Mink J W
Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Prog Neurobiol. 1996 Nov;50(4):381-425. doi: 10.1016/s0301-0082(96)00042-1.
The basal ganglia comprise several nuclei in the forebrain, diencephalon, and midbrain thought to play a significant role in the control of posture and movement. It is well recognized that people with degenerative diseases of the basal ganglia suffer from rigidly held abnormal body postures, slowing of movement, involuntary movements, or a combination of these a abnormalities. However, it has not been agreed just what the basal ganglia contribute to normal movement. Recent advances in knowledge of the basal ganglia circuitry, activity of basal ganglia neurons during movement, and the effect of basal ganglia lesions have led to a new hypothesis of basal ganglia function. The hypothesis states that the basal ganglia do not generate movements. Instead, when voluntary movement is generated by cerebral cortical and cerebellar mechanisms, the basal ganglia act broadly to inhibit competing motor mechanisms that would otherwise interfere with the desired movement. Simultaneously, inhibition is removed focally from the desired motor mechanisms to allow that movement to proceed. Inability to inhibit competing motor programs results in slow movements, abnormal postures and involuntary muscle activity.
基底神经节由前脑、间脑和中脑的几个核组成,被认为在姿势和运动控制中起重要作用。众所周知,患有基底神经节退行性疾病的人会出现异常身体姿势僵硬、运动迟缓、不自主运动或这些异常的组合。然而,关于基底神经节对正常运动的具体作用尚未达成共识。近年来,在基底神经节神经回路知识、运动过程中基底神经节神经元的活动以及基底神经节损伤的影响方面取得的进展,导致了一种关于基底神经节功能的新假说。该假说认为,基底神经节并不产生运动。相反,当大脑皮质和小脑机制产生自主运动时,基底神经节广泛地发挥作用,抑制那些否则会干扰预期运动的相互竞争的运动机制。同时,对预期运动机制的抑制在局部被解除,以使该运动得以进行。无法抑制相互竞争的运动程序会导致运动缓慢、姿势异常和肌肉不自主活动。