The precise mechanisms for SIDS, or “crib death,” are not known, although multiple hypotheses have been proposed over the years, including abnormal brainstem respiratory control of arousal, dysautonomia, and malignant cardiac bradyarrhythmias or tachyarrhythmias.2–4 Genetic, developmental, and environmental risk factors for SIDS have been identified, such as premature birth, multiple gestations...

Dear Editor, The sudden infant death syndrome (SIDS)–critical diaphragm failure (CDF) hypothesis (1,2) continues to attract attention 5 years after the publication of the original article in this journal, and several colleagues have contributed perspectives and insights to the hypothesis (3–6). The basic premise of the SIDS-CDF hypothesis is that the diaphragm is a vital organ that must continu...

CONTEXT The serotonergic (5-hydroxytryptamine [5-HT]) neurons in the medulla oblongata project extensively to autonomic and respiratory nuclei in the brainstem and spinal cord and help regulate homeostatic function. Previously, abnormalities in 5-HT receptor binding in the medullae of infants dying from sudden infant death syndrome (SIDS) were identified, suggesting that medullary 5-HT dysfunct...

Genetic studies in Sudden Infant Death Syndrome (SIDS) have been motivated by clinical, epidemiological, and/or neuropathological observations in SIDS victims, with subsequent pursuit of candidate genes in five categories: (1) genes for ion channel proteins based on electrocardiographic evidence of prolonged QT intervals in SIDS victims, (2) gene for serotonin transporter based on decreased ser...

BACKGROUND The pathomechanism of sudden infant death syndrome (SIDS) has not been clarified yet. The high rate of early progenitor cells in carotid body has been reported as a pathognomic feature for SIDS. AIM AND STUDY DESIGN: The morphometric analysis was done by NIKON Eclipse microscope with a morphometric program Lucia G. SUBJECTS This study was designed to investigate the structure and d...

OBJECTIVE Vaccination does not cause sudden infant death syndrome (SIDS). However, SIDS peaks at 2 months of age, when vaccination encounters are frequent. There are no published estimates using population data on age of death and immunization coverage to indicate to practitioners how often coincident vaccination may occur by chance. This study aimed to determine the probability that an Austral...

The authors investigated risk profiles of sudden infant death syndrome (SIDS) as a function of age at death. A case-control study carried out in the Tyrol region of Austria enrolled 99 infants who died of SIDS between 1984 and 1994 and 136 randomly selected controls. Early and late SIDS (< 120 days of age vs. > or = 120 days) were defined according to the clear-cut bimodal age-at-death distribu...

The association between Long QT syndrome (LQTS) and sudden infant death syndrome (SIDS) remains highly topical and even polarizing. Because the landmark Italian study of the QT interval and SIDS triggered extensive controversy, there has been a substantial and commendable effort to establish LQTS as one of the true causes of SIDS. The motivation underlying this effort is based on the fact that ...

UNLABELLED Despite the large reduction in SIDS mortality, which occurred in the early 1990s following the 'Back to Sleep' campaigns, SIDS remains the leading cause of death in the postneonatal age group. This paper describes the position in the 1980s, the contribution of the New Zealand Cot Death Study, what should be recommended and the current research priorities. CONCLUSION SIDS is prevent...

This study was designed to assess whether development of the central nervous system (CNS) is delayed in victims of the sudden infant death syndrome (SIDS). We selected the parameter of myelination because it is a continuously changing and readily accessible marker of CNS development in the SIDS age-range. We assessed myelination blindly in 61 SIDS and 89 autopsy controls. In 62 sites the degree...