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PubMed1998

Increased density of somatostatin binding sites in respiratory nuclei of the brainstem in sudden infant death syndrome.

Sudden infant death syndrome is the primary cause of mortality in children aged one to six months in industrialized countries. Although the etiology of this syndrome is still unknown, subtle abnormalities in the neuronal circuitry involved in the control of respiratory activity are suspected. Since stereotaxic administration of somatostatin in the brainstem of rat and cat produces fatal apnea, we have compared the densities of somatostatin binding sites in the respiratory centers of 11 cases of sudden infant death syndrome and six control infants without neuronal disease. The density of binding sites was measured in 17 structures of the pons and medulla oblongata by means of quantitative in vitro autoradiography using iodinated [Tyr0,D-Trp8]somatostatin-14 as a radioligand. The density of somatostatin binding sites was significantly higher in the medial and lateral parabrachial nuclei in the sudden infant death syndrome group than in the control group. In six other nuclei, the median of the receptor density was higher in the sudden infant death syndrome group than the maximum values measured in the control group. The presence of high concentrations of somatostatin binding sites in several respiratory nuclei of the brainstem in approximately half of the sudden infant death syndrome victims suggests that the decrease in receptor density that normally occurs during ontogeny was delayed in these infants. In particular, the high level of somatostatin binding sites in the medial and lateral parabrachial nuclei of sudden infant death syndrome suggests that the delayed maturation of these receptors may be associated with a deficit of the hyperventilatory response to hypoxia.

Animals↗
PubMed2002

[Intrauterine hypoxia and sudden infant death syndrome].

Sudden infant death syndrome (SIDS) or crib or cot death are synonyms for the sudden, unexpected and unexplained death of an infant. The incidence of SIDS has been estimated to be from 1-2% to 3%. Protracted intrauterine hypoxia or recurrent hypoxic insults during fetal life undoubtedly influence the development of the central nervous structures as a tissue most susceptible to hypoxia, although well developed mechanisms of defense against hypoxia exist during the fetal life. The mechanisms underlying SIDS include neurologically compromised infants who are deprived of compensatory mechanisms during sleep, sustaining a hypoxic insult with alterations in neurotransmitter receptors within the regions involved in chemoreception and cardiovascular control. Changes in the brain result from perinatal prolonged hypoxia (persistent reticular pathways in the pons and medulla, astroglia in the brainstem, gliosis of brain nerve nuclei, defects in neurotransmitter receptors, neuronal apoptosis, microthrombosis, and hypoxic ischemic lesion). Hypoxic perinatal risk factors for SIDS included passive and active exposure to cigarette smoking in pregnancy, abuse of drugs, alcohol, coffee and medication in pregnancy, intrauterine growth retardation, perinatal hypoxia with or without resuscitation, preeclampsia, anemia in pregnancy, prematurity, multiparity, multiple pregnancy, pregnant women aged < 20 years and > 35 years, cardiocirculatory, pulmonary and endocrine diseases in pregnancy, and short time interval between two pregnancies. As cigarette smoking has been demonstrated to lead to fetoplacental insufficiency, which result in fetal hypoxia, it is concluded that hypoxia is a precondition for the occurrence of SIDS. Prenatal exposure to cigarette smoke decreases maternal red blood cell count, and concentrations of tyrosine and selenium, reduces fetal and neonatal cerebral blood flow, and increases maternal MCV, leukocytosis, especially neutrophils, monocytes and lymphocytes, maternal and fetal heart rate, systolic and diastolic blood pressure, resistance index in umbilical artery, fetal hemoglobin, cytokine, serotonine, dopamine, catecholamine, hypoxanthine, endorphin and interleukin-6. Pregnancy at a risk of hypoxia, especially in heavy smokers, is a major risk factor for SIDS, and such pregnancy requires close and intensive antenatal monitoring.

Female↗
PubMedDate not supplied

Cardiovascular causes for sudden infant death.

Although sudden infant death syndrome (SIDS) is a cause for sudden infant death, other causes should be ruled out before diagnosing SIDS. Cardiac causes for sudden infant death include viral myocarditis, congential heart disease particularly congential aortic stenosis, endocardial fibroelastosis, and anomalous origin of the left coronary artery from the pulmonary artery. Other cardiac conditions that may result in sudden death include rhabdomyomas of the heart in tuberous sclerosis and conduction system disorders. The most frequent conduction system disorders resulting in sudden death include histiocytoid cardiomyopathy, congential heart block that may be associated with maternal lupus erythematosus, arrhythmogenic right ventricular dysplasia, noncompaction of the left ventricle, and long QT syndromes.

Arrhythmias, Cardiac↗
PubMed1991

Basement-membrane thickening of the vocal cords in sudden infant death syndrome.

Sudden infant death syndrome remains the leading cause of death in infants between the ages of 1 month and 1 year. Diagnosis at autopsy is usually reached by process of elimination, as no obvious cause of death is recognized. The larynges of 23 sudden infant death syndrome victims, as well as 6 infants and 3 fetuses who died of other known causes, were examined in this study. While thickening of the basement membrane of the vocal cords was apparent in all sudden infant death syndrome victims, no such finding was present in the larynges of infants and fetuses dying of other causes. Thus, it is suggested that basement-membrane thickening may serve as a diagnostic tool for identification of sudden infant death syndrome at autopsy.

Basement Membrane↗
PubMed2002

Congenital myasthenic syndrome associated with episodic apnea and sudden infant death.

The sudden infant death syndrome has multiple etiologies. Some congenital myasthenic syndromes can cause sudden infant death syndrome by apnea, but the frequency of this etiology is unknown. We report here a young patient with sudden respiratory crises culminating in apnea followed by recovery, against a background of no or variable myasthenic symptoms without dyspnea. One sib without myasthenic symptoms and one sib who only had mild ptosis died previously during febrile episodes. Studies reported by us elsewhere traced the proband's illness to mutations in choline acetyltransferase. Here, we describe in detail the morphologic investigations and electrophysiologic findings, which point to a presynaptic defect in acetylcholine resynthesis or vesicular filling, in the proband. Analysis of DNA from a sib who previously died of sudden infant death syndrome revealed the same choline acetyltransferase mutation. Thus, mutations in choline acetyltransferase may be a cause of sudden infant death syndrome as, theoretically, could other presynaptic myasthenic disorders.

Acetylcholine↗
PubMed1996

[DTP vaccine and infant sudden death syndrome. Meta-analysis].

BACKGROUND: At the beginning of 1994, five cases of sudden infant death syndrome after DTP immunization appeared in Spain. In order to study a causal relationship a meta-analysis of the different studies that assess this possibility has been conducted. METHODS: The selection criteria was epidemiological study, case-control or cohort, assessing risk of sudden infant death syndrome in immunized versus non-immunized infants or risk of sudden infant death syndrome in recently immunized infants versus immunized infants beyond 30 days. Pooled risk ratios were calculated from adjusted risk ratios, when available, of the different studies, by a meta-analysis according the method described by Greenland. RESULTS: One cohort and four case-control studies were selected. Pooled risk ratio for immunized versus non-immunized infants was 0.67 (95% CI = 0.60-0.75). When comparing risk of sudden death syndrome in up to 30 days immunized infants versus more than 30 days immunized infants, the pooled risk ratio was 1.00 (95% CI = 0.84-1.20). CONCLUSIONS: DTP-immunization does not seem to increase the risk of sudden infant death syndrome. The risk of sudden infant death syndrome is not greater in the first thirty days following immunization. These data indicate a lack of association between DTP immunization and sudden infant death syndrome.

Case-Control Studies↗
PubMed1995

Cytokines may give insight into mechanisms of death in sudden infant death syndrome.

There are a number of postulated causes of sudden infant death syndrome, including bacterial toxins, defects in thermoregulation and hypersensitivity. This paper formulates the hypothesis that analysis of cytokine profiles in suspected sudden infant death syndrome victims may give an insight into mechanisms of death. These cytokine profiles may also help to identify specific causes of sudden infant death syndrome or indicate that different causes act in concert in individual cases.

Allergens↗
PubMed2002

Synergistic effect of influenza a virus on endotoxin-induced mortality in rat pups: a potential model for sudden infant death syndrome.

Sudden infant death syndrome is the most common cause of postneonatal infant mortality in the developed world. It is a diagnosis of exclusion with peak age of incidence between 2 and 6 mo. Fifty to 63% of these infants have a preexisting upper respiratory tract infection before death. We hypothesized that the immature immune system may be altered by a primary infection, preventing a protective response after secondary challenge. To mimic dual infection, we used a nonlethal strain of a rat-adapted influenza A virus and a sublethal dose of endotoxin to establish a model that results in pathology and death in 12-d-old rat pups similar to that seen in infants dying of sudden infant death syndrome. Mortality only occurred when specific criteria such as timing between infectious insults and developmental age of the pup were met. Results suggest that mortality is caused by a rapid systemic shock event rather than lung-specific damage. Gross pathologic findings such as lung petechiae and liquid blood around the heart on necropsy were consistent with those seen in infants dying of sudden infant death syndrome. Histopathologic lesions including subendocardial hemorrhage and mild cortical thymocyte necrosis were found with greater severity and frequency in dually challenged animals. Macrophage subpopulation in rat-adapted influenza A virus-inoculated animals was significantly elevated in the spleen at the time of death. Our model suggests that the developing immune system can be primed to respond in an exaggerated way to a second immune challenge resulting in unexpected death.

Animals↗
PubMed1997

Can risk factors for over-heating explain epidemiological features of sudden infant death syndrome?

Sudden infant death syndrome is characterized by a number of epidemiological features that have defied simple explanation. Overheating is believed to play a role in its causation. Overheating can be caused by changes in heat production, changes in insulation of the infant, or changes in the external environmental temperature. Risk factors may influence any of these variables. A model is proposed which links risk factors for overheating to the epidemiological distribution of sudden infant death syndrome. This model might account for the frequently reported association between formula-feeding and sudden infant death syndrome.

Body Temperature Regulation↗
PubMed2005

Incongruent cerebral growth in sudden infant death syndrome.

Sudden infant death syndrome remains a leading cause of post-neonatal mortality in developed countries. Its etiopathogenic mechanisms are unknown. In this neuropathologic study, we noticed that the weights of the brains of infants who died from sudden infant death syndrome (n = 97) were invariably heavier in comparison with those of a group of age-matched controls (n = 23) issuing from the same local population. Brain edema was not a major element, and there were no significant microscopic or macroscopic cerebral anomalies in the brains from either of the study groups. Head circumference did not show a parallel increase in infants with sudden infant death syndrome. The excessive brain weight might reflect abnormal cerebral development and could be detrimental to vital neural control. In a previous study, we disclosed cytokine overexpression in the brains of these victims. Whether increased brain weight is linked to cytokine up-regulation remains, however, a moot case and merits further exploration.

Brain↗
PubMed1988

Deaths from sudden infant death syndrome on public holidays and weekends.

Deaths from sudden infant death syndrome (SIDS) between 1979 and 1984 were tabulated by month for weekdays, weekends and public holidays. Examination of deaths by day of the week showed the weekend had more deaths than the weekdays (chi 2 = 26.3, df = 6, p = 0.0002) and that this pattern occurred in both the under three months and three-11 months age group. There were 40 deaths on the 78 public holidays in the six years under study. Modelling the data showed that there was no difference between the number of deaths on holidays compared to weekends.

Holidays↗
PubMed2002

[Sudden infant death syndrome].

Sudden infant death syndrome (SIDS) is a disease of unknown cause. The occurrence of SIDS is rare during the first month of life, increases to a peak between 2 and 4 months old, and then declines. The following have been consistently identified across studies as independent risk factors for SIDS: prone sleep position, sleeping on a soft surface, maternal smoking during pregnancy, young maternal age, bedsharing, prematurity and/or low birth weight, and male sex. Although the cause of the sudden infant death syndrome is multifactorial, contemporary hypotheses include defects in arousal or cardiorespiratory control. The interesting is hypothesis that prolongation of the QT interval may have a role in the pathogenesis of SIDS.

Birth Order↗
PubMed2005

Unexpected perinatal death and sudden infant death syndrome (SIDS): anatomopathologic and legal aspects.

This work intends to be a review of the recent histopathological findings elicited by research into sudden and unexpected perinatal death and sudden infant death syndrome (SIDS) that have dictated a novel approach to the inherent problems by pathologists, especially those entrusted with forensic medical authority. The new approach stems from the recent advances made in the understanding of neuro- and/or cardiac-conduction-system diseases present in unexpected perinatal death and SIDS. These demand that an accurate morphologic examination be performed of these structures, which modulate respiratory, cardiovascular, digestive, and arousal activities, in all victims of sudden death. A histopathologic study of an ample register of cases of victims of sudden death, either perinatally or in early infancy, has demonstrated frequent alterations both of the autonomic nervous system (especially hypoplasia of the arcuate nucleus) and of the cardiac conduction system (accessory atrioventricular pathways). The present research provides an in-depth study of the many still-controversial aspects underlying perinatal unexpected death and SIDS and is recommended for professionals working in the forensic field, whose greater insight into this problem will allow more complete medicolegal documentation.

Autonomic Nervous System↗
PubMed2006

[The advances in the neuropathology of sudden infant death syndrome].

Sudden infant death syndrome is known as sudden death in 12 months postnatal without obvious cause, the cause of death and differential diagnosis of still couldn't be indefinite so far. In this paper, the recent studies on the SIDS neuropathology using immunohisto-chemical technology were reviewed in order to suggest the lethal patho-physiologic derangement or mechanism in SIDS involves dysfunction of sleep-related cardio-respiratory homeostatic controls or failure to arouse. Thus the main cause of SIDS lies in central nerve system, but not unique cause.

Brain↗