Cerebello-frontal cortical projections in humans studied with the magnetic coil.
tion of noradrenergic inhibition in the spinal cord  have been implicated. Despite the uncertainty of clonidine's mechanism of action in treating spasticity, there is substantial evidence pointing to the usefulness of this drug. Our case series is the first to document a role for clonidine in treating MS patients with spasticity. While previous reports [2-6] described clonidine's efficacy in treating spasticity secondary to spinal cord injury or brain-stem disease, spasticity in MS could be secondary to both spinal cord and brain involvement. It is of note in our patients that high doses of baclofen had failed to be effective when these patients responded positively to clonidine. To establish the role of clonidine in the treatment of spasticity in MS patients, a controlled trial is indicated. The drug may provide the clinician with another useful option when dealing with difficult and resistant cases of spastic MS patients.