• dystonia;
  • bradykinesia;
  • corticospinal excitability;
  • EMG patterns;
  • transcranial magnetic stimulation


Current models of basal ganglia dysfunction in primary dystonia propose that the excessive muscle activity results from an increase in the excitability of the primary motor cortex. Neurophysiological and neuroimaging studies, however, have shown consistently reduced movement-related sensorimotor cortical activity. To explore this paradox, we used transcranial magnetic stimulation (TMS) to examine changes in corticospinal excitability preceding and during ballistic movements of the wrist in 9 patients with primary dystonia affecting the arm and 9 matched control subjects. The onset time, rate of rise, and duration of changes in the excitability of corticospinal projections to the agonist muscle were normal in the patients with dystonia. Increases in excitability were selective to the initial agonist muscle, suggesting that the spatial recruitment of corticospinal neurons was normal. Nonetheless, movements were slower in the patients by an average of 26%. The onset of the first agonist muscle burst was normal in magnitude and timing but the activity in this muscle subsequently became attenuated as movement progressed. Muscle activity in antagonist and proximal muscles of the upper arm was reduced significantly in the dystonia patients. These findings support the view that movement preparation and initiation at the level of the primary motor cortex is normal in patients with dystonia. Bradykinesia could not be attributed to co-contraction or overflow of activity and was associated with reduced rather than excessive muscle activity. © 2004 Movement Disorder Society