Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Quantitative analysis of reticular dendritic spines was performed on rapid Golgi impregnated neurons in 7 brainstem areas from 61 sudden infant death syndrome (SIDS) and 34 control infants. Throughout the first postnatal year, mean spine density in SIDS was significantly greater than the mean density in controls (P less than 0.0001). There were significantly higher values of spine density in SIDS compared to controls (P less than 0.0001) in both term and preterm infants. Within the SIDS brainstem itself, the density of dendritic spines was significantly different (P less than 0.05) between two medullary regions and between reticular and non-reticular formation areas. Among these brainstem areas in controls, there was no significant difference. Our findings indicate an immature developmental pattern of increased dendritic spine density in the SIDS brainstem which may be responsible for abnormal central respiratory and arousal control. These significant quantitative differences in spine density are considered in the present study to represent an anatomical substrate of brainstem immaturity in the multifactorial pathogenesis of SIDS.
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PMID:Brainstem immaturity in sudden infant death syndrome: a quantitative rapid Golgi study of dendritic spines in 95 infants. 397 32

Cerebral cortical function was prospectively examined by electroencephalography (EEG) in 3 subgroups of 257 infants at risk for sudden infant death syndrome (SIDS). Group 1 consisted of apparently healthy infants with near-miss SIDS episodes; Group 2 consisted of siblings of SIDS victims; and Group 3 consisted of neurologically suspect infants with apnea. The usual abundance and distribution of sharp EEG transients (SETs) were determined from 69 Group 1 infants. EEGs were interpreted as abnormal in the presence of ictal apnea, excessively abundant SETs, or immaturity of EEG background for conceptional age. Ninety percent of infants in Group 1 had entirely normal EEGs. There was no significant difference in the abundance or distribution of SETs between infants with normal breathing patterns and those with excessively periodic respirations. Nonictal apnea was recorded in 7% of Group 1 infants. The unexpected diagnosis of ictal apnea was confirmed in 2 Group 1 infants (1.2%), and 5 (2.9%) had excessive SETs but no recorded seizures. Only 4 infants (2.3%) had abnormally immature EEGs for conceptional age. Nonictal apnea occurred in 5 of 33 (15.2%) Group 3 infants and ictal apnea was confirmed in 2 others (6.1%). We conclude that the majority of Group 1 and 2 infants have normal cerebral cortical activity between and during apnea and that central nervous system cortical immaturity, as measured by EEG, plays no important role in the pathogenesis of SIDS. SETs are commonly recorded in these infants and must be conservatively interpreted. However, an EEG examination was critical in establishing the unexpected diagnosis of ictal apnea in a small percentage of Group 1 and 3 infants and materially influenced subsequent evaluation, management, and prognosis.
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PMID:Cerebral cortical function in infants at risk for sudden infant death syndrome. 404 Nov 62

According to national mortality statistics and to epidemiologic surveys main causes of infant mortality are congenital malformations, prematurity with its immaturity related morbidity, asphyxia, and, more recently, the sudden infant death syndrome. In all these situations the full scale of possible preventive measures has not been exhausted. This applies, in particular, to disorders in the perinatal period. What is needed is a greater awareness of risks, more gynecological interest in the baby and better teamwork between gynecologist and pediatrician; this also means a more effective use of available resources. Infant mortality rate still could be reduced by 50 percent.
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PMID:[Infant mortality- course, causes, improvement possibilities]. 668 28

The study was aimed to evaluate possible relation between the probability of brain stem gliosis at the autopsy in infants who died of SIDS and of other known causes of death and some major infants characteristics. 131 infants (78 boys, 53 girls) who died in St. Petersburg in 1983 to 1989 of SIDS and 60 infants (37 boys, 23 girls) who died suddenly during the same period of time of other than SIDS known causes of death without signs of inborn malformations, tumours and intrauterine infections entered the study. Stepwise logistic regression was used in data analysis. No statistically significant association was found between the probability of brain stem gliosis and the following explanatory variables: gender, gestational and calendar age, weight at birth and at death. It was shown that the probability of brain stem gliosis depended of the cause of death (whether SIDS or not) and postconceptional age, two variables interacting. The probability of brain stem gliosis decreased with growing postconceptional age in the infants from both groups, less prominent in SIDS babies. The findings may serve an argument that delayed brain myelination and maturation is more often the case in the babies who died of SIDS, and that excessive brain stem gliosis may serve a marker of biological immaturity in a part of SIDS victims.
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PMID:Brain stem gliosis in the victims of sudden infant death syndrome (SIDS): a sign of retarded maturation? 775 48

The nasal cavities were examined in 56 cases of sudden infant death syndrome (SIDS) and 26 control cases and the following criteria were compared: inflammatory infiltration of the nasal mucosa (SIDS 59%--controls 65%; P = 0.577), diapedesis of inflammatory cells (SIDS 38%--controls 42%; P = 0.678), epithelial desquamation (SIDS 62%--controls 85%; P = 0.043); hyperemia (SIDS 66%--controls 65%; P = 0.951) and hypersecretion of the seromucous glands (SIDS 55%--controls 69%; P = 0.233). Only epithelial desquamation was found significantly more often in the controls than in SIDS cases, but these alterations are unspecific and are influenced by the postmortem interval. The intensity of rhinitis was not different between the SIDS and control groups. The frequency of rhinitis is therefore not specific for the sudden infant death syndrome, and seems to be merely a result of the high incidence of upper respiratory tract infections in this age group. We speculate, however, that infections of the nose in conjunction with other factors, such as prone position, covering of the head, hyperthermia, parental smoking and immaturity of the central nervous system, could play a role in the pathogenesis of the sudden infant death syndrome.
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PMID:Infections of the upper respiratory tract in cases of sudden infant death. 854 64

To investigate the recurrence of sudden infant death syndrome (SIDS) among siblings, the authors analyzed data for all 352,475 mothers whose first and second single births were reported to the Medical Birth Registry of Norway during 1967-1988. Recurrence of stillbirths from the 16th week of gestation onward and infant deaths other than SIDS were also studied. Relative risk of recurrence for SIDS was 5.8 (95% confidence interval (CI) 2.1-13.2); for asphyxia- and immaturity-related infant deaths, 12.5 (9.2-17.4); for congenital malformations, 7.2 (4.7-11.0); and for other causes of infant death, 8.0 (2.0-22.1). Deaths due to infections did not recur. Similar categories of infant deaths had higher overall relative risk, 9.1, compared with 1.6 for dissimilar categories. Previous early stillbirth (16-27 weeks) had a high recurrence (relative risk (RR) = 21.8, 95% CI 17.5-26.9), while late stillbirth (> or = 28 weeks) had lower recurrence (RR = 4.6, 95% CI 3.7-5.8). Previous SIDS was associated with an increased risk of all other types of loss. In contrast, previous late stillbirth and previous asphyxia- and immaturity-related infant deaths were associated with a reduced risk of subsequent SIDS (RR = 0.31, 95% CI 0.08-0.84, and RR = 0.23, 95% CI 0.01-1.13, respectively). In conclusion, as with other infant and fetal deaths, SIDS deaths showed strong sibship aggregation consistent with a genetic susceptibility in subsets of SIDS that may interact with environmental factors. The authors also suggest common pregnancy-specific risk factors for late stillbirths, asphyxia- and immaturity-related infant deaths, and SIDS.
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PMID:Population-based recurrence risk of sudden infant death syndrome compared with other infant and fetal deaths. 868 99

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 distribution. Inadequate antenatal care, low parental social and educational level, and the prone sleeping position were risk conditions that applied to both early and late SIDS. A marked seasonal variation (winter preponderance) was the most outstanding feature of late SIDS. A gestational age of < 37 weeks (odds ratio (OR) = 8.4, 95% confidence interval (CI) 2.6-26.0), repeated episodes of apnea (OR = 5.7, 95% CI 1.2-27.0), low birth weight (< 2,500 g) (OR = 3.4, 95% CI 1.1-11.0), a family history of sudden infant death (OR = 2.9, 95% CI 1.1-7.5), and maternal smoking during pregnancy (OR = 2.2, 95% CI 1.0-4.5) were associated with early SIDS. This study identified two distinct subgroups of SIDS infants characterized by different risk conditions and ages at death. These results underline a multiple-cause hypothesis for SIDS etiology which involves a genetic predisposition, immaturity in the first months of life, and environmental factors acting at various ages.
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PMID:Sudden infant death syndrome: risk factor profiles for distinct subgroups. 1020 29

SIDS (Sudden Infant Death Syndrome) is the major cause of death in young, apparently healthy, infants, yet its etiology and pathogenesis remain unknown. SIDS peaks at 2-4 months, is more prevalent in the winter months and typically occurs in the early morning hours when most babies are asleep, suggesting that sleep may be part of the pathophysiological mechanism of SIDS. The sleep patterns of infants at high risk for SIDS were analyzed to test the hypothesis that there are abnormalities specific to nighttime sleep which may be indicative of a central nervous system (CNS) deficit that contributes to a high frequency of SIDS during the night. Electrophysiological sleep variables were recorded at monthly intervals in 1-6 months-old infants during the peak age of SIDS. The risk group (R) was resuscitated from a potentially life-threatening Sudden A-Ventilatory Event (S.A.V.E.) and compared to a group of control infants (C) with no family history of SIDS. The data representing four equal time intervals from 11 p.m.-11 a.m. show an abrupt, statistically significant increase in REM sleep from 2-5 a.m. in R infants. In C infants, time spent in REM sleep after 2 a.m. becomes progressively shorter while NREM sleep is proportionately longer. From 11 p.m.-2 a.m., however, R and C infants do not differ either in the duration or in the percent of total sleep time (TST) of REM sleep. We hypothesize that these REM sleep abnormalities in vulnerable infants are indicative of a pervasive CNS immaturity. The higher prevalence of SIDS in the cold winter months and in the early morning hours, when darkness is prolonged, is discussed in relation to the possible involvement of the circadian rhythm of melatonin.
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PMID:SIDS, abnormal nighttime REM sleep and CNS immaturity. 963 61

The immaturity of the control of the autonomic nervous system has been suggested as one of the key factors in the pathophysiology of sudden infant death syndrome (SIDS). Therefore, the attenuated control of respiration may also cause more slow oscillatory breathing among infants at risk of SIDS. In this study, patterns of respiratory activity (RAV) and heart rate variability (HRV) were examined in Medilog-records prospectively obtained from 22 tape recordings made on 16 babies subsequently suffering from SIDS and from 22 matched control babies. A total of 248 signal segments, 120 s in duration, representing the state of regular breathing were visually selected for further analysis. The digitised signal sets were detrended, Fast-Fourier-transformed and autospectra as well as cross-spectra for the HRV and HRV were computed. The RAV and HRV were examined at two spectral bands: (1) a low frequency (LF) band 0.03-0.17 Hz (1.8-10 cycles/min) and (2) a high frequency (HF) band 0.3-1.3 Hz (18-90 cycles/min). Different parameters of each band were tested in the spectral analysis of cardiorespiratory control. The LF/HF-ratio of the spectral peak area of the respiratory activity and the LF/HF-ratio of the spectral band area of the respiratory activity were greater in the SIDS group when compared to the controls. No significant intergroup differences were found in the parameters of HRV, or the cross-spectral parameters. Interestingly, the technique appeared helpful in displaying that the victims of SIDS had a significantly greater amount of slow oscillation in the continuous respiratory signal (1.05+/-1.89 vs. 0.41+/-0.57, P=0.02). In the victims of SIDS the respiratory control system seems to be less stable and cause more slow oscillatory breathing and this can be detected using spectral analysis of respiratory activity even during breathing that visually seems to be regular.
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PMID:Increased amplitude modulation of continuous respiration precedes sudden infant death syndrome -detection by spectral estimation of respirogram. 1019 26

Sudden infant death syndrome (SIDS) is frequently associated with a mild infection, the incidence peaking during the third month of life. We hypothesize that the neonatal immaturity of both the acute febrile response and hypothalamus promote neonatal protection from SIDS. Vagal afferents modify the febrile response. Vagotomized rodents displayed a loss of febrile responsiveness in a 'non-sensing' brain. The failure of a 'non-sensing' brain to react to elevated blood pyrogens leads to failure of the febrile response and to a shock-like state. SIDS infants may appear well yet, within hours of this observation, may be found dead. There is a mismatch between the acute febrile response and hypothalamic hypoactivation. The discrepancy increases with development. There is an elevated cytokine response in endothelial cells which induces nitric oxide (NO) production and retarded development of the hypothalamus. Cigarette smoke also induces NO production and retards hypothalamic development by augmented apoptosis. Zinc inhibits this effect in mouse thymocytes. Fetal haemoglobin (HbF) induces hypoxia, which is a stimulator of the immune response while vasodilator gases (carbon monoxide (CO), NO) reduce hypothalamic function. The hypothalamic failure to sense elevated blood pyrogens induces toxic shock - a feature of SIDS.
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PMID:Sudden infant death syndrome: hypothalamic failure to sense elevated blood pyrogens. 1045 40


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