Transcranial brain stimulation is used increasingly as a potential therapeutic intervention for a variety of conditions. Because studies have shown that the after-effects of stimulation can be prolonged when repeated sessions are given 
, therapy is almost always designed around daily stimulation delivered for weeks or more. The effects of a single session of stimulation are often assumed as valid predictors of long-term changes that might be expected in a therapeutic protocol 
. However, there is some evidence that the effects of long-term treatment may differ in quality from those of a single session. In depression, effects of repetitive transcranial magnetic stimulation (rTMS) in excess of those of placebo can only be observed after several weeks of treatment. Similarly, a progressively developing response to therapeutic brain stimulation can be observed after implantation of deep brain stimulation (DBS). Maximum clinical effects of DBS in dystonia, as well as Tourette syndrome and obsessive compulsive disorder, may take months to develop 
. Indeed, in dystonia, implantation of DBS may initiate progressive changes in underlying motor physiology that are not apparent when testing acutely 
The present experiments examined whether repeated sessions of rTMS can promote slow reorganisation in the motor system of patients with writer's cramp (WC). This is a clinically relevant condition in which rTMS to the dorsal premotor cortex (PMd) has already been tested as a potential therapeutic intervention. Although small effects of a single session of have been reported 
, repetitive sessions over consecutive days are usually required for clearer therapeutic effects 
. We ask whether repeated sessions of rTMS lead to cumulative effects on typical pathophysiological hallmarks of dystonia that cannot be observed after a single intervention.
Our intervention targeted PMd since functional imaging studies have often revealed that it is hyperactive during movement in patients with dystonia 
. However the underlying mechanism of hyperactivity in PMd and its role in causing dystonia remain unclear. It could be an intrinsic premotor deficit or reflect abnormal interaction in a wider motor network. We therefore assessed effects of multisession premotor suppression on both premotor and motor cortex to gain some insight into possible motor network reorganisation in dystonia.
We applied cTBS to PMd for 5 days and measured effects on physiological markers of dystonia: the network interaction from PMd-M1, and the increased plasticity and reduced inhibition within M1 in WC patients 
. cTBS is generally believed to suppress the stimulated cortex 
, although recent reports using protocols slightly different from that used in the current study suggest that the response to TBS protocols is variable and the effect of cTBS may not be always inhibitory 
. We hypothesised that PMd suppression might restore PMd-M1 connectivity. This would not only be evident as a normalisation in M1 intracortical inhibition as we have observed previously in a single session cTBS study 
, but also might reduce overactive M1 plasticity that is so common in dystonia.