also demonstrate an increase in the number of cortical sites from where an MEP of the paretic hand can be obtained (Traversa et al., 1997; Liepert et al., 1998, 2000b; Wittenberg et al., 2003). Another study demonstrated that TMS pulses to ipsilesional dorsal premotor cortex can produce much greater delays in reaction time in stroke patients with infarcts in motor cortex but preserved premotor cortices than in healthy controls (Fridman et al., 2004). Furthermore, TMS to the premotor cortex in the intact cortex produces MEPs in the ipsilateral (paretic) hand (Caramia et al., 2000), suggesting that the contralesional premotor cortex also plays a role in motor activation after stroke. The importance of the contralesional hemisphere was also demonstrated in a study by Lotze et al (2006), who evaluated the impact of inhibitory rTMS to various locations in the contralesional hemisphere in patients who had recovered fully from subcortical strokes. They found that stimulation of the contralesional M1, dorsal premotor cortex, and superior parietal lobule all produced significant decreases in performance of motor tasks by the ipsilateral hand (that was affected by the stroke). Taken together, these studies suggest that the excitability of the lesioned hemisphere is altered after a stroke,
