Increased spring constant could be related to either real change in K as well as a change in the threshold location. In spasticity, experimentally it appears that clinical spasticity is mainly related to changes in threshold rather than spring constant. Change in threshold might be caused by changes in motor neuron or gamma loop. Velocity dependance does not seem to be a large component. A 5 fold increase in speed causes only a slight increase in force.
Mechanisms are much less clear than in spinal cord.
These may be a fragment of pattern generators used during stance phase of locomotion. Drugs currently in use for Spasticity Many monoamines excite motor neurons and inhibit interneurons. Its original rationale was presynaptic inhibition of sensory input. However, also now realized that may have direct post-synaptic effect on motor neurons, as it directly blocks plateau potentials, and it suppresses both interneurons and motorneurons. Glycine and Gaba are two inhibitory receptors in spinal cord.