Recovery following stroke has two distinct periods: the immediate recuperative phase taking effect within the first few days, and the delayed phenomenon occurring several days later. The first phase is thought to be a secondary to resolution of brain edema and diaschisis, while the latter phase is believed to be due to neural plasticity. Neural plasticity comprises primarily neurite growth and synaptogenesis. While there have been controversial studies regarding the existence and exact nature of neural plasticity, several researchers have established behavioral recovery after stroke as a function of neuronal remodeling, that would include dendritic growth and increase in synaptic population. Nororepinephrine plays a key role in both phases of stroke recovery. Antagonist such as clonidine and alpha-1 agonists impair functional recovery when administered in the immediate post-stroke period. Sympathomimetic drugs such as amphetamines have been shown to increase functional performance that correlates with neuronal (and synaptic) growth in the brain. Most of these studies have been performed on rats, with limited work performed on human subjects. The exact dosage and timing of administration of amphetamines in the post-stroke period remains to be defined. Nonetheless, amphetamines remain a viable and exciting option for in the post-stroke “recovery” period.