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

This paper is a study of child abuse and neglect from the perspective of the child. Generally, the mistreatment of children was associated with "poor care" from parents, attributed mainly to immaturity, marital problems, alcohol abuse, unemployment, drug abuse and lack of money. Differences in attribution are noted between males and females, and some differences are noted by the age of the child. When factors other than the causes given by the children were taken into account, mistreatment was significantly related to family break-up, as well as long-term disinterest and lack of affection from the parents. When the children were asked for their "worst experience in life," the most common responses were "abuse" "family break-up," and for the juvenile offenders "getting charged with a crime."
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PMID:Causes of child abuse and neglect. 139 16

Data on 178 term and 34 preterm infants born to methadone-maintained mothers were analyzed to assess the effects of neonatal opiate abstinence in infants of varying gestational ages. More mothers in the term group (79%) than in the preterm group (53%) had abused other drugs during pregnancy (p less than 0.001). Mean (+/- SD) gestational age was 39.5 weeks +/- 1.4 for term infants and 34.3 weeks +/- 2.6 for preterm infants. On the basis of a semiobjective symptom scoring scale, term infants had more severe abstinence symptoms and more prominent central nervous system manifestations than preterm infants. The severity of abstinence symptoms correlated with maternal methadone dosage in both term and preterm infants. Maternal multiple drug abuse (e.g., heroin, cocaine) did not influence severity of abstinence symptoms in either group. More term infants (145/178) than preterm infants (20/34) required treatment for these symptoms (p less than 0.005). In 13 of 178 term infants, compared with 1 of 34 preterm infants, abstinence-related seizures developed. Peak severity occurred 1 to 2 days earlier in term than in preterm infants. A less severe abstinence syndrome in preterm infants may be due to (1) developmental immaturity of either dendritic ramifications, specific opiate receptors, or neurotransmitter function, or (2) reduced total drug exposure during the intrauterine period.
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PMID:Neonatal opiate abstinence syndrome in term and preterm infants. 204 Sep 31

This discussion addresses the questions of the parinatal, neonatal, and infant health and development of children born to adolescent mothers as related to other biologic and social factors. Medical and legislative plans for adolescent mothers and their infants must be based on assessment of both mortality and morbidity of the infants born to adolescent mothers. Focus here is on neonatal data on 55,711 pregnancies collected by the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke; neonatal data from the University of Kansas Medical Center covering 4000 pregnancies, 770 of which were gestations in teenage mothers; and obstetric, perinatal, and neonatal data concerning 6087 pregnancies in 1976, 1977, and 1978 at the Regional Perinatal Center at the University of Rochester. Ample evidence suggests a strong association between maternal age and birth weight. In particular, Hardy and Mellits found a higher frequency of low birth weight infants born to young black women. Interactions with other variables, including parity, clearly illustrate that firstborn infants are lighter than subsequent infants up to a maternal age of 35. Hoffman et al. have demonstrated that American women 18 years and under show a tendency to have infants of shorter gestational age than women 19-24 years of age. Cigarette smoking, alcohol and drug abuse, prolonged rupture of membranes, seizure disorders, and gonorrhea were significantly more frequently diagnosed in teenage mothers. The studies showed that behavioral and medical complications in the mothers were more powerful determinants of infants born with weight of less than 2500 gm than maternal age alone. In sum, when maternal and fetal growth retarding factors are taken into account among mothers of specific age categories, no biologic disadvantage appears unique to adolescent mothers. Findings fail to support the often expressed view that the mother's biologic immaturity is the main factor responsible for excessive fetal and neonatal deaths in infants born to very young mothers. Proportionately more infants born to adolescent mothers required admission to the intensive care or special care nurseries at the University of Rochester hospital than did infants born to mothers in their 20s (15.77% versus 13.9%). The data suggest that the mothering skills and child rearing practices of adolescent childbearing women have yet to be evaluated adequately.
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PMID:The infants of adolescent mothers. 736 May 10

Although initiation of drug abuse occurs primarily during adolescence, little is known about the central effects of nicotine and other abused drugs during this developmental period. Here evidence, derived from studies in rodents, is presented that suggests that tobacco use initiation during early adolescence results from a higher reward value of nicotine. The developmental profiles of the rewarding effects of other abused drugs, such as cocaine, differ from that of nicotine. Using in situ hybridization to quantify mRNA levels of the immediate early gene, cfos, the neuronal activating effects of nicotine in limbic and sensory cortices at different developmental stages are evaluated. Significant age changes in basal levels of cfos mRNA expression in cortical regions are observed, with a peak of responding of limbic cortices during early adolescence. A changing pattern of nicotine-induced neuronal activation is seen across the developmental spectrum, with unique differences in both limbic and sensory cortex responding during adolescence. An attentional set-shifting task was also used to evaluate whether the observed differences during adolescence reflect early functional immaturity of prefrontal cortices that regulate motivated behavior and psychostimulant responding. The finding of significantly better responding during adolescence suggests apparent functional maturity of prefrontal circuits and greater cognitive flexibility at younger ages. These findings in rodent models suggest that adolescence is a period of altered sensitivity to environmental stimuli, including abused drugs. Further efforts are required to overcome technical challenges in order to evaluate drug effects systematically in this age group.
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PMID:Adolescent development of forebrain stimulant responsiveness: insights from animal studies. 1525 85

Risk taking behavior increases during adolescence, which is also a critical period for the onset of drug abuse. The central serotonergic system matures during the adolescent period, and its immaturity during early adolescence may contribute to adolescent risk taking, as deficits in central serotonergic function have been associated with impulsivity, aggression, and risk taking. We investigated serotonergic modulation of behavior and presynaptic serotonergic function in adult (67-74 days old) and adolescent (28-34 days old) male rats. Fenfluramine (2 mg/kg, i.p.) produced greater anxiogenic effects in adult rats in both the light/dark and elevated plus maze tests for anxiety-like behavior, and stimulated greater increases in extracellular serotonin in the adult medial prefrontal cortex (mPFC) (1, 2.5, and 10 mg/kg, i.p.). Local infusion of 100 mM potassium chloride into the mPFC also stimulated greater serotonin efflux in adult rats. Adult rats had higher tissue serotonin content than adolescents in the prefrontal cortex, amygdala, and hippocampus, but the rate of serotonin synthesis was similar between age groups. Serotonin transporter (SERT) immunoreactivity and SERT radioligand binding were comparable between age groups in all three brain regions. These data suggest that lower tissue serotonin stores in adolescents limit fenfluramine-stimulated serotonin release and so contribute to the lesser anxiogenic effects of fenfluramine.
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PMID:Adolescent male rats are less sensitive than adults to the anxiogenic and serotonin-releasing effects of fenfluramine. 2310 47

Adolescence, defined as a transition phase toward autonomy and independence, is a natural time of learning and adjustment, particularly in the setting of long-term goals and personal aspirations. It also is a period of heightened sensation seeking, including risk taking and reckless behaviors, which is a major cause of morbidity and mortality among teenagers. Recent observations suggest that a relative immaturity in frontal cortical neural systems may underlie the adolescent propensity for uninhibited risk taking and hazardous behaviors. However, converging preclinical and clinical studies do not support a simple model of frontal cortical immaturity, and there is substantial evidence that adolescents engage in dangerous activities, including drug abuse, despite knowing and understanding the risks involved. Therefore, a current consensus considers that much brain development during adolescence occurs in brain regions and systems that are critically involved in the perception and evaluation of risk and reward, leading to important changes in social and affective processing. Hence, rather than naive, immature and vulnerable, the adolescent brain, particularly the prefrontal cortex, should be considered as prewired for expecting novel experiences. In this perspective, thrill seeking may not represent a danger but rather a window of opportunities permitting the development of cognitive control through multiple experiences. However, if the maturation of brain systems implicated in self-regulation is contextually dependent, it is important to understand which experiences matter most. In particular, it is essential to unveil the underpinning mechanisms by which recurrent adverse episodes of stress or unrestricted access to drugs can shape the adolescent brain and potentially trigger life-long maladaptive responses.
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PMID:Controversies about the enhanced vulnerability of the adolescent brain to develop addiction. 2434 19

Alcoholism, which is defined as the recurring harmful use of alcohol despite its negative consequences, has a lifetime prevalence of 17.8%. Previous studies have shown that chronic alcohol consumption disrupts various brain functions and behaviours. However, the precise mechanisms that underlie alcoholism are currently unclear. Recently, we discovered "pseudo-immature" brain cell states of the dentate gyrus and prefrontal cortex (PFC) in mouse models of psychotic disorders and epileptic seizure. Similar pseudo-immaturity has been observed in patients with psychotic disorders, such as schizophrenia and bipolar disorder. Patients with alcoholism occasionally exhibit similar psychological symptoms, implying shared molecular and cellular mechanisms between these diseases. Here, we performed a meta-analysis to compare microarray data from the hippocampi/PFCs of the patients with alcoholism to data from these regions in developing human brains and mouse developmental data for specific cell types. We identified immature-like gene expression patterns in post-mortem hippocampi/PFCs of alcoholic patients and the dominant contributions of fast-spiking (FS) neurons to their pseudo-immaturity. These results suggested that FS neuron dysfunction and the subsequent imbalance between excitation and inhibition can be associated with pseudo-immaturity in alcoholism. These immaturities in the hippocampi/PFCs and the underlying mechanisms may explain the psychotic symptom generation and pathophysiology of alcoholism.
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PMID:Transcriptomic immaturity of the hippocampus and prefrontal cortex in patients with alcoholism. 2829 46

Evidence obtained in recent decades has demonstrated that the brain still matures in adolescence. Changes in neural connectivity occur in different regions, including cortical and subcortical structures, which undergo modifications in white and gray matter densities. These alterations concomitantly occur in some neurotransmitter systems and hormone secretion, which markedly influence the refinement of certain brain areas and neural circuits. The immaturity of the adolescent brain makes it more vulnerable to the effects of alcohol and drug abuse, whose use can trigger long-term behavioral dysfunction. This article reviews the action of alcohol and drug abuse (cannabis, cocaine, opioids, amphetamines, anabolic androgenic steroids) in the adolescent brain, and their impact on both cognition and behavioral dysfunction, including predisposition to drug abuse in later life. It also discusses recent evidence that indicates the role of the neuroimmune system response and neuroinflammation as mechanisms that participate in many actions of ethanol and drug abuse in adolescence, including the neurotoxicity and alterations in neurocircuitry that contribute to the dysfunctional behaviors associated with addiction. The new data suggest the therapeutic potential of anti-inflammatory targets to prevent the long-term consequences of drug abuse in adolescence.
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PMID:Impact of neuroimmune activation induced by alcohol or drug abuse on adolescent brain development. 3046 86