PARKINSONIAN SYMPTOMATOLOGY - AN ANATOMICAL AND PHYSIOLOGICAL ANALYSIS
PARKINSONIAN SYMPTOMATOLOGY - AN ANATOMICAL AND PHYSIOLOGICAL ANALYSIS
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DOI：
10.1111/j.1749-6632.1988.tb32998.x
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发表时间：
1988-01-18
影响因子：
5.2
通讯作者：
DELONG, MR
中科院分区：
文献类型：
--
作者：
MILLER, WC;DELONG, MR
帕金森综合征包括运动功能障碍，如运动不能、运动迟缓、震颤和强直、眼球运动障碍和认知障碍。很难理解一个相对较小且特异性的中脑多巴胺神经元损伤如何会产生如此多样的综合征。最近的发展允许重新审视这个问题：（1）对基底神经节和大脑皮层之间的解剖关系的理解增加，（2）使用神经毒素MPTP开发出合适的帕金森病灵长类动物模型。近年来，一个功能分离的平行基底神经节-丘脑皮层回路系统被提出。在这个方案中，基底神经节和丘脑的相关部分被视为更大的皮质-皮质下回路的组成部分，其最终影响指向特定的皮质区域。因此，基底神经节的功能贡献必须根据它们对这些皮质区的影响来考虑。此外，基底神经节功能紊乱，如帕金森氏病等神经系统疾病，一定部分是由异常的皮质输出引起的。最近开发的MPTP模型帕金森病提供了机会，研究基底神经节内的神经元活动的变化，并进一步描绘这种疾病的病理生理基础。在下面的讨论中，我们将根据这些新获得的数据来考虑帕金森病的损害。
The parkinsonian syndrome includes disturbances of motor function such as akinesia, bradykinesia, tremor and rigidity, disturbances of eye movements, and cognitive impairment. It is difficult to understand how a relatively small and specific lesion of midbrain dopamine neurons could produce such a diverse syndrome. Tko recent developments permit a reexamination of this question:(1) the increased understanding of the anatomical relations between the basal ganglia and the cerebral cortex, and (2) the development of a suitable primate model of parkinsonism using the neurotoxin MPTP. In recent years, a system of functionally segregated parallel basal ganglia-thalamocortical circuits has been proposed. In this scheme, the basal ganglia and the related portions of the thalamus are viewed as components of larger cortico-subcortical circuits whose ultimate influences are directed upon specific cortical areas. It therefore follows that the functional contributions of the basal ganglia must be considered in terms of their influences on these cortical areas. Moreover, disturbances in basal ganglia function, as occur in neurological diseases such as Parkinson’s disease, must result in part from abnormal cortical output. The recent development of the MPTP model of Parkinson’s disease has provided the opportunity to study the changes in neuronal activity within the basal ganglia and to delineate further the pathophysiologic basis of this disorder. In the following discussion, we will consider the impairments in Parkinson’s disease in light of this newly acquired data.