In spinal injury, descending motor commands from the cortex to the spinal cord are disrupted. There exists however an equally important descending motor system, one from the brainstem that is primarily system for setting the appropriate levels of excitability in spinal neurons. Injury of this brainstem system results in highly aberrant behavior of the spinal motor networks. As a result, any remaining descending commands from the cortex are distorted and produce inappropriate outputs. The spinal cord itself generates certain types of motor commands, the most important of which is the basic pattern for locomotion. The spinal central pattern generation for locomotion is also highly dependent on the brainstem input. A third aspect of brainstem control of the spinal cord is exerted on the pattern of sensory input from the limbs. Our recent studies (e.g. Hyngstrom et al Nature Neuroscience; Hyngstrom et al, Journal of Physiology) show that loss of brainstem input severely distorts the pattern of sensory input. Normally, the motoneurons that innervate ankle extensor muscles receive a tightly focused input, predominately from ankle muscles. Thus rotating the ankle, as done in our experiments by a robotic arm (Figure 1, left) generates a strong synaptic current in ankle extensor motoneurons (first set of movements, trace labeled "Normal"; there are two deflections in the current trace because the ankle flexion/extension, as well as the other movements, were repeated twice). Rotations of knee and the hip produced very little effect. Note that the 6 degrees of freedom of the robotic arm allowed the rotations to be selective to individual joints (green segments in the stick figures at the top) while the other joint angles remained constant (black segments). In sharp contrast, following acute spinal injury (lower trace), the response to ankle rotation remained but there was an overall increase in noise and the response from hip rotation became aberrantly large. Fortunately, the primary source of descending control of the pattern of synaptic input is via brainstem axons that release serotonin or norepinephrine. A number of drugs that mimic these endogenous neurotransmitters are available for use in human subjects and we are presently investigated their effectiveness in restoring function in spinal injury.
In the figure shown here, a previously unappreciated aspect of distortion of spinal ciruits is illustrated, namely that the pattern of sensory input