Sleep-onset central sleep apnea is not uncommon phenomenon, and is usually regarded as a normal sleep pattern. Dysrhytymic breathing is frequently seen at sleep onset. Any process that leads to frequent sleep-wake transitions over the course of the night (such as insomnia) may increase the number of central apneas. Although the exact mechanism is still unclear, rapid loss of the wakefulness drive to breathe and unstable carbon dioxide set point results in central apnea/hypopnea leading to hypercapnia which induces subsequent hyperventilation secondary to arousals. If the following hypocapnia cross the apnea threshold, then central sleep apnea resumes. In this brief review, I will address the underlying physiology influencing sleep-onset central sleep apnea and its clinical implications.