The study was based on the hypothesis that cerebellar hypoxia may play a role in sudden infant death syndrome resulting in morphological changes of the cerebellar cortex, especially with respect to Purkinje cell density. In the morphological evaluation of the Purkinje cell layer, special consideration was additionally given to secondary alterations (i.e., macrophage and/or astrocyte reaction). A total of 12 sudden infant death syndrome cases were compared with an age- and sex-matched control group. The Purkinje cell density was evaluated by determining the number of these cells per surface unit on parasagittal sections in both hemispheres. The myelomonocytic and glial reaction was demonstrated by immunohistochemical methods using lysozyme as leukocyte and macrophage markers and glial fibrillary acidic protein as an astrocyte marker. Qualitatively, no alterations resembling a macrophage or glial cell reaction were detected in sudden infant death syndrome. No differences between the right and left cerebellar hemisphere could be established in the victims of sudden infant death syndrome nor in the controls. The number of Purkinje cells per 0.352 mm2 cortex was higher in the younger victims of sudden infant death (younger than 45 weeks of gestation) than in all matched controls. A statistically significant difference in Purkinje cell density, however, could not be established, and, especially, no indications of hypoxia were observed in the cerebellar cortex.