Naumann M, Pirker W, Reiners K, Lange K W, Becker G, Brücke T
Department of Neurology, Bayerische Julius-Maximilians-Universität Würzburg, Germany.
Mov Disord. 1998 Mar;13(2):319-23. doi: 10.1002/mds.870130219.
There is increasing evidence that a dysfunction of the dopaminergic system may be involved in the pathogenesis of idiopathic dystonia. To visualize possible alterations of the pre- and postsynaptic side of striatal dopaminergic synapses, SPECT studies using the radiotracers [123I] epidepride and [123I] beta-CIT were performed in 10 patients with idiopathic cervical dystonia. Eleven age- and sex-matched subjects served as controls. [123I] Epidepride is a new highly affine marker of D2 receptors, and [123I] beta-CIT binds to dopamine transporters on dopaminergic nerve endings. [123I] Epidepride binding was significantly reduced in both striata of dystonia patients compared with controls (p < 0.05). In contrast, striatal [123I beta-CIT uptake did not differ from controls. We conclude that dopaminergic dysfunction in idiopathic focal dystonia mainly involves postsynaptic mechanisms and suggest a disturbance of the indirect pathway of the motor circuit resulting in a disinhibited thalamocortical stimulation.
越来越多的证据表明，多巴胺能系统功能障碍可能参与特发性肌张力障碍的发病机制。为了观察纹状体多巴胺能突触突触前和突触后可能存在的改变，对10例特发性颈部肌张力障碍患者进行了使用放射性示踪剂[123I]表哌立登和[123I]β-CIT的单光子发射计算机断层扫描（SPECT）研究。11名年龄和性别匹配的受试者作为对照。[123I]表哌立登是一种新型的高亲和力D2受体标记物，[123I]β-CIT与多巴胺能神经末梢上的多巴胺转运体结合。与对照组相比，肌张力障碍患者双侧纹状体中[123I]表哌立登结合显著降低（p<0.05）。相比之下，纹状体[123I]β-CIT摄取与对照组无差异。我们得出结论，特发性局灶性肌张力障碍中的多巴胺能功能障碍主要涉及突触后机制，并提示运动回路间接通路紊乱导致丘脑皮质刺激去抑制。
