Sudden infant death syndrome (SIDS) is a leading cause of death in infants, although the mechanisms leading to death remain unclear. Multiple theories have emerged over time, with one of the most influential hypotheses being the triple risk model. This model, first devised in 1972 and later revised in 1994 by Filiano and Kinney, is still widely used in assisting with conceptualising and understanding sudden death in infancy. This model has evolved over time, with each version stressing that SIDS is likely to occur when certain risk factors coincide, suggesting that the lethal mechanisms in SIDS are likely to be multifactorial. All versions of the triple risk model from 1972 to the present have emphasised the complexity of SIDS and serve as useful guides for current and future research into the enigma of sudden and unexpected death in infancy.

Sudden infant death syndrome remains the leading cause of death in infants under 1 year, and underlying pathophysiological mechanisms are poorly understood. The current study investigated the hypothesis that co-sleepers die more rapidly from causes such as suffocation from overlaying by comparing levels of reactive astrogliosis in the medulla of infants who died sleeping alone to those who died co-sleeping. The amount of glial fibrillary acidic protein (GFAP) staining in alone sleepers was significantly higher than shared sleepers in 3 specific areas of the medulla, the inferior vestibular nucleus, the medial vestibular nucleus and the cochlear nucleus. Given that glial fibrillary acidic protein elevations follow a delayed time course, this suggests that death in co-sleepers was more rapid, not allowing for reactive gliosis to occur. This provides evidence of pathological differences in mechanisms of death in infants who are classified as having died from sudden infant death syndrome, suggesting potential need for refinement of categorization of these cases.

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