The Serotonin Brainstem Hypothesis for the Sudden Infant Death Syndrome

Abstract

AbstractThe sudden infant death syndrome (SIDS) is the leading cause of postneonatal infant mortality in the United States today, with an overall rate of 0.39/1000 live births. It is defined as the sudden and unexpected death of an infant <12 months of age that remains unexplained after a complete autopsy, death scene investigation, and review of the clinical history. The serotonin brainstem hypothesis has been a leading hypothesis for SIDS over the last 2 decades. Our laboratory has studied this hypothesis over time with a variety of tissue techniques, including tissue receptor autoradiography, high performance liquid chromatography, Western blot analysis, immunocytochemistry, and proteomics. The purpose of this article is to review the progress in our laboratory toward supporting this hypothesis. We conclude that an important subset of SIDS infants has serotonergic abnormalities resulting from a “core lesion” in the medullary reticular formation comprised of nuclei that contain serotonin neurons. This lesion could lead to a failure of protective brainstem responses to homeostatic challenges during sleep in a critical developmental period which cause sleep-related sudden death.