The young human brain is highly plastic and thus brain lesions during development interfere with the innate development of architecture, connectivity and mapping of functions and trigger modifications in structure, wiring and representations (for review, see Payne & Lomber, 2001). In childhood the motor cortex and/or corticospinal tract is the most common site of brain damage and the pre- or immediately peri-natal period is the most common time for brain damage to occur. It is now increasingly appreciated that the corticospinal system is capable of substantial reorganization after lesions and that such reorganization is likely to underlie spontaneous partial recovery of function (Terashima, 1995; Eyre et al., 2001, 2002; Raineteau & Schwab, 2001). In the mature nervous system synaptic plasticity in pre-existing pathways, and the formation of new circuits through collateral sprouting of lesioned and unlesioned fibres, are the principal components of this recovery process (Raineteau & Schwab, 2001). In the developing nervous system it is clear that there is much greater potential for plasticity, which may involve plasticity not only of the motor areas of the ipsilesional cerebral cortex but also of the contralesional cortex, corticospinal tract formation and the development of spinal cord networks (Benecke et al., 1991; Carr et al., 1993; Cao et al., 1994; Lewine et al., 1994; Maegaki et al., 1995; Terashima, 1995; Muller et al., 1997, 1998; Nirkko et al., 1997; Graveline et al., 1998; O'Sullivan et al., 1998; Hertz-Pannier, 1999; Holloway et al., 1999; Wieser et al., 1999; Balbi et al., 2000; Chu et al., 2000; Eyre et al., 2000a, 2001; Thickbroom et al., 2001).