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Control of Posture and Gait by the Basal Ganglia: Pathophysiological Mechanisms Implicated in Parkinson's Disease Kaoru Takakusaki 1 , Mirai Takahashi 1 , Shusei Fukuyama 1 , Tomohiro Noguchi 1 , Ryosuke Chiba 1 1Department of Physiology, Division of Neuroscience, Asahikawa Medical University Keyword: パーキンソン病 , ドーパミン , アセチルコリン , 中脳歩行誘発野 , MLR , 脚橋被蓋核 , PPN , 歩行パターン生成器 , CPG , Parkinson's disease , dopamine , acetylcholine , mesencephalic locomotor region , pedunculopontine tegmental nucleus , central pattern generator pp.1067-1079
Published Date 2022/9/1
DOI https://doi.org/10.11477/mf.1416202185
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Abstract

Regulation of posture-gait control by the basal ganglia (BG) plays a critical role in the acquisition of automatically executed context-dependent learned motor acts, technically referred to as habit formation. Patients with Parkinson's disease (PD) show posture-gait disturbances and progressively lose habitual behaviors. Injury to dopamine (DA) neurons in the midbrain is implicated as the primary pathophysiological mechanism underlying PD; therefore, DA actions in the BG play a pivotal role in optimal BG function. In this commentary, we discuss the mechanism underlying BG-modulated regulation of cognitive posture-gait control by the cerebral cortex through the cortico-BG loop and the basic posture-gait mechanisms underlying the actions of the brainstem and spinal cord via the BG-brainstem projection. The BG primarily regulates excitability of the cerebral cortex and brainstem through its DA-mediated inhibitory action. Based on these considerations, we describe the pathophysiological mechanisms that contribute to posture-gait disturbances in PD. Recent clinical studies suggest that posture-gait disturbances may be attributable to functional disconnection between the BG and the cerebral cortex and brainstem. Injury to various neurotransmitter systems in addition to the DA system and significant alpha-synuclein (Lewy body)-induced degeneration of the brainstem neurons may worsen posture-gait control impairment in PD.


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電子版ISSN 1344-8129 印刷版ISSN 1881-6096 医学書院

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