The role of auditory neural input in sudden infant death syndrome: a brief review and hypothesis

We present the hypothesis that auditory neural input is important to maintain diencephalically mediated sleep respiratory function during a critical period in infant development, and that attenuation of these stimuli due to sleep practices, sleep environment, or auditory system dysfunction may contribute to the development of sudden infant death syndrome (SIDS). It is hypothesized that severely attenuated auditory neural input leads to respiratory deregulation and/or bradycardia in the at-risk infant, leading to subsequent intermittent and chronic sleep hypoxia. The hypoxia leads to damage of the auditory system, particularly the cochlea, which further attenuates auditory neural input, leading to a potentially fatal vicious cycle. This hypothesis integrates a wide variety of epidemiological, psychophysical, acoustic and pathophysiological research related to SIDS.