A current hypothesis that the sudden infant death syndrome (SIDS) is a sleep apnea syndrome precipitated by defective control of involuntary respiration prompted the present study in which "reactive gliosis" in sections of the medulla oblongata of 45 SIDS victims was quantitated and compared with that in 20 control infants. Six anatomic regions were studied; five are related and one is unrelated to neural control of involuntary respiration. Increased numbers of "reactive" astrocytes were found in the SIDS group when the counts for all regions were combined (P = .04). Counts were also significantly higher in the SIDS victims for each of three regions alone: (1) the hilum of the inferior olivary nucleus (P = .01); (2) a lateral region (P = .02); and (3) the nucleus of the tractus solitarius (P = .03). The region with the greatest statistical difference, the inferior olivary hilum, has no recognized role in the control of involuntary respiration. There were no consistent associations between reactive astrocyte counts and specific clinical, socioeconomic, and pathologic variables. Characterization of the SIDS group whose counts exceeded that of the highest control infant also did not uncover distinguishing features. This study reinforces previous observations that, at least statistically, an abnormality of the brainstem occurs in a group of SIDS victims in contrast to a group of control infants, but also discloses considerable overlap in the numbers of such cells between these two groups.