The mechanisms underlying failure in sudden infant death syndrome may involve inadequate compensatory motor responses to a hypotensive challenge; the insult may result from a shock-like sequence, or from a ventilatory challenge that leads to a hypotensive event. Structures ordinarily not considered in mediating breathing or cardiovascular control, especially cerebellar-related structures, may play a critical role in compensatory responses, and underlie the position-dependent risk for SIDS. Dysfunction in affected brain areas appears to arise prenatally from a compromised fetal environment, with a nicotinic component contributing to the deficient mechanism. Physiologic characteristics of infants who later succumb to SIDS, and cardiovascular events associated with the fatal scenario suggest a failure of interaction between somatomotor and autonomic control mechanisms in infants at risk for the syndrome. A failure of compensatory motor actions to overcome a profound hypotension, perhaps mediated by cerebellar mechanisms that regulate blood pressure, may underlie-the fatal event.