Stroke is the leading cause of serious long-term disability in the US, leaving less than half of survivors able to return directly home. 1 Stroke recurrence, estimated as high as 17% over 5 years, also remains unacceptably high. 1 The use of lytic drugs and endovascular devices have revolutionized the care of select stroke patients in the acute setting. However, enormous challenges remain in changing the trajectory of stroke recovery for the vast majority of patients who do not qualify or remain disabled after these treatments, and also in preventing the accumulating disability associated with stroke recurrence. The role of sleep disorders in stroke outcome and recurrence has become a pressing question. Despite estimates of greater than 50% prevalence of sleep disorders after stroke, only about 6% of stroke survivors are offered formal sleep testing and an estimated 2% complete such testing in the 3-month post-stroke period. 2 The reasons for the low rate of screening are at least partly related to the lack of awareness regarding sleep disorders among stroke providers (Figure 1). This review evaluates the role of sleep disorders, including sleep disordered breathing (SDB) and sleep-wake cycle disorders, in stroke etiology and examines the impact of their treatment on stroke outcome. Physiology and anatomy of breathing during sleep During sleep, ventilation is reduced compared to wake, in parallel with the restorative and toning-down changes that occur to heart rate, temperature and blood pressure. Volitional or behavioral input on breathing are absent during sleep; only brainstem neurons, peripheral chemoreceptors and respiratory muscle afferents regulate breathing. 3 Groups of chemoreceptive neurons in the brainstem, including those of the dorsolateral pons, nucleus solitarius and ventral medullary respiratory column, respond to changes in the partial pressure of carbon dioxide and oxygen and thereby serve as a pacemaker regulating the breathing rhythm. 4 Along with effects on the breathing pattern, these brainstem neurons cause a reduction in the upper airway tone at sleep onset through reduced activity of airway dilator muscles, especially the genioglossus, which forms the bulk of the tongue. 3 Alternatively, the chemoreceptive neurons of the brainstem can detect increased carbon