Improvement of clinical function following neural insult is commonly observed. However, recovery of clinical function cannot be completely explained by resolution of structural damage local to the site of the lesion. Following focal injury, dynamic alterations of activity in different brain regions have been observed, consistent with the phenomenon of neuroplasticity. This neuroplasticity is an intrinsic property of the central nervous system that is also present during adult life and allows the remodeling of specific brain networks in a putative attempt to optimize cortical function in response to injury.1 When this plasticity genuinely aids clinical recovery, or maintains clinical function in the presence of persistent structural damage, it is known as compensatory plasticity. However, when observed, it may also represent a noncompensatory or even malcompensatory process. The value of compensatory neuroplasticity lies in its theoretical potential as a target for therapeutic intervention that could conceivably enhance functional recovery after brain injury.