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

Several studies in the last ten years have been directed towards a better understanding of sleep disorders in childhood. Defining sleep disorders in this age is difficult in dependence of relevant differences in sleep patterns at subsequent developmental stages. In new-borns total sleep time is fairly equal during night and day. Normally, day-time sleep gradually decreases over the first three years of life, such that night-time sleep progressively increases till the age of four, and similar to adult sleep-time by adolescence. The most frequent sleep disorders observed in childhood are parasomnias, that, thought to be a CNS sign of immaturity, tend to be quite predictable, recurring in the same families and not even influenced by environmental stimuli. These disorders included: a) arousal disorders, that generally emerge from delta sleep or relate to arousals occurring during NREM sleep, very common in childhood and fairly common in adulthood either; b) somnambulism and somniloquy, that have many common characteristics: first of all, they have the potential to generate a great sense of discomfort and fear in parents watching a child who suddenly sits up in bed eyes-opened but 'unseeing'; c) nocturnal enuresis, that is substantially not a problem of depth of sleep, despite many parents believe. Although narcolepsy is more common in adolescence, many studies have demonstrated that narcoleptic symptoms may begin in childhood. Narcoleptic symptoms in children are similar in their appearance to those predominant in adults, but their expression may be different because of CNS maturational factors. Historical descriptions of the OSAS evidenced since the beginning the importance of neurobehavioral complications associated with the cessation of airflow at the nose and mouth accompanied by respiratory effort, deriving from upper airway obstruction which occurs during sleep.
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PMID:Sleep disorders in childhood: a review. 1216 81

Apnea of prematurity (AOP) remains a major clinical problem in present day neonatology that warrants frequent evaluations and imposes challenges in therapeutic strategies. Although the pathogenesis of AOP is poorly understood, it is probably a manifestation of physiologic immaturity of breathing control rather than a pathologic disorder. Immature breathing responses to hypoxia, hypercapnia and exaggerated inhibitory pulmonary reflexes in preterm infants might also contribute to the occurrence or severity of AOP. Recent data suggest a role for genetic predisposition. Although typically resolve with maturation, the role of bradycardia and desaturation episodes associated with AOP in the development of sleep disorder breathing and neurodevelopmental delay needs further clarification. Pharmacological treatment with methylxanthines and CPAP remain the mainstay for treatment of AOP. However, recent studies have implicated central inhibitory neuromodulators including prostaglandins, GABA and adenosine in its pathogenesis, the fact that might provide future specific targets for treatment. This review will summarize new insights involving these issues as well as others involving the pathogenesis, treatment strategies and consequences of apnea in premature infants.
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PMID:Neonatal apnea: what's new? 1878 Mar 39

Apnea of prematurity (AOP) is a developmental sleep disorder which is yet to be completely understood. Although there is some evidence of brainstem immaturity, there is nothing to suggest that infants with AOP have gross deficits in respiratory control. It appears, however, that the early (and frequent) occurrence of hypoxemia during apnea in preterm infants is related to their low expiratory lung volume, which falls even further during apnea, while the accompanying bradycardia results from this combination of apnea and hypoxemia. Feeding is an important trigger for AOP. While hypoxemia during feeding is most likely related to an immature coordination between sucking, swallowing and breathing and potentially also to an immature laryngeal chemoreflex, hypoxemia after feeding may be caused by diaphragmatic fatigue; gastro-esophageal reflux only rarely plays a role. The time course of AOP, i.e., its increased occurrence during the second and third rather than the first week of life, together with data from physiological studies, also suggests a role for diaphragmatic fatigue. Additional factors include upper airway obstruction, persistence of the fetal response to hypoxia, i.e., ventilatory depression, and the close proximity between the eupneic and apneic CO(2) thresholds in neonates. Observational data cannot provide definite answers on cause-and-effect issues but may provide a starting point for further studies into mechanisms involved in AOP and for the development of new therapeutic interventions. First, however, we need to better define how much AOP can be tolerated in an infant without endangering neurodevelopment.
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PMID:Apnea of prematurity: What can observational studies tell us about pathophysiology? 2062 58

Sleep-disordered breathing includes disorders of breathing that affect airway patency, e.g. obstructive sleep apnoea syndrome, and also conditions that affect respiratory drive (central sleep disorders) or cause hypoventilation, either as a direct central effect or due to peripheral muscle weakness. Obstructive sleep apnoea syndrome (OSAS) is an increasingly-recognised clinical entity affecting up to 5.7% of children, which, if left untreated, is associated with adverse effects on growth and development including deleterious cognitive and behavioural outcomes. Evidence exists also that untreated OSAS impacts on cardiovascular risk. Close attention should be paid to assessment and investigation of this relatively common condition, instigating early and appropriate treatment to children with OSAS. First-line treatment in younger children is adenotonsillectomy, although other treatment options available include continuous positive airways pressure (CPAP), anti-inflammatory therapies (nasal corticosteroids and anti-leukotrienes), airway adjuncts and orthodontic appliances. Central sleep-disordered breathing may be related to immaturity of respiratory control and can be associated with prematurity as well as disorders such as Prader-Willi syndrome. In some cases, central apnoeas occur as part of a central hypoventilation disorder, which may be inherited, e.g. Congenital Central hypoventilation Syndrome, or acquired, e.g. Arnold-Chiari malformation, brain tumour, or spinal injury. The treatments of central breathing problems depend upon the underlying aetiology.
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PMID:Investigation and management of childhood sleep apnoea. 2447 Jul 27