Central Pattern Generation of Locomotion: A Review of the Evidence

We have studied manual motor function in a man deafferented by a severe peripheral sensory neuropathy. Motor power was almost unaffected. Our patients could produce a very wide range of preprogrammed finger movements with remarkable accuracy, involving complex muscle synergies of the hand and forearm muscles. He could perform individual finger movements and outline figures in the air with high eyes closed. He had normal pre- and postmovement EEG potentials, and showed the normal bi/triphasic pattern of muscle activation in agonist and antagonist muscles during fast limb movements. He could also move his thumb accurately through three different distances at three different speeds, and could produce three different levels of force at his thumb pad when required. Although he could not judge the weights of objects placed in his hands without vision, he was able to match forces applied by the experimenter to the pad of each thumb if he was given a minimal indication of thumb movement. Despite his success with these laboratory tasks, his hands were relatively useless to him in daily life. He was unable to grasp a pen and write, to fasten his shirt buttons or to hold a cup in one hand. Part of hist difficulty lay in the absence of any automatic reflex correction in his voluntary movements, and also to an inability to sustain constant levels of muscle contraction without visual feedback over periods of more than one or two seconds. He was also unable to maintain long sequences of simple motor programmes without vision.

Timing of the repetitive movements that constitute any rhythmic behavior is regulated by intrinsic properties of the central nervous system rather than by sensory feedback from moving parts of the body. Evidence of this permits resolution of the long-standing controversy over the neural basis of rhythmic behavior and aids in the identification of this mechanism as a general principle of neural organization applicable to all animals with central nervous systems.

Because of new data, anatomical and functional models of the basal ganglia in normal and pathological conditions (e.g. Parkinson's and Huntington's diseases) have recently come under greater scrutiny. An update of these models is clearly timely, taking into consideration not only changes in neuronal discharge rates, but also changes in the patterning and synchronization of neuronal discharge, the role of extrastriatal dopamine, and expanded intrinsic and input/output connections of these nuclei.