Kato M
Department of Clinical Neurophysiology, Faculty of Medicine, Kyushu University.
Nihon Rinsho. 1997 Jan;55(1):26-31.
The structural organization and neuronal circuit of the basal ganglia were reviewed, and the neural mechanisms for the clinical syndromes of Parkinson's disease were discussed. Dopamine depletion in parkinsonian patients causes an increase in neuronal activities in the globus pallidus internal segment and the substantia nigra pars reticulata, resulting in an inhibition of neurons in the thalamus and pedunculopontine nucleus, and developing akinesia and rigidity. Distorted integral information processes in the striatum and different involvement patterns of the two pathways of the information flow, the direct and indirect pathways, may cause diversity of the extrapyramidal syndromes in basal ganglia diseases. Also discussed was an instructional role of dopamine in generating a relevant voluntary movement by modulating the striatal neurons.
回顾了基底神经节的结构组织和神经回路，并讨论了帕金森病临床综合征的神经机制。帕金森病患者多巴胺耗竭导致苍白球内侧段和黑质网状部神经元活动增加，从而抑制丘脑和脚桥核中的神经元，进而产生运动不能和强直。纹状体中整体信息处理过程的扭曲以及信息流的直接和间接两条途径的不同参与模式，可能导致基底神经节疾病锥体外系综合征的多样性。还讨论了多巴胺通过调节纹状体神经元在产生相关随意运动中的指导作用。
