Experiments utilizing TMS have provided insights into the network mechanisms of stroke recovery, as well as factors that may inhibit this process. Intriguingly, studies using paired-pulse TMS have demonstrated that in cortical strokes, short-interval intracortical inhibition is decreased in the acute stage, whereas intracortical facilitation is unchanged, suggesting that the balance of excitability in these cortical circuits is shifted towards excitation (Cicinelli et al., 1997; Liepert et al., 2000b, 2000a; Nardone & Tezzon, 2002; Manganotti et al., 2002). However, other studies have demonstrated that the cortical silent period is initially prolonged, suggesting increased inhibition (Braune & Fritz, 1995; Traversa et al., 1997; Ahonen et al., 1998; Liepert et al., 2000a; Nardone & Tezzon, 2002); this prolongation normalizes with clinical recovery (Traversa et al., 1997; Classen et al., 1997; Cicinelli et al., 1997; Byrnes et al., 2001). Stroke patients undergoing rehabilitation 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
