Respiratory depression may occur after use of most opioid drugs, but only one case of prolonged apnea after intraoperative administration of the ultra-short-acting opioid, remifentanil, has been reported [1]. We present a neurosurgical patient with prolonged postoperative apnea that was probably caused by remifentanil. A 70-year-old man (height 168 cm, weight 50 kg) with a complicated history of multiple neurosurgical and radiation treatments for a parasellar chordoma underwent emergency ventriculoperitoneal shunting for acute hydrocephalus. Two weeks previously, he had undergone tracheostomy under general anesthesia with propofol, sevoflurane, and remifentanil, with no postoperative respiratory depression. The anesthetic protocol used in the instance reported here was the same as the one used previously. Anesthesia was induced with propofol 60 mg, remifentanil 0.3 µg/kg per minute, and rocuronium 30 mg and was maintained with end-tidal sevoflurane concentration 1 vol% and remifentanil 0.05–0.1 µg/kg per minute. No opioids other than remifentanil were administered. The surgery lasted 60 min and was completed without complications, with normal blood pressure and bladder temperature throughout. On awakening from anesthesia, the patient had prolonged apnea that did not respond to sugammadex but was successfully reversed by naloxone. Because of the naloxone-reversible nature of the apnea, absence of any opioids other than remifentanil, and absence of other common factors associated with delayed awakening, it is likely that the respiratory depression was caused by remifentanil. The pharmacogenetic variant suggested by Nelson et al. [1] as a cause of abnormal response to remifentanil could be excluded because there