Gamma-motorneurons are always active, even in resting brain states - this is a characteristic of facilitatory brain regions (generally more caudal regions). Other brain regions provide an inhibitory effect... cortex, basal ganglia, cerebellum (generally more rostral regions). With loss of the cerebrum's inhibitory effect, gamma-motorneurons exhibit unopposed excitatory action.
Increased gamma-motorneuron firing contracts intrafusal muscle fibers, which increases the sensitivity of the muscle spindle to passive stretch.
Thus, any stretch of the muscle initiates a primed myotatic stretch reflex and shortens the muscle. This is the mechanism of spasticity, and much of the mechanism of hyperreflexia. The other component is the likely loss of inhibitory influences from higher brain regions directly on alpha-motorneurons, which helps to localize the segmental myotatic stretch reflex to the specific muscle group stimulated. Loss of this inhibitory effect probably contributes to the hyperreflex, and also the involvement of nearby muscle groups ('triple reflex') as some myotatic reflex arcs are likely divergent.
I guess that is the gist of it without getting into specific neurotransmitters at each step, or describing the myotatic reflex arc in more detail.
