Sudden Infant Death Syndrome (SIDS) Essay -- Crib Death SIDS

Sudden Infant Death Syndrome (SIDS) Sudden Infant Death Syndrome (SIDS) or "crib death" is an abrupt and inexplicable death of an apparently healthy infant. Most of the cases involve infants from ages 1-12 months, and the event occurs during the night. Various theories have been postulated from research results but without consistency of the etiology. Since the death is sudden, prior diagnostic criteria or patterns are not available for correlation, although some near-miss infants have been followed. A number of possibilities have been documented in current literature, to include beta-endorphin changes, abnormal temperature regulation, pineal abnormalities, carotid body irregularities, lead poisoning, elevated fetal hemoglobin, brainstem immaturity, and cerebral hypoperfusion. The following is an overview of these pathologies in their relation to Sudden Infant Death Syndrome. As with most physiological processes, several intermediate steps can lead to a certain event, thus making the mechanism more controlled. However, as more steps that are required, there arises a greater number of possible problems. SIDS is no exception. Most literature supports the view that victims of SIDS suffer a failure of the automatic control of respiration, producing periodic apnea and eventually death. Neural control of respiration involves three anatomical structures (Armstrong et al., 1982~. The first is the motor system, which contains the neurons which initiate and maintain respiration. These include the dorsal motor nucleus of the vague, the nucleus tractus solitarius, the nucleus ambiguous, the nucleus retro-ambiguous, the reticulo-spinal tracts in the anterior and lateral columns and the anterior horn cells of the cervical and thora... ...16:1122-1126, 1978. Koceard-Varo, G. The physiological role of the pineal gland as the masterswitch of life, turning on at birth breathing and geared to it the function of the autonomic nervous system. The cause of SIDS examined in this context. Medical Hypothesis, 34:122-126, 1991. Myer, E., Morris, D., et. al. Increased cerebrospinal fluid beta-endorphin immunoreactivity in infants with apnea and in siblings of victims of Sudden Infant Death Syndrome. J. Pedia., 111:660-666, 1987. Quattrochi, J., McBride, P., and Yates, A. Brainstem immaturity in Sudden Infant Death Syndrome: A quantitative rapid Golgi study of dendritic spines in 95 infants. Brain Research, 325:39-48, 1985. Takashima, S., Armstrong, D., Becker, L., et. al. Cerebral hypoperfusion in the Sudden Infant Death Syndrome? Brainstem gliosis and vasculature. Ann. Neurol., 4:257-262, 1978.