Goto S, Matsumoto S, Ushio Y, Hirano A
Department of Neurosurgery, Kumamoto University Medical School, Japan.
Neurology. 1996 Oct;47(4):1032-6. doi: 10.1212/wnl.47.4.1032.
In this study, we examined the topographic involvement of the putaminal projection neurons and their axons in the globus pallidus and substantia nigra, which we visualized by calcineurin immunostaining, in the basal ganglia of patients with striatonigral degeneration (SND). In all cases examined, there was a marked decrease in number of calcineurin-immunopositive neurons in the caudal and lateral portion of the putamen. Also, marked depletion of calcineurin-immunoreactive putaminal efferents was consistently present in the posteroventrolateral portions of the globus pallidus interna (GPi) and externa, and in the ventrolateral portion of the substantia nigra pars reticulata (SNr) topographically corresponding to the putaminal lesion. In view of the functional model of the basal ganglia "motor" circuit, these findings suggest that subregional deafferentation of the GPi/SNr (i.e., basal ganglia output nuclei) from putaminal inputs may be responsible for parkinsonism in patients with SND.
在本研究中，我们通过钙调神经磷酸酶免疫染色观察了纹状体黑质变性（SND）患者基底节中壳核投射神经元及其轴突在苍白球和黑质中的局部受累情况。在所有检查的病例中，壳核尾部和外侧部分钙调神经磷酸酶免疫阳性神经元的数量明显减少。此外，在苍白球内侧部（GPi）和外侧部的后腹外侧部分，以及与壳核病变在地形上相对应的黑质网状部（SNr）腹外侧部分，始终存在钙调神经磷酸酶免疫反应性壳核传出纤维的明显缺失。鉴于基底节“运动”回路的功能模型，这些发现表明，来自壳核输入的GPi/SNr（即基底节输出核）的局部传入缺失可能是SND患者帕金森症的原因。
