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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A hypothesis is present that explains Sudden Infant Death Syndrome (SIDS) as an outcome of biological immaturity. This hypothesis fits the known characteristics of SIDS and does not conflict with other possible explanations of its genesis.
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PMID:Generalized view of the origins of the sudden infant death syndrome. 229 83

A 15-year-old boy with 18 q-syndrome manifesting a status epilepticus is reported. He has been already diagnosed as epilepsy because of grand mal seizures at six months earlier, and abnormal EEG findings. Unilateral status epilepticus developed at 15 years of age, which were characterized by alternative repetition of horizontal nystagmus to the right and clonic convulsion of the right (mainly upper) extremities every several minutes. Ictal EEG showed continuous 2 Hz high voltage slow waves superimposed by spikes and polyspikes which transformed to localized, irregular spike discharges in the left occipital region at the end of the status. The chromosomal study revealed a partial deletion of the long arm of No. 18. He had severe mental retardation, and a typical karyotype for 18 q-syndrome with reduced prominence of the midface region, short stature and whorls on all finger tips. The immaturity of the brain probably relates to this kind of unilateral status epilepticus.
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PMID:[A case of 18 q-syndrome associated with status epilepticus]. 280

Epidemiological studies indicate that the incidence of seizures is highest early in life. This report discusses the experimental data derived from studies of focal epileptogenesis of the immature brain in tandem with ongoing maturational changes. During development, neurons have characteristic neurophysiological properties. Local interictal discharges are long in duration, lack a stereotypic morphology, and have limited fields. Yet the immature brain is very susceptible to the development of bilateral, although asynchronous, seizures and status epilepticus induced by amygdala kindling or by convulsant drugs. This increased seizure susceptibility may be due to a functional immaturity of a substantia nigra, GABA-sensitive output system. The morbidity of convulsions occurring early in life may not be as grave as previously thought in terms of subsequent acquisition of "normal" developmental milestones. The propensity to develop recurrent convulsions in adulthood is not related to the severity of a single seizure in infancy. Although multiple severe seizures may predispose animals to the development of seizures later in life, this is not a unique feature of the immature brain, since it also occurs in the adult brain. Finally, there is evidence that the immature brain may respond to anticonvulsant drugs differently from its mature counterpart; these findings emphasize the need to develop new antiepileptic therapies that take into account the maturational state of the brain.
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PMID:Epileptogenesis and the immature brain. 330 93

Animal experimental studies conducted at the turn of the century resulted in the use of magnesium sulphate as an anticonvulsant in humans. In U.S. clinics, parenteral administration of magnesium sulphate became a routine procedure in the treatment of eclampsia and pre-eclampsia. This treatment has proved very effective in treating convulsions in pregnancy provided an adequate dosage was given amounting to up to 60 g daily. Mother and infant mortality were largely eliminated. Numerous clinical studies showed a negligible side effect rate. Side effects in the foetus: These are due to penetration of magnesium into the foetal blood circulation. Reports on an inhibition of cardiac rate fluctuation and changes in calcium levels have been contradictory, and hence not generally accepted. It is claimed that the parathormone level may drop slightly. Isolated reports on foetal magnesium intoxications associated with depression of breathing, slackness and hyporeflexia often prompt the conclusion that this disease pattern had been due to immaturity and asphyxia. Generally, foetal magnesium blood levels do not correlate well with signs of magnesium intoxication. Urine excretion is greatly slowed down in foetal immaturity. Side effects in the mother: Short-term relaxing action on the uterus has been described frequently. High dosages have been successfully used in arresting labour if there is a tendency to premature birth. Increase in uterine blood flow was seen after administration of magnesium sulphate in animal experiments. Magnesium is said to reduce blood coagulation by influencing fibrinolysis and thrombocyte resistance. However, a somewhat enhanced loss of blood during birth is said to be more likely due to relaxation of the uterus than to a disturbance of blood coagulation. Rapid intravenous injection causes short-term flushing, nausea and vomiting. Short-acting drops in blood pressure are possible. The cardiac output is said to increase at the conventional dosage level whereas the peripheral resistance drops due to vasodilation. Increases and decreases in heart rate have been reported, but in most cases no changes were seen. Changes in ventricular action time occur with toxic doses only, which can lead to cardiac arrest in the diastole. Other toxic signs are hyporeflexia, depressed breathing and CNS depressions which may result in coma. Hyporeflexia always occurs before the other toxic signs appear, so that it can be used as a clinical control criterion. Calcium gluconate, given via the IV route, is a good and rapid-acting antidote.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Use of magnesium sulfate as an anticonvulsant in severe pregnancy toxemia and eclampsia]. 655 75

A three-component, competing-risk mortality model, developed for animal survival data, fits human life table data for all ages over a range of mean life spans from 16 to 74 years. The competing risks are a novel exponentially-decreasing hazard, dominant during immaturity; a constant hazard, dominant during adulthood; and an exponentially increasing Gompertzian hazard, dominant during senescence. By fitting the model to a specific life table using non-linear techniques, estimates of the five model parameters and their standard errors obtain; the proportion of deaths expected from each hazard alone may then be calculated. Preliminary analysis of 13 life tables indicates that for human populations under heavy stress, with very short mean life spans of about 20 years, the three hazard components account for roughly equal numbers of deaths; for modern populations, with mean life spans of about 75 years, nearly all deaths are due to the hazard of senescence. Factor analysis of the correlation matrix of parameter values for the 13 populations shows a two-factor structure. One factor involves only the multiplicative constants (initial values) of the three hazards, but not the hazard rates of change; the second factor involves only the parameter of the immaturity hazard and the rate of acceleration of the senescence hazard, but not the constant hazard nor the multiplicative constant (initial value) of the senescence hazard.
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PMID:Parameters of mortality in human populations with widely varying life spans. 664 50

The reported incidence of Bronchopulmonary dysplasia (BPD) varies from 5% to 68%. The different criteria used to define BPD are responsable for these discrepancies: some Authors include only patients with a clinical and radiological picture that fits the stage IV, as originally described by Northway, others use a more liberal approach and include all patients with manifestations of chronic pulmonary disease. We observed BPD in 12 of 22 (54%) survivors infants of very low birth weight (mean 1115 gm) and gestational age (mean 29,2 weeks). The infants were all born between November 1979 and March 1981. According to Ehrenkranz et al., we classified the radiological findings as severe, moderate and mild. We believe that the etiology of BPD in very low birth weight infants is multifactorial. However, pulmonary oxygen toxicity and immaturity are the most important causes.
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PMID:[Bronchopulmonary dysplasia in very low birth weight infants]. 692 45

The purpose of this study was to investigate the developmental differences in seizure susceptibility in mice and the roles of the histaminergic neuron system in inhibition of convulsions in development. First, we studied developmental differences in electrically-induced seizures. Since the 14-day-old mice showed a different seizure pattern from that of older mice, we evaluated the seizure susceptibility of mice older than 21 days. The durations of all the convulsive phases were significantly increased in 21- and 30-day-old mice, compared with older mice. Second, pyrilamine (or mepyramine), ketotifen, and d-chlorpheniramine, centrally-acting H1-antagonists, increased the durations of all the convulsive phases in the 21- and 30-day-old mice, but did not increase duration in 42-day-old mice. Terfenadine and astemizole, H1-antagonists that hardly enter the brain, did not affect the durations of all the convulsive phases in 21-, 30- and 42-day-old mice. The proconvulsant effect of centrally-acting H1-antagonists in 21- and 30-day-old mice were considered to be mediated via the central H1-receptors. Thus, the histaminergic neuron system may have an important physiological role in inhibition of seizures in 21- and 30-day-old mice which have higher seizure susceptibility. This would compensate for the immaturity of the other protective neuron systems such as NMDA receptor complexes and GABA receptors. In conclusion, the present findings support the view that the central histaminergic system plays a role in inhibition of convulsions.
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PMID:Proconvulsive effects of histamine H1-antagonists on electrically-induced seizure in developing mice. 787 Oct 20

In an attempt to identify causes of perinatal mortality and thence devise preventative strategies on the island of Jamaica, a study was made of the 1847 singleton perinatal deaths occurring over the 12-month period between 1 September 1986 and 31 August 1987. Complications of the pregnancy were elicited by questioning the mother as well abstracting data from the antenatal and clinical obstetric records. The deaths were classified using the Wigglesworth categorisation and the three largest groups were chosen for special study: antepartum fetal deaths, deaths of live birth from immaturity and deaths from intrapartum asphyxia. The medical features of the pregnancies were compared with data similarly obtained from 9919 women delivering singletons in the 2 months of September and October 1986 and who survived the first week of life. Unadjusted statistically significant associations were found with maternal syphilis, vaginal infection or discharge, bleeding in the first two trimesters, bleeding in the third trimester, lowest haemoglobin, highest diastolic and first diastolic blood pressures, highest level of proteinuria, diabetes and antenatal eclampsia. Logistic regression taking account of social, environmental and health behaviour variables showed the following significant relationships. Antepartum fetal death was associated with adjusted odds ratio (AOR) for syphilis 2.88 [95% confidence interval (CI): 1.91, 4.32], bleeding in third trimester 3.86 [2.73, 5.44], highest diastolic blood pressure (P < 0.0001), highest level of proteinuria (P < 0.0001), lowest Hb (P < 0.0001) and antenatal eclamptic fits AOR 4.62 [1.47, 14.50]. Deaths from immaturity were independently associated with bleeding < 28 weeks AOR 3.50 [2.39, 5.13], bleeding 28 + weeks AOR 1.93 [1.16, 3.22], highest diastolic blood pressure (P < 0.01) and highest level of proteinuria (P < 0.0001). Infection featured in deaths associated with intrapartum asphyxia, with syphilis AOR 2.17 [1.44, 3.26] and vaginal infection/discharge (P < 0.01) independently associated; other strong associations were bleeding < 28 weeks AOR 2.10 [1.57, 2.81], bleeding 28 + weeks AOR 2.32 [1.62, 3.33], highest diastolic blood pressure (P < 0.0001), first diastolic blood pressure (P < 0.0001) and antenatal eclampsia AOR 6.70 [2.63, 17.13]. For all perinatal deaths combined, independent features were syphilis AOR 2.06 [1.49, 2.85], vaginal infection/discharge (P < 0.001), bleeding < 28 weeks AOR 2.01 [1.60, 2.53], bleeding 28 + weeks AOR 2.65 [2.02, 3.48], highest diastolic blood pressure (P < 0.0001), first diastolic blood pressure (P < 0.0001), proteinuria (P < 0.0001) and antenatal eclampsia AOR 4.22 [1.76, 10.14]. The results help identify areas for monitoring and identifying pregnancies at highest risk.
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PMID:Medical conditions present during pregnancy and risk of perinatal death in Jamaica. 807 3

Benign neonatal familial convulsions comprise a distinct epileptic syndrome with an autosomal mode of transmission. The electroclinical signs of seizures in this syndrome are not yet well defined. In 3 children from two families presenting with benign neonatal familial convulsions, 14 seizures were recorded during electroencephalographic (EEG)-video sessions. All seizures occurred during sleep, after a short arousal reaction. Seizures started with bilateral, symmetrical flattening of the EEG for 5 to 19 seconds; simultaneously there was apnea and tonic motor activity. The EEG flattening was followed by a long (1-2-minute) bilateral discharge of spikes and sharp waves; simultaneously, there were vocalizations, chewing, and focal or generalized clonic activity. The prominence of EEG and motor abnormalities varied between the left and the right from one seizure to the next in any given child. The seizures stopped without EEG or clinical postictal depression. These electroclinical observations suggest that the convulsions of benign neonatal familial convulsions are a form of generalized tonic-clonic seizure whose expression may be asymmetrical, probably because of the immaturity of the corpus callosum or other structures ensuring seizure synchronization.
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PMID:Electroclinical signs of benign neonatal familial convulsions. 825 May 33

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.
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PMID:Pathophysiological mechanisms of brain damage from status epilepticus. 838 2


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