Chick embryos between the 15th and 20th day of incubation were subjected to hypothermia of 20°C followed by nitrogenous hypoxia until the cerebral EEG showed no fluctuations of potential. The embryos were exposed to ah 15 or 30 min later. Body temperature was raised to 30°C and maintained there for 1 hr before being raised to 36"C, during which time 2 types of sehure episodes of rhythmic waves appeared. Type I was characterized by an ontogenetically later appearance (after the 15th day), larger amplitude, spike and slow wave patterns, a frequency of .3-3.5 Hz with the slowest in the younger embryos, and a duration of 1 to several minutes. Type I1 was characterized by an earlier ontogenetic appearance, small amplitude, a frequency of 1-30 Hz, and a duration of a few seconds to several minutes. None of these seizure episodes was observed after body temperature had reached 36°C. About the 17th day of incubation, the physiological components responsible for producing EEG patterns during episodes seem to undergo an abrupt maturational change indicated by the increase in percentage of embryos undergoing Type I episodes, and by changes in frequency of waves and duration of episodes.The observation has been repeatedly made that in developing animals hypoxic stress causes the earlier cessation of function of ontogenetically newer structures in the central nervous system (