Pharmacologic and ElectroPhysiologic studies over the past 20 years have shown Tizanidine to be a potent, Central-acting MyoTonolytic agent that principally affects Spinal PolySynaptic Reflexes.
This action arises from Agonistic activity of the compound at NorAdrenergic alpha 2 receptors, resulting in both direct impairment of Excitatory Amino Acid release from Spinal InterNeurons and a concomitant Inhibition of Facilitatory CoeruleoSpinal Pathways.
Similar alpha 2-receptor-mediated Inhibition of InterNeuronal activity appears to underlie the additional AntiNociceptive and AntiConvulsant activity of Tizanidine reported in several species and test paradigms.
Despite its structural and biochemical similarity to Clonidine, the Cardiovscular properties of Tizanidine are mild and transitory in relation to its activity as a muscle relaxant.
These findings, together with a possible greater separation between MyoTonolytic and general CNS depressant activity than with other agents, make Tizanidine a valuable addition in the pharmacologic treatment of Spasticity.
