Background. Parkinson disease (PD) is characterized by hypometric movements resulting from loss of dopaminergic neurons in the substantia nigra. PD leads to decreased activation of the supplementary motor area (SMA); the net result of these changes is a poverty of movement. The present study determined the impact of 5？Hz repetitive transcranial magnetic stimulation (rTMS) over the SMA on a fine motor movement, handwriting (writing cursive “l”s), and on cortical excitability, in individuals with PD. Methods. In a cross-over design, ten individuals with PD were randomized to receive either 5？Hz or control stimulation over the SMA. Immediately following brain stimulation right handed writing was assessed. Results. 5？Hz stimulation increased vertical size of handwriting and diminished axial pressure. In addition, 5？Hz rTMS significantly decreased the threshold for excitability in the primary motor cortex. Conclusions. These data suggest that in the short term 5？Hz rTMS benefits functional fine motor task performance, perhaps by altering cortical excitability across a network of brain regions. Further, these data may provide the foundation for a larger investigation of the effects of noninvasive brain stimulation over the SMA in individuals with PD. 1. Introduction Hypometric movements, resulting in diminution of letter size, reduced speed and slow acceleration, typically characterize handwriting in individuals with Parkinson disease (PD) [1–5]. Deficits in handwriting begin with hypometric movements and then may progress to micrographia as PD severity progresses. Specifically, hypometric movements may be related to the impaired ability to maintain adequate muscle force and to process concurrent and forthcoming movement information while writing. Given that individuals with PD suffer from hypometric handwriting [1], we selected this task to consider the effects of noninvasive brain stimulation on hand function. Normally, the basal ganglia (BG) play a role in the kinematic scaling of movements [6], but in individuals with PD, suboptimal BG function due to dopamine depletion leads to widespread changes in interconnected brain regions that include decreased activity in the supplementary motor area (SMA) and reduced efferent feedback in the basal ganglia-thalamocortical motor loop [7]. Consequently, individuals with PD show altered activation patterns in the SMA [8–15] and overall less corticocortical excitability [8–10, 12]. Taken together, changes in activation patterns across a broad cortical network and sub-optimal BG function lead to hypometric movements
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