Mother‐child interaction is associated with neurocognitive outcome in extremely low gestational age children

Early mother‐child interaction is one of the factors suggested to have an impact on neurocognitive development of extremely low gestational age (ELGA) children. Our aim was to examine associations of mother‐child interaction with neurocognitive outcome, neurological impairments and neonatal brain injuries in ELGA children. A prospective study of 48 ELGA children, born before 28 gestational weeks (26.3 ± 1.2 weeks, birth weight 876 g ± 194 g), and 16 term controls. Brain MRI was performed at term‐equivalent age. At two years of corrected age, the mother‐child interaction was assessed in a structured play situation using the Erickson Scales and Mutually Responsive Orientation Scales. Neurocognitive outcome was assessed with Griffiths Mental Developmental Scales (GMDS) and Bayley Scales of Infant and Toddler Development ‐ Third Edition (BSID‐III) and with Hempel neurological examination. Among ELGA children, higher quality of dyadic relationship and maternal sensitivity, responsiveness, and supportiveness were associated with positive neurocognitive outcome measured both with GMDS and BSID‐III (adjusted p < 0.05). This association remained after adjusting for mother's educational level. Neurological impairments at two years, white matter or gray matter abnormalities in MRI at term‐equivalent age, and grade III‐IV intraventricular hemorrhage during the neonatal period were not associated with mother‐child interaction. This study emphasizes the importance of the quality of mother‐child interaction after extremely preterm birth for neurocognitive development. Neonatal brain injury and neurological impairments were not associated with worse parent‐child interaction after two years.     

Cognitive development in absence epilepsy during long-term follow-up

Absence epilepsy (AE) has been associated with lower than average cognitive functioning, which are clinically relevant in some and may predispose to problems later in life. This study aimed to assess cognitive development during long-term follow-up in children with AE. Thirty-one children with AE, who had undergone two neuropsychological assessments between 2010 and 2017 were analyzed retrospectively. Cognitive measurements were 1.7 ± 0.95 years apart. The difference in neurocognitive test scores was assessed on a group level and on an individual level using reliable change methodology. Results show that sustained attention was lower at the first measurement compared to the normative mean. Sustained attention improved during follow-up and 7 out of 14 children showed improvement after correction for practice effects. Receptive vocabulary showed a decline over time, but did not differ from the normative mean. Significant lower mean group scores were present for performance IQ, perceptual organization, processing speed, simple reaction times, and visual motor integration, while being stable over time in the majority of children. Cognitive development was not associated with seizure freedom. Mild-to-severe academic underachievement was present in 65% and comorbidities that might affect learning in 38%. This study in children with AE showed improvement in sustained attention during long-term follow-up while other cognitive weaknesses persisted over time, regardless of seizure freedom.     

共情的神经生物基础

共情指个体感知或想象他人的情感, 并部分体验到他人感受的心理过程。共情包括情感共情和认知共情两个独立成分。情感共情的神经网络包括前脑岛(AI)、前扣带回(ACC)以及镜像神经系统(MNS), 认知共情的核心脑区是腹内侧前额叶(vmPFC)。共情的神经网络在个体发展中逐渐成熟并受到认知评价的调节。另外, 催产素和催产素受体基因多态性与共情密切联系。未来应该深入研究躯体感觉皮质在疼痛共情中的作用, 共情和亲身情感体验的神经网络的区别, 开展催产素改善共情缺陷个体的干预研究, 采用脑成像基因技术研究基因多态性与共情神经网络的关系以及提高共情研究范式的生态效度。     

Adolescent Neurodevelopment and Psychopathology

Adolescence is a high-risk period for the onset of psychopathology. The occurrence of depression increases markedly in the years following the onset of puberty, and most individuals who are eventually diagnosed with a psychotic disorder show a marked rise in adjustment problems during adolescence. It is well established that puberty involves increases in the secretion of gonadal hormones. More recently, research has shown that stress hormones show a similar normative rise following puberty. Accumulating findings indicate that the postpubescent period is also characterized by significant neurodevelopment; there are changes in brain structure and function that are partially a consequence of hormonal factors. Researchers are now challenged to elucidate the neural mechanisms relating postpubertal neurodevelopment with the elevations in risk for psychopathology that characterize adolescence. One plausible mechanism is the effect of hormones on gene expression. The normal neuromaturational processes observed in adolescence partially reflect the effect of gonadal hormones on the expression of genes that control brain development. Hormone surges following puberty may also trigger the expression of genes that code for brain abnormalities that give rise to mental disorders.     

The Impact of Early Life Stress on the Neurodevelopment of the Stress Response System

The focus of this article is on the impact of early life stress on the neurodevelopment of the stress response mechanisms of the brain. The functioning of the stress response system and mechanisms of neurodevelopmental change are described. The theoretical and clinical implications of the reviewed literature are discussed.     

THE AMAZING PLACENTA: EVOLUTION AND LIFELINE TO HUMANNESS

The placenta arose during mammalian evolution, which is recent in evolutionary terms. Genetic changes underlying placental development remain identifiable by the new science of comparative genomics (approximately post-2000). Randomly arising features of genomes including endogenous retroviruses and transposable elements have provided structural genes and gene-regulatory motifs responsible for innovations in placental biology. Stochastic genetic events indeed contribute to new functionality. Theologically, random mutations are part of the strategy by which the divine purpose for humanity is attained. Placental function critically underlies human brain development, and suboptimal function, associated with environmental conditions and maternal distress, contributes to mental health deficits in the offspring. Many enter life with handicaps arising from contingent events in utero, mandating understanding, compassion, and socioemotional support, imperatives native to moral including biblical values. The extended period of development afforded by placentation enables prenatal parenting, with implications for sensitive and devoted parental commitment.     

Schizophrenia: A Neurodevelopmental Perspective

Diverse lines of research suggest that schizophrenia is a genetically influenced neurodevelopmental disorder. Family, twin, and adoption studies suggest that most cases of schizophrenia involve a genetic diathesis that is necessary but not sufficient for development of the disorder. Histological, neuroimaging, and neuropsychological findings converge in providing evidence for medial-temporal and frontal lobe dysfunction that likely predates the onset of psychosis. Behavioral phenomenology and neurobiology suggest that dopamine plays a crucial moderating role between these structural abnormalities and functional impairment. Recently, investigators have used animal models and clinical syndromes to integrate these findings into neurodevelopmental models of schizophrenia that hold great potential for yielding etiological insight.