Sudden infant death syndrome (
SIDS) is characterized by a lack of any known morphological or functional organ changes that could explain the lethal process. In the present study we investigated the hypothesis of an association between hypoxic/ischemic injury and
SIDS deaths. In a previous study, we could demonstrate by quantitative immunohistochemistry a distinct drop in
microtubule-associated protein (MAP2) reactivity in neurons of adult, human brains secondary to acute hypoxic-ischemic
injuries. Here we applied the same method on sections of the frontal cortex and hippocampus of 41 brains of infants younger than 1 year of age. For each brain area 100 selected neurons were evaluated for their MAP2 reactivity in the different layers of the frontal cortex and in the different segments of the hippocampus. Three groups were compared: (1)
SIDS victims (n = 17), (2) infants with
hypoxia/
ischemia (control group one; n = 14), (3) infants without hypoxic/ischemic injury (control group two; n = 10). The
SIDS group and hypoxic/ischemic group exhibited a general reduction in the number of MAP2 reactive neurons in comparison with the non-hypoxic/ischemic injury group. The
SIDS group also had a significantly lower (P < 0.05) number of reactive neurons in the CA2 and CA3 areas of the hippocampus than did control group two. No difference was detected between the
SIDS group and control group one. The
SIDS brains were thus found to display hypoxic/ischemic features without however providing evidence as to the cause of the
oxygen reduction.