/1073858402008003014.
Parkinson's disease (PD) is caused by the degeneration of the dopaminergic neurons in the substantia nigra. Loss of dopaminergic innervation leads to hyperactivity in the internal segment of the globus pallidus (GPi), the main output nucleus of the basal ganglia and to a profound disturbance in the function of motor circuits. Lesions of the GPi (or in its upstream modulator, the subthalamic nucleus) can greatly improve the motor symptoms of PD presumably by reducing this pathological activity. Paradoxically, high-frequency electrical stimulation of the GPi (deep brain stimulation, DBS) mimics the effects of pallidotomy and has become an accepted therapeutic technique. The mechanisms underlying the beneficial effects of pallidal DBS are not known. Various mechanisms that might account for inhibiting or disrupting the pathological pallidal outflow by high-frequency DBS have been proposed ranging from depolarization block to stimulation-evoked release of GABA, and these are discussed.
帕金森病（PD）是由黑质中多巴胺能神经元变性引起的。多巴胺能神经支配的丧失导致苍白球内侧部（GPi）过度活跃，GPi是基底神经节的主要输出核，进而导致运动回路功能严重紊乱。GPi（或其上游调节核，即丘脑底核）的损伤可能通过减少这种病理活动而极大地改善帕金森病的运动症状。矛盾的是，GPi的高频电刺激（深部脑刺激，DBS）模拟了苍白球切开术的效果，并已成为一种公认的治疗技术。苍白球DBS有益效果的潜在机制尚不清楚。已经提出了各种可能解释高频DBS抑制或破坏病理性苍白球输出的机制，从去极化阻滞到刺激诱发的GABA释放，本文将对这些机制进行讨论。
