Central sleep apnea (CSA) describes a group of conditions in which cessations in air flow occur without respiratory effort. In contrast, obstructive sleep apnea patients have ongoing respiratory effort during respiratory events. However, considerable overlap exists in the pathogenesis and clinical presentation of obstructive sleep apnea and CSA. A good working knowledge of the mechanisms underlying CSA is important for optimal clinical care. In general, CSA can be classified into those with excessive drive (eg, Cheyne-Stokes breathing) versus those with inadequate drive (eg, sleep hypoventilation syndrome). One critical factor contributing to the cessation of air flow during sleep is the concept of the apnea threshold, such that a P(aCO(2)) value below a certain level will lead to cessations in breathing. P(aCO(2)) can fall below the chemical apnea threshold when drive is excessive (eg, robust chemosensitivity) or when hyperventilation is occurring (eg, following arousal). Another important factor is the loss of the so-called wakefulness drive to breathe, such that some rise in P(aCO(2)) is likely to occur at the onset of sleep. A variety of factors contribute to this rise, including upper-airway collapse and diminished chemosensitivity (particularly during rapid-eye-movement sleep). In patients with low central drive, this further loss of drive at sleep onset can lead to marked hypercapnia in some cases. The treatment of CSA is also reviewed in some detail, including a role for positive airway pressure (eg, bi-level positive airway pressure in hypoventilation patients) and optimization of medical therapy (eg, in Cheyne-Stokes breathing). A paucity of research exists in this area, emphasizing the opportunities for young investigators who are interested in this field.