Transcranial magnetic stimulation of the motor sytem in focal dystonia

Several lines of evidence suggest that focal task-specific hand dystonia represents a model for maladaptive plasticity of the sensorimotor cortex. A dysfunction of homeostatic processes that stabilize the properties of neuronal circuits may be a candidate mechanism to trigger and maintain these maladaptive changes. To test this hypothesis, we combined transcranial direct current stimulation (TDCS) and repetitive transcranial magnetic stimulation (rTMS) at a rate of 1Hz to probe “homeostatic-like“ mechanisms in the intact primary motor cortex (M1) in patients with writer's cramp. Confirming our previous work (Siebner et al.; J Neurosci 2004;24:3379–85), healthy controls showed a “facilitatory“ response to anodal TDCS pre-conditioning and a subsequent period of rTMS reduced corticospinal excitability. Conversely, “inhibitory“ pre-conditioning with cathodal TDCS reversed the after effect of rTMS leading to an increase in corticospinal excitability. Patients with writer's cramp, a focal task-specific dystonia affecting handwriting, showed an abnormal responsiveness of the M1 to both, TDCS and rTMS. (i) Only anodal TDCS produced a normal facilitatory effect on corticospinal excitability, whereas “inhibitory“ cathodal TDCS had no after effect on corticospinal excitability. (ii) Regardless of the type of pre-conditioning, rTMS did not modify corticospinal excitability. In particular, though anodal TDCS produced a “normal“ facilitatory response, subsequent 1Hz rTMS did not reverse the increase in excitability produced by anodal pre-conditioning, indicating a deficiency of homeostatic mechanisms in the M1 in patients with writer's cramp. Our results indicate that impaired “homeostatic-like“ regulation of motor cortical excitability may be involved in maladapitive plasticity in task-specific hand dystonia.