The generation of the neuronal signals in motor neurons that cause muscle relaxant contractions are dependent on the balance of synaptic excitation and inhibition that the motor neuron receives. Spasmolytic agents generally act by either enhancing the condition of inhibition, or reducing the level of excitation.

Inhibition is enhanced by mimicking or enhancing the actions of endogenous inhibitory substances, similar of the same kind with GABA. Because they may act at the level of the cortex, brain stem or spinal cord, or all three areas, they have traditionally been referred to as 'centrally-acting' muscle relaxants.

However, it is now known that not every agent in this class has CNS activity (e.g. dantrolene), so this name is inaccurate.

Because of the enhancement of inhibition in the CNS, most spasmolytic agents have the side-effects of sedation, drowsiness and may cause dependence with long term use. Several of these agents also have abuse potential, and their prescription is strictly controlled.0