MECHANISMS WITHIN THE HUMAN SPINAL-CORD SUPPRESS FAST REFLEXES TO CONTROL THE MOVEMENT OF THE LEGS

Passive locomotor-like movement induces depression of the gain of a fa st conducting spinal sensorimotor path in humans. It was hypothesized that this gain control is mediated through a spinal circuit. In the fi rst experiment, passive pedalling motion was rapidly initiated in eigh t able bodied subjects. Soleus I-I-reflexes (used to reveal the gain o f the short latency stretch reflex) were recorded over the first 250 m s after the movement started. Significant depression in H-reflex magni tude was observed by 50 ms after the onset of movement. On the basis o f the timing, this gain attenuation was likely mediated through a spin al circuit. In a second experiment we tested chronic quadriplegics wit h clinically complete lesions of the spinal cord. Of five subjects tes ted, three expressed the reflex and all three showed significant inhib ition with passive pedalling movement (mean depression was to 39% of c ontrols). Both the rapid onset of the gain change (Expt. 1) and the pr esence of movement-induced inhibition in individuals with spinal lesio ns (Expt. 2) provide evidence that this component of human locomotor c ontrol is located in the spinal cord. The initiating source is probabl y somatosensory receptor discharge due to the movement.