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

Respiratory adaptation during sleep improves with growth. The most vulnerable period for respiratory adaptation to sleep is from birth to 3 months of age. Factors that favor vulnerability are immaturity in ventilatory control and high rib cage compliance which impairs its effectiveness for ventilation. Improvement in respiratory adaptation during sleep is rapid during the first year of life. Sleep, and especially active (REM) sleep, is a risk period for respiratory disturbances in infants. Numerous factors may trigger apparent life threatening events. Respiratory disorders such as bronchiolitis, upper airway obstruction, and bronchopulmonary dysplasia impair respiratory adaptation during sleep. Treatment of respiratory disorders in infants must take into account the exacerbation of respiratory disturbances during sleep.
 ...
PMID:Respiratory adaptation during sleep in infants. 211 10

The aim of the present study was to examine whether immaturity of cardiorespiratory control corresponds to a less mature behavioural state pattern and/or to less efficient feeding behaviour. Fifty-four infants were observed and data polygraphically recorded for 6 hours; a feeding session was included. It was found that infants with immature cardiorespiratory control spent more time in REM-sleep, less time in the active awake state, and were more likely to be inefficient feeders. In addition, 100 infants were observed for risk signs of sudden infant death syndrome and their parents were asked to answer a questionnaire on the sleeping and feeding behaviour of their infants. The majority of the infants with immature cardiorespiratory control were described as bad feeders but good sleepers. We conclude that gathering information about sleeping and feeding behaviour is useful when screening for immaturity of cardiorespiratory control.
 ...
PMID:Feeding, behavioural state and cardiorespiratory control. 338 29

All-night sleep polygraphs, except the first night, were recorded for 15 patients with idiopathic nocturnal enuresis and 10 normal controls. Relations between sleep and the mechanism by which nocturnal enuresis is caused, with special emphasis on the occurrence of rhythmic slow waves (RSW), was studied. The following results were obtained. (a) There was no significant difference between the two groups in the proportions of the electroencephalographic (EEG) sleep stages, under the same conditions. (b) Nocturnal enuresis occurred with almost the same frequency in all sleep stages except stage 1 sleep and was higher in the second and third cycles. (c) Immediately before a nocturnal enuretic event, 6-7 Hz RSW continued for as long as 15-40 s in NREM sleep, or 3-5 Hz RSW was observed in REM sleep. (d) RSW was observed in enuretics and controls, and decreased with increase in age. However, RSW occurred more often, and age-related decrease was delayed in enuretic children. (e) RSW was induced by stimuli such as changes in sleep stages or body movement. During RSW, the variance of heart rate and respiration tended to be low. These results and the similarity between RSW and diffuse rhythmic theta suggest that RSW may be an expression of the process of maintaining a given sleep stage in children. These results may also be caused by the immaturity of the sleep mechanism in enuretic children. The long-lasting RSW on the sleep EEG was considered to be a sign of the onset of nocturnal enuresis.
 ...
PMID:Rhythmic slow wave observed on nocturnal sleep encephalogram in children with idiopathic nocturnal enuresis. 343 57

A description is first given of respiratory activity in the fetus and its control. Evidence suggests that when the fetus makes respiratory movements, it is in a state comparable to REM sleep in the newborn and adult and that in the alternating periods of apnoea, it is in quiet sleep. It does not appear that the respiratory movements are normally regulated by chemical or reflex, e.g. Hering Breuer, inputs though they are enhanced by CO2 and depressed by hypoxia. In the apnoeic periods, breathing movements are virtually impossible to elicit by chemical or reflex means. Evidence from examination of peripheral inputs indicates that: the carotid body chemoreceptors are inhibited at receptor level, stimulation of the aortic chemoreceptors affects the circulation only and although pulmonary stretch receptors are active and are excited by inflation of the fetal lung, such inflation does not affect discharge in medullary respiratory units or phrenic nerve. Since there is no real evidence of immaturity of the respiratory system in late gestation and since chemical and most reflex inputs appear to provide an adequate stimulus, it is most probable that the periods of apnoea are caused by an inhibitory process, possibly of supra-pontine origin which acts close to medullary respiratory units and effectively inhibits the operation of the automatic component. This inhibitory process may operate periodically; or continuously and be periodically overridden in REM sleep. After birth, breathing is normally continuous and sensitive to lung inflation, CO2 and after a variable delay, to hypoxia. This may be due to the lifting of the inhibitory process allowing activation of the automatic component. However, there is evidence that even in normal, full term infants, full maturation of the automatic component is not complete until about three months of age and in the meanwhile, breathing tends to be imperfectly regulated and subject to damped oscillations when disturbed.
 ...
PMID:Respiratory sensitivity before and after birth. 681 77

The pineal nonapeptide hormone arginine vasotocin (AVT) (100 ng/kg) administered intra-nasally (IN) to healthy prepubertal boys, dramatically increased the amount of REM sleep, decreased REM sleep latency, and induced REM periods at sleep onset. Neither arginine vasopressin (AVP) nor oxytocin administered IN at the dose of 100 ng/kg was able to reproduce the effects of AVT, demonstrating its high specificity. Methergoline, a selective central 5-hydroxytryptamine (5-HT) receptor blocker, administered IN at the dose of 100 ng/kg, completely prevented AVT induction of REM sleep. Fluoxetine, a specific 5-HT uptake inhibitor, administered IN at the dose of 25 microgram/kg, 10 min after AVT, greatly potentiated the effects of AVT in inducing REM periods at sleep onset and in increasing the amount of REM sleep and the percentage of dream reports. It is suggested that AVT induces REM sleep in prepubertal boys by interfering with 5-HT neurotransmission and that the high sensitivity of prepubertal boys to AVT reflects an immaturity of REM triggering centers.
 ...
PMID:REM sleep induction in prepubertal boys by vasotocin: evidence for the involvement of serotonin containing neurons. 697 70

The laryngeal chemoreflex was studied during quiet and REM sleep and wakefulness in premature newborn lambs. The response to reflex stimulation with a 5 sec-water infusion was evaluated during 30 sec, as % change in ventilation, heart rate and blood pressure. Apnea, hypertension and bradycardia were more pronounced during sleep than during wakefulness, when arousal was not associated with the stimulation. The response was similar during quiet and REM sleep. Arousal, which occurred in 24 and 31% of the tests respectively, resulted in a response comparable to that seen during wakefulness. The respiratory drive was evaluated by measurement of the mean inspiratory flow and was found to be decreased during both sleep states when compared to wakefulness. We propose that during sleep in the newborn period there is a decreased ability to respond to asphyxia possibly due to a functional immaturity of the arterial chemoreceptors. This results in a low incidence of arousal and a delayed termination of the pronounced poststimulus apnea resulting from laryngeal chemoreflex stimulation.
 ...
PMID:Reflex apnea from laryngeal chemo-stimulation in the sleeping premature newborn lamb. 711 Jul 84

Hare's (1970) REM deficit theory in psychopathy was investigated. The repeated finding of EEG slowing in waking psychopaths has been interpreted as reflecting cortical immaturity, cortical underarousal, and an intense need for sensory stimulation of psychopaths. REM sleep has been implicated in cortical maturation during development and in daily cortical maintenance. Hare postulated a possible REM deficit in psychopaths to account for their apparent cortical abnormalities. Three groups of incarcerated criminals were investigated: psychopaths with normal waking EEGs (n = 8), psychopaths with abnormal EEGs (n = 9), and nonpsychopaths with normal EEGs (n = 6). The sleep stages of each inmate were recorded for one baseline and two experimental nights. No significant differences were found in the sleep patterns of these groups using stepwise, multiple discriminant analysis. The psychopaths with abnormal EEGs tended to have the highest REM time and REM% of the inmates, contrary to Hare's theory.
 ...
PMID:REM sleep and EEG abnormalities in criminal psychopaths. 720 15

Both the pineal nonapeptide hormone arginine vasotocin (AVT) (2.5 micrograms) administered intra-nasally and the pineal indole melatonin (50 mg) administered intravenously to three male narcoleptics (two with auxiliary symptoms and one with sleep attacks only), dramatically increased the amount of REM sleep and decreased REM sleep latency. The duration of the sleep onset REM periods in the two narcoleptics with auxiliary symptoms increased by more than 100 percent after AVT and melatonin administration. In the narcoleptic with sleep attacks only both AVT and melatonin induced REM periods at sleep onset. The hypothesis is advanced that narcolepsy represents an impairment of the melatonin-AVT control in the induction and circadian organization of REM sleep associated with an immaturity of REM triggering centers.
 ...
PMID:Vasotocin, melatonin and narcolepsy: possible involvement of the pineal gland in its patho-physiological mechanism. 730 33

Phylogenetic studies in placental and marsupial mammals have demonstrated three major correlates of increased REM sleep time across these species. These are high amounts of non-REM sleep time, safe sleep conditions and immaturity at birth. While these variables explain approximately 30% of the variance in REM sleep time across these orders, these relations are violated when animals other than placentals are included. Birds are small, many have safe sleeping situations and are certainly immature at birth, yet they have less REM sleep than the vast majority of mammals. The echidna is immature at birth, has high amounts of non-REM sleep and safe sleeping conditions, yet has been reported to have no REM sleep. Our recent studies in the echidna indicate that REM and non-REM sleep did not evolve sequentially, but rather evolved as a differentiation of a primitive state which held the seeds of both sleep states. The echidna sleeps with an activated brainstem and EEG synchronized forebrain. Future studies of sleep phylogeny need to compare the behavior of key neuronal groups across the sleep cycle, since these results indicate that EEG variables and sleep state durations may given an inadequate picture of the nature of brain activity during sleep.
 ...
PMID:Phylogeny and the function of REM sleep. 754 15

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.
 ...
PMID:SIDS, abnormal nighttime REM sleep and CNS immaturity. 963 61


1 2 Next >>