Neurologic functions improve in most patients days and weeks after onset of a stroke. This can not be explained by recovery of the early salvageable ischemia zone. The most likely mechanism is relearning, a process in which healthy brain takes over functions lost with the infarct. Experimental studies indicate that this recovery can be modulated by pharmacological agents. NMDA antagonists and GABA agonists found to reduce infarct size in stroke models may have a harmful effect on relearning and neurologic recovery. This should be considered when clinical trial protocols are designed.